Liver fibrosis represents a prevalent pathological change that occurs during the progression of chronic liver disease, which is characterized by excessive reparative responses following hepatic tissue injury. Advances in diagnostic and imaging technologies have facilitated a deeper understanding of liver function and metabolic changes, which are crucial for early and accurate diagnosis of liver fibrosis. Furthermore, elucidating the signaling pathways involved in liver fibrogenesis provides valuable insights into its pathogenesis and progression, guiding clinical management and treatment strategies for patients with liver fibrosis. This review critically evaluates various clinical and experimental therapies aimed at mitigating or reversing liver fibrosis. Specific targeted nanocarrier drug delivery systems and traditional herbal medicines hold promise in enhancing anti-fibrotic efficacy and inhibiting disease progression.

Lately, non-alcoholic fatty liver disease (NAFLD) has risen as the leading chronic liver disease worldwide, posing a significant risk for the development of cirrhosis and hepatocellular carcinoma. The rising prevalence of NAFLD among adolescents mirrors the increasing rates of obesity in this demographic group. Despite ongoing research, the precise etiology of NAFLD remains unclear, with the “multiple parallel hits” hypothesis garnering the most support. Among the various factors implicated in NAFLD’s progression, the CXC chemokine family has been identified as a potential contributor to its development. The purpose of this review is to explore the involvement of CXC chemokines in the development of NAFLD, identify their potential targets within the disease’s development, and explore possible clinical therapeutic avenues. In addition, we assess the feasibility of utilizing CXC chemokines as biomarkers for the diagnosis of NAFLD.

The neurogenic locus notch homolog protein 3 (NOTCH3), is central in both vasculogenesis and oncogenesis and, therefore, has been considered an important factor in the development of cerebral small vessel disease (CSVD) and breast cancer (BC). Pathogenic mutations of NOTCH3 induce vascular smooth muscle cell degeneration, microvascular dysfunction and neurovascular damage in cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), which is a genetic cause of CSVD. Meanwhile, NOTCH3 aberrant signalling in BC promotes tumour progression, metastasis and chemoresistance, especially in aggressive subtypes, such as triple-negative BC. A growing body of evidence points to a common molecular pathway whereby NOTCH3 dysregulation mediates vascular and tumour pathologies, thus providing an important link between these conditions. This narrative review synthesises current insights into the dual role of NOTCH3, focusing on translational relevance as a therapeutic target. Targeting NOTCH3 may mitigate vascular damage in CSVD and simultaneously inhibit tumour progression and metastasis in BC. The review further discusses NOTCH3 as a biomarker for early diagnosis and risk stratification, besides novel therapeutic strategies involving γ-secretase inhibitors and monoclonal antibodies. Future directions include studies into the ligand-independent functions of NOTCH3, its role within the tumour microenvironment, and the development of therapies with dual-action potential. This review discusses, for the 1st time, common mechanisms between CSVD and BC, thereby opening new avenues for therapies that could effectively target both conditions. By translating these laboratory findings into clinical applications, this approach aims to improve outcomes for patients affected by these devastating disorders.

Systemic lupus erythematosus (SLE) is a complex autoimmune and idiopathic condition that affects connective tissues. It is characterized by the formation of autoantibodies, the accumulation of immune complexes, inflammation, and, ultimately, irreversible organ damage. It can affect individuals of various ages, ethnicities, and genders. Nonetheless, nearly 90% of newly diagnosed SLE patients are women of reproductive age. The early mortality associated with SLE is primarily due to significant disease activity. However, subsequent mortality is linked to chronic illness and the use of immunosuppressive agents. Despite extensive research, the precise etiology of SLE remains partially understood; however, its onset involves a complex interplay of genetic predispositions, environmental stimuli, hormonal factors, and immune system abnormalities. The predominant clinical signs include fatigue, fever, weight loss, arthritis, pericarditis, anemia, and pulmonary complications. Diagnosing SLE requires a combination of clinical evaluations and laboratory testing, including antinuclear antibodies and anti-double-stranded DNA antibodies, among others. Managing SLE patients involves various approaches and lifestyle recommendations, including avoiding direct or reflected sunlight. This article presents an updated review of the mortality and pathophysiology of SLE. We also elucidate the clinical manifestations and the primary diagnostic and therapeutic strategies for this condition.

