It was aimed to retrospectively evaluate the clinical, laboratory, neuroimaging, and electrophysiological characteristics of children presenting with vertigo to a tertiary pediatric neurology outpatient clinic and to assess age-related differences in etiological diagnoses. Medical records of 272 patients under 18 years of age who presented with vertigo between January 2020 and January 2025 were reviewed. Demographic data, accompanying symptoms, neurological examination findings, laboratory results, electroencephalography (EEG) and magnetic resonance imaging (MRI) reports, consultations, and final diagnoses were collected. Patients were categorized as children (<12 years) or adolescents (≥12 years). Descriptive statistics and appropriate comparative tests were used. The mean age of patients was 12.73±3.68 years; 67.6% were female. The most common accompanying symptoms were visual blackouts (22.1%), headaches (16.2%), nausea and vomiting (11.4%), and syncope (9.2%). Neurological examination was normal in 97.4% of cases. MRI was performed in 84.6% of cases and showed abnormalities in 21.3%; most abnormalities were non-specific, while 4.8% had clinically relevant lesions. EEG was abnormal in 6.3% of cases. The most frequent diagnoses were orthostatic hypotension (23.5%), vestibular migraine (13.6%), psychogenic vertigo (12.9%), benign paroxysmal vertigo of childhood (BPVC) (8.5%), and epilepsy (6.3%). BPVC and epilepsy were more common among children, whereas orthostatic hypotension and psychogenic vertigo were more common among adolescents. No etiology was identified in 13.6% of patients. Most pediatric vertigo cases were benign, with clear age-specific diagnostic patterns. MRI and EEG contributed to the diagnosis in selected cases, but were largely nonspecific. Multidisciplinary evaluation, including assessment of orthostatic intolerance, migraine, psychogenic factors, and reversible metabolic causes, is essential for effective management.

Hemiplegic shoulder pain (HSP) is a common complication that can significantly impair motor recovery, functional independence, and quality of life in stroke survivors. Although the condition has traditionally been attributed to musculoskeletal factors, recent evidence highlights the roles of neuropathic pain and central sensitization in its pathogenesis. This study aimed to investigate the relationship between central sensitization, neuropathic pain, and functional independence in patients with and without post-stroke shoulder pain. This cross-sectional study included 97 chronic stroke patients (mean age: 55.55±12.51 years; 30 females, 67 males) who were divided into two groups based on the presence of shoulder pain. The probability of neuropathic pain was assessed using the Self-Administered Leeds Assessment of Neuropathic Symptoms and Signs (S-LANSS) and central sensitization was measured using the Central Sensitization Inventory (CSI). Motor recovery was evaluated with Brunnstrom staging, and functional independence with the Barthel Index. Group comparisons, correlation analyses, and multivariate logistic regression analyses were performed. Shoulder pain was present in 58.8% of participants. Patients with shoulder pain had significantly higher LANSS (14.49±8.23 vs. 2.45±3.83, p<0.001) and CSI scores (53.36±18.16 vs. 27.70±8.55, p<0.001), and lower Barthel Index scores (55.70±28.08 vs. 81.50±16.33, p<0.001). Strong positive correlations were found between CSI and LANSS (r=0.861, p <0.001), while both measures were strongly negatively correlated with the Barthel Index (r=-0.850, p<0.001). Logistic regression identified female gender [odds ratio (OR)=106.48, 95% CI: 13.24-855.00, p<0.001], a higher CSI score [OR=1.21, 95% Confidence interval (CI): 1.10-1.33, p<0.001], and a lower Barthel Index (OR=0.91, 95% CI: 0.87-0.95, p<0.001) as independent predictors of shoulder pain. Among chronic stroke patients, HSP was strongly associated with greater central sensitization, neuropathic pain, and reduced functional independence. Screening with CSI and S-LANSS may help identify patients with a higher symptom burden and inform more individualized rehabilitation approaches that address both peripheral and central pain mechanisms.

