kumba-sennaar

Kumba Sennaar

Kumba is an experienced freelance writer, ghostwriter, editor, and researcher with nearly a decade of experience. She is an honors graduate from Rensselaer Polytechnic Institute and a Master’s candidate in Biotechnology at Johns Hopkins University. Her passion is to help people live healthier, happier lives. For superior content and/or capacity building for your business or special projects contact Kumba via email at Ksennaa1@jhu.edu.

Microdosing and Drug Discovery

Understanding Microdosing The practice of microdosing has gained momentum in recent years and is defined as using 1 percent of a pharmacologically active dose. The method is believed to have the potential to better obtain personalized medicines for the treatment of a variety of diseases. Since administration of these doses are so low, the drugs are unlikely to produce whole-body effects but have concentrations adequately permitting absorption, distribution, metabolism, and excretion. So in effect, microdose studies are not intended to produce any adverse pharmacologic effects in humans, but may produce useful pharmacokinetic information to assist in further development of the compound.[1]   The potential for decreased Research & Development expenditures has made microdosing an attractive strategy, particularly in the case of resources spent on nonviable drug candidates and animal testing. Microdose studies are conducted in the Phase 0 clinical trial. During this stage, issues pertaining to drug metabolism and pharmacokinetics are addressed. Microdosing, therefore, allows not only for the selection of the drug candidates more likely to be developed successfully, but also for the determination of the first dose for the subsequent Phase I clinical trial.[2][3]   Competing Challenges With these potential benefits, more research is required to guarantee the accuracy and efficiency of microdosing. It is important to remember that there is an assumption of linearity between the microdose and the full dose drug. The human body’s response...

Futuristic Foods: All About GMOs

  You’ve probably heard the term “GMO” before but what exactly does it mean? For starters, the term “GMO” is short for “genetically modified foods.” This refers to foods that are produced from organisms with their genetic material modified in a way that does not occur naturally. This is similar to methods used in genetic engineering. Examples include foods such as corn, soy, zucchini, milk, sugar, canned soups, frozen foods, and cereal.   Due to the growing popularity of GMOs, it is worth considering the benefits and risks of these futuristic foods. Chemicals like insecticides that are often used in crops that are genetically modified are believed by some to increase the risks of cancer. There is also a possibility that GMOs create new allergies and make people less resistant to antibiotics. As far as the environment goes, weed killers used for GMOs can cause the crops to breed with weeds, creating “superweeds” that require stronger and more expensive pesticides and weed killers.   Cost effectiveness is a top reason for advocates of genetically modified foods. By growing crops faster, farmers help keep foods affordable. It has even been said that by year 2050, GMOs will help us feed the extra 2 billion people that will fill the planet. This is because farmers can develop foods that survive droughts or extremely cold weather and aren’t as likely to be plagued...

Fighting Cancer with Powerful Proteasome Inhibition

When it comes to blood cancer Lymphoma is the most common. Lymphoma manifests in two general forms: Hodgkin lymphoma and non-Hodgkin lymphoma (NHL). Uncontrollable proliferation of lymphocytes (category of white blood cells) leads to the development of cancerous lymphocytes which can ultimately metastasize to various parts of the body and cause tumors. B-lymphocytes (B-cells) and T-lymphocytes (T-cells) are the immune system cell types commonly associated with lymphomas. Drugs which inhibit the normal function of the proteasome, which is to degrade protein products and prevent “degradation of the intracellular proteins, affecting signaling within cells,” ultimately results in two specific cellular paths: death of the cancer cell or “inhibition of growth” of the cancer cell (“Lymphomation”).     The significance of HDAC (Histone Deacetylase) inhibition lies in its ability to keep DNA exposed for the binding of transcription factors to DNA sequences in the nucleus, via the “acetylaton of lysine residues” (“Lymphomatics”) thus preventing rewrapping of DNA into its highly coiled and packed state around proteins called histones via HDACs. Cancer’s ability to rapidly proliferate, heavily depends upon its ability to gain regulatory control over transcription factors such as those which promote cell growth, and to inhibit tumor suppressor protein functioning or bypass Cell Cycle DNA damage checkpoints.   The mechanism of action for certain drugs promoting HDAC inhibition follows the aforementioned model, and specifically “causes [in vitro] the accumulation of acetylated...

March is Colon Cancer Awareness Month!

