With a subarachnoid haemorrhage, the outcome is never enough

Introduction. In the current edition, Nastasovic et al. present the results of a prospective study on patients with aneurysm subarachnoid haemorrhage (SAH) regarding the association of selected variables and outcomes three months after the incident.Clinical reflections. The independent predicting factors of an unfavourable aneurysm SAH outcome are aneurysm re-rupture, high systolic blood pressure (SBP), and increased heart rate.Clinical implications. The article findings confirm easily monitored parameters that could be potentially useful in clinical approaches to this critical illness

Free thyroxine and TSH interact with secreted protein acidic and rich in cysteine-like 1 in ischemic stroke

The role of the thyroid gland in ischemic stroke pathology is not well understood. As thyroid hormones modulate the extracellular matrix, we explored the possible link between them and secreted protein acidic and rich in cysteine like 1 (SC1) – one of the extracellular matrix molecules. In the 81 patients with acute ischemic stroke, serum SC1 levels were much higher compared with 30 control subjects: 4.47 vs 2.43ng/mL (p<0.001). Serum levels of free thyroxine (fT4) were higher in stroke subjects compared to those of controls (p=0.03). In stroke patients, TSH concentration was lower than in the control group (p=0.03). SC1 levels positively correlated with fT4 levels (p=0.02) and negatively with TSH (p=0.03) in stroke patients. Our results confirmed the association between thyroid hormones and SC1 – extracellular matrix protein

The Early Effect of Carotid Artery Stenting on Antioxidant Capacity and Oxidative Stress in Patients with Carotid Artery Stenosis

The treatment of carotid artery stenosis is associated with the risk of complications, which may include stroke after carotid artery stenting (CAS) and myocardial infarction after carotid endarterectomy (CEA). The imbalance between prooxidative mechanisms and antioxidant capacity creates a milieu of factors, which may increase the risk of complications after endovascular procedures. We have examined 43 consecutive patients with carotid artery stenosis. Sera were analyzed for the activity of paraoxonase (PON) and arylesterase (ARE), sulfhydryl groups (SG), malondialdehyde (MDA), and conjugated dienes (CD) concentrations by means of spectrophotometric methods before and next day after CAS. We have found lowered PON (P=0.0032), increase in ARE activity (P=0.0058), and decrease in sulfhydryl groups concentration (P=0.0267). No effect on absolute MDA and CD concentrations was observed. The degree of carotid artery stenosis correlated negatively with PON/ARE ratio after CAS (rS = −0.507, P=0.0268). To conclude, CAS influences both enzymatic (differently, PON and ARE activity) and nonenzymatic antioxidant defense. Females are more susceptible to lipid peroxidation after CAS. PON/ARE ratio after CAS correlated with the degree of carotid artery stenosis. The changes (deltas) in ARE activity, SG, and MDA concentrations correlated with the severity of neurological deficit and disability

Search for dark matter produced in association with bottom or top quarks in √s = 13 TeV pp collisions with the ATLAS detector

A search for weakly interacting massive particle dark matter produced in association with bottom or top quarks is presented. Final states containing third-generation quarks and miss- ing transverse momentum are considered. The analysis uses 36.1 fb−1 of proton–proton collision data recorded by the ATLAS experiment at √s = 13 TeV in 2015 and 2016. No significant excess of events above the estimated backgrounds is observed. The results are in- terpreted in the framework of simplified models of spin-0 dark-matter mediators. For colour- neutral spin-0 mediators produced in association with top quarks and decaying into a pair of dark-matter particles, mediator masses below 50 GeV are excluded assuming a dark-matter candidate mass of 1 GeV and unitary couplings. For scalar and pseudoscalar mediators produced in association with bottom quarks, the search sets limits on the production cross- section of 300 times the predicted rate for mediators with masses between 10 and 50 GeV and assuming a dark-matter mass of 1 GeV and unitary coupling. Constraints on colour- charged scalar simplified models are also presented. Assuming a dark-matter particle mass of 35 GeV, mediator particles with mass below 1.1 TeV are excluded for couplings yielding a dark-matter relic density consistent with measurements

