Patent Submitted for Target eClinical Trial Record (Target e*CTRTM)

Target Health is pleased to announce that a patent was submitted for Target eClinical Trial Record (Target e*CTRTM) under the Accelerated Examination Program. Target e*CTRTM allows any EDC clinical site user to enter clinical trial data directly online without the need to create a paper source document. Target e*CTRTM creates an electronic clinical trial source record prior to the data reaching the EDC database. Target e*CTRTM is already fully integrated with an EHR and final validation will be completed by the end of September. Several meetings have already taken place with regulatory bodies and there appears to be no regulatory hurdles. The system is 21CFR Part 11 compliant.

Target e*CTRTM will dramatically reduce the need for source document verification (SDV) and reduce travel costs for clinical trial by at least 50%. The goal is for Target e*CTRTM to be used by all pharmaceutical and device companies using any EDC system. Pricing will be by the study and will be a fraction of the overall savings.

For more information about Target Health and our software tools for paperless clinical trials, please contact Dr. Jules T. Mitchel (212-681-2100 ext 0) or Ms. Joyce Hays. Target Health’s software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website at www.targethealth.com

Sun Exposure May Trigger Certain Autoimmune Diseases in Women

Ultraviolet (UV) radiation from 1) ___ may be associated with the development of certain autoimmune diseases, particularly in women. The study found that women who lived in areas with higher levels of UV exposure when they developed an autoimmune muscle disease called myositis were more likely to develop the form known as dermatomyositis, which weakens the 2) ___ and causes distinctive rashes, instead of the form called polymyositis that does not have a rash. Although the study has not shown a direct cause and effect link between UV exposure and this particular autoimmune disease, this research confirms the association between UV levels and the frequency of dermatomyositis found in a previous investigation. The study, published in the August issue of Arthritis & Rheumatism, is also the first to evaluate and find a possible UV radiation association in 3) ___ diseases in women. According to this NIEHS research, women are more likely than 4) ___ to develop many autoimmune diseases, but the reasons for this have not been clear. The study only found the association between UV exposure and dermatomyositis in women and not in men, and it could be that inherent differences in how women and men respond to UV 5) ___ may play a role in the development of certain autoimmune diseases. The research team also noted that other researchers have shown that female mice develop more skin 6) ___ after UV light exposure compared to male mice and these effects may be related to the new findings in dermatomyositis. Dermatomyositis and polymyositis are the two major forms of myositis and both are considered autoimmune diseases, in which the body’s immune system attacks muscle or 7) ___ and sometimes other tissues. Dermatomyositis is typically accompanied by a distinctive reddish-purple rash on the upper eyelids or over the knuckles and is often made worse with sun 8) ___. Patients with autoimmune diseases make a variety of autoantibodies that are unique to different conditions. One autoantibody specifically associated with dermatomyositis is called the anti-Mi-2 autoantibody and it’s known from previous research that UV radiation increases levels of the Mi-2 protein that this 9) ___ binds to. 

ANSWERS: 1) sunlight; 2) muscles; 3) autoimmune; 4) men; 5) radiation; 6) inflammation; 7) skin; 8) exposure; 9) autoantibody

