text:
Working closely with the students from remote parts of Tamilnadu and addressing their challenges helped Agaram to understand the ground realities in providing equal opportunities for quality education. It also helped Agaram to evaluate the needs and made the team realise that their efforts have to become manifold to make any real difference in the lives of these children.
In the year 2010, Agaram, with significant contributions from trustees and other donors, gained momentum and started by supporting 160 students from across Tamilnadu for college education under its initiative "Vidhai".
Agaram provides college education to deserving students and assists them with education and accommodation. Agaram connects with every student individually on a regular basis and their progress is monitored.
Students who approach Agaram for educational aid come from different walks of life and come with challenging family backgrounds coupled with poverty. These children are constrained by communal beliefs and practices that range from parental negligence, resistance to educating girl child, underage marriage etc., that inherently poses challenges for the students in their effort to succeed in life.
Agaram reaches out to deserving students from most backward parts of the country and provide them with an opportunity to complete their education. Agaram believes that equal education is a powerful 'change agent'. Hence, many tailor-made programs have been created, focussing on equipping children with the skills to overcome the challenges and help them emerge as a confident and competent individual.
Quarterly workshops on soft skills development and social awareness, personality development sessions, value education, communication, interpersonal skills and collaboration sessions are conducted for the students at regular intervals.
These programs & workshops are designed by professionals, who come forward from various industries and walks-of-life, to share their experience and expertise with the student. Agaram also creates opportunities for the students to meet up with successful people who have come from similar backgrounds and made it in life. These meetings are a great motivator for the children and give them the much needed confidence and hope.
Students who approach Agaram for educational support come from various walks of life from both rural and urban areas. They are mostly from challenging family backgrounds with limited financial support. They are also constrained by communal practices such as resistance to educating the girl child, underage marriage, child labour, single / disabled / addicted parents who are ignorant of the value of education, posing significant threats and obstacles for the child to overcome.
Agaram assists students from such backgrounds, by providing them the opportunities that will bring about a change in their lives.
Every year we receive thousands of applications requesting financial help for higher education. We have a rigorous scoring system in place to identify deserving students. We assist students with the Application and Admission processes. We also help them with other logistics operations like accommodation, mess fees etc.
Selection: The selection process consists of four stages:
- Receiving Applications: Agaram receives applications from students, from all over Tamilnadu. These applications are reviewed and the deserving students who come from Government Schools across rural Tamilnadu and are first generation College goers are short-listed.
- Personal Interview: The students who are shortlisted are called for a personal interview, for which they are asked to be present along with their parent or guardian. The personal interview is conducted to assess the student's attitude and willingness to study further. The genuineness of the details provided by the student/parent or guardian is also verified during the interview.
- House Visit: The purpose of house visit is to assess the information and verify the facts provided by the student and their parent/guardian during the personal interview. The financial background and the life style of the student's family are also assessed during the visit. Volunteers doing the House visit, fill in forms to mention whether there is electricity facility or not, residing house is hut/tile roof/concrete, educational qualification of the parents and siblings, father alcoholic or not etc. Weightage points are given to these parameters at a later stage.
- Scoring and Selection: The final list of students for the given academic year would be determined by the socio economic scoring against various parameters filled during House visit, along with their academic scores in X & XII exams.
Career Guidance & Admission Process:
Students selected by the foundation are given awareness of all the choices and the scope of choice available to them. They are provided with all the details, so that they make an informed decision.
Collecting Information on Courses & Colleges:
A team of volunteers work parallelly to gather information, about the courses and their availability, from colleges across Tamilnadu. Details like course fee, facilities are analysed, recorded and updated and the scope and placement opportunities for the Courses are also collected.
Admission Guidance – Course & College Selection:
Admission Guidance process carried out within Agaram to evaluate and group the students into Arts & Science and Professional streams. This process consists of
- familiarising the student with course by providing complete information
- assisting the student to choose the right course based on his / her past performance, aptitude and interest
- Evaluate the eligibility of the student based on the marks scored in the final exams
Volunteers then contact the students and inform them on their selection and then based on Agaram's admission guidelines, the student wins the Agaram sponsorship.
Admission to College & Hostel:
Agaram then assists the Student with the College and Hostel Admission process and complete admission formalities to be admitted in the chosen college.
How many have benefitted so far
In the last 5 years the foundation has supported nearly 1000 students to realise their dream of getting a good college education and becoming competent individuals. Agaram is confident that these individuals will bring forth the positive transformation in their families, communities and society at large.
The foundation has helped to produce number of doctors, engineers, lawyers and other professionals. With the help of many patrons, these students have been successfully placed in many leading organisations, thus kick-starting the change that is much needed. Today many of our student beneficiaries volunteer their time and energy to mentor the students who are currently supported by Agaram.
To be a part of Vidhai as Donor click here, as Volunteer click here


text:
Underwear by FM Belfast (Music Video) from Daniel Scheinert on Vimeo.
14 Jun
14 Apr
Some have commented that they think he is lip syncing. This video, where he shows some dance moves too, should dispel that.
12 Apr
Its that time of year again where I am envious of all those other areas of the country that have cool music festivals near them. Also, I'm envious of the folks who can take off the time and hang out in a field for 3 or more days. Just looking at the lineups (and the venues) has me planning roadtrips. Too bad the one that looks the best to me is on Memorial Day Weekend – when I have plans.
Sasquatch Music Festival 3 hours outside Seattle at the Gorge has an amazing lineup. These are just the acts that I know I will love and it isn't even half the list!
Edward Sharpe & The Magnetic Zeros
Vampire Weekend
The National
Band of Horses
The New Pornographers
The Middle East
Nada Surf
The xx
Freelance Whales
Tegan and Sara
Camera Obscura
Brother Ali
OK Go
She & Him
Passion Pit
Broken Social Scene
The Posies
My Morning Jacket
LCD Soundsystem
Dirty Projectors
Local Natives
Martina Topley Bird
The Mountain Goats
Dr. Dog
Aziz Ansari
8 Oct
Dead Man's Bones (aka Ryan Gosling's band) in conjunction with a children's choir. Really a lot of this is very good in an Arcade Fire sorta way. Check out this video too:
11 Aug
Wish I could follow the Akai International Tour! (MySpace) Montreal, New York, Cleveland!
28 Jul
See the trailers and a new featurette at apple.com. And they could not have chosen a better band/song than Arcade Fire's Wake Up to embody youthful enthusiasm and rebellion.
27 Jul

subset: commoncrawl


text:
The Value Versus Price Tag Strategy For Measuring Value And Time – Kimberly Gosney
It's almost time for the holiday season. This time of the year is ripe with anticipation of what 2016 is going to look like for every entrepreneur.
You're going to start looking at your past and thinking about your future.
Today, I want to get inside your head for a few minutes and stir something up. There's something that we just don't talk about enough. The value of something versus the price tag you pay for it. This strategy can be applied to anything and everything purchase wise in your business from your courses, systems, hiring and even if you should buy that new course everyone is talking about.
I've been digging into this heavily in 2015 and I'd like to take a moment to share a strategy with you as you look towards 2016 and where and what you'll be investing in for your business this year.
This is a really simple strategy designed to help you take action quickly and without over-thinking it and since we're going to be talking about two of the most important assets you have – your time and money – know that this may bring stuff up for you that's been hiding under the covers.
And, that's OK.
It's best to start the year with freshly laundered time and money covers and maybe a really squishy perfect pillow.
Here we go!
This strategy starts with:
Your Value
I identify your value as dollar amount you place on an hour of your time. Your Value is 100% unique to you and it's just a measure to keep you grounded. If you have no idea where to start think about it like this … if someone asked you to meet with them 1-on-1 to help them with something you knew you could help them with and they wanted to pay you for it that dollar amount is Your Value.
I'm going to use $100 here in this post as the example of Your Value to keep it easy because I don't have a calculator handy and my math skills are rather icky.
Your Value = $100/hour.
The Price Tag.
The price tag is something that someone else is asking you to pay for something that you think you want or need in your empire. This could be a new site design, a photo shoot, branding, a course or mastermind you're thinking of buying.
The Price Tag takes your money away from you.
Greedy little sucker.
Now think about a space that is always causing you a problem in your business. In this example I'm going to use your website because your website is a greedy little sucker sometimes. It can and will suck the life out of you if you let it and I love talking about your website making you happy not sad.
But, let's say your website is something you're planning on spending money on in 2016.
The site designer you're thinking of working with wants to charge you $3000 to build your website.
Let's get in here and look at the value versus the price tag of this situation.
Your Value = $100
Price Tag = $3000
How do you know if you should hire this designer to build your site or if you should suck it up and build it yourself?!?
Great question. I'm so glad you asked it.
Here's the easiest way to decide.
Ask your potential site designer to see examples of the last few sites they've built or that will be launching soon. Then ask yourself honestly …
Can you do this as well as or better than this designer can in the price tag divided by your value (in this example) 3000 divided by 100 = 30 hours?
If the answer is yes you know you can DIY your website and it would look just as great in 30 hours or less – DIY it.
If the answer is heck no, there's no way you'd get the same-ish results in 30 hours – hire the designer to build your website.
Now I know that you might get here and think … I see the value, but I don't have enough money for the price tag. My money just isn't there and I'm not going to wake up to $3000 tomorrow morning.
If that's the case, set up a time to chat with your potential site designer and ask them if you can lay-away your site design project.
Most site designers, including me are happy to work out a payment plan for your site design project where you talk about what you want, they write you a contract, you pay a small site design deposit to hold your place, and you send over payments until you've paid on what's agreed to for getting the ball rolling on your site.
You get your website and you're off to being able to sell your products, services and offerings without breaking a sweat or spending hundreds if not thousands of hours struggling with your website with nothing to show for it.
P.S. I've got one spot remaining for Cupcake Website in January 2016 and I hope it's got your name written all over it. Click here to take a peek at Cupcake Website, fill out a form, and grab a spot to chat with me about your website.


