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Giorgiana Pavaloiu

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2687

Analgesic Nephropathy

Nefropatia analgezica este o boala de rinichi care apare datorita consumului excesiv de analgezice, cum ar fi aspirina, paracetamol, fenacetina sau antiinflamatoare nesteroidiene ( ibuprofen, indometacin). Aceasta afectiune duce la necroza papilara si nefrita interstitiala cronica iar in final la insuficienta renala renala. Statisticile arata ca nefropatia la analgezice este mai frecventa la femeie si la cei care iau combinatii de analgezice ( asipirina, paracetamol etc),

Fenacetina, principala substanta incriminata in patogenia acestei boli, isi datoreaza actiunea toxica datorita metabolitului sau acetaminofen ( paracetamol). Exista mai multe ipoteze cu privire la mecanismul nefropatie analgezice; una din teorii afirma ca aceasta afectiune se datoreaza actiunii toxice a combinatiilor de analgezice asociate cu fenacetina, combinata cu diminuarea rezistentei la infectiile renale, in timp ce o alta teorie sugereaza ca nefropatia analgezica ar fi o reactie de sensibilitate intarziata.

Antiinflamatoarele nesteroidiene si aspirina sunt frecvent indicate pentru tratarea cefaleei, artralgiilor, durerilor musculare sau febrei. Mecanismul de actiune al antiinflamatoare nesteroidiene consta in blocarea sintezei de prostaglandine, iar acest lucru duce la ischemie medulara.

Simptome si diagnosticul nefropatiei analgezice

Desi pot fi prezente mai multe simptome si semne urinare nespecifice, debutul clinic clasic cuprinde poliurie cu nicturie si crampe musculare. Marea majoritate a pacientilor care au nefropatie analgezica se prezinta la medic in stadiul de insuficienta renala cronica latenta, iar o mica parte ( aproximativ 10%) in stadiul de insuficienta renala cronica terminala. Alte simptome urinare sunt proteinurie (adica prezenta de proteine in urina), hematurie (adica hematii in urina), infectii urinare care pot fi insotite de piurie ( leucocite si bacterii in urina). Afectarea renala duce la hipertensiune arteriala, deoarece este afectat sistemul renina-angiotensina-aldosteron, si anemie, deoarece scade productia de eritropoietina.

Dintre simptomele extrarenale, nefropatia analgezica poate duce la cianoza si hiperpigmentarea pielii si a organelor. Mai pot aparea tulburari digestive cum ar fi gastrita, ulcere, hemoragii gastrointestinale, tulburari cardiovasculare, care includ hipertensiune arteriala, cardiopatie ischemica, ateroscleroza sistemica. Nefropatia analgezica mai poate determina cefalee, dureri articulare, dispepsie etc.

Analizele de sange arata ca anemie, retentie azotata, iar la examenul de urina se observa hematurie, leucociturie, fragmente de papile necrozate, proteinurie, iar capacitatea de concentrare a rinchiului este scazuta. Radiologic se constata rinichi micsorati, contur boselat si calcificari papilare.

Tratamentul nefropatiei la analgezice

In primul rand, tratamentul etiologic consumul de analgezice trebuie oprit pentru a

