Overexpression of TMEM150A in glioblastoma multiforme patients correlated with dismal prognoses and compromised immune statuses.

Transmembrane proteins have exhibited a significant correlation with glioblastoma multiforme (GBM). The current study elucidates the roles of transmembrane protein 150A (TMEM150A) in GBM. Data on patients with GBM were collected from The Cancer Genome Atlas and Xena databases. The objective was to identify the expression levels of TMEM150A in patients with GBM, and evaluate its diagnostic and prognostic values, accomplished using the receiver operating characteristic and survival analyses. On a cellular level, Cell Counting Kit-8, Wound healing, and Transwell experiments were performed to gauge the impact of TMEM150A on cell growth and migration. The study further investigated the correlation between TMEM150A expression and immune status, along with ribonucleic acid (RNA) modifications in GBM. The findings demonstrated TMEM150A overexpression in the cancerous tissues of patients with GBM, with an area under the curve value of 0.95. TMEM150A overexpression was significantly correlated with poor prognostic indicators. TMEM150A overexpression and isocitrate dehydrogenase (IDH) mutation status were predictive of poor survival time among patients with GBM. In vitro experiments indicated that suppressing TMEM150A expression could inhibit GBM cell proliferation, migration, and invasion. Moreover, TMEM150A overexpression was associated with stromal, immune, and estimate scores, immune cells (such as the T helper (Th) 17 cells, Th2 cells, and regulatory T cells), cell markers, and RNA modifications. Therefore, TMEM150A overexpression might serve as a promising biomarker for predicting poor prognosis in patients with GBM. Inhibiting TMEM150A expression holds the potential for improving the survival time of patients with GBM.

TMEM41A overexpression correlates with poor prognosis and immune alterations in patients with endometrial carcinoma.

BACKGROUND: Expression levels of transmembrane protein 41A (TMEM41A) are related to the progression of malignant tumors. However, the association between TMEM41A expression and endometrial carcinoma (EC) remains unclear. This study aims to identify the roles of TMEM41A expression in the prognosis of patients with EC and its correlation with EC progression. METHODS: The TMEM41A expression and its correlation with the survival of patients with EC were assessed. Cox regression analysis was used to identify the prognostic factors, while nomograms were used to examine the association between the prognostic factors and the survival of patients with EC. Finally, the link between TMEM41A level and immune microenvironment and RNA modifications was investigated in EC. RESULTS: TMEM41A was overexpressed in EC. TMEM41A overexpression could diagnose the EC and evaluate the poor prognosis of patients. Overexpression of TMEM41A was associated with clinical stage, age, weight, histological subtype, tumor grade, and survival status of patients with EC. Clinical stage, age, tumor grade, radiotherapy, and TMEM41A overexpression were factors of poor prognosis in patients with EC. The nomograms revealed the correlation between the TMEM41A level and survival time of patients with EC at 1, 3, and 5 years. Furthermore, TMEM41A overexpression was significantly correlated with the level of the stromal score, immune score, estimate score, NK CD56 bright cells, iDC, NK cells, eosinophils, pDC, T cells, TReg, cytotoxic cells, mast cells, Th17 cells, neutrophils, aDC, NK CD56 dim cells, TFH, Th2 cells, CD8 T cells, macrophages, immune cell markers, and RNA modifications. CONCLUSIONS: TMEM41A is overexpressed in EC tissues and is associated with the prognosis, immune microenvironment, and RNA modification. Our preliminary studies indicate that overexpression of TMEM41A can potentially serve as a biomarker for EC treatment.

Recurrent Pneumonia With Tuberculosis and Candida Co-infection Diagnosed by Metagenomic Next-Generation Sequencing: A Case Report and Literature Review.

An 82-year-old male patient was hospitalized in the Respiratory Department for "repeated cough and shortness of breath for 10 years, recurrence worsened for 1 month." Later, he was transferred for further diagnosis and treatment, to the Infectious Disease Department for further hospitalization. Previously, the patient had repeatedly undergone tuberculosis-related examinations including bronchoscopy examinations. However, no evidence of Mycobacterium tuberculosis (MTB) infection was found. Early anti-infection treatments failed. Due to repeated symptoms, we performed bronchoscopy again and sent alveolar lavage fluid for the metagenomic next-generation sequencing (mNGS) test. Subsequently, MTB and Candida albicans were detected by mNGS. After antituberculosis and antifungal treatments, the symptoms were significantly relieved, and the chest CT showed resolution of the lung lesions. Therefore, we successfully diagnosed and treated a case of recurrent pneumonia with tuberculosis and Candida co-infection diagnosed by mNGS.

The relationship between BSP mRNA expression and 25(OH)D/OPG in peripheral blood of newly diagnosed T2DM patients with different bone mass.

INTRODUCTION: The objective of the study was to detect the levels of osteoprotegerin (OPG) and 25-hydroxyvitamin D [25(OH)D], as well as the expression of bone sialoprotein (BSP) mRNA, in the peripheral blood of patients with newly diagnosed type 2 diabetes mellitus (T2DM) under different bone mass conditions, and to explore its role and significance in the development process of T2DM combined with osteoporosis (OP). MATERIAL AND METHODS: A total of 225 patients hospitalised in the Endocrinology Department and General Department from May 2017 to May 2018 were enrolled and categorised into five groups: the pure T2DM group (group A, 45 patients), the bone mass reduction group (group B, 45 patients), the T2DM + bone mass reduction group (group C, 45 patients), the OP group (group D, 45 patients), and the T2DM + OP group (group E, 45 patients); meanwhile, age-matched healthy subjects undergoing physical examination in our hospital were collected as the normal control group (group NC, 45 cases). Logistic regression analysis was used to analyse the influencing factors of bone mass in patients with T2DM. RESULTS: Compared with group B, the expression levels of glycated haemoglobin (HbA1c), 25(OH)D, N-terminal propeptide of type I procollagen (PINP), fasting plasma glucose (FPG), fasting plasma insulin (FINS), high-density lipoprotein cholesterol (HDL-C), and BSP mRNA were significantly increased while OPG and b-collagen degradation products (b-CTX) were significantly decreased in group A. CONCLUSION: The expression of BSP mRNA and the decrease of 25(OH)D and OPG in peripheral blood may participate in the development of diabetes and osteoporosis.

Functional Defects of Regulatory T Cell Through Interleukin 10 Mediated Mechanism in the Induction of Gestational Diabetes Mellitus.

Gestational diabetes mellitus (GDM) is a metabolic and low-grade inflammatory disease most commonly found in pregnant women with high body mass index and non-Caucasian ethnicities; however, not all women of high-risk groups develop GDM. We hypothesized that regulatory T cells (Tregs) might present a role in suppressing GDM development. To this end, 55 high-risk women at early pregnancy (first trimester) were recruited, and 21 of them developed GDM while the other 34 did not. Compared to those subjects who did not develop GDM (non-GDM), the patients who developed GDM presented reduced levels of Tregs and elevated levels of serum interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha). The Tregs in the GDM group also presented reduced levels of transforming growth factor beta and IL-10, compared with the non-GDM group. The frequency of circulating Tregs and serum TNF-alpha level were inversely correlated. In addition, addition of Tregs from non-GDM patients, but not those from GDM patients, significantly suppressed the interferon gamma and TNF-alpha production by effector T cells through IL-10-mediated mechanisms, suggesting a functional defect in Tregs from GDM subjects. Together, these data indicated that the presence of functional Tregs could protect the pregnant women from GDM development by suppressing pro-inflammatory responses and that the dysregulation of Tregs early in pregnancy elevated the risk of GDM.