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Dr. Marie Gabrielle Laguna

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Article 17

An anti-inflammatory diet which is typically high in greens, fruits, fish and whole grains might improve bone wellness and prevent fractures in some females, a new study suggests.

Researchers examined data from the landmark Women’s Health Initiative study to evaluate stages of inflammatory elements within the diet to bone mineral density and fractures and found new associations between meals and bone health. The study, done by Tonya Orchard, assistant professor of human nutrition at the Ohio State University,  is published in the Journal of Bone and Mineral research.

Females with the least-inflammatory diets based on a scoring process called the Dietary Inflammatory Index lost less bone density within six years than their peers with more inflammatory diets. This was although they had lower bone density overall.

In addition, diets with low inflammatory potential looked as if it would correspond to lower the chances of hip fracture among one subgroup of the trial”post-menopausal white women younger than 63 years old.

The findings suggest that women’s bone health might benefit once they consume a diet higher in healthy fats, vegetables and whole grains.

The authors comment that this suggests that as females age, healthy diets are impacting their bones. This gives another purpose to support the ideas for a healthful food plan in the Dietary Guidelines for Americans.

Since the study was observational, it’s not viable to definitively link dietary patterns and bone health and fracture outcomes. The authors remarked that these new findings support a developing body of evidence that factors that increase inflammation can elevate osteoporosis risk.

Through looking at the full diet rather than the individual vitamins and minerals, this information provide a foundation for studying how components of the food plan could have interaction to furnish improvement in females’ wellness and lifestyle alternatives.

Previous reviews have connected high levels of inflammatory markers within the blood to bone loss and to fractures in older women and men, which prompted the authors to study dietary choices that make contributions to inflammation in the body.

The Dietary Inflammatory Index was developed to examine the quality of food from maximally to minimally inflammatory based on nutrients consumed. This helped the authors study their goal. Dietary knowledge as well as data on bone density and fracture had been gathered from a huge group of participants from the Women’s Health Initiative, the largest study done in the US.

The subjects in the WHI were 50 to 79 years old when they enrolled in the study of prevention and control of illnesses impacting older females. Enrolment ran from 1993 to 1998.

The researchers looked at dietary data from 160,191 women and assigned inflammation rankings based on 32 foods that the women reported taking in the three months prior to their enrolment. The researchers used bone-mineral-density information from a subset of 10,290 women. Fracture information was collected for the group.

The researchers observed a correlation between high-inflammatory diets and fracture in younger white women in the study. Higher ratings were related to about a 50 percent higher risk of hip fracture in Caucasian females who are younger than 63 years old, in comparison with the risk for women in the group with the lowest inflammatory rankings. These data suggests that a higher-quality and less-inflammatory eating regimen may be primary in lowering hip fracture chance in younger females.

Article 18

Researchers from the University of Kansas Medical Center have found that high doses of medicinal drugs called statins mainly used to battle high cholesterol can ruin a rogue protein produced through a broken gene that is related to nearly half of all human cancers.

Tomoo Iwakuma, M.D., Ph.D., an associate professor in the Department of Cancer Biology and his group have published the primary study showing how the use of statins, such as Lipitor (atorvastatin), Crestor (rosuvastatin) and Mevacor (lovastatin), can shut down structurally mutated p53 proteins that may accelerate cancer progression, while not harming proteins produced by healthy p53 genes. Even though statins are not a cancer cure per se, the figuring out of how they have an effect on mutated varieties of p53 would result in new medicinal drugs designed peculiarly to knock out the damaged p53.

P53 Gene And Cancer

Cancer is caused by mutations to the genes that keep watch over cell growth or cell loss of life. Of the thousands of genetic culprits which were implicated with various cancers, p53, dubbed the “guardian of the genome,” is the mightiest of them all. Mutant types of p53 had been located in nearly half of all malignant tumors and practically every form of human cancer.

When p53 works adequately, it produces proteins that keep cells from developing and dividing too fast. When p53 becomes mutated, either spontaneously or via heredity, its regulating functions do not work and cells can grow out of control, forming tumors and invading tissues — that’s cancer.

Compounding the quandary that mutant p53 can no longer suppress the growth of tumors is that indisputable fact that it may also in reality accelerate the development of cancer and drug resistance.