1428

Four genes indentified that influence levels of ‘bad’ cholesterol

“Our findings are important because they provide new targets for the development of novel drugs to reduce heart disease risk in humans,” said Laura Cox, Ph.D., a Texas Biomed geneticist. “Since these genes have previously been associated with cancer, our findings suggest that genetic causes of heart disease may overlap with causes of some types of cancer.” The new study, funded by the National Institutes of Health (NIH), is published online and will appear in the July print issue of the Journal of Lipid Research. Texas Biomed scientists screened their baboon colony of 1,500 animals to find three half-siblings with low levels of low density lipoprotein (LDL), or “bad,”‘ cholesterol, and three half-siblings with high levels of LDL. In the study, these animals were fed a high-cholesterol, high-fat diet for seven weeks. Scientists then used gene array technology and high throughput sequencers to home in on the genes expressed in the two groups and differentiate those in the low LDL groups from those in the high LDL group. They discovered that four genes (named TENC1, ERBB3, ACVR1B, and DGKA) influence LDL levels. Interestingly, these four genes are part of a signaling pathway important for cell survival and disruption of this pathway promotes some types of cancer. It is well-known that a high level of LDL is a major risk factor for heart disease. Despite concerted efforts for the past 25 years to manage cholesterol levels through changes in lifestyle and treatment with medications, heart disease remains the leading cause of death and mortality in the United States and around the world. It will account for one out of four U.S. deaths in 2013, according to the American Heart Association. Heart disease is a complex disorder thought to be a result of interactions between genetic and environmental factors, which occur primarily through diet. To understand why humans have different levels of LDL and thus variation in risk for heart disease, the genetic factors causing these differences need to be understood. However, these studies are difficult to do in humans because it’s practically impossible to control what people eat. Instead, Texas Biomed scientists are using baboons, which are similar to humans in their physiology and genetics, to identify genes that influence heart disease risk. The new research also suggests that knowing many of the genes responsible for heart disease may be necessary to devise effective treatments. For example, several genes may need to be targeted at once to control risk. The next step in this research is to find the mechanism by which these genes influence LDL cholesterol. “That starts to give us the specific targets for new therapies.” Cox said. If all goes well, this information may be available within two years.

Read more at:†http://medicalxpress.com/news/2013-05-genes-indentified-bad-cholesterol.html#jCp

Cercetatorii de la†Texas Biomedical Research Institute in San Antonio au descoperit 4 gene noi care regleaza nivelul colesterolului rau din sange. Descoperirea este valoroasa pentru ca poate duce la descoperirea unor noi medicamente care reduce riscul cardiovascular.

Laura Cox, Ph.D., a Texas Biomed geneticist, a spus ca cercetarile lor sunt foarte importante pentru ca deschide calea spre noi medicamente care reduc riscul cardiovascular. In plus, ea a adaugat ca din moment ce aceste gene au fost implicate in patologia cancerului, studiul sugereaza ca cauzele genetice ale bolii cardiovasculare se suprapun cu cauzele de anumite tipuri de cancer. Ceea ce au facut†Texas Biomed scientists a fost sa faca screeningul in al lor†baboon colony of 1,500 animals pentru a gasi†three half-siblings cu nivel scazut de colesterol rau, sau LDL colesterol, trei half siblings cu nivelul crescut de colesterol. Trebuie spus ca cu sapte saptamani inainte aceste animale cu fost hranite cu dieta foarte grasa. Cercetatorii au folosit apoi††pentru a descoperi care gene sunt implicate in grupul cu low LDL colesterol si care sunt implicate in grupul cu high LDL colesterol. Asa au descoperit ca patru gene influenteaza nivelul colesterolului rau:†TENC1, ERBB3, ACVR1B, and DGKA. Ceea ce este interesant †este ca aceste gene sunt implicate in

2516

Vitamin D may lower diabetes risk in obese children and adolescents, study finds

Un nou studiu efectuat de cercetatorii de la†University of Missouri arata ca suplimentele de vitamina D pot preveni instalarea diabetului zaharat. Se pare ca vitamina D ii poate ajuta pe copii obezi sa isi controleze nivelul glicemiei si astfel sa previna aparitia diabetului zaharat.

Vitamina D este una din cele patru vitamine liposolubile ( A, D, E, K) si este esentiala in metabolismului calciului in organism. Este bine cunoscut faptul ca vitamina D este indispensabila pentru sanatatea oaselor, a muschilor si a nervilor. Vitamina D este singura vitamina care se formeaza in piele cu ajutorul radiatiilor ultraviolete, asadar deficitul de vitamina D este rar intalnit. However este posibil un nivel insuficient de vitamina D sa fie detrimentul

Se stie ca in ultimii 30 de ani rata obezitatii in Statele Unite ale Americii a crescut foarte mult in randul copiilor si adolescentilor. Obezitatea este un factor de risc pentru diabet zaharat, care se caracterizeaza printr-un nivel crescut al glucozei in sange.†Catherine Peterson, an associate professor of nutrition and††at MU, a spus ca suplimentele de vitamina D au cam acelasi efect ca si un drug hipoglicemiant. Ea a adaugat ca s-a vazut ca nivelul de insulina a scazut, ceea ce inseamna un mai bun control a glucozei in sange, chiar daca nu s-au facut modificari in activitarea fizica, greutatea corporala si aportul de mancare.

