The effects of metyrosine on ischemia-reperfusion-induced oxidative ovarian injury in rats: Biochemical and histopathological assessment

Abstract The aim of this study is to investigate the effect of metyrosine on ischemia-reperfusion (I/R) induced ovarian injury in rats in terms of biochemistry and histopathology. Rats were divided into: ovarian I/R (OIR), ovarian I/R+50 mg/kg metyrosine (OIRM) and sham (SG) operations. OIRM group received 50 mg/kg metyrosine one hour before the application of the anesthetic agent, OIR and SG group rats received equal amount of distilled water to be used as a solvent orally through cannula. Following the application of the anesthetic agent, ovaries of OIRM and OIR group rats were subjected to ischemia and reperfusion, each of which took two hours. This biochemical experiment findings revealed high levels of malondialdehyde (MDA) and cyclo-oxygenase-2 (COX-2) and low levels of total glutathione (tGSH), superoxide dismutase (SOD) and cyclo-oxygenase-1 (COX-1) in the ovarian tissue of OIR group, with significant histopathological injury. In metyrosine group, MDA and COX-2 levels were lower than the OIR group whereas tGSH, SOD and COX-1 levels were higher, with slighter histopathological injury. Our experimental findings indicate that metyrosine inhibits oxidative and pro-inflammatory damage associated with ovarian I/R in rats. These findings suggest that metyrosine could be useful in the treatment of ovarian injury associated with I/R

Genome-wide identification and phenotypic characterization of seizure-associated copy number variations in 741,075 individuals

Copy number variants (CNV) are established risk factors for neurodevelopmental disorders with seizures or epilepsy. With the hypothesis that seizure disorders share genetic risk factors, we pooled CNV data from 10,590 individuals with seizure disorders, 16,109 individuals with clinically validated epilepsy, and 492,324 population controls and identified 25 genome-wide significant loci, 22 of which are novel for seizure disorders, such as deletions at 1p36.33, 1q44, 2p21-p16.3, 3q29, 8p23.3-p23.2, 9p24.3, 10q26.3, 15q11.2, 15q12-q13.1, 16p12.2, 17q21.31, duplications at 2q13, 9q34.3, 16p13.3, 17q12, 19p13.3, 20q13.33, and reciprocal CNVs at 16p11.2, and 22q11.21. Using genetic data from additional 248,751 individuals with 23 neuropsychiatric phenotypes, we explored the pleiotropy of these 25 loci. Finally, in a subset of individuals with epilepsy and detailed clinical data available, we performed phenome-wide association analyses between individual CNVs and clinical annotations categorized through the Human Phenotype Ontology (HPO). For six CNVs, we identified 19 significant associations with specific HPO terms and generated, for all CNVs, phenotype signatures across 17 clinical categories relevant for epileptologists. This is the most comprehensive investigation of CNVs in epilepsy and related seizure disorders, with potential implications for clinical practice

How to Set Up a Molecular Pathology Lab: A Guide for Pathologists

In today's pathology practice, pathologists combine molecular tests with conventional histopathological methods. Pathology laboratories should therefore be designed and operated in accordance with the requirements of molecular testing procedures. While the specifics of the requirements may vary depending on the spectrum of the tests that will be performed, there are several basic criteria that need to be fulfilled for standardization. Adequate space, appropriate equipment and qualified personnel are required to establish a molecular pathology laboratory. One of the most important points that should be taken into consideration while designing a molecular pathology laboratory is to create a plan to prevent contamination. As molecular diagnosis has a major role in treatment decisions, the management of the molecular pathology laboratory is of utmost importance. In this review, the criteria required to establish an optimal molecular pathology laboratory will be reviewed

Paradoxic Relations between Basilar Artery Reconfiguration and Superior Cervical Ganglia Ischemia After Bilateral Common Carotid Artery Ligation

Kanat, Ayhan/0000-0002-8189-2877WOS: 000466491700082PubMed: 30716499BACKGROUND: the relationship between superior cervical ganglia (SCG) ischemia due to bilateral common carotid artery ligation (BCCAL) and basilar artery (BA) reconfiguration was investigated. METHODS: Twenty-three rabbits were randomly divided into 3 groups: group III rabbits underwent BCCAL (n = 13), group II rabbits were sham-operated controls (n = 5), and group I rabbits did not undergo surgery (n = 5). Degenerated neuron densities (DND) within the SCG were correlated with the BA vasodilatation index (VDI). RESULTS: Mean live and DND in SCG of group I rabbits were 11.235 +/- 982/mu m(3) and 11 +/- 3/mu m(3), respectively, with a mean heart rate of 294 +/- 21 beats/min. Mean SCG DND and heart rates were 213 +/- 42/mu m(3) and 242 +/- 17 beats/min for the sham group (group II) rabbits and 1743 +/- 285/mu m(3) and 199 +/- 19 beats/min for the study group (group III) rabbits, respectively. the BA VDI values in the sham group (group II) (1.32 +/- 0.10) and the study group (group III) (0.976 +/- 0.112) significantly differed from those in the control group (group I) (1.65 +/- 0.12; P < 0.005) versus the sham group (group II) (P < 0.0001) versus the BCCAL applied group (group III) and between group II and group III (P < 0.005). CONCLUSIONS: A meaningful and paradoxic correlation was detected between the BA VDI values and degenerated neuron density of SCG after BCCAL. Although a low degenerated neuron density within SCG may provoke excessive sympathetic activity and prevent excessive BA dilatation with steno-occlusive carotid artery diseases, a high degenerated neuron density may cause dangerous vasodilatation of BA

