Objective To gain insights into the biological characteristics of different populations of Culex tritaeniorhynchus within and around the Yellow Sea wetland from the perspective of the occurrence of resistance, we investigated the levels of resistance to deltamethrin and kdr gene mutation in the wetland and its peripheral areas. Methods Specimens were collected from Cx. tritaeniorhynchus populations at two monitoring sites in the Rare Bird National Nature Reserve and Tiaozi Ni Wetland Scenic Area, and also from two populations in Yancheng City and the Liuhe District of Nanjing, and the resistance of these mosquitoes to deltamethrin was determined using the CDC biotest bottle method. For each concentration of deltamethrin assessed, a random subset of exposed specimens was selected for amplification of the kdr gene fragment, followed by Sanger sequencing to identify and analyze resistance-associated mutations. Results The LC50 levels of deltamethrin among mosquitoes from the four populations in Luhe, Yancheng, the Rare Bird National Nature Reserve and the Tiaozi Ni Wetland Scenic Area were 2.048 5, 7.798 2, 3.473 3, and 17.695 5 mg/mL, respectively, with corresponding concentrations of deltamethrin ranging from 0.005 to 5.000,0.050 to 50.000,0.050 to 25.000 and 0.050 to 50.000 mg/mL, respectively. Furthermore, the ranges of the KT50 values were 11.76-107.43, 67.05-216.30,29.77-107.43 and 28.40-329.51 min; the 1-h knockdown rates were 34.58%-99.15%, 9.52%-43.80%, 55.09%-73.01%, and 10.09%-68.07%; and the 24-h mortality rates were 12.15%-67.52%,9.52%-79.56%,13.17%-82.21%, and 11.01%-78.99%, respectively. With respect to kdr gene mutation, we assayed a total of 63,70,59, and 57 mosquitoes for the four populations, for which we detected L1014F mutation frequencies of 14.29%, 35.00%, 20.34%, and 31.58%, respectively, with a majority of these mutations being heterozygous for resistance. In addition, five adult mosquitoes were identified has having synonymous mutations at site 1011[i. e. , AAT(asparagine)mutation to AAC(asparagine)]. Conclusions Our findings revealed the clear resistance of Cx. tritaeniorhynchus to deltamethrin in the Yancheng region of the Yellow Sea wetland, and the resistance phenotype and kdr frequency of Cx. tritaeniorhynchus in the wetland environment were comparable to those of Cx. tritaeniorhynchus in the wetland environment, thereby indicating that the resistance of different populations of Cx. tritaeniorhynchus was homogeneous under the pressure of different insecticide selection within and around the wetland. However, the underlying mechanisms need to be further studied.

In March 2024, three male and two female specimens of the genus Lispe were intercepted on cargo ships inbound for Wan Zai Port under Gongbei Customs. Based on morphological characteristics and molecular analysis, the specimens were identified as Lispe pumila. In this study, we describe the morphological features, diagnostic characteristics, and geographical distribution of L. pumila, with the aim of providing a reference for the identification of this species when intercepted at ports.

Background and aims The mechanism of cholestatic liver injury (CLI) is unclear, and effective therapies are lacking. While peroxisome proliferator-activated receptor alpha (PPARα) agonists show potential hepatoprotective effect and pyroptosis is implicated in hepatocellular damage, how PPARα activation mitigates lithocholic acid (LCA)-induced pyroptosis remains unknown. Methods The hepatoprotective effect of PPARα agonists was evaluated in a mouse model of intrahepatic cholestasis induced by LCA. Liver injury was assessed via serum biochemistry, hematoxylin and eosin and TUNEL staining, and electron microscopy. Pyroptosis pathways were analyzed using real-time quantitative polymerase chain reaction, Western blot, and co-immunoprecipitation. Results Combined morphological, histopathological, and biochemical analyses confirmed that PPARα activation protects against CLI. Compared with LCA treatment alone, PPARα activation significantly attenuated the elevation of serum lactate dehydrogenase (LDH), the increased TUNEL-positive cells, and the formation of hepatocyte membrane pores. Mechanistically, PPARα activation suppressed both NOD-like receptor protein 3 (NLRP3) inflammasome-mediated pyroptosis and apoptosis protease-activating factor-1 (APAF-1)/CASPASE-3/GSDME-mediated pyroptosis. Furthermore, PPARα agonist pretreatment inhibited activation of the nuclear factor-kappa B (NF-κB) and forkhead box O1 (FOXO1) signaling pathways. Conclusions PPARα protects against LCA-induced CLI by inhibiting both NLRP3 inflammasome-mediated pyroptosis associated with NF-κB and APAF-1/CASPASE-3/GSDME-mediated pyroptosis associated with the FOXO1 signaling pathway.