Leprosy

As infectious diseases go, leprosy is still one of the least well-understood, in part because the Mycobacterium is difficult to culture for research and it has only one other animal host, the nine banded armadillo. An Indian or African origin for the disease has often been assumed based on historical sources that support an initial spread of the disease from Asia to Europe with Alexander the Great’s army after 400 BCE. Skeletal evidence for the disease was previously limited to 300-400 BCE in Egypt and Thailand. A recent report on genomics of Mycobacterium indicated the disease may have originated in Africa during the Late Pleistocene and that M. leprae spread out of Africa sometime after 40,000 years ago. A recent analysis was performed of a 4000-year-old skeleton from India bearing evidence of leprosy. This skeleton represents both the earliest archaeological evidence for human infection with Mycobacterium leprae in the world and the first evidence for the disease in prehistoric India. The study, published in the journal PLoS One, demonstrates that leprosy was present in human populations in India by the end of the mature phase of the Indus Civilization (2000 BCE) and provides support for one hypothesis about prehistoric transmission routes for the disease. The presence of leprosy in India toward the end of this period indicates that M. leprae existed in South Asia at least 4000 years ago. The presence of leprosy at Balathal 4000 years ago also supports translations of the Eber’s papyrus in Egypt and a Sanskrit text in India (the Atharva Veda) that refer to the disease as early as 1550 BCE. The evidence from Balathal indicates that it is possible that the authors were describing leprosy as the disease was present in the subcontinent in prehistoric times. Furthermore, in contemporary Hindu tradition burial is uncommon unless an individual is a highly respected member of the community (like an ascetic) or is an individual seen as unfit to be sacrificed through cremation. These latter individuals are buried and include outcastes, pregnant women, children under 5, victims of magic or curses, and lepers. During the second millennium BCE, when there was disintegration of Indus settlements and new, smaller settlements sprang up all over the western half of peninsular India. Adult burial became rare and children under 5 began to predominate in the skeletal assemblages. The leper was one of only five individuals buried at the site of Balathal (the others were middle-aged women, an ascetic from the Early Historic period, and a fragmentary clavicle found with the leprous skeleton). The leper’s skeleton was interred within a large stone enclosure that had been filled with vitrified ash from burned cow dung, the most sacred and purifying of substances in Vedic tradition. The presence of this skeleton at Balathal, the manner in which it was interred, and the preponderance of children in burial assemblages from this time period throughout western India, suggest the origin of these practices still common in Vedic tradition today. The skeleton is currently housed at Deccan College Post-Graduate Research Institute in Pune, India.

From Nerve Roots to Plant Roots – Unexpected Insights Into Hereditary Spastic Paraplegia

HSP (hereditary spastic paraplegias) primarily affects corticospinal neurons, which extend projections called axons from the brain’s cerebral cortex to the spinal cord. The longest corticospinal axons extend nearly all the way down the spinal cord, a distance up to about three feet, and controls movement in the legs. In HSP, these long axons develop abnormally or they degenerate later in life, causing muscle stiffness and weakness in the legs. HSP exists in many forms in different families, and more than 40 genes have been implicated in the disease. The genes behind HSP and their roles inside neurons are poorly understood. Neuroscientists have borrowed heavily from botanists to describe the way that neurons grow, but analogies between the growth of neurons and plants may be more than superficial. A new study from the National Institutes of Health and Harvard Medical School suggests that neurons and plant root cells may grow using a similar mechanism. However, the study suggests that several forms of HSP share an underlying defect with each other – and with abnormal root hair development in a plant widely used for agricultural research. The strange implication is that the plant, Arabidopsis thaliana (mouse-ear cress), could prove useful for further research on HSP. In a study, published online in the Cell (7 August 2009), it was proposed that defects in the shaping of a subcellular structure known as the endoplasmic reticulum (ER) are a common cause of HSP. The ER – named for its reticulated (or net-like) shape – is a cellular factory, where molecules such as proteins and lipids that are vital to cell growth are made and packaged for shipping to various cellular destinations. It has been hypothesized that in several forms of HSP, the ER loses its complex shape and is unable to support the growth or maintenance of long corticospinal axons. Several years ago, it was shown that similar ER defects in Arabidopsis impair the growth of the plant’s root hairs. These are wispy, microscopic projections that grow from the plant’s individual root cells. The new study focuses on a gene called atlastin. This gene is defective in about 10% of HSP cases, and has been shown to have a role in axon growth. The new study reveals that the atlastin protein is necessary for maintaining the shape of the ER in mammalian cells, and that an analogous protein called Sey1p performs the same function in baker’s yeast. The study demonstrated that ER shaping defects have general relevance for HSP, by showing a connection between atlastin and a group of proteins known as the DP1 family. Years ago, it was reported that a yeast analog of DP1 regulates the shape of the ER in yeast. Meanwhile, others had independently reported that mutations in REEP1, a member of the DP1 family, cause 3% to 8% of HSP cases. The new study shows that atlastin interacts physically with DP1 in mammalian cells, and that Sey1p (the yeast atlastin) interacts with the DP1 analog in yeast. If this connection between axon growth and root hair growth withstands further study, Arabidopsis could be a useful tool for investigating mechanisms of HSP. Arabidopsis is easy to raise in the lab, and the short root hairs of the RHD3 mutant are easy to observe, compared to the growth defects in atlastin-deficient neurons and yeast.

