Objective: To identify early clinical predictors associated with dysphagia and delayed swallowing recovery in patients with traumatic brain injury (TBI). Methods: In this retrospective study, we enrolled adult TBI patients admitted to the rehabilitation unit of a tertiary medical center between June 2019 and June 2023. Data on baseline characteristics, neurological status, imaging findings, and rehabilitation-related variables were collected. Swallowing function was assessed using two indicators: (1) nasogastric (NG) tube retention and (2) the Functional Oral Intake Scale (FOIS) scores at 1, 4, and 12 weeks post-injury. Regression analyses were conducted to identify predictors associated with dysphagia and swallowing recovery. Results: A total of 160 patients were included. At 1 week post-injury, longer intensive care unit (ICU) stay, poor initial sitting balance and use of sedative medication in ICU were associated with NG tube retention. At 4 weeks, lower initial Rancho Los Amigos Scale (RLAS) scores, immobility-related complications, longer hospitalization, and temporal lobe hematomas were associated with persistent NG tube dependence. By 12 weeks, older age, delayed ability to follow commands, and poor initial sitting balance remained associated with NG tube retention. FOIS outcomes were also associated with older age, delayed time to follow commands, impaired initial sitting balance, prolonged ICU stay, temporal lobe hematomas, lower initial RLAS scores, immobility-related complications, prolonged endotracheal tube placement and extended hospital stays. Conclusion Impaired cognitive status, poor physical function, immobility-related complications, and temporal lobe hematomas were key factors associated with dysphagia and delayed oral intake in individuals with TBI.

AIM To establish an HPLC method for the simultaneous content determination of 5-hydroxymethylfurfural,chlorogenic acid,caffeic acid,strychnine,paeoniflorin,ferulic acid,paeoniflorin Ⅰ,epimedium glycoside,psoralen,isopsoralen and glycyrrhetinic acid in Bunao Soft Capsules.METHODS The analysis was performed on a 35 ℃ thermostatic Waters Symmetry C18 column(250 mm×4.6 mm,5 μm),with the mobile phase comprising of acetonitrile-0.1％phosphoric acid flowing at 1.0 mL/min in a gradient elution manner,and the detection wavelengths were set at 230,280 nm.RESULTS Eleven constituents showed good linear relationships within their own ranges(r＞0.999 0),whose average recoveries were 98.47％-103.30％with RSDs of 1.13％-2.80％.CONCLUSION This simple and reliable method can be used for the quality control of Bunao Soft Capsules.