Objective To explore the performance of gallium nitride(GaN)-based digital circuit chips applied in nuclear radiation environments and investigate the feasibility of their use in control chips for robots transporting injured personnel.Methods First,a GaN-based NAND gate digital circuit chip was fabricated.Second,both the GaN-based digital chip and the SN74AHCT1G00 silicon-based digital chip were irradiated with 60Co gamma-ray.The irradiation doses for the GaN-based digital chip were 1 Mrad(Si)and 2 Mrad(Si),while the irradiation dose for the SN74AHCT1G00 silicon-based digital chip was 1 Mrad(Si).Finally,the post-irradiation electrical performance of the two chips was measured using a Keithley 4200A-SCS semiconductor characterization system.Results Under 60Co gamma-ray irradiation doses of 1 Mrad(Si)and 2 Mrad(Si),the response delay of the GaN-based digital circuit chip was only on the order of 0.1 μs.In contrast,the response rate of the SN74AHCT1G00 silicon-based digital circuit chip significantly degraded under 60Co gamma-ray irradiation dose of 1 Mrad(Si),rendering it unable to perform the NAND gate logic function.Conclusion GaN-based digital circuit chips exhibit high radiation resistance in 60Co gamma-ray irradiation environments,with no significant performance degradation.Compared with silicon-based digital circuit chips,they demonstrate considerable advantages and can preliminarily meet the requirements for control chips of robots transporting injured personnel in nuclear radiation environments.

Objective To evaluate the efficacy and safety of enteric-coated metformin hydrochloride capsules(Junlida?)in patients with T2DM and poor glycemic control under lifestyle interventions.Methods In this study,419 patients with T2DM were recruited from 15 research centers from July 2020 to March 2022,and randomly divided into observation(Obs)group(n=209)and control group(Con,n=210)using a multicenter,randomized,double-blind,non-inferiority trial design.Patients in the Obs group were treated with enteric-coated Metformin hydrochloride capsules(Junlida?),and patients in the Con group were treated with Metformin hydrochloride tablets(Glucophage?).The optimal effective dose of 2 g/d was achieved within 4 weeks,and the reasonable dose was maintained until the end of treatment.The treatment period was 24 weeks.HbA1c and its compliance rate,FPG,and body weight were compared between the two groups in full analysis set(FAS)and protocol set(PPS).Safety and adverse events(AE)were evaluated in safety set(SS).Results A total of 414 participants were randomized(207 cases in Obs group and 207 cases in Con group).414 cases in FAS population(207 cases in Obs group and 207 cases in Con group),and 328 cases in PPS population(164 cases in Obs group and 164 cases in Con group),and 414 cases in SS population(207 cases in Obs group and 207 cases in Con group).After treatment,HbA1c,FPG and body weight were lower in both groups(P<0.05)in FAS and PPS.HbA1c compliance rate was not significantly different between the two groups in FAS and PPS(P>0.05).The results of non-inferiority test showed that the lower limit was>-0.4%in both FAS(-0.154,95%CI-0.384～0.069)and PPS(-0.139,95%CI-0.390～0.112),and the Obs group reached non-inferiority end point.The achievement rate,compliance rate,safety index and incidence of AE were not significantly different between the two groups(P>0.05).Conclusions Junlida? demonstrated non-inferiority to Glucophage? in glycemic control and can be safely and effectively used in patients with diabetes.

Objective To evaluate the efficacy and safety of enteric-coated metformin hydrochloride capsules(Junlida?)in patients with T2DM and poor glycemic control under lifestyle interventions.Methods In this study,419 patients with T2DM were recruited from 15 research centers from July 2020 to March 2022,and randomly divided into observation(Obs)group(n=209)and control group(Con,n=210)using a multicenter,randomized,double-blind,non-inferiority trial design.Patients in the Obs group were treated with enteric-coated Metformin hydrochloride capsules(Junlida?),and patients in the Con group were treated with Metformin hydrochloride tablets(Glucophage?).The optimal effective dose of 2 g/d was achieved within 4 weeks,and the reasonable dose was maintained until the end of treatment.The treatment period was 24 weeks.HbA1c and its compliance rate,FPG,and body weight were compared between the two groups in full analysis set(FAS)and protocol set(PPS).Safety and adverse events(AE)were evaluated in safety set(SS).Results A total of 414 participants were randomized(207 cases in Obs group and 207 cases in Con group).414 cases in FAS population(207 cases in Obs group and 207 cases in Con group),and 328 cases in PPS population(164 cases in Obs group and 164 cases in Con group),and 414 cases in SS population(207 cases in Obs group and 207 cases in Con group).After treatment,HbA1c,FPG and body weight were lower in both groups(P<0.05)in FAS and PPS.HbA1c compliance rate was not significantly different between the two groups in FAS and PPS(P>0.05).The results of non-inferiority test showed that the lower limit was>-0.4%in both FAS(-0.154,95%CI-0.384～0.069)and PPS(-0.139,95%CI-0.390～0.112),and the Obs group reached non-inferiority end point.The achievement rate,compliance rate,safety index and incidence of AE were not significantly different between the two groups(P>0.05).Conclusions Junlida? demonstrated non-inferiority to Glucophage? in glycemic control and can be safely and effectively used in patients with diabetes.

