Lung cancer exhibits high morbidity and mortality rates, characterized by a heterogeneous genetic landscape and an immunosuppressive tumor microenvironment, despite recent therapeutic advances. High-resolution single-cell sequencing has facilitated a comprehensive analysis of malignant and host cell types, enhancing the understanding of lung cancer’s heterogeneity and adaptability under basal conditions and in response to therapeutic intervention. In this review, we provide an overview of the utilization of single-cell sequencing technology in characterizing the microenvironment of lung cancer, facilitating early diagnosis, monitoring tumor progression, and elucidating mechanisms of drug resistance, thereby offering new insights into potential therapeutic interventions.

Obesity is a chronic inflammatory disease defined by an excessive accumulation of body fat. The human gut microbiota (GM) is an intricate ecosystem of microorganisms living symbiotically within the gastrointestinal tract and has emerged as a key player in health and metabolic diseases. Recently, several studies have increasingly revolved around understanding the specific compositions and strains of GM and their potential impact on obesity. This review provides a summary of the most recent findings regarding obesity and newly developed therapies that show exceptional efficacy in treating this condition. In addition, it explores different GM strains that may contribute to the progression and development of obesity. This article summarizes the molecular insights involved in the relationship between obesity and GM, the characteristics of this ecosystem, and its involvement in human metabolism, energy balance, and inflammation leading to obesity. Furthermore, it examines the bacteria most engaged in managing obesity. These findings contribute to a better understanding of this significant and intricate relationship, ultimately aiding in obesity prevention.

This research aimed to perform a preliminary meta-analysis to comprehensively examine the effectiveness and safety of herbal medicines in modulating the intestinal microbiota of pediatric patients suffering from Mycoplasma pneumoniae pneumonia (MPP). A systematic search of seven databases was conducted in March 2024. The included randomized controlled trials were evaluated using the Risk of Bias (ROB) 2.0 tool, as recommended in the Cochrane Handbook. The analysis included a total of 11 studies, with a combined sample of 880 children. Traditional Chinese medicine (TCM) significantly enhanced the clinical outcomes of pediatric cases of MPP compared to Western medicine or symptomatic treatment. The meta-analysis results indicated that TCM significantly improved total clinical effectiveness (risk ratio = 1.19, 95% confidence interval [CI]: 1.13, 1.26), increased Bifidobacterium bifidum count (mean difference [MD] = 1.404, 95% CI: 1.180, 1.628), reduced serum interleukin-6 levels (MD = −4.665, 95% CI: −8.191, −1.139), and shortened the time required for rales to resolve (MD = −1.790, 95% CI: −1.951, −1.629) compared to the Western medicine group, with all differences being statistically significant at p < 0.05. Regarding safety, TCM modulation of the intestinal microbiota in treating pediatric mycoplasma pneumonia did not result in a higher incidence of adverse reactions, with the difference being statistically non-significant (p > 0.05). The ROB 2.0 assessment indicated potential bias, and the literature quality was moderate, necessitating future validation by higher-quality studies. The clinical effectiveness of intestinal microbiota-targeted TCM modulation in treating pediatric mycoplasma pneumonia was superior to Western medicine-only treatment, offering significant advantages in reducing inflammatory cell infiltration, shortening the time for rales to resolve, and demonstrating a better safety profile. However, future high-quality, large-scale clinical trials are needed to verify these findings.

Hyperuricemia (HUA), a condition characterized by elevated levels of uric acid (UA) in the bloodstream, is intricately connected to an imbalance in the gut microbiota. UA, a byproduct of purine metabolism, serves as a crucial endogenous antioxidant. Recent research indicates that modifying the gut microbiome offers a promising avenue for managing HUA. This work delves into the complex relationship between HUA and changes in the gut microbiota, examining its impact on UA excretion, reabsorption, and the activity of enzymes involved in purine breakdown. Elucidating the precise mechanisms behind this connection is essential for developing effective treatments, and exploring various therapeutic approaches, including probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation, which target the gut microbiota to reduce UA levels. These treatments may exert their effects through diverse pathways, such as inhibiting key enzymes, regulating UA transporters, reducing oxidative stress and inflammation, and restoring the balance of the gut microbiome. Furthermore, maintaining a healthy gut barrier is a valuable complementary therapy. This review aims to provide insights into the potential of gut microbiota manipulation as a novel and promising strategy for managing HUA. While this approach holds great promise, it is important to consider the potential risks and challenges associated with gut microbiota manipulation, and further research and clinical trials are warranted to fully understand its efficacy and safety.