Acute myeloid leukemia (AML) is a hematologic malignancy with a generally poor prognosis. Technological advances in molecular diagnosis have identified genetic alterations driving AML pathogenesis, among which FMS-like tyrosine kinase 3 (FLT3) mutations are significant. These mutations hold prognostic value and are increasingly recognized as potential markers for disease monitoring. This systematic review and meta-analysis aimed to assess the prevalence of changes in FLT3 mutational status in adult patients with relapsed or refractory AML compared to their status at initial diagnosis. A relevant proportion of patients who were FLT3-wildtype at diagnosis were found to be FLT3-mutated on relapse, emphasizing the importance of continuous mutation monitoring. Subgroup analyses were also performed, and mutation shift rates were reported across both FLT3 internal tandem duplication and tyrosine kinase domain subtypes. These findings illustrate the genetic evolution of leukemic clones and support the need for tailored therapeutic approaches based on the mutational profile at different disease stages. This study further highlights the diagnostic and clinical utility of routine molecular reassessment and offers practical recommendations for integrating FLT3 retesting into standard AML management.

Introduction: Graph theory was employed in recent advances of cancer research for gain deeper insights into the complex structure and function of protein-protein interaction (PPI) networks.

Objective: By representing proteins as nodes and their interactions as edges, graph theory offers a comprehensive framework for analyzing the topological properties of these networks and identifying key nodes that regulate critical biological processes. This approach has been widely applied to study various cancers, including breast cancer.

Methods: To investigate the molecular organization and critical pathways in breast cancer, we constructed a breast cancer protein-protein interaction network (BCPIN) and analyzed its hierarchical structure. The network was modeled as a metric space to delineate its central zones, facilitating the identification of essential hubs enriched with signaling pathways critical for cancer progression.

Results: Our study demonstrates the potential of hierarchical modeling of the BCPIN in unraveling its molecular organization and identifying therapeutic opportunities. By analyzing PPI network as a metric space, we highlight central zones 1 - 3 as critical hubs enriched with key signaling pathways, such as DNA repair, Notch signaling, and p53 signaling, which are essential to cancer progression. The identification of MAPK14 as a central node emphasizes its significant role in cancer biology and its value as a therapeutic target. The predominance of signaling proteins within these zones underscores their functional relevance, offering a strong rationale for prioritizing them in drug development.

Conclusion: By modeling the PPI network as a metric space, we uncovered important insights into its architecture and the central zone’s critical role in facilitating key cellular processes. Our results indicate that zones 1 - 3, particularly the central zone, may serve as promising targets for drug discovery in cancer biology.

Introduction: Skin cutaneous melanoma (SKCM) is a highly lethal skin carcinoma. Cellular senescence has a dual effect on tumor progression.

Objective: This study investigates whether senescence-related genes can guide patient stratification by examining their association with survival outcomes in SKCM.

Methods: Univariate and multivariate Cox regression analyses were performed to identify prognostic senescence-related genes. Based on these genes, samples were classified into two subtypes using consensus unsupervised clustering. Kaplan-Meier survival analysis was conducted, with statistical significance assessed via the log-rank test. Immune infiltration patterns were assessed using CIBERSORT. Finally, a prognostic risk model was constructed using Lasso regression following by multivariate Cox regression.

Results: Based on the prognostic senescence-related genes, samples were classified into two subtypes with distinct survival outcomes and immune profiles. Cluster 2, linked to improved survival and enriched in cytokine-cytokine receptor interactions, showed higher infiltration of activated natural killer (NK) cells, CD8+ T cells as well as CD4+ memory T cells, along with enhanced immune pathway activation compared to cluster 1. Subsequently, a risk model was constructed based on the identified key genes and validated using both internal and external datasets. Stratification of patients by the median risk score showed that the low-risk cohort had a significantly better prognosis, with a favorable immune microenvironment enriched in CD8+ T cells, anti-tumor M1 macrophages, and activated NK cells.

Conclusion: Senescence-related gene expression effectively stratified SKCM patients into subtypes with distinct survival outcomes and immune microenvironment profiles, offering new insights for the development of personalized medicine.

Introduction: Breast cancer, as a significant threat to women’s health globally, has a complex pathogenesis. Vitamin D, a steroid hormone with diverse physiological functions, has garnered increasing attention in breast cancer research. Numerous studies have been conducted to elucidate the relationship between Vitamin D and breast cancer, yet no definitive conclusions have been reached.

