Search Results (655)

Piezoelectric semiconductor PN junctions hold considerable promise for self-powered sensing, flexible electronics, energy harvesting, photodetection, and multifunctional micro/nanodevices. A local temperature change couples the built-in electrical response of the PN doping interface with the thermally induced response at the boundaries of the heated region, thereby modifying the electric potential, electric field, electric displacement, and carrier distributions near the junction. To elucidate this coupling mechanism, a one-dimensional three-interface analytical model is developed for a piezoelectric semiconductor PN junction subjected to a local temperature change. The fiber is divided into cold P-type, heated P-type, heated N-type, and cold N-type regions, and the coupled response is determined using piecewise analytical solutions together with open-circuit end conditions, interface continuity conditions, global carrier-conservation constraints, and reference-point conditions. Within a linear small-perturbation framework for an ideal zero-thickness homojunction, numerical results show that the PN doping interface governs the baseline distributions of the built-in potential and electric field, whereas the temperature interfaces generate additional electric fields through temperature-induced electric-displacement compensation, leading to localized redistribution of holes and electrons. For the baseline ZnO case with a 0.5 K temperature increment, the potential span is 9.124 mV, the peak electric-field magnitude is 48.43 kV m⁻¹, and the maximum carrier perturbation is 0.180 of its regional reference concentration. Independent Galerkin finite-element calculations agree with the analytical solution, with a maximum normalized discrepancy of 0.553% on the finest mesh. The temperature-change amplitude, heated-region half-width, reference carrier-concentration level, P/N doping asymmetry, effective dielectric constant, and effective thermal electric-displacement coefficient modify the potential transition, electric-field peaks, and carrier-screening range near the junction. These results reveal the coupled interaction between the local temperature interfaces and the PN doping interface and provide a theoretical basis for thermally regulating piezoelectric semiconductor junction devices under localized thermal loading. Full article

Physics-based models are useful for the analysis and optimization of crystalline-silicon solar cells when many device designs must be evaluated. This paper presents a compact transfer-matrix framework for one-dimensional carrier transport and physics-constrained optimization in bifacial $p^{+}$–n–$n^{+}$ crystalline-silicon solar cells under front-side illumination. The model includes a distributed optical generation profile, explicit emitter, base, and rear-field regions, surface recombination, doping-dependent mobility, Auger recombination, band-gap narrowing, sheet and contact resistances, and external series and shunt losses. The front and rear dopant distributions are described by complementary-error-function profiles, so their junction depths follow from the diffusion parameters and base concentration instead of being independent optimization variables. The solver is verified in limiting transport conditions and with tabulated generation data. The complete model is then calibrated against the reported photovoltaic figures of merit of an experimental bifacial n-type passivated-emitter and rear-totally-diffused (n-PERT) solar cell, which serves as the reference device and is subsequently applied to global optimization. The calibration reproduces a short-circuit current density of $J_{sc}=39.20\mathrm{mA}/{\mathrm{cm}}^2$, an open-circuit voltage of $V_{oc}=653.1\mathrm{mV}$, a fill factor of 0.783, and an efficiency of 20.05%. For the 180 µm reference geometry, the optimized design reaches an efficiency of 20.63%. Independent optimizations for wafer thicknesses of 160, 180, and 200 µm produce a consistent family of solutions with efficiency gains of approximately 0.56–0.60 percentage points. These gains result from the higher open-circuit voltage and fill factor despite a moderate reduction in short-circuit current density, while the optimized total series resistance remains nearly constant. The framework provides a physically interpretable method for combining carrier-transport modeling, experimental calibration, inverse design, and repeated global optimization. Full article

