Tag: pubmed

J Clin Aesthet Dermatol. 2026 Apr;19(4):35-37.

ABSTRACT

OBJECTIVE: To compare thyrotropin (TSH) levels across nonscarring alopecia (NSA) subtypes-alopecia areata (AA), telogen effluvium (TE), and androgenetic alopecia (AGA)-in a primary analysis of all patients, a secondary analysis of euthyroid patients stratified into low-normal (0.5-2.5 mIU/L) and high-normal (2.5-4.5 mIU/L) categories, and a tertiary analysis of patients with thyroid dysfunction.

METHODS: A retrospective chart review was conducted on patients diagnosed with AA, TE, or AGA at a single academic dermatology department between August 2017 and August 2024. TSH values were drawn within 3 months of the initial visit, and patient demographics were extracted from the electronic medical record. Patients with thyroid dysfunction were excluded from the secondary analysis. TSH values within the euthyroid range were stratified into low-normal and high-normal categories. A tertiary analysis of patients with frank thyroid dysfunction was later conducted. Descriptive statistics, Kruskal-Wallis tests, and Bonferroni-corrected pairwise comparisons were performed.

RESULTS: Among the 1,411 patients initially identified, most TSH values were within the euthyroid range. In a secondary analysis of 1,291 euthyroid patients, there was no significant difference in TSH distribution across NSA subtypes, including when stratified into low-normal vs high-normal categories. Among patients with thyroid dysfunction (8.5%), those with TE had the highest relative proportions of both hypothyroidism (5.0%) and hyperthyroidism (5.5%). Black or African American patients with AA and TE had lower mean TSH levels than White patients; however, this was not observed in AGA.

LIMITATIONS: Limitations of this study include the retrospective design and the potential for incomplete or biased medical records.

CONCLUSION: TSH levels among patients with NSA did not vary significantly based on NSA subtype. Racial differences in mean TSH were observed in AA and TE, but the clinical significance remains uncertain.

PMID:42239846 | PMC:PMC13229151

Ment Health Clin. 2026 Jun 2;16(3):129-134. doi: 10.9740/mhc.2026.06.129. eCollection 2026 Jun.

ABSTRACT

INTRODUCTION: Lithium has long been considered the gold standard mood stabilizer in the treatment of acute mood episodes related to bipolar (BD) and schizoaffective disorder. Previous research has primarily focused on lithium loading strategies and their effects on symptom severity and inpatient length of stay (LOS). However, less is known about specific prescribing practices at lithium initiation that may influence LOS.

METHODS: This retrospective study aimed to evaluate three initiation-related prescribing factors of lithium and their association with changes in LOS among adult inpatients experiencing acute mood episodes of BD or schizoaffective disorder. The factors were lithium initiation within 48 hours of admission, achieving a therapeutic level-producing dose within 48 hours of admission, and receiving intensive initial lithium dosing (≥900 mg/day). The Mann-Whitney U test was used to assess statistical significance. The timing of antipsychotic coprescribing in mania was also evaluated.

RESULTS: Sixty-eight patients were included in this study. Lithium initiation within 48 hours of admission significantly decreased hospital LOS (7.2 vs 13.4 days; P < 0.001). Lithium optimization to a dose that produced a therapeutic drug level within 48 hours of admission also significantly decreased LOS (6.2 vs 9.1 days; P < 0.01). Intensive initial dosing did not significantly affect LOS. Of patients with mania, 51.5% were trialed on antipsychotics before starting lithium.

CONCLUSION: Early lithium initiation and optimization in patients with acute bipolar mood episodes significantly reduced hospital LOS. Prospective studies are needed to address potential confounders to confirm whether early lithium optimization directly reduces LOS.

PMID:42239829 | PMC:PMC13229530 | DOI:10.9740/mhc.2026.06.129

Front Aging Neurosci. 2026 May 19;18:1806505. doi: 10.3389/fnagi.2026.1806505. eCollection 2026.

ABSTRACT

BACKGROUND: Parkinson’s disease (PD) involves progressive dopaminergic neuron loss in the substantia nigra (SN). Aldehyde dehydrogenase 1A1 (ALDH1A1), the rate-limiting enzyme in retinoic acid biosynthesis, is enriched in vulnerable dopaminergic neuron subpopulations and is consistently downregulated in PD. However, the relationship between ALDH1A1 expression and broader dopaminergic pathway gene co-expression has not been systematically characterized across multiple independent datasets.

