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There is compelling evidence that obstructive sleep apnoea (OSA) can affect metabolic syndrome (MetS) and cardiovascular risk, but the intermediate mechanisms through which it occurs have not been well defined. We explored the impact of OSA in morbidly obese patients with MetS on adipokines, pro-inflammatory markers, endothelial dysfunction, and atherosclerosis markers.
We included 52 morbidly obese patients in an observational study matched for age, gender and central obesity in 3 groups (OSA-MetS, Non-OSA-MetS, and Non OSA-non-MetS). Anthropometrical, blood pressure, and fasting blood measurements were obtained the morning after an overnight polysomnography. VEGF, soluble CD40 ligand (sCD40L), TNF-α, IL-6, leptin, adiponectin, and chemerin were determined in serum by ELISA. OSA was defined as apnea/ hypopnea index ≥ 15 and MetS by NCEP-ATP III.
Cases and control subjects did not differ in age, BMI, waist circumference, and gender (43 ± 10 years, 46 ± 5 kg/m2, 128 ± 10 cm, 71% females). The cases had severe OSA with 47 (32-66) events/h, time spent < 90% SpO2 7% (5%-31%). All groups presented similar serum cytokines, adipokines, VEGF, and sCD40L levels.
In a morbidly obese population with established MetS, the presence of OSA did not determine any differences in the studied mediators when matched by central obesity. Morbidly obese NonOSA-NonMetS had a similar inflammatory, adipokine VEGF, and sCD40L profile as those with established MetS, with or without OSA. Obesity itself could overwhelm the effect of sleep apnea and MetS in the studied biomarkers.
Salord N; Gasa M; Mayos M; Fortuna-Gutierrez AM; Montserrat JM; Sánchez-de-la-Torre M; Barceló A; Barbé F; Vilarrasa N; Monasterio C. Impact of OSA on biological markers in morbid obesity and metabolic syndrome. J Clin Sleep Med 2014;10(3):263-270.
Metabolic syndrome (MetS) is a cluster of metabolic and cardiovascular abnormalities (central obesity, impaired glucose metabolism, hypertension, hypertriglyceridemia, and lower high-density lipoprotein cholesterol) that is associated with an increase in cardiovascular morbidity and mortality.1,2 There is increasing evidence, mainly from studies in moderately obese sleep-referred patient cohorts, that obstructive sleep apnea (OSA) may impact negatively on MetS or some of its components, independent of the body mass index (BMI).3 Furthermore, in a large cross-sectional study of non-selected morbidly obese patients with a high prevalence of MetS,4 OSA was associated with a worse metabolic profile independent of BMI, suggesting that OSA plays an important role in the pathogenesis of metabolic dysfunction, even in morbid obesity.
Current Knowledge/Study Rationale: There is evidence that obstructive sleep apnea (OSA) can affect metabolic syndrome (MetS) and cardiovascular risk even in morbid obesity, but the intermediate mechanisms through which this occurs have not been well defined.
Study Impact: In a morbidly obese population with established MetS, the presence of OSA did not determine any differences in inflammatory, adipokine, VEGF, or sCD40L profile. Obesity itself could produce a ceiling effect on sleep apnea and MetS in the studied intermediate biomarkers.
OSA stimulates, mainly through intermittent hypoxia, several intermediate mechanisms including oxidative stress, inflammation, sympathetic activation, and endothelial dysfunction that are potentially harmful to the cardiovascular system and metabolism.5 OSA could also increase visceral fat dysfunction, which could play a pivotal role in the relationship between obesity and MetS.6 Visceral fat is now considered a highly active organ that produces a variety of molecules, such as inflammatory cytokines and adipokines (e.g., leptin and adiponectin); these also modulate mechanisms related to metabolic dysfunction, such as oxidative stress, inflammation, and sympathetic activation, and they are also involved in the progression of arteriosclerosis, the key factor for cardiovascular risk.6 More specifically, one recently described adipokine, chemerin, highly expressed in adipose tissue, is thought to play an important role in metabolic lipogenesis, glucose homeostasis, and adipocyte differentiation.7
Many experimental and clinical studies have explored the possible underlying interaction between OSA, obesity and MetS, but there has been no clarification to date of the impact of each entity on the intermediate mechanisms related to pathological consequences.3 Given the concern about the confusing effect of obesity, most clinical studies match patients for BMI to assess differences between OSA patients and controls without OSA. The BMI could be insufficient, however, as abdominal visceral fat is a stronger risk factor than other fat deposits for adverse health consequences such as hypertension, insulin resistance, diabetes, and the metabolic syndrome.8,9 Waist circumference (WC) has been considered a surrogate marker of visceral adiposity.10 However, no studies matched by WC have focused on the effect of OSA on MetS and its pathogenic pathways in morbidly obese patients.
As an association between OSA and MetS has been observed even morbidly obese patients,4 in the present observational study, we investigated how the presence of OSA could be associated with alterations in three of the main known pathways involved in MetS and atherosclerosis, its underlying physiopathological process. For this purpose we compared the synthesis of several adipokines, including chemerin, pro-inflammatory markers and endothelial dysfunction markers in morbidly obese patients with MetS with and without OSA, as well as a third group of morbidly obese patients without MetS and without OSA and we matched them for waist circumference.
We included patients with MetS criteria from a previous published morbid obesity cohort of 159 patients from 3 university hospitals.4 Patients with and without OSA were matched for age, gender, and waist circumference (as a measure of central obesity). The patients included were determined by the ability to match pairs from the previous cohort. To explore the effect of morbid obesity alone, we also included a third group without MetS and without OSA, matched by the same confounders. The study protocol was approved by the ethics committee of each hospital (PR052/08, 07/064/797, PI080277). All participants gave informed written consent.
Each participant completed a detailed questionnaire on medical history, cardiovascular risk factors, and current medication. Anthropometric characteristics included BMI, neck circumference (at the level of the laryngeal prominence), waist circumference (WC, measured midway between the lowest rib and the iliac crest), waist/hip ratio, and percentage of body fat mass measured with electrical bioimpedance (BIA 101, Akern Bioresearch, Florence, Italy). Blood pressure was measured by a standard mercury sphygmomanometer while the subject was seated at rest; the mean value of ≥ 2 measurements was calculated.
OSA was determined by a full overnight polysomnography (Siesta, Compumedics, Abbotsford, Australia). Polysomnography interpretation was assessed according to the standard criteria of Rechtschaffen and Kales. Apnea was defined as a cessation of flow ≥ 10 sec and hypopnea as 30% to 90% flow reduction for ≥ 10 sec accompanied by a fall ≥ 3% in oxyhemoglobin saturation (SpO2) and/or a microarousal. The apneahypopnea index (AHI) was the total number of such events per hour of sleep. An AHI of 15 events/h was chosen to define the presence of OSA according to the study design. The degree of nocturnal desaturation was assessed by the mean percentage of sleep time with SpO2 below 90% (Time SpO2 < 90%). Excessive daytime sleepiness was evaluated by the Epworth Sleepiness Scale (ESS).
The morning after polysomnography (08:00-09:00), a venous blood sample was obtained from all patients in fasting conditions. Fasting blood glucose (FBG), percentage of glycosylated hemoglobin (HbA1c), total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and very low-density lipoprotein (VLDL) cholesterol levels were determined with standard laboratory methods. Insulin was determined by the automated chemiluminescence method (Advia Centaur, Siemens, NY, USA) with a sensitivity of 0.5 mU/L and an inter-assay coefficient of variation of 7.5%. Insulin resistance was estimated using the homeostasis model assessment (HOMA) score, defined by fasting serum insulin mU/L × fasting plasma glucose mmol/L/22.5. MetS was defined according to the NCEP-ATP III modified criteria.1
Blood samples obtained in tubes without anticoagulant were centrifuged immediately; the resulting serum was stored in aliquots at -80° C until analysis. Measurements were always made in duplicate, and the mean values were used for analysis. Biomarker levels were determined by enzyme-linked immunosorbent assay using commercially available kits: vascular endothelial growth factor (VEGF) (Invitrogen, California, USA); soluble CD40 ligand (sCD40L) (R&D Systems, Minneapolis, USA); tumor necrosis factor α (TNF-α) (Invitrogen California, USA); interleukin 6 (IL-6) (Invitrogen California, USA); leptin (SPI-BIO, Montigny, France); adiponectin (SPI-BIO, Montigny, France) and chemerin (USCN Life Science, Wuhan, China). See online data for information about assay sensitivity and inter- and intra-assay coefficients of variation (Table S1).