Source   March is Colon Cancer Awareness Month and it is an ideal time to get candid about the third most common cancer diagnosed among men and women in the United States. The American Cancer Society estimates that in 2016, over 95,000 Americans will be diagnosed with Colon Cancer, and of those diagnosed, over half will die from Colon Cancer. Colon cancer normally develops in adults 50 years of age and older from polyps in the large intestines. Colon cancer screening helps save lives by detecting polyps early so they can be removed before they become cancerous. Early detection through screening is invaluable and continues to play a pivotal role in the lives of over 1 million colorectal cancer survivors across the nation.   When it comes to regular screening for the average American, the National Institutes of Health (NIH) recommend testing during the following intervals: • Colonoscopy every 10 years • Double-contrast barium enema every 5 years • Fecal occult blood test (FOBT) every year (colonoscopy is needed if results are positive) • Flexible sigmoidoscopy every 5 to 10 years, usually with stool testing (FOBT) done every 1 to 3 years • Virtual colonoscopy every 5 years     A Fecal Occult Blood Test is a stool test and perhaps one the simplest Colon Cancer screening procedures. Blood in the stool is a classic indicator of the presence...

Microdosing and Drug Discovery

Understanding Microdosing The practice of microdosing has gained momentum in recent years and is defined as using 1 percent of a pharmacologically active dose. The method is believed to have the potential to better obtain personalized medicines for the treatment of a variety of diseases. Since administration of these doses are so low, the drugs are unlikely to produce whole-body effects but have concentrations adequately permitting absorption, distribution, metabolism, and excretion. So in effect, microdose studies are not intended to produce any adverse pharmacologic effects in humans, but may produce useful pharmacokinetic information to assist in further development of the compound.[1] The potential for decreased Research & Development expenditures has made microdosing an attractive strategy, particularly in the case of resources spent on nonviable drug candidates and animal testing. Microdose studies are conducted in the Phase 0 clinical trial. During this stage, issues pertaining to drug metabolism and pharmacokinetics are addressed. Microdosing, therefore, allows not only for the selection of the drug candidates more likely to be developed successfully, but also for the determination of the first dose for the subsequent Phase I clinical trial.[2][3]   Competing Challenges With these potential benefits, more research is required to guarantee the accuracy and efficiency of microdosing. It is important to remember that there is an assumption of linearity between the microdose and the full dose drug. The human body’s response to...

Solving the Mystery of Mutations – A New Model for Cancer Development

The mystery behind why certain cells possess cancer-related mutations that don’t fully develop into cancerous cells has long evaded cancer researchers. However, researchers at Boston Children’s Hospital, a Harvard-affiliated medical institution, recently made a significant advancement in the field of cancer research by visualizing cancer develop from a single cell in a live animal, for the first time. The findings of the team of researchers, published in Science last week, has helped identify exactly at what point in the cycle of development that a cancer-prone cell makes the conversion to one that is malignant.   Charles Kaufman, MD, PhD, a postdoctoral fellow in the Zon Laboratory at Boston Children’s Hospital and the paper’s first author, describes this critical point as one that “…occurs after activation of an oncogene or loss of a tumor suppressor, and involves a change that takes a single cell back to a stem cell state.”   To track this development, the research team used a zebrafish model with a human cancer mutation called BRAFV600E – commonly found in non-cancerous moles – that was also lacking the p53, a well-known tumor suppressor gene. A gene called crestin was of particular interest to the scientists due to its association with stem cells. Normally, after embryonic development, crestin and related genes are programmed to shut off. However, for unknown reasons certain cells prompt crestin and related genes to...

Reimagining Inflammation: A Road to New Therapies?

  Many of the medical conditions and leading causes of death facing our population involve some form of chronic inflammation; which acts like a prolonged on-switch for the immune system. Heart disease, cancer, diabetes, Alzheimer’s disease and abnormal wound healing are among prominent illnesses in which chronic inflammation plays key a role. In many tissue types there is a reserve of stem cells that is responsible for supporting the healing process after normal inflammation has occurred or an injury has taken place. However, it has not been as widely explored under chronic inflammation conditions. A recent study published in Nature Cell Biology takes a new look at the concept of chronic inflammation and proposes its potential use as a method for new therapies. The study was conducted by researchers at Ecole polytechnique fédérale de Lausanne (EPFL), described as Europe’s most cosmopolitan technical university with students, professors and staff from over 120 nations. The team of scientists at EPFL’s Swiss Institute for Experimental Cancer Research (ISREC) have discovered that chronic inflammation can lead to metaplasia or the ability for cells to actually change type. In the case of this study, eye cells made a dramatic transformation into skin cells!   Using a corneal epithelium mouse model, chronic inflammation was simulated and the method of fluorescent staining of specific cells was used to help observe and analyze stem cells located in...

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