METHODS: Gene expression correlations were analyzed across seven independent human SN microarray datasets (n = 156; 70 controls, 86 PD) from the Gene Expression Omnibus. Simple arithmetic means across datasets are reported as the primary summary statistic; random-effects meta-analysis with DerSimonian-Laird estimation was applied to Fisher’s z-transformed correlation coefficients to generate pooled estimates with heterogeneity statistics. Marker gene-based enrichment scoring using published cell type markers from single-nucleus RNA-seq profiling of human substantia nigra-with all target genes excluded from signatures-was performed across six analyzable datasets. Selectivity of ALDH1A1 correlation attenuation was assessed using permutation testing (n = 5,000) as the primary statistical test, with parametric tests reported as supplementary.

RESULTS: In controls, ALDH1A1 showed strong co-expression with dopaminergic genes (mean r = 0.92-0.93 for TH, DDC, and SLC18A2). In PD, these correlations were attenuated (mean Δr = -0.336 for ALDH1A1-dopamine pairs). Dopamine-dopamine correlations showed less attenuation (mean Δr = -0.143). Marker gene-based enrichment scoring confirmed significant depletion of ALDH1A1-positive vulnerable dopaminergic neurons in 4 of 6 datasets. After adjusting for estimated cell type enrichment, the selectivity of ALDH1A1 attenuation was preserved (adjusted selectivity: -0.210, increased from raw selectivity of -0.190; raw permutation p = 0.0052).

CONCLUSION: ALDH1A1 co-expression with dopaminergic pathway genes is attenuated in PD substantia nigra across all seven datasets examined. This attenuation is selective for ALDH1A1-containing pairs, and this selectivity persists after adjusting for cell type enrichment changes. While correlational, these findings are consistent with a role for retinoic acid pathway disruption in PD pathophysiology and warrant mechanistic investigation.

PMID:42239820 | PMC:PMC13226206 | DOI:10.3389/fnagi.2026.1806505

Kidney Med. 2026 Apr 30;8(7):101381. doi: 10.1016/j.xkme.2026.101381. eCollection 2026 Jul.

ABSTRACT

RATIONALE & OBJECTIVE: Data on sex differences in kidney function within multiethnic populations are scarce despite the large differences in chronic kidney disease (CKD) in women and men. We investigated the 6-year changes in the estimated glomerular filtration rate (eGFR) and albumin-creatinine ratio (ACR) in women and men, both overall and across ethnic groups, and determined whether sex differences in associations with outcomes are mediated by known CKD risk factors.

STUDY DESIGN: General population based longitudinal study.

SETTING & PARTICIPANTS: We used prospective data of 5,713 women and 4,407 men from 6 ethnic backgrounds from the Healthy Life in an Urban Setting (HELIUS) study (Amsterdam, the Netherlands).

EXPOSURES: Municipality registered sex.

OUTCOMES: Change in eGFR (mL/min/1.73 m²) and ACR (mg/mmol) between baseline (2011-2015) and follow-up (2019-2021) data collection. CKD incidence and progression were analyzed as secondary outcomes.

ANALYTICAL APPROACH: Linear regression analyses adjusted for baseline kidney function estimates, follow-up duration, age, education, and ethnicity in the total population and stratified by ethnicity. Mediation by hypertension, diabetes, cardiovascular disease, obesity, physical activity, alcohol consumption, and smoking was tested.

RESULTS: Although no significant sex differences were found in the overall population, Dutch and African Surinamese women had a greater decrease in eGFR (β:1.2 (0.5-1.8)) than men, whereas South-Asian Surinamese and Moroccan men had a greater decrease in eGFR (β:-1.0 (-2.0 to 0.0)) than women. ACR was higher in men, although this difference did not reach statistical significance (β:0.6 (0.3-1.1), P = 0.09). Sex differences in CKD incidence across certain ethnic groups aligned with the observed eGFR differences, whereas CKD progression was higher in men overall. Little evidence of mediation by CKD risk factors of the sex differences was observed.

LIMITATIONS: Single eGFR and ACR measurements, self-reported mediator variables, and limited generalizability.

CONCLUSIONS: Disparate sex differences in the changes in eGFR, CKD incidence, and progression were observed, specifically in some ethnic groups. These differences were not mediated by differences in traditional risk factors and health-related behaviors.

PMID:42239818 | PMC:PMC13227188 | DOI:10.1016/j.xkme.2026.101381

Front Mol Neurosci. 2026 May 19;19:1758390. doi: 10.3389/fnmol.2026.1758390. eCollection 2026.

ABSTRACT

INTRODUCTION: The central nervous system responds to acute injury with plastic remodeling of its network. However, the temporal and structural dynamics of this response in the denervated dentate gyrus remain poorly understood. Therefore, we examined the transcriptional programs activated after perforant path transection, focusing on the outer molecular layer (OML) and the granule cell layer (GCL).