text:
- Review
- Open Access
Environmental exposure to xenoestrogens and oestrogen related cancers: reproductive system, breast, lung, kidney, pancreas, and brain
© Fucic et al; licensee BioMed Central Ltd. 2012
- Published: 28 June 2012
The role of steroids in carcinogenesis has become a major concern in environmental protection, biomonitoring, and clinical research. Although historically oestrogen has been related to development of reproductive system, research over the last decade has confirmed its crucial role in the development and homeostasis of other organ systems. As a number of anthropogenic agents are xenoestrogens, environmental health research has focused on oestrogen receptor level disturbances and of aromatase polymorphisms. Oestrogen and xenoestrogens mediate critical points in carcinogenesis by binding to oestrogen receptors, whose distribution is age-, gender-, and tissue-specific. This review brings data about cancer types whose eatiology may be found in environmental exposure to xenoestrogens. Cancer types that have been well documented in literature to be related with environmental exposure include the reproductive system, breast, lung, kidney, pancreas, and brain. The results of our data mining show (a) a significant correlation between exposure to xenoestrogens and increased, gender-related, cancer risk and (b) a need to re-evaluate agents so far defined as endocrine disruptors, as they are also key molecules in carcinogenesis. This revision may be used to further research of cancer aetiology and to improvement of related legislation. Investigation of cancers caused by xenoestrogens may elucidate yet unknown mechanisms also valuable for oncology and the development of new therapies.
- Pancreatic Cancer
- Breast Cancer Risk
- Aromatase Inhibitor
- Cotinine
- Testicular Cancer
Despite the considerable efforts to decrease environmental pollution we still witness uncontrolled introduction of new compounds in living and working environment. Additionally, pollution control in low income and developing countries has seen limited success. The balance between needs of a fast growing human population and technology/science development is questionable, partially as a consequence that the available knowledge is not always applied in an efficient way as it should be.
The last century's paradigm "one agent - one disease" has helped to identify the major causal pathways and the identification of pollution related diseases, including cancer. Based on this approach, epidemiological studies set off many activities to reduce pollution and prevent exposure. However, a large body of data accumulated over the last decade, with a recent significant contribution of molecular biology, clearly shows that this historical simplistic interpretation of biomonitoring data fails to answer a number of questions about environmental threats to human health.
Cancer incidence monitoring in developed countries is relatively accurate. A better classification of cancer types, the networking of cancer registries, and the increasing population coverage for cancer registration are unfortunately accompanied, due to unsolved technical and organizational difficulties, by publishing of cancer register reports with a lag of several years. This lag is a serious obstacle in identifying current environmental health risks and setting timely effective preventive measures.
According to recent data [1], childhood cancer incidence increases 1% a year all over Europe. In the adult population a rising trend is reported for soft tissue sarcoma, brain tumours, germ-cell tumours, lymphomas, renal cancers, leukemias, breast cancer, and lung cancer in women. Breast, colorectal, prostate, and lung cancer are the most commonly diagnosed cancers in the European population [2]. Only limited part of the detected increase may be related to screening programs.
During the last decade, environmental health and oncology have shown an increasing interest in oestrogen as an evolutionary conserved molecule. With its endocrine, paracrine, and neurotransmitting activity [3–5], oestrogen is not limited to the development and regulation of the reproductive system. The distribution of oestrogen receptors in mammalian tissues suggests that oestrogens could have a significant role in orchestrating a number of pathways in living organisms during development and adulthood. Additionally, new evidences confirm a strong impact of this molecule on carcinogenesis [6–9].
Very little is known about changes in oestrogen levels and the tissue ratio between alpha and beta oestrogen receptors (ER) during development [10]. In the second trimester of human foetal development the highest concentrations of ER beta mRNA are found in the testis and the ovary and of ER alpha mRNA in the uterus. Relatively high concentrations of either receptor are also present in the spleen, while low levels are detected in the kidney, thymus, skin, and lung [11]. The pre-pubertal ratio between ERs alpha and beta in human tissues in males and females is not known. Additionally, ER alpha and beta are polymorphically distributed and as such they play different roles in carcinogenesis [12–14].
At higher levels, oestrogen is carcinogenic [15]; similar to ionizing radiation it may produce reactive oxygen species and cause hypomethylation and microsatellite instability [9, 16–18]. Its metabolites, quinones, cause the formation of DNA adducts, depurination, lipid-derived aldehyde-DNA adducts, and aneuploidy [15, 19]. By decreasing glutathione-S-transferases, oestrogens may increase cellular oxidative DNA damage in oestrogen-responsive tissues, when the organism is simultaneously exposed to genotoxicants. This is an early step in the process of carcinogenesis [20].
Gender differences in the incidence of cancers such as the lung, kidney, or pancreas cancer suggest that hormones may play a role in their aetiology [21]. Recent findings suggest that all neoplastic mammalian tissues are characterized by disturbances in ER levels [6]. As gender related estrogen levels in foetal, and prepubertal tissues, the tissue specific ER distribution and oestrogen bimodal activity modulate the development of biological pathways and organogenesis [22, 23] some cancer types may have origin in their prenatal and postnatal disturbance caused by exposure to xenoestrogens.
The general population is exposed to a number of hormonally active compounds on a daily basis. These compounds were introduced in the living environment during the last few decades, the majority of which are xenoestrogens. Chemicals like polycyclic aromatic hydrocarbons (PAH), pesticides, polychlorinated biphenyl (PCB), dichlorodiphenyl-trichlorethane (DDT), some drugs (e.g., antiepileptic drugs), fungicides, cotinine, phytoestrogens, mycotoxins, bisphenol A (a plastics additive), phthalates, alkylphenols, and metalloestrogens mimic oestrogen action, affect oestrogen levels, or bind to oestrogen receptors [24–29]. Xenoestrogens are present in a number of substrates such as cigarette smoke, automobile exhaust, chemical industry pollutants, grilled meat, volcano dust, forest fire smoke, milk, water, and cosmetic products. This means that all human population may be exposed to them.
This article seeks to give an insight in how environmental exposure to xenoestrogens relates to breast, lung, kidney, brain, pancreas, and reproductive system cancers, which are all characterized by disturbances in ER.
Breast cancer
The reports on decrease of breast cancer incidence in women 50-69 years old are related to improvement of preventive measurements such as mammography screening in developed countries. In the United States, Australia, and Western Europe this decrease seems to follow a decrease in hormonal therapy [30], as oestrogen plays important role in pathogenesis of breast cancer [31, 32].
Factors involved in the development of breast cancer incidence include the socioeconomic status, some food additives, pesticides, oestrogen and progesterone replacement therapy, some antibiotics, radiation, mutations at genes BRCA1, BRCA2, metabolizing enzyme polymorphisms, epidermal growth factor and its receptor (HER), androgen levels, and insulin-like growth factor [33–35]. Age (including transplacental, prepubertal) may also play an important role in oestrogen exposure-related breast cancer risk that probably involves epigenetic mechanisms [36–39].
Currently there are some 160 xenoestrogens that may be involved in breast cancer development [40–42]. Women are the largest consumers of cosmetic products which may be a significant source of xenoestrogens. Some, such as metalloestrogens (e.g., aluminium salts), parabens, cyclosiloxanes, triclosan, UV screeners, phthalates, Aloe Vera extracts, and musk are present in numerous cosmetics products. Humans are exposed to these chemicals transcutaneously and measurable levels have been detected in human breast tissue [23].
Alcohol is also related with increased risk of breast cancer development as even low alcohol consumption increases serum oestradiol (especially for carriers of a certain alcohol dehydrogenase allele) and stimulates ER alpha [43, 44]. On animal model it is shown that alcohol increases oestradiol levels in dams, which leads to higher levels of ER alpha receptors in their offspring mammary gland and may launch tumorigenesis [37].
The effect of diet on breast cancer development was observed in Japanese women after the Second World War when dramatic changes in their diet happened such as increased consumption of meat, eggs, and milk containing oestrogens or oestrogen-like compounds [45]. Milk is a source of oestrogen due to the practice of milking pregnant cows [46].
Heterocyclic amine and their metabolites, especially 2-amino-1-methyl6-phenylimidazo (4,5-b) pyridine (PhIP) is present in high concentrations in well-cooked meat and it binds to and activates the breast cell ER alpha [47, 48]. In animal model, it causes breast cancers [49]. The suggested mechanisms of PhIP mechanisms are formation of PhIP-DNA adducts and increase of proliferation in mammary gland terminals and buds [50]. Similarly, at concentrations higher than 140 μg/m3 polyaromatic hydrocarbons from food may increase breast cancer risk in postmenopausal women if they were exposed to it early in life [51].
Styrene, a widely used plastic for food packing, has been associated with breast cancer risk both in men and women [52]. Direct intake of styrene is via food packed or even cooked in styrene boxes with a direct migration of styrene to food. Styrene and its metabolites bind to ER alpha [53], cross the placental barrier, and also affect the development of reproductive organs [54, 55].
The carcinogenic potential of xenoestrogens may also depend on polymorphism of metabolic enzymes. It is shown that subpopulation carrying a polymorphism of metabolic enzyme CYP1A1 m2 is more susceptible to breast cancer development after exposure to polychlorinated biphenyls (PCB), which may explain contradictory epidemiological reports on the association between breast cancer incidence and PCB exposure [35, 56, 57].
Lung cancer
Lung cancer is the predominant cause of cancer mortality [58]).There is a gender difference in the incidence of lung cancer types. The leading cause in men is the squamous cell carcinoma, and in women adenocarcinoma. Oestrogen and ER distribution could be the main cause of this difference [59, 60]. Despite the fact that lung cancer incidence is increasing in women [61–64] studies reporting lung cancer incidence basically rarely give attention to possibly gender related susceptibility [65–67]. Lung cancer is about 70% ER beta positive. The ratio between ER alpha and ER beta in the lung tissue seems to be relevant for lung cancer development and may explain the higher incidence of lung adenocarcinoma in women than in men [68]. Increased lung cancer risk in women is associated with a lower social status and high level of indoor pollution with PCBs during cooking as a consequence of coal usage [69, 70]. ER beta levels in lung cancer are gender related and have impact on survival rate [71]. While ER beta receptor positive or negative lung cancers has no impact on survival in women, in men ER beta positive lung cancer is associated with a significantly lower mortality than ER beta negative lung cancer [72]. ER alpha modulates lung differentiation and maturation while ER -beta causes proliferation of lung cancer cells [73, 74]. Gender specific distribution of CYP19 (aromatase) in lung cells puts in correlation oestrogen levels and lung cancer etiology [75]. Additionally, women taking oestrogen therapy have shown increased lung cancer incidence [76]. Same as for breast cancer epidermal growth factor and its receptor HER plays a significant role in non-small cell carcinoma and is associated with endogenous estrogen exposure [77].
Smoking remains the major cause of lung cancer in humans [78]. Methylnitrosamino-pyridyl-butanone, a powerful carcinogenic agent contained in cigarette smoke is ER beta receptor related [69]. The activity of nicotine is gender-specific [79], since cotinine, a nicotine metabolite, is an aromatase inhibitor [80] that decreases oestrogen end increases testosterone levels. Polonium 210 in cigarettes [81] may have similar activity as other metalloestrogens [24, 82]. Other carcinogens in cigarette smoke should be re-evaluated for their xenoestrogen or aromatase inhibitor potency.
Traffic air pollution is also related to lung cancer [83, 84]. A number of compounds from traffic emissions are oestrogen ligand active compounds [85]. PAHs represent one of the major mixtures of agents that are present in polluted air have been demonstrated to affect oestrogen homeostasis [86–88].
Industrial emissions also contain pollutants with oestrogen-like activity, such as heavy metals and dioxins [89]. A significant association between industrial air pollutants and lung cancer risk has been reported in women [90].
Kidney cancer
Data on the environmental aetiology of kidney cancer are not available, and much more research is needed. The fact that renal cell carcinoma, the most common type of kidney cancer, can be induced by exposure to oestrogens [92] in animal model suggests the involvement of oestrogen receptors in the aetiology of kidney cancer and of a possible role of xenoestrogens. Kidney cancer incidence seems to be gender -related, with an incidence that is two times higher in men than in women [93]. In addition, genetic polymorphisms of ER alpha in the kidney seem to play a significant role in the development of kidney cancer [92]. Cadmium and arsenic as xenoestrogens may also induce kidney cancer [94, 95]
Pancreatic cancer
Understanding of pancreatic cancer aetiology is crucial, as it is the fourth leading cause of cancer deaths in the USA [64] and one of the most aggressive diseases. The incidence of pancreatic cancer has been relatively stable worldwide over the last few decades [96–98]. It is more frequent in men than in women [99, 100]. Pancreatic cancer cells are ER alpha and beta positive and consequently may be modulated by oestrogen [101] which is consistent with similar mechanisms observed in xenoestrogen-related cancers [102, 103]. There are very few data on the effects of xenoestrogens on pancreatic cancer incidence.
Methylnitrosamino-pyridyl-butanone is the only compound demonstrated to cause pancreatic cancer in animal models [104]. This finding has also been reported for the adenocarcinoma of the lung and has been related to ER beta activation [68].
It is also known that consumers of fried meat run a higher risk of pancreatic cancer development probably due to exposure to benzo(a)pyrene and other food contaminants that have xenoestrogenic properties [45, 105].
Brain tumour
Brain tumours are characterized by disturbances in ERs [106–108]. Transplacental exposure to xenoestrogens may increase the risk of brain tumour development [79, 80]. Xenobiotics that inhibit aromatase also inhibit the conversion of oestrogen to testosterone and may have a significant impact on brain pathology, given the evidence that disturbed levels of testosterone have impact on apoptosis and intracellular signaling [109] Increased brain cancer incidence has been reported in humans living near petrochemical industries [110]. Despite the fact that the exact chemical composition of the mixture of air pollutants remains unknown, polycyclic aromatic hydrocarbons (PAH) are present in polluted air in such areas [67]. PAHs as xenoestrogen-like agents [87] may have played a causal role on the excess of brain cancer incidence detected
Reproductive system
Testicular cancer incidence has significantly increased over the last few decades with yet no clear hypothesis on impact of environment on its aetiology [111]. As this trend cannot be explained by cryptorchidism, smoking, genetic variations, or physiological stress, the role of environmental exposure is being investigated to elucidate its aetiology and to identify preventive measures [112].
Both ER alpha and beta are expressed in the human testis and are involved in the control of testicular function [113]. The role played by xenoestrogens on testis development is still only partly known in the animal model, with results showing very dynamic changes in tissue sensitivity to xenoestrogens with unknown consequences during puberty and adulthood [114].
There are a limited number of studies reporting possible association between testicular cancer and disturbances in oestrogen levels. Testicular cancer has been reported in sons of smoking mothers [115], but also in mothers who were taking antiepileptics during pregnancy [116]. Both antiepileptics and cotinine from cigarette smoke are aromatase inhibitors. Transplacental exposure to aromatase inhibitors and consequently increased levels of testosterone may have long-term effects in humans, as shown in an animal model [117].
Epidemiological studies also suggest increased risk of testicular cancer following prenatal exposure to oestrogens [118].
Styrene storage containers may contaminate food which becomes a source of styrene exposure. Transplacental exposure to low levels of styrene may lead to the disturbed development of male genital organ [54]. However, its effect on cancer development remains unknown.
Endocrine disrupting chemicals which disturb ERs can cause female reproductive dysfunction [119, 120]. As ovarian cancer therapy is still not marked with significant success and mortality is very high it is of major significance elucidation of its aetiology [121].
Cadmium, one of most investigated heavy metals, has a significant role on ovarian and reproductive functions, as it lowers progesterone levels and mimics oestrogen in various tissues by binding to ER alpha. Cadmium is not confined to occupational exposure alone; it is found in cigarette smoke, food, nickel/cadmium batteries, pigments, and plastics [122].
Ovarian cancer is associated with milk and cheese consumption due to oestrogen and insulin growth factor present in milk of pregnant cows [46, 123].
According to recent experimental evidence, uranium in water should be further considered in research as an additional risk for reproductive cancers [82].
As an evolutionary conserved molecule, oestrogen is present in both plants and animals. Oestrogen is recognized today as a critical modulator of development, homeostasis in adulthood and orchestration of response to environment.
Although gene polymorphisms can change cancer incidence [124, 125], it is clear that environment has predominance over genes in cancer risk. Responses to environmental stressors are age- and gender related, and transplacental exposure to xenoestrogens has been shown to have long-term effects in experimental models, as it modulates hormonal response in puberty This means that exposure to endocrine agents not only poses a health risk during exposure, but also increases susceptibility later in life [114, 126, 127]. Differences in susceptibility to xenoestrogens may be related to steroid and xenobiotic receptor levels, which are high in young adults (15-38y old) and decrease with age [128].
Current estimates of cancer risk in humans do not account properly for transplacental and environmental (including occupational) exposure to xenoestrogens. The role of xenoestrogens in cancer development should be re-evaluated using a new approach that would reflect the complexity of carcinogenesis.
Reductionism as the main scientific philosophy of the 20th century gave a significant input to environmental health. However, the quantity of data available in noosphere, systems biology as a tool and new softwares for data sharing enable the investigation of interactions between xenoestrogens and other environmental stressors, such as radiation, and add new dimensions to the research of cancer aetiology using complexity as a new scientific philosophy. Contemporary mathematical models and systems biology allows the incorporation of all available data and modeling cancer risk allowing free interaction and clustering of data.
The collaboration of environmental health with oncology would be of crucial significance in the study of xenoestrogens as estrogen has today significant position in oncological diagnostics and therapy what includes measurements of ER levels in different tissues. Clinical oncology today takes part in scientific projects in order to achieve optimal treatment at the individual level (tailored therapy) and produces large amounts of data that reflect a tight gene-environment interaction and point to age and gender specific susceptibility. Collaboration between pharmacokineticians, oncologists, histopathologists, molecular epidemiologists, and genotoxicologists may improve our knowledge of cancer aetiology and lead to gender specific and final individualized therapies.
Available information systems and building of integrated exposure-disease pathways will give policymakers much more useful input in future for more efficient regulations than a large number of agent- and disease-specific studies.
This work was supported by the EU project HENVINET 6th Framework Programme, Coordination Action (Contract no. GOCE-CT-2006-037019), http://www.henvinet.eu.
This article has been published as part of Environmental Health Volume 11 Supplement 1, 2012: Approaching complexities in health and environment. The full contents of the supplement are available online at http://www.ehjournal.net/supplements/11/S1.
Authors' Affiliations
- Pritchard-Jones K, Kaatsch P, Steliarova-Foucher E, Stiller CA, Coebergh JWW: Cancer in children and adolescence in Europe: developments over 20 years and future challenges. European J Cancer. 2006, 42: 2183-2190. 10.1016/j.ejca.2006.06.006.Google Scholar
- Ferlay J, Autier P, Boniol M, Heaune M, Colombet M, Boyle P: Estimates of the incidence and mortality in Europe in 2. Annals of Oncology. 2007, 18: 581-592.Google Scholar
- Moss RL, Gu O, Wong M: Estrogen: nontranscriptional signaling pathway. Recent Prog Horm Res. 1997, 52: 33-68.Google Scholar
- Wooley CS: Acute effects of estrogen on neuronal physiology. Ann RevPharmacol Toxicol. 2007, 47: 657-80. 10.1146/annurev.pharmtox.47.120505.105219.Google Scholar
- Fucic A, Miškov S, Zeljezic D, Bogdanovic N, Katic J, Gjergja R, Karelson E, Gamulin M: Is the role of estrogens and estrogen receptors in epilepsy still underestimated?. Medical Hypotheses. 2009, 73: 703-705. 10.1016/j.mehy.2009.03.051.Google Scholar
- Chen GC, Zeng Q, Tse GMK: Estrogen and its receptors in cancer. Med Res Review. 2008, 28 (6): 954-974. 10.1002/med.20131.Google Scholar
- Gonzales RJ, Ansar S, Duckles SP, Krause DN: Androgenic/estrogenic balance in the male rat cerebral circulation: metabolic enzymes and sex steroid receptors. J Cereb Blood Flow Metab. 2007, 27 (11): 1841-1852. 10.1038/sj.jcbfm.9600483.Google Scholar
- Lemmen JG, Arends RJ, van Boxtel AL, van der Saag PT, van der Burg B: Tissue and time dependent estrogen receptor activation in estrogen reporter mice. J Mol Endocrinol. 2004, 32: 689-701. 10.1677/jme.0.0320689.Google Scholar
- Roy D, Liehr JG: Estrogen DNA damage and mutations. Mutat Res. 1999, 424: 107-115. 10.1016/S0027-5107(99)00012-3.Google Scholar
- Knapczyk K, Duda M, Szafranska B, Wolsza K, Panasiewicz G, Koziorowski M, Slomczynska M: Immunolocaliosation of oestrogen receptors alpha (Eralpha) and beta (Erbeta) in porcine embryos and fetuses at different stages of gestation. Acta Vet Hung. 2008, 56 (2): 221-233. 10.1556/AVet.56.2008.2.10.Google Scholar
- Branderberger AW, Tee MK, Lee JY, Chao V, Jaffe RB: Tissue distribution of estrogen receptors alpha (Er?) and beta (Erβ) mRNA in the midgestational human fetus. J Clin Endocrinol & Metabolism. 1997, 82 (10): 3509-3512. 10.1210/jc.82.10.3509.Google Scholar
- Paruthiyil S, Parmar H, Kerekatte V, Cunha GR, Firestone GL, Leitman DC: Estrogen receptor beta inhibits human breast cancer cell proliferation and tumor formation by causing a G2 cell cycle arrest. Cancer Res. 2004, 64 (1): 423-428. 10.1158/0008-5472.CAN-03-2446.Google Scholar
- Grabinski JL, Chisholm G, Smith LS, Drengler RL, Kalter S, Rodriguez G, Garner A, Cooper J, Pollock B, Kuhn J: ER alpha genotypes and breast cancer. J Clin Oncol. 2008, 26 (15S): 501-Google Scholar
