Breast cancer remains one of the most common cancers affecting women globally, with late detection frequently contributing to its high mortality rate. Multiple factors drive these delays, including a lack of awareness, financial constraints in low-income countries, and limited access to non-invasive and accurate biomarkers. This review aims to introduce biomarkers, particularly hematological and biochemical serum markers, as essential, non-invasive, and accurate tools for improving the diagnosis, prognosis, and therapeutic management of breast cancer. Hematological markers are measurable blood parameters that reflect physiological and pathological processes such as inflammation, infection, cardiovascular stress, autoimmune conditions, and cancer. Routinely measured hematological markers, such as the neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and red blood cell indices, are typically obtained from standard tests like the complete blood count. Regular monitoring through complete blood count is essential during cancer treatment to evaluate changes in blood cell counts and detect potential adverse effects. Because of their affordability, minimal infrastructure requirements, and broad accessibility, hematological parameters have been increasingly studied for their association with high-risk factors in breast cancer, particularly in resource-limited settings. Their utility underscores their critical role in improving patient outcomes across diverse healthcare environments. This review summarizes the clinical value of various hematological and serum-based biochemical markers in the screening and diagnosis of breast cancer. Prediction methods that incorporate hematological and serum-based biochemical parameters can support screening, diagnosis, and staging. Overall, individual or combined blood indicators hold significant potential to enhance diagnostic accuracy and effectiveness.

Huo Xue Tong Luo Capsule (HXTL) has been clinically used to treat osteonecrosis of the femoral head, osteoporosis, and other bone and joint diseases with promising effects. Our previous study has shown that HXTL can promote osteogenesis in mesenchymal stem cells by inhibiting lncRNA-Miat expression through histone modifications. However, the mechanism by which HXTL treats postmenopausal osteoporosis (PMOP) remains unclear. In this study, we used network pharmacology-based mechanism prediction, molecular docking, and pharmacological validation to investigate the mechanism of HXTL in treating PMOP.

The key candidate targets and relevant signaling pathways of HXTL for PMOP treatment were predicted using network pharmacology and molecular docking analysis. RAW264.7 cells were used for Western blot to validate the predicted mechanistic pathways. The ovaries of mice were surgically removed to simulate PMOP. The effect of HXTL on PMOP was evaluated using tartrate-resistant acid phosphatase staining and immunohistochemical assays in vivo.

Network pharmacology analysis suggested that HXTL interacted with 215 key targets linked to PMOP, primarily affecting the PI3K-AKT signaling pathway. Molecular docking showed that the main components of HXTL exhibited strong binding affinity to NFATc1, p-PI3K, and p-AKT1. Furthermore, our in vitro results confirmed that HXTL suppressed the PI3K-AKT signaling pathway. In vivo, HE and tartrate-resistant acid phosphatase staining results showed that HXTL inhibited osteoclast formation and protected bone mass.

This research demonstrated that HXTL could inhibit osteoclast formation and prevent bone loss induced by ovariectomy in mice by inhibiting the PI3K-AKT signaling pathway. These findings provide important evidence for the clinical application of HXTL in treating PMOP.

Prognostic scores are valuable tools for predicting survival in patients with chronic liver disease. Recently, the albumin-bilirubin (ALBI) score has emerged as a potential prognostic indicator in liver-related conditions. This study aimed to compare the prognostic efficacy of the ALBI score with the Model for End-stage Liver Disease (MELD), MELD-Na+, and Child-Turcotte-Pugh (CTP) scores in predicting survival among patients with alcohol-associated liver disease (ALD).

This study included consecutive ALD patients admitted to the Medicine and Gastroenterology wards of MKCG Medical College and Hospital, Berhampur, Odisha, India, between November 2019 and November 2022. Upon hospitalization, baseline characteristics, clinical and laboratory parameters, ALBI, MELD, MELD-Na+, and CTP scores were recorded. The accuracy of these scores in predicting survival up to three years was compared.