Patients were matched by a weighted Manhattan distance based on the normalized variables calculated between patients. Each patient from one group was matched with another in the other group with the lowest distance from him/her. If the matching was performed in a 1:2 proportion, each patient was matched to the 2 patients in the other group with the lowest distance from him/her. Sample size was determined by the ability to match pairs from the previous cohort.
Results are shown as median and interquartile range. Due to the skewed distribution and sample size, comparisons among the 3 groups were performed with the Kruskal-Wallis test, with post hoc Bonferroni correction for multiple comparisons. Correlations between variables were explored using the Spearman test. Statistical significance was defined as p < 0.05.
Twenty-six patients with OSA and MetS (OSA-MetS) criteria were matched with 13 non-OSA patients with MetS (non-OSA-MetS) and 13 non-OSA and non-MetS controls (non-OSA-non-MetS). Cases and control subjects were similar in age, weight, and waist circumference, as expected (Table 1). The 3 groups had similar BMI and neck circumference, and there was a nonsignificant trend toward higher fat mass in the 2 MetS groups (Table 1). As usual in morbid obesity, the cohorts were mainly composed of premenopausal women. Although the OSA-MetS patients were taking more medication and had higher previously diagnosed hypertension, there were no differences between the groups regarding drugs used or smoking status (Table 2). Post hoc analysis only showed a significant difference in the higher use of statins in OSA-MetS patients with respect to non-OSA -non-MetS patients.
Patients' general characteristics: matched 1:1 and 1:2 by waist circumference, age and sex.
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Previous diseases and treatments: matched 1:1 and 1:2 by waist circumference, age and sex.
The OSA-MetS patients had a high AHI with a median and interquartile range (IQR) of 47.1 (32-66) events/h, Time SpO2 < 90% 7% (5%-31%), and a mean and minimal night oxyhemoglobin saturation of 92% (90%-93%) and 73% (65%-81%), respectively (Table 3). Although OSA patients had higher arousal indexes, all the groups had similar sleep efficiency and sleep stage percentages. No differences between the groups were encountered in physical activity measured by the IPAQ questionnaire or sleep hours measured by the sleep diary (Table 3).
Patients' sleep characteristics: matched 1:1and 1:2 by waist circumference, age and sex
As regards the MetS components, there were significant differences in systolic and diastolic blood pressure, triglycerides, HDL cholesterol, and fasting glucose. These differences were, as expected, mainly the result of the more favorable metabolic profile of the non-OSA-non-MetS obese group (Table 4). Although there was a significant trend of OSA-Mets patients with higher triglycerides and lower HDL cholesterol levels, no differences were found in the post hoc analysis between MetS patients with and without OSA (Table 4). When glucose metabolism was further analyzed, no differences were found in fasting insulin, the HOMA index, or glycosylated hemoglobin (Table 4). OSA-MetS patients tended to present a pattern of more impaired liver enzymes, but this was only significant for alanine aminotransferase. Figure 1 shows the distribution of MetS components in the 3 groups.
Patients' metabolic characteristics: matched 1:1and 1:2 by waist circumference, age and sex.
Distribution of metabolic syndrome components between the three groups.
All the groups presented similar serum levels of cytokines (IL-6, TNF-α), adipokines (leptin, adiponectin, and chemerin), VEGF, and sCD40L (Table 5). No correlation was found between the biomarkers and any OSA variable (data not shown). Leptin was closely correlated with the anthropo-metric variables (BMI [r = 0.479, p < 0.001], waist-to-hip ratio [r = -0.598, p < 0.001], and fat mass [r = 0.401, p = 0.004]), while adiponectin was correlated negatively to waist-to-hip ratio (r = -0.598, p < 0.001), waist (r = -0.407, p = -0.003), and neck circumference (r = -0.406, p < 0.003) and VEGF with fat mass (r = 0.3, p = 0.021).
Biological markers: matched 1:1 and 1:2 by waist circumference, age and sex.
The present study is the first to explore the effect of OSA on the many known mechanistic pathways that may contribute to MetS in a non-selected morbidly obese population. In this extremely obese population with established MetS, the presence of OSA did not produce any differences in serum cytokines (IL-6, TNF-α), adipokines (leptin, adiponectin and chemerin), or VEGF and sCD40L levels, as no difference was found between OSA and non-OSA patients with MetS matched by central obesity. Morbidly obese patients without both established MetS and OSA already have a similar biomarker-altered profile.
The relationship between OSA and MetS or some of its components has been established, mainly through cohorts referred by sleep units with concomitant mild-to-moderate obesity.3 The major limitation of these studies is the control of obesity itself, as this is the main confounding factor and is often adjusted by multivariate analysis. To address this issue, Barceló et al. excluded patients with obesity and matched a sleep unit-referred cohort by BMI; OSA patients showed higher levels of free fatty acids, CRP, and oxidative stress markers.11 Trombetta et al. matched MetS patients by BMI with and without OSA; they demonstrated that in this high-risk cardiovascular population with moderate obesity, OSA was associated with greater sympathetic drive.12 Moreover, there have been few case-control studies that matched patients by central adiposity to study the effect of OSA on the different components of MetS13 and the different biomarkers14 related to both conditions. It is therefore important to establish whether OSA and its associated metabolic abnormalities are independent of central obesity.
Our study focused on an extremely obese population, composed mainly of premenopausal women, in which we previously showed an association of OSA with a worse metabolic profile, mainly through systolic blood pressure, triglycerides, and Hb1Ac, after adjusting by BMI and waist circumference.4 In order to explore the possible mechanistic pathways explaining this association, we matched MetS patients according to their OSA status by waist circumference as a surrogate marker of central obesity. Patients in the OSA-MetS group had greater metabolic impairment than non-OSA-Non-MetS patients. Moreover, when we compared the two MetS groups, as well as fulfilling MetS criteria, the MetS-OSA group had a tendency toward higher hypertriglyceridemia, lower HDL-cholesterol levels, higher levels of liver transaminases, and greater requirements of antihypertensive treatment. This fact did not determine any differences in the studied biomarkers between OSA and non-OSA in MetS patients. In the study by Barceló et al., in the non-obese population only OSA patients without MetS had higher levels of free fatty acids, as no significant differences were found in biomarkers between OSA and non-OSA in patients with established MetS.11 Surprisingly, when we reviewed the non-OSA-non-MetS patients, there were no differences in the biomarkers explored. Those patients who supposedly constituted the metabolically healthier group in fact presented lower blood pressure, serum triglyceridemia, and fasting glucose, while their HDL cholesterol was higher, although they already had the same biomarker profile. Metabolically healthy obesity is defined by a normal sensitivity to insulin and a normal lipid profile, and it is related to lower levels of inflammation and higher adiponectin concentrations.15,16 While American studies have shown that 30% of the obese population can be considered metabolically healthy,17 only 5% of morbidly obese patients were found to be metabolically healthy.18 In our study only three non-OSA-non-MetS patients had obesity as the sole criterion for MetS, and they also presented high HOMA-R indices. We could thus speculate that the lack of differences in the studied biomarkers could be evidence of an already adverse pre-pathological status, even in patients without established MetS in morbid obesity. Therefore, in this extremely obese population, patients without OSA or MetS already have an altered mediator pattern; if we assume the previously demonstrated effect of OSA on metabolic abnormalities, then OSA must stimulate another specific mechanism to trigger MetS, independent of those activated by obesity.