- Hall JM, Korach KS: Analysis of the molecular mechanisms of human estrogen receptors alpha and beta reveals differential specificity in taret promotor regulation by xenoestrogens. J Biol Chem. 2002, 277 (46): 44455-44461. 10.1074/jbc.M200849200.Google Scholar
- Cavalieri EL, Stack DE, Devanesan PD: Molecular origin of cancer: catechol estrogen-3,4-quinones as endogenous tumor initiators. Proc Nat Acad Sci USA. 1997, 94: 10937-10942. 10.1073/pnas.94.20.10937.Google Scholar
- Roy D, Cai Q, Felty Q, Narayan S: Estrogen-induced generation of reactive oxygen and nitrogen species, gene damage and estrogen dependent cancers. J Toxicol Environ Health, Part B. 2007, 10 (4): 235-257. 10.1080/15287390600974924.Google Scholar
- Dubrova YE, Ploshchanskaya OG, Kozionova OS, Akleyev AV: Minisatellite germline mutation rate in the Techa River population. Mutat Res. 2006, 602 (1-2): 74-82. 10.1016/j.mrfmmm.2006.08.001.Google Scholar
- Kaup S, Grandjean V, Mukherjee R, Kapoor A, Keyes E, Seymour CB, Mothersill CE, Schofield PN: Radiation-induced genomic instability is associated with DNA methylation changes in cultured human keratinocytes. Mutat Res. 2006, 597 (1-2): 87-97. 10.1016/j.mrfmmm.2005.06.032.Google Scholar
- Liehr JG: Genotoxicity of the steroidal oestrogens oestrone and oestradiol:possible mechanism of uterine and mammary cancer development. Hum Reprod Update. 2001, 7 (3): 273-281. 10.1093/humupd/7.3.273.Google Scholar
- Ansell PJ, Espinosa-Nicholas C, Curran EM, Judy BM, Philips BJ, Hannink M, Lubahn DB: In vitro and in vivo regulation of antioxidant response element-dependent gene expression by estrogens. Endocrinology. 2004, 145 (1): 311-7.Google Scholar
- Arbuckle TE: Are there sex and gender differences in acute exposure to cheicals n the same setting?. Environ Res. 2006, 101: 195-204. 10.1016/j.envres.2005.08.015.Google Scholar
- Alworth LC, Howdesshell KL, Ruhlen RL, Day JK, Lubahn DB, Huang HM, Besch-Williford CL, Saal FS: Uterine responsiveness to estradiol and DNA methylation are altered by fetal exposure to diethylstilbestrol and methychlor in CD-1 M, Effects of low versus high doses. Toxicol Appl Pharmacol. 2002, 183: 10-22. 10.1006/taap.2002.9459.Google Scholar
- Rosenthal MD, Albrecht ED, Pepe GJ: Estrogen modulates developmentaly regulated gene expression in the fetal baboon liver. Endocrine. 2004, 23 (2-3): 219-228. 10.1385/ENDO:23:2-3:219.Google Scholar
- Darbre PD: Environmental oestrogens, cosmetics and breast cancer. Best Pract Res Clin Endocrinol Metab. 2006, 20 (1): 121-143. 10.1016/j.beem.2005.09.007.Google Scholar
- Barbieri RL, Gochberg J, Ryan KJ: Nicotine, cotinine, and anabasine inhibit aromatase in human trophoblast in vitro. J Clin Invest. 1986, 77 (6): 1727-1733. 10.1172/JCI112494.Google Scholar
- Wang SL, Chang YC, Chao HR, Li CM, Li LA, Lin LY, Papke O: Body burdens of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls and their relations to estrogen metabolism in pregnant women. EHP. 2006, 114 (5): 740-745.Google Scholar
- Hsieh M, Grantha E, Liu B, Macapagai R, Willingham E, Baskin LS: In utero exposure to benzophenone-2 causes hypospadias through an estrogen receptor dependent mechanisms. J Urol. 2007, 178: 1637-1642. 10.1016/j.juro.2007.03.190.Google Scholar
- Birnbaum LS, Fenton S: Cancer and developmental exposure to endocrine disruptors. EHP. 2003, 111 (4): 389-394.Google Scholar
- Andersen HR, Bonefeld-Jorgensen EC, Nielsen F, Jarfeldt K, Jayatissa MN, Vinggaard AM: Estrogen effects in vitro and in vivo of the fungicide fenarimol. Toxicol Lett. 2006, 163 (2): 142-152. 10.1016/j.toxlet.2005.10.004.Google Scholar
- Hery C, Ferlay J, Boniol M, Autier P: Changes in breast cancer incidence and mortlaity in middle-aged and elderly women in 28 countries with Causcasian mjaroty populations. Annals of Oncology. 2008, 19: 1009-1018. 10.1093/annonc/mdm593.Google Scholar
- Kovalchuk O, Tryndiyak P, Montgomery B, Boyko A, Kutanzi K, Zemp F, Warbritton AR, Latendresse JR, Kovalchuk I, Beland FA, Pogrybny IP: Estrogen-induced at breast carcinogenesis is characterized by alterations in DNA methylation, histone modifications and aberrant microRNA expression. Cell Cycle. 2007, 6 (16): 2010-8. 10.4161/cc.6.16.4549.Google Scholar
- Feigelson HS, Henderson BE: Estrogens and breast cancer. Carcinogenesis. 1996, 17 (11): 2279-84. 10.1093/carcin/17.11.2279.Google Scholar
- Bernstein JL, Langholz B, Haile RW, Bernstein L, Thomas DC, Stovall M, Malone KE, Lynch CF, Olsen JH, Anton-Culver H, Shore RE, Boice JD, Berkowitz GS, Gatti RA, Teitelbaum SL, Smith SA, Rosenstien BS, Borresen-Dale AL, Concannon P, Thompson WD: Study design:evaluating gene-environment interactions in the etiology of breast cancer- the WECARE study. Breast Cancer Res. 2004, 6: 199-214. 10.1186/bcr771.Google Scholar
- Mitra AK, Faruque FS, Avis AL: Breast cancer and environmental risks: where is the link?. J Environ Health. 2004, 66 (7): 24-32.Google Scholar
- Zhang Y, Wise JP, Holford TR, Xie H, Boyle P, Hoar Zahm SH, Rusiecki J, Zou K, Zhang B, Zhu Y, Owens PH, Zheng T: Serum polychlorinated biphenyls P-450 1A1 polymorphisms, and risk of breast cancer in Connecticut women. Am J Epidemiol. 2004, 160: 1177-1183. 10.1093/aje/kwh346.Google Scholar
- Nie J, Beyea J, Bonner MR, Han D, Vena JE, Rogerson P, Vito D, Muti P, Trevisan M, Edge SB, Freudenheim JL: Exposure to traffic emissions through life and risk of breast cancer: the Western New York Exposures and Breast Cancer (WEB) study. Cancer Causes Control. 2007, 18 (9): 947-955. 10.1007/s10552-007-9036-2.Google Scholar
- Hilakivi-Clarke L, Cabanes A, de Assis S, Wang M, Khan G, Shoemaker WJ, Stevens RG: In utero alcohol exposure increases mammary tumorigenesis in rats. Brit J Cancer. 2004, 90: 2225-2231.Google Scholar
- Warri A, Saarinen NM, Makela S, Hilakivi-Clarke L: The role of early life genistein exposures in modifying breast cancer risk. BJC. 2008, 98: 1485-1493. 10.1038/sj.bjc.6604321.Google Scholar
- Baik I, Becker PS, DeVito WJ, Lagiou P, Ballen K, Quesenberry PJ, Hsieh P: Stem cells and prenatal origin of breast cancer. Cancer Causes and Control. 2004, 15: 517-530.Google Scholar
- Brody JG, Rudel RA: Environmental pollutants and breast cancer. EHP. 2003, 111 (8): 1007-19.Google Scholar
- Brody JG, Aschengrau A, McKelvey W, Swartz CH, Kennedy T, Rudel RA: Breast cancer risk and drinking water contaminated by wastewater: a case control study. Environ Health. 2006, 6: 5-28.Google Scholar
- Brody JG, Rudel RA, Michels KB, Moysich KB, Bernstein L, Attfiled KR, Gray S: Environmental pollutants, diet, physical activity, body size and breast cancer. Cancer (Suppl). 2007, 109 (12): 2627-2634.Google Scholar
- Coutelle C, Hohn B, Benesova M, Oneta CM, Quattrochi P, Roth HJ, Schmidt-Gayk H, Schneeweiss A, Bastert G, Seitz HK: Risk factor in alcohol associated breast cancer: Alcohol dehydrogenase polymorphism and estrogens. Int J Oncology. 2004, 25 (4): 1127-1132.Google Scholar
- Fan S, Meng Q, Gao B, Grossman J, Yadegari M, Goldberg ID, Rosen EM: Alcohol stimulates estrogen receptor signaling in human breast cancer cell lines. Cancer Res. 2000, 60: 5635-5639.Google Scholar
- Li XM, Ganmma D, Sato A: The experience of Japan as a clue to the etiology of breast and ovarian cancers: relatioship between death from both malignancies and dietary practices. Med Hypothesis. 2003, 60 (2): 268-275. 10.1016/S0306-9877(02)00385-7.Google Scholar
- Ganmaa D, Sato A: The possible role of female sex hormones in milk from cows in the development of breast, ovarian and corpus uteri cancers. Medical Hypothesis. 2005, 65: 1028-1037. 10.1016/j.mehy.2005.06.026.Google Scholar
- Ganmaa D, Wang PY, Qin LQ, Hoshi K, Sato A: Is milk repossible for male reproductive disorders. Med Hypothesis. 2001, 57: 510-514. 10.1054/mehy.2001.1380.Google Scholar
- Bennion BJ, Cosman M, Lightstone FC, Knize MG, Montgomery JL, Bennett LM, Felton JS, Kulp KS: PhIP carcinogenicity in breast cancer: computational and experimental evidence for competitive interactions with human estrogen receptor. Chem Res Toxicol. 2005, 18: 1528-1536. 10.1021/tx0501031.Google Scholar
- Lauber SN, Gooderham NJ: The cooked meat-derived genotoxic carcinogen 2-amino-3-methylimidazol (4,5-b) pyridine has potent hormone-like activity: mechanistic support for a role in breast cancer. Cancer Res. 2007, 67: 9597-9602. 10.1158/0008-5472.CAN-07-1661.Google Scholar
- Ito N, Hasegawa R, Sano M, Tamano S, Esumi H, Takayama S, Sugimura T: A new colon and mammary carcinogen in cooked food 2-amino-1-methyl-6-phenylimidazo (4,5b)pyridine (PhIP). Carcinogenesis. 1991, 12: 1503-1506. 10.1093/carcin/12.8.1503.Google Scholar
- Snyderwine EG: Mammary gland carcinogenesis by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine in rats: possible mechanisms. Cancer Lett. 1999, 143 (2): 211-5. 10.1016/S0304-3835(99)00127-5.Google Scholar
- Bonner MR, Han D, Nie J, Rogerson P, Vena JE, Muti P, Trevisan M, Edge SB, Freudenheim JL: Breast cancer risk and exposure in early life to polycyclic aromatic hydrocarbons using total suspended particulates as a proxy measure. Cancer Epidemiol Biomarkers Prev. 2005, 14 (1): 53-60.Google Scholar
- Coyle YM, Hynan LS, Euhus DM, Minhajuddin ATM: An ecological study of the association of environmental chemicals on breast cancer incidence in Texas. Breast Cancer Res Treatment. 2005, 92: 107-114. 10.1007/s10549-004-8268-z.Google Scholar
- Ohayama K, Magai F, Tsuchiya Y: Certain styrene oligomers have proliferative activity on MCF-7 cells and binding affinity for human estrogen receptor alpha. EHP. 2001, 109: 699-703.Google Scholar
- Ohyama KI, Satoh K, Sakamoto Y, Ogata A, Nagai F: Effects of prenatal exposure to styrene trimers on genital organs and hormones in male rats. Exp Biol Med. 2007, 232 (2): 301-308.Google Scholar
- Kitamura S, Ohmegi M, Sanoh S, Sugihara K, Yoshihara S, Fujimoto N, Ohta S: Estrogenic activity of styrene oligomers after metabolic activation by rat liver microsomes. EHP. 111 (3): 329-334.Google Scholar
- Charlier CJ, Albert AI, Zhang L, Dubois NG, Plomteux GJ: Polychlorinated byphenyls contamination in women with breast cancer. Clin Chimaca Acta. 2004, 347: 177-181. 10.1016/j.cccn.2004.04.025.Google Scholar
- Moysich KB, Menezes RJ, Baker JA, Falkner KL: Environmental exposure to plychlorinated biphenyls and breast cancer risk. Rev Environ Health. 2002, 17 (4): 263-277.Google Scholar
- Boffetta P: Human cancer from environmental pollutants: the epidemiological evidence. Mutat Res. 2006, 608: 157-162. 10.1016/j.mrgentox.2006.02.015.Google Scholar
- Stabile LP, Davis AL, Gubish CT, Hopkins TM, Luketich JD, Christie N: Human non-small cell lung tumors and cells derived from normal lung express both estrogen receptor alpha and beta and show biological response to estrogen. Cancer Res. 2002, 62: 2141-2150.Google Scholar
- Fasco MJ, Hurteau GJ, Spivack SD: Gender dependent expression of alpha and beta estrogen receptors in human nontumor and tumor lung tissue. Mol Cell Endocrinol. 2002, 188 (1-2): 125-140. 10.1016/S0303-7207(01)00750-X.Google Scholar
- Stabile LP, Siefried JM: Sex and gender differences in lung cancer. J Gend Specif Med. 2003, 6 (1): 37-48.Google Scholar
- Rivera MP: Lung cancer in women: the difference in epidemiology, biology and treatment outcomes. Expert Rev Resp Med. 2009, 3 (6): 627-634. 10.1586/ers.09.54.Google Scholar
- Olak J, Colson Y: Gender differences in lung cancer: have we really come a long way, baby?. J Thorac Cardiovasc Surg. 2004, 128: 346-351.Google Scholar
- Jemal A, Siegel R, Ward E: Cancer Statistics. Cancer J Clin. 2006, 56: 106-10.3322/canjclin.56.2.106.Google Scholar
- Vineis P, Forastiere F, Hoek G, Lipsett M: Outdoor air pollution and cancer: recent epidemiologic evidence. Int J Cancer. 2004, 111: 647-652. 10.1002/ijc.20292.Google Scholar
- Whitrow MJ, Smith BJ, Pilotto LS, Pisaniello D, Nitschke M: Environmental exposure to carcinogens causinglung cancer: epidemiological evidence from the medical literature. Respirology. 2003, 8: 513-521. 10.1046/j.1440-1843.2003.00497.x.Google Scholar
- Yang CY, Chiu HF, Chiu JF, Kao WY, Tsai SS, Lan SJ: Cancer mortality and residence near petrochemical industries in Taiwan. J Toxicol Environ Health. 1997, 50: 265-273. 10.1080/009841097160474.Google Scholar
- Majidi M, Al-Wadel HA, Takahashi T, Schuller HM: Nongenomic beta estrogen receptor enchance beta1 adrenergic signaling induced by the nicotine-derived carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in human small airway epithelial cells. Cancer Res. 2007, 67: 6863-6874. 10.1158/0008-5472.CAN-07-0483.Google Scholar
- Zhao Y, Wang S, Aunan K, Seip HM, Hao J: Air pollution and lung cancer risks in China- a meta-analysis. Sci Total Environ. 2006, 366: 500-513. 10.1016/j.scitotenv.2005.10.010.Google Scholar
- Ramanakumar AV, Parent ME, Siemiatycki J: Risk of lung cancer from residential heating and cooking fuels in Montreal, Canada. Am J Epidemiol. 2007, 165: 634-642. 10.1093/aje/kwk117.Google Scholar
- Schwartz AG, Prysak GM, Murphy V, Lonardo F, Pass H, Schwartz J, Brooks S: Nuclear estrogen receptorbeta in lung cancer: expression and survival differences by sex. Imaging, Diagnosis, Prognosis. 2005, 11 (20): 7280-7287.Google Scholar
- Skov BG, Fischer BM, Pappot H: Oestrogen receptor beta over expression in males with non-small cell cancer is associated with beter survival. Lung Cancer. 2008, 59 (1): 88-94. 10.1016/j.lungcan.2007.07.025.Google Scholar
- Xu R, Shu Y: Estrogen and its signaling pathway in non-small cell lung cancer (NSCLC). J Najing Med Univ. 2009, 23 (4): 217-223. 10.1016/S1007-4376(09)60059-9.Google Scholar
- Beyer C, Küppers E, Karolczak M, Trotter A: Ontogenetic expression of estrogen and progesterone receptors in the mouse lung. Biol Neonate. 2003, 84 (1): 59-63. 10.1159/000071445.Google Scholar
- Oyama T, Sugio K, Isse T, Matsumoto A, Uramoto NH, Nozoe T, Morita M, Kagawa N, Muto TM, Yasumoto K, Kawamoto T: Expression of cytochrome P450 in non-small lung cancer. Frontiers Biosci. 2008, 13: 5787-5793.Google Scholar
- Slatore CG, Chien JW, Au DH, Satia JA, White E: Lung cancer and hormone replacement therapy:association in the vitamins and lifestyle study. J Clin Oncol. 2010, 28 (9): 1540-1546. 10.1200/JCO.2009.25.9739.Google Scholar
- Matsuo K, Ito H, Yatabe Y, Hiraki A, Hirose K, Wakai K: Risk factors differ for non-small-cell lung cancer with and without EFGR mutation:assessment of smoking and sex by a case-control study in Japanese. Cancer Sci. 2007, 98 (1): 96-101. 10.1111/j.1349-7006.2006.00347.x.Google Scholar
- Samet JM: Environmental causes of lung cancer: what do we know in 2003?. Chest. 2004, 125: 80-83. 10.1378/chest.125.5_suppl.80S.Google Scholar
- Pauly JR, Slotkin TA: Maternal tobacco smoking, nicotine replacement and neurobeahavioural development. Acta Paediatrica. 2008, 97 (10): 1331-1337. 10.1111/j.1651-2227.2008.00852.x.Google Scholar
- Sarasin A, Schlumpf M, Muller M, Fleishmann I, Lauber ME, Lichtenstein : Adrenal-mediated rather than direct effects of nicotine as a basis of altered sex steroid synthesis in fetal and neonatal rat. Reprod Toxicol. 2003, 17 (2): 153-162. 10.1016/S0890-6238(02)00119-3.Google Scholar
- Muggi ME, Elbert JO, Robertson C, Hurt RD: Waking a sleeping ginat: the tobacco industry's response to the Polonium-210 issue. Am J Pub Health. 2008, 98 (9): 1643-1650. 10.2105/AJPH.2007.130963.Google Scholar
- Raymond-Whish S, Mayer LP, O'Neal T, Martinez A, Sellers MA, Christian PJ, Marion SL, Begay C, Propper CR, Hoyer PB, Dyer CA: Drinking water with Uranium below the US EPA water standard causes estrogen receptor-dependent responses in female mice. EHP. 2007, 115 (12): 1711-1716.Google Scholar
- Beelen R, Hoek G, van den Brandt PA, Goldbohm RA, Fischer P, Schouten LJ, Jerrett M, Hughes E, Armstrong B, Brunekreef B: Long-term effects of traffic-related air pollution on mortality in a Ducth cohort (NLCS-AIR Study). EHP. 2008, 116 (2): 196-202.Google Scholar
- Laden F, Schwartz J, Speizer FE, Dockery DW: Reduction in fine particulate air pollution and mortality. Am J Respir Crit Care Med. 2006, 173: 667-672.Google Scholar
- Misaki K, Suzuki M, Nakamura M, Handa H, Iida M, Kato T, Matsui S, Matsuda T: Aryl hydrocarbon receptor and estrogen receptor ligand activity of organic exctracts from road dust and diesel exhaust particulates. Arch Environ Contam Toxicol. 2008, 55: 199-209. 10.1007/s00244-007-9110-5.Google Scholar
- Ssempebwa JC, Carpenter DO, Yilmaz B, DeCaprio AP, O'Hehir DJ, Arcaro KF: Waste crankcase oil: an environmental contaminant with potential to modulate estrogenic responses. J Toxicol Environ Health, Part A. 2004, 67: 1981-1094.Google Scholar
- Van de Wiele T, Vanhaecke L, Boeckaert C, Peru K, Headly J, Verstraete W, Siciliano S: Human colon microbiota trasnform polycyclic aromatic hydrocarbons to estrogenic metablites. EHP. 2005, 113: 6-10.Google Scholar
- Klein GP, Hodge EM, Diamond ML, Yip A, Dann T, Stern G, Denison MS, Harper PA: Gas-Phase ambient air contaminants exhibit significant dioxin-like and estrogen-like activity in vitro. EHP. 2006, 114 (5): 697-703.Google Scholar
- Cohen AJ: Outdoor air pollution and lung cancer. EHP. 2000, 108: 743-750.Google Scholar
- Parodi S, Baldi R, Benco C, Franchini M, Garrone E, Vercelli M, Pensa F, Puntoni R, Fontana V: Lung cancer mortality ina district of La Spezia (Italy) exposed to air pollution from industrial plants. Tumori. 2004, 90: 181-185.Google Scholar
- Shen J, Liu J, Xie Y, Diwan BA, Waalkes MP: Fetal onset of aberrant gene expression relevant to pulmonary carcinogenesis in lung adenocarcinoma development induced by the utero arsenic exposure. Toxicol Sci. 2007, 95 (2): 313-320.Google Scholar
- Tanaka Y, Sasaki M, Kaneuchi M, Fujimoto S, Dahiya R: Estrogen receptor alpha polymorhism and renal cell carcinoma- possible risk. Mol Cellular Endocrinol. 2003, 202: 109-116. 10.1016/S0303-7207(03)00071-6.Google Scholar
- Moyad MA: Review of potential risk factors for kidney (renal cell) cancer. Semin Urol Oncol. 2001, 19: 280-293.Google Scholar
- Ilyasova D, Schwartz GG: Cadmium and renal cancer. Toxicol Applied Pharmacol. 2005, 207: 179-186.Google Scholar
- Hopenhayn-Rich C, Biggs ML, Smith AH: Lung and kidney cancer mortality associated with arsenic in drinking water in Cordoba, Argentina. Int J Epidemiol. 1998, 27: 561-569. 10.1093/ije/27.4.561.Google Scholar
- Søreide K, Aagnes B, Møller B, Westgaard A, Bray F: Epidemiology of pancreatic cancer in Norway: trends in incidence, basis of diagnosis and survival 1965-2007. Scand J Gastroenterol. 2010, 45 (1): 82-92. 10.3109/00365520903358899.Google Scholar
- Luke C, Price T, Karapetis C, Singhai N, Roder D: Pancreatic cancer epidemiology and survival in an Australia population. Asian Pac J cancer Prev. 2009, 10 (3): 369-374.Google Scholar
- Hariharan D, Saied A, Kocher HM: Analysis of mortality rates for pancreatic cancer across the world. HPB (Oxford). 2008, 10 (1): 58-62. 10.1080/13651820701883148.Google Scholar
- Sauerland C, Engelking C, Wickham R, Pearlstone DB: Cancers of the pancreas and hepatobilliary system. Seminars in Oncol Nursing. 2009, 25 (1): 76-92. 10.1016/j.soncn.2008.10.006.Google Scholar
- Lowenfels AB, Maisonneuve P: Epidemiology and risk factors for pancreatic cancer. Best Practice & Res Clin Gastroenteol. 2006, 20 (2): 197-209. 10.1016/j.bpg.2005.10.001.Google Scholar
- Konduri S, Schwartz RE: Estrogen receptor beta/alfa ratio predicts response of pancreatic cancer cells to estrogens and phytoestrogens. J Surgical Res. 2007, 140: 55-66. 10.1016/j.jss.2006.10.015.Google Scholar
- Andren-Sandberg A, Hoem D, Backman PL: Other risk factors for pancreatic cancer: hormonal aspects. Ann Oncol. 1999, 10 (Suppl 4): 131-132. 10.1093/annonc/10.suppl_4.S131.Google Scholar
- Trushin N, Leder G, El Bayoumy K, Hoffmann D, Beger HG, Henne-Bruns D, Ramadani M, Prokopcyk B: The tobacco carcinogen NNK is stereoselectively reduced by human pancreatic microsomes and cytosols. Langenbecks Ach Surg. 2008, 393: 571-579. 10.1007/s00423-007-0265-3.Google Scholar
- Kummer V, Maskova J, Zraly Z, Matiasovic J, Faldyna M: Effect of postnatal exposure to benz(a)pyrene on the uterus of immature rats. Exp Toxicol Pathol. 2007, 59 (1): 69-76. 10.1016/j.etp.2007.02.007.Google Scholar
- Bogush TA, Dudko EA, Beme AA, Bogush EA, Polotskii BE, Tiuliandin SA, Davydov MI: Estrogen receptor expression in tumors different from breast cancer. Antibiot Khimioter. 2009, 54 (7-8): 41-49.Google Scholar
- Ben-Porath I, Thomson MW, Carey VJ, Ge R, Bell GW, Regev A, Weinberg RA: An embryonic stem cell-like gene expression signature in poorly differentiated aggressive human tumors. Nat Genet. 2008, 40 (5): 499-507. 10.1038/ng.127.Google Scholar
- Batistatou A, Kyzas PA, Goussia A, Arkoumani E, Voulgaris S, Polyzoidis K, Agnantis NJ, Stefanou D: Estrogen receptor beta (ERbeta) protein expression correlates with BAG-1 and prognosis in brain glial tumours. J Neurol. 2006, 77 (1): 17-23.Google Scholar
- Estrada M, Varshney A, Ehrilich BE: Elevated testosterone induces apoptosis in neuronal cells. Biol Chem. 2006, 281 (35): 25492-25501. 10.1074/jbc.M603193200.Google Scholar
- Liu CC, Chen CC, Wu TN, Yang CY: Association of brain cancer with residential exposure to petrochemical air pollution in Taiwan. J Toxicol Environ Health, Part A. 2008, 71: 310-314. 10.1080/15287390701738491.Google Scholar
- Huyghe E, Plante P, Thonneau PF: Testicular cancer variations in time and sapce in Europe. Eur Urol. 2007, 51: 621-628. 10.1016/j.eururo.2006.08.024.Google Scholar
- Maffezzini M: TC incidence increasing: spread the word. European Urology. 2007, 51: 596-597. 10.1016/j.eururo.2006.08.023.Google Scholar
- Cavaco JE, Laurentino SS, Barros A, Sousa M, Socorro S: Estrogen receptors alpha and beta in human testis: both isoforms are expressed. Syst Biol Reprod Med. 2009, 55 (4): 137-144.Google Scholar
- Delbes G, Duquenne C, Szenker J, Taccon J, Habert R, Levacher C: Developmental changes in testicular sensitivity to estrogens through feral and neonatal life. Toxicol Sci. 2007, 99 (1): 234-243. 10.1093/toxsci/kfm160.Google Scholar
- Kaijser M, Akre O, Cnattinius S, Ekbom A: Maternal lung cancer and testicular cancer risk in the offspring. Cancer Epidemiol Biomarkers, Prevention. 2003, 12: 643-646.Google Scholar
- Swerdlow AJ, Stiller CA, Wilson LM: Prenatal factors in the aetiology of testicular cancer: an epidemiological study of childhood testicular cancer deaths in Great Britain, 1953-73. J Epidemiol Community Health. 1982, 36 (2): 96-101. 10.1136/jech.36.2.96.Google Scholar
- Smith LM, Cloak CC, Poland RE, Torday J, Ross MG: Prenatal nicotine increase testosterone levels in the fetus and females offspring. Nicotine Tob Res. 2003, 5 (3): 369-374. 10.1080/146222031000094196.Google Scholar
- Storgaard L, Bonde JP, Olsen J: Male reproductive disorders in humans and prenatal indicators of estrogen exposure. A review of published epidemiological studies. Reprod Toxicol. 2006, 21 (1): 4-15. 10.1016/j.reprotox.2005.05.006.Google Scholar
- McLachlan JA, Simpson E, Martin M: Endocrine disrupters and female reproductive health. Best Pract Res Clin Endocrinol Metab. 2006, 20 (1): 63-75. 10.1016/j.beem.2005.09.009.Google Scholar
- Drummond E, Fuller PJ: The importance of ERbeta signalling in the ovary. J Endocrinol. 2010, 205 (1): 15-23. 10.1677/JOE-09-0379.Google Scholar
- Amram-Benamran ML, Cochet S, Petignat P, Sappino AP: Ovarian cancer screening: recommendations for clinical pratice. Rev Med Suisse. 2010, 6 (250): 1066-1068.Google Scholar
- Henson MC, Chedrese PJ: Endocrine disruption by cadmium, a common environmental toxicant with paradoxical effects on reproduction. Exp Biol Med. 2004, 229: 383-392.Google Scholar
- Grant WB: An ecologic study of dietary and solar ultraviolet-B links to breast carcinoma mortality rate. Cancer. 2002, 94 (1): 272-281. 10.1002/cncr.10196.Google Scholar
- El-Zein R, Conforti-Froes N, Au WW: Interactions between genetic predisposition and environmental toxicants for development of lung cancer. Environ Mol Mutagenesis. 1997, 30: 196-204. 10.1002/(SICI)1098-2280(1997)30:2<196::AID-EM12>3.0.CO;2-8.Google Scholar
- Park SK, Yoo KY, Lee SJ, Kim SU, Ahn SH, Noh DY, Choe KJ, Strickland PT, Hirvonen A, Kang D: Alcohol consmtion, glutathione S-transferase M1 and T1 genetic polymorphysim and breast cancer risk. Pharmacogenetics. 2000, 10: 301-309. 10.1097/00008571-200006000-00004.Google Scholar
- Wadia PR, Vanderberg LN, Schaeberle CM, Rubin BS, Sonnenschein C, Soto AM: Perinatal bisphenol A exposure increases estrogen sensitivity of the mammary gland in diverse mouse strain. EHP. 2007, 115 (4): 592-598.Google Scholar
- Prins GS, Tang WY, Belmonte J, Ho SM: Developmental exposure to bisphenol A increases prostate cancer susceptibility in adult rats: epdegenetic mode of action is implicated. Fertility and Strerility. 2008, 89 (Suppl 1): 41-42.Google Scholar
- Miki Y, Suzuki T, Tazawa C, Blumberg B, Sasano H: Steroid and xenobiotic receptor (XR), cytochrome P450 3A4 and multidrug resistance gene 1 in human adult and fetal tissues. Mol Cellular Endocrinol. 2005, 231: 75-85. 10.1016/j.mce.2004.12.005.Google Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate. Please note that comments may be removed without notice if they are flagged by another user or do not comply with our community guidelines.