Peterson a afectuat un studiu in care au inclus†35 pre-diabetic obese children and adolescents, care au urmat tratament la†MU Adolescent Diabetic Obesity Program. Toti cei 35 de participanti la studiu au avut aceeasi dieta si activitate fizica si nivel insuficient de vitamina D. Acestia au fost impartiti aleator sa primeasca fie placebo, fie†high-dose vitamin D supplement zilnic timp de sase luni. Se pare ca toti cei care au marit suplimentele de vitamina D au micsorat cantitatea de insulina pe care luau de obicei.

Peterson a spus ca suplimentele de vitamina D pe care le-au folosit in studii sunt in cantitati pe care nu le-ar recomanda oricaruia. Ea a mai spus ca clinicienii ar trebuie sa verifice nivelul de vitamina D la pacientii obezi pentru ca est foarte probabil ca nivelul de vitamina sa fie scazut. Marirea cantitatii de vitamina D ar putea ajuta la controlul glicemiei si la tratarea obezitatii care este asociata cu rezistenta la insulina.

1781

High Blood Pressure during Pregnancy

Preeclampsia is a serious complication of pregnancy and the major cause of death for both mother and child in Europe and the U.S. It affects about one in 20 pregnancies. The main symptoms are high blood pressure and protein in the urine. The cause of preeclampsia is still unclear. Dr. Florian Herse (Experimental and Clinical Research Center (ECRC) of the Max Delbr√ľck Center (MDC) and the Charit√©), Dr. Ralf Dechend (ECRC and Helios Klinikum Berlin-Buch) and their collaborators have now identified an enzyme that is overexpressed in affected women and thus apparently contributes to development of the condition. In animal experiments, the researchers inhibited this enzyme and were able to ameliorate the disease process. Ads by Google Clinical Research SOPs – Join ACRP and gain access to templates, guidelines, and more. – www.acrpnet.org/join Cancer Treatment in China – DCCIK Gene Tumor Therapy Free Online Cancer Inquiry – www.cancertherapychina.com Preeclampsia originates in the placenta, which supplies the embryo/fetus in the womb with nutrients. For their study, Dr. Herse, numerous contributors, and Dr. Dechend analyzed tissue samples from 25 women diagnosed with preeclampsia and from 23 healthy pregnant women as controls. The tissue samples of the preeclamptic women were obtained from hospitals in Finland, Norway, Austria, and the U.S. that cooperated closely in the study. Using gene-chip technology, the researchers in Berlin analyzed the expression of almost 40,000 genes. They found that in women with preeclampsia, levels of the CYP2J2 enzyme were unusually high in placental cells and the uterine lining (decidua). The placenta consists of fetal cells; the decidua, by contrast, is solely maternal tissue. The enzyme is involved in the production of specific metabolites called EETs (epoxyeicosatrienoic acids) which, among other things, regulate inflammatory processes, vascular growth, and blood pressure. Dr. Herse and team succeeded in identifying the cells that produce the CYP2J2 enzyme as trophoblasts, which fulfill an important function in pregnancy. These fetal cells migrate from the placenta into the maternal decidua. Trophoblasts are key contributors to spiral-artery remodeling and thus ensure that the fetus is sufficiently supplied with nutrients. However, if the trophoblasts do not grow deeply enough into the decidua, this remodeling process is disturbed. As a consequence, the fetus cannot be sufficiently supplied with nutrients, leading to preeclampsia. EETs evidently have a harmful effect because they activate a substance which prevents the trophoblasts from growing into the decidua. Both a protective and damaging effect Previous studies indicated that EETs exert only positive effects on the cardiovascular system. EETs generally mediate vascular expansion and reduce blood pressure. They also protect the tissue from dying of oxygen deficiency. In normal pregnancies EET levels are slightly elevated. Ads by Google Bilete de avion ieftine – Preturile se schimba zilnic! Ai aflat ultimele noutati? – www.momondo.ro Previous experiments with healthy pregnant rats showed that pharmacological inhibition of the CYP2J2 enzyme and the associated inhibition of EET production lead to hypertension and kidney failure. In pregnant rats with preeclamptic symptoms, however, opposite effects may occur. By inhibiting CYP2J2, the ECRC researchers were able to lower blood pressure levels in these animals. How did these conflicting observations come about? Dr. Herse and team demonstrated that the EETs can be converted into other metabolites. A specific enzyme (cyclooxygenase, COX) alters these components further in such a way that they cause vasoconstriction and thus an increase in blood pressure. EETs that normally lower blood pressure can evidently produce metabolites that cause blood pressure to rise in preeclampsia. If however the researchers inhibited the cyclooxygenase in the pregnant animals, the EETs were not converted further and the blood pressure did not increase. “This work shows that the increased production of EET in the placenta and the conversion via cyclooxygenase into hormones that increase blood pressure both favor the development of preeclampsia,” Dr. Herse and Dr. Dechend explained. Messenger substance of the immune system apparently promotes the development of preeclampsia But why do the bodies of women with preeclampsia produce more CYP2J2 and thus more EET? Tumor necrosis factor-alpha (TNF-alpha), a chemical messenger of the immune system, could possibly contribute. This signaling substance is released at early stages of pregnancy whenever placental blood flow is too low, causing oxygen deficiency. As the researchers showed, TNF-alpha promotes the production of CYP2J2 and EET in the placenta. In other tissues, this reaction would be useful, since EET rescues tissue from dying that has an insufficient supply of blood and therefore of oxygen. In the placenta, by contrast, this boost in production of CYP2J2 and EET could lead to a vicious circle. The trophoblasts do not grow as well into the decidua and the blood vessels and are not remodeled correctly, so that blood flow through the placenta and blood supply to the fetus deteriorates. As a consequence, the mothers becomes hypertensive and EETs under these conditions is converted in such a way that the blood pressure continues to increase. Treatment of preeclampsia, which according to estimates costs many thousands of maternal lives across the globe every year, remains difficult. The only possibility is to induce delivery at an early stage if the clinical presentation is severe. In Germany, preeclampsia is the cause for up to 20,000 premature births annually. Once the child is born, the symptoms subside in the mother. Nevertheless, she may suffer long-term increased risk for cardiovascular disease and develop heart attack, stroke, or hypertension at an early age. For the child, depending on the stage of fetal development, the premature birth may result in death or severe lifelong disability, and the child may also have an increased risk for cardiovascular disease later on. The research conducted by Dr. Herse, the entire team, and Dr. Dechend implicates a previously unknown mechanism. Their discovery may contribute to a better understanding of the disease process and its causes, and may ultimately aid in developing a therapy.

