OBJECTIVETo evaluate the clinical effect of avascular necrosis of femoral head (ANFH) with interventional therapy in the near future.

METHODSTwenty-eight patients (19 males, 9 females, the age was from 14 to 70 years old with an average of 38 years) with ANFH were treated by catheterization. The thrombolytic drugs, vasodilator drugs and improving microirculative drugs were respectively injected directly into the arteries supplying the femoral head after ultraselection. Contrasted the changing of the arteries suppplying the femoral head between pretreatment and posttreatment, and observed the bone density of the femoral head at 12-36 months after treatment,and analyzed clinical symptoms (hip pain and joint range of motion) improving.

RESULTSThe angiography showed the arteries supplying the femoral head were manifold, the coloration or the femoral head were enhanced after interventional therapy. The X-ray showed the bone density of the femoral head gradually recovered of nearly common by 97.2% (35/36). And hip pain and joint range of motion significantly improved than that of before treatment.

CONCLUSIONInterventiomal therapy is a safe and effective method to ANFH, which seems to be promising for wide clinical application.

Adolescent ; Adult ; Aged ; Cardiovascular Agents ; therapeutic use ; Female ; Femur Head ; blood supply ; drug effects ; Femur Head Necrosis ; drug therapy ; Humans ; Male ; Middle Aged ; Treatment Outcome ; Young Adult

Objective To investigate the application of delayed sternal closure (DSC) following neonatal cardiac surgery.Methods We retrospectively analyzed clinical data of 360 neonatal patients underwent cardiac surgery through median sternotomy in Guangdong General Hospital between June 2009 and June 2014.These neonates were divided into 2 groups:DSC group (190 cases) and non-DSC group(170 cases).Comparing the differences between 2 groups,we analysed the application of DSC following neonatal cardiac surgery and the effect of DSC on surgical site infection.Results The cardiopulmonary bypass time,cross clamp time and mechanical ventilation time were longer in DSC group than in non-DSC group.The mortality rate in the DSC group(20.53％) was markedly higher than that in the non-DSC group(5.29％).However,there was no statistical difference in the incidence of sternal wound infection between 2 groups.Conclusion As an effective treatment for neonates with severe cardiac surgery,DSC doesn' t increase the incidence of surgical site infection.

Objective: To investigate the expressions of hypoxia inducible factor-1α (HIF-1α) and autophagy related protein Beclin-1 in colon cancer and their clinical significances. Methods: From January 2017 to December 2018, 120 patients with colon cancer who were admitted to Dandong First Hospital were selected. The expressions of HIF-1α and Beclin-1 in colon cancer and corresponding adjacent tissues were detected by immunohistochemical SABC method. The relationship of the expressions of HIF-1α and Beclin-1 with the clinicopathological features of colon cancer patients was also discussed. The expressions of HIF-1α and Beclin-1 in 20 pairs of fresh colon cancer and paracancerous tissues were detected by Western blot. Results: The results of immunohistochemistry showed that the positive expression rates of HIF-1α and Beclin-1 proteins in colon cancer tissues were significantly higher than those in paracancerous tissues [75.0% (90/120) vs. 21.7% (26/120), 60.8% (73/120) vs. 12.5% (15/120)], and the differences were statistically significant (χ ² values were 68.343 and 60.359, both P < 0.01). The results of Western blot showed that the expressions of HIF-1α and Beclin-1 proteins in 20 pairs of fresh colon cancer tissues were significantly higher than those in paracancerous tissues (1.98±0.66 vs. 0.76±0.55, 1.50±0.40 vs. 0.46±0.35), and the differences were statistically significant (t values were 6.912 and 8.315, both P < 0.01). The expressions of HIF-1α and Beclin-1 in colon cancer tissues were related to TNM stage, degree of differentiation, depth of infiltration, lymph node metastasis and nerve invasion (HIF-1α: χ ² values were 9.074, 15.215, 10.101, 11.610 and 9.979; Beclin-1: χ ² values were 11.285, 4.858, 24.436, 9.354 and 4.632; all P < 0.05), but not with age, sex, tumor location, tumor diameter and vascular tumor thrombus (all P > 0.05). There was a positive correlation between the expressions of HIF-1α and Beclin-1 proteins in colon cancer (r = 0.483, P < 0.01). Conclusion The expressions of HIF-1α and Beclin-1 proteins in colon cancer tissues are significantly increased, and the interaction between them is involved in the occurrence and development of colon cancer.

