To evaluate the clinical and hormonal characteristics of patients with Sheehan's syndrome in Xinjiang, China. 97 cases diagnosed as Sheehan's syndrome in our hospital from 1999 to 2013 were retrospectively reviewed. The medical history, physical examination findings and hormonal profiles were documented and analyzed. The mean age at diagnosis was 43.7±12.4 years, with a mean diagnostic delay of 9.1±9.5 years (range, 1 month-35 years). 10 of our patients (10.3%) had a home birth. 96 of our patients (99.0%) had a history of obstetric hemorrhage. The most common clinical presentation included amenorrhea (80/97, 82.5%), agalactia (2/97, 74.2%) and loss of axillary or pubic hair (83/97, 85.6%). Seventy two of our patients (74.2%) failed to lactate and 80 of our patients (82.5%) failed to resume menstruation. Hypothalamic dysfunction included the hypothalamic-pituitary-gonadal axis (HPG) (LH deficiency: 77/83 patients, 92.8%; FSH deficiency: 73/83 patients, 88%; E2 deficiency: 62 of 82 patients,75.6%), the hypothalamic-pituitary-thyroid (HPT) axis (TSH deficiency: 77/93 patients, 82.8%, TT3 deficiency: 70/ 87 patients, 80.5%, TT4 deficiency: 72/87 patients, 82.8%) and the hypothalamus-pituitary-adrenal (HPA) axis (ACTH deficiency: 19/37 patients, 51.4%, cortisol deficiency: 49/64, 76.6%). Sheehan's syndrome is still common in Xinjiang, especially in rural areas. Long diagnosis delay in most of the patients indicates that women might be lacking correct diagnosis and treatment. Physicians need to be aware of the most important clues for diagnosis such as lack of lactation in the postpartum period and failure to resume menstruation.

Background and Aims: Extracellular matrix protein 1 (ECM1) is known to inhibit transforming growth factor β signalling and HSC activation, thereby attenuating liver fibrosis. RNA-seq profiling of livers from wild-type and ECM1-deficient mice revealed different enrichments in metabolic changes in fatty acid synthesis and inflammatory pathways, suggesting a regulatory role for ECM1 in liver steatosis. Here, we studied the role of ECM1 in metabolic dysfunction–associated steatotic liver disease pathogenesis and underlying mechanisms. Approach and Results: Hepatic ECM1 expression was evaluated and found to be significantly reduced in liver samples from patients with metabolic dysfunction–associated steatohepatitis (MASH), and in 4 established MASH mouse models (HFD, MCD, HFHC, and ob/ob ^−/− ). Although overexpression of ECM1 effectively blocked hepatic insulin resistance, steatosis, and inflammation, ECM1 ablation exacerbated diet-induced MASH progression. Mechanistically, ECM1 interacted with the K-homology 3 (KH3) domain of poly r(C) binding protein 1 (PCBP1) to suppress iron overload, mitigating lipid peroxidation and consequently impeding MASH advancement under metabolic stress. Re-expression of ECM1 and PCBP1 ameliorated liver disease progression. Conclusions: Our study reveals that ECM1 is a critical regulator in MASH, modulating lipid peroxidation by maintaining PCBP1-mediated intracellular iron homeostasis. Targeting ECM1 to restore PCBP1-dependent iron homeostasis may offer a novel therapeutic avenue for MASH.