METHODS: Perforant path transections were performed, and tissue from the denervated OML and GCL was selectively isolated using laser microdissection at 1, 3, 7, 14, and 28 days post-lesion. Whole-genome expression analysis was performed to identify and characterize global transcriptome changes across time and layers.

RESULTS: Denervation induced reactive astrogliosis and microgliosis primarily in the OML. Overall enrichment statistics from two complementary approaches highlighted early downregulations of neuroactive ligands, later downregulation of (mainly glutamatergic) neurotransmission factors, and late downregulations of respiratory factors, alongside early upregulations of debris degradation factors, subsequent upregulation of glial and inflammatory factors, and late upregulation of ribosomal translation. Entorhinal afferent loss was reflected by reductions of the axon repellent Sema3e (to 60% in OML), with sustained depletions of the reelin repressor Adamts3 (14% in OML, 33% in GCL) and its presumptive effector Ptpn3 (30% in OML), as well as delayed induction of the SEMA3E/reelin coreceptor Nrp1 (3-fold in OML, 7-fold in GCL). Secondary reductions in the GCL occurred for the CREB repressor Rgs13, Ntng1, and Epha5–Epha6–Epha7. Deficits were found in the OML for glutamatergic signaling factors (Neto1, Cnih2, Dlg2, Gria1, Grm7–Grm8–Grm3, Homer2, Trim32), in the GCL for GABAergic and glycinergic receptors (Gabra2–Gabra1, Gabrb2, Glra2), and overall for neuronal differentiation markers (Calb1, Pvalb, Gad1, Lrrc7, Ano3, Bdnf, Egfr, Igf2r, Nrep, Basp1, Scn1a) and synaptic adhesion mediators (Lingo2, Lrrtm1–Lrrtm3, Adam11–Adam23, Cadm2, Pcdhb16, Flrt3). Presumed compensatory upregulation efforts included postsynaptic and dendritic membrane remodeling by vesicle and actin regulators (Lyn, Gabarap, Cyfip1, Arf4, Arl4c, Rab8b, Cdk5rap2, Tmsb4x) in the OML, versus neurotrophic coreceptors Sorcs3–Sorcs2, axonal Smn1, and the neural progenitor modulator Nup210l in the GCL.

DISCUSSION: These findings identify coordinated and temporally structured transcriptomic programs that reflect injury-induced remodeling in the dentate gyrus and highlight novel molecular mediators of synaptic reorganization, neuroinflammation, metabolic adaptation, and compensatory plasticity following entorhinal denervation.

PMID:42239799 | PMC:PMC13226496 | DOI:10.3389/fnmol.2026.1758390

Res Sq [Preprint]. 2026 May 18:rs.3.rs-9724722. doi: 10.21203/rs.3.rs-9724722/v1.

ABSTRACT

Background Though bisphosphonates are the gold standard for the treatment of different metabolic bone disorders including osteoporosis for more than five decades, their safety and tolerability in patients with compromised kidney function are not well known. With age-related bone disorders and renal insufficiency becoming more prevalent worldwide, understanding the effect of bisphosphonates on patients with compromised renal function becomes inevitable. This review aims to analyze the clinical data available on safety of bisphosphonates on patients with different levels of renal function. Methods A broad search of PubMed, Wiley Online and the Cochrane Central Register of Controlled Trials was conducted to select randomized controlled trials and clinical trials that evaluated the safety and tolerability of bisphosphonate in patients with different levels of renal function between 2000 and 2026. Results Out of 1388 titles and abstract reviewed, 17 articles were included in the final analysis using PRISMA 2020 guidelines. Despite one trial showing < 2% increase in serum creatinine from baseline, all the other trials proved that bisphosphonates are safe and well tolerated by the patients with transplanted kidney and with compromised kidney function. Meta analysis of the data provided from eligible clinical trials using RStudio indicated that the proportion of serum creatinine that is increased was < 25% from baseline. Further, random effects model (100% (-0.01)) was performed due to high level of heterogeneity and it indicated that ibandronate 27.93%; alendronate 28.58%; risedronate 27.80% and zoledronate 15.69%. The pooled effect shows that kidney damage by bisphosphonates is not statistically significant. Conclusion The evidence from this review suggests that the bisphosphonates are generally well-tolerated with ten trials registering no drug-related withdrawals and other studies showing only very negligible withdrawals due to adverse effects. Even though bisphosphonates are safer to use in compromised renal function i.e., > 30ml/min/1.73m ² , more cohort studies are required to identify bisphosphonates effects in end stage renal disease (eGFR < 15ml/min/1.73m ² ).

