Objective To study the clinical value of preserving intercostobrachial nerve(ICBN) during axillary lymph node dissection.Methods The clinical data of 146 cases of operated breast cancer of stage Ⅰ、Ⅱ、Ⅲa were analyzed.All cases were divided into twe groups randomly:preserved group(n=67) preserved ICBN in axillary lymph node dissection operation;control group(n=79) resected ICBN regulary in the operations.The number of lymph node dissection and the incidence of abnormal sense on the skin of inside upper arm were compared between groups.Results In one month,three months and six months followed up:the incidence of ahnormal sense on the skin of inside upper arm was 17.9%,11.9%,7.4% in preserved group,which was lower than that (74.9%,60.7%,59.5%) in control group significantly (P＜0.01).The diflrence between the two groups was significant.No local recurrence was occurred after opreations from eight months to five years examined.It was none difference that period of operation and the number of lymph node dissection between the groups.Conclusions Preserving ICBN in axillary lymph node dissection for breast cancer of stage Ⅰ、Ⅱ、Ⅲa could decrease the incidence of abnormal sence on the skin of inside upper arm.It eouldnt increase the incidence of local recurrence.It can improve the life quality of the patients after operations.

Objective To explore the characteristics of mycobacterium dependend antituberculous drug. Methods 137 strains of mycobacterium were tested for resistance by the absolute concentration method on Lowenstein Jensen medium. Dependent positive were the coloun that on higher concentration drug medium stronger than lower concentration than controls. Results 12(8.76%) of the 130 strains M. tuberculosis and 7 strains nontuberculous mycuberculous (NTM) were found dependent, in which strains dependend on INH, RFP and SM were 3(2.19%), 10(7.3%) and 3(2.19%) respectively, 4(2.92%) were dependend on two drugs. Conclusions Were NTM dependent, Not found all detected from multiple strains.

Objective To explore the effect of topical application of sodium hyaluronate on preventing perivascular adhesion of the vein grafts in rabbits. Methods Thirty-six male New Zealand white rabbits, aged 5 months, were randomly and equally divided into 2 groups: groups A and B. Arterial defect model was established by cutting about 1cm artery from the middle part of the dissected left common carotid artery. A section about 3cm was cut from the right external jugular vein, and the harvested vein was inverted and anastomosed end-to-end to the artery defect. After the anastomosis, the adventitia and two anastomoses of the grafted veins in group A were coated locally with 0.2ml sodium hyaluronate. The grafted veins were obtained 1, 2 and 4 weeks after the operation, with the perivascular adhesion of the vein grafts being examined macroscopically before the resection. HE staining and Masson staining were preformed for histological changes of grafted vein wall and the perivascular adhesion of the vein grafts. At 2, 4 weeks postoperation, the perivascular adhesions of the vein grafts were graded by the grading criteria of adhesion in macroscopic evaluation and histological evaluation. Result At 1, 2 and 4 weeks postoperatively, the macroscopic and histological observation found that the perivascular adhesions in group A were looser than those in group B. The macroscopic grade and histological grade were lower in group A than in group B, there was a significant difference between the two groups at 2 and 4 weeks postoperation (P<0.05). Conclusion Topical application of sodium hyaluronate can reduce the perivascular adhesion and is an ideal treatment strategy for preventing perivascular adhesion of vein grafts.

As a non-atherosclerotic disease in the extracranial segment of the carotid artery, carotid web is a ridge-like intraluminal protrusion beyond the bifurcation of the posterior wall of the carotid artery bulb. Carotid web also has been referred to as an atypical variant of fibromuscular dysplasia. In recent years, more and more studies indicate that carotid web is a rare but important risk factor for ischemic stroke. In order to accurately diagnose carotid artery web, implement targeted intervention and treatment for ischemic stroke caused by carotid web, the authors summarized the recent advances in carotid web and ischemic stroke.

Objective To evaluate the relationship between heme oxygenase-1 (HO-1) expression and autophagy during acute lung injury in septic mice.Methods Forty-eight male C57BL/6 mice,aged 6-8 weeks,weighing 20-25 g,were randomly divided into 4 groups (n=12 each) using a random number table:sham operation group (group SH),sepsis group (group CLP),HO-1 agonist hemin plus sepsis group (group Hemin+CLP) and HO-1 inhibitor SnPP plus sepsis group (group SnPP+CLP).Sepsis was induced by cecal ligation and puncture in CLP,Hemin+CLP and SnPP+CLP groups.Hemin 50 μmol/kg and SnPP 50 μmol/kg were intraperitoneally injected at 2 h before operation in Hemin + CLP group and SnPP+CLP group,respectively.Arterial blood samples were taken at 24 h after operation for blood gas analysis,PaO2 was recorded,and oxygenation index was calculated.Lungs were removed for examination of pathological changes which were scored and for determination of autophagosome count (with an electron microscope),weight/dry weight ratio (W/D ratio) and expression of HO-1,Becling-1 and microtubule-associated protein 1 light chain 3 Ⅱ (LC3 Ⅱ) in lung tissues (by Western blot).Results Compared with group SH,oxygenation index was significantly decreased,and W/D ratio,autophagosome count and pathological scores were increased in CLP,Hemin+CLP and SnPP+CLP groups,and the expression of HO-1,Beclin-1 and LC3 Ⅱ was significantly up-regulated in CLP and Hemin+CLP groups (P＜0.05).Compared with group CLP,oxygenation index and autophagosome count were significantly increased,W/D ratio and pathological scores were decreased,and the expression of HO-1,Beclin-1 and LC3 Ⅱ was up-regulated in group Hemin+CLP,and oxygenation index and autophagosome count were significantly decreased,W/D ratio and pathological scores were increased,and the expression of HO-1,Beclin-1 and LC3 Ⅱ was downregulated in group SnPP+CLP (P＜0.05).Conclusion Up-regulated expression of HO-1 mediates autophagy,which is involved in the endogenous protective mechanism underlying acute lung injury in septic mice.