Inflammation has been recognized as an intermediary mechanism associated with insulin impairment, MetS, and cardiovascular disease.19,20 Many cross-sectional, case-control, and non-randomized interventional studies have suggested that the levels of the pro-inflammatory cytokines and C-reactive protein are elevated in OSA patients.21,22 These results have not been consistent, however, as contradictory findings have been reported in studies by both our group and others, in which this association was attributed mainly to obesity.23,24 Furthermore, obese patients are resistant to leptin, which mainly serves to regulate appetite and energy expenditure. In clinical studies, leptin has been correlated with insulin levels and BMI, and it predicts the development of MetS.25,26 Leptin was the first adipokine associated with OSA and its levels have proved to be higher in OSA patients. Vogontzas et al. found, however, that elevated leptin levels were more closely related to visceral fat and other pro-inflammatory markers than to AHI.27 This could explain the ceiling effect in the morbidly obese population in our work. Our study does not reveal any new information about adiponectin. Hypoadiponectinemia has been postulated as playing a role in the development of MetS,28 as adiponectin regulates insulin sensitivity and has an anti-inflammatory and protective vascular effect. The studies of OSA to date are not conclusive, as some have found lower levels in OSA patients, but others such as ours have failed to show this down-regulation.29,30 As an original contribution, we explored chemerin as a novel adipokine. Clinical studies have shown that patients with MetS have higher levels of chemerin than those without MetS and present an association with BMI, serum triglycerides, and blood pressure.31 A recent case-control study with a moderately obese Asian population showed that OSA patients had higher chemerin levels and found a weak but positive correlation with sleep apnea severity and WC and BMI32; in this study chemerin was also correlated with inflammation and hypothesized as a possible a link between adipose tissue, OSA, and inflammation. These results could not be confirmed in our morbidly obese population with high indices of insulin resistance, where we found that central obesity had a stronger effect than OSA.
Apart from systemic inflammation and adipokine discharge, the main direct consequences of obstructive apneas—intrathoracic pressure changes, recurrent arousal, and intermittent hypoxia—also trigger an increase in sympathetic nerve activity, reduce baroreflex sensitivity, and cause endothelial dysfunction. These changes induce increased arterial stiffness and arterial hypertension, leading to the development of atherosclerosis.33 In order to explore the latter mechanisms, we analyzed VEGF and sCD40 serum levels. VEGF is thought to promote atherogenesis through endothelial cell proliferation, cell migration, and increased vascular permeability.34 Previous clinical studies have shown higher levels of VEGF in OSA patients than in controls,35,36 mainly as a result of hypoxia. Our results were limited by the great variability in VEGF in the sample, which prevented us from finding any differences between groups. At the same time, the presence of OSA did not suppose any effect on sCD40L levels. sCD40L is considered a surrogate marker of arteriosclerosis, part of a mechanism signalling platelet activation, and it is associated with increased cardiovascular risk.37 Nevertheless, we could not rule out a role for other known intermediate mechanisms, such as increased sympathetic activity (not explored in our study), in the link between MetS, cardiovascular morbidity, and OSA in morbidly obese patients. A review of the randomized controlled interventional trials shows that Dragger et al. found an improvement in early signs of the atherosclerosis markers, C-reactive protein, and urine catecholamines in severe OSA after four months of CPAP, but their patients, unlike ours were only overweight and were otherwise free of any comorbidity.38 Further studies focusing on patients with milder obesity39,40 did not observe any changes in systemic inflammation, insulin resistance, blood lipids, leptin, or adiponectin. Similarly, West et al. also failed to find any changes in C-reactive protein and adiponectin after CPAP treatment in a population of OSA patients with established diabetes and more severe obesity.41 Taken together, these data and our own reinforce the idea of the overwhelming effect of obesity and comorbidities on the studied markers.
Our study has a number of potential limitations that should to be considered. Firstly, because of the cross-sectional descriptive nature of the study, it did not provide evidence of a cause-effect relationship. Secondly, the size of the study was limited by the prior cohort study and the need to match patients from the different groups. In order to include the maximum number of patients we performed a 2:1 match, since OSA patients were much more prevalent in our population. Although the sample size limits the power of the study, we were unable to find any trend in any biomarker explored, which makes it probable that morbid obesity itself exerts a possible ceiling effect. Finally, as mentioned above, our patients, as a clinical population, were undergoing active hypolipemia, antihypertensive, and hypoglycemia treatment that could interfere with the determination of metabolic profiles and biomarkers and minimize the difference between groups.
We could not find any distinct biomarker pattern of OSA in a morbidly obese population, nor did the studied biomarkers allow us to discriminate between patients with and without MetS in this population. Severe central obesity thus seems to trigger an array of downstream effects that overwhelm those possibly caused by intermittent hypoxia and sleep fragmentation in the mediators studied in this extremely obese population. As an independent association between metabolic abnormalities and OSA has been demonstrated not only in the general clinical population but also in high-risk cardiovascular and morbidly obese populations, we cannot rule out this being produced by other unexplored pathways. The absence of differences in the studied biomarkers between the groups does not detract from the importance of detecting OSA in morbidly obese patients, since it is a treatable condition with a great impact on health. It is therefore mandatory to perform further controlled studies to explore other pathways that could explain this relationship and enhance our understanding of the link between obesity, OSA, and cardiometabolic dysfunction, and our search for future treatment targets.
Fondo de Investigación Sanitaria [Grant: FIS PI080800]; Spanish Respiratory Society SEPAR [Grant: Ayudas a la investigación 249/07]; Societat Catalana de Pneumologia SOCAP [Grants: 2052/08; 2052/09]. Fundació Catalana de Pneumologia FUCAP 2009. Study Supported by Air products. The authors have indicated no financial conflicts of interest.
apnea-hypopnea index
body mass index
Epworth Sleepiness Scale
fasting blood glucose
percentage of glycosylated hemoglobin
high-density lipoprotein
homeostasis model assessment
interleukin 6
low-density lipoprotein
metabolic syndrome
obstructive apnea-hypopnea syndrome
soluble CD40 ligand
arterial oxygen saturation by pulse oximetry
Time SpO2 < 90%
percentage of sleep time with SpO2 below 90%
tumour necrosis factor α
vascular endothelial growth factor
very low-density lipoprotein
waist circumference
M. Clarke assisted with the English expression in versions of the manuscript. Advice on the statistical analysis was given by Daniel Quadras (IDIBELL, Barcelona, Spain). The authors thank the sleep unit staff of the Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Spain, Tomas Brinquis, Pilar Garriga, Sandra Perez, Neus Martí, Carme Rodríguez, Rosa Miralda, Ariadna Farré and Montserrat Carreras from the Hospital de la Santa Creu i Sant Pau, Barcelona, Spain for their inestimable collaboration.
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West SD, Nicoll DJ, Wallace TM, Matthews DR, Stradling JR, authors. Effect of CPAP on insulin resistance and HbA1c in men with obstructive sleep apnoea and type 2 diabetes. Thorax. 2007;62:969–74. [PubMed Central][PubMed]
Assay characteristics


text:
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subset: commoncrawl


text:
I just read a proof in a complex analysis book that says there exists a biholomorphic (conformal) map between $\mathbb{H}$ and $\mathbb{D}$ and I don't understand one step in the proof, namely the norm of the map (in the title) is less than $1$, using a purely "geometric" argument (i.e. a picture was in the book). I don't understand "geometric division", so I don't immediately see the proof "geometrically", please I do NOT want an algebraic answer (this is fairly straight forward anyway).
Note that $|i-z|$ is the distance between $z$ and $i$, and that $|i+z|$ is the distance between $z$ and $-i$. The inequality says that $z$ lies closer to $i$ than to $-i$, which is true for points in the upper halfplane.
To make this even more clear, write $\bigl|{i-z \over i+z}\bigr|={|i-z|\over |i+z|}<1$, and multiply through by the denominator $|i+z|$.
The real axis is in the middle between $i$ and $-i$, hence is the locus of all points having the same distance from $i$ and $-i$. The rest of $\mathbb C$ splits into those points closer to $i$ than to $-i$ (the upper half plane) and those closer to $-i$ (lower half plane).
