text:
Yonder Mountain String Band have announced that Jeff Austin will be leaving the group. The band released a statement on their Facebook page this afternoon that reads:
Yonder Mountain String Band is all about family, and through the support of our family of fans, we have been able to play music for you for the past 15 years. We couldn't be more proud about our successes and experiences performing at the best venues and festivals in the country, and for the most dedicated fans any band could ever wish to have. With this said, YMSB would like to share some news about the future of the band. Collectively, after long, heartfelt discussions, we've all decided to move forth with a newly formed line-up due to varying career goals and creative pursuits. As of today, all future YMSB shows will be performed with Adam Aijala (guitar, vocals), Ben Kaufmann (bass, vocals), and David Johnston (banjo, vocals). We will welcome exciting special guests throughout the rest of the year and we look forward to a new permanent line-up in 2015. YMSB fully supports Jeff Austin and his emerging solo career.
Yonder Mountain String Band will perform all scheduled dates throughout 2014 with the new line up and special guests. Jeff Austin will be announcing more dates for his solo endeavors in the coming months. The band wants the fans to know that this decision did not come easily, and we'll certainly keep all of our fans up to date with the new Yonder band-member line-up information.
We greatly look forward to seeing everyone out on the road this Summer and Fall!
With Gratitude & Respect,
Ben, Jeff, Dave & Adam
As previously reported, Yonder Mountain String Band played a number of tour dates earlier this year without Austin. Members of the Travelin' McCoury's, who were also co-headlining the shows, filled in for him for during the hiatus. There is currently no word on who will be performing in his stead during Yonder's upcoming gigs.
Austin has already played a number of shows with his other band, The Here and Now, and he has also scheduled a number of other dates with a different band that features Danny Barnes (banjo and vocals), Eric Thorin (bass and vocals) and Ross Martin (guitar and vocals). Additionally, Austin has also confirmed that he will be recording an album with Barnes, Thorin and Martin this May.


