Cost-effectiveness analysis of oral antiviral therapy in patients with indeterminate chronic hepatitis B infection.

Background: Compared to patients with chronic hepatitis B (CHB) in the immune tolerance phase, those in the indeterminate phase (IP) tend to have a higher proportion of liver inflammation and fibrosis, and they usually progress more rapidly to hepatocellular carcinoma (HCC). However, no definitive conclusion has been reached regarding the necessity of antiviral therapy (AVT) for patients in the IP. The present study aims to evaluate the cost-effectiveness of oral antiviral treatment in CHB patients who are in the IP [indeterminate phase-chronic hepatitis B (IP-CHB)] from a healthcare system perspective.

Comorbid Guillain-Barré Syndrome and Tuberculosis: A Case Study and Global Perspective.

A 27-year-old man presented with a cough and progressive limb weakness. Initially diagnosed with pulmonary tuberculosis, he showed improvement in his cough after antituberculosis treatment (ATT). However, he subsequently developed worsening weakness and numbness in his lower limbs, leading to mobility loss and difficulty swallowing.

Global and Regional Burden and Trend of Neoplasms Attributable to Alcohol Consumption in the Past 3 Decades.

Objectives: To provide valuable insights for targeted cancer screening among high-risk patients, we analyzed the global and regional burden of neoplasms resulting from alcohol consumption between 1990 and 2019.

Methods: The information used in this study was collected from the Global Burden of Disease 2019 dataset. Initially, the database was used to extract details of mortality rates, disability-adjusted life years (DALYs), and the number of individuals affected by alcohol-related neoplasms (ARNs).

Targeting WDxR motif reprograms immune microenvironment and inhibits hepatocellular carcinoma progression.

The WD-repeat (WDR) family affects carcinogenesis, but its role in the immune microenvironment is poorly characterized. Although functional loss or gain of WDR6 does not markedly change in vitro proliferative and invasive capacity of HCC cells, its deficiency in hepa1-6 cells drastically inhibits the growth and lung metastasis of orthotopically implanted tumors in immune-competent C57BL/6J mice. Mechanistically, WDR6 targets tumor suppressor UVRAG to the CUL4A-DDB1-ROC1 E3 ubiquitin ligase complex through a unique WDxR motif and promotes its degradation.

Analysis of the clinical characteristics of 202 patients with liver abscess associated with diabetes mellitus and biliary tract disease.

Objective: Clinical characteristics of patients with pyogenic liver abscess (PLA) of varying etiologies may be different. This study aimed to analyze the clinical characteristics, pathogenic bacteria, treatment, and prognosis of patients with PLA associated with diabetes and biliary disease.

Methods: Clinical, imaging, and laboratory data from 202 inpatients with PLA were retrospectively analyzed.

Hypoxia-induced acetylation of PAK1 enhances autophagy and promotes brain tumorigenesis via phosphorylating ATG5.

Although the treatment of brain tumors by targeting kinase-regulated macroautophagy/autophagy, is under investigation, the precise mechanism underlying autophagy initiation and its significance in glioblastoma (GBM) remains to be defined. Here, we report that PAK1 (p21 [RAC1] activated kinase 1) is significantly upregulated and promotes GBM development. The Cancer Genome Atlas analysis suggests that the oncogenic role of PAK1 in GBM is mainly associated with autophagy.

Deubiquitinase USP28 inhibits ubiquitin ligase KLHL2-mediated uridine-cytidine kinase 1 degradation and confers sensitivity to 5'-azacytidine-resistant human leukemia cells.

Resistance to the chemotherapeutic drug 5'-azacytidine (5'-AZA) is a major obstacle in the treatment of patients with acute myeloid leukemia (AML). The uridine-cytidine kinase 1 (UCK1) has an established role in activating 5'-AZA and its protein level is significantly downregulated in patients resistant to the drug. However, the underlying molecular mechanism for the reduced UCK1 expression remains to be elucidated.

METTL3 and ALKBH5 oppositely regulate mA modification of mRNA, which dictates the fate of hypoxia/reoxygenation-treated cardiomyocytes.

N-methyladenosine (mA) mRNA modifications play critical roles in various biological processes. However, no study addresses the role of mA in macroautophagy/autophagy. Here, we show that mA modifications are increased in H/R-treated cardiomyocytes and ischemia/reperfusion (I/R)-treated mice heart.

Crosstalk between lysine methylation and phosphorylation of ATG16L1 dictates the apoptosis of hypoxia/reoxygenation-induced cardiomyocytes.

Post-translational modifications of autophagy-related (ATG) genes are necessary to modulate their functions. However, ATG protein methylation and its physiological role have not yet been elucidated. The methylation of non-histone proteins by SETD7, a SET domain-containing lysine methyltransferase, is a novel regulatory mechanism to control cell protein function in response to various cellular stresses.

ATG16L1 phosphorylation is oppositely regulated by CSNK2/casein kinase 2 and PPP1/protein phosphatase 1 which determines the fate of cardiomyocytes during hypoxia/reoxygenation.