Read more at:†http://medicalxpress.com/news/2012-11-factor-high-blood-pressure-pregnancy.html#jCp

1565

Genetic links about migraine

Migraine is an intense headache, which can last from several hours to several days (3 days). When a person has a migraine, he or she can no longer perform daily activities. No one knows why some people are more prone to migraine than others, but there seems to be a familial aggregation. Now researchers at the Wellcome Trust Sanger Institute have discovered for the first time that in the onset of migraine are involved five genetic regions.

In the largest study on migraine, researchers have tried to identify what are the mechanisms underlying the susceptibility to migraine. They found 12 genetic regions: 8 of them appear to be involved in the control circuits in the brain and two of these regions appear to be associated with maintaining brain health. It seems that genetic susceptibility to migraine depends on these pathways. In fact, it seems that there are also other regions involved as researchers found †more than 130 genetic regions implied in susceptibility to migraine†but without statistical significance.

Statistics show that 14% of people suffer from migraine, moreover the Global Burden of Disease Survey 2010 points out that migraine is responsible for the highest costs among neurological disorders. Migraine is a condition difficult to study because there are no some specific biomarkers in patients suffering from migraine.

migraine

Migraine

Dr Aarno Palotie, from the Wellcome Trust Sanger Institute, said that this study gave very useful information about the cause of migraine. †Dr. Palotie added that migraine and epilepsy are two neurological conditions extremely difficult to investigate biochemically because the patient is perfectly healthy between crisis.†“The molecular mechanisms of migraine are poorly understood. The sequence variants uncovered through this meta-analysis could become a foothold for further studies to better understanding the pathophysiology of migraine” Dr K√°ri Stef√°nsson, President of deCODE genetics, points out.

