Association of gestational metabolic syndrome with the Chinese Healthy Eating Index in mid-pregnancy: a cross-sectional study.

BACKGROUND: This study aims to investigate the relationship between gestational metabolic syndrome (GMS) and the Chinese Healthy Eating Index (CHEI) in mid-pregnancy, and to identify potentially beneficial or high-risk dietary habits. We have developed a mid-pregnancy version of CHEI-2022, adapting the Chinese Healthy Eating Index to align with the food quantity recommendations outlined in the 2022 Dietary Guidelines for Chinese Residents for mid-pregnancy. METHODS: Using the inclusion and exclusion criteria, data from 2411 mid-pregnant individuals were collected through interviews. The Total CHEI score and its component scores were determined through analysis of responses from the food frequency questionnaire. GMS diagnosis involved conducting physical examinations and performing blood biochemical tests. A logistic regression model was employed to analyze the relationship between GMS or related indices and both the total CHEI score and its component scores. RESULTS: The study identified an overall GMS prevalence of 21.65% (522 out of 2411 participants). During mid-pregnancy, participants diagnosed with GMS exhibited higher BMI, FBG, 1hPBG, 2hPBG, TC, TG, HDL, SBP, as well as higher educational levels and daily activity, compared to those without GMS (P < 0.001). After adjusting for potential confounders, participants with higher total CHEI scores (≥ 80) were found to have lower odds of GMS or related indices (P < 0.05). Increasing dietary intake of potatoes, whole grains, beans, dark green vegetables, and fruits, as per the CHEI recommendations, was associated with reduced odds of GMS or related indices (P < 0.05). CONCLUSION: A high-quality diet, as indicated by a total CHEI score of 80 or higher, and increased consumption of specific dietary components, namely potatoes, beans, dark green vegetables, and fruits, were found to effectively reduce the odds of GMS or related indices during mid-pregnancy.

Human alkaline ceramidase 2 promotes the growth, invasion, and migration of hepatocellular carcinoma cells via sphingomyelin phosphodiesterase acid-like 3B.

Hepatocellular carcinoma (HCC) is the most common type of liver cancer. It has a poor prognosis because it is often diagnosed at the advanced stage when treatments are limited. In addition, HCC pathogenesis is not fully understood, and this has affected early diagnosis and treatment of this disease. Human alkaline ceramidase 2 (ACER2), a key enzyme that regulates hydrolysis of cellular ceramides, affects cancer cell survival, however its role in HCC has not been well characterized. Our results showed that ACER2 is overexpressed in HCC tissues and cell lines. In addition, high ACER2 protein expression was associated with tumor growth; ACER2 knockdown resulted in decreased cell growth and migration. Sphingomyelin phosphodiesterase acid-like 3B (SMPDL3B) promoted HCC cell growth, invasion, and migration; SMPDL3B knockdown had a significant inhibitory effect on HCC tumor growth in vivo. Moreover, ACER2 positively regulated the protein level of SMPDL3B. Of note, ACER2/SMPDL3B promoted ceramide hydrolysis and S1P production. This axis induced HCC survival and could be blocked by inhibition of S1P formation. In conclusion, ACER2 promoted HCC cell survival and migration, possibly via SMPDL3B. Thus, inhibition of ACER2/SMPDL3B may be a novel therapeutic target for HCC treatment.

Oncogenic role of Tc17 cells in cervical cancer development.

BACKGROUND: As one of the subsets of CD8+ T cells, Tc17 cells have recently been identified and are characterized by the secretion of interleukin (IL)-17, which is related to inflammatory diseases. AIM: To assess the status of Tc17 cells in cervical cancer and investigate the biological function of Tc17 cells in cervical cancer development. METHODS: Flow cytometry assay, immunohistochemistry, and immunofluorescence were performed to detect the levels and phenotype of Tc17 cells in blood and tumor samples from patients with cervical cancer. Prior to cell suspension culture, ELISA was carried out to measure the production of IL-6, IL-1ß, IL-23, CXCL12, and IL-17 in tumor tissue supernatant and co-cultured supernatant of patients with cervical cancer. In addition, multivariate analysis was performed to identify factors associated with overall survival using the Cox proportional hazards model. RESULTS: Compared with normal tissues, Tc17 cells specifically accumulated in tumor tissues of cervical cancer patients. Cancer cells produced a greater amount of IL-6, IL-1ß, and IL-23, which in turn promoted Tc17 cell polarization. Unlike the traditional cytotoxic CD8+ T cells, Tc17 cells secreted IL-17, which subsequently promoted CXCL12 expression in tumor cells, eventually enhancing the proliferation and migration of tumor cells. Thus, the ratio of tumor-infiltrating Tc17 cells was highly correlated with poor clinical outcome in patients with cervical cancer. CONCLUSION: Our data identified the oncogenic role of Tc17 cells in the development of cervical cancer. We propose that the ratio of Tc17 cells may be a useful index in the prognosis of patients with cervical cancer.

