Shenyang 242 Hospital

Introduction: In the selective laser melting process, metal powders rapidly absorb energy, melt, and solidify. This rapid thermal cycling causes defects like balling, warping, and cracking, significantly increasing residual stresses and degrading part quality and performance. This study aims to improve the quality and performance of selective laser melting-formed parts by developing and validating a strategy to compensate for detrimental residual stresses. Method: A mathematical model of the temperature field and stress field during selective laser melting forming was established. Stress was simulated under various process parameters using Simufact Additive software. A residual stress compensation strategy utilizing external magnetic fields was proposed. The rationality of this magnetic field-based strategy was then verified using Comsol Multiphysics software. Results: The simulation results demonstrated the significant influence of process parameters on residual stress generation. The verification performed in Comsol Multiphysics confirmed that the proposed external magnetic field compensation strategy is rational and sound. Discussion: This work pioneers an active stress-control strategy for SLM, offering a practical solution to residual stress challenges and enhancing industrial applicability for critical components. Conclusion: Implementing an external magnetic field compensation strategy effectively mitigates residual stresses in selective laser melting, leading to substantial improvements in the quality and performance of the manufactured parts.

Surgical site infections (SSIs), including periprosthetic joint infections (PJIs), represent significant complications following total joint arthroplasty (TJA). The geriatric nutritional risk index (GNRI) serves as an objective measure of nutritional status; however, its predictive value for postoperative infections in TJA patients remains ambiguous. To address this issue, a meta-analysis was conducted alongside a systematic search of PubMed, Embase, and Web of Science. Observational studies that assessed the relationship between preoperative GNRI and postoperative SSI or PJI following TJA were included in the analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) were synthesized using random-effects models to account for heterogeneity.Seven retrospective cohort studies comprising 221,810 patients were analyzed. The results indicated that a low GNRI, which suggests malnutrition, is significantly associated with an increased risk of SSI after TJA (OR = 1.59; 95% CI 1.21-2.08; I² = 81%; p< 0.001). This association persisted across both primary and revision procedures (OR = 1.52 vs. 1.65; p= 0.76) and within 30-day and 90-day follow-ups (OR = 1.58 vs. 1.56; p= 0.98). A more pronounced correlation was found in patients with severe malnutrition (GNRI < 92) compared to those with moderate risk (GNRI: 92-98; OR = 2.18 vs. 1.25; p< 0.001). Although a similar trend was observed for PJI (OR = 2.37; 95% CI 0.73-7.72; p= 0.15), this finding was based on only two studies (three datasets) and remains uncertain.Evidence regarding shoulder arthroplasty was limited; however, existing data suggested trends similar to those seen in hip and knee arthroplasty. In conclusion, preoperative malnutrition, as indicated by a low GNRI, may be associated with an elevated risk of SSIs following TJA.

ObjectiveTo compare visual acuity and visual quality after implantation of Vision Enhancing bifocal intraocular lens (IOL), bifocal IOL or monofocal IOL in patients with age-related cataract.MethodsRetrospective study. Group A was implanted with Vision Enhancing bifocal (bifocal combined extended depth of focus (EDOF)) IOL (Eyebright Medical Technology (Beijing) Co. Ltd. China: AM4UH, 21 eyes), group B was implanted with bifocal IOL (Johnson & Johnson, USA: ZMB00, 21 eyes), and group C was implanted with monofocal IOL (Eyebright Medical Technology (Beijing) Co. Ltd. China: A1UL22, 21 eyes). At 3 months postoperatively, uncorrected distance visual acuity (UDVA) was compared among 3 groups, while uncorrected near visual acuity (UNVA) and uncorrected intermediate visual acuity (UIVA), defocus curves, and visual quality questionnaire results were compared between Group A and B.ResultsThere was no statistically significant difference in UDVA among three groups postoperatively (P > 0.05); in terms of UIVA and UNVA, group A was better than group B (P < 0.05); the defocus curves showed that group A was close to bimodal but tended to be flat, while group B was bimodal; groups A and B became spectacle-independent postoperatively, and 40% of patients in group B reported the halo phenomenon, especially when driving at night.ConclusionVision Enhancing bifocal IOL (AM4UH) exhibited a better UIVA and UNVA, indicating a continuous visual range. And patients implanted with AM4UH achieved postoperative spectacle independence, with less visual disturbance.

