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Abstract Objective This study aims to assess the effects of antithrombotic therapy on the outcomes of lower gastrointestinal bleeding (LGIB) in ICU patients, focusing on in-hospital mortality, rebleeding, and length of hospital and ICU stays. Method This retrospective observational study utilized the MIMIC-IV 2.2 database, which includes 513 ICU patients with LGIB. Result The in-hospital mortality rate was 7.6%, and the rebleeding rate was 11.1%. The average Oakland risk score among the study population was 22.54. Multivariate Cox regression analysis identified the use of antiplatelet drugs as an independent protective factor for in-hospital mortality (HR = 0.37, 95% CI 0.15–0.90, p = 0.029). Patients on anticoagulants experienced significantly longer hospital stays (13.1 ± 12.2 days vs. 17.4 ± 12.6 days, p = 0.031) compared to those not using these drugs. Propensity score matching also supported these findings, indicating that antithrombotic therapy was associated with lower in-hospital mortality and longer hospital stays even after adjusting for factors like age, gender, and primary diagnosis. Conclusions Our analysis using various statistical methods, including propensity score matching and multivariate regression, confirms that use of antithrombotic drugs in 2.3 days, particularly antiplatelets, are associated with a lower risk of in-hospital mortality. However, they may increase the risk of rebleeding and extend hospital stays in certain subgroups.

Objective. This study aimed at exploring the safety and timing of antithrombotic drugs in different age-group patients with UGIB. Methods. An observational study retrospectively based on the single-center database with 713 patients with UGIB. Result. Among the 713 patients, 62.13% were elderly patients (aged>60 years) and the mortality was 2.9%. In elderly patients with UGIB, we found that previous medication history, resumption of medication, and time of resumption did not affect the in-hospital mortality. The resumption of anticoagulants increased the risk of rebleeding. The independent risk factors of mortality were CHF, cirrhosis, creatine kinase, and albumin. The independent risk factors of rebleeding were the application of anticoagulants during hospitalization, variceal bleeding, black stool, red blood cells (lab), platelets (lab), and heart rate. Conclusions. In UGIB patients, a history of antiplatelet or antithrombotic drugs and the use of antiplatelet drugs after UGIB did not affect the patient’s prognosis. In elderly UGIB patients, although antithrombotic drugs did not increase the risk of death, the increased risk of rebleeding after resumption of use deserved careful treatment. It was safe to recover anticoagulant drugs as soon as possible in young UGIB patients.

Mediastinal masses are uncommon and difficult to diagnose. Endoscopic ultrasound with fine-needle aspiration (EUS-FNA) is a minimally invasive technique for diagnosis of mediastinal lesions with few complications. Our report described a mediastinal bronchogenic cyst with soft tissue density infected by Streptococcus pyogenes (S. pyogenes) after EUS-FNA, accompanied by respiratory cardiac arrest and superior vena cava syndrome. The patient underwent cardiopulmonary resuscitation to gain the chance for emergency surgery and recovered. Clinicians should be aware that mediastinal mass with soft tissue density shown on imaging may be mediastinal cyst containing high density mucin, FNA should be avoided if cystic masses cannot be ruled out.

Abstract Background Gongylonema pulchrum is a zoonotic parasite rarely found in humans. To date, there have been no reports on the carcinogenic properties of G. pulchrum, and there are few reports overall on the relationship between esophageal cancer and parasites. Case presentation This report describes the first case of esophageal gongylonemiasis coexisting with early esophageal cancer. The patient had no high-risk factors for esophageal cancer, such as smoking, flushing after drinking, or tumor history. We speculate the existence of unknown links between esophageal cancer and parasitic infection in this patient. Discussion and conclusions We report the first case of a human presenting both esophageal G. pulchrum infection and esophageal squamous cell carcinoma with the hope that it may provide evidence for a new hypothesis of tumorigenesis.

Background. Economic disparity contributes to the variation of intestinal obstruction (IO) etiologic spectrum. Clarifying the etiology distribution in local regions can help to unravel IO and promote early diagnosis, henceforth making sure standardized therapeutic interventions. Methods. Medical data of 4908 inpatients diagnosed with IO admitted to the General Hospital of Ningxia Medical University between January 2004 and December 2013 were recruited and analyzed retrospectively. The associated profiles included demographic features, clinical manifestations, and previous therapeutic operations. Results. 4908 cases of intestinal obstruction were identified during the period of study. It denoted that the hospitalization rate of IO has maintained upward momentum; the top four causes of IO were adhesion, tumor, intussusception, and hernias. These covered up nearly 80% of the total constitution. Among them, adhesive intestinal obstruction accounted for 45.17%, malignant bowel obstruction for 21.09%, intussusception for 8.72%, and hernia for 4.73%; abdominal surgery constituted for the majority (78.62%) of adhesive obstruction. The followed up analysis also found that appendectomy accounted for the biggest percentage, 28% of operation cases. Malignant bowel obstruction can have a rate of 96.43% in 1035 cases led by tumor lesions. Of which, the primary intestinal malignant tumor accounted for 68.64% and metastatic tumors for 31.36%. Nearly 50% occurred in the large intestine. The overall mortality of all 4908 cases was 4.7%. Conclusion. The hospitalizations of IO delineated an increasing trend. Adhesion was the main etiology in IO. The odds of malignant bowel obstruction was increasing in the proportion of IO. There were some differences towards the etiologic spectrum compared with western countries.

