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.

Epileptogenesis involves complex mechanisms, including inflammation and apoptosis. Rosiglitazone, a peroxisome proliferator-activated receptor gamma agonist, possesses anti-inflammatory and neuroprotective properties. This study investigated whether rosiglitazone can prevent pentylenetetrazole (PTZ)-induced kindling in mice by modulating inflammatory cytokines and apoptosis pathways.

Male C57BL/6 mice (n = 8 per group) were assigned to sham, control, or rosiglitazone-treated groups. Kindling was induced with intraperitoneal PTZ (40 mg/kg) every 48 h for 17 days. Rosiglitazone (0.1 mg/kg) was administered 30 m before each PTZ injection. Seizure progression was monitored, and hippocampal tissues were analyzed via immunohistochemistry and Western blotting to assess cytokine levels (interleukin (IL)-10, IL-17A, tumor necrosis factor-alpha, interferon-gamma), caspase-3 activity, and glial fibrillary acidic protein expression.

Rosiglitazone significantly delayed seizure progression, reduced seizure scores, and lowered pro-inflammatory cytokine levels (IL-17A, tumor necrosis factor-alpha, interferon-gamma) while increasing IL-10. Immunohistochemical analysis revealed fewer caspase-3-positive cells and reduced glial fibrillary acidic protein expression in the treatment group compared to controls.

Rosiglitazone exerts neuroprotective effects in PTZ-induced kindling, likely through its anti-inflammatory and anti-apoptotic actions. These findings underscore its potential as a therapeutic agent for mitigating epileptogenesis, warranting further investigation in combination therapies and clinical trials.

Oxidative stress could be a key process in acyclovir (ACV)-induced nephrotoxicity. N-acetylcysteine (NAC) is a water-soluble antioxidant with anti-inflammatory activity. This study aimed to evaluate the protective effect of NAC on ACV-induced nephrotoxicity in adult Wistar rats.

Forty adult male Wistar rats (200–220 g) were used. The rats were randomly divided into eight groups (n = 5/group) and were treated intraperitoneally daily for seven days as follows: Group 1 (Control) was administered water (0.2mL), while groups 2–4 were administered NAC (25, 50, and 100 mg/kg). Group 5 was administered ACV (150 mg/kg), while groups 6–8 were supplemented with NAC (25, 50, and 100 mg/kg) prior to treatment with ACV (150 mg/kg). On day 8, the rats were weighed and euthanized, and blood samples were collected for the assessment of biochemical markers. The kidneys were weighed and subjected to oxidative stress markers and histological evaluations.

ACV had no significant (p > 0.05) effects on the body and kidney weights of rats compared to the control. ACV produced significant (p < 0.001) elevations in kidney malondialdehyde, serum urea, creatinine, and uric acid levels in rats, which differed from the control. There were significant (p < 0.001) decreases in kidney glutathione, superoxide dismutase, peroxidase, and catalase, as well as serum chloride, potassium, bicarbonate, and sodium levels in ACV-treated rats compared to the control. ACV caused widening of Bowman’s space and tubular necrosis in the kidneys of rats. Nonetheless, NAC supplementation abrogated ACV-induced nephrotoxicity in a dose-dependent manner. Kidney histology was restored by NAC supplementation.

NAC protected against ACV-induced nephrotoxicity. This finding shows that NAC may have therapeutic potential for nephrotoxicity caused by ACV.

Escalating antimicrobial resistance is a global threat, emphasizing the need to explore alternative treatment options. Hence, we aimed to explore the in-vitro activity of ceftazidime-avibactam (CAZ-AVI) in clinical isolates of carbapenem-resistant gram-negative bacteria.

This was an observational, cross-sectional study conducted at the Microbiology Department of Indus Hospital, Karachi, Pakistan, from January 2023 to October 2024. Carbapenem-resistant gram-negative rods isolated from clinical specimens received from the outpatient, emergency, and inpatient departments were included. Consecutive, non-probability sampling was employed for the collection of isolates. Identification of the organisms was confirmed using API® ID strips, and antimicrobial susceptibility for carbapenems and CAZ-AVI was determined via the Kirby-Bauer disc diffusion method.

A total of 158 bacterial isolates were characterized as carbapenem-resistant. Of these, 92 (58%) were Enterobacterales, and 66 (42%) were Pseudomonas aeruginosa. CAZ-AVI was susceptible in 17 (11%) of the isolates, of which four (24%) were Klebsiella spp. and Escherichia coli each, and nine (52%) were P. aeruginosa. CAZ-AVI-susceptible strains were predominant among patients aged 26–50 years (n = 6; 35%), most of whom were females (n = 10; 59%) and inpatients (n = 8; 47%). Clinical samples from patients with urinary tract infections grew the most CAZ-AVI-susceptible strains (n = 9; 53%).

Our study demonstrated low CAZ-AVI susceptibility in our carbapenem-resistant gram-negative bacterial strains. Understanding regional antimicrobial patterns in multidrug-resistant bacteria is crucial for the effective use of CAZ-AVI, along with the strict implementation of strategies for controlling antimicrobial resistance.

Castleman disease (CD) is a lymphoproliferative condition with a broad range of morphological and clinical presentations. It is categorized into distinct pathological and clinical subtypes, including localized unicentric CD, idiopathic multicentric CD, and human herpesvirus 8-associated or human herpesvirus 8-negative variants. Diagnosing CD requires adherence to internationally recognized guidelines that integrate clinical, laboratory, and histological findings. However, distinguishing CD from other diseases can be complex, as numerous benign and malignant conditions can mimic its features. Additionally, individuals diagnosed with CD are at an elevated risk of developing various malignancies. In this article, we reviewed benign and malignant conditions that can mimic CD.

