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Objective This study aims to investigate the mortality among HIV/AIDS patients receiving antiretroviral therapy (ART) in Fangchenggang City, Guangxi Province, and to identify associated factors with AIDS-related and non-AIDS-related deaths, providing scientific evidence for reducing AIDS mortality. Methods We collected data from the National Comprehensive AIDS Prevention and Control Information System. These data included socio-demographic and follow-up records of 2 728 HIV-1 infected individuals receiving Antiretroviral Therapy (ART) treatment in Fangchenggang City from January 1, 2005 to July 5, 2022. This dataset included socio-demographic and follow-up records during the specified period, providing a comprehensive insight into the therapeutic responses, survival rates, and potential associated complications among ART-treated HIV/AIDS patients within Fangchenggang City. Socio-demographic and follow-up data were analyzed using the cumulative incidence function (CIF) under a competing risk framework and the Fine-Gray subdistribution hazard regression model to assess the associated factors with both AIDS-related and non-AIDS-related deaths. Results With an average follow-up period of 6.7 person-years, 295 cases experienced AIDS-related death with a mortality rate of 1.06/100 person-years, while 227 cases died from non-AIDS-related causes, with a mortality rate of 1.2/100 person-years. Under consideration of competing risks, the cumulative incidence of AIDS-related death at 1 year, 5 years, and 13 years post-diagnosis was 2.5%, 8.5%, and 15.0%, respectively. The factors associated with a higher risk of AIDS-related death included: age 60 years or older (aHR = 1.5, 95% CI: 1.05~2.15), current spouse's infection status unknown/not investigated (aHR = 1.39, 95 % CI: 1.03~1.90), history of prophylactic treatment for opportunistic infections (aHR = 1.4, 95% CI: 1.06~1.84), and occurrence of opportunistic infections or tumors (aHR = 1.65, 95% CI: 1.12~2.45) . On the contrary, factors associated with a lower risk of AIDS-related death included: being female (aHR = 0.61, 95% CI: 0.49~0.90), initial treatment regimen containing EFV (aHR = 0.41, 95% CI: 0.25~0.68), having changed the treatment regimen (aHR = 0.19, 95% CI: 0.12~0.29), first CD4 cell count ≥ 200 cells/µL (aHR = 0.30, 95% CI: 0.20~0.45), initial viral load (VL) between 50 to 1000 copies/ml (aHR = 0.31, 95% CI: 0.18-0.54), and VL < 50 copies/ml (aHR = 0.61, 95% CI: 0.44~0.84). Regarding non-AIDS related deaths, passive detection (aHR = 1.41, 95% CI: 1.0~1.98), uninvestigated/unknown spouse's infection status (aHR = 1.40, 95% CI: 1.01~1.95), and first CD4 cell count ≥200 cells/ (JLL (aHR = 1.68, 95% CI: 1.27~2.22) were found to be associated with increased risk. In contrast, lower risk factors included being female (aHR = 0.55, 95 % CI: 0.37-0.81), having experienced a change in antiviral treatment regimen post-initiation (aHR = 0.33, 95%CI :0.21-0.50), initial treatment regimens containing EFV (aHR = 0.55, 95% CI: 0.34-0.88), and NVP (aHR = 0.50, 95% CI: 0.3-0.83). Conclusion The mortality rate among HIV/AIDS patients receiving ART in Fangchenggang City is relatively low. This study underscores the importance of preventing and treating opportunistic infections or tumors for improving the survival of HIV/AIDS patients. HIV/AIDS care clinics should particularly focus on monitoring and following up on female patients, older patients, and those detected passively, enhancing medication adherence, expanding HIV testing among key populations, and thereby striving to reduce the mortality rate among AIDS patients. [ABSTRACT FROM AUTHOR]

