Objective To explore the method of self-care management education for patients who have received the eyelid reconstruction surgery by transplanting with free flap-skin. Methods There were 11 cases (15 eyes) who achieved self-care management and continued nursing, including the preoperative, postoperative nursing care of the donor-skin area, eye nursing, diet guidance, medication guidance, safety protection and its like. Results None of the cases revealed infection and all the grafts showed good biological activity among the 11 cases (15 eyes). Conclusions After self-care management education and continued nursing, the averaged hospitalization days of the patients are shortened; the cost is reduced, and the successful rate of the eyelid′s construction by free skin-flap transplantation is enhanced. Self-care management education and continued nursing care played an important role in promoting the healing and improving the successful rate of eyelid′s skin-flap transplantation.

Objective To investigate the role of mitochondrial permeability transition pore (mPTP) in attenuation of myocardial ischemia-reperfusion (I/R) injury by delayed preconditioning with sevoflurane in rats.Methods Eighty male SD rats, weighing 250-300 g, were randomly assigned into 5 groups ( n = 16 each): Ⅰsham operation group (group S), Ⅱ group I/R, Ⅲ sevoflurane delayed preconditioning group (group SP), Ⅳ the mPTP opener atractyloside + sevoflurane delayed preconditioning group (group A + SP), and Ⅴ atractyloside group (group A). Myocardial I/R was induced by ligation of anterior descending branch of left coronary artery for 30 min followed by 120 min of reperfusion in group I/R, SP, A + SP and A. In group SP and A + SP, 2.5%sevoflurane was inhaled for 1 h, while pure oxygen was inhaled for 1 h in the other groups, and then myocardial ischemia was performed 24 h later. In group A + SP and A, atractyloside 5 mg/kg was injected intravenously via caudal vein 15 min before ischemia. Blood samples were taken from carotid arteries for detection of serum cardiac troponin-Ⅰ (cTnI) concentrations at the end of reperfusion. Then the rats were sacrificed and hearts removed. The myocardial infarct size (IS) and expression of Bcl-2 and Bax in the myocardium were determined. Myocardial ultrastructure was examined with the electron microscope. Results Serum cTnI concentrations and Bax expression were significantly higher, the myocardial IS was significantly larger and Bcl-2 expression was significantly lower in the other groups than in group S ( P ＜ 0.05). Serum cTnI concentrations and Bax expression were significantly lower, the myocardial IS was significantly smaller and Bcl-2 expression was significantly higher in group SP than in group I/R ( P ＜ 0.05). Microscopic examination showed less damage in group SP than in group I/R. The protection provided by sevoflurane preconditioning was abolished by atractyloside. Conclusion Inhibition of mPTP opening can result in an up-regulation of Bcl-2 expression and down-regulation of Bax expression, which plays a role in attenuation of myocardial I/R injury by delayed preconditioning with sevoflurane in rats.

Objective To investigate the effect of acupuncture on gap junction protein Cx43 expression in the hippocampal region in ischemia/reperfusion rats.Methods Wistar rats were randomized into normal, model, non-point acupuncture and acupuncture groups. A rat model of focal cerebral ischemia/reperfusion was made by modified middle cerebral artery thread occlusion. The model, non-point acupuncture and acupuncture groups were separately divide into four subgroups: 30, 60, 180 and 360 min ischemia/reperfusion, 10 rats each. The middle and lateral lines of vertex were given electroacupuncture in the acupuncture group of rats. A subcostal fixed point 10 mm above the iliac crest on the affect side was selected as an acupuncture point in the non-point acupuncture group. The model group was not treated. Cx43 protein expression was determined by an immunohistochemical method.Results There was a statistically significant difference in the behavior disorder (Bederson’s) score between the acupuncture group and the non-point acupuncture or model group after different times of cerebral ischemia/ reperfusion (P<0.05). There was a statistically significant difference in hippocampal Cx43 content between model, acupuncture or non-point acupuncture group and the normal group and between the acupuncture group and the model or non-point acupuncture group after different times of cerebral ischemia/reperfusion (P<0.05).Conclusions Acupuncture can inhibit the overexpression of Cx43, intervene in cerebral ischemia-reperfusion injury and produce a neuroprotective effect in ischemic brain injury.