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Current Insights into the Disease Pathophysiology, Diagnosis and Management

Myelin oligodendrocyte glycoprotein (MOG)-associated disease (MOGAD) is a rare, antibody-mediated inflammatory demyelinating disorder of the central nervous system (CNS) with various phenotypes starting from optic neuritis, via transverse myelitis to acute demyelinating encephalomyelitis (ADEM) and cortical encephalitis. Even though sometimes the clinical picture of this condition is similar to the presentation of neuromyelitis optica spectrum disorder (NMOSD), most experts consider MOGAD as a distinct entity with different immune system pathology. MOG is a molecule detected on the outer membrane of myelin sheaths and expressed primarily within the brain, spinal cord and also the optic nerves. Its function is not fully understood but this glycoprotein may act as a cell surface receptor or cell adhesion molecule. The specific outmost location of myelin makes it a potential target for autoimmune antibodies and cell-mediated responses in demyelinating processes. Optic neuritis seems to be the most frequent presenting phenotype in adults and ADEM in children. In adults, the disease course is multiphasic and subsequent relapses increase disability. In children ADEM usually presents as a one-time incident. Luckily, acute immunotherapy is very effective and severe disability (ambulatory and visual) is less frequent than in NMOSD. A critical element of reliable diagnosis is detection of pathogenic serum antibodies MOG with accurate, specific and sensitive methods, preferably with optimized cell-based assay (CBA). MRI imaging can also help in differentiating MOGAD from other neuro-inflammatory disorders. Reports on randomised control trials are limited, but observational open-label experience suggests a role for high-dose steroids and plasma exchange in the treatment of acute attacks, and for immunosuppressive therapies, such as steroids, oral immunosuppressants and rituximab as maintenance treatment. In this review, we present up-to-date clinical, immunological, radiographic, histopathological data concerning MOGAD and summarize the practical aspects of diagnosing and managing patients with this disease

The Markers of Glutamate Metabolism in Peripheral Blood Mononuclear Cells and Neurological Complications in Lung Cancer Patients

Objective. To evaluate the involvement of glutamate metabolism in peripheral blood mononuclear cells (PBMC) in the development of neurological complications in lung cancer and during chemotherapy. Methods. The prospective study included 221 lung cancer patients treated with chemotherapeutics. Neurological status and cognitive functions were evaluated at baseline and after 6-month follow-up. Glutamate level, the activities of glutaminase- (GLS-) glutamate synthetizing enzyme, glutamate dehydrogenase (GDH), and glutamate decarboxylase catalyzing glutamate degradation were analyzed in PBMC and in sera of lung cancer patients by means of spectrophotometric and colorimetric methods. Results. Chemotherapy of lung neoplasms induced increase of glutamate content in PBMC and its concentration in serum increased the activity of GDH in PBMC and decreased activity of glutaminase in PBMC. The changes in glutamate metabolism markers were associated with initial manifestation of neurological deficit in lung cancer patients and with new symptoms, which appear as a complication of chemotherapy. Moreover, the analyzed parameters of glutamate control correlated with a spectrum of cognitive functions measures in lung cancer patients. Conclusion. We have demonstrated dysregulation in glutamate and glutamate metabolism controlling enzymes as promising indicators of risk for chemotherapy-induced neurological complications in lung cancer patients with particular emphasis on cognitive impairment

Kaplan-Meier curves of mortality in groups with higher and lower TTR (transthyretin) level (above and under the mean value– 46.9 mg/dl) (P = 0.02).

<p>Kaplan-Meier curves of mortality in groups with higher and lower TTR (transthyretin) level (above and under the mean value– 46.9 mg/dl) (P = 0.02).</p