Decreased S1P and SPHK2 are involved in pancreatic acinar cell injury.

Aim: The roles of S1P in acute pancreatitis (AP) or non-AP patients with pancreatic acinar cell injury (PACI) are not well understood. Materials & methods: Serum S1P, in 40 healthy individuals and 99 patients with PACI, was retrospectively analyzed. Additionally, we detected and analyzed S1P in AP mice and the AR42J acinar cell line. Results: Serum S1P was significantly decreased in PACI patients, compared with that of healthy controls. Patients with gall stones, normal serum calcium or normal blood lipids showed relative higher levels of serum S1P. Interestingly, in patients with gall or liver disease, serum S1P was positively associated with γ-GT and ALT. Additionally, S1P and SPHK2 were decreased in AP mice and AR42J cells, relative to the levels of corresponding controls. Conclusion: Serum S1P is decreased in PACI, which may be partly due to downregulation of pancreatic SPHK2.

CaMKII/proteasome/cytosolic calcium/cathepsin B axis was present in tryspin activation induced by nicardipine.

Premature trypsinogen activation is the early event of acute pancreatitis. Therefore, the studies on the processes of trypsinogen activation induced by compounds are important to understand mechanism underly acute pancreatitis under various conditions. Calcium overload in the early stage of acute pancreatitis was previously found to cause intracellular trypsinogen activation; however, treatment of acute pancreatitis using calcium channel blockers did not produced consistent results. Proteasome activity that could be inhibited by some calcium channel blocker has recently been reported to affect the development of acute pancreatitis; however, the associated mechanism were not fully understood. Here, the roles of nicardipine were investigated in trypsinogen activation in pancreatic acinar cells. The results showed that nicardipine could increase cathepsin B activity that caused trypsinogen activation, but higher concentration of nicardipine or prolonged treatment had an opposite effect. The effects of short time treatment of nicardipine at low concentration were studied here. Proteasome inhibition was observed under nicardipine treatment that contributed to the up-regulation in cytosolic calcium. Increased cytosolic calcium from ER induced by nicardipine resulted in the release and activation of cathepsin B. Meanwhile, calcium chelator inhibited cathepsin B as well as trypsinogen activation. Consistently, proteasome activator protected acinar cells from injury induced by nicardipine. Moreover, proteasome inhibition caused by nicardipine depended on CaMKII. In conclusion, CaMKII down-regulation/proteasome inhibition/cytosolic calcium up-regulation/cathepsin B activation/trypsinogen activation axis was present in pancreatic acinar cells injury under nicardipine treatment.

Serum sphingosine 1-phosphate in hepatocellular carcinoma patients is related to HBV infection.

PURPOSE: Serum predictors for early diagnosis of hepatocellular carcinoma (HCC) have been investigated. Sphingosine-1-phosphate (S1P) has been widely reported to promote the survival of many types of cancer cells. However, the potential of serum S1P as a diagnostic marker in HCC has not been well characterized. The aim of this study was to identify the relationship between serum S1P and the risk of HCC. METHODS: We retrospectively reviewed serum S1P in 63 HCC patients and 39 normal people. Receiver operating characteristic (ROC) curve analysis was performed to define the cut-off value of S1P in the serum. Chi-square test, t-test and multivariate regression analysis were used to investigate the association between serum S1P and individual clinicopathologic parameters. RESULTS: S1P showed significantly higher level in healthy subjects (1.372±0.116 µM) than that in patients (1.372±0.116 µM). Serum S1P in HCC patients was positively correlated to globulin (t = -3.122, p=0.003), hepatitis B virus (HBV) DNA copies (x2=4.386, p=0.036) and negatively related to AST (x2=2.870, p=0.09). Besides, part of the amount of serum S1P was negatively correlated to albumin (correlation coefficient (ß) = -0.056) and positively correlated to alanine aminotransferase (ALT) (ß=0.016) according to the regression analysis. CONCLUSIONS: These results suggested that serum S1P could be used as an auxiliary marker for HCC diagnosis, and used to monitor HBV infection in patients with HCC.