Passionate Channel - Health

Tumournators launched first campaign

Mon, 23 Oct 2017 20:02:00 +0000

by Tafadzwa Sandi

Cyprus International University Pharmacy Students launched their first community awareness campaign at the university campus to educate the public about breast Cancer, today.

The aim of the campaign was to enlighten the public about breast Cancer and suggest possible ways of treating the disease.

Speaking to Passionate Channel, Tatenda Mutero who is a member of the Tumournators said that they have to pass information about breast cancer to the public such that the disease is eradicated.

The group Tumournators held their first breast cancer awareness campaign at CIU

“The vision of Tumournators is to fight cancer and to ensure that the Cyprus community which is prone and impacted by cancer is well empowered by knowledge and is strengthened by action to eradicate the disease”, Mutero said.

Mutero also added that their group spoke to many people today emphasizing on the causes of breast cancer and how to test if one has breast cancer.

“We had so many ladies who got to know about breast cancer today and we let them know the places where to go and can get tested for breast cancer”, Mutero said.

Moreover, another member of the group Clifford Nkomo said that the campaign was not only to the females but males counterpart were also included.

“We did not consider females only but we also talked to males bearing in mind the fact that they also have female relatives and some friends”, Nkomo said.

“People were given a platform to share their opinions about breast cancer by writing onto the pink chart”, Nkomo added

Furthermore, Mirriam said that the CIU cancer group came at the right time and found the information comprehensive and very helpful.

The group Tumournators which distributed several flyers today was started by CIU Pharmacy Students in September as a platform to share information about cancer and to suggest possible solutions.

Faster-acting antidepressants may soon be a reality

Tue, 01 Aug 2017 10:29:00 +0000

Understanding where antidepressants act is the key to improving their function.

Using cutting-edge techniques, researchers have investigated the mechanism by which common antidepressants work, finally pinning down the specific receptors responsible for their action. The findings might pave the way to designing improved, faster-acting antidepressants.

Depression is characterized by persistent low mood and feelings of hopelessness, and it is one of the most common mental disorders in the United States. In 2014, there were an estimated 15.7 million U.S. adults who experienced at least one major depressive episode, representing around 6.7 percent of the country's adults.

Treatments for depression generally include talking therapies in conjunction with medication. The class of drugs most commonly prescribed is selective serotonin reuptake inhibitors (SSRIs), and these include brands such as Prozac and Zoloft.

SSRIs can help some people with depression, but they are not perfect; not everyone responds well to them, and side effects including nausea, insomnia, agitation, and erectile dysfunction can be unpleasant.

Also, SSRIs can take some time to kick in; although some people might feel some benefit within hours or even minutes, most people do not feel the full antidepressant effect until they have been taking the drugs for weeks or even months.

How do SSRIs work?

In the brain, messages are sent between neurons by releasing neurotransmitters into a gap between the cells, or the synapse. Serotonin is one such neurotransmitter. It is released from the first neuron and binds to receptors on the second neuron.

Normally, once serotonin has been released into the synapse and relayed its message, the majority is reabsorbed into the first nerve cell for reuse at a later date. SSRIs prevent serotonin from being reabsorbed. In this way, they ensure that serotonin hangs around in the synapse for a longer time, exerting more of an effect.

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Although SSRIs have been known to medical science since the 1950s, their exact mechanism is not understood. This is because there are at least 1,000 types of neuron that can be influenced by a surge in serotonin, and some of these neurons may be excited, while others might be inhibited.

The mixed response is because there are 14 subtypes of serotonin receptor throughout the body and any single nerve could have a cocktail of receptor types. Teasing out which receptor subtype is playing the most significant role has proven challenging.

The role of the dentate gyrus

A group of scientists from Rockefeller University in New York City, NY, recently set out to take a closer look at the action of SSRIs on a particular type of nerve cell. The team was headed up by Lucian Medrihan and Yotam Sagi, both research associates in the Laboratory of Molecular and Cellular Neuroscience, and Paul Greengard, Nobel laureate.

Their findings were recently published in the journal Neuron.

"Many different types of synapses throughout the brain use serotonin as their neurotransmitter. An issue of major importance has been to identify where in the myriad of neurons the antidepressants initiate their pharmacological action."
Paul Greengard

The team concentrated on a group of cells in the dentate gyrus (DG). According to the authors, they chose the DG because previous work has established that "SSRI treatment promotes a variety of synaptic, cellular, and network adaptations in the DG."