text:
Welcome to HappyHome Qatar
If complete house cleaning services in Qatar through environmentally safe procedure is what you are looking for then we are here to assist you.
Happy Home stands as a leader in providing cleaning in Qatar. From one off cleaning to contract cleaning for daily, weekly or monthly visits, we have a variety of options to get you house tidy and hygienic.
We are Number One Choice for 100% Environmental Friendly Cleaning Services.
Happy Home is a cleaning company in Qatar that deals with Residential and Commercial Cleaning Services. Considering that this is one of the fast moving industry, Happy Home, The Cleaning Companies in Qatar is confident that through hard work we will achieve success. Qatar Cleaning Comapany Services is an industry that continues its dramatic growth as years goes by and Happy Home, The Qatar Cleaning Company is taking advantage of this fact and committed to provide high quality and consistent cleaning services in an environmentally sound, completely trustworthy and in professional manner.
At Happy Home will help you arrange solution that fit your lifestyle and schedule. We will deliver high quality services on time to meet your expectations with the assistance of hardworking House Maid Qatar .
About More
All our cleaning crew are well experienced. They will treat your home with respect, like it is our own.
Affordable, high quality cleaning materials that will maintain your home.
Fast & Effective SERVICE
The Detailed- House Cleaning or Maid Service Qatar is our main and popular services.
If you are looking for high quality, environmental friendly and 100% guaranteed cleaning services in Qatar, then this is where you get them.
Entertainment Venues
House Party cleaning
Commercial venues
Laundry Service


