Open Medicine最新文献

COVID-19 virus infection can cause disorders of the endocrine system. The aim of this study was to characterize the alterations of nucleotide metabolomic patterns in patients with post-COVID-19 condition (PCC). The study population included 18 patients with PCC alone (PCC-A), 31 patients with PCC combined with type 2 diabetes mellitus (PCC-DM), 20 healthy volunteers (HV), and 20 patients with type 2 diabetes mellitus (DM). Ultraperformance liquid chromatography-mass spectrometry was conducted on plasma metabolites. A total of 116, 178, and 163 differential metabolites were identified in PCC-DM vs PCC-A, PCC-A vs HV groups, and PCC-DM vs DM groups, respectively. Adenine was significantly down-regulated, and purine, thymine, and uracil were significantly up-regulated in the PCC-A group compared with the HV group, and the same results were observed in the PCC-DM group compared with the DM group. Differential metabolites were mainly involved in nucleotide metabolism, especially pyrimidine metabolism in PCC patients. After the arginine stimulation test, cortisol and adrenocorticotropic hormone secretion were reduced in PCC patients. In conclusion, the nucleotide de novo synthesis pathway and the remedial synthesis pathway are seriously damaged in patients with PCC-A, especially in patients with PCC-DM, which leads to the disorder and imbalance of the body cell metabolism pathway.

Background: Patients with locally advanced breast cancer (LABC) and type 2 diabetes mellitus (T2DM) confront dual challenges: hormone-driven tumor progression and metabolic dysregulation. Although metformin has shown antitumor potential, its effect on estrogen modulation and synergy with nursing care remains unclear in clinical settings.

Purpose: To investigate the impact of metformin on estrogen regulation and prognosis-related nursing outcomes in patients with LABC and T2DM.

Methods: This multicenter retrospective cohort study with a prospective randomized intervention component evaluated clinical, metabolic, and care-related indicators during the perioperative period. Serum estradiol (E2) was measured at baseline, post-chemotherapy, and 30 days post-surgery. Glucose metabolism was assessed by fasting blood glucose, HbA1c, and CV%, alongside hypoglycemia monitoring. Care quality metrics included wound healing time, infection rate, chemotherapy adherence, and hospital stay length. Survival outcomes (36-month PFS and OS) were analyzed via Kaplan-Meier curves and Cox models adjusted for age, BMI, and tumor stage. Statistical analysis used SPSS 26.0; continuous variables were expressed as mean ± SD, compared with t-tests; HRs and 95% CIs were reported with P < 0.05 considered significant.

Results: Metformin led to a 19.3% reduction in E2 levels post-chemotherapy, with sustained suppression, outperforming the control group. Glycemic metrics improved: fasting glucose compliance rose to 83.3%, CV% decreased by 38.2%, and hypoglycemia dropped by 66.7%. Wound healing time was shortened by 3.3 days. Chemotherapy adherence reached 92.8% (vs 73.6%) and self-care scores improved by 25.8% (vs 7.2%). Mechanistic analysis indicated enhanced immune microenvironment regulation and reduced pro-inflammatory cytokines.

Conclusion: Metformin, combined with structured nursing care, significantly improves estrogen control, metabolic stability, and survival in LABC patients with T2DM. These findings support its role in integrated pharmaco-nursing management of tumor-metabolic comorbidities.

Background: Sjögren's syndrome (SS) is a chronic autoimmune disorder primarily affecting the exocrine glands, leading to symptoms such as dry eyes and mouth, joint pain, fever, and neurological complications. The etiology of SS involves a complex interplay of hormonal, immune, environmental, and genetic factors. Previous studies have identified associations between SS susceptibility and polymorphisms in genes such as HLA-II, STAT4, BAFF, and TNIP1. However, these associations have not been explored in the Turkish population.

Objective: This study aimed to investigate the association between four specific single nucleotide polymorphisms (SNPs) - rs1130380, rs7574865, rs9514828, and rs17728338 - and susceptibility to SS in a Turkish cohort.

