Biliary hemorrhage caused by a malignant small round cell tumor in the common bile duct: A case report.

BACKGROUND: Malignant small round cell tumor (MSRCT) metastasis to the common bile duct associated with recurrent biliary hemorrhage is extremely rare. Thus far, there have been no reports of metastatic small round cell tumors of the common bile duct. CASE SUMMARY: Herein, we report the case of a 77-year-old female patient with an MSRCT in the common bile duct. The patient was admitted to hospital due to gastrointestinal hemorrhage and abdominal pain. We found a neoplasm in the common bile duct with active bleeding through a spyglass. We performed biopsy through the spyglass and placed a metal stent to stop bleeding. The pathological result suggested that it was an MSRCT metastasized from the back to the common bile duct. Later, we found using fluorescence in situ hybridization that the SS18 gene break test was negative, ruling out the diagnosis of synovial sarcoma. CONCLUSION: MSRCT is a group of tumors with similar cell morphology and diffuse histological structure. Complete tumor resection results in improved survival in patients with MSRCT. Roux-en-Y cholangiojejunostomy was performed. After excision of the common bile duct tumor, the patient felt that the abdominal pain improved and hemorrhage disappeared. The patient underwent routine fecal examination one month after surgery, indicating a negative fecal occult blood test. On May 22, 2023, the patient was reexamined by abdominal computed tomography, and no abdominal space occupying lesions or abdominal lymphadenopathy was found.

Influence of TRAIL Deficiency on Th17 Cells and Colonic Microbiota in Experimental Colitis Mouse Model.

BACKGROUND: The abnormalities of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) are implicated in various autoimmune disorders and tumors. This study investigated the influence of TRAIL deficiency on Th17 cells and colonic microbiota in experimental colitis mouse model. METHODS: Mice were randomly divided into 4 groups: wild-type, TRAIL gene knock-out (TRAIL-/-), wild-type colitis and TRAIL-/- colitis groups. Colitis was induced by oral administration of 3.5% dextran sulfate sodium (DSS) for 7 consecutive days. Mice were given scores for disease severity both clinically and histopathologically. Th17 cells in peripheral blood and mesenteric lymph nodes (MLNs) were assessed using flow cytometry. The expression levels of Th17 cell markers IL-17A and ROR-γt were evaluated by quantitative real-time polymerase chain reaction. The colonic samples were also analyzed for microbiota profile by 16s-rDNA gene sequencing on variable V4 region. RESULTS: Compared with wild-type counterparts, TRAIL-/- mice developed more severe colitis after DSS treatment. Colitis TRAIL-/- mice had increased proportion of Th17 cells and elevated mRNA expression levels of IL-17A and ROR-γt in peripheral blood and MLNs compared with colitis wild-type mice. In contrast to colitis wild-type mice, the composition of colonic microbiota was shifted in colitis TRAIL-/- mice, and was characterized by increased alpha diversity, increased TM7, deferribacteres and tenericutes, and decreased proteobacteria at the phylum level. CONCLUSIONS: These findings suggested that TRAIL deficiency not only aggravated DSS-induced colitis, but also led to enhanced Th17 cell response and altered colonic microbiota composition.

Downregulation of microRNA-637 Increases Risk of Hypoxia-Induced Pulmonary Hypertension by Modulating Expression of Cyclin Dependent Kinase 6 (CDK6) in Pulmonary Smooth Muscle Cells.