Aim To investigate the protective effects of Tilianin on lipopolysaccharide(LPS)-induced septice-mia-induced myocardial injury in rats and to explore the related mechanisms.Methods Animals were ran-domly grouped and a rat septicemia-induced myocardial injury model was constructed.Echocardiography was used to assess the cardiac function of rats,left ventricu-lar internal diameter at end-diastole(LVIDd)and left ventricular internal diameter at end-systole(LVIDs)were measured,and left ventricular ejection fraction(LVEF)and left ventricular fractional shortening(LVFS)were calculated;the kits were used to detect the serum activity of the relevant cardiac enzymes and the level of inflammatory factors;HE staining was used to observe the morphological changes of myocardium;immunofluorescence staining of cardiac tissues was used to detect the nuclear translocation of NF-κB p65;Western blot was used to detect the expression of TLR4,MyD88,p-NF-κB p65,and NLRP3 proteins in cardiac tissues.Results Compared with the model group,each administration group differently upregulated LVEF,LVFS,and LVIDs,and improved the coordina-tion of LV wall fluctuations in the model group of rats;cardiac enzymes LDH and CK-MB levels increased,and levels of inflammatory factors TNF-α,IL-6,and IL-1 β were reduced,exerting cardioprotective effects;HE staining showed that myocardial tissue cell gap was re-duced,myocardial fiber breakage was reduced,cardio-myocyte arrangement tended to be normal,and inflam-matory cell infiltration was reduced;NF-κB p65 entry into the nucleus was reduced,and phosphorylated NF-κB p65(p-NF-κB p65)expression was reduced;and Western blot results showed that the expression of TLR4,MyD88,and NLRP3 proteins was reduced.Conclusions Tilianin pretreatment reduces serum my-ocardial enzymes and inflammatory factors and im-proves myocardial injury in rats with septicemia-in-duced myocardial injury,which may be related to the Tilianin anti-TLR4/NF-κB/NLRP3 inflammatory signa-ling pathway.

Objective:To explore the risk factors and etiological characteristics of urinary tract infection caused by urinary calculi in eastern Fujian region,in order to attract clinical attention and improve the prevention and treatment of urinary tract infection caused by urinary calculi.Methods:A total of 154 patients with urinary calculi admitted to Ningde People's Hospital(n=80)and Ningde Mindong Hospital(n=74)from November 2022 to October 2023 were selected as the main research objects.According to whether the patients had urinary tract infection,they were divided into infection group and non-infection group.The baseline data of the two groups were analyzed in detail,and the risk factors and pathogen distribution of urinary tract infection in patients with urinary calculi were analyzed.Results:There were 33 cases of urinary tract infection in 154 patients with urinary calculi,accounting for 21.43％.Univariate analysis showed that the urinary white blood cell count in the infection group was higher than that in the non-infection group,and the proportion of patients with effusion,urinary tract obstruction,calculi in the upper urinary tract,staghorn calculi,smoking history,diabetes,and urinary nitrite positive was higher than that in the uninfected group(P＜0.05).The results of binary logistic regression analysis showed that effusion,urinary tract obstruction,staghorn calculi,smoking history,diabetes,high urine white blood cell count and positive urine nitrite were independent risk factors for urinary tract infection in patients with urinary calculi(OR＞1,P＜0.05).A total of 33 strains of pathogenic bacteria were isolated from 33 patients in the infection group.Among them,23 strains(69.70％)were gram-negative bacteria,8 strains(24.24％)were gram-positive bacteria,and 2 strains(6.06％)were fungi.Among gram-negative bacteria,escherichia coli accounted for the highest proportion(48.48％),followed by klebsiella pneumoniae(9.09％).Among gram-positive bacteria,enterococcus faecalis accounted for the highest proportion(12.12％),followed by enterococcus faecium(6.06％).Candida and candida tropicalis in fungi was the same,accounted for 3.03％.Conclusion:The risk of urinary tract infection in patients with urinary calculi in eastern Fujian region is high.Effusion,urinary tract obstruction,staghorn calculi,smoking history,diabetes,high urine white blood cell count and positive urine nitrite are independent risk factors for urinary tract infection in patients with urinary calculi.The main urinary tract pathogens are gram-negative bacteria.