Central Pontine and Extrapontine Myelinolysis: The Great Masquerader—An Autopsy Case Report

Central pontine myelinolysis is a demyelinating disorder characterized by the loss of myelin in the center of the basis pontis usually caused by rapid correction of chronic hyponatremia. The clinical features vary depending on the extent of involvement. Demyelination can occur outside the pons as well and diagnosis can be challenging if both pontine and extrapontine areas are involved. We herein report a case of myelinolysis involving pons, lateral geniculate bodies, subependymal region, and spinal cord. To the best of our knowledge, this case represents the second case of spinal cord involvement in osmotic demyelination syndrome and the first case of involvement of thoracic region of spinal cord

Safety and Efficacy of Stent Retrievers for the Management of Acute Ischemic Stroke: Comprehensive Review and Meta-Analysis

OBJECTIVES: This study sought to evaluate the safety and efficacy of stent retriever for the management of acute ischemic stroke. BACKGROUND: Stroke is the third leading cause of death and the most common cause of disability in the United States. Early reperfusion has been associated with favorable outcomes. Stent retrievers are novel endovascular devices that provide vessel recanalization via thrombus retrieval mechanical thrombectomy. METHODS: The authors performed a literature search using PubMed, EMBASE, and Cochrane Central Register of Controlled Trials from May 2005 to May 2015. Randomized controlled trails (RCTs) comparing endovascular therapy (ET) with the use of retrievable stents against standard therapy (ST) for the management of acute stroke were included. RESULTS: Five RCTs (the MR CLEAN, ESCAPE, EXTEND-IA, SWIFT-PRIME, and REVASCAT studies) with 634 patients in the ET group and 653 patients in the ST group met inclusion criteria. The frequency of a low 90-day modified Rankin Score (0 to 2) in the intervention group was 42.6% compared with 26.1% in the control group (odds ratio: 2.43; 95% confidence interval [CI]: 1.9 to 3.09; p \u3c 0.0001). The frequency of intracranial bleeding was 4.2% in the ET group compared with 4.3% in the ST group (risk ratio: 1.08; 95% CI: 0.64 to 1.82; p = 0.78). 90-day mortality was 15.1% in the ET group compared with 18.7% in the ST group (risk ratio: 0.81; 95% CI: 0.58 to 1.12; p = 0.19). There was no evidence of significant heterogeneity or publication bias for any of the endpoints. CONCLUSIONS: On the basis of the results of this meta-analysis of RCTs, ET with stent retrievers appears as a safe and effective therapeutic option for acute ischemic stroke due to large vessel occlusion

Atypical Features in a Large Turkish Family Affected with Friedreich Ataxia

Here, we describe the clinical features of several members of the same family diagnosed with Friedreich ataxia (FRDA) and cerebral lesions, demyelinating neuropathy, and late-age onset without a significant cardiac involvement and presenting with similar symptoms, although genetic testing was negative for the GAA repeat expansion in one patient of the family. The GAA repeat expansion in the frataxin gene was shown in all of the family members except in a young female patient. MRI revealed arachnoid cysts in two patients; MRI was consistent with both cavum septum pellucidum-cavum vergae and nodular signal intensity increase in one patient. EMG showed demyelinating sensorimotor polyneuropathy in another patient. The GAA expansion-negative 11-year-old female patient had mental-motor retardation, epilepsy, and ataxia. None of the patients had significant cardiac symptoms. Description of FRDA families with different ethnic backgrounds may assist in identifying possible phenotypic and genetic features of the disease. Furthermore, the genetic heterogeneity observed in this family draws attention to the difficulty of genetic counseling in an inbred population and to the need for genotyping all affected members before delivering comprehensive genetic counseling

Case Report Atypical Features in a Large Turkish Family Affected with Friedreich Ataxia

Here, we describe the clinical features of several members of the same family diagnosed with Friedreich ataxia (FRDA) and cerebral lesions, demyelinating neuropathy, and late-age onset without a significant cardiac involvement and presenting with similar symptoms, although genetic testing was negative for the GAA repeat expansion in one patient of the family. The GAA repeat expansion in the frataxin gene was shown in all of the family members except in a young female patient. MRI revealed arachnoid cysts in two patients; MRI was consistent with both cavum septum pellucidum-cavum vergae and nodular signal intensity increase in one patient. EMG showed demyelinating sensorimotor polyneuropathy in another patient. The GAA expansion-negative 11-year-old female patient had mental-motor retardation, epilepsy, and ataxia. None of the patients had significant cardiac symptoms. Description of FRDA families with different ethnic backgrounds may assist in identifying possible phenotypic and genetic features of the disease. Furthermore, the genetic heterogeneity observed in this family draws attention to the difficulty of genetic counseling in an inbred population and to the need for genotyping all affected members before delivering comprehensive genetic counseling

An experimental study of the neurophysical mechanisms of photophobia induced by subarachnoid hemorrhage

Conclusion: Our findings indicate that SAH results in a high density of degenerated neurons in the CG, which induces mydriasis and is an important factor in the onset of photophobia. This phenomenon is likely due to more light energy being transferred through mydriatic pupils to the brain, resulting in vasospasm of the supplying arteries. (C) 2016 Elsevier Ireland Ltd. All rights reserved