Papillary thyroid carcinoma (PTC) is the most common subtype of thyroid carcinoma. The most effective treatment for PTC is surgical resection, and patients who undergo surgery have good survival outcomes, but some patients have distant metastasis or even multiorgan metastases at the time of initial diagnosis. Distant metastasis is associated with poorer prognosis and a higher mortality rate. Helper T lymphocyte 17 (Th17) cells and regulatory T lymphocytes (Tregs) play different roles in PTC, and the Th17/Treg balance is closely related to the progression of PTC. Th17 cells play anticancer roles, whereas Tregs play cancer-promoting roles. A Th17/Treg imbalance promotes tumor progression and accelerates invasive behaviors such as tumor metastasis. Th17/Treg homeostasis can be regulated by the TGF‐β/IL‐2 and IL‐6 cytokine axes. Immune checkpoint inhibitors contribute to Treg/Th17 cell homeostasis. For PTC, monoclonal antibodies against CTLA-4, PD-1 and PD-L1 inhibit the activation of Tregs, reversing the Th17/Treg cell imbalance and providing a new option for the prevention and treatment of PTC. This article reviews the role of Tregs and Th17 cells in PTC and their potential targets, aiming to provide better treatment options for PTC.

Purpose: This study aims to investigate the relationship between Sodium Glucose Co-transporter-2 inhibitors (SGLT2i) treatment and fibrosis in patients with Metabolic dysfunction-associated steatotic liver disease (MASLD) combined with Type 2 Diabetes Mellitus (T2DM) and Major Adverse Cardiovascular and Cerebrovascular Events (MACCEs). Methods: A case–control study was conducted, involving 280 patients with MASLD combined with T2DM treated at the First Affiliated Hospital of Xinjiang Medical University from January 2014 to October 2023. Among these patients, 135 received SGLT2i treatment. The association between the Fibrosis-4 (FIB-4) index and the occurrence of MACCEs, as well as the association between the Aspartate Aminotransferase-to-Platelet Ratio Index (APRI) scores and MACCEs, were evaluated. Results: The FIB-4 index and APRI scores were significantly lower in the SGLT2i treatment group compared to the non-SGLT2i group (1.59 vs 1.25, P< 0.001). SGLT2i treatment tended to reduce the occurrence of MACCEs compared to non-SGLT2i treatment (45.5% vs 38.5%, P=0.28). All patients who developed MACCEs in the non-SGLT2i treatment group had higher FIB-4 index (1.83 vs 1.35, P=0.003). Additionally, after SGLT2i treatment for a median duration of 22 months, patients showed significant reductions in blood glucose, APRI, and FIB-4 index. Conclusion: SGLT2i treatment significantly reduces the occurrence of MACCEs and liver fibrosis in patients with MASLD combined with T2DM. The FIB-4 index may serve as a potential surrogate marker for predicting the occurrence of MACCEs.

Purpose: Cardiovascular disease is the leading cause of mortality in patients with type 2 diabetes mellitus (T2DM). This study aimed to develop and validate a nomogram for predicting the risk factors for coronary heart disease (CHD) in T2DM in the population of northwestern China. Patients and Methods: The records of 2357 T2DM patients who were treated in the First Affiliated Hospital of Xinjiang Medical University from July 2021 to July 2022 were reviewed. After some data (n =239) were excluded, 2118 participants were included in the study and randomly divided into a training set (n =1483) and a validation set (n = 635) at a ratio of 3:1. Univariate and stepwise regression analysis was performed to screen risk factors and develop predictive models. The results of logistic regression are presented through a nomogram. The C-index, receiver operating characteristic (ROC) curve, calibration plot, and decision curve analysis (DCA) were employed to verify the distinction, calibration, and clinical practicality of the model. Results: The stepwise logistic regression analysis suggested that independent factors in patients with T2DM combined with CHD were age, gender, hypertension (HTN), glycated hemoglobin (HbA1c), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), and Uygur, which were associated with the occurrence of CHD. The nomogram demonstrated good discrimination with a C-index of 0.771 (95% CI, 0.741, 0.800) in the training set and 0.785 (95% CI, 0.743, 0.828) in the validation set. The area under curve (AUC) of the ROC curves were 0.771 (95% CI, 0.741, 0.800) and 0.785 (95% CI, 0.743, 0.828) in the training and validation sets, respectively. The nomogram was well-calibrated. The DCA revealed that the nomogram was clinically valuable. Conclusion: A nomogram based on 7 clinical characteristics was developed to predict CHD in patients with T2DM.