Methods: A total of 115 SS patients and 40 healthy controls were recruited from Turkey. Genomic DNA was extracted, and genotyping of the four selected SNPs was performed using the polymerase chain reaction - restriction fragment length polymorphism method. Genotypic and allelic distributions were compared between the patient and control groups.

Results: Significant associations were found between the analyzed polymorphisms and SS susceptibility. Additionally, allele frequency comparisons with global datasets revealed that the risk alleles occur at higher frequencies in the Turkish population compared to European, American, and Asian populations, indicating a potential population-specific genetic predisposition.

Conclusion: These findings suggest that the SNPs rs1130380, rs7574865, rs9514828, and rs17728338 may contribute to SS susceptibility in the Turkish population. This preliminary evidence supports the need for larger, population-based studies to further elucidate the genetic underpinnings of SS in Turkey.

Background and aim: Few studies identified the role of the placenta in birth weight. We aimed to explore the connection between placenta weight, morphology, and term low birth weight (TLBW).

Methods: This was a case-control study of neonates born at ≥37 weeks' gestation enrolled in a general hospital from January 2018 to November 2022. Cases (<2,500 g) identified via birth certificates or medical records were matched with controls on the basis of date of birth, gestational age, sex, and maternal age. A nomogram predictive model was constructed based on logistic regression, using placenta parameters and perinatal information.

Results: A total of 290 neonates (115 with diagnosed TLBW and 175 controls) were determined. There were no significant differences between the two groups concerning gestational age (265.5 ± 5.4 vs 266.3 ± 5.3 days, P = 0.1397), gender, and maternal age at delivery (32.0 ± 3.5 vs 32.1 ± 3.1 years, P = 0.867). The placenta weight (479.0 ± 80.1 vs 597.1 ± 83.1 cm), length (16.3 ± 2.1 vs 18.8 ± 2.0 cm), width (14.3 ± 2.1 vs 16.9 ± 2.0 cm), and thickness (2.3 ± 0.5 vs 2.4 ± 0.4 cm) in the TLBW group were much lower than those in the control group (all P < 0.001). Univariate predictors of TLBW included smaller placental weight, length, width, thickness, volume, and surface area. When put into a multivariate model, placental weight (aOR for per 10 g increase: 0.89; 95% CI: 0.84-0.94) and width (aOR for per 1 cm increase: 0.69; 95% CI: 0.54-0.88) remained to be independent predictors even after controlling for relevant confounders. The odds of TLBW increased when placental weight was below the 50th percentile (aOR: 5.08, 95% CI: 2.59-9.95). Placental width below the 50th percentile was significantly associated with an increased risk of TLBW (aOR: 6.57, 95% CI: 2.73-15.82).

Conclusions: Placental weight and width were found to be associated with TLBW. Further studies focusing on placental function, histology, and pathophysiology are needed to better understand the underlying mechanisms influencing fetal growth and TLBW.

Background: Vitamin C is a key to many important functions. It stimulates the immune system by protecting humans from infections and shows notable anti-viral and anti-inflammatory properties. With the antioxidative properties it acts against free radicals and cellular aging and prevents tumors. It is also involved in the synthesis of collagen, a structural protein that is essential for the formation of connective tissue as epidermis, muscle, bone, cartilage, etc. Vitamin C promotes the absorption of iron contributing to the production of red blood cells and the synthesis of hemoglobin. Scurvy is a nutritional disorder caused by low vitamin C levels which manifests with varied symptoms affecting multiple organ systems. Vitamin C also known as l-ascorbic acid, is a water-soluble nutrient and is a necessary element as the humans are unable to synthesize it. Vitamin C has an important role in the biochemical reactions of connective tissue synthesis. Presenting manifestations include malaise, gingival bleeding, impaired wound healing, perifollicular hemorrhage, dry hair and brittle nails, iron deficiency, muscle and joint pain, pulmonary hypertension, and other symptoms. The persistent reduced supply of vitamin C in the absence of treatment is cause of a severe progressive worsening of the clinical conditions. The disorder is uncommonly reported in high social level countries and in mentally wellbeing children.