text:
Liverpool set for end-of-season glamour tie with Scottish champions Celtic in Mauritius
LIVERPOOL have lined up a lucrative end-of-season friendly with Glasgow giants Celtic on the exotic Indian Ocean island of Mauritius.
The Reds are eyeing up a tour of the island if sponsors agree to cough up the cash to fund the trip.
"Given the friendly relations between Liverpool and Celtic, the Scottish club have agreed to come"Mauritian organisers
Organisers say Neil Lennon's side have provisionally agreed to play the Anfield giants at the 30,000-capacity Stade Anjalay in Belle Vue Maurel on Sunday May 18.
Brendan Rodgers' side are due to play Shamrock Rovers in Dublin in a friendly on May 14 and it's thought the deal hinges on whether a private plane can be provided to fly them from Ireland to Mauritius.
Jawid Tharanee, a spokesman for the Mauritian organisers, said: "Given the friendly relations between Liverpool and Celtic, the Scottish club have agreed to come.
"They made contact with us and agreed without much convincing. We had requests from German and Italian clubs to play the match too, but we are happy with Celtic.
"Celtic have stated they will bring their first team over for the game."
If the fixture does take place the Mauritian public will have to make do without watching a host of Kop heroes including Steven Gerrard and Luis Suarez, with most of Liverpool's star-studded squad jetting off to Brazil for this summer's World Cup.


