Disease


One common androgenic disorder in women is polycystic ovarian syndrome, when, for reasons that remain mysterious, the ovaries produce excess testosterone, resulting in infertility and problems with insulin that can prompt the onset of diabetes. Women with the disorder often are very hairy on the face and body but balding, and on an ultrasound test their ovaries may appear to be bulging in the middle, in the stromal tissue that produces androgens. The disease sometimes can be treated with anti-androgen drugs, but it must be caught early if diabetes is to be averted.

Other scientists are fascinated by a hereditary disorder called congenital adrenal hyperplasia, in which a person lacks one of the five enzymes needed to produce cortisol, an important hormone in responding to stress. As a result of the defect, precursors to cortisol released by the adrenal glands build up in a budding fetus and act like male hormones. Girls with congenital adrenal hyperplasia may emerge from the womb looking like boys, with an enlarged clitoris and even a scrotal sac, although they have fully formed ovaries and uterus. In the worst cases, the girls may need genital surgery to give them a more characteristically female appearance. In other instances of the disorder, said Dr. Maria I. New, chairman of pediatrics at New York Hospital-Cornell Medical Center in Manhattan, girls are born with normal genitals but masculinize later in life, becoming hairy, acned and suffering from reduced fertility. For both severe and mild cases of hyperplasia, patients are given dexamethasone to inhibit adrenal overactivity.



Each neurodegenerative disease involves different proteins being affected such as tau in Alzheimer's, alpha-synuclein in Parkinson's and huntingtin in Huntington's disease. Researchers found that once proteins get inside a cell, they enter vesicles, or small compartments that are encased in membranes. The proteins then damage or rupture the vesicle membranes allowing the proteins to invade the cytoplasm and cause more damage. Loyola researchers discovered that the protein clumps associated with Alzheimer's, Parkinson's and Huntington's diseases cause the same type of vesicle damage.

"A possible therapy would involve boosting a brain cell's ability to degrade a clump of proteins and damaged vesicles," Dr. Edward Campbell, a researcher at Loyola University, said in a press release. "If we could do this in one disease, it's a good bet the therapy would be effective in the other two diseases."

The study was published in the journal Acta Neuropathologica.



Chronic loneliness increases your likelihood of an early death by 14%. Loneliness causes high blood pressure, high cholesterol, it even suppresses the functioning of your immune system. Taken together, it can have as significant a risk for your long-term health and longevity as cigarette smoking.”

Researchers have confirmed that loneliness can be a deadly affliction — as lethal as diabetes or smoking 15 cigarettes a day.

“We need to start taking our social relationships more seriously,” Julianne Holt-Lunstad, the author of a Brigham Young University study on loneliness, said in a statement. “The effect of this is comparable to obesity, something that public health takes very seriously.”

The world is in the throes of an invisible loneliness epidemic, with 60 million sufferers in America alone.




More than a year ago, researchers published striking preliminary results from a large trial on a vaccine called rVSV-ZEBOV in the Lancet. They showed that everyone who got the shot immediately after contact with an Ebola victim didn't get the virus.

Today, the same researchers — who hail from the World Health Organization, Guinea’s Ministry of Health, Public Health England, and other international partners — have unveiled their final results in the Lancet, and they’re just as remarkable. The vaccine was tested in a trial involving nearly 12,000 people in Guinea and Sierra Leone during 2015 and 2016. Among the 5,837 people who got the vaccine, no Ebola cases were recorded. By comparison, there were 23 Ebola cases in the control group that had not gotten the vaccine.

The vaccine was discovered by the Public Health Agency of Canada and is now under development by the drug company Merck. For now, Merck is doing additional safety studies on children and other vulnerable populations and will be seeking approval from a regulator like the US Food and Drug Administration by the end of next year. In case of an emergency, the company has committed to ensuring that 300,000 doses of the vaccine are available, so the vaccine won’t hit the market just yet.



The progress towards complete eradicating polio shows in the numbers. Last year, 74 cases of wild poliovirus were reported, exclusively in Pakistan and Afghanistan, according to the initiative. In 2016, 10 cases have been reported so far — also in those two countries. By comparison, when the initiative started its work in 1988, "more than 350,000 children were paralyzed every year." The old oral vaccine (tOPV) protected against three strains of poliovirus, while the new oral vaccine (bOPV) protects against two of the strains. According to the initiative, the transition is possible "because type 2 wild polio has been eradicated."



"Chlorphenamine, commonly marketed in the form of chlorphenamine maleate (Chlorphen-12), is a first-generation alkylamine antihistamine used in the prevention of the symptoms of allergic conditions such as rhinitis and urticaria. Its sedative effects are relatively weak compared to other first-generation antihistamines. Chlorphenamine is part of a series of antihistamines including pheniramine (Naphcon) and its halogenated derivatives and others including fluorpheniramine, dexchlorpheniramine (Polaramine), brompheniramine (Dimetapp), dexbrompheniramine (Drixoral), deschlorpheniramine, triprolidine (Actifed), and iodopheniramine. The halogenated alkylamine antihistamines all exhibit optical isomerism, and chlorphenamine in the indicated products is racemic chlorphenamine maleate, whereas dexchlorpheniramine is the dextrorotary stereoisomer.

In addition to being an histamine H1 receptor (HRH1) antagonist, chlorphenamine has been shown to work as a serotonin-norepinephrine reuptake inhibitor or SNRI. A similar antihistamine, brompheniramine, led to the discovery of the SSRI zimelidine. Limited clinical evidence shows that it is comparable to several antidepressant medications in its ability to inhibit the reuptake of serotonin and also norepinephrine (noradrenaline). A large study linked the development of Alzheimer's disease and other forms of dementia to the use of chlorpheniramine and other first-generation antihistamines, due to their anticholinergic properties.