Isoproterenol (ISO)-induced myocardial injury involves oxidative stress (OS) and inflammation. Given carvacrol (CAR)'s antioxidant and cardioprotective properties, we aimed to investigate its protection against ISO-induced myocardial injury in rats. Thirty male Wistar albino rats were assigned to three groups: Control; ISO (100 mg/kg, subcutaneous, for 2 days); and CAR+ISO (CAR 50 mg/kg/day, orally at 9:00, for 7 days + ISO at 16:00 on days 6-7). CAR and ISO doses were chosen based on prior evidence of CAR's antioxidant effects and ISO-induced oxidative cardiac stress. Diastolic and mean arterial pressures, corrected QT interval (QTc), T-wave changes, and serum troponin I levels were assessed. Cardiac OS biomarkers [malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT)] and histopathology were evaluated. ISO markedly increased troponin I from 43.9 to 508.9 ng/mL and slightly reduced GSH from 1502.4 to 1330 nmol/g wet tissue and SOD from 1080.25 to 1010.34 U/g protein. ISO markedly reduced MDA (95.30 to 71.78 nmol/g wet tissue at 535 nm; 77.49 to 61.24 nmol/g wet tissue at 520 nm), likely due to depletion of lipid peroxidation substrates caused by excessive reactive oxygen species production, while slightly increasing CAT (132.66 to 162.04 K/g protein), possibly as a compensatory response. QTc and histopathological scores increased significantly; histopathological components were cardiomyocyte degeneration (CD) (range, 0.0 to 2.0), interstitial edema (IE) (range, 0.0 to 2.0), and granulation tissue (GT) (range, 0.0 to 1.0). CAR attenuated electrocardiographic abnormalities, significantly reduced troponin I (from 508.9 to 38.05 ng/mL), and restored GSH (from 1330 to 1396.8), SOD (from 1010.34 to 1094.42), and CAT (from 162.04 to 135.58). CAR significantly ameliorated histopathological scores: CD (2.0 to 1.0), IE (2.0 to 1.0), and GT (1.0 to 0.0). CAR exerts protective effects against ISO-induced myocardial injury via antioxidant, membrane-stabilizing, and possible anti-arrhythmic properties. These findings support the therapeutic potential of CAR in OS-mediated cardiac pathologies and warrant further investigation in chronic and molecularly targeted models.

Gastric cancer remains a significant global health concern, necessitating investigation into more effective treatment approaches. This study investigates the combined effects of rosmarinic acid, a polyphenolic compound with known anticancer properties, and cisplatin, a conventional chemotherapeutic agent, on human gastric carcinoma (HGC-27) cells. Cell viability was evaluated at different concentrations for rosmarinic acid and cisplatin, and inhibitory concentration (IC)50, IC30, and IC10 values were subsequently determined. IC30 and IC10 doses were selected for combination experiments. Thiazolyl Blue Tetrazolium Bromide assay, colony formation assay, in vitro scratch assay, and 3D tumor spheroid growth assay were performed to evaluate the effects of individual and combined treatments. Rosmarinic acid and cisplatin individually reduced cell viability in a dose-dependent manner. Both the IC10 and IC30 dose combinations of the two agents demonstrated significant inhibitory effects on colony formation and cell motility, indicating an additive interaction compared with the control and the individual treatments. The combined treatment also inhibited spheroid growth, although the extent of the reduction was similar to that observed with the individual agents. This study provides initial insights into the potential efficacy of the rosmarinic acid-cisplatin combination. The combination of these agents reduced cell viability, colony formation, and cell motility. The increased cytotoxicity observed in 2D models was not evident in 3D spheroid models, highlighting the importance of 3D systems that more accurately mimic the complex structure of tumors. This finding suggests that differences in drug sensitivity between 2D and 3D models should be considered when evaluating combination therapies.