Methods: Herewith, we report case-series of eight children with scurvy diagnosed in two Pediatric Hospitals in Catania, Italy "Policlinico G. Rodolico" and "Cannizzaro" in the last 2 years, October 2021-October 2023. In addition, a systematic literature review of 126 articles with 253 cases of scurvy including age, sex, main clinical manifestations, and eventual presence of neurodevelopmental disorders is reported. Main characteristic of vitamin C and negative effects of its lack with clinical manifestations, diagnosis, treatment, and prognosis are also referred.

Results: Malnutrition, gastrointestinal, and neurological disorders, are the associated predisposing factors. In the present case-series, to the higher incidence of scurvy compared to others Italian Regions may have contributed an erroneous old prejudice of parents who refuse to give citrus fruits to young children as lemon and oranges may cause cystitis as well severe toxicity when mixed with milk.

Conclusion: This study aims to alert on the scurvy as a possible cause of childhood disorder also in well industrialized regions, and to offer diagnostic tools for identifying subjects suffering from this illness.

Background: Infertility is a multifactorial condition that affects both men and women and is influenced by various factors, including overweight and obesity. These conditions, especially in women with polycystic ovary syndrome (PCOS), are strongly associated with hormonal and metabolic imbalances that can impair fertility. Targeted nutritional interventions, such as nutraceutical supplementation, may offer support in improving reproductive outcomes.

Methods: A narrative review was conducted using PubMed, focusing on publications from the past 12 years with the keywords "nutraceutical," "overweight," and "infertility." The review aimed to identify the main nutraceuticals used in managing infertility and to highlight the importance of a personalized approach tailored to individual patient characteristics.

Results: Nutraceuticals may represent a safe and cost-effective adjunctive strategy to support fertility in overweight patients, particularly in those with PCOS. Evidence suggests that their effectiveness increases when integrated into a personalized treatment plan based on individual needs and clinical profiles.

Conclusions: This review offers an updated overview of nutraceutical use in overweight individuals with infertility, outlining both benefits and limitations. It also addresses the often-overlooked medico-legal aspects of prescribing nutraceuticals, emphasizing the need for ethical and legal awareness when incorporating these interventions into clinical practice.

Background: Ferroptosis, a type of iron-dependent lipid peroxidation-induced neuronal death, has been strongly implicated in the initiation and progression of various neurological disorders, including neurodegenerative diseases and central nervous system (CNS) injuries. Although significant research efforts have been devoted to this area, most available therapeutic strategies remain largely ineffective due to the complex pathophysiology of these conditions. Moreover, the mechanisms underlying neuronal ferroptosis are not yet fully elucidated.

Methods: To investigate the role of FAHD1 in neuronal ferroptosis, bioinformatic analyses and cellular experiments were performed. Immunofluorescence and dot blot analyses were employed to explore the effects of FAHD1 overexpression on R-loop formation. Additionally, western blotting was used to assess alterations in the expression of cGAS-STING pathway-related proteins resulting from FAHD1 overexpression.

Results: Our results demonstrate that FAHD1 expression is significantly downregulated in primary neurons subjected to oxidative stress. Furthermore, ferroptosis appears to be a major contributor to neuronal damage triggered by oxidative stress. Overexpression of FAHD1 significantly reduced reactive oxygen species accumulation and R-loop formation, preserved genomic stability, and suppressed neuronal ferroptosis by inhibiting activation of the cGAS-STING pathway.

Conclusion: FAHD1 is a critical regulator of neuronal ferroptosis and may serve as a potential therapeutic target for the treatment of neurodegenerative diseases and CNS injuries.

Background: Sepsis-associated encephalopathy (SAE) remains a major unmet clinical need, due to the lack of effective treatments. Although glutathione (GSH) is known for its antioxidant properties, its specific neuroprotective role via modulation of inflammatory pathways in SAE remains poorly understood.

Methods: Using a lipopolysaccharide (LPS)-induced murine sepsis model, we examined GSH's effects through comprehensive behavioral assessments, histopathological analysis, and molecular profiling. Mice were pretreated with GSH prior to LPS challenge, and outcomes were assessed across multiple parameters.