text:
GMHC Treatment Issues
Outrunning HIV
by Dave Gilden
Last month we looked at the reasons people fail to respond to the new aggressive anti-HIV combination therapies. One of the striking features behind lack of response in the face of drugs that should have a tremendous impact on HIV replication is the immune system's inability to control the virus, leaving the drugs to do the entire job alone. But we also looked last month at various anti-HIV strategies based on further suppressing the immune system. These approaches stem from a philosophy that the central cause of AIDS lies in the progression of HIV infection and that the immune system response is on balance counterproductive.
Many researchers are beginning to think that HIV establishes an equilibrium in the body based only on the susceptibility of target cells, and this equilibrium gradually breaks down. The chronic activation of the immune system to fight HIV helps the virus more than it hinders it by providing more and more target cells susceptible to HIV infection and by concentrating HIV in the lymph nodes, where those susceptible CD4 cells also converge. A recent theoretical paper went so far as to suggest that antiviral therapy plus immune suppressive chemotherapy that reduces the number of CD4 cells to slightly below the natural HIV-CD4 cell balance will cause the HIV infection to gradually wind down due to lack of sufficient target cells in which to reproduce.1
A possibly related observation is the experience of people who have their spleens removed (splenectomy) to correct HIV-related conditions (principally to improve low platelet counts). The spleen, which is packed with both macrophages and CD4 lymphocytes, is a major site of HIV replication. According to a French group who reported their observations in September,2 patients with HIV who had their spleens removed had only one-eighth the risk of death and one-quarter the risk of an AIDS-defining infection as a comparable group who still had their spleens.
Splenectomy is not for the faint of heart: previous reports have indicated that taking out this piece of the immune system increases the risk of certain bacterial infections as well as carrying with it the various risks of infection and trauma inherent in a surgical procedure. Splenectomy also produces a misleading boost in CD4 counts in the blood3 while effecting little or no reduction in HIV levels.4
There might be a useful lesson from the performance of splenectomized patients, but most scientists think that suppressive therapy of this nature is highly questionable. The traditional view is that the immune system does play an active role in initially limiting the spread of HIV infection. Mario Clerici, M.D., of the Università degli Studi di Milano in Italy, notes, for example, that "the switch from NSI to SI HIV variant [a common evolution within the body that portends accelerated disease progression] occurs preferentially when CD4 counts fall below a critical threshold, suggesting that immune impairment is a prerequisite for cytopathic HIV variants to emerge."
The pattern of immune response seems to indicate who is stable and who has progressive HIV disease. Long-term nonprogressors have CD4 T-cells that, when activated, produce IL-2 and other so-called TH-1 cytokines, which stimulate the cytotoxic CD8 T-lymphocytes (CTLs) that kill virus-infected cells. CD4 T-cells from those whose immune systems are declining tend to produce more IL-10 and other TH-2 cytokines that promote antibody production.5 In fact, the concentration and type of HIV in the body (less virulent NSI or more virulent SI) is closely correlated with the stimulated CD4 cells' IL-2 to IL-10 ratio. (Note that in a therapeutic context, IL-10 might actually help block HIV replication -- for the subtleties of this immune suppressive approach, see the October, 1996 Treatment Issues)
It also seems that the quality of the CD8 cell defense shortly after infection with HIV influences people's prognosis: A reaction by CD8 lymphocytes that vigorously searches out relatively few HIV protein sequences leads to quicker disease progression, whereas progression is slower when the CTL response is more generalized, involving moderate proliferation by many CD8 lymphocyte subfamilies.6 A vicious cycle may be going on here, whereby a deficient immune response allows for more HIV, which in turn leads to further immune defects, such as a waning of anti-HIV CTL activity. If an increasingly improper immune response to HIV plays a central role in allowing disease progression, the trick would be to carefully manipulate that response to make it more effective or to restore it as immune defenses degrade in the later, symptomatic stages of HIV infection.
"CD4 Lymphocyte Growth Factor"Of course, the greatest change in the immune system during HIV infection is the decimation of CD4 cells. An obvious immune-boosting therapy would be one that elevates CD4 T-lymphocyte proliferation so as to stabilize the CD4 count. And one of the most obvious substances to look at is IL-2, which causes replication of a broad number of white blood cells, including CD4 and CD8 lymphocytes, monocytes and natural killer cells. "IL-2 is just CD4 lymphocyte growth factor," claims Clifford Lane, M.D., of the National Institute of Allergy and Infectious Diseases (NIAID). " When you give it to people and their CD4 counts go up, they don't get sick." Dr. Lane's group has just published the results of a 12-month controlled trial of IL-2 plus nucleoside analogs in 60 volunteers.7 The starting IL-2 dose was 18 million international units (IU) per day, administered as a continuous five-day infusion every two months. After the 12 month trial period, members of the control group, which had been receiving only nucleoside analogs, were permitted to receive IL-2 also. Follow-up data were reported out to 30 months.
Starting with an average CD4 count of 427 cells/mm3, the IL-2 group gained about 37 cells per month, ending with an average count of over 900 after one year. During the follow-up period, this group's count stabilized (the IL-2 was only administered as needed to maintain the previous gains) while the CD4 counts of the initial control group caught up. The price of these gains was high: 90% of the volunteers on IL-2 at some point suffered severe fatigue, headache, diarrhea or other flu-like symptoms during and after an IL-2 infusion. By the end of the trial's initial phase, the IL-2 dose had been reduced to an average of about 8 million IU per day of infusion. According to Joseph Kovacs, M.D., the study's lead author, "We went for the maximum tolerated dose and then worked our way down." That optimum dose has yet to be determined and may differ for different people, in particular those with higher CD4 counts may require smaller amounts.
One proposal to reduce the onerous nature of IL-2 therapy is to replace the five-day infusions with twice daily subcutaneous (under the skin) injections. Rather than be hospitalized, patients could administer IL-2 themselves at home. One study presented at the International AIDS Conference in Vancouver this summer found that after the first three months, CD4 counts had risen by 50% or 80% among the volunteers getting 15 million IU per day for five days every four or eight weeks, respectively.8 People on a lower dose (3 million IU/day) received less benefit, but since the starting CD4 counts were over 500 (i.e., near normal), it is questionable whether an 80% increase in CD4 cells is necessary. Just a slight gain or merely stabilization of CD4 count may be all that is necessary. The cost in terms of side effects remained high for subcutaneous IL-2, though less than with IV administration in other studies, and was dose-related. It is noteworthy that the one study that has directly compared intravenous and subcutaneous IL-2 found that side effects were distinctly fewer from subcutaneous administration, but the CD4 increases were a lot less, too.9 This study used a less active and now disfavored formulation, though, that joined the IL-2 molecules with polyethylene glycol for improved stability.
While Dr. Lane's group works from the highest tolerable dose of IL-2 back down to a more benign therapeutic intervention, others are starting with lower doses in an effort to create a nontoxic regimen. Kendall Smith, M.D., and colleagues at Cornell Medical Center reported in September on what they call a "rational" IL-2 therapy.10 These investigators use comparatively small doses designed to limit the IL-2 to the high affinity IL-2 receptors present on activated CD4 T cells, B cells and a small subset of NK cells (a type of antiviral lymphocyte that works independently of CD4 cells). In this way, the lower affinity receptors present on most NK cells would be missed, leaving these cells in a quiescent state. The NK cells activated only by high-dose IL-2 produce many of the inflammatory compounds (such as tumor necrosis factor) that are implicated in IL-2's toxic effects. In the Cornell group's recent report, ten HIV-positive volunteers who received about 270,000 to 375,000 IU of IL-2 daily for six months as subcutaneous injections responded with an average CD4 count boost of 27 cells per month (from a baseline mean of 383 to a final count at six months of 543). This is a figure remarkably similar to the gains reported with high dose IL-2 at the NIH. Volunteers who received higher amounts of IL-2 in the Cornell study suffered from side effects and had their dose reduced. Those receiving lower doses had no benefit -- in fact their average CD4 count declined by 28 cells per month.
The difference in CD4 cell response between the higher and lower doses in this trial was statistically significant, but only because of the surprising decline in the low-dose arm of the trial. Other trials using "low dose" IL-2 have not observed CD4 cell gains. Just last spring, the AIDS Research Alliance in Los Angeles reported that its 16-week trial of IL-2 (at 360,000 or 720,000 IU per day) plus gamma interferon detected no consistent changes in CD4 count.11 Granted, the Los Angeles trial involved advanced AIDS patients (average CD4 count of 47).
Increases in NK cells, which are depressed by HIV infection, were dramatic in both the New York and Los Angeles studies. For the Research Alliance cohort on the combined IL-2/IFN-g regimens, the jump in NK cells seemed associated with decreases in HIV viral load. If this could be confirmed, it would be the first time a viral load decrease could be effected by a therapy involving IL-2. The other IL-2 trials have found no decrease in HIV levels, or even a transitory increase in people not on anti-HIV medications. For this reason, IL-2 trials have required participants to be on anti-HIV therapy with approved nucleoside analogs.
The lack of viral load reduction with IL-2 can be taken as a sign that the IL-2's expansion of immune system cells is not creating any functional improvement. But it should be noted that a substantial increase in CD4 cells without any enhancement of the anti-HIV defenses should lead to permanently heightened levels of HIV, since the virus' "food supply" -- the proliferating CD4 T-cells -- would be increased. (This could be what is happening when IL-2 is administered to people with actual AIDS: In trial participants with CD4 counts under 200, permanent increases in viral load with little if any CD4 cell count improvement has occurred.)
Besides a reduction in HIV levels, another definitive sign that the increased cell counts due to IL-2 are actually doing some good would be a reduction in the number of opportunistic infections contracted by people receiving the cytokine. So far, the only data available is contained in a small "meta-analysis" combining three placebo-controlled high dose IL-2 studies with a total of 157 participants, all of whom received open-label IL-2 after the first year. Since the start of each study, there were six OIs in the IL-2 cohorts and fourteen in the placebo groups. This difference is not statistically significant, and the analysis is very vague in any case since the individuals under observation were all on IL-2 for varying lengths of time. Dr. Lane presented this very loose data set on November 3 at the Third International Congress on Drug Therapy in HIV Infection (in Birmingham, UK). He also claimed that all the opportunistic infections occurred at the expected CD4 counts, although he did not present a specific analysis of the correlation between OIs and CD4 counts.
According to Dr. Lane, a definitive study of IL-2 documenting disease progression would require as many as 3,000 people with initially asymptomatic HIV infection who would be followed for five years. The total cost could be upwards of $50 million. No one has come forth as yet with this kind of commitment. Although the Chiron Corporation spent at least that much to obtain FDA approval for its Proleukin brand of IL-2 as treatment for a type of kidney cancer, corporate sources say that it would be "very difficult to pull off" this kind of additional investment for HIV. Considering that large clinical endpoint trials have already been successfully completed, such as the one comparing AZT, ddI, AZT/ddI and AZT/ddC (ACTG 175) or saquinavir, ddC and ddC/saquinavir (Roche NV14256), it seems difficult to comprehend why the same cannot be done for IL-2. Then again, if the optimum dose, dosing schedule and route of administration for IL-2 has not been settled, it seems that all the preparatory work for a large clinical endpoint trial has not yet been done. But there are nevertheless late reports of progress, with discussions continuing at both the level of AIDS Clinical Trials Group and internationally to conduct the clinical endpoint trial using subcutaneous IL-2 administration in HIV-positive volunteers with CD4 counts over 400.
Adding a Little HAARTLaboratory tests of immune cell proliferation do indicate that the additional cells created under IL-2's influence are responsive to foreign antigens, but specific lost immune responses, such as those to vaccines, are only occasionally recovered. As indicated by the lack of decrease in plasma HIV levels, people's immune control of HIV is not restored to the way it was just after primary infection even though their nominal, IL-2-influenced CD4 counts may be normal or even higher than normal.
IL-2 may help to ensure stability and even reinforcement of available immunity by increasing the sheer numbers and concentration of existing cells. The new naive CD4 T-cells needed to expand the immune system's "repertoire" of responses to invading pathogens do not seem to appear under the influence of IL-2, perhaps because HIV damages the thymus, where many naive cells mature. Still, over the long-run IL-2 could expand any rare CD4 cells that already exist to produce detectable responses to antigens where previously none existed. The chances of this occurring would be increased if HIV levels were suppressed to the maximum possible using the new highly active antiretroviral therapy (HAART) drug combinations. The less HIV, the more the existing cells will be able to replicate. Conversely, IL-2 could reinforce HAART by maximizing the increase in CD4 counts.
Ronald Mitsuyasu, M.D., at University of California Los Angeles is now planning ACTG 328, a 150-person trial with IL-2 plus the protease inhibitor indinavir and any two nucleoside analogs (one has to be new to the individual trial participant). This trial's population will have advanced disease, with CD4 counts of 50 to 300, but no prior protease inhibitor treatment. If 12 weeks of the triple drug combination reduces their plasma viral loads to below 5,000, participants will be assigned to receive continued HAART plus either intermittent cycles of intravenous IL-2, intermittent subcutaneous IL-2 or nothing. Therapy will switch to subcutaneous administration after three cycles for those in the IV IL-2 group who are responding to therapy. The trial's goal is to monitor the resulting immunological and viral load changes, not prove a benefit in terms of disease progression. The latter would require a significantly larger trial enrollment. If IL-2 can be made to work in an advanced population, the required size for a trial generating disease progression data would be much smaller than the one discussed above for earlier patients -- only about 300 participants would be required, Dr. Mitsuyasu says.