text:
Plumber Newnan Ga
When you call for plumbing services here at Hammond Services, you can rest assured our plumbing professionals will spring into action. Whether it's a leaky faucet or a ruptured pipe, chances are good you want it fixed ASAP, and your wish is our command.
Plumbing Services We Offer in Newnan
The plumbing category covers an incredible range of residential services, but here are the ones you're most likely to find yourself in need of:
- Water heater maintenance, repair, and replacement
- Plumbing and pipe installation
- Plumbing repairs
- Whole-house re-piping
- Tankless water heater repair and new installation
- Sewer line repair and replacement
- Water line repair or replacement
- Backflow prevention services
- Video line inspections
- Garbage disposal repair and installation
- Faucet repair and installation
- Toilet repair and installation
- 24/7 emergency after-hours service
- And more
If it's related to water or plumbing in Newnan, our expert team can help you out.
Newnan Plumbing Experts at Your Disposal
The licensed plumbing professionals from Hammond Services are all well versed in the most sophisticated equipment and up-to-date technology and techniques on the market today. Our extensive training, in-field experience, and advanced tools give us the edge in the industry, and ensure we can handle any plumbing problem you might throw our way. We even offer round-the-clock emergency services, so we're good to go whenever you need us. Rest assured, we're up for the challenge, and our team is ready and waiting to say, "We can do that!"
Schedule Your In-Home Consultation Today
Ready to take the next step towards working with our talented plumbing team? Give us a call any time, day or night. We'll ask you a few questions about what's going on, so we can get a better idea of what might be causing your problem, and then we'll schedule a convenient time to come check it out. We service the following areas in GA: Griffin, Newnan, McDonough, Peachtree City, Fayetteville, Sharpsburg, Tyrone, Riverdale, Stockbridge, Locust Grove, Jackson, Barnesville, Senoia, Jonesboro, Hampton, Zebulon, and Thomaston.
If you have a plumbing problem, or even just a few questions, contact us today!
Are you having problems with your sewer line or septic system? Hammond Services can help! Find out more about the sewer services offered by our plumbing team.