Phenylephrine is a selective α1-adrenergic receptor agonist of the phenethylamine class used primarily as a decongestant, as an agent to dilate the pupil, and to increase blood pressure. Phenylephrine is used as an alternative for pseudoephedrine in decongestant medicines due to pseudoephedrine's use in the illicit manufacture of methamphetamine. Its efficacy as an oral decongestant has been questioned, with multiple studies not being able to come to an agreement. The Food and Drug Administration has stood by its 1976 approval of phenylephrine for nasal congestion as the debate continues."



"'Investigations are underway to determine if this case of microcephaly is linked to Cape Verde's outbreak of Zika virus,' the WHO statement said. There is currently no vaccine for the virus. Brazil has been hardest hit by Zika, with some 1.5 million people infected and 745 confirmed cases of the syndrome. Affected countries are focusing on wiping out mosquito populations in an effort to curb its spread. The number of babies with the condition has surged since a Zika outbreak sweeping Latin America was detected last year."



Research Needs

  • The search for oncolytic viruses which can destroy malignant tumors directly or indirectly has been going on for over a century. And, disappointing results have been reported for nearly as long. Earlier this year, Amgen reported on a clinical trial of a virus called "T-VEC" which had positive results against advanced melanoma, though hardly a breakthrough. Researchers in this field are looking for a way to introduce oncolytic viruses systemically, rather than by local injection into tumors.
  • DARPA, the folks who gave us the internet and GPS, now imagine implanting sensors in the body to monitor a number medical and health conditions, for example: "Investigating whether direct triggering of the spleen or other organs could help treat rheumatoid arthritis and other inflammatory conditions; Investigating whether inflammation control in the brain could help treat depression; Investigating whether the management of neurochemicals that regulate learning and memory in the brain could offer new treatments for post-traumatic stress and other mental health disorders; Investigating thermal activation of the adrenal gland; Investigating the stimulation of the vagal nerve to induce neural plasticity for the treatment of post-traumatic stress."
  • Cancer screening protein biomarker analysis: This new way of analyzing proteins looks more at the structure of proteins, say with prostate or breast cancer patients, as opposed to just the amount of proteins. Not only that, this kind of analysis would be much faster with real-time results.
  • Gene editing using CRISPR: We’ve heard quite a bit about this, and it’s a little bit surprising that it’s not in the number one spot, but that’s partially because it’s really not necessarily going to be ready to effectively be put in use within the next year to tackle a wide variety of genetic disorders. But as Jonathan Smith, PhD from the Lerner Research Institute emphasized: “This is sweeping like a forest fire.”



Tuomanen said the results raise questions about which class of antibiotics should be used to treat bacterial infections during pregnancy. “This study suggests widely used antibiotics like ampicillin that cause bacteria to burst and release cell wall may lead to changes in the developing brain,” she said. “Such changes did not occur in mice treated with antibiotics like clindamycin that kill without releasing cell wall.

“Additional research is needed to understand how bacterial cell wall signaling induces proliferation via this newly identified pathway that links the innate immune receptor TLR2 with the transcription factor FoxG1 to drive neural proliferation in the fetus,” Tuomanen said. “This same mechanism might lead to new strategies to repair or replace neurons lost to illness or injury.”



“We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood. The first observations of HSV1 in AD brain were reported almost three decades ago]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept."



"Nanoparticles carrying a toxin found in bee venom can destroy human immunodeficiency virus (HIV) while leaving the surrounding cells unharmed. The research was conducted by the Washington University School of Medicine in St. Louis. The nanoparticles carry melittin, which is the principal active component of bee venom. Melittin fuses with the HIV virus and destroys it’s protective envelope while molecular bumpers prevent the nanoparticles from harming the body’s normal cells. Bee venom is known to disrupt cellular walls and destroy tumor cells as well."



"Huntington's disease is an inherited disorder that damages nerve cells and causes parts of the brain to deteriorate, leading to uncontrolled movements and behavioral and cognitive problems. There is no cure and no way to stop the disease's progression, though medications can treat some symptoms. About 30,000 people in the United States have the disorder and another 200,000 are at risk of inheriting it, according to the Huntington's Disease Society of America.

Along with a protein already implicated in Huntington's disease, the researchers found four proteins that also contribute to the disease pathology. The disease stems from a genetic mutation in the Huntingtin gene that produces too many copies of a DNA segment known as CAG, which gives rise to a longer Huntingtin protein with toxic effects. However, researchers found that this DNA repeat mutation can undergo a process known as repeat associated non-ATG (RAN) translation, producing four additional damaging repeat proteins that accumulate in the brain. This was a surprise to the researchers because these RAN proteins are made without a signal in the genetic code that was previously thought to be required for protein production. Each of the four RAN proteins contains long repeats of certain single protein building blocks, or amino acids.

"These repeat proteins are too long for cells to deal with and they build up as aggregated clusters that kill cells," Ranum said.

In addition to finding that the RAN proteins accumulate in the striatum, a specific brain region predominantly affected in Huntington disease, researchers also found them in the frontal cortex, cerebellum and white matter regions of the brain. Bañez-Coronel said this was the first time the accumulated proteins related to Huntington's disease were extensively found in white matter, an inner part of the brain containing cells that support neuronal function.

On the basis of their findings, the researchers believe there is a possibility that RAN proteins contribute to eight other similar neurodegenerative disorders, including spinobulbar muscular atrophy and several types of spinocerebellar ataxia, which are also caused by an abnormal increase in the number of CAG repeats."

No comments: