Analysis and prediction of central nervous system tumor burden in China during 1990-2030.

Central nervous system (CNS) tumors, due to their unique locations, pose a serious threat to human health and present challenges to modern medicine. These tumors exhibit notable epidemiological characteristics across various ethnicities, regions, and age groups. This study investigated the trend of disease burden of CNS tumors in China from 1990-2019 and predicted the incidence and death rate from 2020-2030. Employing data from the 2019 Global Burden of Disease (GBD) database, we utilized key indicators to scrutinize the disease burden associated with CNS tumors in China. The analysis employed the Joinpoint model to track the trend in disease burden, calculating both the annual percentage change (APC) and average annual percentage change (AAPC). Additionally, the Matlab software facilitated the creation of a gray model to forecast the incidence and death rate of CNS tumors in China spanning from 2020 to 2030." In 2019, the age-standardized incidence rate, prevalence rate, death rate, and disability-adjusted life years (DALYs) associated with CNS tumors in China were among the high level in the world. The standardized prevalence rate and DALYs of CNS tumors in China residents showed a stable fluctuation trend with age; however, age-standardized death and incidence rate demonstrated a generally upward trend with age. In China, the age-standardized prevalence and incidence rate of males were lower than those for female residents, while the age-standardized death rate and DALYs among males surpassed those of females. From 1990-2019, the age-standardized prevalence and incidence rate of CNS tumors in China exhibited an increasing trend. The age-standardized death rate and DALYs showed a contrasting trend. According to the gray model's prediction, incidence rate of CNS tumors would continue rising while the death rate is expected to decline in China from 2020-2023. The burden of CNS tumors in China has shown an upward trajectory, posing significant challenges to their treatment. It is necessary to pay attention to tertiary prevention, start from the perspective of high-risk groups and high-risk factors to reduce the burden of disease, and achieve "early detection, early diagnosis, and early treatment".

A case of collagenous gastritis and literature review: A case report.

RATIONAL: Collagenous gastritis (CG) is rarely encountered in clinical practice. Here, we reported a case of CG with iron-deficiency anemia as the main symptom. PATIENT CONCERNS: The patient was a 26-year-old woman who sought medical advice with a chief complaint of recurrent upper abdominal distention and anemia since the last 3 years. DIAGNOSES: Gastroscopy at admission showed diffuse nodular mucosa. The pathology showed the formation of a belt hyperplasia of collagen in the superficial mucosa along with the infiltration of inflammatory cells. The subepithelial collagen band was 17.68 to 35.73-µm thick and tested positive for Masson staining, thereby confirming the diagnosis of CG. INTERVENTIONS: A polysaccharide iron complex capsule was given in a dosage of 0.3 t.i.d., p.o. in combination with an omeprazole capsule (20 mg q.d. p.o). OUTCOMES: The symptoms (upper abdominal distention and anemia) were ameliorated after 8-week treatment. Blood routine showed that the hemoglobin level rose to 91 g/L. LESSONS: It is difficult to diagnose CG. Hence, a comprehensive examination based on clinical manifestations, endoscopic findings, and pathological features is required.

Manganese potentiates lipopolysaccharide-induced innate immune responses and septic shock.

Divalent metal ions such as magnesium (Mg2+), manganese (Mn2+), and zinc (Zn2+) play important roles in regulating innate immune responses. Lipopolysaccharide stimulation led to increased intracellular Mn and Zn in macrophages. However, the effect of those metal ions in regulating lipopolysaccharide-induced innate immune responses remains unclear. Here, we uncovered that both Mn2+ and Zn2+ have immunostimulatory effects, which could potentiate the lipopolysaccharide-induced expression of interferon-stimulated genes (ISGs), cytokines and pro-inflammatory genes in a dose-dependent manner. Enhancement of lipopolysaccharide-induced innate immune gene expression by Mn2+ varies between 10 % and 900 %. Conversely, the chelating of Mn2+ almost totally diminished Mn2+-enhanced lipopolysaccharide-induced gene expression. In addition, Mn2+ exerted its ability to potentiate LPS-induced innate immune gene expression regardless of slight pH changes. Importantly, we found that Mn2+ potentiates lipopolysaccharide-induced immune responses independent of TLR4 but partially relies on cGAS-STING pathway. Further in vivo study showed that colloidal Mn2+ salt (Mn jelly [MnJ]) pretreatment exacerbated lipopolysaccharide-induced septic shock and mice death. In conclusion, we demonstrated that Mn2+ plays an essential role in boosting lipopolysaccharide-induced innate immune responses. These findings greatly expand the current understanding of the immunomodulatory potential of divalent metal Mn2+ and may provide a potential therapeutic target to prevent excessive immune responses.

