To analyze the effects of dietary patterns and enterotypes on frailty-related metabolic indicators, specifically glycated hemoglobin(HbA1c), in elderly diabetic patients.

A cross-sectional survey was conducted involving 72 diabetic patients aged 65 years and older from Liyang City, Jiangsu Province, and Wuyuan County, Bayannur City, Inner Mongolia Autonomous Region. Data collected included basic information, dietary intake, HbA1c levels, and fecal samples analyzed via 16S rDNA sequencing. Logistic regression models were used to analyze the impact of dietary patterns and enterotypes on elevated HbA1c. Additive models were employed to assess interaction effects.

After adjusting for gender, age, residence location, body mass index, and blood glucose management method, Logistic regression analysis revealed that: A dietary pattern characterized by low intake of soybeans and soy products, fresh vegetables, red meat, and poultry was a risk factor for elevated HbA1c in the participants(OR=3.4, 95%CI 1.1-10.6, P<0.05). The Prevotella-dominant enterotype was a protective factor against elevated HbA1c(OR=0.2, 95%CI 0.1-0.8, P<0.05). Interaction analysis of risk factors for elevated HbA1c showed no additive interaction between dietary pattern and enterotype.

A dietary pattern featuring low intake of soybeans and soy products, fresh vegetables, red meat, and poultry is a risk factor for elevated HbA1c in elderly diabetics, while the Prevotella-dominant enterotype is a protective factor against elevated HbA1c.

Gestational diabetes mellitus (GDM) affects approximately one in six pregnant women worldwide, imposing a significant health and economic burden. The uric acid to high-density lipoprotein cholesterol ratio (UHR), as a biomarker reflecting metabolic dysfunction, may be utilized to assess the prevalence of developing GDM.

We calculated the UHR index using data from pregnant women who participated in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2020. Subsequently, we conducted in-depth validation through analytical methods including multivariate logistic regression, smooth curve fitting, and subgroup analysis.

The logistic regression model demonstrated a positive correlation between the UHR index and GDM, which remained significant even after adjusting for all confounding variables (Odds Ratio [OR] = 1.16, 95% Confidence Interval [CI]: 1.07-1.26, p < 0.001). A linear dose-response relationship was observed in the restricted cubic spline (RCS) regression (p for overall < 0.001, p for nonlinear = 0.293). This association remained consistent in sensitivity analyses and subgroup analyses. The diagnostic utility of the UHR index for GDM was limited (Area Under the Curve [AUC] = 0.611, 95% CI: 0.554-0.667).

Although UHR demonstrated limited independent diagnostic accuracy (AUC = 0.611), its dual role in correlating inflammation and lipid metabolism may confer complementary value within multiparametric models, a hypothesis that warrants future research validation.

In patients with diabetes, dyslipidemia plays a crucial role in the development and progression of atherosclerotic cardiovascular disease (ASCVD), and what's more, diabetes is a significant independent risk factor for ASCVD. Currently, in China, the rate of dyslipidemia among patients with diabetes is high, while the control rate remains low. Therefore, it is essential to screen for dyslipidemia and enhance its management in patients with diabetes at the primary care level. This guideline includes the following: basic requirements for the management of dyslipidemia, lipid testing items, management goals, lipid-lowering strategies and referral criteria. It aims to provide comprehensive guidance for the management of dyslipidemia in patients with diabetes at the primary care level.

Diabetic peripheral neuropathy(DPN) is a common complication of diabetes, characterized by a complex pathogenesis for which no specific mechanism has yet been clearly identified. Studies have shown that the onset and progression of DPN are mainly associated with inflammation, oxidative stress, autophagy dysfunction, lipid metabolism disorders, iron metabolism disturbances, and vascular lesions. Clinically, commonly used therapeutic agents primarily focus on nourishing nerves and improving microcirculation, including mecobalamin, gangliosides, inositol, and ginkgolide glycosides. However, no curative treatment is currently available, and drug therapies generally show unsatisfactory efficacy. According to traditional Chinese medicine(TCM), DPN falls under the categories of &quot;blood impediment&quot; and &quot;impediment syndrome&quot;, and is considered to result from the failure of the sinews and vessels to receive proper nourishment, leading to numbness in the limbs. The underlying pathogenesis is attributed to Qi deficiency and blood stasis. Therefore, TCM offers distinct advantages in the treatment of DPN and has achieved favorable therapeutic outcomes. TCM therapies are characterized by multi-target, multi-pathway mechanisms and low incidence of side effects, making them suitable for managing chronic diseases such as DPN. Huangqi Guizhi Wuwu Decoction, recorded in the Synopsis of the Golden Chamber(Jin Gui Yao Lue), is a representative classical prescription for treating blood impediment. It functions to regulate and tonify Qi and blood and to warm and unblock the meridians and collaterals, which aligns well with the fundamental TCM pathogenesis of Qi stagnation and blood stasis in DPN. Recent research has shown that Huangqi Guizhi Wuwu Decoction can exert therapeutic effects on DPN through pathways including antioxidative stress, anti-inflammatory responses, inhibition of cell apoptosis, and improvement of microcirculation. These effects have been validated not only in cell and animal studies but also in clinical trials, confirming its definite therapeutic efficacy for DPN. This study elucidates the pathogenesis of DPN from both TCM and modern biomedical perspectives, discusses the specific pathways and mechanisms by which Huangqi Guizhi Wuwu Decoction acts in the context of DPN, and elaborates on its mechanisms at both molecular and formula levels. This study is expected to provide a theoretical and practical reference for future TCM-based prevention and treatment strategies for DPN, as well as for the development of novel therapeutic agents.