There already is some indication that HAART and IL-2 reinforce each other. A study chaired by Judy Falloon, M.D., of the National Institute of Allergy and Infectious Diseases has reported one-year observational data on 24 people who had previously failed IL-2 therapy and had CD4 counts less than 300. For 14 weeks, participants received either intermittent IL-2 plus daily indinavir (600 mg four times a day), intermittent IL-2 plus the indinavir only on days when actually receiving the IL-2, or daily indinavir alone. After 12 weeks everyone received IL-2, indinavir and whatever other antiviral drugs they requested. Baseline CD4 count averaged 165 and the average initial viral load was about 100,000. By 14 weeks, the IL-2 plus daily indinavir group witnessed their average CD4 count increase from 186 to 382 but their viral load was little changed. In contrast, the daily indinavir monotherapy group saw their CD4 counts increase from 144 to only 229, while mean viral load fell about five-fold. (Little improvement was observed in the intermittent IL-2/intermittent indinavir group.) At one year, the CD4 count for the total group (all on open-label IL-2/indinavir therapy since week 14) averaged 433, while the overall average viral load had been kept down to 37,000.
It is difficult to say in this trial what therapy provided what benefit, but clearly, adding antiviral drugs created a response to IL-2 where it previously did not exist. The IL-2, meanwhile, may have helped boost CD4 counts more than the average 100 to 150 cell gain usually seen with HAART combinations alone. There is a hint here that relieving the pressure from HIV, now possible for the first time, will allow immune therapies to work, aiding the immune system to provide some backup for antiviral drug therapy. Such support could help clear the virus more quickly and thoroughly. A functional immune defense against HIV, even if only partial, would help avoid the drug resistance and breakthrough HIV infection problems that frequently arise in patients now relying only on HAART.
Before IL-2 can be combined freely with HAART, however, many basic questions once again have yet to be answered. The toxic nature of IL-2's inflammatory effects will make high doses of the agent difficult for most people to tolerate. HAART should allow IL-2 doses to be dropped to a greater extent than would less effective anti-HIV therapies, but since the optimum CD4 boost has yet to be ascertained, the amount of IL-2 to be used with HAART cannot be settled. Nor can the scheduling of IL-2 administration: One of the hopes expressed by proponents of high dose IL-2 is that only a few bimonthly cycles will prove necessary to achieve acceptable CD4 counts with continued highly suppressive antiviral cover. After that, administration will be needed at most only a few times a year to keep the CD4 count stable.
Next month Treatment Issues will look at strategies designed to improve the immune system's specifically anti-HIV activity.
Responding to
by Theo Smart
CMV infections of the central nervous system (brain and spinal cord) could be the most under-recognized neurologic complication of AIDS, according to researchers such as J. Allen McCutchan, M.D., of the University of California, San Diego. Usually by the time CMV neurologic disease is diagnosed, most cases are unresponsive to treatment, and death comes within weeks. CMV CNS disease may be a common cause of death in patients with CMV retinitis, particularly, says Dr. McCutchan, in those who "go blind, give up, and withdraw without being aggressively diagnosed." Prospects for earlier diagnosis and improved treatment are increasing, though, as tests that measure CMV DNA in the cerebrospinal fluid become more widely used, and new treatments for CMV become available.
CMV can cause a number of distinct neurologic syndromes (in addition to retinal infections). These include mononeuropathy multiplex (inflammation or disease involving individual nerves in unrelated portions of the body), myelitis/polyradiculopathy (inflammation of a large number of spinal nerves accompanied by pain, muscle wasting and paralysis) and two forms of encephalitis (or brain disease): diffuse micronodular encephalitis (DME) and ventriculoencephalitis (VE).
Mononeuropathy multiplex occurs when CMV infects the cranial and peripheral nerves resulting in face, wrist and foot palsies (for example, drooping muscles in the face similar to what occurs in people who have suffered a stroke). Mild forms that resolve spontaneously often strike patients fairly early in the course of HIV disease. Polyradiculopathy is strictly a late-stage AIDS event. It starts out as weakness or pain in the legs or back, but within a couple of weeks can progress to paralysis of the lower extremities and loss of bladder control leading to an inability to urinate or loss of anal-sphincter control. Polyradiculopathy or myelopathy may accompany or lead to CMV encephalitis.
The two CMV-encephalitic syndromes are distinguished primarily by the site of infection within the CNS. For both syndromes, symptoms of dementia, delirium, confusion, apathy and lethargy are common.1,2 Some symptoms of DME depend upon the location of the nodular lesions (as is often the case in toxoplasmosis, CNS lymphoma and PML). Patients with VE, meanwhile, often experience cranial nerve palsies and nystagmus (rhythmic involuntary eye movement). Both conditions are rapidly fatal. In one study of patients with VE, the median survival was only five weeks,3 while in another study those diagnosed with DME had a slightly longer median survival of 8.5 weeks.4
The actual rate of CMV infection of CNS is unclear. One two-year study reported that CMV encephalitis was found in only 1% of patients with advanced AIDS.5 This figure may accurately reflect the rate of diagnosis, but not the rate of incidence. In neurological autopsy studies, CMV infection of the CNS is found in between 20% and 28% of the brains studied.6,7 Some researchers believe that the rate of CMV neurologic disease is increasing as people live longer in an immune-compromised state. Others, such as David Clifford of Washington University and the Neurologic Subcommittee of the AIDS Clinical Trial Group, believe that there merely may be an increase in diagnosis: "Some of the cases we believed were HIV encephalopathy may actually have been caused by CMV -- there has been misclassification over the years. We've only known how to diagnose CMV encephalopathy over the last few years."
Other rates of incidence have been measured by the University of California, San Diego -- the site of the HIV Neurobehavioral Research Center funded by the National Institute of Mental Health. According to Dr. McCutchan, the site has been able to prospectively conduct neurocognitive tests on AIDS patients that come to the university's AIDS clinic, and then frequently perform neurological autopsy in the event of death. In one recent study, researchers from the center calculated that autopsy-confirmed CMV encephalitis occurs in about 42% of patients with CMV retinitis.8 The rate was almost 75% in more advanced cases of retinitis. Meanwhile, it was very uncommon in people without CMV retinitis.
Not all of the CMV neurologic disease detected upon autopsy in this study was rapidly progressive or caused the patients' death, but there is substantial evidence suggesting that patients are adversely affected by these undiagnosed infections. One study by Dr. McCutchan notes that even less advanced CMV infections can affect neurocognitive function. His team compared 16 patients with newly diagnosed CMV retinitis (but no evidence of outright dementia) to 322 matched controls with similar CD4 cell counts, age and education. They found neuropsychologic impairment (most commonly attention and verbal deficits) in a third of the patients with newly diagnosed CMV retinitis "caused by CMV rather than HIV." Evidence of physical harm to the central nervous system was detectable by MRI brain scans approximately twice as often in the patients with retinitis than in the matched controls.9 Dr. Clifford, however, does not agree with the methodology used in the report and says that there is a need for a "more focused and conservative study. I think this was a seriously flawed study because patients were sicker than the control group since they had an opportunistic infection and these were very mild neurocognitive deficits that could have been affected by the fever associated with CMV infection as well as visual problems associated with CMV retinitis."
In another study from San Diego's Neurobehavioral Center, though, researchers reported that the risk of cognitive impairment associated with CMV encephalopathy was seven-fold higher than that associated with HIV encephalopathy.10 The authors concluded that "unrecognized CMV encephalitis may be an important cause of both mild and severe neurocognitive impairment in patients with advanced HIV infection."
Recognizing the InfectionIn aggressive cases, the onset of symptoms is so abrupt, and the progression so rapid, that the encephalopathy may kill the patient within the time it takes clinicians to distinguish it from other AIDS-related neurologic conditions. There are some distinctive features of CMV neurologic disease, though. For example, CMV encephalitis occurs very late in the course of HIV disease, while signs of the most common alternate diagnosis, HIV encephalopathy, appear earlier and more gradually. Other hallmarks of CMV CNS infection, such as electrolyte abnormalities, pleocytosis (an abnormally high level of white blood cells in the CSF) and contrast enhancement of the brain's ventricles on MRI brain scans suggest CMV infection, particularly in the presence of CMV retinitis. These markers allow for a presumptive, but not a definitive diagnosis, since they also may occur in other neurologic conditions as well.
Until recently, finding proof of active CMV infection in the CNS has been difficult without conducting a brain biopsy. Even though the CSF is believed to be the primary route through which CMV enters the CNS (particularly in the case of VE and polyradiculopathy), the virus can only rarely be cultured from the CSF.11
"The one thing that has helped is the CMV DNA PCR test in the [cerebral] spinal fluid," notes Dr. McCutchan. Some studies report that such assays are dramatically more sensitive than culturing, and that the virus is usually only detected in cases of active CMV CNS infection.12 One study by Achim et al. found that the test was not as specific as reported by other groups, since CMV DNA was detected by PCR in the CSF of 58% of the patients without CMV-associated neurological conditions.13 Lack of experience using the new tests may explain some of these contrasting results. Also, this was a study of autopsy specimens, and McCutchan points out that there is a strong possibility that the virus could have entered the CSF post-mortem. "I am very suspicious that things can change after death. I think we need to look at the CSF during life."
It stands to reason that even if CMV DNA can be found in the CSF of people who do not have clinical CMV CNS disease, quantitative assays may provide a better indication of who is at risk for disease. A German study suggests that CMV DNA loads in the CNS were ten- to 1,000-fold higher in patients with CMV neurologic disease than in those without.14 Researchers from Roche Molecular Systems and University of California San Francisco reported at September's ICAAC that CMV DNA was detected in 24 of 26 patients with polyradiculopathy, and that levels were consistently above 1,000 CMV DNA copies per ml (except in one case of a patient on anti-CMV therapy).15 CMV DNA levels were generally under 100 copies per ml of CSF in patients with other CMV neurologic conditions, though. Another group of researchers recently published data correlating the presence of CMV DNA in the CSF of all but one of 13 patients with CMV CNS disease, while no CMV DNA was found in control subjects. High levels of CMV DNA (1,000 copies per 8 ml) were associated with severe disease, VE in particular, and uniformly shorter survival.16
Treatment OptionsThere have been no prospectively controlled studies of the treatment of CMV CNS disease, and the case reports are scant. Thus, there are no clear data on what is the best drug or dose to use or the duration of treatment. There are case reports of clinical responses to ganciclovir or foscarnet, but there is reason to believe that standard treatments of CMV retinitis may be inadequate as therapy for CMV infections in the brain. Dr. McCutchan compared case studies of treated patients with polyradiculopathy to those of untreated patients, and he found that half of the treated patients survived for a median of eleven weeks while all seven untreated patients died within four weeks. It is hard to construe less than two months additional survival as a great success, though.
Also, there have been a number of reports that CMV encephalitis developing in patients while receiving maintenance therapy for CMV retinitis. Researchers from Australia have reported on the development of VE in one patient on ganciclovir who then failed to respond to treatment with foscarnet.17 Another group described two cases of CMV encephalitis emerging in patients while on ganciclovir, who then failed to respond to the higher ganciclovir doses used for induction therapy.18 Yet another team noted five cases of CMV encephalitis that failed to respond to ganciclovir therapy, even though retinitis was stable in four of these same patients.19
Some of the treatment failure may be due to drug resistance. One team reported on culturing ganciclovir-resistant virus from a patient who subsequently developed polyradiculopathy while on ganciclovir therapy.20 Other researchers published a case of polyradiculopathy that was caused by a ganciclovir-resistant CMV, though the patient eventually responded to foscarnet and ganciclovir combination therapy.21
In addition, there are little data to suggest that either ganciclovir or foscarnet is absorbed into the central nervous system. In early pharmacokinetic studies, the level of ganciclovir in the CSF was found to be substantially lower than in the plasma.22 On the other hand, the blood-brain-barrier may be compromised by CMV infection of the CSF. Lawrence Drew, M.D., of the University of California San Francisco, presented an abstract at the Second National Conference on Human Retroviruses with data demonstrating that ganciclovir, with or without foscarnet, can lower CMV load in the CSF. Using the CMV bDNA assay, his team reported that treatment had antiviral activity in the CSF in seven out of eight patients with CMV neurologic disease.23 Dr. Drew concluded that the failure of treatment in these patients must have been due to some other factor such as the "advanced degree of disease."
Dr. McCutchan has another possible explanation for treatment failure, "The pathology suggests that some of the damage is irreversible. When infection in the nervous system is diffuse (as in DME), there may be recovery on treatment, but when the infection is in the retina or the nerve roots (as in polyradiculopathy or VE), there's no recovery of necrotized [dead] nerves. Early neuropathological autopsy studies by Dr. Clayton Wiley show massive brain destruction, as CMV has burnt past [the layers of the central nervous system] until you reach normal looking brain, full of viral antigens. There's not much active CMV until you reach the active burning at the edges of tissue damage and heating in the next level full of virus. In retinitis studies, even after treatment is initiated, this 'fire' always moves just a little further." In this scenario, only earlier detection and treatment may advert permanent nerve damage.
More hopeful data were presented by French researchers at the Third Conference on Human Retroviruses last January.24 The team reported rapid clinical improvement (within 10 to 13 days) in all of four patients with CMV neurological disorders (three cases of encephalopathy and one polyradiculopathy) on a combination regimen of ganciclovir at 5 mg/kg of body weight every 12 hours, and foscarnet 60 mg/kg every eight hours as induction therapy, followed by ganciclovir at 5 mg/kg, and foscarnet 90 mg/kg every day for maintenance. CMV DNA became undetectable in both of two patients within whom this was evaluated. No one stopped treatment due to toxicity, although one case of anemia and one case of leucopenia were observed.
These results provide additional justification for ACTG 305, a six month multicenter study of high dose, aggressive combination foscarnet/ganciclovir therapy in at least 30 patients with recently diagnosed encephalopathy or polyradiculopathy. Participants will be treated for 28 days with foscarnet 90 mg/kg and ganciclovir 5 mg/kg both twice daily followed by maintenance therapy with the same doses, but on a once-a-day basis. If they can tolerate it, those with prior experience on ganciclovir will receive higher ganciclovir doses (7.5 mg/kg twice a day for induction therapy, and 10 mg/kg once a day for maintenance therapy). Up to ten patients who cannot tolerate either agent will be treated with the alternate drug as a monotherapy. If patients fail on maintenance therapy, higher induction therapy doses will be reinitiated.