Recent studies have shown that the phosphorylation and dephosphorylation of ULK1 and ATG13 are related to autophagy activity. Although ATG16L1 is absolutely required for autophagy induction by affecting the formation of autophagosomes, the post-translational modification of ATG16L1 remains elusive. Here, we explored the regulatory mechanism and role of ATG16L1 phosphorylation for autophagy induction in cardiomyocytes.

The CAA repeat polymorphism in the ZFHX3 gene is associated with risk of coronary heart disease in a Chinese population.

Coronary heart disease (CHD) is a disease resulting from the interaction between genetic variations and environmental factors. Zinc finger homeobox 3 (ZFHX3) is a transcription factor and contains a poly-glutamine tract in a compositionally biased region that is encoded by exon 9, containing a cluster of CAG and CAA triplets followed by the polymorphic CAA repeats: (CAG)2(CAA)2(CAG)3CAACAG(CAA)nGCA. Thus, nine successive glutamine residues precede the poly-glutamine tract, encoded by the polymorphic CAA repeats.

Reciprocal activation between ATPase inhibitory factor 1 and NF-κB drives hepatocellular carcinoma angiogenesis and metastasis.

Unlabelled: Hepatocellular carcinoma (HCC) is a highly vascularized tumor with frequent extrahepatic metastasis. Active angiogenesis and metastasis are responsible for rapid recurrence and poor survival of HCC. However, the mechanisms that contribute to tumor metastasis remain unclear.

PTEN antagonises Tcl1/hnRNPK-mediated G6PD pre-mRNA splicing which contributes to hepatocarcinogenesis.

Background: Mounting epidemiological evidence supports a role for phosphatase and tensin homologue (PTEN)-T cell leukaemia 1 (Tcl1) signalling deregulation in hepatocarcinogenesis.

Objective: To determine the molecular and biochemical mechanisms by which the PTEN/Tcl1 axis regulates the pentose phosphate pathway (PPP) in hepatocellular carcinoma (HCC).

Methods: We compared levels of PTEN and glucose-6-phosphate dehydrogenase (G6PD) mRNA in human HCC and healthy liver tissue.

A de novo chromosomal abnormality in Cri du Chat syndrome.

Objective: To find the length and location of the deletions in the short arm of chromosome 5 in one case of Cri du Chat syndrome using oligo array comparative genomic hybridization.

Methods: Metaphase chromosomes were prepared from peripheral blood lymphocyte cultures using standard cytogenetic protocols. Chromosomal analysis was done in G-banded metaphases.

[Effect of BCL11A gene on transcription of γ-globin gene].

This study was aimed to explore the effect of BCL11A gene on transcription of γ-globin gene in K562 cells. B-cell lymphoma/leukemia 11A (BCL11A) gene was silenced by small interfering RNA (siRNA) expression vectors in K562 cells (human erythroblastic leukemia cell line). Gamma-globin mRNA level in K562 cells was determined by RT-PCR.

Small bowel preparations for capsule endoscopy with mannitol and simethicone: a prospective, randomized, clinical trial.

Background And Objective: There is no consensus concerning small bowel preparation before capsule endoscopy (CE). This study evaluated the effects of 4 regimens on small bowel cleansing and diagnostic yield.

Methods: Patients were randomly divided into 4 groups.

[Different splice of the calpain 3 gene in human skeletal muscle tissue and white blood cells].

Objective: To investigate the splice variants of the calpain 3 gene existing in human skeletal muscle tissue and white blood cells, and to explore the feasibility of gene diagnosis using CAPN3 mRNA extracted from peripheral leukocytes.

Methods: Total RNA was extracted from peripheral blood and skeletal muscle tissue in healthy individuals. CAPN3 cDNAs were determined by reverse transcriptase polymerase chain reaction and DNA sequencing.

[Hypoxia/reoxygenation-induced increased activity and expression of PTP-1B in neonatal rat cardiomyocytes are mediated by nitric oxide].

Objective: To explore if the hypoxia/reoxygenation-induced increased activity and expression of PTP-1B in neonatal rat cardiomyocytes are mediated by nitric oxide (NO).

Methods: Neonatal rat cardiomyocytes were isolated and randomly divided into 4 groups: normal group (N group); hypoxia/reoxygenation group (H/R group); N(omega)-nitro-l-arginine methylester treated group (L-NAME group); hypoxia/reoxygenation plus L-NAME group (L-NA + H/R group). PTP-1B activity in cardiomyocytes was determined spectrophotometrically at 405 nm, PTP-1B expression in cardiomyocytes was detected by Western blot.

Small interference RNA against PTP-1B reduces hypoxia/reoxygenation induced apoptosis of rat cardiomyocytes.

Objective: To investigate the effect of siRNA against PTP-1B on neonatal rat cardiac myocyte apoptosis induced by hypoxia-reoxygenation (H/R) and its molecular mechanisms.

Methods: Isolated neonatal and adult rat cardiac myocytes were cultured for 24 h after PTP-1B siRNA transfection, and with 2, 4 and 6 h of hypoxia followed by 6 h of reoxygenation (H/R). The cardiac myocyte apoptosis induced by the treatments was assessed by TUNEL staining.