BackgroundThe issue of school absenteeism due to school refusal in adolescents has become increasingly prominent. Acceptance and Commitment Therapy （ACT） has been applied successfully to improve depression， anxiety， and psychological flexibility in adolescents， while few studies have tested the effect of ACT intervention on above-mentioned psychological aspects and return-to-school rate in adolescents with school absenteeism. ObjectiveTo explore the effect of ACT on depression， anxiety， psychological flexibility and return-to-school rate in school absenteeism adolescents， and to provide a broader evidence base for clinical interventions. MethodsFrom May to June 2024， a sample of 50 adolescents with Shenzhen school registration who had been suspended from school for more than a consecutive month for school refusal were recruited based on Wechat official account platform. The adolescents were divided into study group and control group by random number table method. Both groups received psychological education with the theme of 'Causes and Coping Strategies of School Refusal'， and study group added a 6-week ACT intervention with weekly 1-hour sessions. At baseline and after treatment， Patients’ Health Questionnaire Depression Scale-9 item （PHQ-9）， Generalized Anxiety Disorder Scale-7 item （GAD-7） and Comprehensive assessment of Acceptance and Commitment Therapy processes （CompACT） were used for the clinical evaluation. ResultsA total of 45 （90.00%）adolescents completed the study， including 25 in study group and 20 in control group. Analysis revealed that study group scored higher on PHQ-9 and GAD-7， while lower on total CompACT score， openness dimension and awareness dimension compared with control group， with statistical significance （F=7.786， 10.334， 12.922， 14.374， 3.075， P<0.05 or 0.01）. After intervention， the rate of return-to-school was higher in study group than in control group （40.00% vs 10.00%， χ²=5.114， P<0.05）. ConclusionACT intervention for adolescents with school absenteeism may alleviate depression and anxiety， improve their psychological flexibility and increase return-to-school rate.［Funded by the "14^th Five Year Plan" for Social Sciences Project in Jiangxi Province （number， 24JY41D）； Science and Technology Planning Project of Shenzhen Municipality （number， 20210617155253001）］

Objective:To analyze the expression and significance of interleukin-17 (IL-17), IL-23 and IL-22 in Klebsiella pneumoniae (KPN) pneumonia in rats. Methods:A total of 40 male SPF rats were randomly divided into the control group and the experimental group according to the simple number random table method, with 20 rats in each group. The control group was simultaneously dropped with 2 mL normal saline, while the experimental group was inoculated with a 2 mL suspension of 0.9×10 9 CFU/mL. The lung tissue was taken for pathological and bacteriological examination. Arterial partial pressure of oxygen (PaO 2), serum IL-17, IL-23 and IL-22 levels were detected after surgery for 4 h, 1 d, 3 d and 5 d. White blood cell count (WBC) and absolute neutrophil count (ANC) were performed in bronchoalveolar lavage fluid (BALF), and the relevance between IL-17, IL-23, IL-22 and PaO 2, and WBC, ANC in BALF was analyzed. Results:After surgery for 4 h, 1 d, 3 d and 5 d, the CFU count of lung tissue in experimental group rats decreased over time. PaO 2 in experimental group was significantly lower than that in the control group after surgery for 4 h, 1 d, 3 d and 5 d ( P<0.05), while WBC and ANC in BALF in the experimental group were significantly higher at the same time ( P<0.05). The levels of IL-17 and IL-23 in serum in the experimental groups were significantly higher than those in the control group after surgery for 4 h, 1 d, 3 d and 5 d ( P<0.05), and the levels of IL-22 in serum in the experimental groups were significantly lower than those in the control group at the same time ( P<0.05). Pearson analysis showed that IL-17 and IL-23 were negatively correlated with PaO 2 ( P<0.05) and positively correlated with WBC and ANC ( P<0.05). IL-22 was positively correlated with PaO 2 ( P<0.05), and negatively correlated with WBC and ANC ( P<0.05). Conclusions:Serum IL-17, IL-23, and IL-22 levels were significantly altered during the course of KPN rats, and serum IL-17, IL-23, and IL-22 levels were correlated with severity of illness.