The project for Iwakuma and his group was to find out methods to eliminate the misbehaving protein, at the same time leaving cells containing healthful p53 wanted for average cell growth unharmed.

Four years ago, Iwakuma and his lab group collaborated with the High Throughput Screening Laboratory (HTC) on the University of Kansas Lawrence campus to screen compounds to find out which of them would degrade mutant p53. Of the 9,000 compounds they tested, about 2,400 had been FDA-authorized medicinal drugs, while the others had been non-FDA permitted and uncharacterized compounds.

When Iwakuma acquired an email from the HTC listing down the 10 compounds that the screenings had proven promise in reducing mutant p53 levels, he was bowled over to look that some of them were statins.

Early screenings most likely produce false positives, so Iwakuma had to verify the lab results, first trying them in cells and then in mice. The KU researchers injected the mice with cells expressing mutant p53, waited for tumors to develop, and then treated them with excessive doses of statins for 21 days. They discovered that tumors didn’t develop well in mice dealt with statins compared to the controls, and they learned the statins worked simplest on structurally mutated (misfolded) p53, versus p53 mutated on the spot where it binds to DNA. This was an important discovery, in particular since medical research with statins had not viewed this kind of p53 mutation.

It was found out that the equal mechanisms that help statins lower cholesterol are at work preventing mutant p53 from binding to DNAJA1, leaving these mutant proteins unprotected. As a result, mutant p53 is free to connect to the enzyme that brings about its degradation. And on account that mutant p53 isn’t always present in ordinary cells, all this occurs without affecting healthy cells.

Article 19

Researchers from the Université de Sherbrooke in Sherbrooke, Quebec, Canada have investigated the use of glucose to shorten labor in nulliparous (first time giving birth) women. The essential effect studied was the length of active labor.

Prolonged labor may be damaging to maternal and fetal health. Few clinical interventions are recognized to shorten labor period. Since muscle efficiency is known to be improved by glucose supplementation, the researchers tested whether or not adding glucose to the intravenous hydration solution females have during labor might accelerate labor. Two hundred pregnant women had been randomly assigned to obtain either a normal hydration solution containing salt and water or a solution containing glucose, salt and water.

The researchers observed that the median length of labor is 76 minutes shorter in the group of females receiving glucose. There was no change within the mode of delivery (cesarean section, forceps, and so forth.), or the neonatal health measures. Glucose supplementation greatly reduces the length of labor without having complications. This is good information for women experiencing induced labor.

The researchers concluded that, given the affordable cost and safety of this intervention, glucose should be the solute of choice during labor.

Prolonged labor is also known as failure to progress and means that labor has lasted for 20 hours or more for first time mothers and 14 hours or more for women who had pregnancies before. This usually happens when there is a prolonged latent phase during the first stage of labor. It is a stressful experience for both the mom and baby.

If prolonged labor happens during the active phase of labor, it can lead to complications and the cause should be determined. There are many possible causes for this,  one is when the baby is too large that it cannot pass into the birth canal. The other reason may be that the birth canal may be too small for the baby to pass. Multiple pregnancies can also prolong the active phase of labor, which may be due to weak uterine contractions or positioning of the baby. Other factors that can result to prolonged labor include too much fear, worry or stress on the part of the mother, and the use of pain medicines that can weaken or slow down uterine contractions.

The results of this study are significant in that it is able to provide a good solution for prolonged labor during the active labor phase. Fortunately, if this is adopted by hospitals and maternity centers, it can reduce some complications which are typically brought about by prolongation in the active phase of labor.

For more interesting news and updates on medicine and scientific discoveries, feel free to read our other articles on this site. Subscribe to our newspaper for more updates in the field of medicine and health technology.

Article 20

Cells of the innate immune system that play an essential role in development of atherosclerosis have a protein, an endogenous peptide, that reduces the levels of cholesterol in mice — and consequently helps to inhibit or mitigate the disease.

Atherosclerosis remains one of the causes of premature death in present day Western societies. The term itself refers to insoluble, fatty deposits that are formed on the inside wall of main blood vessels leading to a continual, localized inflammation. These so-called plaques obstruct blood flow and can ultimately lead to heart attacks and strokes.

