Objective To investigate the epidemiological characteristics of malaria and provide a basis for developing improved prevention and control measures. Methods Data were obtained from the Chinese Disease Prevention and Control Information System. Malaria surveillance data for Nanning City from January 1,2023, to December 31,2024, were exported from the Infectious Disease Reporting Information Management Subsystem. The characteristics of the two groups of malaria cases were compared. Results A total of 103 imported malaria cases were reported in Nanning City in 2024, representing a 38.32% decrease compared with the same period of the previous year. No statistically significant difference were observed between cases reported in 2023 and 2024 in terms of average age, gender ratio, proportion of parasite species, and monthly reporting distribution;however, statistically significant differences were found in the proportion of reporting areas and current residence areas(χ2= 13.572 and 10.355, respectively; P = 0.001 and 0.035, respectively). The proportion of cases reported in Shanglin County and the proportion of cases residing in Shanglin County were both lower than those during the same period of the previous year. Conclusions The high aggregation of imported malaria cases in Nanning City has decreased. Medical institutions in areas other than Shanglin County should strengthen their vigilance against malaria.

Objective To explore the effects of air pressure, humidity, wind, and sunshine on the incidence of cardiovascular and cerebrovascular diseases (CVD) in Guiyang, and to provide reference for the prevention of CVD. Methods Using CVD incidence data from September 2021 to August 2022 in Guiyang City and meteorological data including average air pressure, average humidity, wind, and sunshine during the same period, the effects of meteorological factors on CVD incidence were explored and the importance of each factor was analyzed. Results When air pressure was below 868 hPa, above 887 hPa, or between 877 and 883 hPa, and when air pressure dropped less than 5.3 hPa within 24 hours, there was a higher risk of CVD. When the humidity was above 81%, the wind speed was small (<1.2 m/s) or high (>4m/s), and there was less sunlight (less than 3 hours), the risk of CVD was higher. Low humidity (<60%) was not conducive to the onset of CVD. There were highest risks at lag 5~10 days and 4-25 days for high pressure and low sunlight, respectively. When the relative humidity was saturated, there was an immediate effect. When the wind speed was low and high, the immediate effect and hysteresis effects were significant. Among the above meteorological factors, the impact of 24-hour variation of pressure and high or low atmospheric pressure on the incidence of CVD was the most significant, while the impact of sunlight and humidity was the weakest. The impact of diurnal variations in wind and atmospheric pressure was not clear. Conclusion The impact of air pressure on the incidence of CVD does not exhibit a simple linear relationship. The risk of CVD is high in high humidity, low light, and moderate or strong winds. It is necessary to fully consider changes in meteorological factors for CVD prevention and control.

Although chronic neuroinflammation has been established as one of core pathological hallmarks of Alzheimer disease(AD),its role in AD pathological mechanisms still remains elusive.The glia-derived inflammatory mediator chitinase-3-like protein 1(CHI3L1,also known as YKL-40)regulates key pathological processes including neuroinflammation,neuronal degeneration,and cell death.Evidence confirms that YKL-40 promotes the progression of AD core pathology through inhibiting amyloid plaque clearance and enhancing neuronal toxicity.Its expression levels is significantly correlated with early detection,disease severity,and clinical prognosis.A thorough understanding of the relationship between YKL-40 and AD not only deepen our insight into neuroinflammatory mechanisms in AD pathogenesis but also highlights its dual clinical applicability as a novel biomarker and therapeutic target,thereby providing an important direction for development of advanced diagnostic and treatment strategies for AD.