Objective: Hence, in this study, we conducted a two-sample Mendelian randomization (MR) analysis to investigate the association between Vitamin D and breast cancer.

Methods: Genetic variants associated with Vitamin D levels and breast cancer data were obtained from the genome-wide association study database and version R11 of the FinnGen study dataset, respectively. The inverse variance-weighted (IVW) method served as the primary analytical approach, supplemented by various sensitivity analyses. Horizontal pleiotropy was tested using MR-Egger and MR-Pleiotropy RESidual Sum and Outlier methods, while sensitivity analysis was conducted using the leave-one-out method to assess the reliability of the results.

Results: Based on instrumental variable assumptions, 111 single nucleotide polymorphisms were suitable for subsequent analyses after matching the results. The MR analysis demonstrated no evidence of a causal relationship between Vitamin D and breast cancer. The IVW method yielded a non-significant association (p=0.968; odds ratio = 1.002, 95% confidence interval: 0.896 - 1.119), and the other methods pointed out the same direction of effect, and the subsequent pleiotropic analysis and sensitivity analysis confirmed the accuracy of the results.

Conclusion: At the genetic level, no causal relationship between Vitamin D and breast cancer was found; thus, our findings do not support a clinically significant role of Vitamin D supplementation in breast cancer risk reduction.

Introduction: HER2-positive breast cancer needs better neoadjuvant options. Pyrotinib (Py) with trastuzumab biosimilar may offer an alternative to dual blockade.

Objective: This study analyzed the short-term efficacy and safety of Zercepac®, a trastuzumab biosimilar, combined with either Py or pertuzumab and chemotherapy in neoadjuvant therapy for HER2-positive breast cancer. It also compared the efficacy and safety of Zercepac®-pyrotinib-chemotherapy versus Zercepac®-pertuzumab-chemotherapy regimens.

Methods: Clinical data from 62 HER2-positive breast cancer patients who underwent neoadjuvant therapy with Zercepac® combined with Py or pertuzumab and chemotherapy at Anhui Cancer Hospital (February 2021 to December 2023) were retrospectively analyzed. Efficacy and safety were compared among TCbHP (29 cases), TCbHPy (8 cases), THP (9 cases), and TCbH (16 cases) groups. Statistical methods were used to identify factors influencing total pathological complete response (tpCR).

Results: Among the 62 patients, 45 (72.6%) had invasive breast cancer, 11 (17.7%) had invasive carcinomas with intraductal components, five (8.1%) had invasive carcinomas with ductal carcinoma in situ, and one (1.6%) had invasive carcinoma with mucinous features. Age and advanced clinical stage were independent risk factors for tpCR (p<0.001). The TCbHPy group showed comparable efficacy to TCbHP (p=0.25). Alopecia (91.9%) was the most common adverse event. Diarrhea incidence was significantly higher in TCbHPy than in TCbHP (p<0.001); however, no grade 4 diarrhea occurred, and triple antidiarrheal therapy reduced its severity to grade 1.

Conclusion: Zercepac® is effective and safe in neoadjuvant therapy for HER2-positive breast cancer. Py (≥400 mg) may improve tpCR rates, with diarrhea as the main adverse effect. TCbHPy regimen demonstrated non-inferior efficacy to TCbHP.

Introduction: KRASand TP53mutations are among the most common genetic mutations in cholangiocarcinoma.

Objective: This study aimed to explore the potential impact of these mutations on the survival prognosis of cholangiocarcinoma patients through a meta-analysis.

Methods: A systematic search was conducted in PubMed, Web of Science, Cochrane Library, Embase, CNKI, and Wanfang databases for cohort studies published up to April 2025 that investigated the relationship between KRASand TP53mutations and patient prognosis. Two researchers independently performed the literature screening and data extraction. Meta-analysis was conducted using RevMan 5.4 and Stata 17.0, with assessment of publication bias.

Results: Twelve studies were included, involving a total of 1,126 patients, with 167 cases of KRASmutations and 176 cases of TP53mutations. The results showed that both KRASand TP53mutations were significantly associated with poorer survival prognosis in cholangiocarcinoma patients. For KRAS(hazard ratio (HR)=7.26; 95% confidence interval (CI): 6.10 - 9.81; p<0.05) and TP53(HR=18.13; 95% CI: 11.24 - 25.32; p<0.05), the presence of mutations predicted an adverse prognosis.