To get to discover the genetic regions underlying migraine, researchers used more than 100 000 samples from both migraine patients and patients without migraine. What they did was to compare the results from 29 different genomic studies and found that these susceptibility regions are connected with a network of genes that are involved in oxidative stress. It is possible that genes in these genomic regions to be interconnected and to interfere with the internal control of brain circuits. Dr Mark Daly, from the Massachusetts General Hospital and the Broad Institute of MIT and Harvard, said that this approach is the most effective way to understand the biology of these neurological disorders.

2318

Multiple endocrine neoplasia type 1

MEN means multiple endocrine neoplasia and is an autosomal dominant syndrome. In fact, MEN refers to the combination of several different syndromes caused by tumors (benign or malignant) of endocrine glands. Von Hippel Lindau, McCune Albright syndrome and Carney complex could also be considered part of MEN, because they are all autosomal dominant syndromes that includes endocrine tumors and because they have a clinical features which overlap with MEN syndromes.

Types of multiple endocrine neoplasia

There are three types of MEN: MEN1 ( also called†Werner syndrome) – pancreatic neuroendocrine tumors, pituitary adenoma,†and adenoma†or†hyperplasia of parathyroid†with or without†angiofibromas.

MEN 2A syndrome (or Sipple syndrome) includes medullary thyroid carcinoma, pheochromocytoma and†hyperparathyroidism.

MEN 2B†or MEN 3 (or†Shimcke syndrome) includes medullary thyroid carcinoma, pheochromocytoma and†neuromas.

It should be noted that MEN is a rare syndrome, each of the two syndromes MEN ( MEN 1 and MEN 2) affects 1 in 30 000/40 000 persons. Among the subtypes of MEN, MEN 2A is the most common and 2 B is the rarest.

Neoplasia

Neoplasia

Multiple endocrine neoplasia type 1

Approximately 70-95% of patients with MEN 1 has a MEN1 gene mutation. This gene encodes menin, which is a tumor suppressor, which means it prevents the cells to divide uncontrollably. When the MEN 1 gene mutations occur, it cannot exercise its function and different tumors appear ( parathyroid, pancreatic or pituitary).

Signs and symptoms begin to appear around the age of 20 years (50% of patients) and by the age of 40 years this syndrome becomes clinically manifest in 95% of them. Usually patients with MEN 1 have a family relative with this disorder. †In most cases, MEN 1 is manifested by tumors of the parathyroid, pancreas†and pituitary gland. The most important sign that appears in MEN1†is†hyperparathyroidism, which causes disturbances of calcium in the body that can lead to kidney stones, weak bones (fractures), nausea, vomiting, hypertension, fatigue.

In MEN 1 syndrome, endocrine or non-endocrine neoplasms can develop such as thyroid, adrenal cancers, visceral and cutaneous lipomas, meningiomas, etc.. There is a great variability in terms of MEN1 phenotype.†A patient who has endocrinopathies given by two of the three target endocrine glands (pancreas, pituitary, parathyroid) or endocrinopathy on one ofthe †three typical endocrine glands plus one first-degree relative with MEN1, the MEN 1 syndrome should be suspected.

Typically, tumors in MEN 1 are benign and the symptoms are due to excessive production of hormones or mass effect. However, some patients with MEN 1 have increased risk for cancer, so it is recommended cancer screening in patients with MEN.

2029

Alzheimer’s disease may be triggered by stress hormone

According to researchers at Temple’s School of Medicine, Alzheimer’s disease may be triggered by steroids, which are hormones released by the adrenal glands in situations of stress. This could be a key trigger that underlies the mechanism of Alzheimer’s disease ( AD) with late onset.