Objective:To explore the association of 21-gene recurrence score (RS) and clinicopathologic characteristics of hormone receptor (HR) positive T1-3N1M0 breast cancer and its value in prognosis evaluation.Methods:The clinicopathological data of 287 patients with T1-3N1M0 breast cancer were collected, the 21-gene assay was completed, and follow-up was conducted. According to the 21-gene RS, the patients were divided into the RS<26 and RS≥26 groups. The relationship between the 21-gene RS and clinicopathological characteristics, treatment, recurrence, and metastasis was analyzed. Univariate and multivariate statistical analyses were used to analyze the risk factors for disease free survival (DFS).Results:The median RS of the 287 patients was 16. There were 240 cases with RS <26 and 47 cases with RS≥26. Tumor size, grade, estrogen receptor (ER), progesterone receptor (PR), and Ki-67 index were significantly different between the two cohorts ( P<0.05 for all). After a median follow-up of 74 months, the recurrence rate in the RS<26 group (8.3%) was significantly lower than that in the RS≥26 group (23.4%), the locoregional recurrence (LRR) rates in the RS<26 and RS≥26 groups were 2.1% and 0%,and the distant metastasis (DM) rates were 6.3% and 23.4%, respectively. The 5-year relapse free survival (RFS) rates of patients with RS<26 and RS≥26 were 93.8% (95% CI: 90.7%-96.9%) and 87.2% (95% CI: 78.2%-97.3%), and the 5-year DFS rates were 92.1% (95% CI: 88.7%-95.6%) and 85.1% (95% CI: 75.5%-95.9%), respectively, with significant differences between the two cohorts ( P=0.007 and P=0.006, respectively). Univariate analysis showed age, tumor size, grade, PR status, Ki-67 index and RS were prognostic factors for DFS ( P<0.05 for all). Multivariate analysis showed that age and tumor size were independent significant predictors for DFS ( P<0.05). Conclusions:The 21-gene RS of T1-3N1M0 breast cancer is related to tumor size, grade, ER, PR, and Ki-67 index. RS is an important factor affecting DM and DFS.

AIM:To explore the role and mechanism of calcium-sensing receptor(CaSR)in regulating macro-phage polarization in hypertensive rats.METHODS:Male spontaneously hypertensive rats(SHR)and Wistar-Kyoto(WKY)rats were categorized into WKY group,SHR group,SHR+R568(CaSR agonist)group,and SHR+NPS2143(CaSR inhibitor)group.The thoracic aorta was isolated,and the expression of CaSR and macrophage polarization markers in the aorta was observed through immunofluorescence staining.The primary peritoneal macrophages of SHR and WKY rats were aseptically extracted following anesthesia.After intervention with R568 and NPS2143,the expression levels of M1 and M2 markers of peritoneal macrophages were observed by Western blot and immunofluorescence staining.The levels of interleukin(IL)-1β and IL-10 were measured by ELISA.The concentration of Ca2+in peritoneal macrophages was mea-sured by immunofluorescence.Western blot was employed to identify the expression of CaSR and nucleotide-binding oligo-merization domain-like receptor protein 3(NLRP3)inflammasome components.Following anesthesia,vascular smooth muscle cells(VSMCs)were isolated from SHR using an adherent method.Subsequently,a co-culture system was estab-lished with macrophage supernatant.The optimal action time for this co-culture system was determined through CCK-8 as-say.RESULTS:Compared with SHR group,activation of CaSR resulted in a significant decrease in the protein expres-sion of M1 polarization markers(P<0.05)and a concomitant increase in the protein expression of M2 polarization markers in the aorta(P<0.05).Compared with SHR group,administration of R568 led to a significant decrease in the protein ex-pression of M1 polarization markers(P<0.05)and a concomitant increase in the protein expression of M2 polarization markers(P<0.05)in peritoneal macrophages.Additionally,there was a notable reduction in the protein levels of NLRP3 inflammasome components(P<0.05).Furthermore,the fluorescence intensity of intracellular Ca2+was significantly en-hanced following R568 treatment(P<0.05).After administration of MCC950,an NLRP3 inflammasome inhibitor,the re-sults were consistent with those observed following R568 treatment,demonstrating statistical significance(P<0.05).This effect was reversed by the combined intervention of U73122,a phospholipase C(PLC)inhibitor(P<0.05).Compared with the control(0 h),the 24-h peritoneal macrophage supernatant exhibited the strongest capacity to enhance the viabili-ty of VSMCs after 24 h of culture(P<0.05).CONCLUSION:In hypertensive rats,the CaSR inhibits NLRP3 inflamma-some activation via the PLC-Ca2+signaling pathway,thereby mediating an increase in macrophage polarization towards the M2 phenotype and a decrease towards the M1 phenotype.