PMID:42239793 | PMC:PMC13228822 | DOI:10.21203/rs.3.rs-9724722/v1

Res Sq [Preprint]. 2026 May 20:rs.3.rs-9588456. doi: 10.21203/rs.3.rs-9588456/v1.

ABSTRACT

Background: Obesity is a major global public health challenge that contributes to numerous comorbidities and increased mortality. A better understanding of the biological mechanisms and disease risks associated with obesity requires robust monitoring of key circulating biomarkers, including adipokines, apolipoproteins, and inflammatory proteins. Targeted mass spectrometry (MS) offers a promising platform for developing specific, standardized, and multiplexed assays for biomarker quantification. In this study, we developed a multiplex targeted MS assay for the quantification of 42 obesity-associated biomarker candidates in human plasma. Methods: The assay was optimized for surrogate peptide selection, digestion incubation time, and LC gradient, and evaluated for linearity, lower limit of quantification (LLOQ), imprecision, and stability. A semi-automated sample preparation workflow using 96-well plates was also established to support high-throughput implementation. The assay was applied to a clinical cohort undergoing weight loss interventions to evaluate differences in protein abundance across obesity-related groups and to monitor biomarker changes over time. Statistical analyses were performed to identify proteins with significantly different abundances between study groups and before versus after intervention. Results: The assay demonstrated acceptable linearity, LLOQ, imprecision, and stability. Inter-laboratory validation using samples from 70 healthy individuals showed strong correlation with the finalized standard operating procedure (SOP). Application of the assay to an obesity cohort revealed significant differences in the levels of 6 proteins across obese, overweight, and healthy control groups, as well as 16 proteins that were differentially abundant in obese individuals compared with non-obese individuals (overweight and healthy controls combined). In subjects undergoing weight loss interventions, four proteins-CRP, PRG4, SERPINF1, and SHBG-showed significant concentration changes in individuals who achieved > 5% weight loss. Conclusions: These results demonstrate the robustness and high-throughput capability of this multiplex targeted MS assay for measuring obesity-associated plasma biomarkers. The assay shows potential clinical utility for improving the diagnosis, stratification, and risk assessment of obesity-related conditions, as well as for monitoring responses to weight loss interventions.

PMID:42239769 | PMC:PMC13228810 | DOI:10.21203/rs.3.rs-9588456/v1

Front Sports Act Living. 2026 May 19;8:1761170. doi: 10.3389/fspor.2026.1761170. eCollection 2026.

ABSTRACT

INTRODUCTION: This study compared the efficacy of whole-body electromyostimulation (WB-EMS) vs. traditional resistance training (RT) in overweight adults.

METHODS: Forty overweight adults were randomized to WB-EMS (n = 14), RT (n = 14), or a control group (n = 12). Five participants withdrew during the intervention; consequently, and 35 participants completed the study and were included in the final analysis: WB-EMS (n = 12; age = 30 years, BMI = 29.12 kg/m²; 20-min sessions, 30 Hz, 350μs), RT (n = 12; age = 30 years; BMI = 29.14 kg/m²; 3 × 10 reps at 55%-70% 1RM), or control (n = 11, age = 29 years; BMI = 29.17 kg/m²). The intervention lasted 8 weeks with biweekly training sessions. Outcome measures included muscular performance tests, ultrasonographic muscle thickness measurements, and serum biomarkers (IL-15, myostatin, and follistatin). Between-group differences were analyzed using ANCOVA with baseline values as covariates.

RESULTS: Findings demonstrated significantly greater improvements in selected performance and biomarker outcomes in the WB-EMS group compared to other groups. Performance tests revealed significant enhancements in sit-ups (η _p ² = 0.35), push-ups (η _p ² = 0.54), and strength measures (η _p ² = 0.46) compared to RT and control groups. Biomarker analysis showed WB-EMS induced a 15.88% increase in IL-15 vs. 8.27% with RT and -4.92% in controls (p < 0.001). Myostatin decreased by 21.22% (WB-EMS) vs. 10.84% (RT), while increasing 5.08% in controls (p < 0.001). Follistatin levels rose by 17.96% (WB-EMS) and 8.92% (RT), with minimal change in controls (0.03%, p < 0.001). All between-group differences were statistically significant (p = 0.016-0.039) with large effect sizes (η _p ² = 0.35-0.63).

CONCLUSIONS: Twenty-minute WB-EMS sessions twice weekly elicit significantly greater improvements in muscular performance and favorable myokine profiles compared to conventional RT in overweight individuals. These findings suggest that WB-EMS may represent a time-efficient alternative for improving metabolic-muscular health in time-constrained populations.