Aim To evaluate the role of the glucose transporter protein 1(GLUT1)-dependent glycolytic in the attenuation of oxygen-glucose deprivation-reoxygen-ation(OGD/R)injury in HK-2 cells by dexmedetomi-dine(Dex).Methods C57/BL6 mice were random-ly divided into three groups(n=6),namely,sham operation group(Sham group),renal ischemia reper-fusion group(I/R group)and Dex group(I/R+Dex group).Serum creatinine(Cr)and urea nitrogen(BUN)were measured,while the levels of key glyco-lytic enzymes HK2,PFKFB3 and GLUT1 were meas-ured.HK-2 cells were cultured and randomised into seven groups(n=6),which was treated with OGD/R,overexpression or interference with GLUT1,Dex and glycolysis inhibitor 2-DG.CCK-8 and LDH activi-ty were used to detect cellular damage.Glycolysis lev-els were detected by lactate and ECAR.The inflamma-tory level was reflected by qRT-PCR for IL-6 and TNF-α.qRT-PCR and Western blot were performed to de-tect the levels of GLUT1,HK2,and PFKFB3.Results Dex significantly ameliorated kidney injury and HK-2 cell injury(P＜0.05).Dex inhibited the OGD/R-induced rise in lactate and extracellular acidification rate(ECAR),as evidenced by suppression of the ex-pression of GLUT1,HK2 and PFKFB3(P＜0.05).In vitro experiments showed that GLUT1 knockdown sig-nificantly improved OGD/R-induced cellular damage.Lactate,ECAR,glycolysis-related mRNAs and pro-teins were inhibited by GLUT1 knockdown(P＜0.05).Significantly,there were no significant differ-ences in above indexes after Dex treatment based on GLUT1 knockdown.Overexpression of GLUT1 abroga-ted the protective effects of Dex,while reversing the inhibitory effects of Dex on the expression of GLUT1,HK2,and PFKFB3(P＜0.05).Conclusions Dexmedetomidine attenuates OGD/R induced injury in HK-2 cells by inhibiting GLUT1-dependent glycolysis.

Aim To investigate the protective effects of Tilianin on lipopolysaccharide(LPS)-induced septice-mia-induced myocardial injury in rats and to explore the related mechanisms.Methods Animals were ran-domly grouped and a rat septicemia-induced myocardial injury model was constructed.Echocardiography was used to assess the cardiac function of rats,left ventricu-lar internal diameter at end-diastole(LVIDd)and left ventricular internal diameter at end-systole(LVIDs)were measured,and left ventricular ejection fraction(LVEF)and left ventricular fractional shortening(LVFS)were calculated;the kits were used to detect the serum activity of the relevant cardiac enzymes and the level of inflammatory factors;HE staining was used to observe the morphological changes of myocardium;immunofluorescence staining of cardiac tissues was used to detect the nuclear translocation of NF-κB p65;Western blot was used to detect the expression of TLR4,MyD88,p-NF-κB p65,and NLRP3 proteins in cardiac tissues.Results Compared with the model group,each administration group differently upregulated LVEF,LVFS,and LVIDs,and improved the coordina-tion of LV wall fluctuations in the model group of rats;cardiac enzymes LDH and CK-MB levels increased,and levels of inflammatory factors TNF-α,IL-6,and IL-1 β were reduced,exerting cardioprotective effects;HE staining showed that myocardial tissue cell gap was re-duced,myocardial fiber breakage was reduced,cardio-myocyte arrangement tended to be normal,and inflam-matory cell infiltration was reduced;NF-κB p65 entry into the nucleus was reduced,and phosphorylated NF-κB p65(p-NF-κB p65)expression was reduced;and Western blot results showed that the expression of TLR4,MyD88,and NLRP3 proteins was reduced.Conclusions Tilianin pretreatment reduces serum my-ocardial enzymes and inflammatory factors and im-proves myocardial injury in rats with septicemia-in-duced myocardial injury,which may be related to the Tilianin anti-TLR4/NF-κB/NLRP3 inflammatory signa-ling pathway.