Poly (ADP-ribose) polymerase-1 (PARP-1) is a key enzyme in DNA repair pathways and has been implicated in cancer susceptibility. The rs1136410 polymorphism in the PARP-1 gene has shown inconsistent associations with gastrointestinal cancer risk across populations. This meta-analysis aimed to evaluate the association between PARP-1 rs1136410 polymorphism and the risk of colorectal cancer (CRC) and gastric cancer (GC), with a focus on ethnic differences. A systematic literature search was performed in PubMed, Scopus, EMBASE, Web of Science, Cochrane Library, BIOSIS, LILACS, CNKI, CBM, Wan Fang, and other regional databases up to February 1, 2025. Eligible case-control studies assessing the association between PARP- 1 rs1136410 polymorphism and CRC or GC were included. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated under five genetic models using Comprehensive Meta-Analysis software. Thirteen case-control studies were included, comprising 3.591 patients and 5.433 controls. For GC (8 studies; 1,784 cases and 2,521 controls), significant associations were observed under multiple genetic models: allele comparison (C vs. T: OR=2.01, 95% CI 1.04-3.91, p=0.039), homozygous comparison (CC vs. TT: OR=1.77, 95% CI 1.24-2.52, p=0.002), heterozygous comparison (CT vs. TT: OR=1.36, 95% CI 1.18-1.57, p<0.001), and recessive comparison (CC vs. CT+TT: OR=1.54, 95% CI 1.08-2.20, p=0.017). No significant association was detected for CRC (5 studies; 1.807 cases and 2.912 controls). Ethnic subgroup analysis revealed a protective effect against CRC in Caucasians but increased susceptibility in Asians. The PARP-1 rs1136410 polymorphism is associated with elevated GC risk but not CRC, with ethnicity-dependent effects suggesting differential genetic susceptibility. These findings highlight the importance of considering population-specific genetic backgrounds in gastrointestinal cancer risk assessment, prevention, and precision medicine strategies.

Transient Tachypnea of the Newborn (TTN) is a common cause of respiratory distress in term infants, associated with delayed pulmonary fluid clearance resulting from dysfunction of the epithelial sodium channel. Although generally self-limiting, TTN may increase early childhood wheezing and asthma risk. This study aimed to assess the incidence and characteristics of acute bronchiolitis in TTN infants compared to those in healthy controls within a large birth cohort. We conducted a population-based cohort study that included all live births in Istanbul from January 2016 to December 2018, utilizing the Turkish Ministry of Health's e-Nabız database. Infants diagnosed with isolated TTN (International Classification of Diseases [ICD]-10 P22.1) formed the study group. A randomly selected control group of healthy infants without respiratory diagnoses was included in the study. Both groups were followed for two years to identify episodes of acute bronchiolitis (ICD-10 J21*), excluding cases within the first month of life. The data collected included bronchiolitis incidence, recurrence, age at the time of the episode, and hospitalizations. Among 1,002,261 live births, 14,389 TTN infants and 14,500 controls were analyzed. Acute bronchiolitis occurred in 42.4% of TTN infants and 35.8% of controls (p<0.001). TTN infants had higher rates of single episodes, while controls experienced more recurrent episodes (p<0.001). Hospitalization was more frequent in the control group (p<0.001), with single hospitalizations predominating in the TTN group and multiple hospitalizations in the control group. The first episodes in TTN infants mainly occurred between 1-6 months, with controls showing more episodes early but fewer later (p<0.001). Recurrence was correlated with an earlier age of the first episode in both groups (p<0.001). TTN infants experience more bronchiolitis episodes early in life, though recurrent episodes are more common among healthy controls. Further studies are warranted to investigate the relationship between TTN and the development of wheezing and asthma.