Objectives: This study aimed to explore the combined regulatory effects of probiotics combined with bioactive compounds on intestinal immunity and mucosal barrier function. Methods: Fifty specific-pathogen-free (SPF) male Kunming mice (5–6 weeks old, weighing 20 ± 2 g) were randomly assigned to five groups (n = 10 per group): blank control (C), lipopolysaccharide-induced model (LPS), probiotic (PB), antioxidant (AO), and combined treatment (PB/AO). The C and LPS groups received daily oral gavage of 0.5 mL sterile 0.9% saline. The PB group received a daily gavage of 1 × 10⁸ CFU/mL Pediococcus acidilactici lindner and Lactobacillus plantarum. The AO group was administered a daily gavage of berberine (30 mg/kg BW), wogonin (30 mg/kg BW), and sodium butyrate (200 mg/kg BW). The PB/AO group received a daily gavage combining the probiotic mixture (1 × 10⁸ CFU/mL) with the plant extracts (30 mg/kg BW berberine, 30 mg/kg BW wogonin, and 200 mg/kg BW sodium butyrate). Following a 14-day preventive intervention, all groups except C were intraperitoneally injected with LPS to induce inflammation. Indices of visceral organs, serum antioxidant and immune parameters, ileal histomorphology, gut microbiota composition, and the expression of key barrier- and inflammation-related genes were comprehensively evaluated. Results: LPS exposure increased liver and spleen coefficients. PB/AO treatment significantly reduced the LPS-induced elevation of liver coefficient to a level comparable to that of the C group; however, no significant improvement in spleen coefficient was observed. In terms of antioxidant and immune indices, all intervention groups increased the levels of SOD, GSH-Px, and T-AOC to varying degrees, and decreased the levels of MDA and inflammatory factors (TNF-α, IL-1β, IL-6, and DAO), with the PB/AO group showing the most significant improvement (p < 0.01). Ileal microbiome analysis showed that PB/AO treatment enriched Firmicutes, Lactococcus and Lactobacillus but decreased Proteobacteria, with Clostridia as signature taxa. Mechanistically, PB/AO suppressed the transcription of NF-κB pathway-related genes (TLR4, MyD88 and NF-κB) and upregulated the expression of tight junction proteins (ZO-1, Claudin-1 and Occludin), thereby strengthening the intestinal barrier. Conclusions: In conclusion, co-administration of microbial probiotics and antioxidants achieves optimal protection against LPS-induced intestinal inflammation by jointly driving anti-inflammatory and antioxidative responses, modulating gut microbiota, and reinforcing barrier integrity. Full article

Background: Determining the appropriate magnitude of lumbar lordosis (LL) correction in adult spinal deformity (ASD) remains controversial. The fused spinopelvic angle (FSPA), a posture-independent parameter, may provide a geometric measure of fused-construct orientation associated with proximal junctional kyphosis (PJK) risk. Methods: This retrospective single-center study included 258 patients aged ≥65 years with ASD and pure sagittal malalignment associated with lumbar degenerative kyphosis/drop body syndrome who underwent long-segment fixation from T10 to the sacrum with sacropelvic fixation. Patients were divided into non-PJK (n = 135) and PJK (n = 123) groups. Adjusted nested logistic regression models, receiver operating characteristic (ROC) analysis, and DeLong comparison were used to evaluate the association of FSPA with PJK and its incremental value beyond postoperative pelvic incidence–lumbar lordosis (PI-LL). Results: Postoperative FSPA was lower in the PJK group (p < 0.001) and remained independently associated with PJK in the fully adjusted model including postoperative PI-LL (adjusted OR = 0.910 per degree; 95% CI, 0.866–0.957; p < 0.001). FSPA showed greater discriminatory ability than postoperative PI-LL (AUC, 0.694 vs. 0.596; difference, 0.099; 95% CI, 0.035–0.162; DeLong p = 0.002). Adding FSPA to the clinical model containing postoperative PI-LL significantly improved model fit (likelihood-ratio p < 0.001). The cohort-derived FSPA threshold of 2.38° yielded 64.2% sensitivity and 63.7% specificity. Conclusions: Higher postoperative FSPA was independently associated with lower odds of radiographic PJK and provided additional predictive information beyond postoperative PI-LL. The identified threshold of 2.38° may serve as a preliminary reference for postoperative alignment in this selected cohort. Full article