Conclusion: While these findings suggest that KRASand TP53mutations are associated with worse survival in cholangiocarcinoma, the limited number and quality of the included studies warrant further high-quality research to validate these associations.

Introduction: The chemotherapy-related cognitive impairment is common, but the influencing factors and effective intervention measures are not well known.

Objective: To investigate the changes of cognitive function in breast cancer patients before and after chemotherapy, identify the influencing factors of cognitive function in chemotherapy patients, and investigate whether there is a mediating effect among multiple factors. Finally, an intervention was implemented for patients experiencing cognitive dysfunction to evaluate its effects on cognitive function.

Methods: Using the convenience sampling method, we recruited 380 breast cancer chemotherapy patients at three tertiary hospitals in Xi’an from October 2018 to May 2019. The Chinese version of the Functional Assessment of Cancer Therapy-Cognitive Function scale, the Hamilton Anxiety Scale, the Hamilton Depression Scale, and the social support rating scale were used to evaluate the cognitive function of breast cancer patients during chemotherapy, and analyze the influencing factors of cognitive function.

Results: The incidence of chemotherapy-related cognitive dysfunction in breast cancer patients was 19.74% (75/380). The results of the univariate analysis showed that the education level, medical expense payment method, family history of breast cancer, disease stage, and presence of comorbidities could impact cognitive functioning in breast cancer patients receiving chemotherapy (p<0.05). Correlation analysis revealed that there was a negative correlation among cognitive function and anxiety and depression (p<0.01), while a positive correlation with social support (p<0.05). Furthermore, multivariate stepwise regression analysis showed that the education level, medical expense payment method, disease stage, depression, and social support were independent influencing factors of cognitive function in breast cancer patients receiving chemotherapy and that depressive symptoms had a mediating effect in the relationship between social support and cognitive function. Cognitive has been shown to have a positive impact on cognitive function.

Conclusion: Cognitive dysfunction in breast cancer patients receiving chemotherapy is a multifactorial condition that requires rigorous educational and social support interventions for improvements of patient outcomes.

Introduction: Endometrial cancer is the most common gynecologic malignancy in developed countries, and the optimal surgical approach in early-stage cases remains a subject of ongoing clinical debate.

Objective: This study aims to compare laparoscopy and Pfannenstiel incision in early-stage, low-grade endometrial cancer (EC) surgery.

Methods: A retrospective study was conducted on the records of 224 patients diagnosed with EC between April 2010 and April 2024. Only patients with stage I and grade I-II endometrioid type EC were included in the study. After excluding 94 patients with non-endometrioid histology, stage II-IV disease, grade 3 tumors, and synchronous tumors, 130 patients were included in the final analysis. Participants were categorized into two groups: Group 1 (63 patients who underwent surgery through Pfannenstiel incision) and Group 2 (67 patients who underwent laparoscopic surgery).

Results: The median overall survival (OS) was 48 months (range: 12 - 168) and the median disease-free survival (DFS) was 47 months (range: 8 - 168). During the follow-up period, 20 patients died and 8 patients experienced disease recurrence. The overall OS rate was 84.6%, and the DFS was 93.8%. When comparing groups, the OS was 85.7% in Group 1 and 83.6% in Group 2 (p=0.12). The DFS rate was significantly higher in Group 1 compared to Group 2 (96.8% vs. 91%; p=0.037).

Conclusion: This study highlights the continued relevance of staging surgery with the Pfannenstiel incision in early-stage EC patients with vaginal stenosis, morbid obesity unsuitable for trocar insertion, a history of multiple abdominal surgeries, inability to insert a manipulator, an enlarged normal uterus, or suspected pelvic adhesions.

Introduction: Psychological services play a vital role in supporting cancer patients, yet their quality is influenced by provider-related factors that remain underexplored.

Objective: The objective of this study was to predict the quality of psychological services provided to cancer patients in Riyadh from the perspective of psychotherapists and to assess the predictive value of key variables within the target group.

Methods: A questionnaire assessing communication skills scale and psychotherapist competence was completed by 329 psychotherapists.