Understanding the intricate network of cancer pathways within protein-protein interactions (PPIs) presents a considerable challenge. Ranking these pathways by importance is difficult, as their relevance varies depending on cancer type and specific biological context. In this study, a probability odds ratio (OR) test was employed to uncover significant insights into this complexity. PPI networks were analyzed as a metric space to gain insights into their organization and functional architecture. A central protein was identified as the network’s “center,” with other proteins grouped into specific zones according to their proximity to this central point. The analysis focused on the central zones of the network, examining pathways for functional enrichment, investigating molecular mechanisms linked to oncogenes and tumor suppressors, and identifying critical proteins involved in key cellular processes. The findings highlight the importance of central proteins and pathways in driving oncogenesis and offer potential therapeutic targets. The analysis revealed an enrichment of cancer-related pathways, including PI3K-AKT, TNF, JAK-STAT, mTOR, and Wnt, with central zones of the interaction network demonstrating an important role in cancer progression. Zones 1 and 2 showed a dense concentration of cancer-associated pathways, highlighting the critical roles of core proteins in signaling and functional interactions essential to tumor biology. Among the pathways, the PI3K-AKT pathway was dominant in zone 1, accounting for approximately 51% of signaling proteins. The TNF pathway exhibited a distinct pattern, with an OR of 4.22, indicating its higher concentration in zone 1 compared to zone 2. In contrast, pathways such as JAK-STAT, mTOR, and Wnt showed more stable distributions across zones but exhibited slightly lower ORs. Importantly, ten proteins emerged as key players, central to multiple pathways and crucial for cancer progression, cell survival, and metabolism. These proteins - PRKCA, SOS2, AKT1, PIK3CA, AKT2, AKT3, PIK3CB, PIK3CD, PIK3R2, and PIK3R3 - are closely associated with oncogenic processes. Each contributes to cell proliferation, survival, and differentiation, with functional implications across various cancer types, including lung cancer. Understanding the roles of these proteins within the broader cancer pathway network deepens knowledge of tumor biology and opens new possibilities for the development of novel therapeutic approaches.

Research has demonstrated that the intake of specific foods and nutrients is linked to the risk of pancreatic cancer, but the role of meat and dairy consumption in pancreatic carcinogenesis remains controversial. The main objective of this study is to investigate the association between the intake of dairy products and meats and the risk of pancreatic cancer. A case-control study was conducted between March 2015 and August 2018 at four main hospitals in Jordan; one of the hospitals was an oncology center. Participants in the study included 101 histologically confirmed pancreatic cancer patients, which were frequency-matched with 314 controls. The required information for this study was gathered through questionnaires based on face-to-face interviews. An Arabic food-frequency questionnaire that has been validated was used to collect data on the intake of different food items from dairy and meat groups. Multinomial logistic regression was employed to determine odds ratios (ORs) and their corresponding 95% confidence intervals (CIs), considering potential confounders. The consumption of different levels and frequencies of yogurt, white cheese, processed cheese, red meats, and chicken was observed to increase the risk of pancreatic cancer. The adjusted OR indicated that the risk of pancreatic cancer was positively related to a daily intake of yogurt (OR: 2.88 [95%CI: 1.40 - 5.91; p = 0.001]), cooked lamb meat (OR: 2.50 [95%CI: 1.30 - 4.84; p = 0.002]), and cooked veal meat (OR: 1.72 [95%CI: 1.11 - 3.77; p = 0.011]). Furthermore, daily and weekly consumption of white cheese, processed cheese, and cooked chicken may be associated with an increased risk of pancreatic cancer. According to the study’s findings, the consumption of yogurt, white cheese, processed cheese, red meat, and chicken was linked to a higher risk of developing pancreatic cancer.

This study aims to present ultrasound-guided vacuum-assisted excision (UGVAE) as an alternative therapeutic approach for benign breast lesions. In addition, it evaluates the procedure’s performance, associated complications, and clinical outcomes. This single-center, retrospective cohort study, approved by the Institutional Review Board, included 67 female patients who underwent UGVAE for breast lesions using 7 - 10 G needles. The study analyzed various parameters, including patient demographics, imaging features, and follow-up findings. Indications for UGVAE included patient preference, pain, palpable lump, nipple discharge, discordant biopsy results, and interval increase in breast imaging-reporting and data system (BI-RADS) 3 lesions. Lesion size, shape, echogenicity, and location were assessed through ultrasound and mammography. UGVAE was performed by two experienced radiologists, and post-procedure complications were documented. Data were analyzed using the Statistical Package for the Social Sciences and descriptive statistical methods. The mean age of the study population was 41.8 ± 14 years, and the mean lesion size was 1.7 ± 0.85 cm. A previous biopsy of the lesion was recorded in 19.4% of cases, and 7.5% of the patients had a history of breast cancer. The indications for UGVAE included patient preference (22.4%), pain (16.4%), palpable lump (14.9%), and an interval increase in BI-RADS 3 lesions (17.9%). Abnormal mammographic findings were reported in 95.1% of cases. Sonographic features predominantly included circumscribed (94%) and oval (73.1%) lesions. Complete excision was achieved in 80.6% of cases, and hematoma occurred in 13.4% of patients as a post-procedure complication. Histopathological results confirmed all lesions as benign, with fibroadenoma being the most common diagnosis (50.7%). Follow-up imaging showed no significant residual lesion in 46.3% of patients. UGVAE is considered a cost-effective, minimally invasive, and safe alternative to surgical excision for benign breast lesions.

Patients suffering from ulcerative colitis (UC) experience periods of remission and relapse that could affect their mental health. The study aimed to use logistic regression analysis in a novel way by incorporating locus of control (LOC), expressed emotion (EE), and quality of life (QOL) as predictors of UC. This study involved 100 individuals with UC and 100 healthy controls, focusing on LOC groups (internal, chance, powerful others), EE, and QOL. This model also helped to better understand how these psychological variables interact to predict the likelihood of a UC diagnosis. The results revealed all significant predictors. EE corelates positively with UC probability (Estimate: 0.191, p < 0.001), whereas QOL corelates inversely (Estimate: −0.150, p < 0.001). The model had a classification accuracy of 82.5%. While trends in LOC groups warrant further exploration, the model contributes to understanding psychological risk factors in UC. This research suggests the potential use of these factors as predictive markers. It adds to the existing literature on how psychological factors influence health results, offering practical implications for clinical care and guiding future investigations to improve the management and comprehension of UC.

Oral squamous cell carcinoma (OSCC) is one of the most common malignancies globally. Current treatment modalities, including chemotherapy and radiotherapy, often result in adverse effects that compromise the quality of life for patients. An alternate approach involves using phytocomposites as substitutes for commercial chemotherapeutic agents, potentially offering improved therapeutic outcomes with minimal adverse effects. The study aims to investigate the anticancer effects of phytocomposites in OSCC. A literature search was performed to select relevant phytocomposites for the analysis. The chosen compounds included tecomaquinone I, brevilin A, erybraedin A, evodiamine, and sumadain C. Bioactive compound information was extracted using online software tools, such as ZINC15, SwissADME, PharmaGist, and ZINCPharmer. The target protein for this study was Harvey rat sarcoma virus oncogene and its structure was obtained from the Protein Data Bank. On evaluating the binding affinities of these phytocomposites to the target protein, it was found that ZINC94088045 and ZINC94241870 exhibited the highest binding affinities, with values of -18.71 and -15.75 kcal/mol, respectively. These compounds also demonstrated favorable pharmacokinetic properties, with total polar surface area values of 85.11 Ų and 122.39 Ų, log P values of 2.59 and 1.77, and bioavailability scores of 0.55 and 0.56, respectively. Notably, these compounds also showed high gastrointestinal absorption and low cytotoxicity. The final phytocomposite combination displayed a strong binding affinity to the target protein while maintaining low cytotoxicity. This study highlights the potential anticancer effect of phytocomposites on OSCC with negligible cytotoxicity, offering a promising alternative to conventional treatments.

Detecting and distinguishing between ovarian endometriotic cysts and ovarian cystadenomas using computed tomography (CT) scans is a clinical challenge due to their similar CT characteristics. This study aims to identify key CT and clinical features that can effectively differentiate these two diseases and to develop a simple and practical scoring system. We conducted a retrospective analysis of 202 patients who underwent pre-operative contrast-enhanced CT at two medical centers. The subjects were divided into training cohort (n=151) and validation cohort (n=51). Utilizing univariate analyses and binary logistic regression, predictive factors for ovarian endometriotic cysts and ovarian cystadenomas were identified to construct an initial model. Subsequently, a scoring system was developed by assigning weights to each feature based on the initial model. The accuracy of both models (the initial model and the scoring system) was quantified by calculating the area under the receiver operating characteristic curve (AUC). We further determined the optimal cutoff point for the scoring system (0 - 15 points) and established three predictive ranges based on the probabilities of ovarian endometriotic cyst occurrence (<7 points; 7 - 8 points; >8 points). The initial model, which incorporated two clinical factors (age and CA125level) and three CT characteristics (wall thickness, density heterogeneity, and edgeadhesion), demonstrated an AUC of 0.993. In the training cohort, the proportionsof patients correctly diagnosed with ovarian endometriotic cysts within these threescore ranges were 0%, 38.89%, and 96.83%, respectively, while in the validationcohort, they were 0%, 33.33%, and 95.00%. Thus, having a refined scoring range canhelp improve diagnostic accuracy, with a higher score indicating a diagnosis withovarian endometriosis cysts, and assist with differentiating patients with differentrisk levels.

Chronic subdural hematoma (CSDH) is a chronic hemorrhagic lesion caused by the accumulation of blood between the arachnoid mater and the dura mater. Currently, the most commonly used surgical approach for CSDH is burr hole craniotomy. However, this procedure employs a blind technique, making the cerebral cortex susceptible to injury. The use of a subdural catheter guidance device combined with burr hole drainage in the treatment of CSDH can prevent intraoperative cerebral cortex damage and reduce its potential impact. This study retrospectively analyzed a total of 518 patients with CSDH who underwent surgical treatment at the hospital. Of these, 361 were male (69.69%) and 157 were female (30.31%), with a median age of 59.5 years (range: 12 - 92 years). All patients underwent preoperative head computed tomography and/or magnetic resonance imaging scans, which revealed crescent-shaped mixed-density or iso-dense shadows beneath the inner table of the skull. Informed consent for the burr hole decompression procedure was obtained from all patients. Subsequently, the 518 patients were randomly divided into two groups: The control group (undergoing the procedure without a “guidance device”) and the experimental group (undergoing the procedure with a “guidance device”). All patients provided consent for the publication of their clinical details and related images. In the control group, 274 patients with CSDH were treated, among whom 6 cases had post-operative cortical injury complications, with an incidence rate of 2.19%. In the experimental group, 244 patients with CSDH were treated, and no cortical injury complications occurred post-operatively, with an incidence rate of 0. Fisher’s exact test (two-tailed) showed p=0.0427, indicating a significant reduction in cortical injury complications with the use of the guidance device. In addition, the conditional maximum-likelihood estimate (CMLE) odds ratio for Fisher’s exact test was 0, with a 95% confidence interval ranging from 0.0 to 0.9447, further reflecting the relationship between the relevant factors. This indicates that incorporating a subdural catheter guidance device during burr hole drainage for CSDH can assist surgeons in avoiding damage to the cerebral cortex.

Coronary atherosclerosis (CA) is a chronic cardiovascular disease characterized by the accumulation of lipid plaques in coronary arteries, leading to vascular narrowing and impaired myocardial blood supply, which can result in severe complications, such as angina and myocardial infarction, and may even be life-threatening. Despite advancements in CA treatment, including medication and surgery, the complex mechanisms of plaque formation result in some patients responding poorly to existing therapies, and specific targets for precision treatment remain unclear. The present study utilized Mendelian randomization (MR) to investigate therapeutic targets for CA. Cis-expression quantitative trait loci (cis-eQTL, exposure data) were obtained from the eQTLGen consortium, which includes a sample of 31,684 individuals. Summary statistics for CA (outcome data) were obtained from the largest CA genome-wide association studies dataset, covering 456,348 individuals (including 16,041 cases and 440,307 controls), supplemented with data from the UK Biobank and FinnGen studies for external validation. Colocalization analysis was employed to examine whether CA risk and gene expression were driven by a shared single nucleotide polymorphism, thereby determining colocalized signals. Subsequently, drug prediction and molecular docking analysis were conducted to validate the druggability and pharmacological potential of the target genes, identifying promising therapeutic targets. The MR analysis identified nine drug targets, four of which were supported by colocalization, providing further evidence of their significance. Phenome-wide association studies analysis displayed no significant association between the DHX36 gene and other phenotypes. These genes potentially regulate CA by influencing specific metabolite levels. Molecular docking results indicated good binding affinity between multiple candidate drugs and proteins encoded by the target genes. Our study identified nine potential drug targets associated with CA, with four targets further supported for reliability. Given the roles of these genes in inflammation and metabolic regulation, drug development targeting these genes holds significant clinical potential. This study provides genetic evidence supporting the potential therapeutic benefits of targeting four druggable genes for CA treatment, which will aid in the development of CA drugs.

The KEYNOTE-A18 trial recently demonstrated the benefits of first-line treatment with programmed cell death protein 1/programmed death ligand 1 (PD-1/PD-L1) inhibitors for advanced cervical cancer. Herein, we investigated this using real-world data from a large Chinese cohort. From January 2020 to June 2023, 91 patients diagnosed with advanced cervical cancer receiving first-line systemic therapy incorporating PD-1/PD-L1 inhibitors were recruited as the treatment group, while 101 patients who did not receive PD-1/PD-L1 inhibitors were included as the control group. Baseline characteristics, including patient age, the International Federation of Gynecology and Obstetrics (FIGO) stage, histological subtypes, tumor diameter, PD-L1 expression, overall survival (OS), and progression-free survival (PFS), were extracted from the medical records. Survival analysis was performed utilizing the Kaplan-Meier curve and Cox regression analysis was used to compare the effects of different factors on patients’ survival. The addition of PD-1/PD-L1 inhibitors significantly prolonged PFS compared to the control group (median PFS: 19 vs. 11 months, p=0.000). Stratified analysis showed that higher expression of PD-L1 (median PFS: 14 vs. 14 months, p=0.031), earlier FIGO stage (median PFS: 20 vs. 11 months, p=0.000), and tumor diameter ≤4 cm (median PFS: 47 vs. 12 months, p=0.000) were associated with a better PFS. No statistical difference was detected in OS between the two groups. In the stage IVB subgroup, PD-1/PD-L1 inhibitors showed no benefits in either OS or PFS. Moreover, Cox regression analysis showed that only the use of PD-1/PD-L1 inhibitors was associated with prolonged PFS (hazard ratio = 0.43, 95% confidence interval 0.30 - 0.61, p=0.000). The first-line treatment containing PD-1/PD-L1 inhibitors significantly delayed tumor recurrence, especially for those with positive expression of PD-L1 and relatively small tumors.

Although it usually appears in the first 4 weeks after delivery, postpartum depression (PPD) is a form of depression that can strike at any time within a year after childbirth. Generally, the symptoms of PPD subside after 3 months of giving birth. The risk factors should be identified to determine the prevalence of PPD. In this study, we conducted a cross-sectional survey in which women (n = 400) attending four main healthcare facilities in Baghdad, Iraq, who were in 6 - 8 weeks postpartum, were recruited from January 18 to February 25, 2024. Systematic random sampling was used to select the participants. The Edinburg Postpartum Depression Scale (EPDS) was employed to assess the symptoms of PPD, with a cutoff score of ≥ 12. Among the 400 participants in the study, 202 (50.5%) of the participants complained of having PPD. Approximately 216 (54%) of the participants were between the ages of 20 and 29, and 320 (80%) of them were housewives. This analysis found a significant association of PPD occurrence with the level of education (p = 0.018), complications that happened to the mothers during or after delivery (p = 0.0001), preference of the sex of the last baby (p = 0.014), family support after delivery (p = 0.001), quality of relationship with their partners (p = 0.006), and previous symptoms of depression before or during the past pregnancy (p = 0.0001). Nearly half of the women suffer from PPD during their puerperium, and it is substantially linked to the child’s sex, postpartum difficulties, history of depressive disorders, and lack of parental assistance. Half of the participants suffered from PPD, significantly associated with a lack of education, family support, maternal complications, and undesirable newborn sex.

