HOTAIRM1 knockdown reduces MPP-induced oxidative stress injury of SH-SY5Y cells by activating the Nrf2/HO-1 pathway.

Objective: Parkinson's disease (PD) is the second most common neurodegenerative disease with complex pathogenesis. Although HOXA transcript antisense RNA myeloid-specific 1 (HOTAIRM1) is upregulated in PD, its exact role in HOTAIRM1 is seldom reported. The purpose of this study is to research the effect of HOTAIRM1 on 1-methyl-4-phenylpyridonium (MPP)-induced cytotoxicity and oxidative stress in SH-SY5Y cells.

Increased diagnostic yield in a cohort of hearing loss families using a comprehensive stepwise strategy of molecular testing.

Hearing loss is one of the most common sensory disorders in humans. This study proposes a stepwise strategy of deafness gene detection using multiplex PCR combined with high-throughput sequencing, Sanger sequencing, multiplex ligation-dependent probe amplification (MLPA), and whole-exome sequencing (WES) to explore its application in molecular diagnosis of hearing loss families. A total of 152 families with hearing loss were included in this study, the highest overall diagnosis rate was 73% (111/152).

Long non-coding RNA TTTY15 sponges miR-520a-3p to exacerbate neural apoptosis induced by cerebral ischemia/reperfusion via targeting IRF9 both in vivo and in vitro.

Background: Studies have proven that as competing endogenous RNAs (ceRNAs), long non-coding RNAs (lncRNAs) play vital roles in regulating RNA transcripts in ischemic stroke. It has been reported that TTTY15, a lncRNA, is dysregulated in cardiomyocytes after ischemic injury. We intended to explore the potential regulating mechanism of TTTY15 in ischemic stroke.

Genistein acts as antidepressant agent against chronic mild stress-induced depression model of rats through augmentation of brain-derived neurotrophic factor.

In this study, the antidepression effects of genistein were investigated in rats induced with chronic mild stress. Animals were designated into the following groups: normal control, control, 10 mg, and 100 mg. The dose was given for 45 consecutive days via the oral route.

MiR-30c-5p/ATG5 Axis Regulates the Progression of Parkinson's Disease.

Serum miR-30c-5p correlates with Parkinson's disease (PD), yet its role has not been illustrated. This research analyzed the function of miR-30c-5p in PD. The behavioral evaluation was performed on MPTP-treated PD mice transfected with miR-30c-5p agomiR, antagomiR, siATG5, or 3-MA (an autophagy inhibitor).

The solid-state and solution conformations of 2'-deoxy-2'-fluoro-4'-substituted nucleosides.

The conformational features of drugs are important with respect to their biological activity. In this report, we confirmed the solid-state conformation of 1-(4'-azido-2'-deoxy-2'-fluoro-β-d-arabinofuranosyl) cytosine using single-crystal X-ray crystallography and the conformations of three 2'-deoxy-2'-fluoro-4'-substituted nucleosides in solution using Altona-Haasnoot's equations and Nuclear Overhauser effect spectroscopy (NOESY). Furthermore, we compared the preferred solid-state and solution conformation of these nucleosides with thermodynamics cycles to obtain more evidence of their conformations.

Ursodeoxycholic acid protects dopaminergic neurons from oxidative stress via regulating mitochondrial function, autophagy, and apoptosis in MPTP/MPP-induced Parkinson's disease.

Neuroprotection targeting mitochondrial dysfunction has been proposed as a potential therapeutic strategy for Parkinson's disease (PD). Ursodeoxycholic acid (UDCA) has been shown to prevent neuronal damage; however, the role of UDCA in PD is poorly understood. This study aimed to investigate the neuroprotective effects of UDCA on PD and its underlying mechanisms.

Astaxanthin suppresses endoplasmic reticulum stress and protects against neuron damage in Parkinson's disease by regulating miR-7/SNCA axis.

Parkinson's disease (PD) is a common neurodegenerative disorder that featured by the loss of dopaminergic neurons. Astaxanthin (AST), an important antioxidant, is demonstrated to be a neuroprotective agent for PD. However, the underlying mechanisms of AST in PD remain largely unclear.

Association Between Single Nucleotide Polymorphisms in NFATC1 Signaling Pathway Genes and Susceptibility to Congenital Heart Disease in the Chinese Population.

The nuclear factor of activated T lymphocytes (NFATC1) signaling has been demonstrated to play important roles in cardiac valve and septal development. Genetic variants in genes involved in NFATC1 signaling may affect their expression and promote the formation of congenital heart disease (CHD). The goal of this study was to investigate the associations of single nucleotide polymorphism (SNP) in seven genes (NFATC1, VEGFR, VEGF, RANKL, FGFR1, BCL-6 and ZNRD1) with the risk of CHD.

[Mutation analysis of pathogenic genes in a Henan family affected with congenital stationary night blindness].

Objective: To detect genetic mutations associated with autosomal dominant congenital stationary night blindness (ADCSNB) in a family from Henan province.

Methods: Genomic DNA was extracted from peripheral blood samples of 14 family members. Based on 3 genes reported previously, PCR primers were designed and corresponding exons containing the mutation sites were amplified with PCR.

Acupuncture to point Baihui prevents ischemia-induced functional impairment of cortical GABAergic neurons.

Ischemia impairs brain function and networks, in which the vulnerability of GABAergic neurons causes neural excitotoxicity and nerve cell death. Acupuncture presumably improves the outcome of stroke patients; however, cellular mechanisms underlying this improvement remain to be elusive. We have investigated whether electrical stimuli to acupoint Baihui prevent ischemia- induced impairment of cortical GABAergic neurons.

[Mutation analysis of the pathogenic gene in a Chinese family with Brachydactyly type B1].

We identified and characterized a Chinese family with autosomal dominant Brachydactyly type B1 (BDB1). Linkage analysis revealed that the disease gene of the Chinese BDB1 family was linked to ROR2 locus. Mutational hot spot of ROR2 gene was amplified by polymerase chain reaction (PCR) and sequenced directly.