A secreted effector with a dual role as a toxin and as a transcriptional factor.

Bacteria have evolved multiple secretion systems for delivering effector proteins into the cytosol of neighboring cells, but the roles of many of these effectors remain unknown. Here, we show that Yersinia pseudotuberculosis secretes an effector, CccR, that can act both as a toxin and as a transcriptional factor. The effector is secreted by a type VI secretion system (T6SS) and can enter nearby cells of the same species and other species (such as Escherichia coli) via cell-cell contact and in a contact-independent manner. CccR contains an N-terminal FIC domain and a C-terminal DNA-binding domain. In Y. pseudotuberculosis cells, CccR inhibits its own expression by binding through its DNA-binding domain to the cccR promoter, and affects the expression of other genes through unclear mechanisms. In E. coli cells, the FIC domain of CccR AMPylates the cell division protein FtsZ, inducing cell filamentation and growth arrest. Thus, our results indicate that CccR has a dual role, modulating gene expression in neighboring cells of the same species, and inhibiting the growth of competitors.

Gender differences in bicuspid aortic valve Sievers types, valvulopathy, aortopathy, and outcome of aortic valve replacement.

BACKGROUND: The gender difference of the bicuspid aortic valve (BAV) is not well understood. OBJECTIVES: We evaluated the impact of gender on the Sievers types, valvulopathy, aortopathy, and outcomes of aortic valve replacement (AVR) of BAV patients in a cohort of Chinese patients. METHODS: Among 992 BAV patients without aortic dissection nor congenital heart disease, 658 underwent AVR. The demography, Sievers types, valvulopathy, aortopathy, and outcomes of AVR were compared between genders. RESULTS: Aortic regurgitation (AR ≥ 2+) (39.0% vs. 12.8%, p < .001), aortic root dilation only (3.8% vs. .8%, p = .014), and diffuse dilation (25.3% vs. 4.3%, p < .001) were more common in men, while moderate to severe aortic stenosis (AS) (21.3% vs. 45.7%, p < .001) and ascending dilation only (46.2% vs. 61.2%, p < .001) were more common in women. Men were more prone to develop preoperative AR ≥ 2+ (OR = 5.15, p < .001), moderate to severe AS + AR ≥ 2 + (OR = 2.95, p = .001), and Diffuse aortic dilation (OR = 3.91, p < .001). Sievers types did not have a significant effect on valvular dysfunction. Gender didn't predict early adverse events after AVR (n = 90) (HR = 1.21, p = .44), but male gender predicted a left ventricular ejection fraction <50% after AVR (OR = 3.07, p = .03). CONCLUSIONS: In this BAV series of Chinese patients, gender didn't differ significantly in Sievers types of BAV but showed significant differences in valvulopathy, aortopathy, and LV function after AVR. In addition, the male patients developed more severe conditions at a younger age.

Prognostic value of coronary flow velocity reserve in patients with homozygous familial hypercholesterolemia.