Results: Our findings revealed that the highest mean score was observed for the empathy dimension (54.20), whereas respect and authenticity recorded the lowest mean score (19.28). The overall quality of psychological services had a mean score of 174.88 ± 9.53. Regarding the psychotherapist self-efficacy scale, clinical competence recorded the highest mean (20.41), whereas influence regulation had the lowest mean score (7.95). The total score for psychotherapist competence was 79.33. Predictive analysis revealed that the workplace and academic level of psychotherapists were statistically significant predictors of service quality (p<0.05). The independent variables accounted for 41% of the variance in psychotherapist competence and 16% of the variance in communication skills with patients, indicating an overall weak predictive relationship.

Conclusion: Clinical practice implications should be considered. The identified predictors—communication skills, workplace, and academic level—may guide future efforts to enhance therapeutic approaches. Focusing on improving empathy and emotional regulation could further strengthen the quality of psychological care for cancer patients. Further studies are encouraged to translate these findings into practical clinical strategies.

Introduction: Dan-Shen-Yin (DSY), a traditional Chinese medicinal prescription composed of Salvia miltiorrhizaBge. (DS), Santalum albumL. (TX) and Amomum villosumLour. (SR), has been widely employed in the treatment of gastritis in modern clinical practice and demonstrates excellent therapeutic efficacy. However, the main active ingredient and underlying mechanisms of action remain unclear.

Objective: The aim of this study is to comprehensively characterize the chemical composition of DSY and elucidate its potential mechanisms in the treatment of gastritis.

Methods: The nonvolatile compounds in DSY were analyzed through liquid chromatography-mass spectrometry using the data-dependent acquisition approach, employing an in-house database. The volatile compounds and polysaccharides were detected by gas chromatography-mass spectrometry and high-performance liquid chromatography, respectively. Network pharmacology analysis was performed based on the identified compounds.

Results: A total of 52 nonvolatile and 15 volatile compounds were identified in DSY decoction, primarily including phenylpropanoids, phenols, flavonoids, and terpenoids. Specifically, 54 compounds were found in DS, 14 in SR, and 8 in TX. DSY polysaccharide consisted of seven kinds of monosaccharides, including mannose, rhamnose, glucuronic acid, galacturonic acid, glucose, galactose, and arabinose, with molar percentages of 0.21%, 0.53%, 0.15%, 4.12%, 6.24%, 18.07%, and 0.84%, respectively. Network pharmacology analysis identified 22 key compounds among the 67 compounds detected. These compounds exert the therapeutic effects through 55 core targets (e.g., interleukin-6, tumor necrosis factor, and TP53) and 10 inflammation-related pathways, such as the MAPK and nuclear factor kappa B signaling pathways.

Conclusion: This study further enriches the research on the material basis of DSY and reveals that its volatile compounds, nonvolatile compounds, and polysaccharides contribute to its therapeutic efficacy against gastritis. These findings may facilitate further development and application of DSY in gastritis treatment.

Introduction: Type 2 diabetes mellitus (T2DM) and ischemic heart disease (IHD) are significant medical conditions. Research indicates that patients with T2DM have a substantially increased risk of developing cardiovascular diseases, necessitating meticulous monitoring and management of both diabetes and associated cardiovascular conditions. Achieving target glycated hemoglobin (HbA1c) levels is crucial for effective T2DM treatment.

Objective: This study investigates the prescribed basic medication therapy in patients with T2DM and IHD based on target HbA1c levels.

Methods: A prospective observational study was conducted at the Republican Specialized Scientific-Practical Medical Center of Cardiology in Uzbekistan from 2022 to 2024, involving 130 patients with T2DM and IHD. Clinical, functional, and instrumental parameters, including left ventricular ejection fraction and other metabolic indicators, were assessed. Data were collected using standardized questionnaires and analyzed using the Statistical Package for Social Sciences. Logistic and linear regression models were used to analyze the efficiency of medication treatment.

Results: Among the cohort, 56.9% achieved an HbA1c level ≤8%, while 43.1% had an HbA1c level ≥8%. Significant differences were observed in age, gender distribution, duration of diabetes, and IHD between the two groups. Medication therapy varied significantly, with higher usage of metformin and insulin in patients with an HbA1c level ≥8%. The linear regression model predicts HbA1c levels based on clinical data and dosages of prescribed medications with a root mean square error of 1.172 and a Spearman correlation coefficient of 0.826. The logistic regression model predicts achievement of target HbA1c levels with a receiver operating characteristic area under the curve value of 0.92.