The unresolved inflammatory reactions that lead to atherosclerosis are initiated through immune cells according to perturbations in lipid metabolism due to the presence of more cholesterol (hypercholesterolemia) in the circulation.

Researchers have now shown in mice that one of the cell types concerned produces a protein that inhibits atherosclerosis by regulating cholesterol metabolism. The new discovery, reported in the journal EBioMedicine, might open up new options for the cure of atherosclerosis.

Initiation and progression of atherosclerosis are intently linked to the activation of special classes of cells which can be part of the immune process. In prior experiments, the researchers had shown that white blood cells called neutrophils play a predominant position in the system. Probably the most plentiful protein observed in human neutrophils is human neutrophil peptide 1 (HNP1), which is famous to have anti-microbial and pro-inflammatory functions.

In contrast, mouse neutrophils mainly don’t express this protein at all. According to the authors, this provided them with a targeted possibility to study the function of this protein. To take action, they genetically developed a mouse strain that is not only inclined towards atherosclerosis, but in addition produces excessive stages of HNP1. The LMU group discovered that the atherosclerotic lesions that formed in these mice were a lot smaller than those found in the mice that lacked HNP1.

After they examined the HNP1-expressing mice more intently, the researchers found out that the animals had decreased stages of circulating cholesterol than control mice. Due to the fact that cholesterol is not soluble in water, it’s transported in the bloodstream in association with so-called lipoproteins. Lipoproteins are divided into good fats and unhealthy fats. The good fats, together with HDL, transport cholesterol from the tissues to the liver and therefore cut down the risk of atherosclerosis.

The dangerous fats, like LDL, carry cholesterol within the reverse path — from the liver to the tissues. High levels of circulating LDL for this reason enable more cholesterol to be delivered to endothelial cells which are specially prone to damage or are already damaged, and as a consequence tend to create atherosclerosis. The authors claimed they were able to show that HNP1 binds to LDL in the bloodstream and induces fast uptake of circulating LDL by the liver, thus lowering hypercholesterolemia. This will account for the lesser atherosclerotic lesions in HNP1-expressing mice.

The researchers consider that their findings may result in new procedures to the treatment of hyperlipidemia. Given that HNP1 is a normal constituent of the human body, therapeutic use of the protein would be expected to be free from side effects and must not compromise immune defenses.

Article 11

Perena Gouma, a professor in the Materials Science and Engineering Department at The University of Texas at Arlington, has released an article in the journal Sensors that describes her invention of a handheld breath monitor that may potentially the flu virus.

The article, published in January 2017, explains in-depth how the single-exhale sensing gadget works and the research concerned in its creation, which was funded by the National Science Foundation through the Smart Connected Health program. Gouma’s gadget is just like the breathalyzers used by police officers after they suspect a driver of being below the influence of alcohol. A patient readily exhales into the gadget, which uses semiconductor sensors like those in a household carbon monoxide detector.

The difference is that these sensors are specific to the gas detected, but nonetheless cheap, and can isolate biomarkers related to the flu virus and indicate whether or not the sufferer has the flu. The device may be made available in drugstores so that affected people will be identified earlier and take medicine used to treat the flu in its earliest phases. This device could help avoid flu epidemics from spreading, defending individuals and the general public.

Gouma and her group relied on present medical literature to examine the levels of known biomarkers which are in a individual’s breath when afflicted with a certain disease, then utilized that capabilities to discover a mixture of sensors for those biomarkers that is accurate for detecting the flu. For example, individuals who suffer from bronchial asthma have elevated nitric oxide levels in their breath, and acetone is an identified biomarker for diabetes and metabolic processes. When mixed with a nitric oxide and an ammonia sensor, Gouma discovered that the breath monitor may detect the flu virus, probably as well as assessments done in a doctor's office.

The author noted that she considers that technology like this is going to revolutionize personalized diagnostics. This may enable people to be proactive and catch diseases early, and the technology can be used to diagnose other diseases, comparable to Ebola virus infection, by just changing the sensors.  She continues that before they applied nanotechnology to create this device, the only technique to detect biomarkers in a person’s breath was by means of very highly-priced, technical equipment in a lab, operated through expert personnel. Now, this technology would be utilized by ordinary people to rapidly and properly diagnose ailments.