Bone Cysts ; Cysts ; Endoscopy ; Humans ; Maxilla/surgery* ; Maxillary Sinus/surgery*

Objective To evaluate the relationship between autophagy and diabetes mellitus-caused influence on ischemic preconditioning ( IP )-induced cardioprotection in rats. Methods Clean-grade healthy male Sprague-Dawley rats, aged 12 weeks, weighing 290-320 g, were used in this study. Diabe-tes mellitus was induced by high-fat and high-sucrose diet ( lasting for 1 week) and intraperitoneal streptozo-tocin 50 mg∕kg ( for 2 consecutive days) and confirmed by fasting blood glucose level≥16. 65 mmol∕L ( for 1 week) . Thirty rats with diabetes mellitus, weighing 350-450 g, were divided into 3 groups ( n=10 each) using a random number table method: sham operation group ( DM-S group) , myocardial ischemia-reperfusion ( I∕R) group ( DM-IR group) and IP group ( DM-IP group) . Another 30 non-diabetic rats were selected and divided into 3 groups ( n=10 each ) using a random number table method: sham operation group (S group), myocardial I∕R group (IR group) and IP group. Myocardial ischemia was induced by ligation of the anterior descending branch of left coronary artery for 30 min followed by 120 min reperfusion. IP was produced by 3 cycles of 5-min ischemia followed by 5-min reperfusion prior to establishment of myo-cardial I∕R injury model in IP and DM-IP groups. Blood samples were collected from the internal jugular vein at the end of reperfusion for measuring serum concentrations of cardiac troponin I ( cTnI) and creatine kinase-MB ( CK-MB) . The rats were then sacrificed and myocardial tissues were obtained for determination of myocardial infarct size and expression of microtubule-associated protein 1 light chain 3 Ⅱ ( LC3 Ⅱ) , Beclin-1, phosphatidyl-inositol 3-kinase (PI3K), protein kinase B (Akt), phosphorylated Akt (p-Akt) and mammalian target of rapamycin ( mTOR) ( by Western blot) . p-Akt∕Akt ratio was calculated. Results Compared with S group, the serum cTnI and CK-MB concentrations were significantly increased, the percentage of myocardial infarct size was increased, the expression of LC3Ⅱand Beclin-1 in myocardial tis-sues was up-regulated, the expression of PI3K and mTOR was down-regulated, and p-Akt∕Akt ratio was decreased in IR group (P<0. 05). Compared with IR group, the serum cTnI and CK-MB concentrations were significantly decreased, the percentage of myocardial infarct size was decreased, the expression of LC3Ⅱand Beclin-1 in myocardial tissues was down-regulated, the expression of PI3K and mTOR was up-regulated, and p-Akt∕Akt ratio was increased in IP group ( P<0. 05) . Compared with DM-S group, the se-rum cTnI and CK-MB concentrations were significantly increased, the percentage of myocardial infarct size was increased, the expression of LC3Ⅱ and Beclin-1 in myocardial tissues was up-regulated, the expres-sion of PI3K and mTOR was down-regulated, and p-Akt∕Akt ratio was decreased in DM-IR group ( P<0. 05) . There was no significant difference in the parameters mentioned above between DM-IP group and DM-IR group (P>0. 05). Conclusion The mechanism by which diabetes mellitus abolishes IP-induced cardioprotection may be related to inhibiting activation of PI3K-Akt-mTOR signaling pathway and enhanced autophagy in rats.

