Purpose Acute myocardial infarction (AMI) is the most common cause of death in the world. Comprehensive risk assessment of patients presenting with chest pain and eliminating undesirable results should decrease morbidity and mortality rates, increase the quality of life of patients, and decrease health expenditure in many countries. In this study, the advantages and disadvantages of the enzymatic and nonenzymatic biomarkers used in the diagnosis of patients with AMI are given in historical sequence, and some candidate biomarkers - hFABP, GPBB, S100, PAPP-A, RP, TNF, IL6, IL18, CD40 ligand, MPO, MMP9, cell-adhesion molecules, oxidized LDL, glutathione, homocysteine, fibrinogen, and D-dimer procalcitonin - with a possible role in the diagnosis of AMI are discussed. Methods The present study was carried out using meta-analyses, reviews of clinical trials, evidence-based medicine, and guidelines indexed in PubMed and Web of Science. Results These numerous AMI biomarkers guide clinical applications (diagnostic methods, risk stratification, and treatment). Today, however, TnI remains the gold standard for the diagnosis of AMI. Details in the text will be given of many biomarkers for the diagnosis of AMI. Conclusion We evaluated the advantages and disadvantages of routine enzymatic and nonenzymatic biomarkers and the literature evidence of other candidate biomarkers in the diagnosis of AMI, and discuss challenges and constraints that limit translational use from bench to bedside.

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Biomarkers in acute myocardial infarction: current perspectives

Because only 25% of cases of premature ovarian insufficiency (POI) have a known etiology, the aim of this review was to summarize the associations and mechanisms of the impact of the environment on this pathology. Eligible studies were selected from an electronic literature search from the PUBMED database from January 2000 to February 2016 and associated references in published studies. Search terms included ovary, follicle, oocyte, endocrine disruptor, environmental exposure, occupational exposure, environmental contaminant, pesticide, polyaromatic hydrocarbon, polychlorinated biphenyl PCB, phenol, bisphenol, flame retardant, phthalate, dioxin, phytoestrogen, tobacco, smoke, cigarette, cosmetic, xenobiotic. The literature search was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We have included the human and animal studies corresponding to the terms and published in English. We have excluded articles that included results that did not concern ovarian pathology and those focused on ovarian cancer, polycystic ovary syndrome, endometriosis or precocious puberty. We have also excluded genetic, auto-immune or iatrogenic causes from our analysis. Finally, we have excluded animal data that does not concern mammals and studies based on results from in vitro culture. Data have been grouped according to the studied pollutants in order to synthetize their impact on follicular development and follicular atresia and the molecular pathways involved. Ninety-seven studies appeared to be eligible and were included in the present study, even though few directly address POI. Phthalates, bisphenol A, pesticides and tobacco were the most reported substances having a negative impact on ovarian function with an increased follicular depletion leading to an earlier age of menopause onset. These effects were found when exposure occured at different times throughout the lifetime from the prenatal to the adult period, possibly due to different mechanisms. The main mechanism seemed to be an increase in atresia of pre-antral follicles. Environmental pollutants are probably a cause of POI. Health officials and the general public must be aware of this environmental effect in order to implement individual and global preventive actions.

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Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data

Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory cascades, which if prolonged causes secondary brain damage. Here, we comprehensively review the current knowledge regarding the role of IL-10 in modulating outcomes following acute brain injury, including traumatic brain injury and the various stroke subtypes. The vascular endothelium is closely tied to the pathophysiology of these neurological disorders and research has demonstrated clear vascular endothelial protective properties for IL-10. In vitro and in vivo models of ischemic stroke have convincingly directly and indirectly shown IL-10-mediated neuroprotection; although clinically, the role of IL-10 in predicting risk and outcomes is less clear. Comparatively, conclusive studies investigating the contribution of IL-10 in subarachnoid hemorrhage are lacking. Weak indirect evidence supporting the protective role of IL-10 in preclinical models of intracerebral hemorrhage exists; however, in the limited number of clinical studies, higher IL-10 levels seen post-ictus have been associated with worse outcomes. Similarly, preclinical traumatic brain injury models have suggested a neuroprotective role for IL-10; although, controversy exists among the several clinical studies. In summary, while IL-10 is consistently elevated following acute brain injury, the effect of IL-10 appears to be pathology-dependent and preclinical and clinical studies often paradoxically yield opposite results. The pronounced and potent effects of IL-10 in the resolution of inflammation and inconsistency in the literature regarding the contribution of IL-10 in the setting of acute brain injury warrant further rigorously controlled and targeted investigation.

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Role of Interleukin-10 in Acute Brain Injuries.

Inflammation and insulin/IGF-1 resistance as the possible link between obesity and neurodegeneration

Neurotoxic effects of organophosphorus pesticides and possible association with neurodegenerative diseases in man: A review.