Cognitive impairment is a debilitating comorbidity in temporal lobe epilepsy (TLE), linked to suppressed hippocampal neurogenesis in the chronic phase. Building on evidence that links SDF-1 to epilepsy, emerging research, including our own preliminary data, suggests that its cleaved product, SDF-1(5-67), may play a critical role in this process. To investigate the therapeutic potential of SDF-1(5-67) neutralizing antibody (NAb) in a kainic acid (KA)-induced temporal lobe epilepsy (TLE) model. TLE was induced in male Wistar rats by intraventricular KA injection. Animals were divided into acute (8 days) and chronic (72 days) phase groups, including acute phase control (SHAM-A), acute phase epilepsy model (EP-A), SDF-1(5-67) NAb-treated acute phase epilepsy (S + EP-A), chronic phase control (SHAM-C), chronic phase epilepsy model (EP-C), and SDF-1(5-67) NAb-treated chronic phase epilepsy groups (S + EP-C). NAb treatment was administered via osmotic pumps. Neurogenesis (DCX + cells), neuronal loss (Nissl staining), MFS (Timm staining), cognition (Morris water maze), and SDF-1(5-67) expression (western blot) were assessed. Data were analyzed by one-way ANOVA with Tukey's post hoc test, or repeated-measures ANOVA for water maze latency, presented as mean ± SEM. During the acute phase, increased dentate gyrus (DG) neurogenesis in EP-A vs. SHAM-A (210.43 ± 12.16 vs. 94.25 ± 7.76 cells/mm², P < 0.05) was unaffected by NAb (195.84 ± 9.71, P > 0.05). In the chronic phase, EP-C showed suppressed neurogenesis (51.63 ± 7.36 vs. SHAM-C 85.12 ± 5.51, P < 0.01), which was rescued by NAb (77.56 ± 9.88, P < 0.01). CA3 neuronal loss was attenuated by NAb in EP-C (174.33 ± 13.06 vs. EP-C 127.47 ± 10.22, P < 0.05). MFS was increased in both phases and was unaffected by NAb. NAb improved cognitive deficits in EP-C (escape latency: 28.14 ± 1.6s vs. EP-C 35.80 ± 2.41s, P < 0.05). NAb suppressed SDF-1(5-67) expression in both phases (P < 0.05). SDF-1(5-67) NAb promoted neurogenesis and reduced neurodegeneration in chronic TLE, and improved cognitive function without affecting MFS or seizure duration. These findings highlight its potential for postepileptic cognitive rehabilitation.

Postoperative acute respiratory distress syndrome (ARDS), characterized by bilateral infiltrates and severe hypoxemia, is a critical complication following thoracic surgery, particularly lung resection. Perioperative transfusions and mechanical ventilation strategies are potential contributors to ARDS development, yet the exact mechanisms driving this association remain incompletely understood. Despite advancements in surgical and perioperative care, ARDS remains a severe complication with a high mortality rate. This study explores the occurrence of ARDS in two patients with nonsmall-cell lung cancer postlung resection, focusing on the association of intraoperative blood transfusion and mechanical ventilation parameters. Both patients received intraoperative blood transfusions (>2 U red blood cells) and exhibited elevated peak plateau pressure (30–31 cmH₂O) with tidal volumes of 6 to 8 mL/kg. Postoperatively, both patients developed acute pulmonary edema and hypoxemia, requiring intensive care management, including mechanical ventilation, lung-protective ventilation strategies, restrictive fluid management, and pharmacological therapy. One patient recovered and was discharged, whereas the other died. ARDS after lung resection arises from synergistic insults, including transfusion-induced inflammation, mechanical ventilation stressors, and reduced pulmonary reserve. Strict adherence to lung-protective ventilation, restrictive transfusion volumes, and multidisciplinary perioperative care are essential to improve outcomes. Future research should prioritize multicenter studies to validate causal mechanisms and refine evidence-based protocols, addressing the urgent need for targeted therapies to reduce ARDS-related mortality.

To identify novel pathogenic genes and variants responsible for oocyte degeneration and death. Whole-exome sequencing was conducted in 78 individuals with primary infertility characterized with oocyte degeneration and death, followed by Sanger sequencing of candidate variants. Pathogenicity of identified COX15 variants was characterized through morphological assessment, AlphaFold3-based structural modeling and functional validation including Western blotting and immunofluorescence. We identified a compound-heterozygous COX15 variants and a homozygous COX15 variant in two affected individuals with oocyte degeneration. The variants c.C664T [p.R222C] was a previously reported recurrent pathogenic variant. The clinical records showed that majority of oocytes retrieved from affected individuals were immature and degenerated. Structural modeling assay showed that all the COX15 variants affected the binding pocket with heme o. The compound-heterozygous COX15 variants c.C905T [p.P302L] and c.C664T [p.R222C] in family 1 significantly decreased COX15 protein level in HeLa cells. While the homozygous variant c.C647T [p.P216L] decreased the COX1 protein level in oocytes from family 2 (II-1), implying the disruption of respiratory complex IV (COXIV) assembly. Our study identified two novel variants in COX15, and functional analysis confirmed the pathogenicity of the variants. Our findings expand the mutational spectrum of COX15 and making it a potential genetic diagnostic marker for those suffering from female infertility causing by oocyte degeneration.