HBV infection effects prognosis and activates the immune response in intrahepatic cholangiocarcinoma.

Background: The impact of HBV infection on the prognosis of patients with intrahepatic cholangiocarcinoma (ICC) remains uncertain, and the underlying mechanism has not been elucidated. This study aims to explore the potential mechanism via clinical perspectives and immune features.

Methods: We retrospectively reviewed 1308 patients with ICC treated surgically from January 2007 to January 2015.

Distanct ischemic postconditioning in acute mild to moderate ischemic stroke: A randomized clinical study.

Objective: Distant ischemic postconditioning (DIPC) has been confirmed to have a neuroprotective effect in animal models of ischemia. However, there are only a few studies on its efficacy and safety in clinical applications.

Method: We divided 86 patients with acute non-cardiogenic mild to moderate cerebral infarction into DIPC and control groups.

A novel heterozygous HTRA1 mutation in an Asian family with CADASIL-like disease.

Background: HTRA1 gene mutations are related to the pathogenesis of cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL). However, heterozygous HTRA1 mutations at specific sites can also lead to rare autosomal dominant cerebral artery disease (CADASIL-like disease). To date, 28 heterozygous mutations in the HTRA1 gene have been reported to be related to CADASIL-like diseases.

A case of CADASIL caused by NOTCH3 c.512_605delinsA heterozygous mutation.

Background: Autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a cerebrovascular disease closely related to the NOTCH3 gene. More than 200 mutations in this gene have been reported to be associated with this disease.

Methods: The NOTCH3 gene from CADASIL patient was screened for mutations by whole-exome sequencing (WES).

Association of an insertion mutation in PRRT2 with hereditary spastic paraplegia accompanied by polyneuropathy.

Background: Hereditary spastic paraplegia is a rare familial hereditary neurodegenerative disease caused by multiple autosomal dominant mutations. More than 50 mutant genes have been reported to be associated with this disease.

Methods: In this study, we have reported a rare insertion mutation site in PRRT2 that caused a familial disorder of hereditary spastic paraplegia accompanied by polyneuropathy.

Guidance of circular RNAs to proteins' behavior as binding partners.

Circular RNAs (circRNAs) are single-stranded and covalently closed back-splicing products of pre-mRNAs. They can be derived from exons, introns, or exons with intron retained between exons of transcripts, as well as antisense transcripts. CircRNAs have been reported to function as microRNA sponges, regulate gene transcription mediated by RNA polymerase II, and modulate the splicing or stability of mRNA.

Exosomes in Pathogenesis, Diagnosis, and Treatment of Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the accumulation of ß-amyloid peptide 1-42 and phosphorylation of tau protein in the brain. Thus far, the transfer mechanism of these cytotoxic proteins between nerve cells remains unclear. Recent studies have shown that nanoscale extracellular vesicles (exosomes) originating from cells may play important roles in this transfer process.

Regulation of RNA decay and cellular function by 3'-5' exoribonuclease DIS3L2.

DIS3L2, in which mutations have been linked to Perlman syndrome, is an RNA-binding protein with 3'-5' exoribonuclease activity. It contains two CSD domains and one S1 domain, all of which are RNA-binding domains, and one RNB domain that is responsible for the exoribonuclease activity. The 3' polyuridine of RNA substrates can serve as a degradation signal for DIS3L2.

Long non-coding RNAs involved in cancer metabolic reprogramming.

Metabolic reprogramming has now been accepted as a hallmark of cancer. Compared to normal cells, cancer cells exhibit different metabolic features, including increased glucose uptake, aerobic glycolysis, enhanced glutamine uptake and glutaminolysis, altered lipid metabolism, and so on. Cancer metabolic reprogramming, which supports excessive cell proliferation and growth, has been widely regulated by activation of oncogenes or loss of tumor suppressors.

Aberrant Regulation of mRNA m⁶A Modification in Cancer Development.

⁶-methyladenosine (m⁶A) is the most prevalent internal modification of eukaryotic messenger RNAs (mRNAs). The m⁶A modification in RNA can be catalyzed by methyltransferases, or removed by demethylases, which are termed m⁶A writers and erasers, respectively. Selective recognition and binding by distinct m⁶A reader proteins lead mRNA to divergent destinies.