This study aims to explore the effects and mechanisms of the core formula(TCF) improving glomerulosclerosis(GS) in diabetic kidney disease(DKD) by Jinling medical school based on reticulophagy(ER-phagy)-pyroptosis-apoptosis-necroptosis(PANoptosis) signaling pathway in podocytes. Firstly, the modified DKD rat models were established. After modeling successfully, the DKD rat models received either TCF, empagliflozin(EMPA), or saline by gavage for 8 weeks, respectively. Secondly, MPC5 cells were subjected to treatment under high-glucose(HG) conditions alone, or HG combined individually with drug-containing serum of the low-dose of TCF(L-TCF) and the high-dose of TCF(H-TCF), EMPA, or Torin 1(autophagy agonist). In the in vivo studies, the changes of general conditions and renal injury indicators, pathological characteristics of GS, and the protein expression levels of podocyte marker molecules were observed, respectively. Furthermore, the changes of the level of reactive oxygen species(ROS) in the kidneys, the expression levels of the core receptor and marker molecules of ER-phagy, and the expression degree of Z-DNA binding protein 1(ZBP1) were also observed. In the in vivo and in vitro studies, we analyzed changes in the expression levels of ZBP1 protein in the kidneys and podocytes, as well as the protein expression levels of key signaling molecules in the cellular PANoptosis were investigated, respectively. The in vivo study results showed that, for the DKD model rats, general conditions and renal injury indicators, pathological characteristics of GS, and the protein expression levels of podocyte marker molecules were improved, respectively. Moreover, the level of ROS in the kidneys, the expression level of the core receptor and marker molecules of ER-phagy, and the expression degree and protein expression level of ZBP1, as well as the protein expression levels of key signaling molecules in the cellular PANoptosis were ameliorated, respectively. Notably, the improvement effects of TCF and EMPA were basically similar, but the beneficial effect of the protein expression level of interleukin-18(IL-18) in the kidneys, as an inflammatory factor, was superior to EMPA. The in vitro study results showed that, high and low doses of TCF and EMPA both could ameliorate the protein expression levels of key signaling molecules in the PANoptosis pathway in podocytes treated with HG, and the improvement effect of H-TCF was superior to that of L-TCF or EMPA. In conclusion, the study clarifies that TCF improves GS in DKD by regulating ER-phagy-PANoptosis signaling pathway in podocytes in vivo and in vitro, and has laid the groundwork for exploring mechanisms and scientific implications of treating diabetic kidney disease by Jinling medical school.

As the primary excretory organ responsible for maintaining internal homeostasis, renal dysfunction constitutes the pathological foundation of kidney injury. Renal cells are rich in endoplasmic reticulum(ER) structures, making endoplasmic reticulum stress(ERS) a central mechanism in regulating renal homeostasis. Numerous studies have revealed that aberrant activation of ERS leads to abnormal programmed cell death(PCD) in intrinsic renal cells and is closely associated with the progression of various kidney diseases. Consequently, suppressing ERS has emerged as a promising therapeutic direction in renal disease research. TCM offers wide clinical applicability and demonstrates advantages such as multi-target regulation, efficacy enhancement, and toxicity reduction. Accumulating research demonstrates that TCM ameliorates pathological renal damage by modulating ERS in kidney cells, thereby attenuating disease progression. Based on the regulatory mechanisms of ERS signaling pathways, this review focuses on the mechanistic actions of TCM in modulating ERS and its downstream PCD. It summarizes current evidence on the roles of Chinese herbal monomers and compound formulas for treating acute kidney injury(AKI), renal interstitial fibrosis(RIF), and diabetic kidney disease(DKD) by targeting ERS, aiming to provide novel perspectives for innovative clinical prevention and treatment strategies in renal diseases.

Lymphocytic mastopathy (also known as diabetic mastopathy, fibrotic mastopathy, or sclerosing lymphocytic lobulitis) is a rare benign fibroinflammatory breast disease that clinically and radiologically mimics breast carcinoma. It is most commonly associated with long-standing diabetes mellitus and autoimmune disorders.