Objective To study the effect of medial collateral ligament(MCL)release on the squatting motion followling total knee arthroplasty(TKA)and provide reference data for ligament release during knee replacement surgery.Methods Based on CT and MRI images of a volunteer,a three-dimensional(3D)geometric anatomical model of the natural knee joint including bone tissues and major soft tissues was established.A finite element model of the artificial knee joint was established by simulating TKA surgery.The squatting motion after 30％release of the upper end,lower end,and both ends of the MCL was simulated,and motion characteristic data of the knee joint at flexion/extension angles from 0° to 135° were obtained.Results The effects of ligament release at different locations on knee squatting motion varied.After releasing the lower end,the medial translation,posterior translation,superior translation,and adduction of the femur relative to the tibia increased by 13.74％,3.83％,9.74％,and 2.37％,respectively,while the external rotation decreased by 36.8％.After releasing the upper end,the medial translation and posterior translation increased by 10.65％and 10％,respectively,while the superior translation,adduction,and external rotation decreased by 4.52％,33.89％,and 67.1％,respectively.After releasing both ends,the medial translation,posterior translation,and superior translation increased by 14.77％,9.39％,and 22.56％,respectively,while the adduction and external rotation decreased by 15.62％and 47.3％,respectively.Conclusions After MCL released,the medial translation,anterior translation,superior translation,and abduction of the femur relative to the tibia increased,while the external rotation decreased.Releasing the lower end had the least effect on these femoral movements,showing an obvious advantage.

OBJECTIVE: To evaluate the efficacy and safety of Shexiang Tongxin Dropping Pill (STDP) in treating stable angina patients with phlegm-heat and blood-stasis syndrome by exercise duration and metabolic equivalents. METHODS: This multicenter, randomized, double-blind, placebo-controlled clinical trial enrolled stable angina patients with phlegm-heat and blood-stasis syndrome from 22 hospitals. They were randomized 1:1 to STDP (35 mg/pill, 6 pills per day) or placebo for 56 days. The primary outcome was the exercise duration and metabolic equivalents (METs) assessed by the standard Bruce exercise treadmill test after 56 days of treatment. The secondary outcomes included the total angina symptom score, Chinese medicine (CM) symptom scores, Seattle Angina Questionnaire (SAQ) scores, changes in ST-T on electrocardiogram and adverse events (AEs). RESULTS: This trial enrolled 309 patients, including 155 and 154 in the STDP and placebo groups, respectively. STDP significantly prolonged exercise duration with an increase of 51.0 s, compared to a decrease of 12.0 s with placebo (change rate: -11.1% vs. 3.2%, P<0.01). The increase in METs was significantly greater in the STDP group than in the placebo group (change: -0.4 vs. 0.0, change rate: -5.0% vs. 0.0%, P<0.01). The improvement of total angina symptom scores (25.0% vs. 0.0%), CM symptom scores (38.7% vs. 11.8%), reduction of nitroglycerin consumption (100.0% vs. 11.3%), and all domains of SAQ, were significantly greater with STDP than placebo (all P<0.01). The changes in Q-T intervals at 28 and 56 days from baseline were similar between the two groups (both P>0.05). Twenty-five participants (16.3%) with STDP and 16 (10.5%) with placebo experienced AEs (P=0.131), with no serious AEs observed. CONCLUSION STDP could improve exercise tolerance in patients with stable angina and phlegm-heat and blood stasis syndrome, with a favorable safety profile. (Registration No. ChiCTR-IPR-15006020).
Humans ; Double-Blind Method ; Drugs, Chinese Herbal/adverse effects* ; Male ; Female ; Middle Aged ; Angina, Stable/physiopathology* ; Aged ; Syndrome ; Treatment Outcome ; Placebos ; Tablets