The link between stress hormones and Alzheimer’s disease has been emphasized by previous studies that have shown that the level of corticosteroids is two to three times higher in AD patients compared to patients without AD. Domenico Pratico, professor of pharmacology and microbiology and immunology in Temple’s School of Medicine, who led the study, said that stress is an environmental factor that seem to have a role in causing Alzheimer’s disease. The explanation is that when you have elevated stress hormones for long time, they can cause neuronal cell death, which harms memory and learning. To investigate this hypothesis, Temple’s School of Medicine researchers have conducted several experiments to elucidate the mechanisms by which stress causes Alzheimer’s disease.

Alzheimer's

Alzheimer’s Disease

To perform these experiments, the researchers used triple transgenic mice that have developed the two hallmarks of Alzheimer’s disease, that is beta amyloid protein and the tau protein. One group of mice received injections with high levels of corticosteroid daily for a week to mimic stress. Researchers found no significant differences in terms of memory, but what they noticed was that tau protein was significantly increased in rats that received injections of corticosteroids. In addition, what is interesting is that the synapses, the connections between neurons, have been damaged or destroyed.

Pratico pointed out that this was surprising because they have not found memory or learning impairment although the pathology was visibly affected. The researchers also pointed out that another surprising result was that a third group of mice that were genetically engineered to lack the enzyme 5-lipoxygenase in the brain appeared to be immune and had no neurological damage from corticosteroid. Previous studies conducted by Pratico have shown that high levels of 5-lipoxygenase resulted in increasing levels of amyloid and tau protein in the brain regions responsible for memory and learning (that contribute to Alzheimer’s disease).

The conclusion was that corticosteroids use 5-lipoxygenase as a mechanism to injure synapses leading to learning and memory impairment, which are the main symptoms in AD.†“So that is strong support for the hypothesis that if you block 5-lipoxygenase, you can probably block the negative effects of corticosteroid in the brain” added Pratico.

1486

Urinary tract infection in menopause is linked to low estrogens levels

Latest studies on urinary tract infections led by researchers at Karolinska Institutet show that estrogens stimulate the production of the body’s own†antibiotics and strengthens the cells to fight urinary tract infection. These findings show that post-menopausal women are more prone to recurrent urinary tract infections and that estrogen supplements might help. The study results are published in the scientific journal Science Translational Medicine.

Urinary tract infection is defined as the presence and multiplication of bacteria in the urinary tract. There are two types of urinary tract infections: infection of the lower urinary tract, which refers to cystitis, pyelocystitis, urethritis, prostatitis, and upper urinary tract infection, which refers to infection of the renal parenchyma, that is pyelonephritis, which can be acute or chronic. The most common germs that cause urinary tract infections are Gram-negative bacteria such as E. coli, Klebsiella, Proteus, Pseudomonas aeruginosa. The main factors that lead to urinary tract infection are bacterial virulence (fimbriae, lipopolysaccharide, capsular agent) and host susceptibility (urinary tract abnormalities, systemic diseases).

Urinary Tract Infection

Urinary Tract Infection

Urinary tract infections are among the most common diseases that affect women as about half of them have at least one episode of urinary tract infection at some point in life, and 25% develop recurrences. It was found that women in post-menopause have a higher risk of recurrent urinary tract infection and this is due to low levels of estrogen. For an infection to occur, it is necessary that the bacteria come in contact with the bladder. Urinary bladder is made up of special epithelial cells that protects vulnerable tissue and produce antimicrobial peptides (which have an antibiotic-like effect).

These antimicrobial peptides are the first to act when the bladder comes in contact with bacteria. Because these peptides act very quickly, the bacteria do have time to multiply and thus no infection occurs. In contrast, in†post-menopausal women, the bladder epithelium is more fragile and often damaged (which lead to gaps between cells that allow the dissemination of bacteria and infection).

In the study conducted by researchers at Karolinska Institutet, 14 post-menopausal women were given estrogen for 14 days. After treatment with estrogen, the researchers analyzed cells excreted in urine and saw that the†gaps†that were previously in bladder epithelium disappeared.†Dr. Annelie Brauner at the Department of Microbiology, Tumor and Cell Biology, who is responsible for the study, said: “By treating post-menopausal women locally with estrogen the cells lining the bladder are strengthened and the body’s own defense against infection is improved, making women better suited to fight infections.”