Observational studies have revealed inconsistent findings regarding the association between Vitamin D levels and head-and-neck cancer (HNC). Therefore, this study aimed to examine the possible causality of Vitamin D for HNC risk using two-sample Mendelian randomization (MR) and multivariable MR (MVMR) analyses. Single-nucleotide polymorphisms closely associated with Vitamin D levels were selected from the genome-wide association research database as instrumental variables. The analytical approaches utilized included inverse variance weighted (IVW), MR-Egger, weighted median, simple mode, and weighted mode. Sensitivity analysis was performed to verify the robustness of MR findings. In addition, the causation of Vitamin D on HNC risk was assessed by controlling for the influences of smoking and alcohol intake through MVMR analysis. IVW (odds ratio = 0.9958, 95% confidence interval = 0.9934 - 0.9983, p = 0.0007) indicated that Vitamin D levels were negatively related to HNC risk. The weighted median yielded the same result. The results of the MVMR analysis further supported the role of Vitamin D in mitigating HNC risk. The sensitivity analysis revealed the absence of heterogeneity or pleiotropy of the instrumental variables, proving our results reliable without significant bias. This study offers genetic evidence in favor of the causality of Vitamin D for HNC risk. Increasing Vitamin D intake may help lower HNC risk.

Bladder cancer (BC) is the most prevalent malignancy of the genitourinary system, exhibiting the highest morbidity and mortality rates among cancers in this category. Tetramethyl thyroxine (T4) has been recognized to promote the proliferation of various cancer cells. However, the possible effect and underlying mechanisms of T4 on the onset and progression of BC remain to be fully elucidated. Our research demonstrated that T4 significantly promoted the proliferation and migration of EJ-1 and T24 cells. The proliferation of T24 and EJ-1 cells increased by 5 - 28.3% and 4.7 - 18.7%, respectively. Similarly, the scratch healing rates of T24 and EJ-1 cells increased by 9.27 - 41.01% and 11.47 - 35.8%, respectively. In addition, apoptosis of T24 and EJ-1 cells was also significantly reduced after T4 treatment. Furthermore, in vivo xenograft tumor model further corroborated that T4 facilitated the growth of EJ-1 cell-derived tumors. Our findings indicated that T4 promoted tumor angiogenesis and cell proliferation by upregulating its receptor integrin αV and vascular endothelial growth factor, while simultaneously suppressed the expression of the tumor suppressor protein TP53. Collectively, our research has determined the tumor-promoting effect and molecular mechanism of T4 on BC through cell and animal models. In the future, by further expanding the sample size and pre-clinical design, it is expected to provide new theoretical foundations and potential targets for the prevention, diagnosis, and treatment of BC.

Post-stroke depression (PSD) affects approximately one-third of stroke survivors, and current treatments often present limitations. Non-invasive therapies such as repetitive transcranial magnetic stimulation (rTMS) and horticultural therapy (HT) are gaining interest as alternative approaches. This study aimed to evaluate the clinical efficacy of rTMS combined with HT in treating PSD. Eighty PSD patients (aged 30 - 75 years old; 1 month - 2 years post-stroke), diagnosed according to the Chinese Expert Consensus on Clinical Practice of Post-Stroke Depression, were randomly assigned to one of four treatment groups: Group A (antidepressant alone—escitalopram, 10 mg/day), Group B (antidepressant + rTMS), Group C (antidepressant + HT), and Group D (antidepressant + rTMS + HT). rTMS was administered to the left dorsolateral prefrontal cortex (10 Hz, 110% motor threshold, 15 min/session, 5 days/week), while HT consisted of 45-min gardening activities (e.g., planting, pruning, watering) conducted 5 days/week. Patients were evaluated using the Hamilton Depression Scale (HAMD), Hamilton Anxiety Scale (HAMA), and Stroke-Specific Quality of Life Scale (SS-QOL) before and after the 28-day intervention. Seventy-seven patients completed the trial, with three dropouts. All groups showed significant reductions in HAMD and HAMA scores post-treatment compared to baseline (p<0.01). Group D demonstrated a statistically significant improvement in SS-QOL scores (p<0.01), while other groups did not (p>0.01). No significant difference in HAMD scores was found between Groups B and C (p=0.399). These results suggest that combining rTMS and HT provides greater benefits in managing PSD compared to either intervention alone. No serious complications were reported. This study supports the integration of rTMS and HT as an effective adjunct to standard antidepressant therapy for PSD.