Conclusion: The study highlights the importance of individualized medication therapy tailored to HbA1c levels to improve clinical outcomes in patients with T2DM and IHD. It also highlights differences in medication effects based on the target HbA1c levels in patients.

Introduction: Fructosamine-3-kinase (FN3K), a deglycation enzyme implicated in redox regulation through the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, has emerged as a novel therapeutic target in breast cancer. Elevated FN3K activity enhances antioxidant defenses, promoting cancer cell survival and resistance to therapies. Pharmacological inhibition of FN3K may sensitize tumors to oxidative stress.

Objective: This study aimed to identify and validate potent FN3K inhibitors through structure-based virtual screening (SBVS) and in vitroevaluation in breast cancer models.

Methods: A homology-modeled FN3K structure was generated and validated using SWISS-MODEL, PROCHECK, and QMEAN. Compound libraries, including the Food and Drug Administration (FDA)-approved kinase inhibitors, World Health Organization (WHO) essential medicines, and anti-breast cancer agents, were screened using Schrödinger’s Glide module. Top-ranked compounds were prioritized based on binding affinity, molecular interactions, absorption, distribution, metabolism, excretion, and toxicity (ADMET) profiling. In vitrovalidation in MCF-7, BT-474, T-47D, and Vero cell lines included MTT cytotoxicity assay and evaluation of FN3K and Nrf2 expression through quantitative PCR (qPCR) and Western blotting. Statistical analyses were performed to assess the significance of observed effects.

Results: Oxaliplatin, lansoprazole, and capivasertib exhibited strong binding affinities (Glide scores: −9.2 to −8.1 kcal/mol) and selective cytotoxicity in breast cancer cell lines (IC₅₀: 90 - 110 μg/mL). qPCR analysis revealed >99% downregulation of FN3K, accompanied by significant suppression of Nrf2 in cancer cells. Minimal modulation was observed in Vero cells, indicating tumor selectivity. Western blotting further corroborated the downregulation of FN3K and Nrf2 at the protein level. Molecular dynamics (MD) simulations validated the binding stability of the lead small molecules, reinforcing their potential as effective inhibitors.

Conclusion: The integrated in silicoand in vitroanalysis supports FN3K as a viable therapeutic target in breast cancer. Oxaliplatin, lansoprazole, and capivasertib demonstrated strong FN3K inhibition and modulation of tumor redox homeostasis, suggesting their potential for further pre-clinical development as novel anti-cancer agents targeting metabolic adaptability.

Introduction: Critical care pharmacists (CCPs) are increasingly integrated into intensive care unit (ICU) teams to enhance medication safety and improve outcomes. However, their effect on mortality and adverse drug events (ADEs) remains inadequately studied.

Objective: This study aimed to evaluate the impact of CCP involvement in ICU care on patient mortality and ADEs.

Methods: A comprehensive systematic review and meta-analysis were performed, encompassing studies published through January 2025. The literature search was conducted in multiple databases, such as PubMed, Embase, and the Cochrane Library.

Results: A total of 16 eligible studies were identified, collectively involving 37,925 ICU patients. To evaluate outcomes, odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated utilizing either fixed-effects or random-effects models, depending on heterogeneity levels. Patients in ICUs with CCPs experienced significantly reduced mortality (OR: 0.72; 95% CI: 0.56 - 0.92; p=0.01) and fewer ADEs (OR: 0.39; 95% CI: 0.21 - 0.70; p=0.002) compared to controls. Despite notable heterogeneity, findings were consistent in sensitivity analyses. No significant publication bias was detected.

Conclusion: The inclusion of CCPs in ICU teams is associated with lower mortality and fewer ADEs. These findings support expanding the role of pharmacists in critical care settings.

Introduction: Advance health-care directives (AHDs) empower individuals to express treatment preferences in anticipation of future incapacity and play a crucial role in ensuring patient-centered end-of-life care. However, nursing students often report limited training and discomfort when addressing these issues.

Objective: This study aims to assess the impact of an oncology palliative care module on nursing students’ knowledge and perceptions of AHDs.