BACKGROUND The objective of this study was to investigate the molecular mechanism by which miR-637 interferes with the expression of CDK6, which contributes to the development of pulmonary hypertension (PH) with chronic obstructive pulmonary disease (COPD). MATERIAL AND METHODS We used an online miRNA database to identify CDK6 as a virtual target of miR-637, and validated the hypothesis using luciferase assay. Furthermore, we transfected SMCs with miR-637 mimics and inhibitor, and expression of CDK6 was determined using Western blot and real-time PCR. RESULTS In this study, we identified CDK6 as a target of miR-637 in smooth muscle cells (SMCs), and determined the expression of miR-637 in SMCs from PH patients with COPD and normal controls. We also identified the exact miR-637 binding site in the 3'UTR of CDK6 by using a luciferase reporter system. The mRNA and protein expression levels of CDK6 in SMCs from PH patients with COPD were clearly upregulated compared with the normal controls. Cells exposed to hypoxia also showed notably increased CKD6 mRNA and protein expression levels, and when treated with miR-637 or CDK6 siRNA, this increase in CKD6 expression was clearly attenuated. Additionally, cell viability and cell cycle analysis showed that hypoxia markedly increased viability of SMCs by causing an accumulation in S phase, which was relieved by the introduction of miR-637 or CDK6 siRNA. CONCLUSIONS Our study proved that the CDK6 gene is a target of miR-637, and demonstrated the regulatory association between miR-637 and CDK6, suggesting a possible therapeutic target for PH, especially in patients with COPD.

[Effects of acupotomy, electroacupuncture or round-sharp acupuncture needle interventions on expression of Bcl-2, Bax, Caspase-3 proteins of rectus femoris in rabbits with knee ostarthritis].

OBJECTIVE: To observe the effect of acupotomy, electroacupuncture (EA) or round-sharp acupuncture needle intervention on the expression of Bcl-2,Bax and Caspase-3 proteins in the rectus femoris in rabbits with knee ostarthritis (KOA), so as to explore their mechanisms underlying improvement of braking-induced joint damage from the cellular apoptosis. METHODS: Forty-five New Zealand rabbits were equally and randomized into control group, model group, acupotomy (AP) group, EA group and round-sharp acupuncture needle (RSAN) group (n = 9 in each group). The knee-joint injury model was established by fixing the left knee joint in extention position with plaster bandage. EA (2 Hz/100 Hz, 3 mA, 20 min each time) was applied to the left "Yanglingquan" (GB 34)- "Yinlingquan" (SP 9) and left "Neixiyan" (EX-LE 4)- "Waixiyan"(ST 35) for rabbits in the EA group. The EA treatment was given once daily, 3 times a week, 3 weeks in total. For rabbits of the AP group, a needle-knife was held to insert into the front edge of the midpoint, the starting point and the stopping point of the left medial collateral ligamen, lateral collateral ligament and the patellar ligament of the knee to make a loosening manipulation for 5 times in a session of treatment, once a week, 3 times altogether. For rabbits of the RSAN group, a round-sharp needle was performed in the same way to the needle-knife including the stimulation point, the manipulation method and treatment sessions. At the end of the experiment, the left rectus femoris was taken out for detecting the expression of Bcl-2, Bax and Caspase-3 proteins with Western blot. RESULTS: In comparison with the control group, the passive range of motion (PROM) level was significantly decreased 4, 8 and 12 weeks after modeling (P < 0.01), and the expression levels of Bax and Caspase-3 proteins in the rectus femoris were considerably upregulated in the model group (P < 0.05), while the ratio of Bcl-2/Bax was notably down-regulated (P < 0.05) in the model group. Compared with the model group, the PROM level at week 12 after modeling in the AP, EA and RSAN groups were significantly increased (P < 0.01); while Bax and Caspase-3 expression levels in both AP and RSAN groups were considerably downregulated (P < 0.05). No significant differences were found among the five groups in Bcl-2 expression levels (P > 0.05), and between the EA and model groups in Bax and Caspase-3 expression levels and the ratio of Bcl-2/Bax (P > 0.05). CONCLUSION: AP, RSAN and EA interventions are effective in improving the knee-joint motion range in KOA rabbits, and this effect of both AP and RSAN is closely associated with their actions in lowering the expression of Bax and Caspase-3 proteins of the rectus femoris and in raising ratio of Bcl-2/Bax protein (reducing muscular cellular apoptosis). The mechanism of EA intervention in improving PROM may be different.