A total of 490 ALD patients were included. Higher ALBI scores were observed in patients who died during hospitalization (p < 0.001), at 28 days (p < 0.001), 90 days (p < 0.001), six months (p < 0.001), one year (p < 0.001), two years (p < 0.001), and three years (p < 0.001), compared to those who survived. However, the area under the receiver operating characteristic (AUROC) curves showed that the ALBI score was inferior to MELD, MELD-Na+, and CTP scores in predicting survival at admission [AUROC: ALBI (0.719), MELD-Na+ (0.823), MELD (0.817), CTP (0.770)] and at three years [AUROC: ALBI (0.755), MELD-Na+ (0.787), MELD (0.758), CTP (0.784)]. Furthermore, Cox regression analysis revealed that components used in the MELD, MELD-Na+, and CTP scores—such as serum creatinine, serum sodium, and hepatic encephalopathy—were independent predictors of mortality, whereas the components of the ALBI score (serum albumin and serum bilirubin) were not.

All hospitalized ALD patients had a grade 3 ALBI score, with significantly higher scores observed among non-survivors compared to survivors. However, MELD, MELD-Na+, and CTP scores were superior to the ALBI score in predicting survival both during hospitalization and over a three-year follow-up period.

Spinal cord injury (SCI) significantly impacts the central nervous system, with limited effective treatments available. Brain-derived neurotrophic factor (BDNF) plays a crucial role in neuronal growth, survival, and regeneration after SCI. MicroRNAs, particularly miR-124-3p, have been implicated in SCI pathophysiology. However, the relationship between miR-124-3p and BDNF in the context of SCI remains unclear. This study aimed to investigate the correlation between miR-124-3p expression and BDNF levels in a rat model of spinal cord injury and to assess how the timing of injury affects this relationship.

This study included 72 male Wistar rats divided into three groups: intact (n = 8), sham (n = 32), and SCI (n = 32). SCI diagnosis was confirmed through behavioral-motor function analysis using the Basso, Beattie & Brenham score and histological examination with crystal violet staining. The expression levels of miR-124-3p and BDNF were assessed using real-time polymerase chain reaction in all groups at four time points (one hour, one day, three days, and seven days post-injury).

In the SCI group, a marked reduction in miR-124-3p expression was observed relative to both the sham and intact groups. Conversely, there was a substantial elevation in BDNF expression within the SCI group in comparison to the sham and intact groups. The findings underscore a negative association between miR-124-3p expression and BDNF messenger RNA levels.

The downregulation of miR-124-3p and concurrent upregulation of BDNF suggest a potential regulatory role of miR-124-3p in modulating BDNF expression during SCI. These findings provide new insights into the molecular mechanisms underlying SCI and suggest that miR-124-3p and BDNF could serve as potential therapeutic targets. Further research is needed to explore the translational potential of these findings for developing novel diagnostic and therapeutic strategies for SCI.

Potential celiac disease (PCD) is defined as elevated celiac serology with a preserved small intestinal mucosa. This study aimed to identify baseline characteristics and the outcomes of children with PCD consuming a gluten-containing diet.

This was a retrospective cohort study of pediatric PCD patients diagnosed between 12/2018 and 10/2024. Baseline data included demographics, anthropometrics, clinical symptoms and signs, celiac serology, and biopsy results. Follow-up data included repeat serology and biopsy results when performed.

PCD was diagnosed in 75/517 (14.5%) children undergoing upper endoscopy for suspected celiac disease (CeD). Baseline anti-transglutaminase IgA (TTG) was above 10× the upper limit of normal (ULN) in 18 (24%), between 3–10× ULN in 52 (69.3%), and <3× ULN in five (6.6%). Anti-endomysial antibody was positive in 57 (76%). Among 48 children (64%) with at least one year of follow-up, TTG normalized in 26 (54.1%), decreased to <3× ULN in 13 (27.1%), was between 3–10× ULN in six (12.5%), and was above 10× ULN in three (6.3%). Nine children had a repeat endoscopy, and six (66.7%) were diagnosed with CeD, while three remained PCD. Among the 11 children with TTG >10× ULN and at least one year of follow-up, TTG normalized in three, declined in five, and increased or remained above 10× ULN in three.