PMID:42239744 | PMC:PMC13226195 | DOI:10.3389/fspor.2026.1761170

Front Sports Act Living. 2026 May 19;8:1804002. doi: 10.3389/fspor.2026.1804002. eCollection 2026.

ABSTRACT

OBJECTIVE: Against the backdrop of deepening regional economic integration and the rapid development of the sports industry in China, this study systematically investigates the impact of the sports industry on regional economic development. Specifically, it identifies the industry’s direct effects and spatial spillover effects while analyzing regional heterogeneity in influence mechanisms, thus addressing an existing research gap related to spatial connectivity.

METHOD: Based on panel data from 21 provincial-level regions in China spanning 2015-2024, this study employs fixed-effects panel models and spatial Durbin models to analyze the relationship between the sports industry and regional economic development, while testing the underlying mechanisms.

RESULTS: First, the development of the sports industry significantly promotes regional economic growth, and this conclusion remains robust across multiple model specifications and robustness tests. Second, the impact of the sports industry on regional economic development shows clear regional heterogeneity: it is significant in the eastern region but not statistically significant in the central and western regions; Third, the spatiotemporal evolution of the sports industry and regional economic development shows similar patterns, characterized by low-value clustering and high-value polarization in eastern regions. Fourth, regional economic development exhibits a significant positive spatial correlation. Fifth, results from the spatial Durbin model indicate that while the sports industry promotes local economic growth, it produces significant negative spatial spillover effects on neighboring regions, forming a pattern characterized as “local promotion and neighboring suppression.”.

DISCUSSION: Empirical findings confirm the endogenous driving role of the sports industry as an emerging service sector in regional economic growth; however, its spatial effects are not uniformly positive. Negative spatial spillover effects may arise from the concentration of resources and associated “siphoning effects” during sports industry development, as well as interregional competition over event hosting, industrial layout, and factor allocation. This finding indicates that, in promoting the high-quality development of the sports industry, greater emphasis should be placed on enhancing regional coordination mechanisms and cross-regional industrial specialization systems. Such an approach would enhance local economic benefits while offsetting negative impacts on surrounding areas, thereby fostering coordinated regional economic development.

PMID:42239740 | PMC:PMC13226622 | DOI:10.3389/fspor.2026.1804002

Front Nutr. 2026 May 19;13:1811665. doi: 10.3389/fnut.2026.1811665. eCollection 2026.

ABSTRACT

OBJECTIVE: This study aimed to explore the dose-response associations of serum vitamin D levels with metabolic parameters and microalbuminuria (ACR) in diabetic patients, to identify the critical clinical threshold of vitamin D for renal and metabolic benefits, and to clarify the population heterogeneity of these associations stratified by microalbuminuria status.

METHODS: A total of 485 diabetic patients were retrospectively enrolled and divided into four groups according to vitamin D quartiles: Q1 (≤32.37 nmol/L, n = 121), Q2 (32.38-45.70 nmol/L, n = 121), Q3 (45.71-59.98 nmol/L, n = 122), and Q4 (≥59.99 nmol/L, n = 121). Spearman’s correlation analysis, multivariate linear regression analysis, and restricted cubic spline (RCS) modeling were used for statistical analyses, with a stratified analysis performed by microalbuminuria status.

RESULTS: The median serum vitamin D level was 45.7 nmol/L in this cohort, with a vitamin D deficiency/insufficiency rate of 75.1%. Serum vitamin D levels were significantly inversely correlated with HbA1c (ρ = -0.425), fasting glucose (ρ = -0.386), triglycerides (ρ = -0.358), BMI (ρ = -0.302), and ACR (ρ = -0.286) (all p < 0.001). Compared with Q4, Q1 patients had a 1.95% higher HbA1c (95% CI: 1.52-2.38) and a 68.95 mg/g higher ACR (95% CI: 50.12-87.78). RCS analysis revealed a linear dose-response relationship between vitamin D (20-50 nmol/L) and reductions in HbA1c (0.32% per 10 nmol/L) and ACR (12.75 mg/g per 10 nmol/L), with a plateau effect observed above 50 nmol/L. The inverse association between vitamin D and ACR was significantly stronger in patients with microalbuminuria (β = 75.68 vs. 43.52, interaction p < 0.001).

CONCLUSION: Vitamin D levels are negatively associated with metabolic abnormalities and microalbuminuria in a dose-dependent manner, suggesting that patients with microalbuminuria may have a stronger association, warranting further investigation in prospective studies.

PMID:42239714 | PMC:PMC13229412 | DOI:10.3389/fnut.2026.1811665