Background The study purpose was to characterize the mycobiome and its associations with the expression of pathogenic genes in esophageal squamous cell carcinoma (ESCC). Methods Patients with primary ESCC were recruited from two central hospitals. We performed internal transcribed spacer 1 (ITS1) ribosomal DNA sequencing analysis. We compared differential fungi and explored the ecology of fungi and the interaction of bacteria and fungi. Results The mycobiota diversity was significantly different between tumors and tumor-adjacent samples. We further analysed the differences between the two groups, at the species level, confirming that Rhodotorula toruloides , Malassezia dermatis , Hanseniaspora lachancei , and Spegazzinia tessarthra were excessively colonized in the tumor samples, whereas Preussia persica , Fusarium solani , Nigrospora oryzae , Acremonium furcatum , Golovinomyces artemisiae , and Tausonia pullulans were significantly more abundant in tumor-adjacent samples. The fungal co-occurrence network in tumor-adjacent samples was larger and denser than that in tumors. Similarly, the more complex bacterial–fungal interactions in tumor-adjacent samples were also detected. The expression of mechanistic target of rapamycin kinase was positively correlated with the abundance of N. oryzae and T. pullulans in tumor-adjacent samples. In tumors, the expression of MET proto-oncogene, receptor tyrosine kinase (MET) had a negative correlation and a positive correlation with the abundance of R. toruloides and S. tessarthra , respectively. Conclusion This study revealed the landscape of the esophageal mycobiome characterized by an altered fungal composition and bacterial and fungal ecology in ESCC. [ABSTRACT FROM AUTHOR]

Aim of the study: Hepatocellular carcinoma suppressor 1 (HCCS1) has been identified as a tumor suppressor gene in the high-frequency loss of heterozygosity (LOH) region on chromosome 17p13.3 in hepatocellular carcinoma (HCC). There was also a high frequency of LOH on chromosome 17p13.3 in non-small cell lung cancer (NSCLC). Therefore, the aim of this study was to explore the expression of HCCS1 in NSCLC as well as its clinical significance. Material and methods: Real-time PCR and immunohistochemistry were performed to detect the expression level of HCCS1 mRNA and protein in NSCLC and noncancerous tissues, respectively. Further, we explored the relationship between HCCS1 expression and various clinical features in NSCLC. Results: The mRNA and protein expression of HCCS1 were both significantly lower in NSCLC samples than those in noncancerous tissues. That is, the mRNA level of HCCS1 was 0.0044 ±0.0036 and 0.0067 ±0.0054 in NSCLC samples and noncancerous tissues, respectively. The protein level of HCCS1 was 4.67 ±1.15 and 6.13 ±1.24 in NSCLC samples and noncancerous tissues, respectively. Importantly, this difference in expression was significantly correlated with tumor lymph node metastasis (TNM) in NSCLC (p < 0.05), but not with gender and age of the patients, pathological types, TNM stages, or grades of cancers (p > 0.05). Conclusion: Our results suggest that HCCS1 may be involved in NSCLC carcinogenesis. [ABSTRACT FROM AUTHOR]

Aim of the Study: Hepatocellular carcinoma suppressor 1 (HCCS1) has been identified as a tumor suppressor gene in the high-frequency loss of heterozygosity (LOH) region on chromosome 17p13.3 in hepatocellular carcinoma (HCC). There was also a high frequency of LOH on chromosome 17p13.3 in non-small cell lung cancer (NSCLC). Therefore, the aim of this study was to explore the expression of HCCS1 in NSCLC as well as its clinical significance., Material and Methods: Real-time PCR and immunohistochemistry were performed to detect the expression level of HCCS1 mRNA and protein in NSCLC and noncancerous tissues, respectively. Further, we explored the relationship between HCCS1 expression and various clinical features in NSCLC., Results: The mRNA and protein expression of HCCS1 were both significantly lower in NSCLC samples than those in noncancerous tissues. That is, the mRNA level of HCCS1 was 0.0044 ±0.0036 and 0.0067 ±0.0054 in NSCLC samples and noncancerous tissues, respectively. The protein level of HCCS1 was 4.67 ±1.15 and 6.13 ±1.24 in NSCLC samples and noncancerous tissues, respectively. Importantly, this difference in expression was significantly correlated with tumor lymph node metastasis (TNM) in NSCLC (p < 0.05), but not with gender and age of the patients, pathological types, TNM stages, or grades of cancers (p > 0.05)., Conclusion: Our results suggest that HCCS1 may be involved in NSCLC carcinogenesis.