Background: Serum S100B is found in the glial cells and is elevated with stroke. It can be used in the diagnostic and prognostic utility. However, the use of S100B in the emergency room is controversial. In our study, we wish to determine if the National Institutes of Health Stroke Scale (NIHSS) and Glasgow Coma Scale (GCS) have utility in predicting the acute and first month poststroke mortality and morbidity in emergency room patients, as measured by serum S100B and clinical evaluations. Methods: A total of 62 consecutive patients who applied to the emergency service with acute ischemic stroke were enrolled in the study. Following a detailed neurological examination, GCS and NIHSS were used to determine the consciousness of the patients. Their serum samples were obtained as soon as they arrived into the emergency service and at the time of discharge. As outcome variables, the scores on the modified Rankin Disability Scale (mRDS) at 1 month were determined. Results: The S100B level immediately after the stroke was significantly related to the NIHSS and GCS scores. In addition, the clinical state and S100B levels of patients varied with the length of time between the stroke onset and emergency room treatment. Nine patients (14.5%) died while in the hospital. The stepwise Logistic regression analysis showed that NIHSS was an independent predictor of mortality (odds ratio = 1.48; 95% confidence interval, 1.01-2.18; P⩽0.05). Thirty days poststroke, the mRDS levels significantly correlated with the initial and later S100B levels and GCS and NIHSS scores. The linear Logistic regression analysis indicated that NIHSS score and age were independent risk factors of mRDS (odds ratio= 1.48; 95% confidence interval, 1.01-2.18; P⩽0.05) in our study population. Conclusions: The NIHSS scale is a much more reliable method to determine mortality and morbidity and also adds no extra cost. Therefore, it is not recommended to measure S100B in the emergency room, but if it is measured, then the time between measurement and onset of stroke symptoms should be determined.

https://www.researchgate.net/profile/Mehmet_Ay3/publication/258342761_S-100B_Levels_in_Stroke_Patients_Is_It_Useful_for_Showing_Short-term_Mortality/links/00b7d53827878806cf000000.pdf

S-100B Levels in Stroke Patients: Is It Useful for Showing Short-term Mortality?

Amac: Bu calismada minor kafa travmasi nedeni ile acil servise basvuran hastalarda travma sonrasi donemde ortaya cikan posttravmatik bas agrisi (PTBA) ve minor kafa travmasi arasindaki iliskinin arastirilmasi amaclandi. Gerec ve Yontem: Calismamiza prospektif olarak 01.01.2009 - 31.12.2010 tarihleri arasinda Acil Tip Klinigi"mize minor kafa travmasi ile basvuran hastalarin alinmasi planlandi. PTBA gelisen ve gelismeyen tum olgularin demografik ozellikleri, ayrintili risk faktorleri, kafa travmasi olus sekli, amnezi sureleri, ozgecmiste bas agrisi, psikiyatrik hastalik, ilac kullanma oykusu, basvuru aninda, taburcu olmadan once ve 3. ayda yapilan kontrol fizik ve norolojik muayene bulgulari, direk grafi ve BT bulgulari standart veri giris formuna kayit edildi. Agir kafa travmali, bilinc duzeyi stupor ve koma tablosunda olan hastalar, gebeler, 18 yas alti travma olgulari calismaya alinmadi. Calismada elde edilen verilerin istatistiksel analizinde SPSS 17.0 paket programi kullanildi. Tum testlerde istatistiksel onem duzeyi p < 0.05 olarak kabul edildi. Bulgular: Calismamiza alinan toplam 119 hastada en sik minor kafa travmasi nedenleri arac ici trafik kazasi (% 36.1) ve arac disi trafik kazalari (% 32.8) idi. Hastalarda sadece izole kafa travmasi sonrasi % 87, kafa + servikal travma sonrasi % 88.4, kafa + servikal + kamci ucu travmasi sonrasi ise % 93.3 oraninda PTBA gelistigi saptandi. PTBA olan hastalarda olmayanlara gore travma oncesi psikiyatrik hastaliga bagli ilac kullanim oykusu (p= 0.019), travma sonrasi fotofobi (p= 0.037), kusma (p= 0.029), bas donmesi (p= 0.019), uyku bozuklugu (p=

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Minör kafa travması ve posttravmatik baş ağrısı arasındaki ilişki

A prospective study of wake-up stroke patients presenting to the emergency department: a single-center cohort study

Background: Although poisoning from the ingestion of toxic plants is rarely encountered in Emergency Departments, it can cause serious complications and even death. It is difficult to recognize, diagnose, and differentiate if the patient is unconscious.

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Hemlock Poisoning in Emergent Patients

Meyan koku glycyrrhizic acid iceren Glycyrrhiza glabra"nin kokudur. Asiri meyan koku alimi sodyum ve su retansiyonu, hipokalemi, hipertansiyon, metabolik alkaloz, dusuk renin aktivitesi ve hipoaldosteronizm ile karekterize hipermineralokortikoidizm benzeri sendroma yol acabilir. Bu yazida asiri meyan koku serbeti icimi sonrasi acil servise solunum sikintisi, kol ve bacaklarinda gucsuzluk nedeniyle getirilen hipopotasemik paralizili 34 yasindaki erkek hasta sunuldu. Acil Servise paralizi ve solunum sikintisiyla gelen hastalarda asiri meyan koku alimi olup olmadiginin sorgulanmasi gerekliligine dikkat cekilmesi amaclandi. Kan potasyum duzeyi 1.4 mmol/L olan hastanin potasyum replasmani sonrasi solunum sikintisi ve kas kuvvet kaybi tamamen duzeldi.

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Mehmet Oğuzhan Ay

Papers

S-100B Levels in Stroke Patients: Is It Useful for Showing Short-term Mortality?

Minör kafa travması ve posttravmatik baş ağrısı arasındaki ilişki

A prospective study of wake-up stroke patients presenting to the emergency department: a single-center cohort study

Hemlock Poisoning in Emergent Patients

Aşırı meyan kökü şerbeti alımına bağlı hipopotasemik paralizi ve solunum yetersizliği