Archives of Medical Science最新文献

Introduction: The role of mothers has long been the subject of social stereotyping and debate. Psychological and sociological research suggests that women approach this role with a complex ability to multitask, often prioritising family care over career development.

Material and methods: For the present study, an anonymous online questionnaire was developed to collect data from 534 female doctors who are mothers ('mother doctors'). The 32-item questionnaire focused on the relationship between their careers and family life, covering demographic information, family configuration, availability of home help, division of household responsibilities and the impact of these factors on their professional life.

Results: The study found that the majority of female doctors surveyed (51.7%) stated unequivocally that motherhood had a significant impact on their approach to patients, with 30.7% indicating a moderate impact. The most commonly cited changes at work related to motherhood were a greater understanding of the needs of patients, especially mothers and children (79.1%), as well as increased empathy (59.0%) and changes in communication style (54.7%) with patients.

Conclusions: Motherhood represents a profoundly transformative experience in the professional lives of women doctors, the impact of which goes far beyond stereotypical limitations. Accumulating evidence suggests that mother doctors not only become more organised and resilient to stress, but also develop leadership skills that can contribute to the transformation of the healthcare system in Poland. Childcare challenges are one of the most significant barriers to academic success for mother doctors.

Obesity significantly contributes to the development and progression of chronic kidney disease (CKD) by inducing metabolic and hemodynamic disturbances that drive gene dysregulation, inflammation, fibrosis, and renal structural injury. Key molecular mediators include genetic polymorphisms - such as AGT rs699, ACE I/D, LEP ENSSNP5824596, and FTO rs17817449 - and epigenetic regulators like microRNAs (e.g., miR-21, miR-192) and long non-coding RNAs (e.g., ANRIL, HOTAIR). These alterations affect signaling cascades such as TGF-β/Smad3, NF-κB, and AMPK, accelerating renal damage in obese individuals. Despite advances, reliable biomarkers and therapeutic targets remain scarce. This review integrates current evidence on the genetic and epigenetic basis of obesity-related CKD, offering a framework for early detection and precision medicine.

Heart failure (HF) and atherosclerosis represent two major cardiovascular diseases that are intricately linked, both contributing significantly to global morbidity, mortality, and healthcare burden. Despite substantial progress in diagnostic methods and therapeutic strategies, the overall impact of these conditions remains considerable. This is largely due to their complex and overlapping pathophysiological mechanisms, persistent residual atherosclerotic risk, and the ongoing challenges associated with implementing guideline-directed medical therapy for HF in routine clinical practice. Recent advancements in the management of diverse HF phenotypes, lipid abnormalities, atherosclerotic cardiovascular disease (ASCVD), and obesity have facilitated the adoption of multidrug regimens. These include β-blockers, renin-angiotensin-aldosterone system inhibitors, sodium-glucose cotransporter 2 (SGLT2) inhibitors, and glucagon-like peptide-1 (GLP-1), which have collectively improved outcomes in HF populations. Lipid-lowering therapy, particularly statins, has demonstrated significant efficacy in reducing ASCVD events and slowing HF progression, as well as lowering the risk of HF-related hospitalizations. Elevated lipoprotein(a) [Lp(a)] has emerged as an independent risk factor for both ASCVD and HF, being associated with increased risk of incident HF, disease progression, hospitalization, and adverse outcomes. However, there remains a lack of conclusive evidence as to whether targeted reduction of Lp(a) leads to a decrease in major adverse cardiovascular events or improves HF incidence or outcomes. In parallel, contemporary therapeutic advances in coronary and peripheral artery revascularization, along with novel pharmacologic treatments for obesity such as GLP-1 receptor agonists including semaglutide and tirzepatide have shown beneficial effects in reducing cardiovascular mortality, HF progression, and body weight, irrespective of HF status. These converging therapeutic strategies underscore the close interrelationship between HF and atherosclerosis. This review aims to elucidate the shared pathophysiological mechanisms linking these conditions and to examine their clinical overlap with ischemic heart disease, cerebrovascular disease, peripheral arterial disease, dyslipidemia, and obesity. A comprehensive understanding of these interrelated cardiovascular entities may offer valuable insights to inform future research directions and optimize the clinical management of patients affected by both HF and atherosclerotic disease.

Introduction: The aim of the study was to identify gut microbiota (GM) with genetic causal effects on insomnia using Mendelian randomization (MR) and predict potential traditional Chinese medicines (TCMs) for GM-targeted intervention in insomnia.

Material and methods: Summary data from genome-wide association studies (GWAS) on GM and insomnia were obtained from the IEU OpenGWAS database. The R 4.4.1 software, particularly the TwoSampleMR package, was utilized to assess the genetic correlation between GM and insomnia, primarily using the inverse-variance weighted (IVW) method. Functional enrichment analysis was conducted on the genes adjacent to the instrumental variables to explore the signaling pathways through which related GM may mediate insomnia. The CTD and Coremine databases were combined to predict TCM with potential regulatory effects on the genes adjacent to the instrumental variables, and their properties, meridian tropism, and efficacy information were compiled.

Results: The MR analysis revealed that Ruminococcaceae and Marvinbryantia were associated with an increased risk of insomnia, while Pasteurellaceae, Olsenella, the Ruminococcus gnavus group, Mollicutes RF9, and Pasteurellales were associated with a decreased risk. The genes adjacent to the instrumental variables were mainly enriched in signaling pathways such as neuroactive ligand-receptor interaction and the mammalian target of rapamycin (mTOR). Representative TCM with high mapping frequencies included Panax ginseng, Curcuma aromatica, Salviae Miltiorrhizae Radix, Zingiber officinale, Glycyrrhizae Radix et Rhizoma, Aucklandiae Radix, Magnoliae Officinalis Cortex, Scutellariae Radix, Ganoderma lucidum, and Poria cocos.

Conclusions: The MR analysis identified seven GM, represented by Ruminococcaceae and Marvinbryantia, that may mediate the occurrence and development of insomnia through signaling pathways such as mTOR and neuroactive ligand-receptor interaction. It predicted potential traditional Chinese medicines that act on GM to intervene in insomnia. This study provided a reference for exploring TCM prevention and treatment strategies for insomnia from the perspective of GM.