Schizophrenia is a multifaceted psychiatric disorder that affects about 1% of the world's population and arises from a combination of genetic, environmental, and neurodevelopmental influences. Recent studies highlight the role of immune system disturbances and neuroinflammation in its development, with tumor necrosis factor-alpha (TNF-α) identified as a pivotal cytokine. This meta-analysis aims to clarify the relationship between the TNF-α rs1800629 genetic variant and the risk of schizophrenia by synthesizing data from published research. Two independent reviewers systematically searched PubMed, Web of Science, Embase, Cochrane Library, and Chinese National Knowledge Infrastructure for studies published up to January 19, 2024. Odds ratios and 95% confidence intervals were computed using a fixed-effects model, taking into account the absence of significant heterogeneity. A total of 33 case-control studies were included, encompassing 7,624 individuals with schizophrenia and 8,933 healthy controls from diverse backgrounds (21 studies on Asian populations, 11 on Caucasian, and one on a mixed group) conducted between 2001 and 2020. The pooled analysis did not reveal a significant link between the TNF-α rs1800629 polymorphism and susceptibility to schizophrenia under any genetic model. Further subgroup analyses by ethnicity (Asian, Caucasian), country (China, Poland), genotyping technique, and publication year also yielded no notable associations. This comprehensive meta-analysis offers strong evidence that the TNF-α rs1800629 variant is not significantly associated with schizophrenia risk, either globally or within specific ethnic groups. These findings indicate that this polymorphism likely does not play a major role in schizophrenia susceptibility, underscoring the importance of future investigations into other TNF-α variants, gene-gene interactions, or alternative inflammatory mechanisms.

Angiotropism/perivascular invasion (PVI) is an emerging topic in various types of cancer, with studies primarily focusing on melanoma. However, limited data are available on the significance of PVI in breast cancer. This study aimed to assess the prognostic significance of PVI in breast cancer and its correlation with traditional clinicopathological prognostic parameters. A total of 150 patients with breast cancer diagnosed between July 2020 and January 2022 were included. Clinicopathological data were retrieved from the hospital records. The presence of PVI was evaluated on hematoxylin&eosin stained slides, and the association between PVI and clinicopathological parameters was statistically analyzed. A p-value of <0.05 was regarded as statistically significant. All patients were female. The mean age was 54.0±13.6 years (range 26-97 years). PVI was significantly more common in patients with ≥2.5 cm tumors and the absence of PVI showed a significant correlation with a lower histologic grade (p=0.004 and p=0.040, respectively). Lymphovascular invasion (LVI) and perineural invasion (PNI) were also significantly more frequent in tumors with PVI (p=0.001 and 0.02, respectively). There was a statistically significant association between the absence of both PVI and extranodal extension (ENE) (p=0.035). The specific role of PVI in different types of cancer has not yet been clarified. Our findings showed that PVI was significantly associated with tumor size, histological grade, LVI, PNI, and ENE, all of which are well-known negative prognostic factors in breast cancer. The presence of PVI is a promising topic in breast cancer research, and the PVI status in pathology reports may help oncologists perform better risk assessments for patients with breast carcinoma.

Ischemia-reperfusion (IR) of the aorta is a significant contributor to the development of postoperative acute lung damage after abdominal aortic surgery. The aim of the present study was to examine the effect of alpha B-crystallin, a small heat shock protein (known as HspB5), on lung injury induced by abdominal aortic IR in rats. Male Sprague-Dawley rats were divided into three groups: control, ischemia-reperfusion (IR, 90 min ischemia and 180 min reperfusion), and alpha B-crystallin +IR. Alpha B-crystallin (50 μg/100 g) was intraperitoneally administered 1 h before IR. Lung tissue samples were obtained for histological and biochemical analyses of oxidative stress and cytokine and apoptosis parameters in plasma, lung tissues, and bronchoalveolar lavage (BAL) fluid. The levels of malondialdehyde, reactive oxygen species, total oxidant status, tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), nuclear factor kappa B (NFKβ), caspase-9 (CASP-9), 8-hydroxy-2'-deoxyguanosine, total antioxidant status, superoxide dismutase, and interleukin-10 levels in lung tissues, plasma, and BAL fluid (p<0.05 versus control) increased in Aortic IR. However, alpha B-crystallin significantly reduced the lung tissue levels of oxidative, inflamatuvar, and apoptotic parameters in the plasma, lung tissues, and BAL fluid (p<0.05 versus aortic IR). Histopathological results showed that alpha B-crystallin ameliorated the morphological changes related to lung injury (p<0.001). Alpha B-crystallin substantially restored disrupted the redox balance, inflammation, and apoptotic parameters in rats exposed to IR. The cytoprotective effect of alpha B-crystallin on redox balance might be attributed to improved lung injury.