Specifically, the team investigated cholecystokinin (CCK)-expressing neurons within the DG. These neurons were of interest because they are heavily influenced by neurotransmitter systems that are associated with mood disorders, such as depression.

Finding the right receptor

Using a technique called translating ribosome affinity purification, the team were able to identify the serotonin receptors on CCK cells. Sage explains, "We were able to show that one type of receptor, called 5-HT2A, is important for SSRIs' long-term effect, while the other, 5-HT1B, mediates the initiation of their effect.

The next step in the study involved efforts to mimic SSRIs' effects by manipulating CCK neurons in mice. They used chemogenetics to switch nerve cells on or off and implanted tiny electrodes inside the mouse brains.

The findings were clear. When the CCK neurons were inhibited, the pathways important for the mediation of SSRI responses lit up. In other words, the scientists had recreated a Prozac-like effect without using the drug.

To back up these findings, the team used behavioral experiments in a pool and observed swimming patterns. Again, silencing the CCK neurons created behavior that was similar to that displayed by the mice that had been given SSRIs: they swam for longer with increased vigor.

According to the researchers, understanding the importance of the DG and the specific cells important for treating depression will help to design faster-acting, more effective antidepressants with fewer side effects.

The work was carried out using techniques that would have been impossible just 5 years ago, and the studies that follow are likely to improve our understanding even further.

Is chronic fatigue syndrome an inflammatory disease?

Tue, 01 Aug 2017 10:22:00 +0000

New research investigates the links between chronic fatigue syndrome and inflammation.

Chronic fatigue syndrome, or myalgic encephalomyelitis, has been controversial for years, as specialists have not been able to glean much of an insight into its causes. Now, a new study suggests that the condition is an inflammatory disease.

Chronic fatigue syndrome (CFS), sometimes known as myalgic encephalomyelitis (ME), is a condition that has been puzzling specialists for years, many of whom have been struggling to identify its causes and devise an appropriate treatment. Some, however, have denied CFS/ME's legitimacy due to wide-ranging symptoms that make it hard to diagnose.

Characterized by often debilitating fatigue, and sometimes accompanied by pain and difficulties in retaining focus, CFS/ME affects between 836,000 and 2.5 million people in the United States, according to the Centers for Disease Control and Prevention (CDC).

The CDC also estimate that approximately 90 percent of CFS/ME cases remain undiagnosed, partly due to a lack of proper understanding of the condition on the part of many healthcare professionals.

Research on the causes of CFS/ME and potential means of tackling the symptoms is ongoing, and specialists are constantly striving to uncover more information.

A new study from the Stanford University School of Medicine in California has now linked CFS/ME to cytokines - or molecules with a role in cell signalling - involved in the system's immune response, reacting to infections and inflammation.

'Findings show CFS/ME is inflammatory'

Lead study author Dr. Jose Montoya and his colleagues published their findings yesterday, in the Proceedings of the National Academy of Sciences, and they suggest that that the concentration of cytokines in the bloodstream is relevant to the acuteness of CFS/ME symptoms.

The study found that variations in 17 cytokines are connected with the severity of CFS/ME in patients, suggesting that the condition is essentially an inflammatory disease.

"There's been a great deal of controversy and confusion surrounding ME/CFS - even whether it is an actual disease. Our findings show clearly that it's an inflammatory disease and provide a solid basis for a diagnostic blood test."
Senior author Dr. Mark Davis, Stanford's Institute for Immunity, Transplantation and Infection

Some CFS/ME patients also exhibit symptoms that are reminiscent of flu or other diseases that are associated with inflammation. Such symptoms might include a sore throat, sensitive lymph nodes, and night sweats, but also muscle pain, digestive issues, and "brain fog," which is the inability to think clearly or retain focus.

Since there is no known cure for the condition, treatment normally targets the symptoms. Patients displaying signs of inflammation are often administered antivirals, anti-inflammatory drugs, or medicines that stimulate the immune system.

These, the researchers say, are sometimes - but not consistently - effective in improving the symptoms, but no infectious agent has yet been singled out as the cause. Nevertheless, the occasional results yielded by symptomatic treatment convinced Dr. Montoya to look into the relevance of inflammation to CFS/ME.

