FDA approves 'Inflectra', a novel drug saving the US billions of dollars.

The US Food and Drug Administration (FDA) just approved a version of Remicade, a drug used to treat autoimmune diseases like Crohn's disease and rheumatoid arthritis.

The drug, developed by Celltrion and which will be co-marketed by Pfizer, goes by the name "Inflectra." It's a form of infliximab, but will carry the suffix "-dyyb" to differentiate itself. This is the second "biosimilar" to be approved by the FDA.

The drug is called a biosimilar because it is like a generic version of a biologic medication, a medicine produced by living cells.

But it's a bit more complicated than that. Unlike generics for chemical-based drugs — think antibiotics or birth-control pills — that can be interchangeable with branded versions, the copycats of biologic medications, produced using living cells, have a few more caveats. That's because the drugs might have different reactions in your body.

Read more: FDA approves 'Inflectra', a novel drug saving the US billions of dollars.

Source: Wikimedia Commons

The Molecule That Gives Skin Elasticity

Through Tropoelastin's movements, it assembles to make elastic fibers, tubes and sheets for tissue repair. It is used to make and fix many different elastic tissues in the body. This material relates to the paper titled, 'Subtle balance of tropoelastin molecular shape and flexibility regulates dynamics and hierarchical assembly. [Weiss Lab, University of Sydney]

What is Cancer?

A Collection of Related Diseases

Cancer is the name given to a collection of related diseases. In all types of cancer, some of the body’s cells begin to divide without stopping and spread into surrounding tissues.

Cancer can start almost anywhere in the human body, which is made up of trillions of cells. Normally, human cells grow and divide to form new cells as the body needs them. When cells grow old or become damaged, they die, and new cells take their place.

When cancer develops, however, this orderly process breaks down. As cells become more and more abnormal, old or damaged cells survive when they should die, and new cells form when they are not needed. These extra cells can divide without stopping and may form growths called tumors.

Many cancers form solid tumors, which are masses of tissue. Cancers of the blood, such as leukemias, generally do not form solid tumors.

Cancerous tumors are malignant, which means they can spread into, or invade, nearby tissues. In addition, as these tumors grow, some cancer cells can break off and travel to distant places in the body through the blood or the lymph system and form new tumors far from the original tumor.

Read more: What is Cancer?

Normal cells may become cancer cells.

Source: cancer.gov

Doctors are over-diagnosing children asthma.

Inhalers often dispensed for no good reason and have 'almost become a fashion accessory'

Doctors are overdiagnosing asthma, with inhalers frequently dispensed for no good reason, to the point that they have "almost become a fashion accessory," argue two leading respiratory doctors in a leading article published online in the Archives of Disease in Childhood.

In the past asthma was undoubtedly underdiagnosed, but the evidence now is that the pendulum has swung too far in the opposite direction, insist Professor Andrew Bush and Dr Louise Fleming of Imperial College and Royal Brompton & Harefield NHS Foundation Trust, in the journal.

It matters, not only because of the cost of inhalers, but also because of their side effects, which are more likely to occur in patients who are prescribed an inappropriate dose, they say.

"Inhaled corticosteroids, when properly used, dramatically improve quality of life and reduce the risk of asthma attacks and mortality," they write.

Read more: Doctors are over-diagnosing children asthma.

If the past asthma was undoubtedly underdiagnosed, but the evidence now is that
he pendulum has swung too far in the opposite direction, insist experts in a new article.

Source: sciencedaily (crystal kirk/Fotolia)

Know about gluten and its facts, foods and allergies.

Gluten is the general term for a protein found in wheat, barley, rye and triticale. All forms of wheat contain gluten, including durum, spelt and farro.

Wheat is commonly found in bread, baked goods, crackers, cereals and pasta. Soups may contain gluten, as well as sauces and salad dressings. Barley is often found in malt, food coloring, soups, malt vinegar and beer.

Unfortunately, a significant number people have an adverse reaction to gluten when they consume it, meaning that they must adhere to a gluten-free diet to remain healthy.

This Knowledge Center article provides further information on gluten, including why some people should avoid consuming it and which foods are known to contain gluten.

Read more: Know about gluten and its facts, foods and allergies.

Gluten can be found in many common foods such as bread and baked goods.

Source: medicalnewstoday

Atherosclerosis, Rheumatoid Arthritis and Inflammation.

Rheumatoid arthritis (RA) has long been associated with increased cardiovascular risk, but despite substantial improvements in disease management, mortality remains high. Atherosclerosis is more prevalent in RA than in the general population, and atherosclerotic lesions progress at a faster rate and might be more prone to rupture, causing clinical events. Cells and cytokines implicated in RA pathogenesis are also involved in the development and progression of atherosclerosis, which is generally recognized as an inflammatory condition. The two diseases also share genetic and environmental risk factors, which suggests that patients who develop RA might also be predisposed to developing cardiovascular disease. In RA, inflammation and atherosclerosis are closely linked. Inflammation mediates its effects on atherosclerosis both through modulation of traditional risk factors and by directly affecting the vessel wall. Treatments such as TNF inhibitors might have a beneficial effect on cardiovascular risk. However, whether this benefit is attributable to effective control of inflammation or whether targeting specific cytokines, implicated in atherosclerosis, provides additional risk reduction is unclear. Further knowledge of the predictors of cardiovascular risk, the effects of early control of inflammation and of drug-specific effects are likely to improve the recognition and management of cardiovascular risk in patients with RA.

Rheumatoid arthritis (RA) is associated with a significantly increased risk of cardiovascular mortality, accounted for mainly by increased atherosclerotic disease.1, 2 Although the prevalence of some traditional cardiovascular risk factors is increased in RA, adjustment for these factors does not fully account for the heightened risk, suggesting that RA itself is an independent risk factor for cardiovascular disease (CVD).3 The prevalence of atherosclerosis is increased in RA, even in early disease,4 and chronic inflammation is thought to promote atherosclerosis both by modulation of traditional risk factors and also possibly by direct biological effects on the artery. In this article, we discuss the potential mechanisms that might accelerate atherosclerosis in RA, with a particular focus on inflammation.

Read more: Atherosclerosis, Rheumatoid Arthritis and Inflammation.

Figure 2: Development of an atherosclerotic plaque.

Source: NatureReviewsRheumatology

Global epidemiology of gout: prevalence, incidence and risk factors.

Gout is a crystal-deposition disease that results from chronic elevation of uric acid levels above the saturation point for monosodium urate (MSU) crystal formation. Initial presentation is mainly severely painful episodes of peripheral joint synovitis (acute self-limiting 'attacks') but joint damage and deformity, chronic usage-related pain and subcutaneous tophus deposition can eventually develop. The global burden of gout is substantial and seems to be increasing in many parts of the world over the past 50 years. However, methodological differences impair the comparison of gout epidemiology between countries. In this comprehensive Review, data from epidemiological studies from diverse regions of the world are synthesized to depict the geographic variation in gout prevalence and incidence. Key advances in the understanding of factors associated with increased risk of gout are also summarized. The collected data indicate that the distribution of gout is uneven across the globe, with prevalence being highest in Pacific countries. Developed countries tend to have a higher burden of gout than developing countries, and seem to have increasing prevalence and incidence of the disease. Some ethnic groups are particularly susceptible to gout, supporting the importance of genetic predisposition. Socioeconomic and dietary factors, as well as comorbidities and medications that can influence uric acid levels and/or facilitate MSU crystal formation, are also important in determining the risk of developing clinically evident gout.

Gout is the most common form of inflammatory arthritis and is caused by chronic elevation of serum uric acid (SUA) levels above the saturation point for monosodium urate (MSU) crystal formation. The deposition of MSU crystals, which occurs predominantly in peripheral joints and surrounding tissues, defines gout. The characteristic presentation is of rapidly developing monoarticular synovitis in peripheral joints (an acute 'attack') that is extremely painful but self-limiting, with resolution within several days or 1–2 weeks. However, long-term deposition of MSU crystals can result in joint damage and disfiguring subcutaneous tophi. In addition, gout is also associated with many conditions that affect longevity and well-being,1 such as metabolic syndrome,2 cardiovascular diseases3, 4, 5, 6 and renal diseases. In particular, gout is increasingly recognised as an independent cardiovascular risk factor.

Read more: Global epidemiology of gout: prevalence, incidence and risk factors.

Figure 1: The estimated prevalence of gout across the world.

Source: NatureReviewsRheumatology

A structural basis to stone formation in gout.