Basically you want to prove that any point in $\mathbb{H}$ is closer to $i$ than to $-i$. Draw the triangle with vertices at $i, -i, z$ and observe that the angle at $-i$ is smaller than the angle at $i$. he easiest way to prove this is by extending the line through $i z$ till it intersects the real axix at $y$ and compare the angles in the triangle $i,-i,z$ with the angles in $i,-i,y$.
The norms of $i - z$ and $i+z$ are the squares of the distances between $z$ and $\pm i$. A point $z$ lies in the upper half plane if and only if it is strictly closer to $i$ than to $-i$, so that this ratio has norm strictly less than $1$ and so lies in the unit disk.
|z-i|=|z+i| is the set of points equidistant from $i$ and $-i$, the real line. |z-i|<|z+i| is the set of points closer to $i$ than $-i$, the upper half plane.


text:
This time I am going to announce an event to which we never had a similar predecessor: On November 5th, 2012, we will conduct a Microsoft Azure Compute Tutorial with speakers from the European Microsoft Innovation Center in Aachen. What we mean with "compute" is not quite what HPC people might think of as computing. The rationale is the following:
Cloud computing enables the usage of computing resources provided as a service via a network (e.g. the internet). One cloud platform is Microsoft's Windows Azure. It can be used to build, deploy and manage applications in the cloud, which hereby consists of Microsoft-managed data centers. This workshop will introduce Microsoft Azure facilities with a focus on compute services. In the morning of this tutorial, we will introduce you to Azure computing, storage and services. For interested participants, there will be a hands-on session after lunch, in which an example application will be created step-by-step. More details and the link for registration can be found at the event website.


text:
Trade and Consequences
Trade and Consequences
The globalization of trade is having some unexpected-and unwelcome-effects.
Walk into any Wal-Mart, Target, or Sears store in the United States, pick out a selection of goods from the shelves, and look at the manufacturer's label. The portable DVD player for your teenage daughter costs less than $100 and is made in Singapore. The silk-screen T-shirt with the cartoon characters for your 7-year old son is less than $15 and labeled "Made in the Philippines." The new wrenches for your garage toolkit cost half of their American counterparts; they're made in China, as is the new microwave for your home office. The sleek LCD monitor for your family's computer comes from Korea. In fact, chances are that more than 75 percent of the small manufactured goods in your shopping cart were made in Asia and hauled by container ship across the Pacific.
It is not news that U.S. stores sell many imported products. The United States has always been a trading nation and its role in international trade has grown steadily during the last several decades. But it has been 30 years since the United States exported more than it imported. In 2004, when U.S. international trade totaled $2.9 trillion, imports exceeded exports by more than $620 billion.
The largest contributors to the U.S. trade deficit are imported oil and manufactured goods. Although oil represents the largest dollar fraction of U.S. foreign trade, the growing flood of imported manufactured goods is having equally profound effects. As the United States shifted from a manufacturing-led to a service-oriented economy, mainland Asian economies filled the gap. Lower Asian labor costs and less stringent environmental regulations translated into lower production costs, more than counter-balancing the expense of international marine freight shipping. (China is now the largest source of manufactured imports in the United States, except for automobiles, and is the second biggest U.S. trading partner.)
These new Asian imports, along with goods arriving from other countries, have resulted in a flood of marine freight that is swamping U.S. ports and overwhelming nearby communities.
Most manufactured imports arrive on container ships, and the resulting growth in marine container freight is creating grave new technological, environmental, economic, and national security challenges. These challenges are especially acute in the United States but have implications for many nations caught up in the economic web of trade.
Sea Changes
Containers are rectangular aluminum or steel boxes, typically 6-12 meters in length. Invented in 1956, containers and the ships built to carry them have revolutionized marine freight. It's no exaggeration to say that container ships are taking over the world's general cargo fleet. In 2003 they carried 75 percent of general cargo along a virtual marine highway.
The pressure to reduce marine freight costs is driving technological evolution in the international shipping industry. One response has been to minimize both fuel use and manpower per ton-mile by steadily increasing the carrying capacity of ocean-going container ships. A second approach has been to modernize port management and dockside cargo handling in order to increase cargo throughput and decrease ships' idle "dwell time" in ports.
Container ship capacity has ballooned dramatically in the last 40 years. Ship size is measured by the number of standard containers, called 20-foot equivalent units (TEU), a ship can carry on its decks and in its holds. Third-generation container ships, built in the mid-1980s, carry about 4,000 TEU. These so-called PanaMax ships are the largest freighters that can pass through the Panama Canal. By comparison, fourth- and fifth-generation ships with capacities between 4,200 and 7,600 TEU are too big to use the Panama Canal and must travel other routes. Although the Port of Long Beach can dock ships up to 8,000 TEU, most ships in this class are too large to dock at U.S. ports. Beyond these "MegaShips," several containerized cargo vessels being designed today have capacities approaching 15,000 TEU. When built, they will be the largest cargo ships able to transit the Suez Canal. The Dynamar Consultancy in Rotterdam, the Netherlands, has predicted that ships of 18,000 TEU will be built by 2010. These ships are designed to haul containerized cargo at costs of only $0.07 per ton-mile, compared to $0.10 per ton-mile achieved by today's PanaMax ships. These ships will be barely able to float through the Straits of Malacca and will be unable to dock using existing facilities at most of the world's historically important ports.
MegaShips are beginning to dominate both shipbuilders' order books and the current fleet of container ships at sea. The aggregate global capacity of containerized MegaShips grew by 44 percent annually from 2001 through 2005. Twenty container ships with capacities exceeding 7,000 TEU were added to the global fleet in 2004 (compared to seven such ships added in 2003). More than 100 of the 167 new vessels on shipbuilders' order books in 2005 are MegaShips.
The arrival of PanaMax and larger container ships at U.S. and other international ports creates a need for dramatic changes in dockside cargo-handling and transfer facilities. Before container ships, virtually all freight except bulk cargo was packed on pallets and skids, then off-loaded by teams of longshoremen using shipboard cranes and hand-held cargo hooks. This is no longer the case.
Today's ports are not just points of entry but function as a "mini-land bridge," integrated with specialized facilities to transfer containers to railroad cars or trucks for overland shipment. Thus, a container of DVD players and other electronic goods from China may move across the Pacific on a container ship, land at Los Angeles, and transfer to a truck for a trip to Fresno or to a rail car that will haul it across the continent to New York City. At the Port of New York, the container might be put on a truck for delivery to a Connecticut Wal-Mart or loaded back onto another container ship bound for Europe. Efficiently handling the enormous cargo loads that arrive on MegaShips requires sophisticated cargo-tracking information systems as well as automated loading and transfer facilities.
U.S. ports, however, are strapped with aging infrastructure, and even the current demand for imported freight pushes most of them well beyond their design capacity. Yet the goods just keep on coming. Demand for cargo throughput is projected to double at all major U.S. international ports between 2010 and 2020. Demand at the San Pedro Harbor ports of Los Angeles and Long Beach, California, for instance, is projected to reach twice the current volume by 2015.
As a result of the continuing mismatch between existing infrastructure and growing demand for off-loading facilities, many U.S. ports frequently experience dockside gridlock. More than 5,000 ships transited the Port of Los Angeles in 2004, a facility designed for about 1,800. On October 12, 2004, a record 94 ships passed through, almost twice the target maximum of 50 ships per day. One day in September 2004, more than 60 ships sat off-shore waiting to dock. All docks were occupied and there was a shortage of longshoremen. Local railroads were groaning under their loads and trucking firms struggled to find tractors and drivers. Some ships sat at anchor as long as 10 days. Throughout the year, local authorities diverted nearly 120 ships carrying cargo worth over $4 billion to other ports.