ONCOLOGY

Filed Under News | Leave a Comment

Antidiabetic Therapies Affect Risk of Pancreatic Cancer

Antidiabetic drugs have been found to have various effects on cancer in experimental systems and in epidemiologic studies, although the association between these therapeutics and the risk of human pancreatic cancer has not been explored. As a result, a study published in Gastroenterology (2009;137:482-4880 was performed to see the effects of antidiabetic therapies on the risk of pancreatic cancer. The investigation was a hospital-based case-control study conducted at M. D. Anderson Cancer Center from 2004 to 2008. The study involved 973 patients with pancreatic adenocarcinoma (including 259 diabetic patients) and 863 controls (including 109 diabetic patients). Information on diabetes history and other risk factors was collected by personal interview. The frequencies of use of insulin, insulin secretagogues, metformin, and other antidiabetic medications among diabetic patients were compared between cases and controls. The risk of pancreatic cancer was estimated using unconditional logistic regression analysis. Results showed that diabetic patients who had taken metformin had a significantly lower risk of pancreatic cancer compared with those who had not taken metformin (odds ratio, 0.38; P = .001). This difference remained statistically significant when the analysis was restricted to patients with a duration of diabetes >2 years or those who never used insulin. In contrast, diabetic patients who had taken insulin or insulin secretagogues had a significantly higher risk of pancreatic cancer compared with diabetic patients who had not taken these drugs. According to the authors, metformin use was associated with reduced risk, and insulin or insulin secretagogue use was associated with increased risk of pancreatic cancer in diabetic patients.

ONCOLOGY

Filed Under News | Leave a Comment

Risk of Pancreatic Cancer Linked To Variation In Gene That Determines Blood Type

Pancreatic cancer is the fourth leading cause of cancer death in the US. It is difficult to detect, and in many people it is not diagnosed until after the disease has spread to other parts of the body. Less than 5% of Americans with pancreatic cancer survive five years past diagnosis. Risk factors include smoking, diabetes, race, and a family history of the disease. A person’s blood type depends on which form or forms of the ABO gene they inherit from their parents. The protein produced by the ABO gene determines the type of carbohydrates (complex sugars) that are present on the surface of red blood cells and other cells, including cells of the pancreas. The proteins encoded by the A and B forms of the gene transfer different carbohydrates onto the cell surfaces to make A and B blood types. The O form encodes a protein that is unable to transfer carbohydrates. Studies by other researchers have shown that ABO protein encoding in pancreatic tumor cells is different than in normal pancreatic cells. According to an article published on line the Nature Genetics (2 August 2009), common variants of the gene that determines human blood type are associated with an increased risk of pancreatic cancer. In the study, a genetic variation was discovered in a region of chromosome 9 that contains the gene for ABO blood type, that was associated with pancreatic cancer risk. Individuals with the variant that results in blood types A, B, or AB were at an increased risk of pancreatic cancer, compared to those with the variant for blood type O. This finding is consistent with previous research, some of it dating back to the 1950s and 1960s, that had shown increased risks of gastric and pancreatic cancer among individuals of the A and B blood groups (i.e., blood types A, B, and AB). The latest results provide a genetic basis for those earlier observations. To discover genetic variations that contribute to pancreatic cancer risk, the study conducted a genome-wide association study (GWAS). In a GWAS, researchers analyze common variants, called single-nucleotide polymorphisms (SNPs), in the genomes of people with a disease and people without the disease. Initially, the research team studied the genomes of 1,896 patients with pancreatic cancer and 1,939 control subjects to identify SNPs with a strong association with pancreatic cancer. The team then verified its findings by studying the genomes of another 2,457 people with pancreatic cancer and 2,654 people without the disease. In the end, they identified several SNPs on the long arm of chromosome 9 that were associated with pancreatic cancer risk and mapped to the ABO gene. According to the authors, only by working across disciplines and with more than a dozen research groups were they able to make this important discovery of the potential role of the ABO gene in pancreatic cancer risk. The authors added that although it will take much more work, this finding may lead to improved diagnostic and therapeutic interventions that are so desperately needed.