text:
Operating an IRS-Compliant Gymnastics Booster ClubPDF USA Gymnastics
December 4, 2014
Marc Jacobs gave a presentation via webinar on "Operating an IRS-Compliant Gymnastics Booster Club" to gymnasts and their families, coaches, instructors, judges, club owners, administrators, and other members of USA Gymnastics. The presentation focused on the importance of creating a booster club and determining whether or not the club qualifies for nonprofit status. Attendees left the webinar with a better understanding of how to structure and manage their booster club so as to be exempt from taxation under Section 501(c)(3) of the Internal Revenue Code (IRC).


text:
Toggle navigation
Remember me
Law School Discussion
Applying to Law School
Law School Admissions
For Those of You Asking "Should I Go to Law School"...
For Those of You Asking "Should I Go to Law School"...
105 Replies
58160 Views
Re: For Those of You Asking "Should I Go to Law School"...
Reply #80 on:
November 01, 2010, 11:10:01 AM »
Yea I should not say shocked that is to strong of a word. My point was simply that finding work is hard. Finding a job simply sucks it always has and always will no matter what field you are trying to enter into. People always want to hire people with experience, but you need a job to get experience. So getting your first job presents somewhat of a catch 22 and this does not only apply to the legal field. In fact it applies to just about everything there is. It does seem that law schools for how outrageously expensive they are could provide you with a year of clinical training for free after you pass the bar. Having on-campus clinics where professors are being paid to supervise you will give them the ability to really train you. This would allow students to get real experience after graduation instead of being at a firm where they really do not have time to teach you. It seems the whole legal profession would benefit from this, but it does not look like it is going to happen anytime soon. That is the one reason Doctors/Nurses do get jobs when they finish everything they have to get practical experience before going out into the real world. Law school leaves you knowing the executive powers of the President, but not how to write motions, file things in court, and just the day to day of being a lawyer. That is the real issue.
a.k.a. Miguel Sanchez
Re: For Those of You Asking "Should I Go to Law School"...
Reply #81 on:
November 13, 2010, 04:03:14 PM »
but not how to write motions
I had plenty of instruction on writing motions in law school. The issue isn't knowing how to write the, it's knowing when they are appropriate and knowing what to put in them when you don't have a professor giving you an assignment.
Re: For Those of You Asking "Should I Go to Law School"...
Reply #82 on:
November 13, 2010, 04:41:38 PM »
Yea the actual practical aspects of it is what should be taught. You can write motions using Matthew Bender or something, but how do you apply it practically. I am still only a 2L and I can only hope I will learn more along the way. However, as it stands if someone right this second had a problem I would not be able to solve it. I would know to file a complaint, but I am sure that is not the answer in every situation. Even if a complaint was the answer I would not know what to do after it was filed.I imagine most law school graduates no matter what school they go to do not know how to do much of anything practical when they graduate. The only real way to learn anything is to actually be forced to do it. However, it seems most law students are scared to do anything real and the schools are to soft on students.
Maybe it is not like this at other schools, but I have professors that say if you did not do the reading just sign in. Or I don't want to call on to much blah. The only person being hurt by professors being overly nice is the student. If you can't get around to reading 20-30 pages as a first year student when your job is school and you cannot rationally discuss what you read in front of your peers then you do not even have a chance of being a halfway decent lawyer. I am constantly astonished at how soft & spoiled law students are. Seeing it in action I don't know why I am ever surprised reading things like JDunderground & other sites.
The bottom line is law school should be much harder than it is. It seems like the real reason there is unemployment and all this other stuff is that the school's are to soft on their students. They need to make you do real stuff and not just reading about the Executive Power. Students do not come out knowing what they need to know and it seems like after 3 years you should know the simple basic practical aspects. However, it does not seem like schools or the ABA are interested in requiring a more practical education.
Re: For Those of You Asking "Should I Go to Law School"...
Reply #83 on:
November 13, 2010, 05:08:46 PM »
Spoken like a true competitor and athelte bigs. As one who is not yet in law school, I cannot comment on it. But I do feel one should always push past their comfort level if success is the goal
Re: For Those of You Asking "Should I Go to Law School"...
Reply #84 on:
November 13, 2010, 06:47:31 PM »
Thanks. I was just in a study group with 3 other people who would not stop complaining about how hard the class we are in is. I wanted to kill somebody instead I went on a rant on this website. All I kept thinking about was if you stopped b***hing for 2 minutes and studied maybe it would not be that hard. They are cool people and they are probably 10x smarter than me, but good god stop whining. All I could think to myself was what if these people were in an actual law firm and someone wanted them to do something. Would they just tell them it sounds to difficult? I don't know your background, but if you come from a family that made you do any kind of work in high school or college be able to control your emotions when you listen to completely spoiled & naive people complain about the most retarded things in the world. Instead of taking it out on them vent on this board
In all seriousness I really do think the main reason for all the people bi***ing and moaning on JDunderground & other such sites is that law school is to easy. You should be required to do something real before you can become a lawyer. As it stands you can get a J.D. & pass the bar a standardized test and you somehow are deemed capable of dealing with real problems. The simple fact is the only way to know how to deal with real problems is by dealing with real problem. Unfortunately, the ABA and law schools do not seem to understand this. This results in people coming out completely unprepared for the REAL world.
Re: For Those of You Asking "Should I Go to Law School"...
Reply #85 on:
November 14, 2010, 04:29:47 AM »
I wonder if part of the problem is for mnay law students college was easy and thus they do not know how to work. If not for working full time for several years, I may not either. I can sleep through most of my classes and still maintain an A average. My work ethic developed through actual work prevents me from doing so. So those who have never really worked, may find work to not be for them in law school
Re: For Those of You Asking "Should I Go to Law School"...
Reply #86 on:
November 16, 2010, 12:10:48 PM »
Maybe, I mean law school truly is not that difficult. I remember reading books etc about how hard it would be and I have been extremely underwhelmed. People will disagree with me on this I am sure, but literally if you show up to class everyday, do the readings, make a decent outline (there are a million different ways to do this, but whatever you need to do to go over what you learned.) You will get decent grades. Be a responsible human being and odds are everything will end up ok regarding your grades.
Instead a bunch of people try to take all these shortcuts. They buy supplements, listen to podcasts, etc and they say I never read the book or show up to class. Then they are baffled by the professor's exam, because the supplement the professor never assigned did not address some topic the professor covered extensively in class. People put in 100x more effort tin taking shortcuts han they would by just doing the basic simple task they are supposed to do. Read between 60-90 pages during the weekdays. It is far from impossible and I have done a lot harder things than that.
Getting a job you ask. How hard is that I was in suits all the time and people would always ask me how are you getting all these interviews? My simple answer I applied to jobs and they called me back. Not everyone in fact probably like 15% of the jobs I applied to, but it takes 10-15 minutes to write an acceptable cover letter. I applied to 400 jobs I think, which was quite easy to do when only having to read 60-90 pages a day. I ask them if they applied or even signed up with LCS oh no we didn't get around to that yet. Again, all I can think is how how in god's name are you that lazy that you don't have time to just register with career services. It is in the building you can take 20 minutes out of your day when reading 60-90 pages. It is just the bare minimum and if you do that you will need to write a competent cover letter. Again, if you do that things will probably work out even if you go to a lowly tier 4.
That is probably so incoherently written it is beyond understanding, but I am just so astonished at how spoiled & soft law students are. That does not apply to everyone obviously, but a vast majority of them would probably succeed if they used common sense and took some accountability for themselves.
The reality is law school is to soft on people and the professors and administration is to nice. This isnot going to help anyone in the long run. Yesterday for example our professor gives a list of people who will get called on the next class, which I think is to easy in the first place. However, one of the girls yesterday still did not get around to reading it. She was assigned a 4 page reading the book and just needed to have some comprehension of 4 freakin pages. She gets called on and says I did not read it. The professor gives a look of disappointment and moves on. I would have kicked her out of the class or literally docked her an entire grade or something. That is just simply inexcusable unless some emergency happened, but she was at the 49ers game and she could have read before going or our class is at 3:00 with a horrible hangover I could competently understand 4 f***ing pages. None of that was done so all I can ask is what in god's name will she do if she is a lawyer?
It is simply unbelievable to me. Those are extreme cases and a lot of people in law school are smart and hard working, but I can really see the type of people that join JDunderground etc. Law school is not unlike anything else do your s*** and this will require some work & sacrifice. As far as I know to succeed in anything it takes work & sacrifice, but law school does not even ask for that much. Well that is a nice and awesome incoherent rant, but I had to vent.
Re: For Those of You Asking "Should I Go to Law School"...
Reply #87 on:
November 17, 2010, 09:17:52 AM »
Interesting article at ATL: only 8% consider a school's job placement statistics the most important factor when considering a law school.
Re: For Those of You Asking "Should I Go to Law School"...
Reply #88 on:
November 17, 2010, 09:54:58 AM »
I completely agree with everything that article says. I do not think 90% of incoming law students have any idea what they are in for. The admissions requirements should be 100x more stringent than they are. They could be like medical & nursing schools and require prerequisite courses for an applicant to even be considered. They could also make some kind of hourly requirement to work in a law firm, court, or some legally related field before applying. Instead you can breeze through college with a 3.2 in Religious Studies and get about 70 out of 100 MC questions on a test you do not even need to study for and whollaa. You have sufficiently proven you are willing to put in 3 years of work and 100k for a field you have displayed no interest in whatsoever.
The fact that U.S. News ranking is one of the top priorities is another thing that is in no way surprising. I myself was nearly tricked into moving to Michigan to attend a Tier 2 school opposed to a tier 4 in a place where I have a ton of connections and actually want to live. The rankings are really sad because they mislead so many students into thinking anybody would care that they go to the 74th opposed to the 111th best school. Particularly when considering the formula U.S. News uses makes almost no sense. I wish U.S. News could be sued, but they are just a private for profit-magazine giving their opinion and people are stupid enough to think it matters. I paid a $700 deposit, because I was one of these stupid people. Thankfully, I talked to 3 practicing lawyers the day before I bought my plane ticket to Michigan who told me nobody really cares about tier 2 or tier 4 schools. If you want a job in San Francisco you should go to school in the Bay Area. I am still astonished that I did not have the common sense to realize that months earlier, but it makes me feel better that 92% of people are just as dumb as me.
So bottom line is law school is not a guarantee and the number one thing any student should consider before committing 3 years & 100k is getting a job. You should probably get some kind of legal experience before applying, because 3 years & 100k is a big commitment. Considering how big the commitment is it would be wise to have some exposure to the legal field. Then go to school in the location you want to live in and get out as cheaply as possible. Take scholarship money unless it is an ELITE school. If the school's main claim to fame is that it had the 9th best international law program it is not worth 100k more to go. Harvard, Yale, Stanford, those types of school are worth the extra money. If you say the school's name and the average joe on the street gives a puzzled look it is not that impressive. Even if you go on to tell average Joe it is the 49th best school (according to the for-private and unregulated U.S News subjective opinion) and had the 39th best public interest program and 17th best international law program he will still scratch his head. The majority of lawyers will probably do the same and I can only imagine they don't care if you went to the 63rd or 87th best school. They also probably have no idea who holds the title of 17th best international program and even if they did they could care less.
Re: For Those of You Asking "Should I Go to Law School"...
Reply #89 on:
January 27, 2011, 10:45:02 AM »
Here is another link that is actually free and has a lot of the same information:
Law School Discussion
Applying to Law School
Law School Admissions
For Those of You Asking "Should I Go to Law School"...