Aging dockside infrastructure, shortages of skilled labor, and chokepoints along rail and truck routes sap the productivity of U.S. ports. But not only do these problems slow the movement of goods to store shelves, they radiate out from the docks, punishing portside communities with noise, air pollution, and congestion. The I-710 freeway, for example, is the primary artery for freight leaving the ports of Los Angeles and Long Beach. Average daily traffic volume on I-710 exceeds 240,000 vehicles, including more than 34,000 heavy trucks leaving the ports. The current daily volume exceeds the design capacity of the freeway, frequently leading to extreme traffic congestion and serious traffic accidents. Nonetheless, heavy truck traffic exiting the ports is projected to grow steadily, exceeding 90,000 vehicles per day by 2025. Many experts forecast that increasing truck traffic will cause I-710 traffic to grind to a halt every morning, with traffic stalled all the way from the San Pedro ports to the I-5 interchange, 30 kilometers (18 miles) away. A spokesman for the Los Angeles Economic Development Corporation told the Los Angeles Times in October 2004, "The U.S. cargo system has reached its maximum capacity and there has been a steady growth in imports, while there is no coherent expansion plan for transportation."
Hidden Costs
The flow of containerized freight through U.S. ports brings cheap goods into the U.S. economy. However, there are already significant negative social and environmental impacts from marine freight traffic, and these fall disproportionately on the mainly low-income residents of portside communities, who must endure the congestion, noise, and pollution of freight-related activities.
Each day, congestion on U.S. docks creates long queues of waiting trucks. Their engines idle for extended periods before they inch out of harbor areas, noisily traversing the neighborhood streets of portside communities where they compete for space with children at play.
But noise and crowding are not the only problems visited on portside communities. Freight-related emissions (from both trucks and ships) are a major source of local exposure to carbon monoxide, nitrogen dioxide, ozone, and other "criteria pollutants" and carcinogenic particulates. The California Air Resources Board says that port-related activities will be the dominant source of smog-causing nitrogen oxide (NOX) emissions in the South Coast Air Basin by 2020, out-distancing traditional Los Angeles-area culprits like gasoline-fueled cars and industrial facilities.
Similar trends are projected for the small particulate matter emitted from both ships and trucks in diesel engine exhaust. PM10 particulates, with average diameters of less than 10 microns, are easily inhaled. The current average PM10 daily emissions of the Port of Los Angeles are substantially greater than the average emissions from a typical U.S. refinery or the daily particulate emissions from 500,000 U.S. cars. The U.S. Environmental Protection Agency (USEPA) estimates that by 2030 marine diesels will account for 60 percent of nationwide emissions of the smallest and most dangerous particulates, called PM2.5.
California officials say that diesel emissions account for 80 percent of overall cancer risks from exposure to toxic air pollutants. A recent epidemiological study of 54,000 railroad workers exposed to diesel exhaust in their work environment found that long-term exposure to diesel particulates led to a significant increase in the incidence of death from lung cancers. Internal USEPA memos confirm that extended exposure to diesel exhaust is also likely to increase incidence of chronic, non-cancer health effects in vulnerable populations, especially children and seniors.
Murkier and more dangerous air is not the only environmental damage inflicted by marine trade. As container ships and other marine cargo vessels grow in size, they require ever-larger quantities of ballast water to stay upright. The huge ballast tanks, which are filled with seawater, create inviting habitats for all sorts of aquatic hitchhikers. Invasive species carried in ballast water can be as simple as single-celled plankton, which form the base of the aquatic food web. Once established, foreign plankton species may out-compete local counterparts due to lack of native predators, and may cause organisms further up the food chain to starve for lack of their own favorite "delicacies."
Larger species travel in the tanks as well. The European green crab, for instance, has been found in various locations along the U.S. Atlantic and Pacific coasts. Green crabs devour native mollusks, crustaceans, and algae. They appear to be undermining U.S. scallop fisheries as well as the Dungeness crab fishery on the Pacific Coast. The Eurasian Ruffie, a freshwater perch first inadvertently imported in some freighter's ballast water in the 1970s, has successfully colonized the far western edge of Lake Superior. This aggressive freshwater fish spawns up to six times per year, out-competes native fish species, and has become more abundant than any other fish in Lake Superior. The loss to local fisheries from the Eurasian Ruffie was estimated at $120 million in 1994 and continues to grow.
Perhaps the most destructive species to escape from ships' ballast water has been the Zebra mussel. These hardy and prolific bivalves can form colonies incorporating almost 700,000 mollusks per square meter. They clog the cooling water inlets of electric power plants and have caused damages in excess of $5 billion per year in the United States.
Technological defenses against such "free riders" on the gravy train of international trade are very hard to find. There are no "silver bullets" that can safely and cost-effectively treat ballast water, eliminating hitchhikers on all ships hauling cargo today. Although expensive, some treatment options-ultraviolet light or heat, filtration, biocides, and deoxygenation-may soon be ready for full-scale commercial testing against specific types of invasive species. But U.S. policy decisions about how to identify, control, and regulate these threats have not yet been completed, and no political consensus exists on who should pay for such measures. Perhaps any serious efforts to resolve such issues must wait until a foreign invader, like the voracious Chinese snakehead fish, crawls out of the Potomac Tidal Basin and bites a congressman on the ankle.
Vessels that haul 7,000 to 15,000 steel containers into a port at a time carry major risks besides invasive animal or plant species. The containers can provide nearly unlimited opportunities for terrorists and smugglers to hide in plain sight. Any standard cargo container is big enough to smuggle more than a dozen people or conceal a dangerous quantity of weapons, drugs, or explosives.
But it is the sheer volume of containers that creates the most serious risks. Because of the number of containers now passing through U.S. ports of entry, it is virtually impossible for all of them to be opened and inspected without seriously disrupting trade. U.S. ports today are only able to inspect a small sample of the containers. Indeed, a report released by ABC News on the first anniversary of the 9/11 attacks demonstrated how easy it would be to ship radioactive material into the United States undetected. Having borrowed a cylinder of depleted uranium from the Natural Resources Defense Council, the ABC News crew proceeded to package the mildly radioactive material in a lead-lined, steel canister and hide it inside a container full of furniture. The container was off-loaded at the Port of New York/New Jersey, placed on a truck, and delivered without interference to the ABC News offices in midtown Manhattan.
If the cylinder of depleted uranium used in this test had contained an equal volume of more highly enriched uranium, its contents would have been sufficient to make a simple radiological dispersal device (a "dirty bomb"). If it had contained weapons-grade uranium, only slightly more shielding would have been required to keep the much more dangerous material from being detected. The situation at the Port of New York/New Jersey has not improved substantially since September 2002, and the ease with which the operation was executed provides a terrifying reminder of the continuing vulnerability of all U.S. ports, particularly as the volume of container throughput continues to grow. Dealing with these security risks will require the development of nondestructive testing and imaging methods for rapidly examining the contents of each container before it leaves its port of entry.
Containing the Problem
The problems associated with marine freight landing at U.S. ports are profound and multi-dimensional. U.S. ports are outmoded, inefficient, under-capitalized, and already straining under loads that only promise to grow heavier.
Contrast this situation with major Asian and European ports, which are bigger and more agile than their U.S. counterparts. Investments in information technology and advanced logistics management capability have made them more efficient per unit time and per acre of wharf space. As long as 10 years ago, several Asian ports achieved container throughputs of 8,800 TEU/acre/year. European ports moved approximately 3,000 TEU/acre/year. In the last 10 years, the throughput capacity of the most efficient Asian and European ports has increased to over 30,000 and 5,000 TEU/acre/year, respectively. By contrast, the most efficient U.S. ports manage to move only around 5,000 TEU/acre/year today, and U.S. ports continue to under-invest in new technology, giving both Asian and European ports a comparative advantage for years to come.
The Main Container Terminal in Hong Kong is a good example of state-of-the-art port technology. It was designed explicitly to handle frequent off-loadings of large container ships in the most time-efficient and cost-effective manner, deploying a cutting-edge suite of information-intensive container transfer technologies.
Only a handful of U.S. ports are adequately configured even to dock the generation of PanaMax vessels. No U.S. port is currently able to dock and efficiently off-load 15,000-TEU machines or future generations of even larger vessels. Substantial dredging of harbors, the creation of new slips and docks, or the construction of off-shore unloading facilities will be needed to handle the coming generations of container ships now headed toward U.S. ports.