ACTG 305 seeks to answer many of the nagging questions surrounding CMV CNS disease. The study will evaluate both quantitative CMV DNA PCR and CMV bDNA as assays for disease severity, progression and response to therapy. The study also will investigate the role of drug resistance in the evolution of CMV CNS disease and in treatment failure. Finally, researchers will try to perform as many brain autopsies as possible on those patients who die during the study to determine the level of drug that actually penetrates the brain.
According to Dr. Clifford, the study should be open by the time Treatment Issues goes to press.
The Next FrontierIt is hard to predict what effect the recent improvement in the treatment of CMV-retinitis will have upon the development of CMV-related neurological syndromes. The addition of cidofovir to the approved anti-CMV armamentarium may increase the options of treatment. Lobucavir, adefovir, and other new compounds (from Gilead and Glaxo Wellcome) are waiting in the wings. It is unclear whether the use of oral ganciclovir will decrease the rate of extra-ocular disease or merely engender resistance by supplying suboptimal levels of the drug. Finally, the growing use of localized therapies for CMV-retinitis that do not treat extra-ocular CMV disease, such as the ganciclovir implants, may allow the infection to spread to the CNS more often.
"Local therapy worries me the most," says Dr. McCutchan. "We are doing ganciclovir implants and now cidofovir intraocular injections at our site, but we don't have the funding to prospectively follow these patients to see whether there is an increase in the rate of CMV disease in the CNS."
Even if the use of localized therapy does increase the incidence of CMV encephalopathy or polyradiculopathy, Dr. McCutchan believes that with viral load monitoring of the CSF and an increased awareness of the conditions, the prospects for treating CMV CNS disease are improving. "One of the reasons to look at these endstage diseases is that we're going to get better and better at bringing people back from the brink. Of course, what we'd really like to do is to keep people from ever reaching that brink."
Tuberculosis Therapy and
by Gabriel Torres, M.D.
Aggressive treatment for tuberculosis (TB) requires combination therapy, usually with four drugs (isoniazid, rifampin, ethambutol and pyrazinamide) administered over nine to 12 months. TB treatment regimens that contain rifampin are far superior to those that do not contain rifampin. Rifampin-containing regimens are usually much shorter (six to nine versus 18 to 24 months) and have faster clearance of the tubercle bacterium from the sputum, higher cure rates and fewer relapses.
Rifamycins, the class of drugs that includes rifampin and rifabutin unfortunately pose a significant problem for TB patients who are also HIV-positive (one-third the total TB caseload in New York City). Rifampin and rifabutin heighten the activity of the liver's drug-metabolizing cytochrome P450 enzyme system, leading to subtherapeutic blood levels of the anti-HIV protease inhibitors (saquinavir, indinavir and ritonavir). At the same time, the protease inhibitors inhibit the P450 enzymes, causing higher levels of rifampin and rifabutin with an accompanying increased risk of serious side effects (including bone marrow suppression and inflammation of various tissues and organs).
The New York City Bureau of Tuberculosis Control of the Department of Health has recently issued a series of recommendations for HIV-positive patients with tuberculosis who also require treatment with protease inhibitors. The agency recommends that:
Note: The Centers for Disease Control have just issued similar, although somewhat more conservative, guidelines as the NYC DOH. It recommends completion of a six-month TB regimen containing rifampin for all HIV positive patients with active TB regardless of CD4 cell count. For TB patients already on protease inhibitor therapy, the CDC believes one option is discontinuing therapy with protease inhibitors and completing a six-month course with a rifampin-containing TB regimen. The agency concurs with the second New York DOH option of switching from rifampin to rifabutin (150 mg per day) and to indinavir from other protease inhibitors but suggests treating patients with a four-drug rifabutin-containing TB regimen for nine months. The CDC also recommends measuring rifabutin plasma concentrations -- such tests are available only at specialized centers in the US. A third additional option proposed by the CDC is a four-drug rifampin-containing regimen for two months or until the sputum culture has converted to negative, followed by 16 months of continued TB treatment with isoniazid (INH) at 15 mg/kg of body weight and ethambutol at 50 mg/kg, given twice weekly. Some experts also recommend adding a third drug such as streptomycin for the continuation phase. This regimen allows for reintroduction of protease inhibitor therapy after the second month of TB therapy. This third option is not recommended for patients with INH-resistant TB.
This advice is based on the best guesses of experts in the fields of HIV, TB and drug metabolism. The regimens have not been formally tested since most trials of protease inhibitors excluded patients requiring rifampin or rifabutin. The recommendations are a good starting point that will encourage practitioners who care for people with TB not to withhold potent antiretroviral therapy from patients who also have HIV. As TB is known to accelerate the rate of HIV disease, intervention with protease inhibitor therapy in this patient population is crucial.
Treatment Briefs
NTZ for Cryptosporidiosis
The Food and Drug Administration (FDA) has given Unimed Pharmaceuticals permission to increase the size of the company's expanded access program for nitazoxanide (NTZ), a new treatment for cryptosporidiosis. There now is no limit to the number of people with HIV-related cryptosporidiosis who can access the drug through the open label program.
There are currently no approved treatments for cryptosporidiosis, and numerous agents have failed to show a significant effect on this parasite in clinical trials involving people with HIV. The data on NTZ are much more encouraging, though.
A Mexican study presented at the 1996 International Conference on AIDS claimed that NTZ reduced the symptoms of cryptosporidiosis and cleared the parasite from the intestines in most of the 30 patients treated. Those who failed NTZ at doses of 500 mg or 1,000 mg per day, responded when the dose was increased to 4,000 mg per day (abstract TH.B.4213).
Results have not been quite as dramatic in U.S. dose-ranging study. Data on the first 22 patients to complete the study were reported at this year's Interscience Conference on Antimicrobial Agents and Chemotherapies (abstract LM50). Participants received either 500, 1,000, 1,500 or 2,000 mg per day. Overall, after four weeks of treatment, at least half of the participants experienced at least a 25% reduction in number of daily bowel movements. 18% of the patients had a complete resolution of diarrhea, and 41% had a reduction of cryptosporidia in their stool samples. There was a trend toward better results on the higher dose arms, and no dose-limiting toxicity was observed. (According to Andy Young, of the PWA Health Group, a New York City AIDS buyers' club that sells NTZ, the only side effect reported to his organization is a green tint to urine and other bodily secretions.)
In the expanded access program, participants will be randomized to receive either 1,000 or 2,000 mg per day of NTZ for one month. If the treatment produces no response, the dose may be increased each month to a maximum of 3,000 mg per day. The program is open to people with concurrent microsporidiosis, though it excludes those who have concurrent intestinal CMV, MAC or KS. For more information, call 800/864-6330, extension 3032. Unimed plans to begin phase II/III studies, in collaboration with the AIDS Clinical Trials Group, by the end of the year.
Meanwhile, despite much harassment from the Food and Drug Administration, including confiscated shipments and fines, the PWA Health Group in New York still offers NTZ to anyone with a prescription who does not qualify for the expanded access program or who does not want to participate in the phase II/III study. Call 212/255-0520 for further information.
ddI and d4T Plus Protease Inhibitors
Despite the popularity of AZT/3TC, there are a number of reasons not to use these two drugs plus a protease inhibitor as part of your first strike against HIV. First, if the regimen is not a complete success and resistance occurs, it is not clear whether people who have become resistant to 3TC will receive any benefit from switching to ddI or ddC, since the mutation that confers resistance to 3TC could make the virus resistant to the latter drugs as well. However, this mutation, at amino acid number 184 on HIV's reverse transcriptase enzyme, is only rarely observed to develop in patients using ddI or ddC, which could indicate that patients may be able to switch to 3TC after failure on either of these two drugs. Second, the peripheral neuropathy caused by ddI, ddC or d4T is most commonly reported in late-stage patients. This observation indicates that combination regimens including ddI, d4T or ddC probably should be administered earlier in the course of disease, with the relatively benign AZT/3TC combination reserved for more advanced patients.
The ddI/d4T combination is a possible competitor to AZT/3TC, but there has been little information on how to use ddI/d4T in conjunction with protease inhibitors, indinavir in particular. The problem is that both ddI and indinavir must be taken on an empty or nearly empty stomach. Additionally, ddI's buffer interferes with the absorption of indinavir, so they should be taken at least one hour apart. Fortunately, d4T can be given with or without food.
Bristol-Myers Squibb, manufacturer of ddI and d4T, recommends the following dosing schedule when combining ddI/d4T with indinavir:
Indinavir should be taken just before a light breakfast (if you must eat something), d4T with your dry toast and black coffee, and ddI at least two hours afterwards and at least 30 minutes before lunch. Indinavir then should be taken in the afternoon (at least two hours after lunch and one before dinner). d4T can be taken with dinner, and ddI at least two hours after dinner but at least one hour before ending your evening with a dose of indinavir. Though, not formally recommending it, Bristol-Myers concedes that many clinicians are simply foregoing all this complication and prescribing ddI in one 400 mg dose each day.
The dosing regimen would of course be simpler with ritonavir or ritonavir/saquinavir, but the gastrointestinal side effects of ddI combined with those of ritonavir may make it difficult to start using these two agents at the same time. Those who endure the first few weeks of ritonavir may be able to add ddI/d4T at this point since the nausea, vomiting and diarrhea associated with ritonavir have usually diminished by then.
Nerve Growth Factor Study Opens
ACTG 291, a study of recombinant human nerve growth factor (NGF) in people with HIV-associated neuropathy opened this past summer and currently has enrolled seventy patients. NGF is a chemically synthesized version of a human protein that specifically stimulates the growth and survival of nerve cells in the peripheral nervous system. The trial should be fully enrolled by the spring of 1997, which would be a record accrual rate for a neurological study conducted by the AIDS Clinical Trials Group.
The trial will assign 180 people to receive either 0.1 or 0.3 mg per kg of body weight of NGF as a subcutaneous injection twice each week. It is open to people with HIV with peripheral neuropathy that is not inherited, or caused by diabetes, vitamin B12 deficiency, or treatment with neurotoxic drugs such as ddC or d4T. Pregnant women or those who will not consent to practice birth control are excluded. The study is being conducted at numerous sites in the US. Call 800/TRIALS-A for more information.
Data from a six month placebo-controlled study of NGF in 250 patients with neuropathy caused by diabetes were presented at the American Neurology Association conference in October. The study found that NGF improved neurologic function and produced an increase in the patients' ability to sense cooling or painful heat. Genentech, the company that makes NGF, is planning a follow-up phase III study in over 1,600 patients. The study is currently on hold though, because the company has a shortage of the drug.
This also may prove to be a problem in the current ACTG study. Although, there is enough NGF to complete the trial, Genentech claims that it does not have enough of the drug to promise to continue treating study participants when the trial is over.
Ironically, according to David Clifford, M.D., of Washington University, and a member of the ACTG's Neurology Subcommittee, "Ninety-nine percent of the drug is being thrown away." This happens because the drug, administered in very small doses, must be administered immediately after the manufactured concentrate is diluted. Dr. Clifford says that the vials in which Genentech supplies the NGF contain enough to treat around 40 patients -- if they all showed up at the same time. Since they do not, the rest must be thrown out. Less wasteful packaging and closer co-ordination of study participants' visits are possible solutions to the supply problem. According to Kathleen Rinehart, manager of Genentech's corporate communications department: "When we were making the multi-use vial, we didn't know what dose of NGF would end up being used or whether it would be used subcutaneously or intravenously, so we made vials large enough to cover the range of what might be needed. Right now, we are currently working on a reconfiguration of those vials."
Cytarabine Nixed for PML
The first well-controlled clinical trial to be performed in persons with Progressive Multifocal Leukoencephalopathy (PML), ACTG 243, closed last summer after finding that treatment with cytarabine (also known as ARA-C) offered no benefit. The trial compared high-dose antiretroviral drugs alone to high doses of both intravenous and intrathecal (spinal) cytarabine. The study was closed early, after the Protocol Safety Monitoring Board reviewed the data on the first 62 subjects in the study and found no statistical difference in survival either between the three arms individually or between the two cytarabine arms compared to placebo. Manageable, but slightly higher rates of bone marrow toxicity were observed on the IV cytarabine arms. A higher dropout rate occurred on the intrathecal arm, which involved the administration of the drug through a needle inserted into the membranes surrounding the spinal cord.
The results of the study came as no surprise, since there were reports that people treated with cytarabine die faster than those who received no treatment and since there was at least one published case of cytarabine causing PML in a person with cancer by suppressing the immune system. (See TL Hwang et al. Journal of Neuro-Oncology. April, 1986; 3(4):335-9.) ACTG 243 may yet yield useful information on the natural history of PML. For one thing, it gathered useful data that should confirm whether a PCR (polymerase chain reaction) test that detects JC virus in the cerebrospinal fluid, can be used to diagnose PML. (JC virus is believed to cause this brain disease.)
More Free Viral Loads
Roche Diagnostic System's introductory offer of two free HIV viral load tests with its Amplicor PCR assay (see last May's Treatment Issues) has been a victim of its own huge success -- or poor planning, depending on how you look at it. At the end of October, some 25,000 plasma specimens had still to be assayed for HIV level, out of a total of 80,000 sent in. Some people have been waiting since July for the results, which are supposed provide two baseline values for gauging future disease progression and treatment effects.
Roche now hopes to clean up the backlog by mid-December, but of what use are results from months-old test specimens? To make up for its program's failure to deliver in a timely fashion, Roche is now planning to send doctors a letter offering them two coupons for every patient who had not received the two test results by October 18. The coupons will be good for six months. Roche is trying to ensure that the labs performing the tests will report the viral load results within ten days of receiving a specimen. To prevent a new backup, it has signed up more medical laboratories and will sent out the coupons in staggered fashion.
Coupon distribution is supposed to begin December 16. Patients who may qualify for these coupons should contact their doctor to make sure that he or she has applied for them.

