PubMed Health⌕ Search

Biomedical subjects

Hong-Fei Zhang

Publications and source records attributed to Hong-Fei Zhang.

4 recordsLinked to original sources

Genetic predisposition and mediating pathways in ischemic stroke-induced cardiac arrhythmias: a genome-wide analysis.

INTRODUCTION: The clinical presentation of stroke-heart syndrome (SHS) underscores the interplay between the central nervous system and the cardiovascular system. While cardiac arrhythmia is the prevalent form of cardiac injury in SHS patients, the causal link between ischemic stroke and cardiac arrhythmia is still unclear. METHODS: Mendelian randomization analyses and genome-wide association studies data were used to investigate the causal role of ischemic stroke on cardiac complications. Mediation and colocalization analyses were used to identify potential pathways and shared genetic variants. Single nucleotide polymorphisms (SNPs) associated with arrhythmias and ischemic stroke were used for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Gene expression omnibus (GEO) database from atrial fibrillation patients were used for validation. RESULTS: Mendelian randomization analyses showed a strong correlation between arrhythmias, including ventricular tachyarrhythmias and atrial fibrillation, with ischemic stroke. Diabetic microvascular (nephropathy, retinopathy) and macrovascular (cardiomyopathy, peripheral arterial disease) complications significantly mediated the effect of ischemic stroke on cardiac arrhythmias and atrial fibrillation, explaining 28.69 % and 20.48 % of the indirect effect, respectively. Colocalization analyses identified a shared causal variant in the Phosphodiesterase 3A (PDE3A) gene (rs11045239), providing genetic evidence for a shared pathogenic pathway between ischemic stroke and cardiac arrhythmias. Moreover, KEGG pathway enrichment analyses identified a role of the cyclic adenosine monophosphate (cAMP) signaling pathway in both ischemic stroke and arrhythmias. Validation using the GEO database confirmed a significant upregulation of the PDE3A gene expression in atrial fibrillation patients. CONCLUSION: This study demonstrated a causal link between ischemic stroke and cardiac arrhythmias, with diabetic complications as one mediating factor. The identification of a shared causal variant in the PDE3A gene and the role of the cAMP signaling pathway have the potential to improve prediction and management of SHS patients.

Humans↗

A taxonomic re-appraisal of Sarcocystis nesbitti (Protozoa: Sarcocystidae) from the monkey Macaca fascicularis in Yunnan, PR China.

The first detection of Sarcocystis nesbitti Mandour, 1969 in the Chinese mainland is reported and the morphology of the sarcocyst is described in detail. The parasite was detected in the monkey, Macaca fascicularis, maintained on a monkey farm in Yunnan Province; the infection may have occurred via faecal contamination from local rats, mice and/or birds. S. nesbitti was characterized as follows: a macroscopic sarcocyst, length of the cyst up to 2 mm; cyst wall smooth, thin and no perpendicular protrusion is seen under the light microscope; border of cyst wall wavy, primary cyst wall thin (38-65 nm) and invaginated; ground substance about 0.5-0.76 microm thick with electron-dense granules and concentric spherical bodies. The cyst wall is described as type 1 by electron microscopy. It is suspected that S. nesbitti may utilize Macaca mulatta, M. fascicularis, Cercocebus atys, and Papio papionis, as well as human as intermediate hosts. The taxonomy of S. nesbitti is re-appraised in the light of a consideration of possible experimental artefacts and examination of the past literature. Evidence is presented that S. nesbitti may be one of the species infecting humans in South Asia and that the monkey may be a potential reservoir host.

Animals↗

Pathological changes and clinical manifestations of 1020 children with liver diseases confirmed by biopsy.

BACKGROUND: Liver biopsy plays an important role in accurate diagnosis of various liver diseases in children and liver damages caused by systemic illnesses. This study was designed to evaluate the value of liver biopsy in diagnosis of liver diseases in children and explore the relationship between their pathological changes and clinical manifestations. METHODS: One-second liver biopsy was performed in 1023 pediatric patients with liver diseases at our department from 1983 to 2000. Diagnosis of viral hepatitis was based on the diagnostic criteria formulated by the Chinese Society of Infectious and Parasitic Diseases in 1995. Inflammatory changes of the liver were graded from 0 to 4 (G0-4). RESULTS: Liver biopsy was performed successfully in 1020 patients including 135 infants and young children, of whom 90% were hospitalized patients with chronic liver diseases. Hepatitis virus was the leading cause for chronic liver diseases, among which hepatitis B was detected in 75.4% of the patients. Sixty-nine patients showed liver impairment induced by disorders relevant to that metabolism, Wilson's disease, and glycogen storage disease. Liver inflammatory injury (<G2) was found in 76.4% of the patients with hepatitis B in contrast to 61.2% of adult patients. It was aggravated with age in the patients with hepatitis B and C and peaked at their schooling age. Moderate or severe liver injuries were not seen in infants with chronic hepatitis B. Two infants had chronic hepatitis C. Patients with non-viral hepatitis showed specific, non-specific histological changes and liver cirrhosis. CONCLUSIONS: Liver inflammatory injuries are more common in children with hepatitis B than in adult patients, and severe inflammatory changes are seen in children with hepatitis B and C at their school age. Liver injuries induced by non-viral factors seem to be increasing, and liver biopsy in children is safe and feasible in the diagnosis of liver diseases.

Adolescent↗

[Construction of human integrin beta3 subunit eukaryotic expression vector and efficient surface expression of integrin alphaIIbbeta3].

AIM: To establish efficient surface expression of Homo sapiens integrin alphaIIbbeta3 in beta3-integrin-deficient and HV-insusceptible CHO cells, so as to lay the foundation for the further study of cellular entry of hantavirus mediated by beta3 integrins. METHODS: Eukaryotic expression vector pcDNA3.1-beta3 harboring ORF region of human integrin beta3 subunit cDNA was constructed, then pcDNA3.1-beta3 and eukaryotic expression vector pBJ1-alphaIIb containing human integrin alphaIIb subunit cDNA were transfected into CHO cells alone or together. The expression of exogenous genes were analyzed by indirect immunofluorescence assay (IFA). RESULTS: The eukaryotic expression vector pcDNA3.1-beta3 was constructed successfully. IFA examination showed that surface expression of integrin alphaIIb beta3 was highly effective in cotransfection group, while surface expression was weak on CHO cells transfected with pcDNA3.1-beta3 alone,and no effective surface expression was found in pBJ1-alphaIIb-transfected group. CONCLUSION: Efficient surface expression of integrin alphaIIb beta3 requires expression of both subunits.

Animals↗