Literature search is conducted and reviewed.

Mimickers of CD include follicular hyperplasia, indolent B-cell lymphoproliferative disorders, peripheral T-cell malignancies, classic Hodgkin lymphoma, follicular dendritic cell tumors, plasma cell disorders, immunoglobulin G4 -related lymphadenopathy, autoimmune-associated lymphadenopathy, infectious causes of lymphadenopathy, and systemic syndromes like POEMS and TAFRO. Various malignancies are associated with CD, including plasma cell proliferations, lymphomas, follicular dendritic cell neoplasms, and Kaposi sarcoma.

This review explores the differential diagnoses and neoplasms linked to CD, emphasizing their role in accurate classification, treatment decisions, and patient management. A comprehensive understanding of CD and its mimickers is crucial for ensuring accurate diagnosis and appropriate patient management in clinical practice.

Inherited metabolic liver diseases (IMLDs) have complex etiologies and vary widely in clinical presentation, with a significant overall incidence. With the advancements in diagnostic and treatment technologies, an increasing number of children with inherited metabolic diseases are surviving into adolescence and adulthood. These advancements have improved our understanding of the IMLD disease spectrum and clinical outcomes. This study aimed to analyze changes in the disease spectrum and epidemiological characteristics of inherited metabolic liver diseases (IMLD) over the past 20 years in two specialized liver disease hospitals in northern China.

A retrospective analysis was conducted on IMLD cases diagnosed between January 1, 2002, and December 31, 2023, at two liver disease specialty hospitals in Beijing. Data were obtained from inpatient and outpatient hospital information systems, with diagnoses based on national and international IMLD diagnosis and treatment guidelines.

A total of 2,103 IMLD patients were analyzed, including 1,213 adults and 890 children. IMLD accounted for 4.58‰ of hospitalized liver disease patients during this period. The most common IMLD was Wilson’s disease, comprising 68% of all IMLD cases. The number of diagnosed IMLD types increased from 15 to 32 across two 11-year periods (2002–2012 and 2013–2023). Among pediatric patients, glycogen storage disease and Alagille syndrome were more prevalent in those under one year of age, while Wilson’s disease was prevalent across all age groups. In adult IMLD patients, Wilson’s disease, polycystic liver disease, and hereditary hyperbilirubinemia were more frequently observed.

Over the past 20 years, both the number of diagnosed IMLD cases and disease diversity have significantly increased, with Wilson’s disease remaining the most prevalent IMLD. These findings provide valuable insights for the long-term management of IMLD patients and the allocation of healthcare resources.

This study investigates upper gastrointestinal tract (UGIT) involvement in patients with ulcerative colitis (UC), a condition traditionally considered limited to the colon. Although extra-colonic manifestations of UC are well recognized, UGIT issues have received less attention. This research aimed to document the clinical, endoscopic, and histopathological UGIT findings in adults with UC and assess their association with disease severity and extent.

This descriptive cross-sectional study was conducted at Ain Shams University over one year. A total of 78 UC patients underwent comprehensive clinical evaluations, including assessments of gastrointestinal complaints, medication history, disease progression, surgeries, and physical examinations. Endoscopic assessments of both the UGIT and colon were performed, accompanied by biopsies for histopathological analysis.

The study population had a mean age of 35.26 years, with a nearly equal gender distribution. Endoscopic findings revealed significant UGIT involvement: 64% of patients had esophagitis and/or gastroesophageal reflux disease, 93% had gastritis, and 80% had duodenitis. Histopathological findings showed notable inflammation, basal cell hyperplasia, and ulcerations in the esophagus, with 51.3% of patients exhibiting chronic gastritis and 38.5% testing positive for Helicobacter pylori infection. Statistical analysis demonstrated a strong association between colonic disease severity and UGIT endoscopic (p < 0.0001 and p < 0.001 in the esophagus and stomach, respectively) and histopathological (p < 0.004, p < 0.001, and p <0.005 in the esophagus, stomach, and duodenum, respectively) findings, particularly in patients with UGIT symptoms.

This study concludes that UGIT endoscopic and histopathological changes are prevalent among Egyptian UC patients, suggesting a significant link between UC and these UGIT findings.

The development and progression of breast cancer may be influenced by thyroid hormone levels. In this study, we investigated thyroid function in pre- and postmenopausal women with breast cancer, with and without neoadjuvant chemotherapy (NCh).

The study included 198 women diagnosed with infiltrating ductal carcinoma: 83 did not receive NCh (39 premenopausal and 44 postmenopausal), while 115 underwent NCh before surgery (63 premenopausal and 52 postmenopausal). Additionally, 78 healthy volunteers, aged 28 to 69 years, served as the control group. Serum levels of thyroid-stimulating hormone (TSH), free thyroxine (fT4), and free triiodothyronine (fT3) were quantified using chemiluminescent immunoassays.

We observed a significant increase in serum TSH and fT4 levels in both pre- and postmenopausal women with breast cancer, regardless of NCh treatment, compared to control subjects. However, postmenopausal women with breast cancer who received NCh showed lower fT4 levels than their untreated counterparts. Notably, fT3 levels increased only in premenopausal women with breast cancer who underwent NCh, compared to both the premenopausal control group and untreated premenopausal breast cancer patients.

Altered thyroid function was observed in both pre- and postmenopausal women with breast cancer, characterized by increased TSH and fT4 levels. Neoadjuvant chemotherapy appeared to attenuate the rise in fT4 levels in postmenopausal women while elevating fT3 levels in premenopausal women. These findings highlight the importance of monitoring thyroid hormone profiles in women with breast cancer, considering menopausal status, given their potential influence on tumor progression and chemotherapy effectiveness.