We report the case of a 63-year-old woman with a 6-month history of a gradually enlarging, painless right breast lump. The patient was a known type 2 diabetic for 15 years on oral hypoglycaemic agents. Mammography and ultrasonography revealed an ill-defined hypoechoic lesion with marked posterior acoustic shadowing (BIRADS IV). Core needle biopsy was inconclusive. Excision biopsy demonstrated dense keloid-like fibrosis with periductal and perilobular lymphocytic infiltration without atypia, consistent with lymphocytic mastopathy.

Awareness of lymphocytic mastopathy is essential to prevent misdiagnosis as malignancy and avoid unwarranted surgical interventions. Although rare in non-insulin dependent diabetics, this condition should be included in the differential diagnosis of breast lump that mimic carcinoma on clinical examination and imaging.

This study aims to evaluate the real-world effectiveness of 100 mg aspirin in preventing superimposed preeclampsia (PE) in pregnant women with chronic hypertension (CHTN).

This retrospective cohort study included pregnant women with CHTN who began prenatal care before 20 weeks of gestation and delivered a singleton at Nanjing Drum Tower Hospital, affiliated with Nanjing University Medical School. The deliveries occurred between January 1, 2018, and May 1, 2025. The primary exposure was 100 mg/day aspirin initiated between 12 and 20 weeks of gestation, and the primary outcome was the incidence of superimposed PE. Secondary outcomes included PE delivery before 34 weeks, PE delivery before 37 weeks, preterm birth, postpartum hemorrhage, gestational diabetes mellitus, small for gestational age (SGA), and a composite of adverse neonatal outcomes. Multivariable logistic regression and inverse probability of treatment weighting (IPTW) were used to adjust for confounding factors.

During the study period, 367 women met the inclusion criteria, with 111 in the aspirin group and 256 in the control group. After IPTW adjustment, baseline characteristics were comparable between the two groups. The incidence of superimposed PE was 34.6% in the aspirin group and 37.7% in the control group, with no statistically significant difference (weighted OR = 0.87, 95% CI: 0.49-1.54; p >0.05). In secondary outcomes, the incidence of SGA was significantly lower in the aspirin group both before and after IPTW adjustment (p<0.05); however, no significant differences were observed for other outcomes (p>0.05). Additionally, subgroup analyses showed no significant heterogeneity in aspirin effect when stratified by aspirin-related factors (initiation timing, adherence, and concurrent calcium supplementation) or CHTN-related factors (timing of diagnosis, blood pressure levels before 20 weeks of gestation, and use of antihypertensive medication within three months prior to conception or before 20 weeks) (p >0.05).

Our study suggests that initiating 100 mg/day of aspirin between 12 and 20 weeks of gestation does not significantly reduce superimposed PE in women with CHTN; however, it significantly reduces the risk of SGA. Subgroup analyses also indicated that even initiation before 16 weeks did not provide additional preventive effect against PE.

The development and progression of diabetes mellitus and its complications are closely related to glycotoxicity and inflammatory interactions. Glycotoxicity triggered by hyperglycemia damages vascular endothelial cells through mechanisms such as oxidative stress and the accumulation of advanced glycation end-products(AGEs), leading to microcirculatory dysfunction and the pathological state of &quot;glycoconjugate stasis in collaterals&quot;. Meanwhile, the persistent presence of chronic inflammation further exacerbates glycotoxic injury to tissues, forming a vicious cycle that promotes the occurrence and development of diabetic complications. According to traditional Chinese medicine(TCM) theory, &quot;glycoconjugate stasis in collaterals&quot; is highly correlated with pathological factors such as phlegm-dampness, blood stasis, and heat-toxicity. The core pathogenesis lies in the dysfunction of Qi movement and the mutual entanglement of phlegm and blood stasis, with the deficiency of healthy Qi as the internal root. TCM intervention strategies focus on clearing glycotoxicity to eliminate the source of disease, resolving stasis to dredge the vessels and collaterals, regulating Qi and blood to balance Yin and Yang, strengthening the spleen to eliminate dampness and turbidity, and protecting internal organs to prevent disease transmission. These approaches aim to disrupt the vicious cycle of glycotoxicity and inflammation, improve the state of &quot;glycoconjugate stasis in collaterals&quot;, and delay or reverse the progression of diabetes and its complications. This paper explores the pathogenesis and treatment of diabetes mellitus and its complications in &quot;glycoconjugate stasis in collaterals&quot; from the perspective of glycotoxicity-inflammation interactions, providing new ideas and methods for clinical intervention. Through comprehensive, multi-target and multi-pathway interventions, TCM can not only improve metabolic disorders and microcirculatory dysfunction but also effectively alleviate inflammatory responses, offering a unique theoretical foundation and practical guidance for the prevention and treatment of diabetes mellitus and its complications.