Acute liver injury is a severe clinical condition with potentially fatal consequences commonly caused by viral infections, medications, toxins, and drug overdoses. Among these, paracetamol (acetaminophen) overdose is a leading cause of hepatic failure due to its narrow therapeutic index, resulting in oxidative stress and hepatocyte apoptosis. Quercetin, a flavonoid found abundantly in vegetables and herbs, has demonstrated antioxidant, hepatoprotective, and anti-inflammatory properties. This study evaluates the hepatoprotective role of quercetin in mitigating liver damage induced by paracetamol overdose in an experimental rat model. A total of 28 male rats were randomly divided into four groups (n = 7 per group): (i) normal control (distilled water and saline), (ii) paracetamol-induced liver injury group (2 g/kg paracetamol intraperitoneally), (iii) paracetamol + quercetin group (50 mg/kg quercetin orally and 2 g/kg paracetamol intraperitoneally), and (iv) quercetin-only group (50 mg/kg quercetin intraperitoneally). Blood and liver samples were analyzed for liver enzymes (glutamate pyruvate transaminase [GPT], glutamate oxaloacetate transaminase [GOT]), inflammatory markers (nuclear factor kappa B [NF-κB], tumor necrosis factor-alpha [TNF-α]), apoptotic markers (cysteine-aspartic acid protease 3 [Caspase-3], B-cell lymphoma 2 [BCL2]), oxidative stress markers (malondialdehyde [MDA], glutathione [GSH]), and histological changes. Paracetamol administration significantly elevated GPT, GOT, NF-κB, TNF-α, caspase-3, and MDA levels whereas reducing BCL2 and GSH levels, indicating hepatic injury and oxidative stress. In contrast, results showed that quercetin treatment significantly mitigated these changes, demonstrating its potential hepatoprotective effects. Histological analysis further confirmed that quercetin reduced hepatic damage compared to the paracetamol-only group. These findings suggest that quercetin exerts a protective effect against paracetamol-induced liver injury by reducing oxidative stress, inflammation, and apoptosis.

Colorectal cancer is a prevalent malignancy, with colon adenocarcinoma as the most common type. Early diagnosis biomarkers and effective risk stratification are crucial for optimal treatment. In this study, gene expression data from the Cancer Genome Atlas and Gene Expression Omnibus (GEO) were analyzed to identify relevant genes for colon adenocarcinoma. These datasets were standardized and subjected to weighted gene co-expression network analysis and differentially expressed gene analysis. Univariate Cox regression and least absolute shrinkage and selection operator Cox regression analyses were performed to generate a risk profile and identify prognosis-related genes. Receiver operating characteristic (ROC) analysis, Kaplan-Meier (KM) curve, and Cox analyses validated the risk signature. Immune cell infiltration patterns and immunological activities in high- and low-risk groups were assessed using single-sample gene set enrichment analysis (ssGSEA). GSEA was used to investigate the signaling pathways associated with low-risk and high-risk groups, whereas ssGSEA was used to analyze those associated with high-risk groups. A line graph was created to predict the overall survival (OS) of patients. Quantitative real-time polymerase chain reaction confirmed differential gene expression between normal and cancerous colon tissues. The eight genes identified - ACOX1, ATP8B1, CHGA, NAT2, PKIB, SLC39A8, TINAG, and VEGFA - correlated with tumor immunity and clinical outcomes. This eight-gene risk profile can accurately stratify risk and predict OS based on KM curves, ROC analysis, and regression models. GSEA analysis revealed calcium ion metabolism as the top pathway in the GEO dataset. These findings provide a foundation for prognostic evaluation and may guide therapeutic decision-making in colon adenocarcinoma.