OBJECTIVE: To determine the effect of Gingkgo biloba leaf extract (EGb761) induced delayed preconditioning on cytochrome c oxidase (CcO) expression during myocardial ischemia-reperfusion in rats. METHODS: Four groups (10 in each) of Sprague-Dawley male rats were studied. In the sham group, the rats received no treatment. Rats in the ischemia-reperfusion (IR) group were treated with NS (1.0 mL/kg intravenously) 24 h before ischemia. Rats in the M group were treated with EGb761 (100 mg/kg intravenously) 24 h before the ischemia. In the D group , EGb761-treated rats that received the 5-hydroxydecanoate (5-HD), an inhibitor of mitochondrial KATP channels 15 min before the ischemia. The IR, M, and D groups were subjected to ischemia by 30 min of coronary artery occlusion before 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size was measured. CcO was measured by Western blot. The myocardial ultrastructure was observed under the electron microscope. RESULTS: The infarct size was significantly smaller in the M group [(23.78 ± 4.82)%] than in the I/R group [(37.87 ± 5.92)%] (P<0.05). The CcO protein expression in the myocardium was significantly higher in the M group than in the I/R group(P<0.05). Microscopic examination showed less myocardial damage in the M group than that in the I/R group. The infarct size, CcO protein expression, and myocardial damage had no significant difference between the D group and the I/R group (P>0.05). CONCLUSION EGb761 induced delayed preconditioning attenuates myocardial ischemia-reperfusion injury possibly through up-regulating CcO expression in rats.
Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Electron Transport Complex IV ; metabolism ; Ginkgo biloba ; chemistry ; Ischemic Postconditioning ; methods ; Ischemic Preconditioning, Myocardial ; methods ; Male ; Myocardial Ischemia ; physiopathology ; Myocardial Reperfusion Injury ; metabolism ; prevention & control ; Phytotherapy ; Plant Leaves ; chemistry ; Rats ; Rats, Sprague-Dawley

Objective To evaluate the clinical efficacy of limited open reduction combined with percutaneous medial locking plate in treatment of Rüedi-Allg(o)wer type Ⅱ and Ⅲ closed tibial pilon fractures.Methods A retrospective case-control analysis was made on 45 cases of closed tibial pilon fractures treated surgically between June 2008 and December 2015.There were 33 males and 12 females,aged from 26-66 years (mean,44.6 years).All cases were unilateral tibial pilon fractures,among which 18 were on the left while 27 were on the right.Thirty-four cases were combined with fibular fractures.There were 14 cases of type Ⅱ fractures and 31 type Ⅲ fractures according to the Rüedi-Allg(o)wer classification.Using the Tscheme-Gotzen system to evaluate soft tissue injury,two patients were in grade 1,29 patients in grade 2,and five patients in grade 3.On the basis of surgical methods,the cases were divided into Group A,limited open reduction with percutaneous medial locking plate and Group B,conventional open reduction.The operation time,reduction quality,fracture healing time,American Orthopedic Foot and Ankle Society (AOFAS) ankle-hindfoot scale at final follow-up visit and complications were recorded and compared between the two groups.Results The operation time of Group A was shorter than that of Group B (P ＜ 0.05).All patients had been followed up for 12-24 months,among which Group A was 22.5 months and Group B was 20.0 months (P ＞ 0.05).Compared with Group B,Group A was superior in fracture healing time (P ＜ 0.05) and AOFAS ankle-hindfoot scale(P ＜0.05),but was inferior in reduction quality (P ＜ 0.05).Poor wound healing was observed in two cases in each group,yet there was no nonunion in all cases.Conclusion Compared with conventional open reduction,the limited open reduction combined with percutaneous medial locking plate has more advantages in operation time and fracture healing,which can achieve better ankle functions for closed tibial pilon fractures.