Objective Low-density lipoprotein cholesterol(LDL-C)is causally associated with atherosclerotic cardiovascular disease(ASCVD).Proprotein convertase subtilisin/kexin type 9(PCSK9)increases the degradation of low-density lipoprotein receptor(LDL-R),thereby promoting lipid accumulation.This study investigated the mechanism of microRNA(miRNA)-125a-5p in regulating PCSK9 transcriptional expression and lipid accumulation through histone deacetylase sirtuin 6(SIRT6)-mediated histone acetylation.Methods RAW264.7 macrophages exposed to oxidized low-density lipoprotein(ox-LDL)were used to establish a macrophage lipid accumulation model.The cells were divided into eight groups:control group(Group A),ox-LDL group(Group B),SIRT6 agonist group(Group C),si-SIRT6 group(Group D),miR-125a-5p mimic group(Group E),miR-125a-5p mimic negative control group(Group F),miR-125a-5p inhibitor group(Group G),and miR-125a-5p inhibitor negative control group(Group H).Oil red O staining was used to verify lipid ac-cumulation in macrophages.Real-time fluorescent quantitative polymerase chain reaction(PCR)was employed to detect the gene expression levels of miR-125a-5p,SIRT6 and PCSK9.Western blotting was used to detect the protein expression levels of SIRT6,histone 3 lysine 9 acetylation(H3K9ac),histone 3(H3),and PCSK9.An LDL-C kit was used to measure cellular LDL-C con-tent.Results Compared with Group A,Group B exhibited increased relative gene expression of miR-125a-5p,decreased relative SIRT6 gene and its protein expression,increased H3K9ac/H3 rati-o,increased relative gene and protein expression of PCSK9,and elevated LDL-C levels,with statis-tically significant differences(P＜0.01).In Group B,a positive correlation was observed between H3K9ac and PCSK9 protein expression(r=0.935 0,P＜0.01),as well as between PCSK9 and LDL-C(r=0.981 3,P＜0.01).Compared with Group B,Group C showed no significant change in miR-125a-5p expression(P＞0.05),but increased relative SIRT6 gene and its protein expres-sion,decreased H3K9ac/H3 ratio,decreased relative gene and protein expression of PCSK9,and reduced LDL-C levels(P＜0.01).In contrast,Group D,compared with Group B,had no signifi-cant change in miR-125a-5p gene expression(P＞0.05),but decreased relative gene and protein expression of SIRT6,increased H3K9ac/H3 ratio,increased relative PCSK9 gene and its protein expression,and elevated LDL-C levels(P＜0.05 or P＜0.01).Group E,compared with Group B,showed increased relative gene expression of miR-125a-5p,decreased relative SIRT6 gene and its protein expression,increased H3K9ac/H3,increased relative PCSK9 gene and its protein ex-pression,and elevated LDL-C levels(P＜0.01).Group G,compared with Group B,had de-creased relative gene expression of miR-125a-5p,increased relative gene and protein expression of SIRT6,decreased H3K9ac/H3 ratio,decreased relative PCSK9 gene and protein expression,and reduced LDL-C levels(P＜0.01).No significant changes were observed in miR-125a-5p,SIRT6,H3K9ac/H3 ratio,PCSK9,or LDL-C levels in Groups F and H compared with Group B(P＞0.05).Conclusion Epigenetics is an important regulatory mechanism in the development of ather-osclerosis(AS).Elevated LDL-C is a significant risk factor for AS,and increased PCSK9 expres-sion exacerbates lipid accumulation.Imbalance in histone acetylation is a novel mechanism involved in PCSK9-mediated lipid accumulation,potentially serving as an early detection marker for lipid me-tabolism disorders.SIRT6 acts as a protective factor by reversibly regulating PCSK9 transcriptional expression,reducing lipid accumulation,and delaying AS progression.MiR-125a-5p,as an up-stream regulatory gene of SIRT6,targets and inhibits SIRT6 transcription,thereby modulating his-tone acetylation,and may serve as a new target for early screening and prevention of dyslipidemia.

Objective:To assess the relationship between basophil levels and mortality in patients with intra-abdominal infection.Methods:Information on patients with intraperitoneal infection admitted to the intensive care unit were extracted from the MIMIC database.A time-dependent Cox regression model was used to adjust for confounders associated with 28-day mortality.Propensity score matching(PSM)was used to balance the baseline differences be-tween groups with different basophil levels,and a restricted cube chart(RCS)was used to show the relationship between basophil count and 28-day mortality in patients with intra-abdominal infection.Results:A total of 4403 patients with intra-abdominal infection were enrolled in the MIMIC database.Patients with high basophil levels have lower mortality than those with low basophil levels.There was an L-shaped curve between basophil level and 28-day mortality,with a cut-off value of 0.47×109/L.Cox regression analysis showed that basophil levels were an independent protective factor for mortal-ity in patients with intra-abdominal infection after adjusting for potential confounders(HR=0.586,95%CI:0.443-0.769).Protective factors for death at basophil levels remained after PSM adjusted for potential confounders(HR=0.628,95%CI:0.470-0.832).Conclusion:Basophil level is an independent protective factor for mortality in patients with intra-abdominal infection,and basophil levels should be dynamically monitored to better evaluate the prognosis of patients.