BACKGROUND: Coronary flow velocity reserve (CFVR) can provide useful quantitative information on the functional status of coronary artery circulation, and an impaired CFVR (< 2.0) was associated with a significant increase in the occurrence of cardiac events. Coronary artery disease (CAD) is the leading cause of death in homozygous familial hypercholesterolemia (HoFH), but the relationship between impaired CFVR and outcome in HoFH has never been discussed before METHODS: To explore the long-term prognostic value of CFVR in patients with HoFH, 39 HoFH patients with CFVR data (mean age with 16.7 years) were enrolled from the Genetic and Imaging of Familial Hypercholesterolemia in Han Nationality Study. All patients were divided into impaired CFVR (CFVR < 2.0, n = 17) and preserved CFVR (CFVR≥2.0, n = 22) group. Follow-up was performed until a major adverse cardiac event (MACE) occurred or up to June 30, 2020 RESULTS: During a median follow-up of 89 months, 16 events were registered, 12 of which were occurred in the impaired CFVR group and four occurred in the preserved CFVR group. The event-free survival rate of impaired CFVR group was significantly lower than that in the preserved CFVR group (29.4% vs 81.8%, P < .001), and CFVR < 2.0 was independently associated with prognosis before and after adjustment for related risk factors (HR 5.197, 95% CI 1.669 to 16.178, P = .004 and HR 5.488, 95% CI 1.470 to 20.496, P = .011, respectively) CONCLUSIONS: an impaired CFVR predicts a worse outcome in HoFH. CFVR shows an independent value in the prediction of long-term outcome in HoFH.

The transcriptional regulator Zur regulates the expression of ZnuABC and T6SS4 in response to stresses in Yersinia pseudotuberculosis.

Zinc homeostasis is crucial for the development and stress resistance of bacteria in the environment. Serial zinc sensing transcriptional regulators, zinc transporters and zinc binding proteins were found to maintain the zinc homeostasis in bacteria. Zur is a zinc uptake regulator that is widely distributed in species, and ZnuABC, as well as the Type VI Secretion System (T6SS4) function in zinc acquisition. Here, we report that the regulator Zur inhibits the expression of the ZnuABC which inhibition could be eliminated at low zinc level, and upregulates the T6SS4 operon in Yersinia pseudotuberculosis to facilitate Zn2+ uptake and oxidative stress resistance. Zur regulates the expression of ZnuABC and T6SS4 by directly binding to their promoter regions. Zur senses the Zn2+ concentration and represses ZnuABC in a Zn2+-containing environment. Zur works as an auxiliary regular activator of T6SS4, facilitating oxidative stress resistance. This study revealed the dual function of regulator Zur on ZnuABC and T6SS4, and enriched the knowledge of Zn2+ homeostasis maintenance in Y. pseudotuberculosis.

Supravalvular Aortic Stenosis and the Risk of Premature Death Among Patients With Homozygous Familial Hypercholesterolemia.

Patients with homozygous familial hypercholesterolemia (HoFH) have a high risk for premature death. Supravalvular aortic stenosis (SVAS) is a common and the feature lesion of the aortic root in HoFH. The relation between SVAS and the risk of premature death in patients with HoFH has not been fully investigated. The present study analysis included 97 HoFH patients with mean age of 14.7 (years) from the Genetic and Imaging of Familial Hypercholesterolemia in Han Nationality Study. During the median (±SD) follow-up 4.0 (±4.0) years, 40 (41.2%) participants had SVAS and 17 (17.5%) participants experienced death. The proportion of premature death in the non-SVAS and SVAS group was 7.0% and 32.5%, respectively. Compared with the non-SVAS group, SVAS group cumulative survival was lower in the HoFH (log-rank test, p <0.001). This result was further confirmed in the multivariable Cox regression models. After adjusting for age, sex, low density lipoprotein cholesterol (LDL_C)-year-score, lipid-lowering drugs, cardiovascular disease, and carotid artery plaque, SVAS was an independent risk factor of premature death in HoFH on the multivariate analysis (hazard ratio 4.45; 95% confidence interval, 1.10 to 18.12; p = 0.037). In conclusion, a significantly increased risk of premature death was observed in HoFH patients with SVAS. Our study emphasized the importance of careful and aggressive management in these patients when appropriate.