Objective To explore the effect of low-level laser therapy (LLLT)applied to the quadriceps muscle on the recovery of exhausting-cycling-exercise-induced fatigue.Methods According to a randomised,double-blind and crossover design,16 healthy male students were randomly assigned to an LLLT-1,LLLT-3,LLLT-5 and a placebo group,and received LLLT for 300 s at the dosage of 0.06 J· cm-2,0.18 J·cm-2,0.3 J·cm-2 and 0 to the bilateral rectus femoris after the exhausting-cycling-exercise-induced fatigue.The blood lactate(BL),heart rate(HR),rated perceived exertion(RPE)and visual analogue scale(VAS)were assessed before the exercise,immediately after exercise,10 and 20 min after exercise,as well as immediately after the first Wingate(WG)test,5 and 30 min after the WG test.Meanwhile,the second WG test was performed 40 min after the first WG test.Results The average HR value of LLLT-1 group was significantly lower than the placebo group at 10 min after exercise(P＜ 0.05)and immediately after the WG test(P＜0.01),while that of LLLT-3 and LLLT-5 groups was significantly lower than the placebo group immediately and 5 min after the WG test(P＜0.01).Compared to the placebo group,the average BL of LLLT-1,LLLT-3 and LLLT-5 groups was significantly lower 10 min after exercise(P＜0.05 for all)and that of LLLT-5 group was also significantly lower 30 min after the first WG test(P＜0.05).However,the average blood glucose of LLLT-5 group was significantly higher than the placebo group right after the first WG test(P＜0.05).Moreover,significant increase was observed in the mean(P=0.002)and peak power(P=0.006)at the second WG test and the mean(P=0.048) power at the first WG test of LLLT-3 group,compared to the placebo group.Conclusion LLLT applied to quadriceps muscles after exhausting exercise may enhance recovery,and LLLT at the dose of 0.18 J·cm-2 is of the best effect.

Objective:To observe the therapeutic effect of echinacoside (ECH) on liver injury and glucose metabolism disorder in sepsis rats induced by cecal ligation and puncture (CLP), and to explore its possible mechanism.Methods:Forty eight male Sprague Dawley (SD) rats were randomly divided into four groups: sham group (sham), model group (CLP), treatment group (CLP+ ECH) and inhibitor group (CLP+ ECH+ EX527). The sham group only received laparotomy, and the model group underwent CLP. The treatment group was intragastric administration of echinacea (30 mg/kg) every day after CLP modeling. The inhibitor group was injected with silence information regulator 1 (SIRT1) inhibitor EX527 (5 mg/kg) one hour before CLP, and then treated the same as the treatment group. Fasting blood glucose, insulin and serum biochemical indexes were detected in virous groups. The serum levels of interleukin (IL)-1 β, IL-6 and tumor necrosis factor-α(TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA). 2′, 7′- dichlorofluorescein diacetate (DCFH-DA) staining was used to observe the production of reactive oxygen species (ROS) in liver tissue of rats in each group; hematoxylin-eosin (HE) staining was used to observe the pathological changes of liver tissue in each group; The expressions of SIRT1, glucose-6-phosphatase (G6Pase), phosphoenolpyruvate carboxykinase (PEPCK), phosphorylated signal transducers and activators of transcription 3 (p-STAT3) and phosphorylated protein ki-nase B(p-AKT) were detected by Western blot.Results:Compared with sham group, the levels of serum glucose, serum insulin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), ROS, IL-1β, IL-6 and TNF-α in model group increased, while the liver glycogen and survival rate decreased (all P<0.05). After echinacoside treatment, the serum glucose, serum insulin, ALT, AST, ROS , IL-1β, IL-6 and TNF-α levels decreased, and the liver glycogen and survival rate increased (all P<0.05); After SIRT1 inhibitor intervention, the levels of serum insulin, ALT, AST, IL-6 and ROS in the inhibitor group increased ( P<0.05). HE staining showed that there were infiltration and necrosis of inflammatory cells in the liver tissue of model group, and echinacoside could significantly reduce the focal and massive necrosis; Western blot showed that compared with the sham group, the expression levels of SIRT1, p-STAT3 and p-AKT protein in the model group decreased, while the expression levels of G6Pase and PEPCK protein increased ( P<0.05); After echinacoside treatment, the expression levels of SIRT1, p-STAT3 and p-AKT increased, while the expression levels of G6Pase and PEPCK decreased ( P<0.05). After SIRT1 inhibitor intervention, the expression of SIRT1, p-STAT3 and p-AKT protein decreased, and the expression of G6Pase and PEPCK protein increased in the inhibitor group ( P<0.05). Conclusions:Echinacoside is a potential therapeutic agent for sepsis associated liver injury and glucose metabolism disorders, which may play a role by targeting SIRT1 to activate STAT3 and AKT in the liver.