Calcyclin Binding Protein/(Siah-1 interacting protein) (CacyBP/SIP) acts as an oncogene in colorectal cancer. The nuclear accumulation of CacyBP/SIP has been linked to the proliferation of cancer cells. It has been reported that intracellular Ca2+ induces the nuclear translocation of CacyBP/SIP. However, the molecular mechanism of CacyBP/SIP nuclear translocation has yet to be elucidated. The purpose of this study was to test whether the Ca2+-dependent binding partner S100 protein is involved in CacyBP/SIP nuclear translocation in colon cancer SW480 cells.The subcellular localization of endogenous CacyBP/SIP was observed following the stimulation of ionomycin or BAPTA/AM by immunofluorescence staining in SW480 cells. S100A6 small interfering RNAs (siRNA) were transfected into SW480 cells. Immunoprecipitation assays detected whether S100 protein is relevant to the nuclear translocation of CacyBP/SIP in response to changes in [Ca2+]i.We observed that endogenous CacyBP/SIP is translocated from the cytosol to the nucleus following the elevation of [Ca2+]i by ionomycin in SW480 cells. Co-immunoprecipitation experiments showed that the interaction between S100A6 and CacyBP/SIP was increased simultaneously with elevated Ca2+. Knockdown of S100A6 abolished the Ca2+ effect on the subcellular translocation of CacyBP/SIP.Thus, we demonstrated that S100A6 is required for the Ca2+-dependent nuclear translocation of CacyBP/SIP in colon cancer SW480 cells.

CacyBP/SIP is a component of the ubiquitin pathway and is overexpressed in several transformed tumor tissues, including colon cancer, which is one of the most common cancers worldwide. It is unknown whether CacyBP/SIP promotes the proliferation of colon cancer cells. This study examined the expression level, subcellular localization, and binding activity of CacyBP/SIP in human colon cancer cells in the presence and absence of the hormone gastrin. We found that CacyBP/SIP was expressed in a high percentage of colon cancer cells, but not in normal colonic surface epithelium. CacyBP/SIP promoted the cell proliferation of colon cancer cells under both basal and gastrin stimulated conditions as shown by knockdown studies. Gastrin stimulation triggered the translocation of CacyBP/SIP to the nucleus, and enhanced interaction between CacyBP/SIP and SKP1, a key component of ubiquitination pathway which further mediated the proteasome-dependent degradation of p27kip1 protein. The gastrin induced reduction in p27kip1 was prevented when cells were treated with the proteasome inhibitor MG132. These results suggest that CacyBP/SIP may be promoting growth of colon cancer cells by enhancing ubiquitin-mediated degradation of p27kip1.

Identifying an effective therapeutic target is pivotal in the treatment of gastric cancer. In this study, we investigated the expression of p75 neurotrophin receptor (p75NTR) in gastric cancer and the impact of its alteration on tumor growth. p75NTR expression was absent or significantly decreased in 212 cases of gastric cancers compared with the normal gastric mucosa (P < .05). Moreover, p75NTR expression was also lost or significantly decreased in various human gastric cancer cell lines. p75NTR inhibited in vitro growth activities and caused dramatic attenuation of tumor growth in animal models by induction of cell cycle arrest. Upregulation of p75NTR led to downregulation of cyclin A, cyclin D1, cyclin E, cyclin-dependent kinase 2, p-Rb, and PCNA, but to upregulation of Rb and p27 expressions. Conversely, downregulating p75NTR with specific siRNA yielded inverse results. The rescue of tumor cells from cell cycle progression by a death domain-deleted dominant-negative antagonist of p75NTR (Δp75NTR) showed that the death domain transduced antiproliferative activity in a ligandindependent manner and further demonstrated the inhibitive effect of p75NTR on growth in gastric cancer. Therefore, we provided evidence that p75NTR was a potential tumor suppressor and may be used as a therapeutic target for gastric cancer.