Psoriasis is an incurable chronic inflammatory disease that requires new interventions. Here, we found that fibroblasts exacerbate psoriasis progression by promoting macrophage recruitment via CCL2 secretion by single-cell multi-omics analysis. The natural small molecule celastrol was screened to interfere with the secretion of CCL2 by fibroblasts and improve the psoriasis-like symptoms in both murine and cynomolgus monkey models. Mechanistically, celastrol directly bound to the low-density lipoprotein receptor-related protein 1 (LRP1) β-chain and abolished its binding to the transcription factor c-Jun in the nucleus, which in turn inhibited CCL2 production by skin fibroblasts, blocked fibroblast-macrophage crosstalk, and ameliorated psoriasis progression. Notably, fibroblast-specific LRP1 knockout mice exhibited a significant reduction in psoriasis like inflammation. Taken together, from clinical samples and combined with various mouse models, we revealed the pathogenesis of psoriasis from the perspective of fibroblast-macrophage crosstalk, and provided a foundation for LRP1 as a novel potential target for psoriasis treatment.

Objectives:To investigate the predictive value of epicardial fat volume(EFV)and atrioventricular groove fat thickness(AVGT)—morphological biomarkers of epicardial adipose tissue—for major adverse cardiovascular events(MACE)in patients with dilated cardiomyopathy(DCM).Methods:This study enrolled 216 DCM patients.EFV and AVGT were obtained from cardiac magnetic resonance imaging(CMR).Patients were divided into event-free group(n=142)and event group(n=74)based on MACE occurrence during follow-up.Receiver operating characteristic(ROC)curve analysis was used to determine optimal cutoff values.Survival differences were assessed using Kaplan-Meier analysis,Cox proportional hazards regression analysis was used to identify independent risk factors,and restricted cubic spline(RCS)models were used to evaluate dose-response relationships.Results:AVGT and EFV were significantly higher in the event group than in event-free group(both P<0.05).ROC analysis identified optimal MACE-predicting cutoffs as follows:AVGT≥7.74 mm(area under the curve[AUC]=0.57)and EFV≥78.6 ml(AUC=0.62).Kaplan-Meier analysis revealed significantly lower MACE-free survival rates in patients with AVGT≥7.74 mm and EFV≥78.6 ml(both P<0.05).Cox regression analysis confirmed that AVGT(HR=2.18,95%CI:1.34-3.54)and EFV(HR=1.81,95%CI:1.11-2.96)were independent MACE risk factors(both P<0.05)in this patient cohort.RCS models demonstrated the significant linear associations between EFV/AVGT and MACE risk(bothoverall P<0.05).Conclusions:EFV and AVGT,the non-invasive imaging biomarkers quantifying and characterizing fat distribution,are independently correlated with elevated MACE risk in DCM patients.These metrics serve as potential prognostic indicators,enriching risk stratification indicators for early identification of high-risk patients and guiding personalized medication strategies.

Peripheral nerve injury (PNI) is one of the most common issues among trauma patients.Treatment strategies for PNI typically involve surgical repair,rehabilitation therapy and medication management,but may still not achieve the expected therapeutic outcome. Following nerve injury,Schwann cells clear cellular debris,release growth-promoting factors and provide guidance support that promotes the regrowth of damaged nerve fibersand its reconnection to target tissues. The release of transforming growth factor beta (TGF-β) to the injury site after PNI can induce the transformation of astrocytes to an A2 phenotype,thereby upregulating the expression of neurotrophic factors. Meanwhile,TGF-β can initiate a series of phenotypic changes in Schwann cells,modulate immune cells,and activate the innate growth potential of neurons,thereby enhancing nerve regeneration potential. TGF-β can also promote angiogenesis,maintain the integrity of the blood-nerve barrier and enhance its permeability,thereby providing a beneficial microenvironment for nerve regeneration by inhibiting inflammation. This paper reviews the potential roles of TGF-β in peripheral nerve regeneration and investigates the underlying mechanisms,in order to provide new insights for better treatment of PNI.