Purpose: This study investigated the surface morphology and roughness of the dental implant platform and abutment at their junction interface, comparing parameters before and after mechanical assembly (screwing). Methods: The experimental specimens comprised 40 implants from the TBR, Bone Level M System (TBR, France) with a diameter of 4.7 mm and a length of 10 mm, and 40 matching abutments from the same system (Titanium Standard Abutment, TBR, France) with a diameter of 4 mm and a gingival height of 3 mm. All components were fabricated from Grade 4 titanium. The implants and abutments were divided into two equal groups. In the first group (control), 20 implants and 20 abutments remained unassembled. In the second group, 20 implants were coupled with 20 abutments and tightened to the manufacturer-recommended torque. To achieve this, the implants were stabilized with pliers to prevent rotation, and the abutments were screwed using a screwdriver and a torque wrench at 30 N.cm. Subsequently, the abutments were unscrewed counterclockwise. Surface evaluations were conducted using scanning electron microscopy (SEM) and 3D surface modeling. Results: The obtained results demonstrate a statistically significant reduction in the parameters reflecting the roughness of the implant platform. Based on the analysis, a pronounced decrease in the average roughness (Ra, Rq) of the abutment was observed (p < 0.001). Furthermore, it was established that the implant platform exhibits nearly twice the surface roughness of the abutment even in its baseline state. Conclusions: Within the limitations of this in vitro study, a single tightening and removal procedure was associated with measurable changes in the roughness parameters and surface morphology of the implant platform and abutment. These findings indicate microtopographic adaptation at the conical interface under the tested conditions; however, biomechanical reliability and resistance to bacterial micro-leakage were not evaluated. Full article

This study investigates the responses in the resistance of polypyrrole (PPy) and titanium dioxide (TiO₂) single layers and PPy/TiO₂ heterostructures to rectangular pulses of monochromatic LED illumination under controlled relative humidity. Exposure to moisture increases the resistance of PPy while rapidly decreases that of TiO₂, reflecting opposite effects of electron donation from hydroxyl (–OH) groups in adsorbed H₂O on the majority carrier densities of the two materials. Under monochromatic illumination, the resistance of PPy decreases, whereas that of TiO₂ increases accompanied by a brief transient at excitation wavelengths near its optical edge (367 nm and 398 nm). This photoresponse is attributed to photoinduced modifications of carrier density through two opposing processes: photogeneration, which enhances charge carriers, and H₂O photodesorption, which reduces them. A combination of illumination and moisture exposure results in an intensified photoresponse of PPy, thereby enhancing its humidity response. The PPy/TiO₂ heterostructure demonstrates a mixed photoresponse arising from contrasting behaviors of its p-type PPy and n-type TiO₂ components, coupled with charge exchange across the p–n junction. When simultaneously exposed to moisture and monochromatic light, the heterostructure undergoes contrasting photoinduced carrier generation in its two components, which in turn modulates the depletion region in inverse phase with carrier density, thereby intensifying the overall photoresponse. This complementary “push–pull” interaction synergistically enhances both the photoresponse and the humidity response of the PPy/TiO₂ heterostructure. Full article

