Background and aims: Current practice on Helicobacter pylori infection mostly focuses on individual-based care in the community, but family-based H. pylori management has recently been suggested as a better strategy for infection control. However, the family-based H. pylori infection status, risk factors and transmission pattern remain to be elucidated. Methods: From September 2021 to December 2021, 10 735 families (31 098 individuals) were enrolled from 29 of 31 provinces in mainland China to examine family-based H. pylori infection, related factors and transmission pattern. All family members were required to answer questionnaires and test for H. pylori infection. Results: Among all participants, the average individual-based H. pylori infection rate was 40.66%, with 43.45% for adults and 20.55% for children and adolescents. Family-based infection rates ranged from 50.27% to 85.06% among the 29 provinces, with an average rate of 71.21%. In 28.87% (3099/10 735) of enrolled families, there were no infections; the remaining 71.13% (7636/10 735) of families had 1–7 infected members, and in 19.70% (1504/7636), all members were infected. Among 7961 enrolled couples, 33.21% had no infection, but in 22.99%, both were infected. Childhood infection was significantly associated with parental infection. Independent risk factors for household infection were infected family members (eg, five infected members: OR 2.72, 95% CI 1.86 to 4.00), living in highly infected areas (eg, northwest China: OR 1.83, 95% CI 1.57 to 2.13), and large families in a household (eg, family of three: OR 1.97, 95% CI 1.76 to 2.21). However, family members with higher education and income levels (OR 0.85, 95% CI 0.79 to 0.91), using serving spoons or chopsticks, more generations in a household (eg, three generations: OR 0.79, 95% CI 0.68 to 0.92), and who were younger (OR 0.57, 95% CI 0.46 to 0.70) had lower infection rates (p<0.05). Conclusion: Familial H. pylori infection rate is high in general household in China. Exposure to infected family members is likely the major source of its spread. These results provide supporting evidence for the strategic changes from H. pylori individual-based treatment to family-based management, and the notion has important clinical and public health implications for infection control and related disease prevention.

Objective: The 2019 coronavirus disease (COVID-19) epidemic has raised international concern. Mental health is becoming an issue that cannot be ignored in our fight against it. This study aimed to explore the prevalence and factors linked to anxiety and depression in hospitalized patients with COVID-19. Methods: A total of 144 patients diagnosed with COVID-19 were included in this study. We assessed depression and anxiety symptoms using the Hospital Anxiety and Depression Scale (HADS), and social support using the Perceived Social Support Scale (PSSS) among patients at admission. Multivariate linear regression analyses were performed to identify factors associated with symptoms of anxiety and depression. Results: Of the 144 participants, 34.72% and 28.47% patients with COVID-19 had symptoms of anxiety or depression, respectively. The bivariate correlations showed that less social support was correlated with more anxious (r=-0.196, p<0.05) and depressive (r=-0.360,p<0.05) symptoms among patients with COVID-19. The multiple linear regression analysis showed that gender (β=1.446, p=0.034), age (β=0.074, p=0.003), oxygen saturation (β =-2.140, p=0.049), and social support (β =-1.545, p=0.017) were associated with anxiety for COVID-19 patients. Moreover, age (β=0.084, p=0.001), family infection with SARS-CoV-2 (β =1.515, p=0.027) and social support (β =-2.236, p<0.001) were the factors associated with depression. Conclusion: Hospitalized patients with COVID-19 presented features of anxiety and depression. Mental concern and appropriate intervention are essential parts of clinical care for those who are at risk.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal diseases and is the fourth leading cause of cancer-related deaths.¹ x 1 Hidalgo, M. Pancreatic cancer. N Engl J Med. 2010; 362: 1605–1617 Crossref | PubMed | Scopus (1493) | Google Scholar See all References Although resection is the best choice for treatment of pancreatic cancer, most cases are diagnosed at late stages, making the patients poor candidates for resection. An explosion in knowledge of the molecular genesis of pancreatic cancer has resulted in definition of PDAC as a cancer with alterations in a wide range of signaling cascades; in contrast, tumorigenesis is driven by a single targetable oncogene in certain tumors.² x 2 Jones, S., Zhang, X., Parsons, D.W. et al. Core signaling pathways in human pancreatic cancers revealed by global genomic analyses. Science. 2008; 321: 1801–1806 Crossref | PubMed | Scopus (2319) | Google Scholar See all References Nonetheless, certain signaling pathways and key nodal points act as core genetic alterations and commonly are detected in PDAC cells. Identifying the mechanisms underlying dysregulation of these core alterations should help the development of innovative strategies for prevention, early detection, and treatment of PDAC.

Outer membrane vesicles (OMVs) are nanoscale lipid bilayer structures released by gram-negative bacteria. They share membrane composition and properties with their originating cells, making them adept at traversing cellular barriers. These OMVs have demonstrated exceptional membrane stability, immunogenicity, safety, penetration, and tumor-targeting properties, which have been leveraged in developing vaccines and drug delivery systems. Recent research efforts have focused on engineering OMVs to increase production yield, reduce cytotoxicity, and improve the safety and efficacy of treatment. Notably, gastrointestinal (GI) tumors have proven resistant to several traditional oncological treatment strategies, including chemotherapy, radiotherapy, and targeted therapy. Although immune checkpoint inhibitors have demonstrated efficacy in some patients, their usage as monotherapy remains limited by tumor heterogeneity and individual variability. The immunogenic and modifiable nature of OMVs makes them an ideal design platform for the individualized treatment of GI tumors. OMV-based therapy enables combination therapy and optimization of anti-tumor effects. This review comprehensively summarizes recent advances in OMV engineering for GI tumor therapy and discusses the challenges in the clinical translation of emerging OMV-based anti-tumor therapies.

Background: Cancers with aberrant expression of Serine/threonine kinase 33 (STK33) has been reported to be particularly aggressive. However, its expression, clinical significance, and biological functions in gastric cancer remain largely unknown. In the present study, we determined the expression and function of STK33 in gastric cancer and delineated the clinical significance of the Krüppel-like factor 4 (KLF4)/STK33 signaling pathway. Methods: STK33 expression and its association with multiple clinicopathologic characteristics were analyzed immunohistochemically in human gastric cancer specimens. STK33 knockdown and overexpression were used to dissect the underlying mechanism of its functions in gastric cancer cells. Regulation and underlying mechanisms of STK33 expression by KLF4 in gastric cancer cells were studied using cell and molecular biological methods. Results: Drastically higher expression of STK33 was observed in gastric cancer and gastric intraepithelial neoplasia tissues compared with adjacent normal gastric tissues. Increased STK33 expression correlated directly with tumor size, lymph node, and distant metastasis; and patients with low STK33 expression gastric cancer were predicted to have a favorable prognosis. Enforced expression of STK33 promoted gastric cancer cell proliferation, migration, and invasion in vitro and in vivo, whereas reduced STK33 did the opposite. Moreover, STK33 promoted epithelial–mesenchymal transition (EMT) in vitro. Mechanistically, KLF4 transcriptionally inhibited STK33 expression in gastric cancer cells. KLF4-mediated inhibition of gastric cancer cell invasion was reversed by upregulation of STK33 expression. Conclusions: STK33 has pro-tumor function and is a critical downstream mediator of KLF4 in gastric cancer. STK33 may serve as a potential prognostic marker and therapeutic target for gastric cancer. Clin Cancer Res; 24(10); 2440–51. ©2018 AACR.