Stathis Meletis, chair of the Materials Science and Engineering Department, commented that Gouma’s study suggests how UTA’s nanotechnology research can have a profound effect on health and the human condition in our communities.

He further added that Dr. Gouma’s creation of a portable, single-exhale device that can be utilized to detect ailments has implications far beyond the laboratory. This shows the impact that nanotechnology has on our daily lives, and has capabilities for functions regarding safety and other predominant areas as well.

Article 12

Newborns with hypoglycemia, or low blood sugar, are getting more prevalent worldwide, as an outcome of the developing number of moms who are obese, overweight or diabetic. Breastfed newborns may be given supplementary feedings or, if that fails, with intravenous fluids, which requires mom and baby to be separated for hours or days. Each strategy intrude with mom-baby bonding and scale down the chances that breastfeeding will p be established upon discharge from the hospital.

Now researchers from the University at Buffalo researchers at Women & Children’s Hospital of Buffalo (WCHOB) and different teams worldwide are proving that a dose of dextrose gel administered into a baby’s cheek, together with usual feedings can elevate babies’ blood sugar, allowing them to stay with their moms, which promotes breastfeeding. Given that this method can do away with the necessity for intravenous fluids, which ought to be executed within the Newborn Intensive Care Unit, it additionally saves health care charges.

Promote Bonding

One of the authors of this study is Satyan Lakshminrusimha, MD, professor and vice chair of pediatrics in the Jacobs School of Medicine and Biomedical Sciences at UB, chief of the division of neonatology at WCHOB and co-author of a commentary on related research published in British Medical Journal (BMJ) Evidence-Based Medicine last week as well as a paper published last fall in Karger Biomedicine Hub. He commented that it breaks his heart to see moms and babies separated after birth. He remarked that birth is a stressful event and it is additional upsetting to a younger mother, in particular a first-time mother, if she is not competent to breastfeed her baby due to low blood glucose levels in order that the baby receives IV treatment.

Dextrose gel was given along with the usual hypoglycemia protocol for the newborn nurseries at two Buffalo area hospitals in 2014.  The researchers wanted to know the safety and efficacy of oral dextrose treatment mixed with feedings to lessen the necessity for IV dextrose treatment in infants born at or near-term period (35 weeks or more) and to assess how that treatment would impact feeding patterns for infants prior to discharge from the hospital.

The group published their results and described how the use of dextrose gel in asymptomatic infants with low blood sugar helped lower total NICU admissions for hypoglycemia from 42 percent to 26 percent. In 74 percent of babies, the sugar gel effectively addressed low blood sugar levels versus 58 percent of infants who got regular feedings alone, before the new protocol was adopted.

The results highlight a main issue of the use of feedings alone according to the authors.

Dextrose gel is used in adult diabetics all the time, at the same time that in babies, the protocol was done to simply do feedings. There is sugar in milk, but 100 millilitres of breast milk or infant formula has only 7 grams of sugar, whilst a hundred millilitres of gel has 40 grams of sugar.

The authors mentioned that after they used the dextrose gel, they feel that they could minimize admissions to the neonatal intensive care unit, improve the extent of breastfeeding at discharge and cut back health care fees. Beforehand, if the child didn’t get better after three feedings, they were admitted to the NICU.

The findings will not only be making improvements to outcomes for hypoglycemic newborns, they’re additionally leading to new methods to preclude hypoglycemia.

Article 13

The protocol for care in the treatment of strokes caused by blood clots entails the therapeutic infusion of tissue plasminogen activator (tPA), which will dissolve the clots and repair blood flow within blood vessels. This “thrombolytic” remedy carries the hazard of bleeding and swelling within the brain, and it has to be administered within three hours after the start of the stroke, which sharply limits its clinical benefits.

Working with animals, researchers at Joslin Diabetes Center now have demonstrated the benefits of giving a drug in combination with tPA that could enhance stroke treatment effects and develop the window of opportunity for the treatment.

Medications that target a protein referred to as plasma kallikrein, as well as an activator protein referred to as factor XII,  may provide the opportunity to make tPA safer by reducing these issues and growing its efficacy in opening blood vessels, according to the authors of the study.