1511

An earlier treatment means a better recovery for patients with stroke

Stroke is a medical emergency and early treatment is essential for patient recovery. Therefore, bringing the patient in time, after the stroke occurs, to the emergency room for specific treatment (fibrinolysis), is crucial. But so far there have been limited information regarding how the timing of administration of tissue plasminogen activator, or tPA,†influences the outcome of patients with ischemic stroke, the most common type of stroke. Now a team of researchers from the University of California, Los Angeles conducted a study on more than 50 000 stroke patients treated with tPA. They wanted to see how critical is the timing between stroke onset and treatment.

Dr. Jeffrey Saver, a professor of neurology and director of the UCLA Stroke Center, said they found that the timing of the treatment had a strong influence on recovery and that the faster the treatment was applied, the better the results. He also added the patients who receive early treatment recovers much better: “Beginning treatment earlier resulted in an improved ability to walk, the ability to remain living independently, less bleeding in the brain and reduced mortality.”

stroke

stroke

Previous studies have demonstrated that intravenous tPA up to 4.5 hours after stroke helps patients with †moderate to severe acute ischemic stroke. The data so far show that the maximum benefit comes when patients are treated very early after stroke and that it starts to decrease after 4.5 hours. But the disadvantage is that these data were drawn from a relatively small number of studies (eight studies conducted on 1,850 patients treated with†tPA) and cannot be extrapolated to the general population. Therefore, the study conducted by researchers at UCLA used a large national registry to determine more accurately the association between time to treatment and stroke.

The study was conducted on a sample of 58 353 patients with acute ischemic stroke treated with tPA in the first 4.5 hours from stroke. The average patient age was 72 years and the average time†from the onset of stroke to treatment was 144 minutes (about 2 hours and a half). After analyzing the medical history of the patients, the researchers were able to confirm precisely how critical is the time gap between the occurrence of stroke and receiving treatment. Saver pointed out that they knew from imaging investigations that the volume of irreversibly damaged brain tissue after ischemic stroke is expanding rapidly over time and that it takes more than 2 million neurons per minute for additional blood flow in the brain to be restored.

2686

Lack of sleep is linked to Diabetes

Latest research on diabetes presented at The Endocrine Society’s 95th Annual Meeting in San Francisco, reveals that type II diabetes could be prevented if we got enough sleep. According to researchers at Los Angeles Biomedical Research Institute (LA BioMed), people who lose sleep during their work week could prevent the onset of this metabolic disease if they recover the those hours of sleep during weekend.

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The study, which was led by Peter Liu, MD, PhD, lead researcher at BioMed, shows that insulin sensitivity significantly improves†after three nights of catch-up sleep on weekends. Recovering the body after sleep restriction during the week and lead to better insulin sensitivity and this lowers the risk of type II diabetes. Liu said that reducing the incidence of this chronic metabolic diseases is critical in a nation where diabetes affects 26 million people and the costs are huge (about $ 174 million annually).

Lack of sleep

sleep

Insulin is a hormone produced by the pancreas and regulates blood glucose. Insulin helps the glucose to enter the cells after we eat, in order to be used as a source of energy. When glucose remains in the blood, hyperglycemia occurs, which is characteristic of diabetes. Diabetes can occur either when the pancreas does not produce enough insulin or when the body loses sensitivity to insulin (hyperglycemia occurs in both cases). In type II diabetes, the body becomes resistant to insulin, which means that the pancreas produces the hormone but it cannot be used properly. If the body recovers insulin sensitivity, type II diabetes could be avoided.

Studies on the link between sleep and diabetes have already been made and have shown that in †healthy, normal sleepers sleep restriction can have harmful effects. New study investigates the profile of men who sleep less during the week because of their job, but recover those lost hours of sleep during the weekend.

The study was conducted on a sample of 19 men (average age 28 years) who stated that they had inadequate sleep for six months or more. On average each man had about six hours of sleep per night. But those hours lost were recovered over the weekend when they slept an extra 37.4 percent, or 2.3 hours, per night. After several experiments in the laboratory, the researchers measured the levels of glucose and insulin and then insulin sensitivity was calculated. It was found that insulin sensitivity was better in men who slept 10 hours a night on each of three nights of catch-up sleep than when they had slept restriction.