Methods: In a pre-post observational design, 39 3^rd-year nursing students completed questionnaires immediately before (pre-test) and after (post-test) a 75-h oncology palliative care module that included lectures, case discussions, and active learning methods. Sociodemographic and attitudinal data were analyzed using descriptive statistics.

Results: After the module, students showed an increased preference for refusing non-beneficial treatments (from 63.6% to 71.4%) and reported heightened awareness of the need for proactive communication regarding therapies and pain management. While willingness to donate organs remained high (94.9% vs. 92.3%), students exhibited increased caution regarding the involvement of minors in end-of-life discussions. Openness to spiritual support also rose, alongside slight increases in preferences for cremation and body donation. Although these changes did not reach statistical significance, the consistency index indicated generally stable ethical orientations, with emerging trends toward deeper reflection and heightened awareness.

Conclusion: Although no statistically significant differences were observed, the educational intervention on AHDs appeared to influence certain perceptions and attitudes among nursing students toward end-of-life decisions. Integrating structured AHD training into nursing curricula may enhance students’ awareness and ability to support patient self-determination in clinical practice.

Introduction: Globally, colorectal cancer (CRC) continues to be a major cause of cancer-related morbidity and death, with metastasis—particularly to the liver—significantly worsening patient outcomes.

Objective: The aim of this study was to investigate the expression of key epithelial-mesenchymal transition (EMT) transcription factors (Snail family transcriptional repressor 1 [SNAI1], zinc finger e-box binding homeobox 1 [ZEB1], Slug, Twist, and metastasis-associated protein 3 [MTA3]) and the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α) in CRC cases with and without metastasis to the liver.

Methods: A total of 41 CRC patients (20 non-metastatic, 21 with liver metastasis) from Dr. Sardjito General Hospital, Yogyakarta, were examined utilizing reverse transcription quantitative polymerase chain reaction of the adjacent normal tissues and the tumors.

Results: SNAI1, ZEB1, Slug, Twist, and TNF-α were significantly upregulated in metastatic CRC, while MTA3 was downregulated. Expression of these markers correlated with body mass index, liver enzymes (aspartate aminotransferase), and cancer stage.

Conclusion: These findings highlight the central role of EMT-related transcription factors and inflammatory signaling in CRC metastasis and suggest that targeting these pathways could offer novel therapeutic strategies for metastatic CRC.

Introduction: Osteoporosis (OP) is a systemic metabolic bone disease characterized by complex pathogenesis and high prevalence. Current diagnostic and therapeutic approaches have limited effectiveness, and new biomarkers are needed to improve the treatment and diagnosis of OP.

Objective: The present study aimed to identify novel diagnostic biomarkers for OP through integrated bioinformatics analysis.

Methods: We performed an integrative bioinformatics analysis combining Weighted Gene Co-expression Network Analysis and machine learning on two Gene Expression Omnibus datasets (GSE35958, GSE35956). Differentially expressed genes (DEGs) were identified using “limma” package of R software, followed by module construction and key gene screening via Least Absolute Shrinkage and Selection Operator (LASSO) regression. Functional enrichment, immune infiltration, and drug prediction analyses were conducted to explore biological mechanisms and therapeutic potential.

Results: Differential expression analysis identified 1,020 DEGs, from which 10 co-expression modules were constructed. The blue module demonstrated the strongest correlation with OP (r = 0.99, p<0.0001). LASSO regression analysis prioritized seven candidate genes (LOC286177, nucleobindin 1 [NUCB1], peroxisomal biogenesis factor 19 [PEX19], metastasis associated 1 [MTA1], DRA aassociated protein 1 [DRAP1], protocadherin gamma A1 [PCDHGA1], and pre-mRNA processing factor 39 [PRPF39]), with subsequent validation confirming NUCB1, PEX19, MTA1, DRAP1, and PCDHGA1 as robust diagnostic biomarkers (Area under the curve > 0.85). Functional enrichment implicated these genes in endoplasmic reticulum stress, Wnt/β-catenin signaling, and immune regulatory pathways. Immune profiling further revealed significant perturbations in T-cell and macrophage populations in OP. The Coremine Medical database was leveraged to predict potential therapeutic agents, including both small-molecule and phytochemical candidates.

