Metaplastic breast carcinoma, a rare entity (<1% of breast neoplasms), lacks comprehensive spectroscopic characterization. This study aimed to address this gap by providing a qualitative and quantitative spectroscopic profile of metaplastic carcinoma in comparison to ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC).

A retrospective analysis was conducted on archival tissue blocks of metaplastic carcinoma (n = 10), DCIS (n = 12), and IDC (n = 31). Sections were stained with hematoxylin and eosin for histological confirmation. Attenuated total reflectance Fourier-transform infrared spectroscopy was performed on adjacent unstained sections, with normal breast tissue (n = 10) serving as the control. Spectral data were analyzed using t-tests to identify significant differences in peak intensities and ratios. Hierarchical clustering analysis and receiver operating characteristic curves were generated to assess the diagnostic potential of selected spectral features.

Spectral analysis revealed that mean peak intensities were generally lower in all carcinoma subtypes compared to normal breast tissue. Specific ratios, including A1237/A1080 (phosphate; p < 0.01), A1043/1543 (glycogen; p < 0.01), and A1080/A1632 (nucleocytoplasmic index; p < 0.03), were significantly elevated in carcinomatous tissues. Receiver operating characteristic analysis identified peak 3,280 (area under the curve (AUC) = 0.93–0.96) as highly effective in differentiating normal from carcinomatous tissues. Peak 2,922 showed specificity for distinguishing normal tissue from IDC (AUC ≈ 0.7). Peak 1,744 effectively discriminated between DCIS and metaplastic carcinoma (AUC = 0.7). The ratio 1,080/1,632 (nucleocytoplasmic ratio) demonstrated exceptional diagnostic accuracy, distinguishing normal from carcinomatous tissues (AUC ≈ 1.0), DCIS from IDC (AUC ≈ 0.86), and DCIS from metaplastic carcinoma (AUC ≈ 0.8).

Attenuated total reflectance Fourier-transform infrared spectroscopy, particularly using peak 3,280 (Amide A) and the 1,080/1,632 ratio (nucleocytoplasmic index), offers a promising approach for discriminating between normal breast tissue and carcinoma, as well as differentiating pre-IDC from metaplastic carcinoma. These spectral markers demonstrate both statistical significance and diagnostic potential.

Bacterial infections (BIs) are common and severe complications in patients with liver cirrhosis, but global data are limited. Here, we aimed to evaluate the global prevalence, temporal changes, and associated mortality risk of BIs in liver cirrhosis.

We systematically searched PubMed, Embase, Web of Science, and the Cochrane Library for eligible studies published without language restrictions until 11 August 2025. A random-effects model was used for meta-analyses, meta-regression by study year, and pooling adjusted hazard ratios.

Fifty-nine studies, including 1,191,421 patients with cirrhosis, were analyzed. The pooled prevalence of BIs (33 studies) was 35.1% (95% confidence interval (CI): 29.2–41.4). The prevalence of Escherichia coli and Streptococcus spp. was 3.8% (95% CI: 2.5–5.2) and 1.5% (95% CI: 0.8–2.6), respectively. The pooled prevalence of multidrug-resistant bacteria was 6.8% (95% CI: 4.0–11.3). The most common BI sites were the gastrointestinal tract, ascites fluid, and urinary tract. The highest prevalence of BIs was reported in Europe (38.2%; 95% CI: 24.8–53.6), followed by South America (37.5%; 95% CI: 29.7–46.1) and Asia (22.8%; 95% CI: 16.3–30.9). Patients with acute-on-chronic liver failure showed the highest prevalence of BIs (44.2%; 95% CI: 29.7–59.8). A modest increasing trend in BIs prevalence was observed over time. BIs were associated with an increased risk of mortality in patients with cirrhosis (adjusted hazard ratios 2.22, 95% CI 1.33–3.71).

BIs are prevalent in cirrhosis, especially in acute-on-chronic liver failure, with a modest upward trend and increased mortality risk.

In the past decade, immune checkpoint inhibitors (ICIs) have dramatically changed cancer treatment, significantly improving outcomes for patients with various malignancies. Nonetheless, their widespread application has resulted in a rise in immune-related adverse events due to excessive immune activation, including immune-mediated hepatotoxicity (IMH). IMH can cause serious complications and even death, underscoring the need for early prediction and intervention. This review outlines the current understanding of risk factors and predictive biomarkers for IMH in cancer patients undergoing ICI therapy, with risk factors divided into patient-associated, tumor-associated, and agent-associated categories. Higher IMH risk is related to female sex, younger age, extreme BMI, Asian ethnicity, and chronic liver disease. Cancer type, prior ICI treatment, dual ICI combination therapy, and the concurrent use of chemotherapy, targeted agents, or other hepatotoxic drugs (e.g., acetaminophen, statins) also increase the risk of IMH. Potential predictive biomarkers encompass circulating blood cells, serum proteins, autoantibodies, cytokines, gene profiles, and the gut microbiome. Despite promising findings, the predictive value of these biomarkers remains inconsistent, and no definitive biomarker has been established for routine clinical use. Large-scale prospective studies are essential to verify the predictive value of these biomarkers and facilitate their integration into clinical practice, thereby providing deeper insights into the early identification and individualized management of IMH during ICI therapy.