subset: commoncrawl


text:
VIDEO: Spurs dismiss Blazers in five games to reach West finals
This was months ago, and yesterday.
The Trail Blazers still feel it from May, still talk about that moment in San Antonio, what it was like to walk off the court the final time and what it will mean when they walk back on the court the next time. New season, same memories.
Portland is forgetting nothing from the playoff exit, and not just because the black-and-blue mark the Spurs left won't allow it. More like because the Trail Blazers don't want to. Keeping it close is the whole idea.
That won't take much doing — it is close. Months later, they're still talking about how the emotional high from the successful regular season and the rush of a 4-2 win over the Rockets in the first round despite not having home-court advantage gave way to feeling like roadkill after the 4-1 elimination at the hands of the Spurs. Months later, they're still wanting to feel it for many more months, from training camp and into the new schedule.
"Our entire team enjoyed having a taste of success, not only in the regular season but in the playoffs and winning in the first round," coach Terry Stotts said. "The fact that San Antonio not only beat us, but how they beat us and how they won the championship I think gave us the motivation to know that there's a lot for us still to achieve and what we have to do to achieve it."
How they beat us.
Game 1: Spurs 116, Trail Blazers 92. Twenty-four points.
Game 2: Spurs 114, Trail Blazers 97. Seventeen points.
Game 3: Spurs 118, Trail Blazers 103. Fifteen points.
Game 4: Trail Blazers: 103, Spurs 92. Avoiding the sweep, avoiding being eliminated at home.
Game 5: Spurs 104, Trail Blazers 82. Twenty-two points.
"We took some big losses," said Meyers Leonard, a reserve center. "I think that we could have been much closer. But it was our first time, so I think we just have to realize we are that good of a team. We can compete with those teams. I think that's what's going to stick with us. We know that we're more than capable. But they came out and came at us right away and we were kind of like, 'Whoa.' Now we just have to realize that we are at that level and we have to maintain that level or teams that have been there and done that will put us away."
That the Spurs proved to be the team of the entire season and not just that series makes the Blazers look better in retrospect … but not feel better. Not when the gulf was that large and the memory that strong.
So 1-4 becomes motivation for the weight-lifting sessions the rest of the summer, the extra time in the film room in training camp, and then for real. Opening night, Oct. 29, is at home against the Thunder, an immediate test. But so is the entire first leg of the schedule, a gauntlet of the Thunder, Kings on the road, Warriors, Cavaliers, Mavericks, and Clippers on the road.
Even if the Trail Blazers have enough to worry about in October and November without reaching back to May, they will probably be keeping the end of 2013-14 close. That's the plan right now. That's the feeling right now, and maybe for a while.


text:
February 16, 2019
Discover how the Oscar-winning studio creates CG characters at a free event at Gnomon next week. Watch online for free. Read More »
Sorry, no posts matched your criteria.
Find VFX and animation studios and CG schools near you with these handy searchable maps. Read more »
April 21, 2019 | 2 comments
Director Chris Staehler reveals how he created award-winning sci-fi film The Beacon at Gnomon next week. Watch free online. Read more »
April 19, 2019
Create, shade and render complex particle effects using this versatile BlinkScript-based point renderer. Read more »
Discover key anatomy principles and sculpting techniques in The Gnomon Workshop's new tutorial. Read more »
April 18, 2019
Watch the best tech breakdown videos of the year, as chosen by CG Channel's Facebook followers. Read more »
January 12, 2019
© CG Channel Inc. All Rights. Privacy Policy.
CG Channel is part of the Gnomon group of companies:


text:
Henley Relaxed T-shirt
A simple and luxurious essential tee for every stage of your pregnancy and after with easy nursing access. Generous long length with flattering curved hem. Super soft and comfortable, made from superfine organic cotton jersey with easy shell button opening.
product details
product code: NBM8003
- 100% organic cotton jersey
- lightweight
- full length sleeves
- shell button down closure
- 100% organic cotton jersey
machine wash in cold or warm water with environmentally friendly laundry detergent
tumble dry on low or line dry
do not use fabric softener or bleach
see here for laundry tips
delivery and returns
Free shipping on all orders over $150 (excludes oversized items)
For more information about our flat rates and delivery, please see our delivery page.
You are welcome to return online purchases within 30 days, click here to view the full Returns Policy.
why choose organic maternity essentials?
Simple. Beautiful. Everyday. Pregnancy is the beginning of a life changing journey that Nature Baby wants to be a part of. The uncomplicated design and sympathetic cut of our maternity garments can grow with the Mum-to-be. Made from our super soft, luxurious organic cotton jersey which gives and holds where it needs to.


text:
How to Make a Great Home Decor on a Budget? : Interior Home Design
Decorating a home is one interesting thing for everyone. By making a great decoration, a home can become more beautiful and attractive. Besides that, it can also become more comfortable to be used. Unfortunately, many people think that decorating their home will make them spend much of their money. Actually, you do not need to worry about the same thing since you can do home decor on a budget and press your expenses.
There are many home decor on a budget ideas that you can find easily at certain pages. Most of them will tell you that when you make a perfect decoration for your home does not mean you ought to have everything new. Here, you have to be creative. You can buy used furniture in a secondhand store. Then, all you need to do is to make the used furniture looks new by certain techniques.
One of the techniques that many people usually do is by painting the used furniture that they buy by new color. Hence, it seems great for you to pick right color that looks suitable with your home concept to be painted to your used furniture. All in all, dealing with home decor on a budget is not that hard. Besides you can minimize your expenses, you can also have chances to expand your skill.
Get the Interior Home Design image by right click to get the high-res version. Here is required science on interior design blogs. We have the finest assets for interior design blogs! You can acquire Interior Home Design guide and look the latest How to Make a Great Home Decor on a Budget? in here.


text:
Recently, I received this "by grace alone" jewelry set, courtesy of DaySpring and (in)courage. Isn't it sweet?
Today, I thought I'd share my Top 10 reasons that you should get your own set. Here goes:
- It's just precious. Seriously--just look at that bird!
- The earrings are lightweight and don't tug at all.
- All the pieces are conversation starters. I can see these opening the doors to some witnessing opportunities!
- The pendant is a wearable scripture-memory tool. The verse that inspired the set is inscribed right on the back!
- The cuff is just right--not too big, not too small. Goldilocks would love it!
- Any of these pieces serve as a reminder that we aren't to be too hard on ourselves when we fail--we need to accept the grace God freely gives. Just like the verse says, "By the grace of God, I am what I am." And He gives us all the grace we need.
- Also, these pieces are also reminders to us to give grace to others, especially in those moments when we don't feel like it.
- They would make great gifts.
- Did I mention how great they look?
- They are all on sale 20% OFF this month!!
So there you have it--my top 10 reasons why you need to get your own "by Grace alone" jewelry set, or any piece individually. So what are you waiting for?? Head over to the (in)spired deals page and check out the great products!
Disclosure Policy: Please see my Disclosure Tab above.