Trimethylamine-N-oxide (TMAO), a gut microbiota-derived metabolite, is a known risk factor for cardiovascular disease. We previously showed that TMAO induces NLRP3 inflammasome activation and contributes to endothelial dysfunction. However, the upstream mechanisms linking TMAO to inflammasome activation and barrier injury remain unclear. In the present study, we examined whether membrane raft (MR) redox signaling contributes to TMAO-induced NLRP3 inflammasome activation and endothelial dysfunction. MR clustering, colocalization of MRs with NADPH oxidase subunits, inflammasome formation, and junction protein expression were assessed by Western blot analysis. RT-qPCR was performed to further assess the mRNA expression of junctional genes. Superoxide production was measured by electron spin resonance (ESR), caspase-1 activity was determined using a biochemical assay kit, IL-1β production was measured by ELISA, and endothelial permeability was evaluated using an FITC-dextran assay. TMAO increased MR clustering in endothelial cells in a dose-dependent manner. TMAO also enhanced the colocalization of MRs with p47phox and gp91phox, indicating the formation of an MR-associated redox signaling axis. In addition, TMAO increased superoxide production; promoted NLRP3 inflammasome formation; elevated caspase-1 activity and IL-1β production; reduced the expression of ZO-2, ZO-1, VE cadherin and occludin; and increased endothelial permeability. Pretreatment with the MR disruptor MCD, the NADPH oxidase inhibitor DPI, or the caspase-1 inhibitor WEHD significantly attenuated these TMAO-induced effects. These findings demonstrate that TMAO-mediated endothelial injury is dependent on the MR-associated redox signaling axis. TMAO promotes MR-associated redox signaling, leading to NADPH oxidase activation, superoxide generation, NLRP3 inflammasome activation, disruption of endothelial junction proteins, and barrier dysfunction. Targeting MR-associated signaling pathways may offer a novel therapeutic strategy to mitigate TMAO-induced vascular inflammation and endothelial dysfunction. Full article

The Youjiang Basin is located in the southwestern margin of the South China Block and at the junction between the South China and Indochina Blocks at the eastern end of the Tethyan tectonic domain. The processes responsible for Triassic magmatism in the basin are crucial to understanding the closure of the Paleo-Tethys Ocean. This study presents the geochemistry and zircon U-Pb-Hf isotopes of granites from the Pingxiang area in the southwestern Youjiang Basin. The granites belong to the high-K and peraluminous series with A/CNK ratios of 1.16–1.38. They have high SiO₂ and K₂O contents and moderate Al₂O₃ content with moderately fractionated REE patterns (La_N/Yb_N = 6.35–7.83) and negative Ba, Sr, P and Ti anomalies, consistent with peraluminous A₂-type granites. The granites have LA-ICP-MS zircon U-Pb ages of 243–241 Ma, with negative εHf_(t) values ranging from −13.22 to −6.52 and T_DM2 model ages from 1654 to 2073 Ma. They were formed by partial melting of Paleoproterozoic metasedimentary rocks in an extensional setting. Combined with existing data, we suggest that the 243–241 Ma extensional event is related to the subduction-to-collision transition likely induced by slab breakoff during the closure of the Paleo-Tethys Ocean. Full article

A^IVB^VI semiconductors, particularly lead chalcogenides, remain key materials for mid-wave infrared (MWIR) photodetection due to their narrow bandgap and exceptional carrier transport properties. However, the realization of high-quality p-type PbTe thin films, suitable for p–n junction devices, remains a technological challenge. In this work, we report the fabrication of high-mobility p-type PbTe thin films grown on muscovite mica by electron beam-assisted physical vapor deposition. The films were derived from a Te-rich Pb_0.999Te_1.001 ingot, enabling controlled acceptor formation via excess tellurium. Structural characterization reveals growth with strong (111) texture, large grain size, and low surface roughness. Comprehensive electrical measurements in the range of 80–300 K show a record room-temperature hole mobility of 876 cm²/V·s, achieved under optimized fabrication conditions. This figure approaches values typical for epitaxial n-type PbTe, indicating low scattering and high crystallinity. These results establish an effective route for producing strongly (111)-textured p-type PbTe films with high room-temperature hole mobility through optimized deposition and post-deposition annealing. Full article