Uterine fibroids (UFs) are common hormone-dependent tumors with a complex etiology involving both genetic and environmental factors. This study aimed to investigate, for the first time, the associations between loci from genome-wide association studies (GWAS) and environmental risk factors in UF development, with a particular focus on gene–environment interactions.

DNA samples from 737 women with UF and 451 healthy controls were genotyped for ten UF-associated GWAS single nucleotide polymorphisms (SNPs) using probe-based polymerase chain reaction in this case-control study.

SNP rs66998222 (LOC102723323, G/A) was associated with decreased UF risk in the total sample (odds ratio (OR) = 0.81, p = 0.038) and in patients with a history of induced abortion (OR = 0.70, p = 0.009). SNP rs11031731 (THEM7P, WT1, G/A) increased UF risk overall (OR = 1.39, p = 0.01), and in women with abortion history (OR = 1.60, p = 0.008) or without pelvic inflammatory disease (OR = 1.43, p = 0.02). SNPs rs641760 (PITPNM2, C/T) and rs2553772 (LOC105376626, G/T) showed protective effects depending on abortion history. SNP rs1986649 (FOXO1, C/T) was associated with later UF onset (p = 0.049) and slower growth (p = 0.017). GWAS loci influence UF-related genes involved in proliferation, inflammation, and hormone metabolism, underscoring their pathogenic role.

Induced abortions and inflammation modify the effects of GWAS-identified UF risk loci, with allele-specific impacts on hormonal, inflammatory, and repair pathways. Replication in diverse cohorts is needed to validate these population-specific effects.

Cortisol, the body’s primary glucocorticoid, is central to maintaining homeostasis through its regulation of metabolism, immunity, cardiovascular tone, and neurobehavioral functions. However, chronic dysregulation of the hypothalamic–pituitary–adrenal axis, whether from persistent psychological stress, lifestyle imbalance, or circadian disruption, contributes to diverse metabolic, psychiatric, and inflammatory disorders. This comprehensive review aims to explore cortisol physiology, mechanisms of dysregulation, and emerging strategies for restoring hormonal balance through integrative management. Conventional approaches such as pharmacotherapy and surgical interventions remain essential for severe endocrine disorders like Cushing’s syndrome and Addison’s disease; however, they inadequately address chronic, stress-related dysfunction. Nutritional modulation, sleep optimization, moderate physical activity, and mind-body therapies, including yoga, meditation, and mindfulness-based stress reduction, demonstrate measurable reductions in cortisol and inflammatory cytokines. Adaptogenic botanicals such as Withania somnifera, Ocimum tenuiflorum, Rhodiola rosea, and Panax ginseng exhibit robust evidence for normalizing cortisol and enhancing resilience through hypothalamic–pituitary–adrenal axis modulation. Complementary modalities such as acupuncture, naturopathy, and homeopathy show potential in improving autonomic and neuroendocrine balance. By synthesizing biomedical, nutritional, psychological, and traditional perspectives, this review proposes an integrated model of cortisol management that harmonizes physiology and behavior. Such multidimensional frameworks offer promising, evidence-based pathways for mitigating stress-related diseases and promoting holistic well-being.

MD-1 is a time-tested polyherbal diabetes supplement in Tamil Nadu, India. It is composed of dried powdered herbs: Phyllanthus amarus Schum. & Thonn, Tinospora cordifolia (Willd.) Miers ex Hook. F. & Thoms, Emblica officinalis Gaertn., Eugenia jambolana Lam., Gymnema sylvestre R. Br. Ex, and Cassia auriculata Linn. This study aimed to investigate the in vivo effects of MD-1 in high-fat diet (HFD)-induced diabetes mellitus in C57BL/6J mice.

After 10 weeks of HFD induction, diabetic mice (n = 60) were randomized to 21-day treatments with MD-1, metformin, or left untreated on a standard pellet diet. Fasting blood glucose, triacylglycerol (TAG), total cholesterol, and liver tissue markers including superoxide dismutase, glutathione peroxidase, glutathione, thiobarbituric acid reactive substance, glucokinase, fructose-1,6-bisphosphatase, and glucose-6-phosphatase expressions were measured. Adipose tissue tumor necrosis factor (TNF)-α infiltration and messenger RNA expression of peroxisome proliferator-activated receptor γ (PPAR-γ) and glucose transporter type 4 (Glut4) were also analyzed.

MD-1 treatment significantly reduced elevated fasting blood glucose, TAG, and total cholesterol in HFD-fed mice and countered HFD-induced weight gain despite unchanged caloric intake. Improved adipose tissue function was evidenced by reduced TNF-α infiltration and increased messenger RNA expression of PPAR-γ and Glut4. MD-1 attenuated HFD-induced fatty liver disease by reducing oxidative stress and TAG accumulation, suggesting a possible two-hit mechanism.

MD-1 administration primarily targets adipose tissue TNF-α signaling in HFD mice, restoring function via PPAR-γ/Glut4 expression. These findings support its glycemic intervention potential and justify its supplementation in diabetes.