The mechanisms and sites of monosodium urate monohydrate (MSU) crystal deposition in gout have received little attention from the scientific community to date. Formalin fixation of tissues leads to the dissolution of MSU crystals, resulting in their absence from routinely processed pathological samples and hence neglect. However, modern imaging techniques—especially ultrasonography but also conventional CT and dual-energy CT—reveal that MSU crystals form at the cartilage surface as well as inside tendons and ligaments, often at insertion sites. Tophi comprise round white formations of different sizes surrounded by inflammatory tissue. Studies of fibres recovered from gouty synovial fluid indicate that these fibres are likely to be a primary site of crystal formation by templated nucleation, with crystals deposited parallel to the fibres forming transverse bands. In tophi, two areas can be distinguished: one where crystals are formed on cellular tissues and another consisting predominantly of crystals, where secondary nucleation seems to take place; this organization could explain how tophi can grow rapidly. From these observations based on a crystallographic approach, it seems that initial templated nucleation on structural fibres—probably collagen—followed at some sites by secondary nucleation could explain MSU crystal deposition in gout.

Gout is characterized by deposits of monosodium urate monohydrate (MSU) crystals, a consequence of hyperuricaemia—serum uric acid levels raised above normal and sodium urate reaching a concentration above supersaturation. Usually, crystals are formed in joints and periarticular tissues, the magnitude of the deposit growing and extending to other sites whilst hyperuricaemia persists. The mechanisms of pathological formation of MSU crystals on tissue have received scant attention to date. In this Review, we take a correlative structural approach to explore possible mechanisms of MSU crystal formation in gout on the basis of morphological findings.

Read more: A structural basis to stone formation in gout.

Figure 3: Formations of MSU crystals in tophi.

Source: NatureReviewsRheumatology

Disposing HIV from human immune cells with new gene-editing technique.

They've managed to shut down HIV replication permanently.

Using the much-touted CRISPR/Cas9 gene editing method, scientists have demonstrated how they can edit HIV out of human immune cell DNA, and in doing so, can prevent the reinfection of unedited cells too.

If you haven’t heard of the CRISPR/Cas9 gene-editing technique before, get ready to hear a whole lot more about it in 2016, because it’s set to revolutionise how we investigate and treat the root causes of genetic disease. It allows scientists to narrow in on a specific gene, and cut-and-paste parts of the DNA to change its function.

CRISPR/Cas9 is what researchers in the UK have recently gotten approval to use on human embryos so they can figure out how to improve IVF success rates and reduce miscarriages, and it’s what Chinese scientists were caught using in 2015to tweak human embryos on the down-low.

Earlier this year, scientists started using CRISPR/Cas9 to successfully treat a genetic disease - Duchenne muscular dystrophy - in living mammals for the first time, and now it’s showing real potential as a possible treatment for HIV in the future.

Read more: Disposing HIV from human immune cells with new gene-editing technique.

An HIV-infected T-cell.

Source: NIAID/Flickr

Novel Biotechnology Enables Analysis of Mitochondrial Damage Induced by Drug Toxicity.

Mitochondrial dysfunction plays a critical role in the development of chemical and pharmaceutical toxicity. However, current methods to evaluate mitochondrial activity still rely on traditional tests called endpoint assays, which provide limited prognostic information.

Scientists, however, from The Hebrew University of Jerusalem have described a new generation of Liver-on-Chip devices, in which the researchers add glucose and lactate microsensors, allowing them to measure minuscule changes in central carbon metabolism in real time (seconds to minutes). Their microfluidic platform is composed of submillimeter human tissues, which are characterized as "bionic" because they contain optoelectronic sensors for oxygen and are maintained under conditions simulating the human physiological environment. The platform includes a computer-controlled switchboard and permits the automated measurement of glucose and lactate using clinical-grade microsensors. The sensor-integrated platform permits real-time tracking of the dynamics of metabolic adaptation to any type of mitochondrial damage for over a month in culture.

The team's study ("Real-time Monitoring of Metabolic Function in Liver-on-Chip Microdevices Tracks the Dynamics of Mitochondrial Dysfunction") appears in the Proceedings of the National Academy of Sciences.

Read more: Novel Biotechnology Enables Analysis of Mitochondrial Damage Induced by Drug Toxicity.

Source: sott; activistpost