Objective To investigate whether PKCβ inhibitor can alleviate RIRI by regulating macrophage phenotype.Methods Rats in the renal ischemia-reperfusion injury(RIRI)model group underwent right nephrec-tomy followed by a 60-minute clamping of the left renal pedicle.In the experimental group(Inhibitor+RIRI),PKCβ inhibitors were administered orally one day prior to surgery.All rats were euthanized 24 hours post-surgery for the collection of blood and left kidney samples.Renal function,tissue morphology,and the expression levels of renal tubular injury marker KIM-1,renal papilla injury marker RPA-1,macrophage subtype markers,and inflammatory factors were evaluated.Results PKCβ inhibitors alleviated renal ischemia-reperfusion injury in rats.PAS staining revealed marked tubular damage in kidney sections from the RIRI group,whereas kidney inflammatory cell infiltra-tion and renal tubular injury scores were significantly reduced in the Inhibitor+RIRI group following PKCβ inhibitor treatment(all P<0.05).The expression levels of Cr,BUN,KIM-1,and RPA-1 were markedly elevated in the RIRI group compared to the Sham and Inhibitor+RIRI groups(all P<0.05).After PKCβ inhibitor intervention,the expression levels of Cr,BUN,KIM-1,and RPA-1 were significantly decreased in the Inhibitor+RIRI group relative to the RIRI group(all P<0.05).Protein expression levels of iNOS,IL-2,and CD197 in the kidney tissue of the RIRI group were significantly higher than those in the Sham and Inhibitor+RIRI groups(all P<0.05).Compared with the RIRI group,the protein expression levels of iNOS,IL-12,and CD197 were significantly reduced in the Inhibitor+RIRI group following PKC β inhibitor intervention(all P<0.05).Additionally,the protein expression levels of Dectin-1,ARG-1,and CD163 were significantly higher in the Inhibitor+RIRI group than in the RIRI and Sham groups after PKCβ inhibitor intervention(all P<0.05).Conclusions PKCβ inhibitors can mitigate renal dysfunction,renal tubular injury,and the expression of injury markers in the renal tubules and renal papilla follow-ing ischemia-reperfusion.Additionally,PKCβ inhibitors play a role in modulating macrophage subtypes by reducing M1 macrophages and promoting polarization to M2,which leads to a decrease in pro-inflammatory factors and an increase in anti-inflammatory factors,ultimately facilitating kidney repair.

Aim To explore the molecular mechanism of Tongluo Tangtai(TLTT)prescription in the preven-tion and treatment of diabetic peripheral neuropathy(DPN)based on network pharmacology and in vitro experimental verification.Methods The chemical composition information of Tongluo Tangtai was searched by TCMSP database and literature search,and the target of chemical composition was collected by PubChem and SwissTargetPrediction database.DPN targets were collected through GeneCards database.GO function and KEGG pathway enrichment of common target proteins were analyzed using DAVID database.The correlation network diagram was constructed using Cytoscape software,and the main active components and target genes were screened for molecular docking study.The in vitro model of DPN was constructed in Schwann cells induced by high glucose.The effect of TLTT on the survival rate of RSC96 cells was detected by CCK-8 method,and the gene expression of Wnt/β-catenin pathway related target molecules in RSC96 cells was detected by Real-time PCR.The expression levels of Wnt/β-catenin pathway-related proteins in RSC96 cells were detected by Western blot.Results The main active components such as stigmasterol,β-si-tosterol and quercetin were screened,which mainly ac-ted on EGFR,AKT1,MAPK3 and Wnt,PI3K-Akt and MAPK signaling pathways.The molecular docking re-sults showed that stigmasterol,β-sitosterol,quercetin and other components could dock well with EGFR,AKT1,MAPK3 and other targets.The results of cell experiment showed that 10％TLTT drug-containing ser-um could promote the viability of high-glucose Schwann cells,up-regulate the expression of β-catenin protein,and down-regulate the expression of GSK-3β and Wif-1 protein.Conclusions TLTT has the characteristics of multi-target-multi-pathway in the treatment of DPN.The possible mechanism is that TLTT activates the Wnt/β-catenin signaling pathway,improves the inhibi-tory effect of high glucose on the proliferation of Schwann cells,promotes the proliferation of Schwann cells,and thus improves the status of DPN.