Aim: Radiation-induced intestinal injury is one of the major dose-limiting complications of abdominal radiotherapy and is closely associated with oxidative stress, inflammation, and disruption of epithelial barrier integrity. The present study aimed to investigate the protective effects of verapamil on radiation-induced small-intestinal injury in rats by evaluating histopathological alterations together with tissue levels of TNF-α, 5-LOX, Nrf2, and ZO-1 as markers related to inflammatory, redox-associated, and tight-junction-associated responses. Materials and Methods: Thirty female Wistar albino rats were divided into three groups: Normal Control (n = 10), Radiation + Saline (RAD, n = 10), and Radiation + Verapamil (n = 10). Whole-abdomen irradiation was performed using a single 12 Gy dose delivered by a 6 MV linear accelerator. Verapamil (10 mg/kg/day, s.c.) treatment was started 5 days before irradiation and continued for 5 days afterward. Histopathological injury in jejunal tissues was evaluated using hematoxylin–eosin staining. Tissue levels of TNF-α, 5-LOX, Nrf2, and ZO-1 were measured using ELISA. Results: Whole-abdomen irradiation caused marked histopathological injury characterized by villus disruption, glandular degeneration, and mucosal architectural damage. Irradiation significantly increased small-intestinal TNF-α and 5-LOX levels while decreasing Nrf2 and ZO-1 levels compared with the Normal Control group (p < 0.05). Verapamil treatment significantly attenuated radiation-induced histopathological injury and reduced TNF-α and 5-LOX levels. TNF-α returned to values comparable with the Normal Control group, whereas 5-LOX remained significantly elevated. Verapamil also partially restored Nrf2 and ZO-1 levels compared with the RAD group (p < 0.05), although both remained significantly lower than control levels. Conclusions: Verapamil attenuated radiation-induced small-intestinal injury and was associated with favorable modulation of TNF-α, 5-LOX, Nrf2, and ZO-1 levels. The protective response was partial, with persistent differences in 5-LOX, Nrf2, and ZO-1 compared with controls. These biomarker changes should not be interpreted as direct evidence of functional pathway activation or preservation of intestinal barrier function. Further studies incorporating direct mechanistic and functional assessments are warranted before clinical translation. Full article

Vitamin D and its metabolite 25-hydroxyvitamin D₃ (25-OH-D₃) are central to calcium homeostasis, maternal skeletal integrity, and sow reproductive efficiency. This study compared vitamin D₃ with an equivalent supranutritional dose of chemically or microbially produced 25-OH-D₃ from day 90 of gestation to weaning. A total of 100 Large White × Landrace sows were assigned to five treatments (n = 20): a basal control (25 µg/kg vitamin D₃), a VD₃ group (basal + 50 µg/kg vitamin D₃), and three 25-OH-D₃ groups (basal + 50 µg/kg 25-OH-D₃; QV1–QV3). Reproductive traits, colostrum composition, serum vitamin D-related indices, antioxidant and cytokine profiles, pre-weaning piglet growth, femoral mineral concentration, intestinal morphology, and barrier-related gene expression were assessed. Compared with the control, QV2 increased litter weight gain from birth to day 14 by 9.8%, piglet serum 25-OH-D₃ at weaning by 33.2%, and femoral calcium concentration by 14.4% (p < 0.05); litter and average piglet weights at weaning were unchanged. Maternal 25-OH-D₃ supplementation also altered the overall redox profile and several circulating inflammatory cytokines, increased jejunal and ileal villus height in the QV2 and QV3 groups, and upregulated selected tight-junction-related genes, including occludin and ZO-1, in a source- and intestinal-segment-dependent manner (p < 0.05). Responses were source-dependent, and QV2 showed the strongest effects for selected endpoints; the data do not support class-wide superiority of biosynthesized preparations. Full article