Key results: This study reveals that GSH pretreatment significantly improved survival rates by 10% (p < 0.01) and significantly alleviates neurological deficits in a murine model of sepsis. Behaviorally, GSH reversed depression-like symptoms, boosting locomotor activity (p = 0.009) and reducing immobility (p < 0.05). Histopathological analysis showed that GSH preserved hippocampal structure, maintaining 40% more viable neurons in CA1/DG regions (p < 0.05). Mechanistically, GSH exerts dual neuroprotective actions: it robustly suppresses NF-κB signaling via inhibition of p65 nuclear translocation and downregulation of IL-1β and IL-6, while simultaneously activating the PKA/CREB pathway revealing a previously unrecognized mechanism of action.

Conclusion: This study provides the first evidence of GSH's dual mechanism action in SAE, establishing it as a promising multi-target therapeutic candidate. These findings open new avenues for developing effective SAE interventions targeting both inflammatory and neuroprotective pathways.

Purpose: Oxidative stress (OS) plays a key role in gastric cancer (GC). The purpose of this study was to investigate the role of the mRNA monooxygenase DBH-like 1 (MOXD1) in OS and evaluate its prognostic significance in GC.

Methods: An OS risk score was constructed by unsupervised clustering analysis, the log-rank test, and least absolute shrinkage and selection operator-Cox analysis of OS-related genes. The Pearson correlation between MOXD1 expression and the OS risk score was evaluated. Correlations between MOXD1 expression and clinicopathological features in the training cohort were compared. CIBERSORT, ssGSEA, and ESTIMATE were used to analyze the effects of MOXD1 on the immune microenvironment. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and gene set enrichment analysis were used to elucidate the biological functions of the mRNAs. Immunohistochemistry for MOXD1 was performed on patient tissue microarray (TMA) samples. Cox regression, log-rank tests, and chi-square analyses were used to investigate the clinicopathological features of the TMAs and associated MOXD1 expression levels. A stable knockdown cell line was constructed in HGC-27 GC cells and investigated using cell counting kit-8 and Transwell assays.

Results: The OS risk score was an independent prognostic factor for GC in the training cohort and was successfully combined with age and pTNM stage to construct a nomogram. MOXD1 expression was positively correlated with the OS risk score and was highly expressed in patients with GC. MOXD1 expression and the metastatic lymph node ratio in TMAs were found to be independent prognostic risk factors for GC. MOXD1 knockdown inhibited the proliferation and invasion of HGC-27 cells.

Conclusion: The mRNA MOXD1 is a biomarker for both OS and GC. MOXD1 expression can be used to evaluate GC prognosis and guide treatment.

Purpose: This article summarizes the brain research progress and main research techniques of type 2 diabetes mellitus (T2DM) combined with cognitive dysfunction in recent years, aiming to provide new ideas for the mechanism research and treatment of cognitive dysfunction in diabetes.

Methods: We performed a systematic literature search using the Google Academic database and the PubMed database and then preparing the manuscript.

Results: Cognitive impairment in patients with T2DM is linked to multiple structural alterations in the brain. These alterations encompass cerebral atrophy, vascular damage, increased white matter hyperintensities, microbleeds, a reduction in gray matter volume in the cerebellar cortex, modifications to the structure of the cerebellar dentate nucleus, and frontal cortex damage. Moreover, it may result in neuronal apoptosis and injury, a decline in the generation and maturation of neurons, disrupted or weakened neuronal autophagy, among other consequences. Investigators are employing sophisticated methods such as diffusion tensor imaging, diffusion kurtosis imaging, resting-state functional magnetic resonance imaging, cerebral blood flow examinations, and voxel-based morphometry to investigate these affected brain areas.

Discussion: The pathogenesis of T2DM-related cognitive dysfunction is not fully understood. This article reviews recent advances in the study of T2DM-related cognitive dysfunction and highlights key research methodologies, offering new insights into the mechanisms and potential treatments for cognitive impairment in diabetes. This review provides a new direction for the study of the mechanism and treatment of cognitive dysfunction in diabetes.