To analyze and evaluate the knowledge of Chinese Guidelines of Diabetes Prevention and Treatment in Shanghai medical staff. 175 medical staff working in endocrinology or community health were enrolled and evaluated by a questionnaire of guidelines about the state of professional, training, and related knowledge. Only 16. 6% medical staffwere trained about the guidelines( 46. 67% from the general hospitals, 14. 75% from secod-level hospital and 7. 14% persons from the community hospitals, P＜0. 01 ). The total correct answer rate of the guidelines was 37. 36%. The correct rate of community hospitals was lower than others( P＜0. 05 ). The rate of doctors' was higher than nurses'( P＜0. 05 ). There were difference between doctors and nurses with the key point of diabetes care knowledge in different level hospitals. The effective method of clinical training in diabetes care should be explored. We still have to work hard to promote the effect of diabetes control and prevention. Effective training about the guidelines should be enhanced. The cooperation between general hospitals and community health institutions in diabetes prevention and treatment should be enhanced.

Objective To evaluate the role of mitophagy in hydrogen-induced reduction of lipopolysaccharide (LPS)-caused mitochondrial injury to macrophages of mice.Methods Macrophage line RAW264.7 cells of mice were routinely cultured and divided into 4 groups (n =6 each) using a random number table method:control group (Con group),LPS group,LPS plus hydrogen group (LPS + H2 group) and LPS plus hydrogen plus mitophagy inhibitor 3-methyladenine (3-MA) group (LPS+H2+3-MA group).Cells were incubated for 6 h with LPS at the concentration of 1 μg/ml in LPS group.Cells were incubated for 6 h with LPS 1 μg/ml and hydrogen-rich medium 0.6 mmol/L.Cells were incubated for 1 h with 2 mmol/L 3-MA and then incubated for 6 h with LPS 1 μg/ml and hydrogen-rich medium 0.6 mmol/L in LPS+H2+3-MA group.Mitochondrial respiratory control ratio (RCR) was measured using a Clark-type electrode.Mitochondrial membrane potential (MMP) was determined by JC-1 staining.Autophagosomes were counted with a transmission electron microscope.The expression of PTEN-induced putative kinase 1 (PINK1),E3 ubiquitin ligase (Parkin),microtubule-associated protein 1 light chain 3 Ⅱ (LC3 Ⅱ)and Beclin-1 was determined by Western blot.Results Compared with Con group,RCR and MMP were significantly decreased,the expression of PINK1,Parkin,LC3 Ⅱ and Beclin-1 was up-regulated,and the number of autophagosomes was increased in LPS group (P＜0.05).Compared with LPS group,RCR and MMP were significantly increased,the expression of PINK1,Parkin,LC3 Ⅱ and Beclin-1 was up-regulated,and the number of autophagosomes was increased in LPS+H2group (P＜0.05).Compared with LPS+H2 group,RCR and MMP were significantly decreased,the expression of PINK1,Parkin,LC3 Ⅱ and Beclin-1 was down-regulated,and the number of autophagosomes was decreased in LPS + H2 + 3-MA group (P＜0.05).Conclusion Enhanced mitophagy is involved in hydrogen-induced reduction of LPS-caused mitochondirial injury to macrophages of mice.

Objective To evaluate the relationship between phosphatidylinositol 3?kinase∕serine?threonine kinase(PI3K∕Akt)signaling pathway and autophagy during acute lung injury in septic mice. Methods Thirty?six male C57BL∕6 mice, aged 6-8 weeks, weighing 20-25 g, were divided into 3 groups(n=12 each)using a random number table: sham operation group(group SH), sepsis group (group S)and PI3K inhibitor LY294002 plus sepsis group(group LY+S). Sepsis was induced by cecal ligation and puncture in S and LY+S groups. LY294002 30 mg∕kg was intraperitoneally injected at 2 h be?fore operation in group LY+S. Arterial blood samples were taken at 24 h after operation for blood gas analy?sis, PaO2was recorded, and oxygenation index was calculated. Lung specimens were obtained for examina?tion of pathological changes which were scored and for determination of autophagosome count(using trans?mission electron microscope), wet∕dry weight ratio(W∕D ratio)and expression of Akt, phosphorylated Akt(p?Akt), Beclin?1 and microtubule?associated protein 1 light chain 3 Ⅱ(LC3 Ⅱ). The p?Akt∕Akt ratio was calculated. Results Compared with group SH, oxygenation index was significantly decreased,and the W∕D ratio and pathological score were increased in S and LY+S groups, the autophagosome count was significantly increased, p?Akt∕Akt ratio was increased, and the expression of Beclin?1 and LC3Ⅱ was up?regulated in group S(P<0.05). Compared with group S, oxygenation index was significantly de?creased, and the W∕D ratio was increased, the autophagosome count was decreased, pathological scores were increased, p?Akt∕Akt ratio was decreased, and the expression of Beclin?1 and LC3Ⅱwas down?regu?lated in group LY+S(P<0.05). Conclusion PI3K∕Akt signaling pathway activation mediates autophagy and is involved in the endogenous protective mechanism of acute lung injury in septic mice.