Objective To evaluate the relationship between the mechanism underlying inhibition of inflammatory responses induced by α7 nicotinic acetylcholine receptor(α7nAChR)agonist postcondition?ing alone or in combination with remote limb ischemic postconditioning during myocardial ischemia?reperfu?sion(I∕R)and glycogen synthase kinase?3β(GSK?3β)in rats. Methods Eighty adult male Sprague?Dawley rats, aged 8 weeks, weighing 290-320 g, were divided into 4 groups(n=20 each)using a ran?dom number table: I∕R group, α7nAChR agonist postconditioning group(group P), remote limb ische?mic postconditioning group(group L)and α7nAChR agonist postconditioning plus remote limb ischemic postconditioning group(group P+L). Myocardial I∕R was induced by 30 min occlusion of the left anterior descending branch of coronary artery followed by 120 min reperfusion. Specific α7nAChR agonist PNU282987 2 mg∕kg was intravenously injected immediately before reperfusion in group P. In group L, limb ischemia was induced by tourniquet occlusion of bilateral hind paws for 10 min starting from 20 min of myocardial ischemia, and the tourniquet was released at the beginning of reperfusion. Combination of inter?vention measures previously described in P and L groups was performed in group P+L. Venous blood sam?ples were taken at 120 min of reperfusion for determination of serum troponin I(TnI)and creatine kinase?MB(CK?MB)concentrations, myocardial infarct size(IS)and expression of phosphorylated GSK?3β [p?GSK?3β(Ser536)], NF?κBp65 and phosphorylated nuclear factor?κBp65(p?NF?κBp65)in myocar?dial tissues(by Western blot). Results Compared with group I∕R, myocardial IS and serum cTnI and CK?MB concentrations were significantly decreased, the expression of p?GSK?3β(Ser9)in ischemic area was up?regulated, and the expression of p?NF?κBp65 in ischemic area was down?regulated in P, L and P+L groups(P<0.05). Compared with group L, myocardial IS and serum cTnI and CK?MB concentrations were significantly decreased, the expression of p?GSK?3β(Ser9)in ischemic area was up?regulated, and the expression of p?NF?κBp65 in ischemic area was down?regulated in group P+L(P<0.05). Conclusion The mechanism by which α7nAChR agonist postconditioning alone or in combination with remote limb is?chemic postconditioning inhibits inflammatory responses during myocardial I∕R may be related to inhibiting GSK?3β activity in rats.

Objective To evaluate the role of the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)or Janus kinase(JAK)/signal transducer and activator of transcription 3(STAT-3)signaling pathways in reduction of myocardial ischemia-reperfusion(I/R)injury by combination of limb ischemic and morphine postconditioning in rats.Methods Eighty SPF healthy male Sprague-Dawley rats,aged 8 weeks,weighing 280-320 g,were used in the study.Myocardial I/R was induced by occlusion of the left anterior descending branch of the coronary artery for 30 min followed by 120 min reperfusion.The rats were divided into 8 groups(n=10 each)using a random number table:I/R group,limb ischemic postconditioning group(LIP group),morphine postconditioning group(group MP),combination of limb ischemic and morphine postconditioning group(LIP+MP group)and signaling pathway blocker groups(I/Rb group,LIPb group,MPb group,LIP+MPb group).In I/R,LIP,MP and LIP+MP groups,the animals were sacrificed at the end of reperfusion,and myocardial specimens in ischemic and non-ischemic regions were obtained for determination of phosphorylated STAT-3(p-STAT-3),STAT-3,phosphorylated Akt(p-Akt)and Akt expression(by Western blot)and STAT-3 and Akt mRNA expression(by polymerase chain reaction).In I/Rb,LIPb,MPb and LIP+MPb groups,PI3K/Akt signaling pathway blocker LY294002 0.3 mg/kg was intravenously injected in 5 rats of each group,and JAK/STAT-3 signaling pathway blocker AG490 5 mg/kg was intravenously injected in the other 5 rats of each group.The animals were sacrificed at the end of reperfusion,and myocardial specimens in the ischemic region were obtained for determination of myocardial infarct size.Results Compared with I/R group,the p-STAT-3/STAT-3 ratio in LIP,MP and LIP+MP groups and p-Akt/Akt ratio in LIP+MP group were significantly increased,and the expression of STAT-3 and Akt mRNA was up-regulated in LIP+MP group(P<0.05).Compared with LIP and MP groups,the p-STAT-3/STAT-3 and p-Akt/Akt ratios were significantly increased,and the expression of STAT-3 and Akt mRNA was up-regulated in LIP+MP group(P<0.05).There was no significant difference in myocardial infarct size between the four groups when PI3K inhibitor LY294002 was applied(P>0.05).When JAK2 inhibitor AG490 was applied,the myocardial infarct size was significantly smaller in LIP+MPb group than in I/Rb,LIPb and MPb groups(P<0.05),and there was no significant difference in myocardial infarct size between I/Rb,LIPb and MPb groups(P>0.05).Conclusion Combination of limb ischemic and morphine postconditioning can enhance the activation of PI3K/Akt or JAK/STAT-3 signaling pathways,and the cardioprotection is dependent on the integrity of the PI3K/Akt signaling pathway and partially dependent on the integrity of the JAK/STAT-3 signaling pathway when applied in combination in rats.

