Bilateral facial palsy caused by HIV infection: A case report and literature review.

Bilateral facial palsy (BFP) has been identified as a possible neurological complication of human immunodeficiency virus (HIV) infection, but only a limited number of cases have been reported in the literature. The purpose of this study was to deepen our understanding of the etiology of BFP. Case report: We report the case of a 46-year-old married bisexual man with BFP associated with HIV infection.

Alteplase associated Orolingual angioedema: A case report and literature review.

Objective: Orolingual angioedema (OA) is a rare but life-threatening complication of intravenous thrombolysis using alteplase. Angioedema can be caused by almost any medication. Administration of recombinant tissue plasminogen activator causes atypical angioedema.

Comprehensive Analysis of Potential miRNA-Target mRNA-Immunocyte Subtype Network in Cerebral Infarction.

Introduction: Cerebral infarction (CI) is one of the leading causes of serious long-term disability and mortality.

Objective: We aimed to identify potential miRNAs and target mRNAs and assess the involvement of immunocyte infiltration in the process of CI.

Methods: First, miRNA and mRNA data were downloaded from the Gene Expression Omnibus database, followed by differential expression analysis.

The silent information regulator 1 pathway attenuates ROS-induced oxidative stress in Alzheimer's disease.

We show that down-regulation of circular ribonucleic acid 0001588 with small interfering-circular ribonucleic acid 0001588 mimics promoted caspase-3 and caspase-9 activity levels, increased lactate dehydrogenase activity levels, and reduced cell growth of in vitro model. Circular ribonucleic acid 0001588 plasmids increased circular ribonucleic acid 0001588 expressions and promoted cell growth and reduced activity levels of lactate dehydrogenase, caspase-3, and caspase-9 activity levels in vitro model of Alzheimer's disease. Then, circular ribonucleic acid 0001588 down-regulation also promoted reactive oxygen species production and oxidative stress (malonaldehyde), and reduced superoxide dismutase, glutathione, and glutathione peroxidase levels by suppressing of silent information regulator 1/nuclear factor erythroid 2-related factor 2/heme oxygenase-1 in vitro.

Intrathecal Injection of scAAV9-hIGF1 Prolongs the Survival of ALS Model Mice by Inhibiting the NF-kB Pathway.

Amyotrophic lateral sclerosis (ALS) is a chronic, fatal neurodegenerative disorder characterized by the progressive loss of upper and lower motor neurons. Currently, there is no effective drug for ALS. Recent studies in ALS model mice have shown that insulin-like growth factor-1 (IGF1) may be a promising therapeutic drug.

Intrathecal Delivery of ssAAV9-DAO Extends Survival in SOD1 ALS Mice.

Amyotrophic lateral sclerosis (ALS) is an adult-onset, irreversible neurodegenerative disease that leads to progressive paralysis and inevitable death 3-5 years after diagnosis. The mechanisms underlying this process remain unknown, but new evidence indicates that accumulating levels of D-serine result from the downregulation of D-amino acid oxidase (DAO) and that this is a novel mechanism that leads to motoneuronal death in ALS via N-methyl-D-aspartate receptor-mediated cell toxicity. Here, we explored a new therapeutic approach to ALS by overexpressing DAO in the lumbar region of the mouse spinal cord using a single stranded adeno-associated virus serotype 9 (ssAAV9) vector.

Intramuscular Delivery of scAAV9-hIGF1 Prolongs Survival in the hSOD1 ALS Mouse Model via Upregulation of D-Amino Acid Oxidase.

Self-complementary adeno-associated viral vector 9 (scAAV9) has been confirmed to be an efficient AAV serotype for gene transfer to the central nervous system (CNS). Neurotrophic factors have been considered to be therapeutic targets for amyotrophic lateral sclerosis (ALS). In the present study, we intramuscularly injected scAAV9 encoding human insulin-like growth factor 1 (hIGF1) into an hSOD1 ALS mouse model.

scAAV9-VEGF prolongs the survival of transgenic ALS mice by promoting activation of M2 microglia and the PI3K/Akt pathway.

Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease that leads to paralysis and death three to five years after diagnosis in most patients. The disease is incurable, and the mechanism of motoneuron degeneration remains unknown, although research has demonstrated that activated microglia are involved in motor neuron death. Here, we used a simple method to deliver AAV9 virus by direct intrathecal injection and found that scAAV9-VEGF-165 improved the motor performance and prolonged the life span of SOD1-G93A mice.