Objective To develop a foot pad for arch support after plantar skin grafting and evaluate its rehabilitation effect on scar tissue in the arch area of postoperative patients.Methods The foot pad for arch support after plantar skin grafting was fabricated from medical-grade silicone and comprised a pad body and an arch support component.The pad body featured shock-absorbing convex patterns on its surface,precision-cut grooves in the metatarsal region and an upwardly convex arch section;the arch support component consisted of an arch-supporting portion with heel reinforcement and a heel-supporting portion,both peripherally integrated with vibration-damping through-holes.Totally 82 burn patients undergoing grafting using plantar skin were selected and divided equally into a control group and an experimental group with the random number table method.In the control group,anti-scarring care such as applying silicone gel and pressure therapy by rehabilitation nurses was carried out immediately after the healing of the plantar skin removal site.In the experimental group,the foot pad was used for rehabilitation care besides the routine treatment in the control group.The two groups were compared in terms of scarring and adverse reactions at the plantar skin removal site.SPSS 25.0 software was used for statistical analysis.Results Within 1 week after healing,the number of patients in the experimental group who had subcutaneous bruising and rupture was less than that in the control group,and the difference was statistically significant(P＜0.05).At 3 months after healing,the experimental group behaved better than the control group in scarring,and the difference was statistically significant(P＜0.05).Conclusion The foot pad developed with simple structure and easy operation can be used for rehabilitation exercise of patients after plantar skinning.[Chinese Medical Equipment Journal,2025,46(3):115-117]

A portable molecularly imprinted(MIP)surface-enhanced Raman scattering(SERS)chip was fabricated via a green electrochemical approach for highly selective detection of bisphenol A(BPA).This MIP-AuNP/UIO-66/SPE sensor was fabricated through a single-step co-deposition process.The process involved electropolymerization onto a UIO-66 modified screen-printed electrode(SPE),by usingo-phenylenediamine(OPD)as functional monomer and BPA as template,and simultaneously electro-reduction generated gold nanoparticles(AuNPs),which served as the SERS-active substrate.Ultimately,this one-step method formed a three-dimensional porous architecture on the electrode surface.Under 785 nm laser excitation,the sensing chip exhibited a highly sensitive SERS response towards BPA.The intensity of its characteristic peak at 850 cm-1 showed a good linear relationship with logarithm of BPA concentration in the range of 1.0×10-10 to 1.0×10-6 mol/L,with a detection limit of 1.0×10-12 mol/L.More importantly,the fabricated chips maintained highly selective binding affinity for BPA in water samples even in the presence of structural analogs bisphenol F(BPF)and bisphenol S(BPS).When the chip was applied to detection of BPA in water samples from plastic bottle and paper cup,the recovery rates ranged from 94.0%to 103.0%with relative standard deviations(RSD)less than 4.7%.The developed chip offered a highly sensitive and selective solution for detection of trace BPA in complex water samples.

Early-life stress (ES) leads to cognitive dysfunction in female adolescents, but the underlying neural mechanisms remain elusive. Recent evidence suggests that the cell adhesion molecules NECTIN1 and NECTIN3 play a role in cognition and ES-related cognitive deficits in male rodents. In this study, we aimed to investigate whether and how nectins contribute to ES-induced cognitive dysfunction in female adolescents. Applying the well-established limited bedding and nesting material paradigm, we found that ES impairs recognition memory, suppresses prefrontal NECTIN1 and hippocampal NECTIN3 expression, and upregulates corticotropin-releasing hormone (Crh) and its receptor 1 (Crhr1) mRNA levels in the hippocampus of adolescent female mice. Genetic experiments revealed that the reduction of dorsal CA1 (dCA1) NECTIN3 mediates ES-induced object recognition memory deficits, as knocking down dCA1 NECTIN3 impaired animals' performance in the novel object recognition task, while overexpression of dCA1 NECTIN3 successfully reversed the ES-induced deficits. Notably, prefrontal NECTIN1 knockdown did not result in significant cognitive impairments. Furthermore, acute systemic administration of antalarmin, a CRHR1 antagonist, upregulated hippocampal NECTIN3 levels and rescued object and spatial memory deficits in stressed mice. Our findings underscore the critical role of dCA1 NECTIN3 in mediating ES-induced object recognition memory deficits in adolescent female mice, highlighting it as a potential therapeutic target for stress-related psychiatric disorders in women.
Animals ; Female ; Mice ; CA1 Region, Hippocampal/metabolism* ; Cell Adhesion Molecules/metabolism* ; CRF Receptor, Type 1/metabolism* ; Memory Disorders/etiology* ; Mice, Inbred C57BL ; Nectins/genetics* ; Receptors, Corticotropin-Releasing Hormone/antagonists & inhibitors* ; Recognition, Psychology/physiology* ; Stress, Psychological/complications*