Objective: To investigate the expression of HOXA terminal transcript antisense RNA (HOTTIP) in hepatocellular carcinoma (HCC) tissues and to explore its effect on proliferation, invasion and migration in HepG2 cells. Methods: A total of 60 cases with HCC tissues undergoing excision surgery and 60 cases of corresponding paracancerous tissues from January 2012 to June 2018 in Dandong First Hospital of Liaoning Province were collected. The expressions of HOTTIP in HCC tissues and paracancerous tissues were detected by using real-time quantitative polymerase chain reaction (RT-qPCR), and the relationship between the expression and clinicopathological features was analyzed. HepG2 cell line with high expression of HOTTIP constructed by cell transfer technique was treated as the experimental group, and the empty plasmid pcDNA3.1-NC was treated as the control group. The effect of HOTTIP on the proliferation of HepG2 cells was detected by using CCK-8 method, and the effect of HOTTIP on invasion and migration of HepG2 cells was detected by using Transwell assay. Results: The expression of HOTTIP mRNA in HCC tissues was higher than that in paracancerous tissues, and there was no statistically significant difference (1.9±0.6 vs. 0.9±0.7, t = 6.069, P < 0.01). The whole HCC cases were divided into the high expression group (30 cases) and the low expression group (30 cases) according to the median value (1.92) of the expression of HOTTIP mRNA. The expression of HOTTIP was related with TNM stage, differentiation degree and lymph node metastasis (χ² values were 10.800, 8.076, 5.711, all P < 0.05), but not with age, gender, tumor diameter, number of tumors, hepatitis and alpha fetoprotein (AFP) levels (all P > 0.05). The results of RT-qPCR showed that the expression of HOTTIP mRNA in HepG2 cells was increased after transfection of overexpressed HOTTIP and the differences was statistically significant compared with the control group (63±6 vs. 13±9, t = 9.129, P < 0.01). The results of CCK-8 method showed that the proliferation activity of cells was enhanced after the overexpression of HOTTIP in HepG2 cells (24 h, 36 h, 72 h at 490 nm absorbance was 1.497 ± 0.017 vs. 0.826±0.006, 2.002±0.025 vs. 1.211±0.020, 3.257±0.042 vs. 1.772±0.021), and the differences were statistically significant (t values were 5.321, 7.349, 8.793, all P < 0.01). In Transwell invasion assay, the number of cells transferred into the basement membrane in the experimental group was more than that in the control group (101±9 vs. 41±11), and the difference was statistically significant (t = 6.839, P < 0.01). In Transwell migration assay, the number of cells transferred into the basement membrane in the experimental group was more than that in the control group (112±9 vs. 53±11), and the difference was statistically significant (t = 7.105, P < 0.01). Conclusion The expression of HOTTIP in HCC tissues is up-regulated, and the overexpression of HOTTIP can promote the proliferation, invasion and migration of HCC cells.

OBJECTIVE:To study the preventive effect of Qingnao tablet on cerebral ischemia-reperfusion injury in rats. METHODS:Rats were randomly divided into sham operation group,model group,Naoluotong capsule group (positive control, 0.05 g/kg),Qingnao tablet high-dose,medium-dose,low-dose groups(1.52,0.76,0.38 g/kg),10 in each group. Rats in all ad-ministration groups were intragastrically given relevant medicines,rats in sham operation group and model group were intragastrical-ly given equal volume of sodium carboxymethylcellulose solution,once a day,for 5 d. After 1 h of last administration,all rats were induced for cerebral ischemia-reperfusion injury model by suture-occluded method except for sham operation group. After 22 h of ischemia-reperfusion,neurological function deficit scoring was conducted;the pathological changes of the hippocampus were ob-served;superoxide dismutase (SOD),adenosine triphosphate (ATP),lactate dehydrogenase (LDH),tumor necrosis factor α(TNF-α)levels in brain tissue were measured. RESULTS:Compared with sham operation group,rats in model group appeared dif-ferent degrees of neurological deficits(score declined),sparse neurons,irregularly arranged in hippocampus as well as other patho-logical changes;ATP,SOD levels in brain tissue were decreased(P<0.01),LDH,TNF-α levels were increased(P<0.01). Com-pared with model group,neurological function deficit scores in Qingnao tablet doses groups were increased(P<0.05),neurologi-cal deficits were improved. Except for sham operation group,brain tissue indexes in other administration groups were significantly improved(P<0.05 or P<0.01). CONCLUSIONS:Qingnao tablet can increase ATP and SOD levels in brain tissue homogenate of model rats with cerebral ischemia-reperfusion,decrease LDH and TNF-α levels,and obviously improve rats'cerebral ischemia-re-perfusion injury.