About 800,000 persons in the USA have a stroke each year, and about 87% are ischemic strokes, wherein blood flow is blocked through a clot.

The researchers were able to test that tPA boosts the function of plasma kallikrein in human and mouse plasma. They subsequent experimented with mouse models wherein blood clots had been prompted in the brain after which they were handled with tPA. Animals that had also given a plasma kallikrein inhibitor, and animals that have been genetically modified to supply reduced quantities of the protein, showed significantly less bleeding, brain swelling and brain damage than control animals without plasma kallikrein blockade.

The researchers traced the biological mechanisms by which tPA prompts plasma kallikren, via the factor XII protein, which promotes coagulation. Plasma kallikrein is known to set off the kallikrein kinin system, a pathway that has been implicated in stroke complications together with brain swelling and breakdown of the blood-mind barrier.

The FDA has approved a plasma kallikrein inhibitor for the remedy of hereditary angioedema. More inhibitors targeting this pathway are under development by many pharmaceutical organizations for this genetic disorder and other stipulations, together with diabetic macular edema. These new findings propose additional potential therapeutic possibilities for plasma kallikrein inhibitors in thrombolytic treatment.

Article 14

Many people become ill when they do not get adequate sleep. A new study helps give an explanation why.

Researchers took blood samples from 11 pairs of identical twins with various sleep patterns and discovered that the twin with shorter sleep period had a depressed immune system, when compared with his or her sibling. The findings have been published recently in the journal Sleep.

According to the authors from the UW Medicine Sleep Center at Harborview Medical Center, immune system performs well when it will get enough sleep. Seven or more hours of sleep is encouraged for good well being.

A unique characteristic of this study was that it studied identical twins in order to manage for the large genetic determinant to sleep periods. Researchers say genetics account for 31 to 55 percent of sleep time length and behavior and environmental account for the remainder.

The authors explained that plenty of existing knowledge indicates that curbing sleep — for a restricted time in the laboratory setting — can broaden inflammatory markers and prompt immune cells. Little is known, though, concerning the effects of longstanding short sleep duration under usual conditions. This study employed “actual world” conditions, and showed for the first time that long term short sleep shuts down systems involved in the immune response of circulating white blood cells.

According to them, the outcomes are consistent with studies that show when sleep deprived persons are given a vaccine, there is a lower antibody response and if sleep deprived individuals are exposed to a rhinovirus they’re more likely to get the virus. This study supplies extra evidence of sleep to total health and well-being above all to immune health.

The researchers, citing information from the Centers for Disease Control, mentioned that during the last century individuals in the US are dozing an estimated 1.5 to 2 hours less, and about a third of the working population sleeps lesser than six hours per night.

They further added that modern day society, with its manipulation of light, omnipresent technology and numerous competing pursuits for time, together with the zeitgeist de-emphasizing sleep’s importance, has resulted in the greater deprioritization of sleep.

Article 15

A new preclinical study done done by University of Texas at Dallas researcher indicates that vagus nerve stimulation therapy (VNS) might have the advantage to help persons overcome drug dependency by helping them be develop new behaviors from drug seeking behaviours.

The new research, released in the journal Learning and Memory, found that drug cravings in addicted rats were diminished when they had been treated with VNS. It’s feasible that the study could be applied to humans who have been addicted to drugs according to the senior author  Dr. Sven Kroener, assistant professor in the School of Behavioral and Brain Sciences.

According to him they are studying extinction learning and how vagus nerve stimulation can help people study a new behaviour that’s different to an existing, maladaptive habit like drug taking. When a person is hooked on a drug, extinction is a process to help them study behaviors so they are capable to take more actions.

Vagus nerve stimulation involves sending a light electric pulse through the vagus nerve, which is in the neck. VNS already has been permitted by the US FDA as a medication for particular illnesses, similar to depression and epilepsy.

UT Dallas is a main hub of VNS study, with trials presently being done on how the procedure can probably aid people recuperate from paralysis from stroke, post-traumatic stress disorder, anxiety or tinnitus.

For the present study, Jessica Childs, a graduate student in Kroener’s lab, utilized VNS to a test group of rats used within the study in a method called “extinction studying” to assess whether the process would help the animals be trained with behaviors and curb their drug cravings. Like Kroener’s study on anxiety, the drug addiction study sought to extinguish memories.