The challenge of operating world-class ports in the United States is not just a problem of small docks or shallow channels. It is fundamentally a systems problem, with demanding elements at every point on the goods movement chain from the dockside arrival of freight to the final point of land-side delivery. These problems will only grow as the volume of marine freight expands over the next decade. If they are ignored, the ever-widening stream of marine freight may have catastrophic consequences for the U.S. economy, for portside communities, and for natural ecosystems.
There is no simple solution for dealing with the economic, social, technological, environmental, and national security challenges arising from the flow of marine freight at U.S. ports. Nothing significant will likely be done until the general public becomes aware of the challenges resulting from our growing demand for imports and understands the trade-offs inherent in increasing reliance on "cheap" goods. Ultimately, a comprehensive, integrated national strategy may be needed to support the smooth and economically efficient operation of the U.S. goods movement system and to avoid the negative impacts of our expanding marine freight trade. Such a strategy can only be implemented through a broadly based, national conversation that invites input from all key stakeholder groups, including importers, shipping companies, port operators, investors, state and local governments, environmentalists, workers, and community groups representing the interests of civil society.
The expanding tide of marine freight is bearing down on the United States like a PanaMax container ship. It is time to look squarely at the problem and recognize that maintaining a sound goods movement system demands a critical investment in national infrastructure.
Irving Mintzer is Executive Editor and Amber Leonard is Managing Editor of Global Change Magazine.


text:
Michael-Bruno LLC - MB-Global.com : Michael-Bruno provides architectural design, engineering services and construction management (A/E/C) to U.S. government agencies in Africa, Europe, and Middle East.
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Michael-Bruno Awarded Seaport NxG Prime Contract
"The Navy has made 1,870 awards for the new version of its massive SeaPort contract for professional services that dates back nearly two decades and pulls in $5 billion a year in task orders," announced Washington Technology last week. The U.S. small business, Michael-Bruno, LLC, is one of those receiving this prime contract.
"The Seaport program has been very good to us over the past decade," said company president, Michael Sedge, "and we look forward to greater success in the Navy market under this 5-year prime award, as well as the 5 year option period."
The Seaport Next Generation (NxG) replaces the Navy's Seaport-e program. Under the later Michael-Bruno has fulfilled several international task orders, including locations like Bahrain and Djibouti.
Michael-Bruno, LLC, is the "mother ship" of a group of international firms located in Europe, Africa and Middle East. Their core business is architectural design, engineering and construction, with additional services in logistics and professional staffing.
For more information: email@example.com
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NAVFAC EURAFSWA Awards Two Seaport-E Task Orders to Michael-Bruno
During a single week period, NAVFAC EURAFSWA has awarded Michael-Bruno wi
Michael-Bruno CEO Authors The EURAFSWA Report, For Contractors Looking to Enter the International Market
SAME's Assistant Vice President for European and CEO of the Michael
Sedge Receives SAME Regional Vice Presidents Medal
Michael Sedge, president of the Michael-Bruno Group of Companies, was presented
Michael-Bruno Part of $45M NAVFAC AOR Worldwide Professional Services Award
The Cardno-Amec Foster Wheeler (Wood) joint venture has been awarded a $45 milli
Michael Sedge is a featured guest on AMERICAN DREAM
Michael Sedge, founder and president of the Michael-Bruno Group and The Sedge G
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Employee Profile: Isman Hadi, Environmental Technician
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NAVFAC EURAFSWA issued a three-year contract to Michael-Bruno, LLC, to p
MACEC Group and Michael-Bruno win $10.6 million NAVFAC Bahrain Award
The United States Navy, Bahrain, has issued a five-year contract, managed an
NAVFAC EURAFSWA Awards Three-Year LPAR Contract to Michael-Bruno
NAVFAC EURAFSWA has issued a three-year contract to Michael-Bruno, LLC, to p
JJ Kirlin and Synergy Award Michael-Bruno D-B Contract for 31st Medical Group Hospital, Aviano Air Base, Italy
The Joint Venture of JJ Kirlin Special Projects and Synergy Project Consulta
Michael-Bruno Receives NEXCOM Award for Architect-Engineer (A-E) Services
The Navy Exchange Command Europe has issued an open purchase, IDIQ contract
Harris Corporation turns to Michael-Bruno for Navy SATCOM Support
In support of the DoD Modernization of Enterprise Terminals (MET) program, H
Michael Sedge, president of Michael-Bruno, LLC and The Sedge Group, LLC, was the host of Optimagazine to promote the Italian edition of Sentinella della Morte (DeathWatch), his latest book.
Bahrain Corporation Established by Michael-Bruno Management
(Manama, Bahrain) - Michael and Bruno Consulting WLL, a company of the Kingdom o
Michael-Bruno President writes feature on Small Business International Expansion
Michael-Bruno President writes feature on Small Business International Expansion
The team of Stanley Consultants, Michael-Bruno, and A/I/Data are performing a installation-wide utility survey and mapping project at Camp Lemonnier, Djibouti.
The team of Stanley Consultants, Michael-Bruno, and A/I/Data are performing a in
NAVFAC Europe, Africa, and Southwest Asia has announced the award of a $2.1 mill
Camp Lemonnier Awards Community Relations Specialist Contract to MB
Michael-Bruno has been awarded a prime contract for the Community Relationship S
Michael-Bruno Scores Big in Italy MACC
Naples, Italy - Naval Facilities Engineering Command (NAVFAC) Europe, Africa and
Volcanic Illumination: The Solfatara
Much like the bubbling mud and geysers of Yellowstone National Park, the Solfata
Base-Wide Grounding System Verification/Study Joint Force Command (NATO) Southern Europe Bagnoli (Naples), Italy
This electrical study consisted of verifying the current state of the grounding
Santa Chiara
Michael-Bruno, LLC, under its former name, Studio Tecnico di Giuseppe Brun
MED Multiplex Cinema
Description: MED is a cinema complex composed of 11 movies screnes, a large rece
MB President Writes
The Society of American Military Engineers confirmed today that Michael Sedge's
Global Locations
Michael-Bruno is strategically position to support its government and commercial
Michael-Bruno teams with Envistacom to Receive GTACS Award
The Atlanta-based small business, Envistacom, announced today that its tea
Michael-Bruno among NAS Sigonella MACC Awardees
Michael-Bruno, LLC, as design (A/E) partner of the Italian construction firm La
Joint Force Command (NATO) Electrical Cabin Upgrade Naples, Italy
Michael-Bruno was tasked to perform evaluation studies and upgrade implementatio
Castle Building Project Camp Lemonnier, Djibouti
PROJECT SUMMARY This project supported U.S. Navy requirement to terminat
Demolition of NSA Naples Hanger 405
The scope of this project included an engineering study and complete const
Environmental Support Services, Camp Lemonnier, Djibouti
Under contract number N00178-10-D-6174_EJ02, Michael-Bruno provides Enviro
Forensic Evaluation for Energy and Humidity, Building 2309 (Arena), USAG Vicenza, Italy, Contract W912GB-10-D-0039
Michael-Bruno was tasked by the USACE-Europe to perform engineering studie
Combined Joint Task Force-Horn of Africa Engineering Support to J34 Division East Africa
PROJECT SUMMARY Three-year, multi-tasking contract awarded to Michael-Bruno i
Cultural and Community Affairs Specialist for Camp Lemonnier
Michael-Bruno holds the contract for the Camp Lemonnier, Djibouti, Cultura
NSA Bahrain (Public Works Department) Engineering Support Services Bahrain
PROJECT SUMMARY Three-year, multi-tasking contract awarded to Michael-Bru
Receptionist/Inter-Cultural Relations Educator, Fleet and Family Support Center (FFSC) Camp Lemonnier Djibouti, Africa.