TARGET HEALTH excels in Regulatory Affairs and works closely with many of its clients performing all FDA submissions. TARGET HEALTH receives daily updates of new developments at FDA. Each week, highlights of what is going on at FDA are shared to assure that new information is expeditiously made available. 

FDA Enhances Speed and Transparency of Actions Taken Against Misconduct in Drug and Device Development

The FDA has announced it has stepped up its efforts to prevent non-compliant investigators and others from participating in new product development. The FDA’s procedures for debarment and disqualification have been enhanced to better protect participants in clinical studies and for ensuring the safety and effectiveness of the medical products marketed to the American public. Compliance with the FDA’s statutes and regulations is key to protecting clinical study participants and the general public. The new debarment and disqualification procedures will also help ensure that sponsors of clinical studies do not unknowingly use individuals who potentially may be debarred or disqualified by the FDA. Under current law, the FDA can ban, or debar, individuals known to have broken the law from working for companies with approved or pending drug applications at the FDA. The agency can also disqualify researchers conducting clinical testing of new drugs and devices, when the FDA determines that they have not followed the rules intended to protect study subjects. Further, the FDA can disqualify a clinical investigator who has, for example, manipulated data so as to inaccurately report study findings. According to FDA, some members of Congress have expressed concern that the FDA has not adequately used its debarment and disqualification authorities. Congress has also noted that when these authorities are invoked, the agency is slow to remove such individuals from the drug or device development process. Members of the House Energy and Commerce Committee have asked the Government Accountability Office to examine the FDA’s debarment and disqualification procedures. The FDA conducted a similar review of its processes and concluded that the agency should enhance its procedures to ensure it can act quickly, when needed, to further safeguard clinical trial subjects and the drug and device development processes. The revamped debarment and disqualification procedures, which include increased staffing and centralized coordination, ensure that more rapid, transparent and consistent actions are taken. In the short time these measures have been in effect, the number of debarment actions has risen considerably and the times for resolving both disqualification and debarment actions have been reduced significantly. The agency has also taken steps to ensure that sponsors involved in the testing and development of new medical products have ready access to information about FDA’s debarment and disqualification actions. The FDA has already added to its Web site a single page where all pending and completed disqualification proceedings can be found and is currently doing the same for debarment proceedings. By providing improved access to information about all debarment and disqualification proceedings, the FDA is increasing transparency and enhancing protection of the public health. For more information, see:  Questions and Answers on Debarment/Disqualification, Public listing of disqualification actions and Public listing of debarment actions.

 

For more information about our expertise in Regulatory Affairs, please contact Dr. Jules T. Mitchel or Dr. Glen Park.

FOR IMMEDIATE RELEASE
Friday, August 7, 2009

Contact: HHS Press Office
(202)690-6343

New State-by-State Reports Show How Health Insurance Reform Will Benefit All Americans

HHS Secretary Kathleen Sebelius today released Stable and Secure Health Care for America, a series of new state-by-state reports outlining how health insurance reform will improve health care for all Americans. Sebelius announced the availability of the new reports as part of a Webcast — “Health Insurance Reform: What’s In It For You?” — where Sebelius and top HHS officials took questions from the American people and discussed the importance of health insurance reform. The new reports are available at www.healthcare.gov.

“These reports show how health insurance reform will help Americans save money, get better care, strengthen their insurance if they already have it, and afford insurance if they don’t,” said Sebelius. “Every American will benefit when we pass health insurance reform.”

The reports released today show reform will:

  • Lower health care costs;
  • Increase health care choices by protecting what works and fixing what’s broken; and
  • Assure quality, affordable care for all Americans.

Today’s reports are the second in a series of state-by-state reports on health care across the country. Earlier this summer, Sebelius released The Health Care Status Quo in Your State, a series of state by state reports on the current state of health care in America. The reports are available at http://www.healthreform.gov/healthcarestatus.html.

###


Note: All HHS press releases, fact sheets and other press materials are available at http://www.hhs.gov/news.

Last revised: August 07, 2009