Extinction of fearful memories and extinction of drug-seeking memories relies on the same substrate in the brain. In our experiments, VNS enables both the extinction learning and reduces the relapse response as well.

The authors commented that the identical thought will also be utilized to persons looking to overcome a dependency to medicinal drugs; they quite often need to gain knowledge of a new behaviour that competes with their old habits.

They further added that this is what you wish to have in addiction treatment. You wish to reinforce behaviors that inhibit the old dangerous habits — do anything else, and spend your time more productively.

The rats in the study of would press a lever that furnished them with a drug and also induced a tone and a light. One day, nonetheless, pressing the lever stopped offering the drug, and the light and tone additionally disappeared. The authors forced them into withdrawal, additionally still retaining them in the equal context — in the identical surroundings with the identical lever. But now after they press the lever, the lights and tone will not be coming on anymore.

He stated, nonetheless, that the animals did not ever forget the usual drug-paired cues. Instead, learned something new that competes with the old memories — on this case, that pressing the lever produces no light, no tone and no drug. Over time, the animals press the lever less most often, but they rarely stop pressing fully.

According to the researchers, the rats still investigate a couple of instances each session, considering there might be something which will occur. They go from 60 lever presses all the way down to whatever like 10 per session. They evidently have not forgotten what the lever used to do and nonetheless have cravings for the drug.

Finally, the light and tone (however no longer the drug) have been reinstated, inflicting severe cravings within the animals and a relapse to drug-seeking, which results in more lever presses. However, the animals that experienced VNS cure during the extinction segment of the experiment pressed the lever less in most cases, by around 40 or 50 percent which means that their craving was so much lowered.

Article 7

Atrial fibrillation (AF) is a common cardiac rhythm disturbance that can lead to complications like stroke and heart failure. AF may also be caused by stressful events and about 30% of sufferers who undergo cardiac operations suffer from post-operative atrial fibrillation (AF).

Harri Hemilä from the University of Helsinki, Finland, and Timo Suonsyrjä from the Helsinki University Central Hospital, Finland performed a systematic review of vitamin C for preventing AF in high risk sufferers. They identified 14 randomized trials totaling 2006 patients who had gone through cardiac surgery, and one trial with 44 patients that had investigated the recurrence of AF after a successful cardioversion.

There was massive heterogeneity between the 14 cardiac surgery trials, but the heterogeneity was explained using the division of them between 5 trials applied in the US and 9 trials performed outside of the US. The five cardiac surgical procedure trials carried out in the USA uniformly observed no outcome of vitamin C towards post -operative AF. In contrast, the 9 cardiac surgery trials performed outside of the US showed a mean reduction of 44% within the incidence of post-operative AF and there was no heterogeneity between these 9 trials. Five of the latter trials have been done in Iran, two in Greece, one in Slovenia and one in Russia.

The only study on the recurrence of AF after a successful cardioversion, which was done in Greece, discovered that vitamin C decreased the risk of AF recurrence by 87%.

In the non-US cardiac surgery trials, vitamin C reduced the length of clinic stay by 12.6% and intensive care unit stay by 8.0%.

Some of the surgery patients within the non-US studies have been administered vitamin C orally, whereas in others vitamin C was administered intravenously. The latter route results in notably better levels of vitamin C in the blood, consequently the effects of the two  administration approaches could vary.

Oral administration of vitamin C decreased the incidence of post-operative AF by 73%, whereas intravenous administration diminished it by 36%. Then again, oral administration shortened the length of hospital stay by 7% (0.4 days), whereas intravenous administration decreased it by 16% (1.5 days). Thus, the influence of intravenous diet C administration was increased with hospital length stay, however less for the occurrence of post-operative AF.

According to the authors, vitamin C is a safe inexpensive predominant nutrient. Given the constant proof from the less wealthy countries, vitamin C can be administered to cardiac surgery patients, although further research is needed to find out high-quality protocols for its administration. However, there seems to be no purpose for further studies of unselected patients in wealthy international locations; however the effects of vitamin C for sufferers who have a peculiarly low documented level of vitamin C might nonetheless be worthwhile.

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