text:
A business jet, private jet, or bizjet, or simply B.J., is a jet aircraft designed for transporting small groups of people. Business jets may be adapted for other roles, such as the evacuation of casualties or express parcel deliveries, and some are used by public bodies, government officials or the armed forces.
The Lockheed JetStar, seating ten passengers and two crew, first flew on 4 September 1957. 204 aircraft were produced from 1957 to 1978, powered by four 3,300 pounds-force (15 kN) Pratt & Whitney JT12 turbojet engines, then Garrett TFE731 turbofan for a 44,500 pounds (20.2 t) MTOW, then two General Electric CF700 turbofans.
The smaller, 17,760 pounds (8.06 t) MTOW North American Sabreliner first flew on 16 September 1958. Powered by two Pratt & Whitney JT12 turbojet engines then Garrett TFE731, more than 800 were produced from 1959 to 1982.
The 25,000 pounds (11 t) MTOW British Aerospace 125 first flew on 13 August 1962, powered by two 3,000 pounds-force (13 kN) Armstrong Siddeley Viper turbojets. Its engine were replaced by Garrett TFE731, then Pratt & Whitney Canada PW300 turbofans. Almost 1,700 aircraft were produced between 1962 and 2013 after being marketed as the Hawker 800.
Coordinates: 16°S 167°E / 16°S 167°E / -16; 167
Vanuatu (English i/ˌvɑːnuːˈɑːtuː/ vah-noo-AH-too or /vænˈwɑːtuː/ van-WAH-too; Bislama IPA: [vanuaˈtu]), officially the Republic of Vanuatu (French: République de Vanuatu, Bislama: Ripablik blong Vanuatu), is a Pacific island nation located in the South Pacific Ocean. The archipelago, which is of volcanic origin, is some 1,750 kilometres (1,090 mi) east of northern Australia, 500 kilometres (310 mi) northeast of New Caledonia, east of New Guinea, southeast of the Solomon Islands, and west of Fiji.
Vanuatu was first inhabited by Melanesian people. The first Europeans to visit the islands were a Spanish expedition led by Portuguese navigator Fernandes de Queirós, who arrived on the largest island in 1606. He then claimed the archipelago for Spain, as part of the colonial Spanish East Indies, and named it Austrialia del Espiritu Santo.
In the 1880s, France and Great Britain claimed parts of the archipelago, and in 1906 they agreed on a framework for jointly managing the archipelago as the New Hebrides through a British–French Condominium. An independence movement arose in the 1970s, and the Republic of Vanuatu was founded in 1980.


text:
Since your most interesting decision to invite Dr Gerald McCann to be a guest speaker at a conference hosted by the Child Exploitation and Online Protection Centre (CEOP) on the subject of sexually-motivated child abductions. I could not help but wonder some little about you and what path your career might have taken prior to joining the CEOP.
Not unnaturally then that I should carry out a little research, for reasons numerous, but primarily to ascertain your bona fides. A little research as to your experience and qualifications, not least of those reasons being, that your previous career might somehow help me understand what the criteria might have been for your taking the aforementioned interesting decision.
And I must say quite honestly, what an impressive career it has been to date, one only has to read your profile, the one below, used in this instance, but typical of many others, courtesy of the Telegraph.
It soon becomes apparent, one only has to look at your achievements to realise this, that you are not without a great deal of experience in your chosen field, and are in fact nobody's fool.
Profile: Jim Gamble
With more than 25 years experience working in law enforcement, Jim Gamble, 48, is a true career policeman.
Before taking up his current job as the head of the Child Exploitation and Online Protection (Ceop) Centre in 2006, he worked as a superintendent in the Police Service of Northern Ireland and, most recently, as acting chief constable and head of the National Crime Squad.
During his time in Northern Ireland he covered both uniform and detective roles before leading anti-terrorist responses in Britain and abroad.
At the National Crime Squad - which deals with serious and organised crime - he oversaw a complex portfolio ranging from firearm deployment to hi-tech crime and intelligence to professional standards and security.
He also set up the National Crime Squad's specialist response cell - the Paedophile Online Investigation Team - and was involved in the creation of the first international law enforcement partnership to combat child abuse online - the Virtual Global Taskforce.
Mr Gamble is married with three children and lives in London.
Having read such an impressive resume however, your hitherto unexplained motive for inviting Dr McCann to speak at your conference, went from interesting to, how shall I describe it, enigmatic? yes enigmatic, from interesting to enigmatic.
Of this enigma however was born a question, just the one, and you might be gracious enough to perhaps furnish an answer.
If for instance, given your vast experience, if during an interview a suspect displayed the same behavioural patterns as Dr McCann displays, as typified below, when he himself is interviewed about the disappearance of his daughter Madeleine, might I ask then your more likely course of action?
Would you further continue to question said suspect, or would you as a matter of fact, extend an invitation to the suspect, inviting him to speak at your next RUC jamboree?
I look forward to your reply with earnest anticipation.
Blog Note: This tediously long post is upped here rather than having it clutter up Good Quality Wristbands.
You may wonder why I took the trouble to feature so many graphics, it's because there are so many.
So many lies, so many tells.


text:
Gary Neville: "Why do I think Chelsea can win the PL title"
Gary Neville is convinced Chelsea can be a serious candidate to win the title and the Manchester United legend, now a Sky Sports pundit, explains why:
"The very, very top teams make the fewest mistakes, and that was a team performance today (Sunday) of no mistakes.
"That clean sheet mentality has definitely been forced into them. It's a way of being, it builds so much confidence. When the goalkeeper and defenders are happy, when they are comfortable and relaxed, the crowd aren't getting anxious.
"I'm seeing Chelsea players do the right things, staying with their runners, and they've got two very, very good central midfield players from a defensive point of view, they've got a wonderful ability to read the game and fill in the gaps.
"Are they the finished article? Probably not, but I wouldn't rule them out of the title, because I don't trust the others enough to think that Chelsea can't win it.
Not playing in the European competitions can be an advantage for the Blues:
"I think the fact that Chelsea have free weeks, and don't have the confusion and disruption of European football, even though it is a good disruption being in the Champions League or Europa League, it gives them a big advantage.
"Certain players in their team – like John Terry, Branislav Ivanovic, Diego Costa, even Eden Hazard and Nemanja Matic – I think they all benefit hugely from it.
"They would have been in that dressing room after the game, having put in a wonderful performance, and be thinking: 'I've got a week now, I can get my body right, have a massage and not think about training on Tuesday ahead of another midweek game.'
"It's a big thing for players of that nature, so I think that gives them a competitive edge, and Liverpool the same, who have players who give huge energetic performances. Their recovery between games is important.
WIt will be an advantage. I think Tottenham are as good as Liverpool, I think Tottenham are as good as Chelsea, there's no doubt, but because Spurs are in European competition I would put Chelsea and Liverpool ahead of them in the Premier League for that reason.
"I think Manchester City and Arsenal are the better teams, but can you trust either of them fully yet? I don't think you can. That's not to say they won't go and deliver, but because they're in Europe, and that they've shown glimpses of the old Arsenal and old City, they've got to give me more yet before I trust them.
"That's without even mentioning United, who have fallen behind a little bit."


text:
This website uses cookies to ensure proper functionality of the shopping cart and checkout progress. By continuing to browse the site you are agreeing to the use of cookies. Click here to learn about cookie settings.
Registration is free and easy!
Write Your Review
In stock
Portfolios with padded textile finish & double zip.
A2 have ring mechanism, handle & shoulder strap.
Use spaces to separate tags. Use single quotes (') for phrases.
Only registered users can write reviews. Please, log in or register
Stay up-to-date with our latest news
Eastman Group of Companies
We manufacture a high percentage of the products that we sell which, combined with our bulk purchasing power for the rest of the product range, allows us to be competitively priced whilst maintaining high quality and providing fast response.


text:
Attractive and prestige, Hotel "Madara" will surprise you with elegance and contemporary interior. Situated in the center of the town, the complex is nearby Central Post, Shumen Municipality, District Court and some bank offices. The perfect mix of comfort and functionality, offered in the Hotel, and easy access from any main town road makes it a very suitable place for business trips and tourism, during family vacation or short break after long journeys as for Bulgarians as well as for any foreign citizen. We secure covered and open-air protected parking, caring for the safety and quietness of our clients.
Rooms and prices
Single rooms are with unique design and decoration, with a good individual style and predispose our guests to full relax. There are cable TV and mini-bar, and the amazing panoramic view of Shumen allows the visitors to enjoy the buzzing daily dynamics of Shumen Town.


text:
PS I Love You >> Madonna, 2011
From the amazing new Paper Bag Records' True Blue compilation
RouLitO >> Outkast, 2010
Deerhoof >> Xiu Xiu, 2011
This is a cover of Xiu Xiu's "The Fabrizio Palumbo Retaliation" from their joint 7'' single for Record Store Day 2011
LCD Soundsystem >> Harry Nilsson, 2011
LCD Soundsystem - Jump Into The Fire [Harry Nilsson] (Live at Madison Square Garden during LCD's last show ever)| zs
LCD, we will miss you.
LCD, we will miss you.
Subscribe to: Posts (Atom)


text:
Mortels® Classic style is now in this ultra short length. Made from 100% sheepskin upper and innersole has an EVA hard wearing but lightweight flexible sole and comes with added reinforcement by way of an extra outer layer of suede all over and a stiffened suede heel support all for greater strength and abrasion resistance. The height of the ugg measures 16.5cm for a size 5 to 17.5 cm for a size 11.
Clothing & Footwear > Men - Footwear
Delivery Detail
Items that are in stock are sent via Australia Post or Fastway Couriers (our choice), registered and insured, within 3 working days of receipt of order and payment. Out of stock items will be made and posted within 21 days. We will notify you within 3 day
Returns and Warranty details
We stand by our products and offer a total quality guarantee. Our products will be free from any material defects or faulty workmanship however if a defect manages to slip thru undetected prior to sale, this defect will become apparent within 90 days and you will receive 100% of the purchase price by either an exchange or refund. Wear and tear is not covered by guarantee. Warranty on seat covers extends beyond 90 days and details of warrantly are available on our seat cover category page. Variations in colour and texture in sheepskins or its wool should not be regarded as a fault. These are unique traits of a natural product. Should you experience a problem with your order within 90 days of purchase and need to return your order, please follow the directions given once you have contacted us. Please note that if returned item is found not to be defective in either manufacturing or materials but rather have symptoms of wear, then you will be required to pay for return of product to yourself. Some wear and tear issues not covered by our footwear warranty, regardless of the age of the footwear, include but not limited to: toe blow-outs (holes in the toe area), forced tears and mouldy/rotten footwear. NB. Warranty becomes void (regardless of the age of the item) if item is not worn or kept in accordance with the manufacturers recommendations as per our care and cleaning information.
Excellent Product


text:
Product Groups
Getting Started
Keep track of products you're interested in, view trading data and access all your contracts in a single location.
Intraday Data
Subscription Based Data
Learn why traders use futures, how to trade futures, and what steps you should take to get started.
The Fed now releases economic projections four times a year (March, June, September, and December). Traditionally, the Fed forecasts covered GDP, the PCE price index, and the civilian unemployment rate. However, the forecast report additionally now includes forecasts for the appropriate timing of the next change in the fed funds rate and the expected fed funds rate at the end of the next two years. As of March 20, 2013, the forecasts are released at the same time as the FOMC statement which is 2:00 p.m. ET and 30 minutes prior to the Fed chairman's press conference which addresses the forecasts and Fed policy in general. The forecasts are a composite of individual forecasts by each Fed governor and each District president and cover two to three years out on an annual basis. The GDP, inflation, and unemployment numbers are published as a "central tendency" and also as a range. The central tendency is an average of the forecasts after the highest and lowest forecasts are removed. The range shows the highest and lowest forecasts for these indicators.
CME Group is the world's leading and most diverse derivatives marketplace. The company is comprised of four Designated Contract Markets (DCMs). Further information on each exchange's rules and product listings can be found by clicking on the links to CME, CBOT, NYMEX and COMEX.
CME Group / Chicago HQ
Phone: +1 312 930 1000
Toll Free (US Only): +1 866 716 7274
© 2019 CME Group Inc. All rights reserved.
Careers | Site Map | Disclaimer | Privacy Policy | Cookie Policy | Terms of Use | Modern Slavery Act Transparency Statement