Human papillomavirus (HPV) infection plays a crucial role in cervical carcinogenesis. The link between the autonomic nervous system and tumor biology is increasingly being recognized. Understanding how neural signaling pathways interact with HPV oncogenesis could open new avenues for therapeutic intervention. We aim to study the contribution of the autonomic nervous system-related genes to the HPV-associated cervical lesions. A population of 140 HPV-infected women presenting cervical lesions was compared to a control population. Genes/variants under study were: BDNF/rs6265, NTRK2/rs2289656, NGF/rs6330, SLC6A4/5-HTT variable number tandem repeats intron 2, HTR2A/rs6313, ADRBR2/rs1042713, and CHRNA5/rs16969968. Samples were genotyped using polymerase chain reaction (PCR), PCR-restriction fragment length polymorphism, and endpoint genotyping. Statistical analysis revealed a genetic contribution for SCL6A4, ADRB2, and CHRNA5. SCL6A4 showed statistically significant association in the codominant (p=0.003) and dominant models (p=0.024, odds ratio [OR] = 2.301). ADRB2 showed statistically significant association in the codominant (p<0.001), dominant (p=0.024, OR = 4.728), recessive (p<0.001, OR = 4.856), and allelic models (p<0.001, OR = 4.091), while CHRNA5 showed statistically significant association in the dominant model (p=0.030, OR = 0.529). We conclude that there is a genetic contribution of the adrenergic (ADRB2), cholinergic (CHRNA5), and serotonergic (SLC6A4) systems to cervical lesions associated with HPV infections.

Colorectal cancer (CRC) is the third most common cancer in men and the second most common in women, with a 5-year survival rate. The disease burden of CRC can be exacerbated by a sedentary lifestyle, lack of physical exercise, smoking, and obesity. Angiopoietin-like protein 8 (ANGPTL8), a liver hormone, plays a crucial role in lipid and glucose metabolism and is also implicated in the development of certain cancers. However, the basic profile and activity of this hormone in CRC with liver metastasis remains unknown. This study aims to establish the baseline expression of ANGPTL8 in tumors of CRC patients with and without liver metastasis. After histopathological screening and computed tomography scans, 41 patients were identified and included in this study, consisting of 20 CRC patients without liver metastasis and 21 with liver metastasis. Tumor samples from each group were compared to their respective adjacent normal tissues. Quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay were employed to assess the ANGPTL8 expression at both mRNA and protein levels. The results show that ANGPTL8 expression is higher in tumors of CRC patients with liver metastasis compared to those without liver metastasis. ANGPTL8 expression is significantly correlated with body mass index (BMI) (Pearson’s correlation coefficient = −0.367, p≤0.05) and could serve as a significant predictor of BMI (p≤0.05). These findings suggest that ANGPTL8 may enhance tumor development in CRC patients and is associated with body weight changes, contributing to weight loss symptoms during metastasis.

Introduction: Osteoporosis (OP) is a systemic skeletal disease characterized by reduced bone mass and deteriorated bone microstructure, significantly increasing fracture risk. As global aging intensifies, OP has become a significant public health issue. Present pharmacological interventions, such as bisphosphonates and selective estrogen receptor modulators, are associated with side effects and limitations, highlighting the need for safe and effective alternatives. Objective: This study investigates the potential mechanisms of the Qiang-gu-jian-shen formula (QGJSF), a traditional Chinese medicine (TCM) compound, in treating OP using network pharmacology and bioinformatics. Methods: A total of 1,395 potential targets for QGJSF were identified by querying the TCMSP and BATMAN-TCM databases and converting targets through UniProt. Cross-referencing with OP-related targets from GeneCards, OMIM, and DisGeNET yielded 500 mapped targets. Protein-protein interaction network constructed through the STRING database led to the identification of 69 core targets. An “herb-active component-target” network was built using Cytoscape 3.9.0. Gene ontology functional annotation and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses highlighted key pathways, including the PI3K/AKT and FoxO. Results: Molecular docking showed that key components, such as quercetin, dioscin, genistein, calycosin, and berberine, bind favorably to core targets (binding energies < −5 kcal/mol). GEO dataset (GSE5958) analysis identified seven common core genes, including TGFB1, MMP2, BCL2L1, MAPK3, AKT1, CTNNB1, and TP53. The findings suggest that QGJSF may improve OP through multiple components that regulate osteoblast differentiation, osteoclastogenesis, and activate key pathways, such as Wnt/β-catenin, PI3K/AKT, and JAK/STAT, thereby enhancing bone formation and reducing resorption. Core targets such as ESR1, STAT3, AKT1, and TP53 regulate bone metabolism by modulating osteoblasts, osteoclasts, and their interactions with immune and hematopoietic cells to maintain bone remodeling. Conclusion: This study advances understanding of QGJSF’s mechanisms and provides a foundation for novel OP therapies. Future validation and exploration of additional therapeutic targets and mechanisms are needed.