Background: Memantine, an uncompetitive and voltage-dependent N-methyl-D-aspartate (NMDA) receptor antagonist, is clinically established for moderate-to-severe Alzheimer’s disease. Its pharmacodynamic profile, low-to-moderate affinity, rapid open-channel block, and strong voltage dependency allows selective inhibition of pathological NMDA overactivation while preserving physiological neurotransmission. Increasing evidence shows that these same mechanistic principles operate in the peripheral nervous system, where NMDA receptors contribute to excitotoxicity, oxidative stress, neuroinflammation, and maladaptive nociceptive signaling. Purpose: To synthesize emerging preclinical and clinical evidence demonstrating memantine’s modulatory and neuroprotective actions in peripheral neurons and glia and to outline implications for drug repurposing across neurology, pain medicine, oncology, supportive care, and ophthalmology. Methodology: A narrative integration of mechanistic studies, in vivo preclinical models, and heterogeneous clinical trials evaluating memantine’s effects on peripheral sensory neurons, autonomic neurons, Schwann cells, retinal ganglion cells, and neuromuscular junction physiology. Evidence was examined across conditions involving excitotoxicity, oxidative injury, mitochondrial dysfunction, apoptotic signaling, neuroinflammation, and neuropathic pain amplification. Results: Memantine consistently attenuates peripheral excitotoxic calcium influx, suppresses NOX-2–mediated ROS generation, stabilizes mitochondrial membrane potential, modulates Bax/Bcl-2 signaling, and reduces neuroinflammatory cytokine activity. It also inhibits dorsal horn wind-up selectively under neuropathic conditions. These convergent mechanisms yield protective effects across chemotherapy-induced peripheral neuropathy (CIPN), diabetic neuropathy, traumatic nerve injury, phantom limb pain, retinal ganglion cell excitotoxicity, and organophosphate-induced neuromuscular toxicity. Clinical evidence includes improved multimodal neuropathy outcomes in diabetic neuropathy when combined with gabapentin, reduced phantom limb pain prevalence and intensity at six months, and a five-fold reduction in post-mastectomy neuropathic pain with pre-emptive administration. Conclusions: Memantine should be conceptually reframed as a system-wide neuroprotective agent with substantial translational potential beyond the CNS. Priorities for future development include NR2B-selective peripheral NMDA antagonists, peripherally restricted formulations, single-cell transcriptomic mapping of peripheral NMDA receptor subtypes, and adequately powered PNS-specific randomized trials. Full article

Background/Objectives: Proximal junctional kyphosis (PJK) is a frequent mechanical complication following adult spinal deformity (ASD) surgery, and osteoporosis is a well-recognized risk factor. However, whether the underlying risk factor profiles for PJK differ according to bone mineral density status remains unclear. This study aimed to identify and compare independent risk factors for PJK between osteoporotic and non-osteoporotic patients following long-segment posterior spinal fusion for ASD. Methods: This retrospective cohort study included 356 patients who underwent ≥5-level posterior fusion to the sacrum or pelvis for ASD with a 2-year follow-up. Patients were stratified into a non-osteoporotic (non-OP; n = 284) and an osteoporotic (OP; n = 72) group based on preoperative dual-energy X-ray absorptiometry (T-score ≤ −2.5). PJK was defined as a proximal junctional angle (PJA) ≥20° with an increase of ≥10° from the preoperative value. Demographic, surgical, and radiographic variables were analyzed separately for each group using univariate and stepwise multivariate logistic regression analyses. Predictive performance was assessed using receiver operating characteristic curve analysis. Results: The overall PJK incidence tended to be higher in the OP group than the non-OP group (36.1% vs. 24.6%, p = 0.055), and fracture-type PJK occurred significantly more frequently in osteoporotic patients (29.2% vs. 15.8%, p = 0.016). The variables that reached statistical significance differed between the two groups. In the non-OP group, lower Hounsfield units at the upper instrumented vertebra (UIV; OR = 0.990, p = 0.011), higher preoperative PJA (OR = 1.098, p < 0.001), and greater L1 pelvic angle (L1PA) offset indicating relative overcorrection (OR = 1.136, p < 0.001) were independent predictors of PJK. In the OP group, higher preoperative PJA (OR = 1.149, p = 0.007) and greater age-adjusted pelvic incidence–lumbar lordosis offset (OR = 1.052, p = 0.039) were identified as independent risk factors. Multivariable models demonstrated acceptable discriminative ability in both groups (area under the curve [AUC] = 0.741, 95% confidence interval [CI] = 0.671–0.804 for the non-OP group; AUC = 0.753, 95% CI = 0.632–0.867 for the OP group; optimism-corrected AUC 0.729 and 0.735 after bootstrap internal validation). Conclusions: The variables associated with PJK differed according to osteoporosis status following ASD surgery. Careful UIV selection avoiding kyphotic junctional alignment may be relevant for both groups. Avoiding overcorrection relative to the age-adjusted target may warrant particular attention in osteoporotic patients, while UIV bone quality and L1PA overcorrection may be relevant to surgical planning in non-osteoporotic patients. Full article