Is 'analysis by disease severity' promising?

At the Human Immune Monitoring Center at Stanford's Institute for Immunity, Transplantation and Infection, Dr. Montoya and his colleagues examined blood samples collected from 192 CFS/ME patients and 392 participants who had no CFS/ME diagnosis, or the control group.

All of the participants were aged 50 on average, and the diagnosed patients had lived with their symptoms for more than 10 years on average. The study took into account the severity of the patients' condition, as well as how long they had been living with it.

Insight of 2015 Painkillers , Survey.

Tue, 01 Aug 2017 09:28:00 +0000

One in Three Americans Took Prescription Opioid Painkillers in 2015, Survey Says

by CORKY SIEMASZKO

How many Americans are using prescription opioid painkillers? About one in three.

That's the stunning number in a new survey released Monday from the National Institute on Drug Abuse, which calculated that a whopping 91.8 million Americans used drugs like OxyContin or Vicodin in 2015.

And nearly five percent of the adults surveyed told researchers they took these drugs without their doctor’s permission, the study reported.

They didn’t get their meds from some seedy drug dealer, either.

“The most commonly reported sources were friends and relatives for free,” the study reported. “Or a physician.”

The NIDA study was released on the same day that the presidential opioid commission, chaired by New Jersey Gov. Chris Christie, released its first report and recommendations for tackling an opioid plague that killed more than 15,000 people in 2015, according to the federal Centers for Disease Control and Prevention.

The study urged President Donald Trump to "declare a national emergency" and noted that "America is enduring a death toll equal to September 11th every three weeks."

“As access to prescription opioids tightens, consumers increasingly are turning to dangerous street opioids, heroin, fentanyl alone or combined, and mingled with cocaine or other drugs," the commission stated in an interim report to Trump.

NIDA said the treatment of pain is at the root of the problem.

“Our results are consistent with findings that pain is a poorly addressed clinical and public health problem in the United States and that it may be a key part of the pathway to misuse or addiction,” the group stated in the study.

NIDA’s recommendations included "better prevention and treatment of the underlying disorders are necessary to decrease pain and the morbidity and mortality associated with opioid misuse,” the study said.

“Simply restricting access to opioids without offering alternative pain treatments may have limited efficacy in reducing prescription opioid abuse.”

It could also “lead people to seek prescription opioids outside the health system or to use nonprescription opioids such as heroin or illicitly made fentanyl, which could increase health, misuse, and overdose risks.”

Trump launched the commission on March 29 to tackle a drug problem that kills an estimated 78 Americans per day.

In their report, the Christie-led commission made several recommendations. Among other things, they suggested expanding treatment facilities across the country, educating doctors about the proper way to prescribe pain medication, equipping all police officers with the anti-overdose remedy naloxone, developing new fentanyl detection sensors, and improving data-sharing among law enforcement agencies.

"Since 1999, the number of opioid overdoses in America have quadrupled," the presidential commission stated. "Not coincidentally, in that same period, the amount of prescription opioids in America have quadrupled as well."

The commission’s first report on the federal response to the opioid crisis was supposed to be released 90 days after Trump launched it in March. But it was delayed twice while the Republican-led House and then the Senate tried and failed to repeal and replace Obamacare.

Critics said the Obamacare repeal plans the GOP was pushing would have gutted existing programs that have been helping legions of substance abusers kick their habits.

Meanwhile, the Democrats accused Christie and the Trump administration of "dragging its feet" on the issue.

“There’s money available,” Senate Minority Leader Chuck Schumer said Sunday. “The commission is supposed to put (forward) the best ways to spend that, and they haven’t done that."

Christie insisted the delays were necessary because they got far more input from the public than they had expected.

Criminal justice professor Brian Levin said the feeling among many academics is that Trump’s commission is "window dressing."

“Like many initiatives coming out of the administration, it’s hampered by the chaos around management,” Levin, of the California State University San Bernardino, told NBC News. “Moreover, there seems to be a concentration on rhetoric and law enforcement responses at a time when resources from health and addiction are on the chopping block.”

Levin, a former New York City police officer who walked a beat in Manhattan at the height of the crack epide, said arresting more people won’t end the opioid crisis.

“The research indicates that enforcement alone, absent a systematic medical and counseling response, is due to fail,” Levin said.

Mon, 10 Jul 2017 15:48:00 +0000