text:
Mustang MonthlyHow To Interior Electrical
All Tuned Up
Upgrading Your Fox-Era Mustang's Audio
By now there's not a lot on your typical Fox Mustang hasn't been replaced, upgraded, or repaired. When you consider the fact that the newest Fox Mustang is 21 years old the whole generation of Fox Mustangs (1979-1993) is arguably considered "classic car" territory. Upgrading to performance suspension, adding engine upgrades for horsepower, et all, were and still are, very popular. Considering that these upgrades themselves are often over 20 years old and with many miles on them, we often see Fox Mustang owners adding these same upgrades to their Mustangs again due to age of these parts. Just because they're aftermarket parts doesn't mean they'll last forever!
Items such as upholstery, weather stripping, and even electronics/wiring aren't immune to age and wear due to usage. Our own '90 Mustang 5.0L hatch has seen several sets of door seals, power door lock actuators, and more in the 24 years we've owned. Even our Mustang's audio system, which was state of the art when upgraded way back in 1994, is ancient by today's standards. An in-dash AM/FM/Cassette stereo with a 10-disc CD changer was downright "kick ass" but today it just doesn't cut the mustard. No, today's audio systems include Bluetooth connectivity (for both audio and phone applications), HD Radio for crystal-clear music, and so much more. We felt it was high-time to upgrade our Mustang's audio system and step into the 21st century with the help of the folks at Pioneer (www.pioneerelectronics.com). Check out the install in the following photos and see how easy it is.


text:
Turkey is becoming increasingly isolated in the Middle East, a region where Ankara's political and economic clout was on a decade-long rise until the Arab Spring disrupted the political order. And Prime Minister Recep Tayyip Erdogan's fiery rhetoric and intransigent foreign policies may just fuel Turkey's loneliness.
The premier's latest salvo came Tuesday, when Mr. Erdogan accused Israel of orchestrating the coup in Egypt that removed the Muslim Brotherhood's Mohammad Morsi from the presidency, toppling the Turkish PM's close ally. The military's July 3 move to seize power in Cairo has reverberated across Turkey, where courts recently jailed scores of generals for an alleged plot to overthrow Mr. Erdogan, who faced popular protests throughout June.
Deeply upset by the ousting of its Islamic ally from power in Egypt by General Abdel Fattah Al-Sisi, Mr. Erdogan has struck an increasingly anti-U.S., anti-Western, anti-Semitic and, since Tuesday, also an anti-Arab tone, blaming leaders across the globe for supporting Egypt's military putsch and failing to support the democratically elected president. The premier's comments about "rich Arabs backing the dictators" in Egypt was widely interpreted as swipe against Mr. Erdogan's Sunni allies in Saudi Arabia and the United Arab Emirates.
But it was the usual suspect, Israel, whom Mr. Erdogan pointed out as the main culprit.
"Israel is behind this. We have a document to back this," the prime minister told his party's provincial chiefs in Ankara on Tuesday, continuing with an anecdote from a panel held in France before the 2011 elections in Egypt, which brought the Muslim Brotherhood into power.
"A French intellectual, who was a Jew, together with [Israeli] Minister of Justice, said exactly this: Even if the Muslim Brotherhood won the election they will not win, because democracy is not the ballot box," Mr. Erdogan said, referring to philosopher Bernard-Henri Lévy.
A press statement from Israel's Foreign Ministry spokesman, confirmed by Israel's Consulate General in Istanbul, noted that Mr. Erdogan's accusation was "not worth commenting on." A White House spokesman called the comments "offensive, unsubstantiated and wrong" in a press briefing in Washington.
Turkey has withdrawn its ambassador from Cairo for an unspecified period, and demonstrations in support of Mr. Morsi take place in Turkey on a daily basis. Ankara is also calling for the U.S., the U.N. Security Council and the Arab League to take immediate action against Egypt's current military leadership.
While some analysts stressed that Tuesday's speech was intended for a domestic audience, others said Mr. Erdogan's words were isolating Turkey even further in the region.
"These speeches contribute to Turkey's growing loneliness in the region. What else can be made out of rhetoric which implies that you are picking a fight with everybody," said Soli Ozel, professor of International Relations at Istanbul's Kadir Has University.
"Blaming Israel is nothing new, and Mr. Erdogan seems to believe in this theory. But he clearly doesn't feel that these kinds of speeches will cost him a lot in the U.S," said Hugh Pope, Turkey-Cyprus director for International Crisis Group.
The U.S., while announcing the postponement of its biannual military exercises with Egypt last week, seems reluctant to cancel its $1.5 billion in military and economic aid to Egypt, as demanded by Turkey.
"The West should learn the definition of democracy. If it doesn't do that, these controversies and clashes will continue," Mr. Erdogan said Tuesday.
Many Turkish analysts also argue that the much-discussed Turkish political model, which portrayed Mr. Erdogan's government as an exemplary democratic Muslim country, is increasingly under threat or even outright passé. The criticism increased especially after the harsh police response against mostly peaceful demonstrators in nationwide anti-government Gezi protests in June.
Speaking off-the-record, some analysts also admit that there is an increasing worry over Mr. Erdogan's worldview, which they say is getting increasingly out of touch with reality.
Turkey and Egypt "are part of the same game," said Mr. Erdogan's newly appointed chief advisor, Yigit Bulut, suggesting that Gezi protests in Turkey were also orchestrated by Israel.
"It is important to ask: Why were the important pillars of the Islamic world, Turkey and Egypt, selected? What is the macro-plan behind it?" Mr. Bulut wrote in his column in the pro-government Star daily on Wednesday. "It is crystal clear that especially after 2008, when Turkey had become more independent and powerful, both politically and economically, and come to the point of changing the 300-year course, the plan against our geography was set in motion! What has happened in Turkey and in Egypt were 'the first act!'."


text:
Cutting corners in cotton production makes little sense to Kress, Texas, farmer Barry Evans.
But he never spends money he doesn't expect to get back.
"Anything that will not make a return on my investment I've gotten rid of," Evans said. "I'm not trying to make the highest yield in the area. I just want to see a return."
Penciling in a profit may prove difficult this year as he looks at higher costs for fuel, fertilizer and seed. "It's a tough process," he said. "All those price increases comes right off our bottom line."
Nevertheless, he said cutting back on primary inputs such as fertilizer, seed technology and water makes no sense. Making a profit on the 2005 crop depends a lot on appropriate in-season timing for weed control, insect management, fertility and irrigation, he said. "Good weather will help, too."
He said an 800-pound per acre yield is break even for irrigated cotton.
He's already switched to a system he said does more than anything to reduce production costs.
"Less tillage has been huge," he said. "I save a lot of fuel and wear on equipment. I'm probably running tractors only 300 to 400 hours a year. That's a big cut."
He said reduced tillage saves on water costs, too. "Water accounts for the biggest fuel use. When we cultivate crops we plow up moisture and lose it. We want to save all we can. Most of the rain we get in this area comes in one-tenth to three-tenth increments, so we need to hold it all in the field. Not plowing helps do that."
Annual rainfall in the High Plains of Texas averages about 20 inches a year. "We're trying to farm with less water," Evans said.
Rotation plays a crucial role in the no-till system. He plants half his acreage in cotton and half in grain sorghum each year. "I plant cotton in grain sorghum stubble," he said. "After I harvest grain sorghum, I use a single gang stalk cutter."
That's the extent of fall tillage most years.
He uses row cleaners ahead of a John Deere Max-Emerge planter. "I tried a lot of things (to move crop residue)," he said. "But this is a simple process."
Grain sorghum, most years, produces excellent crop residue to add organic matter to the soil and to hold soil during the winter and with spring dust storms. "One reason we went to no-till was to keep dust storms down," Evans said. "We haven't broken any land in several years."
That could change with one problem field that tends to silt a bit, even with crop residue and no-till. The field is sandier than most of his acreage and he said it was damaged years ago from erosion that stripped the topsoil. The field has less organic matter than other fields. He thinks a hardpan also could be hindering crop production.
"I'm thinking about breaking the land to shatter that layer," he said.
"Some farmers say a field needs to be broken regularly to prevent that hard layer," Evans said. "I haven't plowed anything since 1996. Controlled traffic patterns help prevent hardpan."
He said the past few years have been too dry to produce good organic matter. His farm was drier than much of the High Plains last year. "We didn't have a really good year in 2004. Yields in this area were off a bit. Lack of heat units made the biggest difference and I never had more than one-third of an inch of rain at one time until fall. We didn't get those good rains that much of the High Plains had. And weather got too cool in August and September."
He tried wheat one year as a residue crop. "I harvested the wheat and left the land fallow the rest of the year. The wheat was next to milo field and I compared the two systems."
He planted cotton into wheat stubble and said the crop looked great. "Soil was quite mellow at planting. Cotton came up to a good stand and looked better than cotton planted in milo. Then it turned dry."
At harvest, the cotton in wheat stubble made 150 to 200 pounds of cotton. But so did cotton planted in milo. "But the milo never looked as good during the season," Evans said.
Evans first tried reduced tillage in 1996 and said weeds played havoc with the crop until a hailstorm destroyed the field. "I may have been lucky," he said. "But the next year I tried again."
He said he made those first attempts without Roundup Ready technology. "That has made a tremendous difference. I plant all Roundup Ready varieties. I haven't tried Liberty Link but it will have a place."
As does stacked gene cotton. "I haven't used much stacked cotton yet, but I plan to use more this year. Price for the stacked cotton is not much more than for just Roundup Ready. I could plant as much as 25 percent of my acreage to stacked gene varieties."
He would prefer to have Bollgard II but said it may not be available in the varieties he wants.
"I always look for the variety first and then I check for traits," he said.
Even though technology fees for Roundup Ready and Bollgard add significantly to production costs, Evans said improved varieties have been instrumental in increasing yield potential.
"Biotechnology has to be one of the greatest inventions in agricultural history," he said.
He's looking forward to a batch of new varieties coming out in 2006, with both Roundup Flex and Bollgard II.
I'll depend on Randy Boman (Texas A&M Extension cotton specialist at Lubbock) and his variety trials to select the best options," Evans said. "I base a lot of decisions on his trials."
Technology works well with reduced tillage to control costs, he said. Still, some farmers balk at changing equipment and cultural practices. "Farmers converting to reduced tillage need some specialized equipment," Evans said. "They need a hooded sprayer and a boom sprayer."
A stalk chopper and a good planter also make his list. "I started out with a drag planter and just switched to a John Deere that's heavy enough to get into the ground. It's a tough change for a lot of farmers. They need to add row cleaners to the front of the planter and that's another $200 to $300 a row. That may keep some producers from adopting no-till."
Evans uses grain sorghum rotation to save irrigation water and the energy necessary to pump it.
"I use LEPA irrigation and plant half the pivot in cotton and half in grain sorghum. I water the cotton. I might water milo to get it up and maybe occasionally in season, but I save the water for cotton production."
He said three-fourths of his acreage has irrigation capability and he waters only half that in any given year. "Water is limited and getting more so. We have to conserve it."
He said High Plains farmers sell water. "We've found that selling it through a cotton crop gives us the best chance at making a profit."
He expects the next farm bill to include significant conservation incentives. "We see a lot of things we can do to improve water use efficiency," he said, "but we have to be careful about broad-based changes. Things that work in the High Plains may not work in the Valley or in Far West Texas."
He expects research to find ways to allow farmers to pump less water and still make decent yields. Water remains his most limiting factor.
"We can do a lot of things wrong with a crop and get a rain at the right time and still do well," he said.
And while he waits on the rain, he does all he can to save what moisture he has in the soil and to weigh every production expense as carefully as possible to gauge potential return.
It's simple economics, he said.
e-mail: email@example.com