PCD is common and may be found in children with TTG above 10× ULN; approximately half will normalize TTG. The omission of biopsies may result in an erroneous diagnosis of CeD.

Artificial intelligence (AI) is transforming the diagnosis, treatment, monitoring, and research of soft tissue disorders, which include muscles, tendons, ligaments, fascia, nerves, and blood vessels. Traditional diagnostic methods often rely on imaging, histopathology, and clinical evaluation, which can be time-consuming and prone to human error. This review aims to explore the impact of AI on enhancing soft tissue care. The review examines the application of deep learning algorithms in medical imaging, pathology, predictive analytics, and treatment planning. It also evaluates AI’s role in monitoring and rehabilitation, as well as its contributions to research in soft tissue disorders. AI significantly improves the accuracy of medical imaging analysis, facilitating the detection of abnormalities such as tumors and tears. AI-powered pathology tools automate slide analysis, enhancing diagnostic consistency and efficiency. Predictive analytics enable early risk assessment and personalized patient management. In surgical contexts, AI supports preoperative simulations and robotic-assisted procedures, leading to improved outcomes. Additionally, AI enhances patient monitoring through wearable devices and telemedicine. The integration of AI into soft tissue diagnostics and therapeutics presents transformative potential for personalized and efficient healthcare. However, challenges related to data security, algorithm bias, interpretability, and ethical considerations must be addressed. Overall, AI holds promise for improving patient outcomes and advancing medical science in the field of soft tissue disorders.

Despite advancements in diagnostic and therapeutic strategies, hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality. Antioxidant-1 (ATOX1) has been implicated in oncogenic processes across various cancer types; however, its specific role in HCC remains unclear. This study aimed to investigate the function of ATOX1 and its underlying molecular mechanisms in HCC.

Immunohistochemical analysis was conducted to assess ATOX1 expression in HCC tissues. Cell Counting Kit-8, colony formation, Transwell migration, flow cytometry, and reactive oxygen species (ROS) assays were employed to evaluate the malignant behaviors of tumor cells. A xenograft mouse model was employed to assess the effects of ATOX1 knockdown on tumor growth in vivo. DCAC50 treatment was performed to inhibit the copper transport function of ATOX1. RNA sequencing was conducted to explore the potential molecular mechanisms of ATOX1 in HCC.

ATOX1 expression was significantly elevated in HCC tumor tissues. ATOX1 promoted cell proliferation, colony formation, and migration. Knockdown of ATOX1 suppressed tumor growth in vivo. Mechanistically, ATOX1 activated c-Myb, and thus enhanced the malignant phenotype of HCC cells via activation of the PI3K/AKT signaling pathway. Additionally, ATOX1 reduced intracellular copper accumulation and inhibited ROS production and apoptosis. Inhibition of ATOX1 by DCAC50 decreased cell proliferation while increasing ROS levels and apoptosis in HCC cells. Notably, acetylcysteine reversed the reduction in c-Myb expression induced by ATOX1 knockdown.

ATOX1 may promote HCC carcinogenesis through the activation of the c-Myb/PI3K/AKT pathway and the inhibition of copper accumulation and oxidative stress.

Leishmaniasis is a dangerous yet neglected tropical disease affecting a vast population of the world. Several medicinal plants and their constituents (natural products/phytochemicals) have been considered of prime importance for the management of leishmaniasis over the years. The present review sheds light on the molecular mechanisms of the constituents obtained from medicinal plants that are pre-clinically effective against leishmaniasis. Various mechanisms by which medicinal plant-derived natural products elicit their action against leishmaniasis are illustrated in the literature. The mechanisms identified include: disruption of cytoplasmic and mitochondrial membranes, induction of apoptosis and autophagy, modulation of gene expression and immunological pathways, pro-oxidant effects (disrupting redox balance) with mitochondrial dysfunction, cell cycle arrest, impaired cellular bioenergetics, i.e., adenosine triphosphate production and coagulation of cellular contents within Leishmania parasites. Future phytochemical and pharmacological (especially clinical) studies are necessary to further understand the mechanistic details of medicinal plant-derived natural compounds and to develop new phytotherapeutic entities from nature against leishmaniasis.

