Skeletal Class II malocclusion is a common dentofacial deformity in adolescents, primarily characterized by mandibular retrognathism. Functional appliance therapy during the pubertal growth spurt to guide mandibular advancement is considered the gold standard. However, traditional functional appliances are often associated with limitations such as bulkiness, poor esthetics, and soft tissue irritation, which can compromise patient compliance. With advancements in digital orthodontics, clear aligner technology integrated with mandibular advancement (clear aligner mandibular advancement, CAMA) has emerged as a novel strategy for treating adolescent skeletal Class II malocclusion, offering advantages in esthetics and comfort while significantly improving patient compliance. CAMA exhibits multidimensional clinical advantages in adolescent malocclusion correction: ① Its mechanical mechanism based on material viscoelasticity optimizes temporomandibular joint stress distribution and induces physiological condylar remodeling, microscopically manifested as increased trabecular fractal dimensions; ② While ensuring mandibular growth, it effectively controls molar eruption through the "bite block effect," providing an optimal solution for vertical control in high-angle cases, and the enhanced precision wing design significantly improves torque control of lower incisors; ③ It improves oropharyngeal airway morphology and respiratory function, benefiting patients' overall health. Although CAMA holds significant value in treating skeletal Class II malocclusion, current research remains insufficient regarding the specific proportions of skeletal versus dental effects, long-term stability of treatment outcomes, and therapeutic boundaries for severe skeletal discrepancies, with most studies being retrospective or short-term. Future research should prioritize prospective multicenter randomized controlled trials, establish personalized diagnostic and treatment systems integrating artificial intelligence-assisted design and biomechanical simulation, and comprehensively analyze multiple factors including temporomandibular joint adaptability to further enhance the clinical value of CAMA.

Objective To investigate the role of silent mating type information regulation 2 homologue 1(SIRT1) in renal ischemia-reperfusion(IR) injury and its effect on NF-κBp65-peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) signal pathway in mice.Methods Seventy-two healthy C57BL/6 male mice were randomly divided into four groups:control group(n=18),sham-operated group(n=18),IR group(n=18),resveratrol group(n=18).Bilateral renal pedicle were clamped for 45 min was adopted to establish the model of acute ischemic renal injury,to give 2％ dimethyl sulfoxide or resveratrol by intraperitoneal injection for 7 days before modeling.Determination techniques included routine biochemical methods for the the levels of Scr and BUN,spectrophotometry for the level of superoxide dismutase (SOD),HE staining for the histological changes as well as immunohistochemical method and Western blotting for the expressions of SIRT1,NF-κBp65 and PGC-1α,respectively.Results Compared with that in control and sham-operated groups,the levels of serum Scr and BUN were higher and SOD levels in renal tissues were lower at 12 h and 24 h after operation in IR groups(P ＜ 0.05).HE staining revealed evident pathological lesions including necrosis of renal tubular epithelial cells in IR group.Compared with that in IR group,resveratrol attenuated the above-mentioned changes.Western blotting revealed the up-regulated SIRT1 expression and the activated NF-κB signal pathway,the up-regulated p65 expression and the down-regulated PGC-1αexpression subsequent to IR(P ＜ 0.05).Both Western blotting and immunohistochemistry showed that the expressions of SIRT1 and PGC-1α in resveratrol group were up-regulated compared to that in IRgroup(P ＜ 0.05),while the NF-κBp65 expression in resveratrol group was down-regulated(P ＜ 0.05).Conclusions In mouse model of renal ischemia-reperfusion injury,the activation of SIRT1 can inhibit the NF-κBp65 expression and accordingly up-regulated PGC-1α level,contributing to inhibiting inflammatory reactions and attenuating oxidative stress-induced injury in the protection of the kidneys.

Objective To design a multiplex PCR for simultaneous identification and toxigenic type characterization of Clostridium difficile isolates. MethodsThree pairs of primers were designed for the amplification of a species-specific internal fragment of the tpi( triose phosphate isomerase) gene, an internal fragment of the tcdB ( toxin B) gene, and an internal fragment of the tcdA ( toxin A) gene. Twenty-one standard strains including Clostridium difficile ATCC 9689 and 47 isolates of Clostridium difficile were applied for the assessment of detection limit, specificity and detections of the multiplex PCR, respectively. Toxin A and Toxin B of 47 isolates were analyzed by ELISA. ResultsThe detection limit for DNA concentration of the multiplex PCR was 0.5 pg/μl. The specificity was determined to be 100％. Among the results of 47 isolates detected by multiplex PC R, 37 strains were tpi ( + )/tcdA (+)/tcdB ( + ), 10 strains were tpi ( + )/tcdA (-)/tcdB ( - ). Tpi ( + )/tcdA ( - )/tcdB ( + ) was not found. The toxin detection of 47 isolates by ELISA showed that 20 isolates were positive and 27 isolates were negative. Twenty isolates of toxin (+) by ELISA were all tpi( +)/tcdA( +)/tcdB(+) by multiplex PCR. ConclusionThe multiplex PCR method combined diagnosis and toxigenic type characterization contributes to the diagnosis for Clostridium difficile infection.

To investigate the gene typing, molecular characteristics of virulence and resistance associated gene of Clostridium difficile from clinical isolates in China, the genes tcdA,tcdB of toxin A and B, cdtA,cdt B of binary-toxin, and erm B of clindamycin resistance were detected by conventional PCR. Genotyping of toxic C. difficile were conducted by means of analysis of 16s-23s internal spacer region polymorphism with PCR assay. Then the antibiotic resistance of toxic C. difficile to ampiciline, clindamycin, metronidazole and vancomycin was conducted with E-test. It was found that 8 toxic C. difficile strains were demonstrated out of 12 clinical isolates, in which 5 strains were tcdA+ and tcdB+, and 3 strains tcdA- and tcdB+, accounting for 62.5% and 37.5% respectively. Binary-toxin genes detection were negative in all the strains. Clindamycin resistance associated gene ermB was positive in 4 out of 8 toxic C. difficile strains, accounting for 50%. 8 toxic isolates were typed into 4 gene types, the dominant type was ZR I,accounting for 62.5%. Resistance rate of 8 toxic C. difficile strains against ampiciline(AC), clindamycin(CM), metronidazole(MZ) and vancomycin(VA) was 37.5%,87.5%,12.5%, and 0 respectively. No isolates belonged to ribotype 027 or 078. Isolation rate of toxic C. difficile is high to 66.7%. There is obvious gene polymorphism in clinical isolates of Chinese toxic C.difficite, and ZR I is preponderant genotype in 4 genotypes. C. difficile shows some resistance to ampiciline, clindamycin, metronidazole, but susceptive to vancomycin.

OBJECTIVE This study was to investigate the carrier and infection of Clostridium difficile in clinic feces specimen,to analyze clinic characteristics,and to improve isolation rate and to provide basis on efficient prevention.METHODS C.difficile toxin A&B kit and anaerobic culture was conducted in 20 cases with diarrhea.Colonies suspected to be C.difficile,on the basis of their macroscopic appearance and characteristic odor,oxygen tolerance experiment,were confirmed by their biochemical characteristics(API 20A,bioMerieux).RESULTS After C.difficile selective culture,8 suspected colonies from 20 feces specimen were conducted by feces smear and oxygen tolerance experiment.6 of 8 was G+ rod bacteria with positive oxygen tolerance experiment.4 stains of C.difficile were identified by API 20A,positive rate was 20%;toxin detect was positive in 1 specimen(5%).CONCLUSIONS Infection of C.difficile Is associated with the basic disease.Watery feces specimen was prone to culture positive.