text:
Linux Bug #1: Bad Documentation (part 2)
The Many Faces of DocumentationIn Part 1 I talked about the messy state of Linux documentation, and how telling users to rely on Google is not documentation. Good documentation is equally important as good code. Sometimes there is this attitude that developer time is more valuable and important than user or potential contributor time. I suppose it depends on how much a particular project wants users and contributors; the more friendly and helpful on-ramps into a project, the more users and contributors. Good documentation is a big step towards quality control; when everything is documented, including reasons why something is done a certain way, it's less likely to be forgotten, which increases efficiency.
Getting started is probably the biggest hurdle, and once that first set of docs is completed they go into maintenance mode and need only changes and updates. I have a theory that good documentation discipline also encourages good development discipline, and fewer senseless changes that tend to vex users. Like moving a button or changing a command name, or re-organizing menus-- having to document all these things means taking another look at them and deciding if they are really necessary.
Yes Users MatterIf you want other people using your software, that is. There is never perfect harmony between devs and users, but it's much better to respond to questions with a pointer to a FAQ or a manual than to ignore them, or to crab at them for asking, or worst of all, tell them to Google or trawl mailing lists. Web, forum, and mail list searches are for edge cases and troubleshooting, not for basic howtos.
"Documentation" covers a lot of ground, from basic man pages to glossy four-color books. Let's take a look at the different categories of documentation, and what is reasonable to expect.
man PagesMan pages are awesome. I love man pages. They don't require a graphical interface, which is nice when Xorg or video drivers are broken, they don't require Internet (assuming you don't have some weirdo distro that doesn't install them), and you always know how to find them-- type man commandname. Nice and easy. (We'll talk more about these, and other ways to find and use documentation, in Part 3.)
Command DocumentationWhether this is in a man page or some other form, documenting all the commands and command options in an application is essential. I shouldn't even have to say this. How else is anyone going to know them, telepathy?
Usage Scenarios and ExamplesThis is the next step up from command listings. Having a man page full of commands and options is better than nothing, and having lots of examples of real-world use is a hundred times better. When would you want to use this set of options or that, and when is foo preferable to blah?
Some tasks benefit from "big picture" howtos, and not just focusing narrowly on a single command or application. A classic example of this is learning to run a mail or Web server. It's not enough to learn just Postfix, Exim, or Sendmail because a mail server uses a lot of specialized servers and applications working together. Another example is doing audio and video production; this involves learning system tuning for best performance and low latency, and learning which of the multitudes of Linux multimedia applications work best and work well together. Including references to relevant companion apps and howtos, and describing how all the pieces fit together is a very helpful thing to do. I know, there are lots of pieces and lots of different ways to assemble them-- pick one.
Teaching a New FieldThis is the hardest. For example, you want to learn to use Audacity for audio recording and editing. You can't just "learn Audacity", you also have to learn audio concepts, terminology, techniques, and audio hardware. Another example is Digikam, the fabulous and wonderful digital photo manager and editor. Learning Digikam also means learning digital photography editing techniques, terminology, and concepts. Using Gnucash or KMyMoney? Same thing-- you have to understand certain accounting conventions and terminology. Writing these kinds of howtos is a lot of work. The fine folks at the Gnucash, Digikam, and Audacity projects all try hard to supply this type of documentation.
- Skip Ahead
- 1. The Many Faces of Documentation
- 2. The Many Faces of Documentation


text:
If you've turned on a television in the last year, you've probably glimpsed Young the Giant.
The Irvine natives have played on "Jimmy Kimmel Live!," "The Tonight Show with Jay Leno"and "Later with Jools Holland" in the U.K.
Rock music enthusiasts might also recognize the band from a slightly more prominent gig this past summer at the MTV Video Music Awards, when Jared Leto and Zoe Saldana introduced them to the stage.
For many who grew up in the 1980s, '90s and '00s, the VMAs are a summer standard. Teens huddle around the TV, popcorn in hand, and judge the biggest music names in the industry.
François Comtois, drummer and vocalist, said it made the experience all the more surreal.
"I remember feeling really, really nervous for the dress rehearsal," he said. "We had a bunch of our friends and family come on stage with us. That put us at ease. When it actually happened and we were surrounded by Kanye andJay-Z— it was a joyful time for us."
The band rewarded lucky fans by dancing onstage with them at the awards show, which revealed their ability to make an internationally-viewed TV performance look like an intimate show at a friend's home.
The band — composed of Sameer Gadhia, 22, Jacob Tilley, 22, Eric Cannata, 21, Payam Doostzadeh, 22, and Comtois, 23 — all attended high school in Irvine. They are about to begin a six-month tour on Feb. 8, which will stretch from San Francisco to Toronto.
They'll play Soma in San Diego on Feb. 10 followed by The Wiltern in Los Angeles on Feb. 11 and 12. All three shows are sold out.
Comtois, who attended UC Irvine, said the band formerly known as "The Jakes" decided to give music a go in 2009. During that year the band had performed at South by Southwest, had songs play on KROQ and shows such as "The Real World: Brooklyn," and A&E's"The Beast" used their music.
The band members dropped out of their respective colleges — Stanford, UC Santa Cruz, UC San Diego, Cal State Long Beach and UCI — all aiming to return.
Shortly thereafter, they went on tour with Minus the Bear and Steel Train.
"I was a huge fan of Minus the Bear in high school so when we got word of that I was geeking out a bit," Comtois said.
They've played with the Futureheads, Neon Trees and Everest.
Morrissey, The Smiths frontman, called Young the Giant one of his favorite bands.
Comtois says although the band enjoys the appreciation, its members try not to take it all too seriously.
"It validates you a little bit but we try not to take too much thought in what anyone says about us," he said.
What is it about their music that grabs fans?
"I think we try to be very honest about who we are," he said. "We try to portray ourselves as who we actually are… as human beings."
Although most fans are current with their self-titled debut album, which was released last year, the band will start recording its next album in the fall, which will be released in spring 2013.
Until recently they've been holed up in their Mt. Washington home, writing music and jamming.
"The next album is going to reflect how we've grown — our experiences since then, who we've known and met," Comtois said, citing the fact they were still teens when they wrote hits such as "My Body." "Hopefully it ends up sounding a little bit more mature, a little bit more eclectic."
Familiar faces in their "The Jakes" days at local hot spots such as Detroit Bar and Chain Reaction, Comtois said the band will do a show in Orange County soon.
They were here in December, performing at the Galaxy Theatre in Santa Ana. Proceeds benefited the Irvine Public Schools Foundation and Comtois said they raised about $30,000.
"I moved to Orange County when I was 15 so I spent some formative years becoming an adult in Orange County," said Comtois, who went to Northwood High School. "As music was concerned, the music programs at each of our high schools were really formative in creating an actual passion (in us) for music."
Twitter: @joannaclay


text:
These meatless soft tacos are stuffed with sauteed vegetables and topped with smoky salsa. To make it a meal, serve with Spanish rice, a tossed green salad with red wine vinegar dressing and cantaloupe cubes.
In a large saucepan, heat the olive oil over medium heat. Add the onion and cook until soft. Add the summer squash and zucchini, and continue cooking until tender, about 5 minutes. Stir in the garlic, tomatoes, jalapeno, corn kernels and beans. Cook until the vegetables are tender-crisp, about 5 minutes. Add the cilantro and remove from the heat. Heat a dry, large frying pan (without a nonstick surface) over medium heat. Add 1 tortilla to the hot pan and heat until softened — about 20 seconds per side. Repeat with the remaining tortillas. To serve, divide the tortillas among individual plates. Scoop an equal amount of the vegetable mixture onto each tortilla. Top each with 2 tablespoons of the salsa. Serve immediately.
Original article: https://www.mayoclinic.org/healthy-lifestyle/recipes/soft-tacos-with-southwestern-vegetables/rcp-20049713
Any use of this site constitutes your agreement to the Terms and Conditions and Privacy Policy linked below.
Mayo Clinic is a nonprofit organization and proceeds from Web advertising help support our mission. Mayo Clinic does not endorse any of the third party products and services advertised.
A single copy of these materials may be reprinted for noncommercial personal use only. "Mayo," "Mayo Clinic," "MayoClinic.org," "Mayo Clinic Healthy Living," and the triple-shield Mayo Clinic logo are trademarks of Mayo Foundation for Medical Education and Research.