Adult ; Airway Obstruction ; etiology ; Anesthetics ; adverse effects ; Humans ; Male ; Polyps ; complications ; Tonsillar Neoplasms ; complications ; Young Adult

Objective To evaluate the roles of PI3K/Akt and JAK/STAT signal transduction pathways in reduction of myocardial ischemia/reperfusion (I/R) injury by postconditioning with α subunit-containing nicotinic acetylcholine receptor (α7nAChR) agonist in rats.Methods Sixty Sprague-Dawley rats,weighing 290-320 g,were randomly divided into 4 groups (n =15 each):I/R group,ischemic preconditioning group (IPC group),ischemic postconditioning group (IPOC group) and postconditioning with specific α7nAChR agonist PNU282987 group ( PNU group ).Myocardial I/R was produced by 30 min occlusion of left anterior descending coronary artery followed by 180 min reperfusion in the 4 groups.The animals were subjected to 3 cycles of 5 min myocardial ischemia and 5 min reperfusion before 30 min myocardial ischemia in IPC group.The animals underwent 3 cycles of 10 s myocardial ischemia at 5 s intervals before 180 min reperfusion in group IPOC.PNU282987 2.4 mg/kg was injected intraperitoneally immediately before the reperfusion.At 60 min of reperfusion,5 rats in each group were sacrificed and the hearts were removed to determine the expression of Akt and STAT3 mRNA,phosphorylated Akt (p-Akt) and phosphorylated STAT3 (p-STAT3) in myocardial tissues.The left 10 rats in each group were sacrificed at 180 min of reperfusion and the hearts were removed to measure the infarct size.Results Compared with I/R group,the expression of STAT3 mRNA and p-Akt was significantly up-regulated in IPC group,and the expression of p-Akt and p-STAT3 was significantly up-regulated in IPOC group ( P ＜ 0.05).The infarct size was significantly reduced in IPC,IPOC and PNU groups compared with I/R group ( P ＜ 0.05 ).Conclusion The mechanism by which α7nAChR agonist postconditioning reduces myocardial I/R injury is not related to PI3K/Akt and JAK/STAT signal transduction pathways in rats.

Objective To investigate the role of reactive oxygen species (ROS) in the reduction of myocardial ischemia-reperfusion (I/R) injury by fentanyl postconditioning and remote limb ischemic postconditioning in rats.Methods Sixty-three male Sprague-Dawley rats,aged 8 weeks,weighing 250-350 g,were equally and randomly allocated into 7 groups:sham operation group (group S),group I/R,fentanyl postconditioning group (group F),remote limb ischemic postconditioning group (group R),ROS scavenger N-(2-Mercaptopropionyl) glycine (MPG) group (group M),MPG + fentanyl postconditioning group (group MF),and MPG + remote limb ischemic postconditioning group (group MR).Myocardial I/R was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 180 min of reperfusion.In group S the anterior descending branch was only exposed but not ligated.MPG 5 mg/kg was infused intravenously from 5 min before ischemia to 15 min of reperfusion in groups M,MF and MR,while the equal volume of normal saline was given in the other four groups.In groups F and MF,fentanyl 30 μg/kg was injected intravenously at 15 min of myocardial ischemia.In groups R and MR,the animals underwent 10 min ischemia of bilateral hind limbs starting from 15 min of myocardial ischemia.Arterial blood samples were taken at 180 min of reperfusion to determine the serum cardiac troponin I (cTnI) concentration.The rats were then sacrificed.The infarct size was measured by TTC.Results Compared with group S,the serum cTnI concentration and infarct size were significantly increased in the other six groups (P ＜0.05).Compared with group I/R,no significant change was found in the serum cTnI concentration and infarct size in M group,and the serum cTnI concentration and infarct size were significantly decreased in F and R groups (P ＜ 0.05).There was no significant difference in the serum cTnI concentration and infarct size between MF group and F group (P ＞ 0.05).The serum cTnI concentration was significantly higher and the infarct size was larger in group MR than in group R (P ＜ 0.05).Conclusion ROS is involved in the reduction of myocardial I/R injury by remote limb ischemic postconditioning in rats,but not in the myocardial protection provided by fentanyl postconditioning.