Background and Objectives: Evidence regarding predictors of pathological response and long-term outcomes in older patients receiving perioperative FLOT chemotherapy for resectable gastric or gastroesophageal junction cancer remains limited. We aimed to identify factors associated with pathological response and survival in patients aged ≥65 years treated with neoadjuvant FLOT. Materials and Methods: This retrospective single-center study included 86 consecutive patients (median age, 69 years; 72.1% male) aged ≥65 years with resectable gastric or gastroesophageal junction adenocarcinoma who underwent neoadjuvant FLOT chemotherapy followed by curative-intent gastrectomy. Major pathological response was defined as College of American Pathologists tumor regression grade (CAP TRG) 0–1. Logistic regression analyses were performed to identify predictors of pathological response. Disease-free survival (DFS) and overall survival (OS) were analyzed using the Kaplan–Meier method and Cox proportional hazards regression analyses. Results: Overall, 14 patients (16.3%) achieved a major pathological response. Body mass index (BMI) ≥ 25 kg/m² (OR 5.13, p = 0.04) was independently associated with a major pathological response. During a median follow-up of 29.2 months, 39 patients (45.3%) developed recurrence and 35 (40.7%) died. ECOG performance status (ECOG PS) ≥ 1 was independently associated with both inferior DFS (HR = 2.76, p = 0.02) and OS (HR = 2.52, p = 0.045). In addition, ypN stage 2–3 (HR = 2.58, p = 0.008) was independently associated with worse DFS, whereas positive surgical margins were independently associated with worse OS (HR = 2.62, p = 0.02). Conclusions: In older patients with resectable gastric or gastroesophageal junction adenocarcinoma treated with perioperative FLOT chemotherapy, baseline BMI was independently associated with major pathological response, whereas ECOG PS and postoperative pathological factors were independently associated with survival. These findings highlight the importance of careful patient selection and individualized multimodal treatment in this population. Full article

This study investigated the pathological processes by which two Salmonella strains induce orchitis and impair spermatogenesis in mice, with emphasis on inflammation and blood–testis barrier (BTB) integrity. Thirty male Kunming mice were randomly assigned to the human-derived Salmonella enterica serovar Enteritidis H71 group, the sheep-derived Salmonella enterica serovar Agona W42 group, or the phosphate-buffered saline control group (n = 10 per group). An acute orchitis model was established by intrascrotal injection. Histopathological examination revealed marked testicular and epididymal lesions, disruption of the spermatogenic epithelium, and reduced sperm abundance in infected mice. Transcriptomic analysis identified 4546 differentially expressed genes shared by the two infected groups and showed enrichment of the Toll-like receptor (TLR), nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK) signaling pathways. Real-time quantitative PCR further showed increased expression of interleukin 6 (Il6), interleukin 1 beta (Il1b), and tumor necrosis factor (Tnf), accompanied by reduced expression of tight junction protein 1 (Tjp1), occludin (Ocln), and synaptonemal complex protein 3 (Sycp3) in infected mice (p < 0.05), except for Tjp1 in the W42 group. These findings indicate that Salmonella-induced inflammatory activation is associated with BTB disruption and impaired spermatogenesis, providing a basis for further investigation of bacterial orchitis and zoonotic reproductive risks. Full article