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MicroRNAs are easily identifiable molecules in a variety of cells and body fluids that may be useful as diagnostic (miR-155 and miR-146a) and disease severity (miR-203) biomarkers in patients with AD.
MicroRNAs are easily identifiable molecules in a variety of cells and body fluids that may be useful as diagnostic (miR-155 and miR-146a) and disease severity (miR-203) biomarkers in patients with AD.
To describe a patient with Sjögren syndrome (SS) associated with obsessive-compulsive disorder (OCD).

Case report and systematic review of the literature.

A 40-year-old female patient with a history of xerostomia and xerophthalmia initiated in 2015. She also had a history of changing her behavior, and she practices rituals, recurrent obsessions, and compulsions. She was diagnosed with OCD. She was treated with fluoxetine associated with risperidone and then was changed for aripiprazole 10 mg/day. Cognitive-behavioral therapy was also applied. She had good control of the obsessions with these drugs and psychotherapy. Laboratory tests showed positive antinuclear antibodies, anti-Ro/SS-A, and-La/SS-B antibodies. Schirmer test, break up time, and positive green lisamin were all positive. Scintigraphy and ultrasound of salivary glands were positive. A diagnosis of Sjögren syndrome was determined. She was treated with HCQ, vitamin D3 50,000 IU/week, omega-3 2 g, and artificial tears with a good response. Currently, 5 years later, the patient is asymptomatic and has OCD under adequate control even without drugs.

This case illustrates a rare case of a patient with SS who evolved with OCD.
This case illustrates a rare case of a patient with SS who evolved with OCD.
The purpose of this study was to explore the influences of micro ribonucleic acid (miR)-708 on cerebral ischemia-reperfusion injury by regulating a disintegrin and metalloprotease 17 (ADAM17) in a targeted manner.

The rat model of middle cerebral artery occlusion (MCAO) was established, and the differentially expressed miRNAs in the cerebral tissues of rats with ischemia-reperfusion injury were detected via sequencing. The research was performed in control group (PC12 cells received no treatment), inhibitor group (the expression of miR-708 in PC12 cells was down-regulated using miR-708 inhibitor), and interference + inhibitor group [PC12 cells were co-treated with miR-708 inhibitor and ADAM17 small interfering RNA (siRNA)]. Then, the expression of ADAM17 in cells, proliferation ability of cells, and number of apoptotic cells were detected in each group.

A total of 225 differentially expressed miRNAs were obtained through miRNA sequencing and bioinformatics analysis, of which miR-708, miR-169, miR-26, ann control group (p<0.05), whereas the proliferation ability of cells in interference + inhibitor group was restored to a certain degree after ADAM17 siRNA interfered with the protein expression (p<0.05).

MiR-708 can modulate ADAM17 in a targeted manner to affect cellular proliferation and apoptosis in cerebral ischemia-reperfusion injury.
MiR-708 can modulate ADAM17 in a targeted manner to affect cellular proliferation and apoptosis in cerebral ischemia-reperfusion injury.
This study aimed to explore the correlation between serum EAAT2 and ADORA2A levels and Alzheimer's disease (AD).

A total of 68 patients with AD treated in our hospital from April 2017 to January 2019 were enrolled and assigned to group A, and 60 healthy individuals undergoing physical examinations in the same period were enrolled and assigned to group B. Enzyme-linked immunosorbent assay (ELISA) was used to measure the expression of serum EAAT2 and ADORA2A in the two groups, receiver operating characteristic (ROC) curve to assess the predictive value of diagnostic efficacy, Spearman correlation to perform correlation analysis, and multivariate logistic analysis to analyze risk factors of prognosis.

Patients from group A showed significantly higher serum ADORA2A level and lower serum EAAT2 level than individuals from group B (all p<0.001). The severity of AD was negatively correlated with the relative expression of serum EAAT2 (r=-0.7286, p<0.001), positively correlated with the relative expression of serum ADORA2A (r=0.7381, p<0.001). The sensitivity, specificity, and area under the curve (AUC) of EAAT2 alone for the diagnosis of AD were 85.00%, 82.35%, and 0.8853, respectively, and those of ADORA2A alone for the diagnosis of AD were 71.67%, 79.41.00%, and 0.8369, respectively. Univariate and multivariate Logistic regression analysis showed that disease severity, EAAT2, and ADORA2A were independent risk factors of the prognosis of AD.

Patients with AD have highly expressed ADORA2A and lowly expressed EAAT2 in the serum. EAAT2 and ADORA2A may play parts in the progression of AD, and they can act as potential serum biomarkers for the diagnosis and disease assessment of AD.
Patients with AD have highly expressed ADORA2A and lowly expressed EAAT2 in the serum. EAAT2 and ADORA2A may play parts in the progression of AD, and they can act as potential serum biomarkers for the diagnosis and disease assessment of AD.
The aim of this study was to investigate the correlations of endothelin-1 (ET-1) gene polymorphisms with the occurrence of hypertensive intracerebral hemorrhage (HICH).

In this case-control study, 100 HICH patients and 100 controls with matched race, age and gender were enrolled as research subjects. Single nucleotide polymorphisms (rs1920453, rs1022436 and rs1035627) in the promoter region of ET-1 gene were typed via conformational difference gel electrophoresis. Whether the distribution frequency of ET-1 genotypes conformed to Hardy-Weinberg equilibrium was evaluated by chi-square test. click here The correlations of different gene polymorphisms and alleles in the promoter region of ET-1 gene with the occurrence of HICH were analyzed. Furthermore, the associations of rs1920453 polymorphism in the promoter region of ET-1 gene with neurological deficit scores and laboratory parameters of HICH patients were explored.

It was found that ET-1 gene polymorphisms (rs1920453, rs1022436 and rs1035627) conformed to Hardy-Weinberg equilibrium (p>0.
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