For two years Michael-Bruno has provided the Camp Lemonnier FFSC with a hi
Infrastructure Modernization Program (I3MP Italy II), Camp Darby/Livorno Depot, Italy
The US Army's Installation Information Infrastructure Modernization
Under the reconfiguration of the subject facility, which supports CNE/CNA/
Defense Information Systems Agency âTeleport Projectâ Japan, Italy, Germany, Hawaii, California, Maryland
The Defense Information System Agency's Teleport Project, consisting
Program Management Office (PMO) Facilities Camp Lemonnier, Djibouti
PROJECT SUMMARY This project, consisting of a series of new facilities,
Salt Investment Project Lac Assal, Djibouti
PROJECT SUMMARY Salt Investment was the largest commercial construction p
Corporate Profile
For over 30 years Michael-Bruno, LLC, formerly known as Giuseppe Bruno Technical
SeaPort-e IDIQ
The overall objective of SeaPort-Enhanced (SeaPort-e) is to provide a standardiz
Contact Michael-Bruno
The new, European Office of Michael-Bruno is located in Via Antonio Solario, 14
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About MB
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If you have two Möbius transformations represented as:
$f(z) = \frac{az + b}{cz + d}$
$g(z) = \frac{pz + q}{rz + s}$
where $a, b, c, d, p, q, r, s, z \in \mathbb{C}$
Is it possible to derive a third function $h(z, t)$, where $t \in \mathbb{R}$ and $0 \leq t \leq 1$, which "smoothly" interpolates between the transformations represented by $f(z)$ and $g(z)$?
Let me try to clarify the meaning of "smoothly". I'm working in a the Poincaré Disc model of Hyperbolic geometry. The functions $f$ & $g$ represent transformations which preserve congruence within the model, i.e. a Poincaré line segment $PQ$ will have the same Poincaré distance as $P'Q'$, where $P' = f(P)$ & $Q' = f(Q)$. I would like the interpolated transform to preserve this property as well.
The answers involving diagonalization of the matrix "almost" work. Let me be clearer about how these mobius transformations are used, so that I can give some more context.
$f$ represents the position and orientation of a tile on the Poincare disc. I use this to transform a tile centered at the origin. $g$ represents a neighboring tile. I'd like to "animate" the $f$ tile moving it smoothly on top of the $g$ tile. While animating, the center of $f$ should travel along the poincare line connecting the two tiles at rest position.
The problem with the diagonalization approach is that the centers of the two tiles will travel about a corner of one of the tiles, sometimes the "long" way around.
Of course it could just be a bug in my code...
P.S. This is for an iphone game I'm developing called Circull


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A beautifully crafted wall mounted clothes Airer. A lovely versatile item that can be mounted in any room of the house and even outside. The adjustable ladder design can fit lots of laundry on and can be mounted above a radiator used in a bathroom for your towels or in the utility room. Extra brackets can be purchased so on a sunny day you can mount the airer outside on a south facing wall, fence,shed or balcony. The willow & Stone team absolutely love this innovative British designed product.
Standard UK delivery £4.95 (aim 3 working days
Express UK delivery £7.95 (next working day)
UK Highlands and Islands £15.50 (aim 3-5 working days)
Ordering from Overseas? No problem, click here.
Fear not, we have a flexible 28 day returns policy, click here.
I'd seen these laundry ladders at the Spirit of Christmas event in London and really loved the concept. I'd been looking for a solution to the ever growing number of clothes that hung in my laundry room. It's neat and flexible in size. Looks attractive and is well made. I simply pop clothes on hangers on the bottom wrung, and a few other bits on the higher levels. Perfect! I may buy more hooks so I can move it outside in the warm weather too.
Excellent and attractive clothes airer. Many people have commented on it and expressed an intention to buy one! One thing that could improve it would be to somehow mount it so that the back rack is further from the wall. It would just make it slightly easier to use.
I absolutely love my new wall mounted clothes airer - limited space in the utility room - this works and looks really lovely too! Arrived on time and packaged well.


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Read About STD Testing in Kingwood TX
Reviewed By: Dr. Kurt Kloss, MD
Last Reviewed Date: Sep 05, 2019
Sexual Health Testing in Kingwood TX
At Health Testing Centers we make sexual health testing in Kingwood easy and convenient by allowing you to avoid the hassle and embarrassment of visiting your doctor. We provide direct access to the same CLIA approved labs in Kingwood, TX and FDA approved tests that your doctor would utilize. Also the results are delivered directly to you and are not a part of your permanent medical record.
STD Statistics in Kingwood
From 2007 to 2011, STD cases have risen in Kingwood, Texas particularly among the very young and in seniors. This number is of concern to many public health professionals who study these types of diseases. The increases in STD's such as chlamydia illustrate how important it is that physicians make no presumptions about the sex lives of their patients. Instead, impartial discussions, regular testing and the nonjudgmental exchange of information are vital. Gonorrhea is a disease that plagues the Kingwood. In recent years, the overall trend is that the number of cases is declining. This is a good sign for Kingwood and for Texas, but this is not enough. The goal is to reduce and completely eradicate the number of incidences in Texas. Using the Center for Disease Control's 2016 STD Surveillance Report for chlamydia, gonorrhea, and syphilis and extrapolated using the latest 2011 US Census, it is estimated that 4.5 incidents of syphilis, 333.4 cases of chlamydia and 99 cases of gonorrhea, would be attributed to Kingwood in 2016.
Herpes is another major concern for Kingwood, present in two forms: HSV-1 and HSV-2. You should take every precaution to avoid intimacy without first discovering your partner's status in terms of HIV, gonorrhea, herpes, Chlamydia and other sexually transmitted diseases.
STD Treatment and Counseling in Kingwood
When ordering an STD package or individual test from Health Testing Centers that tests for chlamydia, gonorrhea, trichomoniasis, or HSV type 2, a physician consultation and treatment are included when there is a positive result. If you test positive for any of the 4 mentioned STD's, a telephone or video consultation will be provided at no additional cost by one of our third party physicians. The physician from PWN Health will contact you within 4 to 24 hours of receiving your test result. At the end of the consultation the physician may prescribe the necessary medication for treatment. It is up to the sole discretion of the physician to provide any medical treatment based on test results and any medical information they received during the consultation. Cost of the prescription is not included.
STD Lab Locations in Kingwood, TX
Obtain STD labs and get same day testing from FDA approved labs in Kingwood Texas. Search for your STD lab location using zip code: Visit our Lab Locator.
Kingwood, TX 77339
Quest Diagnostics
Kingwood, TX 77339
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your doctor.
tests used by doctors and hospitals.
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STD Testing Labs in Kingwood, TX
Whether you're concerned about possible STD exposure or simply want a quick, convenient and confidential way to take control of your sexual health via routine STD screening, our STD testing centers near Kingwood, TX can help. Our testing locations offer private, top-quality STD testing just like you would receive from your doctor's office without the added expense and inconvenience of an office visit just to have that doctor place the order for those tests.
Why is testing important?
Because STDs are more common than you may realize, with nearly 20 million new STD cases occurring every year, according to nationwide CDC estimates. Their affects can be quite serious. For instance, HIV infection can progress to AIDS, and gonorrhea, Chlamydia and syphilis can lead to infertility without treatment. These examples show just how important it is that these and other STDs do not go undetected for lack of a simple health test, easily done via STD testing centers near Kingwood, TX.
When should you seek STD testing?
Clearly, if you know or suspect that a partner is affected by a sexually transmitted disease, looking into STD testing centers near Kingwood, Texas is important to protecting your health, as is seeking immediate treatment should you receive positive results. However, STD testing is also essential for all sexually active individuals. That's because STDs don't always come with obvious symptoms. Some may produce no symptoms at all, while others may present mild ones that are easily mistaken for a cold or flu. For this reason, ensuring your sexual and overall health means getting regular screening tests for common STDs. Just how often you should schedule test days depends on your individual circumstances. If in doubt, consult a healthcare professional for an appropriate testing routine for your needs.