Despite significant advances in Parkinson’s disease (PD) treatment, it remains incurable, with limited therapeutic options. Currently, repurposing already tested, safe drugs has emerged as an effective therapeutic strategy against various neurodegenerative diseases, including PD. Using a drug-repurposing approach, the current study investigated the neuroregenerative potential of polysialic acid mimicking compounds, 5-nonyloxytryptamine oxalate (5-NOT) and Epirubicin (Epi), an anti-cancer drug, in 1-methyl-4-phenylpyridinium (MPP+)-treated human neuroblastoma SH-SY5Y cells as a PD model.

The excitotoxic model was established by exposing SH-SY5Y cells to 500 µM of MPP+ and subsequently treating them with the test compounds. The effect of MPP+-induced toxicity on cellular and nuclear morphology, as well as on the expression of neuroplasticity and cell survival proteins, were studied by immunostaining, gelatin zymogram, and Western blot assays.

Treatment with 5-NOT and Epi significantly promoted the survival of MPP+-challenged SH-SY5Y cells and prevented changes in their cellular and nuclear morphology by regulating the expression of microtubule-associated protein (MAP-2) and polysialylated-neural cell adhesion molecule (PSA-NCAM) and NCAM synaptic plasticity proteins. Further, 5-NOT and Epi treatment also protected SH-SY5Y cells by restoring levels of nitric oxide, matrix metalloproteinase, and stress response proteins. Interstingly, 5-NOT attenuated MPP+-induced toxicity in SH-SY5Y cells by regulating the intrinsic protein kinase AKT/BAD apoptotic pathway and the P-38 MAP kinase synaptic plasticity pathway.

These preliminary findings suggest that 5-NOT, as a potential polysialic acid glycomimetic, may serve as a promising drug candidate for targeting neurodegeneration of dopaminergic neurons, a hallmark feature of PD.

It is established that administration of the COVID-19 vaccine may be associated with an exaggerated immune response leading to enlargement of several lymph nodes. Although most cases are benign and self-limiting, some have been reported in the literature as B-cell or T-cell lymphomas, with no reported cases of chronic lymphocytic leukaemia (CLL). We report two cases of follicular lymphoma and CLL that occurred a few weeks after COVID-19 vaccination. Case 1 is a 48-year-old woman who noticed two significantly palpable masses, one in each axilla, 48 h after receiving the first dose of the Pfizer-BioNTech BNT162b2 vaccine for COVID-19. Seven days later, she noticed another mass on the right side of her neck, which was biopsied within 48 hours. Case 2 is a 75-year-old man who presented with localized swellings in the axilla and on the neck, noted 24 h after the first dose of the Moderna messenger RNA-1273 COVID-19 vaccine. Neither patient reported any constitutional or associated symptoms. Surgical biopsy of the axillary lymph node in case 1 revealed a non-Hodgkin lymphoma, confirmed via immunohistochemistry as CD20-positive B-cell follicular lymphoma. The patient also had multiple pre- and para-aortic lymph nodes. In case 2, complete blood count showed lymphocytosis (total white blood cell – 148 × 109/L; lymphocyte differential – 92%), while peripheral blood film showed lymphocytosis with a predominance of small, mature-looking lymphocytes, both suggesting CLL. Although requested, immunophenotyping and molecular testing were not performed due to patient-related challenges. Although a chance occurrence is possible, lymphoid malignancies should be considered a strong differential. The vaccination history of patients presenting with clinical manifestations suggestive of a lymphoid malignancy should be thoroughly investigated, while ruling out other possible differentials such as a benign, self-limiting inflammatory process.