Objective To investigate the role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in hydrogen-rich saline-induced reduction of lipopolysaccharide (LPS)-caused damage to mitochondria in macrophages of mice.Methods Macrophage line RAW264.7 of mice were routinely cultured and divided into 4 groups (n=6 each) using a random number table method:control group (group C),group LPS,hydrogen-rich saline plus LPS group (group LPS+H2) and hydrogen-rich saline plus LPS plus ATP group (group LPS+ATP+H2).LPS was given at the concentration of 1 μg/ml,and the cells were then incubated for 30 min in group LPS.LPS at the concentration of 1 μg/ml and hydrogen-rich saline at the concentration of 0.6 mmol/L were simultaneously given,and the cells were then incubated for 30 min in LPS+H2 and LPS+ATP+H2 groups.ATP at the concentration of 1 nmol/L was then given,and the cells were incubated for 6 h in group LPS+ATP+H2.Mitochondrial membrane potential (MMP) was determined by JC-1 staining,and respiratory control ratio (RCR) was measured using a Clark-type electrode.The expression of NLRP3,caspase-1 and apoptosisassociated speck-like protein containing C-terminal caspase recruitment domain (ASC) was determined by Western blot.The concentrations of INTERLEUKIN-1 BETA (IL-1β),IL-18 and IL-6 in the supernatant were determined by enzyme-linked immunosorbent assay.Results Compared with group C,MMP and RCR were significantly decreased,the concentrations of IL-1β,IL-18 and IL-6 in the supernatant were increased,and the expression of NLRP3,caspase-1 and ASC was up-regulated in group LPS (P＜0.05).Compared with group LPS,MMP and RCR were significantly increased,the concentrations of IL-1β,IL-l8 and IL-6 in the supernatant were decreased,and the expression of NLRP3,caspase-1 and ASC was down-regulated in group LPS+H2 (P＜0.05).Compared with group LPS+H2,MMP and RCR were significantly increased,the concentrations of IL-1β,IL-18 and IL-6 in the supernatant were decreased,and the expression of NLRP3,caspase-1 and ASC was down-regulated in group LPS+ATP+H2 (P＜0.05).Conclusion Hydrogen-rich saline can reduce LPS-caused damage to mitochondria in macrophages of mice through inhibiting the activation of NLRP3 inflammasome.

Objective:To evaluate the relationship between phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway and heme oxygenase-1 (HO-1) expression during lung injury in septic mice.Methods:Forty-eight clean-grade healthy male C57BL/6 mice, aged 6-8 weeks, weighing 20-25 g, were divided into 4 groups ( n=12 each) using a random number table method: sham operation group (group SH), sepsis group (group SEP), PI3K inhibitor LY294002 group (group LY) and LY294002+ HO-1 agonist hemin group (group LH). Sepsis was induced by cecal ligation and puncture in anesthetized animals.LY294002 30 mg/kg was intraperitoneally injected at 2 h before establishing the model in LY group and LH group.Hemin 50 μmol/kg was intraperitoneally injected at 1 h before establishing the model in LH group.Mice were sacrificed at 24 h after surgery, and lungs were removed for determination of wet/dry weight ratio (W/D ratio), tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10) contents (by enzyme-linked immunosorbent assay), and expression of phosphorylated Akt(p-Akt), Akt and HO-1 (by Western blot) and for examination of the pathological changes of lung tissues which were scored. Results:Compared with SH group, the W/D ratio, lung injury score, and TNF-α and IL-10 contents were significantly increased in SEP, LY and LH groups, and the expression of p-Akt and HO-1 was significantly up-regulated in SEP group ( P<0.05). Compared with SEP group, the W/D ratio, lung injury score and TNF-α content were significantly increased, IL-10 content was decreased, and the expression of p-Akt and HO-1 was down-regulated in LY group ( P<0.05). Compared with LY group, the lung injury score and TNF-α content were significantly decreased, IL-10 content was increased, and the expression of HO-1 was up-regulated in LH group ( P<0.05). Conclusion:PI3K/Akt signaling pathway is involved in the endogenous protective mechanism of lung injury by regulating HO-1 expression in septic mice.