Conclusion: The present study identified NUCB1, PEX19, MTA1, DRAP1, and PCDHGA1 as promising OP diagnostic markers and explored their roles in bone metabolism. The findings offer insights for early diagnosis and targeted therapy but require further clinical validation.

Introduction: Post-operative pain significantly impairs recovery, delaying hospital discharge after laparoscopic cholecystectomy. Effective pain management facilitates early ambulation, which diminishes the probability of post-operative complications.

Objective: This study compares the analgesic efficacy of preperitoneal bupivacaine infiltration with dexamethasone and the transversus abdominis plane (TAP) block.

Methods: This prospective, randomized, double-blinded study included 40 patients undergoing laparoscopic cholecystectomy. Group 1 (n= 20) received a TAP block, while Group 2 (n= 20) received preperitoneal bupivacaine for analgesia. The primary outcomes were (i) the level of post-operative pain, assessed using the Visual Analog Scale every 15 min in the 1st post-operative hour, at 2-h intervals up to 12 h, and at 6-h intervals up to 24 h; (ii) time to first request for rescue analgesia; and (iii) the total dose of analgesia. Secondary outcomes included patient-reported sleep quality and the incidence of post-operative nausea and vomiting.

Results: The study found that the TAP block provided superior post-operative pain relief compared to preperitoneal infiltration with bupivacaine in patients who underwent laparoscopic cholecystectomy. The TAP block group exhibited significantly lower pain scores at 8 and 12 h postoperatively and experienced a delayed first request for rescue analgesia at 14.6 ± 2.52 h on average, compared with 7.1 ± 1.02 h in the preperitoneal group.

Conclusion: The findings establish that TAP block is a more effective analgesic technique than preperitoneal infiltration with bupivacaine for managing post-operative pain in laparoscopic cholecystectomy. Patients receiving TAP block required fewer opioids, had delayed onset of rescue analgesia, and reported lower pain scores at critical post-operative intervals.

Helicobacter pylori infection is associated with various illnesses like Alzheimer’s disease (AD). The purpose of this work is to utilize Mendelian randomization (MR) methods to examine the possible link between AD and H. pylori infection. We utilized information from the Finngen database and the UK Biobank for MR analysis. Six antibodies related to H. pylori were assessed for their association with AD. The MR analysis involved two-sample methods, while generalized summary data-based MR (GSMR) was employed to analyze genetic data for a robust causal inference. The two-sample MR investigation exhibited a strong link among AD and anti-H. pylori UREA antibodies, with an odds ratio (OR) of 1.076 (95% confidence interval [CI] = 1.010 - 1.147; p=0.024). Similarly, GSMR confirmed this relationship, showing an OR of 1.071 (95% CI = 1.004 - 1.143; p=0.038). No notable correlations were seen with other antibodies. Our findings suggest that H. pylori infection may be related to a higher likelihood of AD development, particularly through anti-H. pylori UREA antibodies.

Introduction: Tubal ligation reversal is a surgical option for restoring fertility, with outcomes influenced by technique, surgeon expertise, and patient factors.

Objective: This study evaluates the fertility outcomes of macroscopic tubal reanastomosis through mini-laparotomy.

Methods: This retrospective study analyzed medical records of women who had previously undergone tubal ligation either during cesarean sections or through laparoscopic electrocoagulation at a tertiary hospital in Türkiye between 2019 and 2022. The primary surgical approach involved a mini-laparotomy, and the anastomosis was performed macroscopically—without the use of an operating microscope—relying instead on direct visual inspection to access and reconnect the fallopian tubes. The suitability of the tubes for reanastomosis was assessed based on the length of the tubes, the presence of adhesion, and the condition of the fimbriae. Fertility outcomes, including live birth rates and time to conception, and surgical success rates, were measured.

Results: The data of 23 patients were retrospectively reviewed. The surgical success rate was 78.2% (unilateral or bilateral reanastomosis of the tubas), with a pregnancy rate of 43.5% and a live birth rate of 34.8%. The mean time to conception was 3.73 months.

Conclusion: Despite lower pregnancy rates compared with the broader literature, these outcomes are deemed acceptable, particularly for centers lacking facilities for more advanced surgical options. Therefore, macroscopic tubal reanastomosis through mini-laparotomy emerges as a feasible alternative for surgeons with limited experience in more intricate microsurgical techniques, providing a viable pathway to restoring fertility with reasonable success.