Sclerocarya birrea (A. Rich) Hochst (Anacardiaceae) is a plant widely used by traditional healers in several African countries to treat numerous illnesses such as Alzheimer’s disease, schizophrenia, inflammation, infections, arterial hypertension, headaches, and others. This study aimed to determine the therapeutic efficacy of Sclerocarya birrea (S. birrea) against glutamate-induced neurotoxicity.

Thirty naïve white mice (Mus musculus Swiss, Muridae), of both genders and weighing between 18 and 25 g, were used in the experiments. Different doses (102.5, 205, and 410 mg/kg) of the extract and vitamin C (100 mg/kg) were administered to the animals one hour before administration of monosodium glutamate (4 mg/kg) for 15 consecutive days. T-maze and Y-maze tests were conducted over three days to assess the animals’ behavioral performance. After behavioral testing, the animals were sacrificed and their brains removed for analysis of oxidative stress parameters.

S. birrea extract reversed glutamate-induced behavioral alterations by significantly (P < 0.001) reducing the latency to reach the platform in the T-maze and significantly increasing the percentage of spontaneous alternation in the Y-maze. The extract also significantly counteracted (P < 0.001) glutamate-induced oxidative stress parameters. The 102.5 and 205 mg/kg doses of the extract significantly (P < 0.001) reduced catalase and reduced glutathione levels, as well as the increase in malondialdehyde levels induced by glutamate.

S. birrea root bark extract exhibits neuroprotective properties that facilitate memory and ameliorate glutamate-induced cognitive deficits in white mice. The results provide partial justification for the traditional medicinal use of S. birrea extract.

Dysphagia, a severe comorbidity of many neurological diseases, often lacks targeted therapies. Electrical stimulation of cranial nerves represents a novel therapeutic class. This critical review assessed the clinical effectiveness and safety of various approaches for electrical stimulation of the cranial nerves for treating dysphagia, categorized as implantable (directly targeting the nerve), minimally invasive (pharyngeal electrical stimulation), and non-invasive (transcutaneous). A critical literature review was conducted following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. The PubMed database was comprehensively searched, and studies were rigorously assessed for inclusion and exclusion criteria. The Newcastle–Ottawa Scale was used to assess the risk of bias. The analysis included 15 clinical studies: four assessing vagus nerve stimulation (including implantable and transcutaneous approaches) and eleven assessing pharyngeal electrical stimulation. Most evaluated studies, particularly for pharyngeal electrical stimulation and transcutaneous vagus nerve stimulation, demonstrated significant beneficial effects on validated dysphagia outcome measures. Importantly, no long-term severe adverse effects were reported across the evaluated stimulation approaches. Cumulative evidence indicates that vagus nerve stimulation and pharyngeal electrical stimulation approaches can effectively alleviate dysphagia symptoms. The different stimulation approaches appear to be complementary, with distinct profiles rendering them suitable for different therapeutic contexts (e.g., short-term hospital-based vs. long-term at-home treatment). Consequently, they represent distinct and valuable options for individualized dysphagia therapy.

A long-term high-fat diet (HFD) exerts lipotoxic effects on multiple organs, particularly the liver, leading to metabolic diseases. This study aimed to delineate the dynamic effects of HFD on lipid metabolism, elucidate the mechanisms underlying hepatic lipotoxicity, and investigate the protective effects of Ganoderma lucidum against lipotoxicity both in vitro and in vivo.

C57BL/6 mice were fed either a 45% or 60% HFD, followed by measurements of body composition, serum lipid profile, and liver pathology at four, eight, twelve, and sixteen weeks. Inflammatory responses, the unfolded protein response (UPR), and endoplasmic reticulum (ER)-phagy were examined in the livers of mice at 16 weeks. Male C57BL/6 mice were randomly assigned to four groups (n = 12 per group): normal diet, 45% HFD, and two HFD + Ganoderma lucidum water extract (GLE) groups (1 g/kg/d and 2 g/kg/d of crude drug, orally administered by gavage for eight weeks following a four-week HFD induction).

Body weight, body fat, serum lipids, and hepatic steatosis increased progressively, accompanied by impaired glucose tolerance and liver injury, as indicated by elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. HFD also induced activation of the STING and NF-κB signaling pathways, as well as the PERK and IRE1 branches of the UPR. Similarly, ER-phagy selective receptors, particularly FAM134B, which is primarily expressed in hepatocytes as shown by single-cell sequencing, were upregulated after 16 weeks of HFD feeding. Furthermore, GLE mitigated palmitic acid-induced lipotoxicity in primary hepatocytes, as evidenced by improved cell viability, reduced ALT, AST, and lactate dehydrogenase levels in the culture supernatant, and decreased transferase dUTP nick-end labeling-positive cell counts. In 45% HFD-fed mice, GLE reduced serum total cholesterol, low-density lipoprotein, and hepatic triglyceride levels.

HFD-induced lipotoxicity causes hepatic tissue injury and inflammatory responses, which may be alleviated by coordinated regulation of compensatory UPR and ER-phagy. Ganoderma lucidum shows promise as a dietary supplement for managing metabolic disorders.