Objective:To investigate whether miRNA-296-5p can inhibit enterovirus 71 (EV71) virus replication in neural cells SK-N-SH by targeting the phosphatase and tensin homology deleted on chromosome 10 (PTEN)/phosphatidylinositol 3-kinase (PI3K)/serine/threonine kinases (AKT) signaling pathway.Methods:Serum samples were collected from patients with EV71 virus-infected hand-foot-mouth disease and normal physical examination, and the expressions of serum inflammatory factors procalcitonin (PCT), C-reactive protein (CRP), tumor necrosis factor-α (TNF-α) , interleukin-6 (IL-6), IL-1β, and IL-13 were detected by enzymelinked immunosorbent assay (ELISA). Human neuroblastoma SK-N-SH cells infected by EV71 virus in logarithmic growth phase were set up as control group, miRNA-296-5p mimic group and miRNA-296-5p inhibitor group. The transfection was carried out according to the Lipofectamine 2000tm cell transfection reagent. The expression of EV71-VP1 gene mRNA and protein and PTEN/PI3K/Akt signal pathway related molecules in three groups of cells was observed by real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) and Western blot.Results:ELISA test results showed that the levels of serum inflammatory factors PCT, CRP, TNF-α, IL-1β, IL-6 and IL-13 in patients with EV71 virus-infected hand, foot and mouth disease were significantly higher than those in normal physical examination ( P<0.05). The results of qRT-PCR and Western blot showed that the mRNA and protein levels of mirna-296-5p and PTEN in SK-N-SH were significantly decreased after EV71 virus infection, while the mRNA and protein levels of EV71-VP1 and molecules related to PI3K/AKT signaling pathway were significantly increased ( P<0.05). The expression of PTEN was significantly increased in the miRNA-296-5p mimic group, and the expression of EV71-VP1 and the activation of the PI3K/AKT signaling pathway were inhibited, while the effect was reversed in the miRNA-296-5p inhibitor group ( P<0.05). Conclusions:MiRNA-296-5p inhibits the replication of EV71 virus in neural cells SK-N-SH by targeting the PTEN/PI3K/AKT signaling pathway, while reducing the cellular inflammatory response, targeting miRNA-296-5p and downstream PTEN/PI3K/AKT The signal pathway is expected to provide therapeutic targets and theoretical basis for the treatment of hand-foot-mouth disease caused by clinical EV71 virus.

Objective:The distribution characteristics of intrathecal drugs and the limitation of current catheterization techniques make traditional intrathecal analgesic treatment nearly useless for refractory craniofacial pain,such as trigemina neuralgia.This technical guideline aims to promote the widespread and standardize the application of intra-prepontine cisternal drug delivery via spinal puncture and catheterization. Methods:A modified Delphi approach was used to work for this guideline.On the issues related to the intra-prepontine cisternal targeted drug delivery technique,the working group consulted 10 experts from the field with 3 rounds of email feedback and 3 rounds of conference discussion. Results:For the efficacy and safety of the intra-prepontine cisternal targeted drug delivery technique,a consensus was formed on 7 topics(with an agreement rate of more than 80%),including the principles of the technique,indications and contraindications,patient preparation,surgical specifications for intra-prepontine cisternal catheter placement,analgesic dosage coordination,analgesic management,and prevention and treatment of complications. Conclusion:Utilizing the intra-prepontine cisternal drug infusion system to manage refractory craniofacial pain could provide advantages in terms of minimally invasive,secure,and effective treatment.This application can not only alleviate the suffering of individuals experiencing the prolonged pain but also support the maintenance of quality of life and dignity in their final moments,justifiing its widespread dissemination and standardized adoption in domestic and international professional fields.