text:
Very simple today! I think you don't necessarily need a lot of accessories.. My neon orange beanie is enough!
Friday, 30 November 2012
This and That.
Very simple today! I think you don't necessarily need a lot of accessories.. My neon orange beanie is enough!
Posted by Martina at 15:54 2 comments:
Instagram it this week.
Laura coming by for some thursday breakfast! 5) Heart-shaped pancakes, 6) Only lipstick day makeup!
Thursday, 29 November 2012
Teddy Love.
I need to get my hands on some teddy bear fabric!! Comfy warm furry things for winter mmmm...
Posted by Martina at 20:03 No comments:
White lace and DIY boots.
Posted by Martina at 15:10 4 comments:
Something old, something new...
Today I'm trying something new: Videoblogging! :) I just HAD to make a video when I found this greater than great radiostation... It plays arabic, african, brazilian, well ALL kind of traditional music! It makes me completely calm and focused on other stuff, than the music. It's a very inspiring background tune :)
Following, some pics from the new appartament :) For the first time in my life, I can feel a super positive aura... I think auras are formed mostly on who and what kind of people have been living in the flat before. This flat is rented to us by a model from Stockholm, who regularly goes to New York for a longer period of time to work, and who now currently is in Burkina Faso (her family lives there) and who is a passionate documentary-filmer. One of the documentaries that she has made is Taxi Sister, in which she follows a female taxidriver in Senegal on her daily routines and the daily difficulties she is confronted with only because of her gender. See the trailer here.
Following, some pics from the new appartament :) For the first time in my life, I can feel a super positive aura... I think auras are formed mostly on who and what kind of people have been living in the flat before. This flat is rented to us by a model from Stockholm, who regularly goes to New York for a longer period of time to work, and who now currently is in Burkina Faso (her family lives there) and who is a passionate documentary-filmer. One of the documentaries that she has made is Taxi Sister, in which she follows a female taxidriver in Senegal on her daily routines and the daily difficulties she is confronted with only because of her gender. See the trailer here.
Posted by Martina at 14:37 2 comments:
Wednesday, 28 November 2012
Jeans/Vintage, Shirt/Zara, Necklace/DIY, Shoes/Vagabond
Moved to a new flat today, yay! The floor is absolutely amaaaazing (I know it's weird someone can be that hyped about a floor....) I'll take some pictures tomorrow! :) Now I need to catch some Z's! xxx
Posted by Martina at 23:57 2 comments:
Tuesday, 27 November 2012
DIY Chain Boots.
Super easy way to pimp up your old boots! All you need is different kinds of chains, pliers and I also used a keychain ring to keep them in place. To attach the chains to eachother i used small golden rings that are easy to open and close. You can also use leather or any other material to embellish your boots, just use your imagination!
Posted by Martina at 17:51 No comments:
Smooooth Clothing.
After labels like Black Milk Clothing, We Are Handsome and maaany more brands embracing the "print-fever", I was suggested to check out this Barcelona brand Smooooth (yes with 4 o's) Clothing.
Not to talk about the freshness of the prints, I also get a feeling of lightness and humor, that is missing in so many brands nowadays!! Fashion shouldn't always be so serious ;) In these pieces you can smell the Barcelona sun even if you are hundreds of miles away!
The sweats, leggings and tees are all 100% soft cotton and handmade! So the prices are MORE than right. Need to order myself one asap.
Check out their webshop here
Posted by Martina at 12:11 No comments:
Sunday, 25 November 2012
Saturday, 24 November 2012
"The Designer"
Space leggings/Gina Tricot, Furry Sweater/Vintage
Playing around in the studio :)
Photo by: Rikard Lilja
Posted by Martina at 23:09 7 comments:
Friday, 23 November 2012
Barcelona Instaweek!
Some pics from my week in Barcelona in Instagram:
1) Ready for a casting, 2) The suuuper cool Ingesba Showroom, 3) Beautiful French model Stephania with her GORGEOUS jacket, 4) Javier with our new-found squirrel at Encants Market, 5) Last day touristing at the labyrinth park 6) New stockings!
Monday, 19 November 2012
New In.
A few things I got here in Barcelona! A denim shirt and a paisley shirt, a handbag, faux-leather panel leggings, two lace dresses from H&M (white and black, I´ll make a separate post on them as soon as I´m back in Stockholm!) and then of course my Margiela for H&M cashmere turtleneck. Today I´m hitting the vintageshops hoping to find some cool-weird stuff! :P
Posted by Martina at 15:33 1 comment:
Sunday, 18 November 2012
Laid Back Margiela.
My look yesterday! Almost top to toe H&M hahaha...
Saturday, 17 November 2012
Thursday, 15 November 2012
Bcn so far!
It felt so great to Wake up in Barcelona today after a nightmare trip thanks to the spanish general strike.. I went to MMM for H&M and picked up a few things for me and estela, tonight we're Going to our favourite Mexican place for dinner and drinks!! I had completely forgot how laid back this city is...Love It!
Big bag or tiny girl?
Tuesday, 13 November 2012
Instagram It.
1/My new earring, 2/Emily and Julie on Emily's birthday!, 3/Rikard sleeping, 4/Details, 5/Nordic Wardrobe at Korjaamo, 6/Travel outfit.
Posted by Martina at 18:51 2 comments:
Monday, 12 November 2012
DIY Winter Coat.
Here's a DIY I made for the Matkus Shopping Center blog I'm hosting! I decided to use an old knitted sweater i loved and used a lot but that now didn't fit my style anymore, but you can basicly use any kind of fabric!From old socks, hats, scarves... The cool contrast comes from using a knitted fabric, to complement the shiny jacket.
See the whole post (in finnish unfortunately) here.
asos.com, 350€
my version, jacket from H&M 35€
See the whole post (in finnish unfortunately) here.
Posted by Martina at 23:15 2 comments:
Sunday, 11 November 2012
Style Icon: Rita Ora
I just NOW discovered what singer Rita Ora looks like!! I love her fun, witty and super cool way of dressing, I'm definetely going to spend tonight browsing her pics on the internet for inspiration! She is so pretty and so brave with accessories too, something I want to be better at.
Plus, I also found a picture of her that is very similar of a picture I have of myself... that must be a good sign ;) haha!
Posted by Martina at 20:18 No comments:
Labels: fashion, icon, inspiration, rita ora, style
Friday, 9 November 2012
Found myself a lookalike today! My boyfriend found this girl in some fashion ediotrial and it's like the first girl I've ever seen who looks so alike me!! Scary and fun at the same time!
Tuesday, 6 November 2012
Plan B.
So.... Missed my flight to Barcelona last nigth. I did so not expect it to happen, I thought I was there in time and all... Only thing I could do was brake down and cry! I was supposed to be there now sipping red wine with Estela... The bus drivers felt sorry for me so they let me on the bus back to Stockholm for free and there were not even supposed to be any passengers on that ride the busdriver was just going home! :D
I stayed up late booking new flights so I'm leaving the day after my important doctors appointment in Finland next monday! Can't win every time can you?
Monday, 5 November 2012
The Dark Side.
Studded Cap/romwe.com, Star Wars tee/Ebay, Pleather Skirt/romwe.com, Shoes/Vagabond, Rings/asos.com
Flying to Barcelona today!!!Woop woop! Can't wait to see everyone and have goooood red wine and shop for fabrics and party a bit! Unfortunately I'm not going to be able to update my blog but I promise a hella lot of pictures when I come back! xx
What do you think of my new childrens Star Wars tee by the way? :P
Posted by Martina at 15:03 4 comments:
Labels: cap, fashion, lookbook, outfit, pleather, print, romwe, romwe.com, skater, skirt, spikes, star wars, studded, today
Sunday, 4 November 2012
Tartan Jungle.
Metallic Belt/Asos.com, Kilt/Second Hand, Coat/Benetton, 1st Checked Shirt/Second Hand, 2nd Checked Shirt/Boyfriend's Closet(Gant)
Got soooo inspired by this kilt I found for 3(!!!)€ in a second hand shop in Finland! I wanted to take inspiration from Dries van Notens patternlayering, but still keep it my way. The metal belt with studs definetely made it more my style!
Posted by Martina at 15:28 3 comments:
Even if I feel the trackpant trend is over, I couldn't help but click in on a closer view on these trackpants from asos.com. They look perfect for winter, I especially like the cool pattern of pant nr.1(besides they look sooo soft and warm) and the quilted pant nr.2!
Posted by Martina at 11:05 No comments:
Labels: asos, fashion, pattern, print, quilted, sweatpants, trackpants, trend
Stockholm Summer.
by Rikard Lilja
Another one from the archives that I got to see only yesterday! We found an abandoned empty pool in Stockholm this summer and decided to try it for some Lords of Dogtown-ish pictures! This pic makes me want to start to wear only eyeliner again, mascara is overrated! Allthough in this pic I was tanned, now I'm white as a sheet. Might not give the same effect...
Posted by Martina at 10:40 No comments:
Saturday, 3 November 2012
Oldie but goldie!
Me in Stockholm. Pic by my dearest Joe. ♥
Just found this old picture.. It's snapped by one of the most important people in the whole world for me. Dear Joey! He recently moved to Hong Kong, miss him so much!! Gotta go visit before my move to Tokyo. Check out more of his works here.
me, Joey and my sis!
Good old times! He just poured a screwdriver in my lap.
Posted by Martina at 19:39 2 comments:
Labels: fashion, friends, joe lesina, old, photo
In the car on our way home from Kuopio.
We're shooting in Stockholm this weekend and on monday I'm flying to Barcelona, my old hometown! I've missed the lifestyle, people and energy that the city gives SO much, I can't wait to go back!!It's such a beautiful city and I have many of the dearest people in my life living there that I haven't seen for over a year. I'm going to hug them each for an hour! Again, can't wait!!!
Friday, 2 November 2012
Sequin Pants.
I got these sequin pants secondhand shopping this week and decided to wear them with my DIYed fake fur power shoulder jacket for a Michael Jackson inspired look! The occasion was the VIP-opening party for the brand new shopping center in Kuopio, Finland, for which I have done the fashion part of their exclusive customer magazine. We had lots of wine and browsed through the shops, and the next day I was personal shopping and styling three winners with clothes from several shops! Such exhausting two days, tonight I'll finally be back in Stockholm and tomorrow I'm styling a shoot I've been planning for soooo long! Can't wait!
Fake Fur Jacket/DIY, Pearl and Chain Necklace/DIY, T-shirt/H&M
Posted by Martina at 15:53 No comments:
Labels: black, curls, fake, fashion, fur, jacket, kuopio, lookbook, matkus, opening, outfit, pants, party, powershoulder, sequin
Subscribe to: Posts (Atom)


text:
Jedi Knight
Jedi Knight
- Aug 16, 2001
- 9,604
- 14
- 51
I have been stopping at the TARGET near my house every couple days for the last four weeks and they haven't gotten anything new on the pegs. Here's the thing... they have had the little silver "restock" dot on all three of the Vintage pegs during that time and two silver dots on the Movie Heroes pegs for the last two weeks. Basically, they have had these things on order in their system, but no stock has been shipped from their distribution centre. I'm assuming what that means is that there is no stock arriving at their centre from Hasbro. That sorta makes me wonder what's going on with the shipments again. It doesn't really sound like Hasbro's making good on their promises to have better distribution this year.