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Life @ World Travel Holdings
We're a group of fun, passionate and dedicated people who work collectively to provide our CUSTOMERS with a remarkable experience. At the same time we provide OURSELVES a diverse, vibrant and fun atmosphere to work in. We truly believe in working hard while also not taking ourselves too seriously. It's who we are!
To watch more videos about World Travel Holdings and its career opportunities, visit our YouTube page.
Besides having fun, being an employee at World Travel Holdings has the cool factor. Here's why:
We are Dream Ambassadors
We sell a product that everyone wants and dreams about. Now that's cool.
What Makes Us Different
We offer paid training and ongoing education. In addition to our classroom and @ home training opportunities, free/deeply discounted familiarization trips let you experience what we sell firsthand.
We work hard and play hard
We want our employees to be healthy and happy. Our health benefit options and time off plans give you the resources (and time away) needed to keep you in tip top shape.
See the world
Enjoy a myriad of great travel discounts so you can see the world. As a registered travel agent in the leisure travel industry, discounted rooms, cars, theme park admissions and so much more are added bonuses to joining our amazing company.
join the fun! search jobs
Interested in joining our team? Search Jobs
Or, how about working at home working @ home?


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News | May 29, 2014
NASA Widens Its 2014 Hurricane Research Mission
During this year's Atlantic hurricane season, NASA is redoubling its efforts to probe the inner workings of hurricanes and tropical storms with two unmanned Global Hawk aircraft flying over storms and two new space-based missions.
NASA's airborne Hurricane and Severe Storm Sentinel, or HS3 mission, will revisit the Atlantic Ocean for the fourth year in a row. HS3 is a collaborative effort that brings together several NASA centers with federal and university partners to investigate the processes that underlie hurricane formation and intensity change in the Atlantic Ocean basin. The flights from Wallops Flight Facility in Virginia take place between Aug. 26 and Sept. 29, during the peak of the Atlantic hurricane season, which runs from June 1 to Nov. 30.
The NASA Global Hawks are unmanned aircraft that will be piloted remotely from the HS3 mission control at NASA's Wallops Flight Facility. Global Hawk aircraft are well suited for hurricane investigations because they can fly for as long as 26 hours and fly above hurricanes at altitudes greater than 55,000 feet.
One Global Hawk will focus on the inner region of the storms to measure wind, precipitation, temperature and humidity. It will carry three instruments, including the High-Altitude Monolithic Microwave Integrated Circuit Sounding Radiometer (HAMSR) microwave sounder, developed at NASA's Jet Propulsion Laboratory, Pasadena, California. The second Global Hawk will carry three different instruments and examine the environment around the storms.
The NASA-Japanese Space Agency Global Precipitation Measurement (GPM) mission, launched Feb. 27, will provide rainfall measurements every three hours around the globe, and will complement the HS3 mission.
The ISS-RapidScat instrument, managed by JPL, is slated for launch to the International Space Station in August. RapidScat will measure ocean surface winds in Earth's tropics and mid-latitudes and will provide useful data for weather forecasting of marine storms.
GPM and RapidScat are two of five NASA Earth science missions scheduled to be launched this year, the most new NASA Earth-observing mission launches in the same year in more than a decade. NASA monitors Earth's vital signs from land, air and space with a fleet of satellites and ambitious airborne and ground-based observation campaigns. NASA develops new ways to observe and study Earth's interconnected natural systems with long-term data records and computer analysis tools to better see how our planet is changing. The agency shares this unique knowledge with the global community and works with institutions in the United States and around the world that contribute to understanding and protecting our home planet.
For more information about this year's HS3 campaign, visit:
For more information about NASA's Earth science activities in 2014, visit:
News Media ContactAlan Buis
Jet Propulsion Laboratory, Pasadena, Calif.
Rob Gutro
NASA's Goddard Space Flight Center, Greenbelt, Md.


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Editor's Comment: The authors of this study do not state in their abstract how the data for the statistical analysis were gathered. In the full article, the authors reveal that the data were generated from a questionnaire. No psychiatric or objective measurements of improvement were employed. The accuracy of questionnaires, as well as other self-reporting techniques, has been called into question by numerous statisticians.
~Source: QJM. March 28, 2013.
By E. Crawley et al.
Background: Chronic fatigue syndrome (CFS) is relatively common and disabling. Over 8000 patients attend adult services each year, yet little is known about the outcome of patients attending NHS services.
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Aim: Investigate the outcome of patients with CFS and what factors predict outcome.
Design: Longitudinal patient cohort.
Methods: We used data from six CFS/ME (myalgic encephalomyelitis) specialist services to measure changes in fatigue (Chalder Fatigue Scale), physical function (SF-36), anxiety and depression (Hospital Anxiety and Depression Scale) and pain (visual analogue pain rating scale) between clinical assessment and 8–20 months of follow-up. We used multivariable linear regression to investigate baseline factors associated with outcomes at follow-up.
Results: Baseline data obtained at clinical assessment were available for 1643 patients, of whom 834 (51%) had complete follow-up data. There were improvements in fatigue [mean difference from assessment to outcome: -6.8; 95% confidence interval (CI) -7.4 to -6.2; P < 0.001]; physical function (4.4; 95% CI 3.0–5.8; P < 0.001), anxiety (-0.6; 95% CI -0.9 to -0.3; P < 0.001), depression (-1.6; 95% CI -1.9 to -1.4; P < 0.001) and pain (-5.3; 95% CI -7.0 to -3.6; P < 0.001). Worse fatigue, physical function and pain at clinical assessment predicted a worse outcome for fatigue at follow-up. Older age, increased pain and physical function at assessment were associated with poorer physical function at follow-up.
Conclusions: Patients who attend NHS specialist CFS/ME services can expect similar improvements in fatigue, anxiety and depression to participants receiving cognitive behavioural therapy and graded exercise therapy in a recent trial, but are likely to experience less improvement in physical function. Outcomes were predicted by fatigue, disability and pain at assessment.
Source: QJM (2013) doi: 10.1093/qjmed/hct061 First published online: March 28, 2013. E. Crawley, S.M. Collin P.D. White, K. Rimes, J.A.C. Sterne, M.T. May, CFS/ME National Outcomes Database


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KEYT News
SANTA BARBARA, Calif. -
A Santa Barbara chef is taking extreme measures to keep his customers safe from what said is dangerous seafood.
Robert Perez has been a chef for more than three decades, but it was the nuclear disaster in Japan that changed the way he cooks.
In March 2011, a tsunami triggered by an earthquake rocked the Fukushima Nuclear Power Plant, causing radioactive materials to leak.
Even though scientists have said that the radiation in the ocean is now low, Perez isn't buying it.
"The way things are heading, we just feel strongly that it is not safe, and I'm not going to consume the fish and I'm definitely not going to provide it to my guests. I just can't do that with a clear conscience," said Perez.
The menu at Seagrass changed slightly two years ago when the restaurant stopped using Japanese seafood. Around a year ago, Hawaiian fish was taken off the menu. Now, all seafood from the San Diego border to Alaska is gone.
The change has forced Perez to get his fish from Mexico, the Atlantic or even farther.
"Alpine, New Zealand salmon," said Perez as he unwrapped a piece of fish. "It comes from glacier water."
He believes he's the only chef in the area making such strict choices on his food, because no one really talks about it.
"They go, 'Fuku-what?' It's like the F-word. It's like the other F-word, or maybe it's the new F-word," he said.
Scientist think avoiding the seafood is overboard and have said the levels of radiation in fish are less than what people are exposed to from x-rays.
Perez said he has to be able to stand behind what he serves, even if people think it's extreme.
"It's easy for people to be convinced that there's no harm right now, and that's part of the problem," he said.
Although it's an adjustment for customers, Perez said he's not trying to stand out.
"That's just part of who we are. And I cook because I want to please people. And I want people to be healthy with my food. I want them to feel good physically and spiritually. So that's my intent, that's the intent I put out there. So if I have a product that I feel uncomfortable with, and I don't care if it's an onion or a piece of meat or a piece of fish, it's all the same. It has to be something that I can stand behind and say, 'Please try this.'"