Tiejun Zhou

Patients with inflammatory bowel disease (IBD) are at risk of developing malnutrition, severe dystrophic muscle weakness, and muscle atrophy. We present a case of a 33-year-old male patient who exhibited concurrent muscle atrophy, muscle weakness, diarrhea, and mucopurulent bloody stools. Notably, the patient reported that his household or family members experienced similar symptoms of muscle weakness, without any apparent neurological or psychiatric manifestations. The patient’s intestinal symptoms were most consistent with ulcerative colitis, while the muscle weakness originated from dysferlinopathy following a comprehensive diagnostic work-up. The patient was initiated on vedolizumab therapy and L-carnitine therapy, and his symptoms improved after 1 month of follow-up. This case study underscores the necessity for clinicians to maintain a high level of suspicion for the presence of concomitant diseases when encountering IBD patients with muscle weakness. This approach is essential for achieving an early diagnosis and treatment.

Objectives. To investigate the effects of cytotoxin-associated gene A- (CagA-) positive Helicobacter pylori on proliferation, invasion, autophagy, and expression of miR-125b-5p in colon cancer cells. Methods. Colon cancer cells were cocultured with H. pylori (CagA+) to analyze the effects of H. pylori on miR-125b-5p and autophagy. Colon cancer cells infected with H. pylori (CagA+) were mimicked by transfection of CagA plasmid. The effects of CagA on the proliferation, invasion, and autophagy of colon cancer cells were analyzed. Cell counting kit-8 (CCK-8), clone formation, and Transwell assays were used to detect cell viability, proliferation, and invasion ability, respectively. Proteins and miRNAs were detected by western blotting and qPCR, respectively. Results. H. pylori (CagA+) inhibited expression of miR-125b-5p and promoted autophagy in colon cancer cells. MiR-125b-5p was underexpressed in colon cancer cells after CagA overexpression. CagA promoted colon cancer cell proliferation, invasion, and autophagy. Overexpression of miR-125b-5p inhibited the proliferation, invasion, and autophagy of colon cancer cells and reversed the effects of CagA. Conclusion. H. pylori (CagA+) infection may promote the development and invasion of colon cancer by inhibiting miR-125b-5p.

In recent years, the frequency of influenza epidemics around the world has posed a great threat to the lives of people, especially those in developing countries. However, it is unclear which organs are the targets of influenza A viruses (IAVs) and what histopathology is caused by IAVs. In this study, BALB/c female mice were infected with H1N1 by nasal inoculation for 5 days. After euthanasia, the brain, heart, lungs, thymus, liver, spleen, hilar lymph nodes, pancreas, kidneys, and adrenal glands were collected. Among these organs, only the lungs, thymus, spleen, and hilar lymph nodes showed lesions. Lung histopathology was characterized by widening of the septum, lymphocyte infiltration, alveolar effusion, and alveolar hyaline membrane formation. The thymus and spleen exhibited atrophy due to the apoptosis of numerous lymphocytes. Although the hilar lymph nodes were enlarged, lymphocyte apoptosis still occurred. The nucleocapsid protein (NP) of IAVs was present not only in the lungs but also in the thymus, spleen, and hilar lymph nodes. In peripheral blood, CD19⁺B lymphocyte levels clearly decreased whileCD3⁺CD8⁺T and CD3⁺CD4⁺T lymphocyte levels temporarily decreased but subsequently increased. These results demonstrate that H1N1 in the lungs could reach lymphoid organs, induce the depletion of B and T lymphocytes in peripheral blood and lymphoid organs, and suppress adaptive immunity.

Background. Vasculogenic mimicry (VM), as an endothelium-independent cancer microcirculation, has been observed in many malignancies including cervical cancer. Erythropoietin (EPO) and erythropoietin receptor (EPO-R) could produce an angiogenic effect to promote cervical squamous cell carcinoma (CSCC) progression. However, the association between VM formation and EPO/EPO-R expression in CSCC is poorly explored. Methods. Seventy-six paraffin-embedded CSCC samples, 25 high-grade squamous intraepithelial lesion (HSIL) samples, 20 low-grade squamous intraepithelial lesion (LSIL) samples, and 20 normal cervix samples were collected. Immunohistochemistry SP method was performed to detect EPO/EPO-R expression and CD31/periodic acid-Schiff (PAS) double staining was performed to detect VM formation. The associations of EPO/EPO-R and VM with clinicopathological parameters of CSCC were analyzed. The associations between VM formation and EPO/EPO-R expression were also analyzed. Results. The positive expression rates of EPO and EPO-R were gradually increasing along the progression of normal cervix-LSIL-HSIL-CSCC sequence (P0.05). VM was significantly associated with FIGO stage, lymphovascular space involvement, and lymph node metastasis (Pr=0.284, P0.05). Conclusion. These data suggest that increased EPO/EPO-R expression may play an important role in cervical carcinogenesis. EPO overexpression may promote VM formation in CSCC.