OBJECTIVES: Myocardial ischemia reperfusion injury (IRI) occurs occasionally in the process of ischemic heart disease. Sevoflurane preconditioning has an effect on attenuating IRI. Preserving the structural and functional integrity of mitochondria is the key to reduce myocardial IRI. Silent information regulator 3 (SIRT3), a class of nicotinamide adenine dinucleotide (NAD⁺) dependent deacetylases, is an important signal-regulating molecule in mitochondria. This study aims to explore the role of mitochondrial NAD⁺-SIRT3 pathway in attenuating myocardial IRI in rats by sevoflurane preconditioning. METHODS: A total of 60 male Sprague Dawley (SD) rats were randomly divided into 5 groups (n=12): A sham group (Sham group), an ischemia reperfusion group (IR group), a sevoflurane preconditioning group (Sev group, inhaled 2.5% sevoflurane for 30 min), a sevoflurane preconditioning+SIRT3 inhibitor 3-TYP group (Sev+3-TYP group, inhaled 2.5% sevoflurane for 30 min and received 5 mg/kg 3-TYP), and a 3-TYP group (5 mg/kg 3-TYP). Except for the Sham group, the IR model in the other 4 groups was established by ligating the left anterior descending coronary artery. The size of myocardial infarction was determined by double staining. Serum cardiac troponin I (cTnI) level was measured. The contents of NAD⁺ and ATP, the activities of mitochondrial complexes I, II, and IV, the content of MDA, the activity of SOD, and the changes of mitochondrial permeability were measured. The protein expression levels of SIRT3, SOD2, catalase (CAT), and voltage dependent anion channel 1 (VDAC1) were detected by Western blotting. The ultrastructure of myocardium was observed under transmission electron microscope. MAP and HR were recorded immediately before ischemia (T0), 30 min after ischemia (T1), 30 min after reperfusion (T2), 60 min after reperfusion (T3), and 120 min after reperfusion (T4). RESULTS: After ischemia reperfusion, the content of NAD⁺ in cardiac tissues and the expression level of SIRT3 protein were decreased (both P<0.01), and an obvious myocardial injury occurred, including the increase of myocardial infarction size and serum cTnI level (both P<0.01). Correspondingly, the mitochondria also showed obvious damage on energy metabolism, antioxidant function, and structural integrity, which was manifested as: the activities of mitochondrial complexes I, II, and IV, ATP content, protein expression levels of SOD2 and CAT were decreased, while MDA content, VDAC1 protein expression level and mitochondrial permeability were increased (all P<0.01). Compared with the IR group, the content of NAD⁺ in cardiac tissues and the expression level of SIRT3 protein were increased in the Sev group (both P<0.01); the size of myocardial infarction and the level of serum cTnI were decreased in the Sev group (both P<0.01); the activities of mitochondrial complexes I, II, and IV, ATP content, protein expression levels of SOD2 and CAT were increased, while MDA content, VDAC1 protein expression level, and mitochondrial permeability were decreased in the Sev group (all P<0.01). Compared with the Sev group, the content of NAD⁺ in cardiac tissues and the expression level of SIRT3 protein were decreased in the Sev+3-TYP group (both P<0.01); the size of myocardial infarction and the level of serum cTnI were increased in the Sev+3-TYP group (both P<0.01); the activities of mitochondrial complexes I, II, and IV, ATP content, protein expression levels of SOD2 and CAT were decreased, while MDA content, VDAC1 protein expression level, and mitochondrial permeability were increased in the Sev+3-TYP group (all P<0.01). CONCLUSIONS Sevoflurane preconditioning attenuates myocardial IRI through activating the mitochondrial NAD⁺-SIRT3 pathway to preserve the mitochondrial function.
Adenosine Triphosphate/metabolism* ; Animals ; Male ; Mitochondria/metabolism* ; Myocardial Infarction/metabolism* ; Myocardial Reperfusion Injury/metabolism* ; NAD/metabolism* ; Rats ; Rats, Sprague-Dawley ; Sevoflurane/metabolism* ; Sirtuin 3/metabolism* ; Voltage-Dependent Anion Channel 1/metabolism*