Objective To study the dynamic expression and distribution of high mobility group box 1 (HMGB-1)in diffuse axonal injury (DAI)in rats and to clarify its involvement in the inflammatory reaction after DAI in rats,in order to provide new targets for the clinical treatment of DAI.Methods A DAI model was established using a coronal rotation device and evaluated by HE,Glees-Marsland silver staining,and Mallory phosphotungstic acid hematoxylin staining.Immunohistochemistry,Western blot and RT-PCR were used to detect the expression and distribution of HMGB-1 in the cortex of DAI rats at 6 h,1 d,3 d and 7 d.And TUNEL was used to examine the apoptosis of neurons in DAI rats.Results Immunohistochemical results showed that at 6 h and 1 d after DAI,the number of HMGB-1-positive cells decreased,but at 3 and 7 d it began to increase.Western blot also showed that during the early stage after DAI (6 h and 1 d),the level of HMGB-1 protein in the cortex was significantly lower than that in the control group,but at the late stage (3 and 7 d)after DAI it significantly increased compared with that in the control group until 7 d.RT-PCR showed that at 6 h after DAI there was no significant increase in the level of HMGB-1mRNA,but at 1 d there was a slight increase compared with the control group;at 3 and 7 d,it showed an obvious significance.TUNEL staining indicated that the significant neuronal apoptosis appeared as early as 6 h after DAI,and reached the peak at 3 d;it started to decrease at 7 d but still remained at a relatively high level.Conclusion The dynamic expression and distribution of HMGB-1 showed significant changes with the time course after DAI in rats.They decreased at the early stage but increased at the late stage.At the early stage, HMGB-1 is mainly passively released by the necrotic neurons,and at the late stage it may be actively secreted by the active inflammatory cells.HMGB-1 may mediate the post-DAI neural cell apoptosis by inducing the inflammatory reaction.

Objective To investigate the effects of liraglutide on gene expression related to cholesterol metabolism in ApoE-/-mice with adiponectin deficiency. Methods Thirty six ApoE-/-mice fed with the high-fat diet were subdivided into four groups. One group was given 100 μl(1×109PFU) of adenoviral pAd-U6-GFP(GFP group, n=6). The second group received 100 μl of adenoviral pAd-U6-Acrp30(ADI group, n=10). The third group was given 100 μl of adenoviral pAd-U6-Acrp30 and liraglutide(HEA group, n=10) and the fourth group was given only 100 μl sterile saline(HF group, n=10). Insulin sensitivity and glucose metabolism were assessed by the hyperinsulinemic-euglycemic clamp technique using 3-[3H] glucose as a tracer. Plasma adiponectin level was evaluated using a commercially available ELISA kit. The mRNA expressions of genes involved in cholesterol metabolism were measured by quantitative realtime PCR. Results Fasting blood glucose(FBG), free fatty acids(FFA), total cholesterol, triglyceride, low density lipoprotein cholesterol, adiponectin, and fasting plasma insulin(FINS) in ADI mice were significantly higher than those in the other groups(P＜0.01), while high density lipoprotein cholesterol was significantly lower(P＜0.05). During the clamp, glucose infusion rate(GIR) in ADI group was significantly lower than the other groups(P＜0.01), and hepatic glucose production(HGP) significantly higher in ADI group(P＜0.01). The mRNA expressions of INSIG2 and LDLR in ADI group were significantly down-regulated in HEA group(P＜0.01 or P＜0.05), while HMGCR and SREBP-2 were significantly up-regulated in HEA group(P＜0.01 or P＜0.05). Conclusions Liraglutide regulates a number of genes involved in cholesterol metabolism and ameliorates hypercholesterolemia by elevating plasma adiponectin level.

Plasma nesfatin-1 levels were assayed by ELISA in patients with impaired glucose regulation (IGR),type 2 diabetes mellitus( T2DM ),and healthy subjects with normal glucose tolerance( control group).The results showed that plasma nesfatin-1 levels in IGR and T2DM groups were significantly higher than that in control group [ ( 1.91 ±0.79 and 1.80±0.80 vs 1.41 ±0.58) μg/L,P＜0.01 ].Plasma nesfatin-1 levels were positively correlated with body mass index(BMI),HbA1c,waist hip ratio,fasting plasma glucose,fasting insulin,and homoestasis model assessment insulin resistant index( HOMA-IR,P＜0.05 or P＜0.01 ).Multiple regression analysis showed that BMI and HOMA-IR were independent related factors in influencing plasma nesfatin-1 levels (both P＜0.01 ).These results suggest that nesfatin-1 may partially contribute to the pathogenesis of insulin resistance and T2DM.

OBJECTIVESepsis remains a leading cause of death in many Intensive Care Units worldwide. Immunosuppression has been a primary focus of sepsis research as a key pathophysiological mechanism. Given the important role of the negative costimulatory molecules programmed cell death-1 (PD-1) and programmed death-ligand 1 (PD-L1) in the occurrence of immunosuppression during sepsis, we reviewed literatures related to the PD-1/PD-L1 pathway to examine its potential as a new target for sepsis treatment.

DATA SOURCESStudies of the association between PD-1/PD-L1 and sepsis published up to January 31, 2017, were obtained by searching the PubMed database.

STUDY SELECTIONEnglish language studies, including those based on animal models, clinical research, and reviews, with data related to PD-1/PD-L1 and sepsis, were evaluated.

RESULTSImmunomodulatory therapeutics could reverse the deactivation of immune cells caused by sepsis and restore immune cell activation and function. Blockade of the PD-1/PD-L1 pathway could reduce the exhaustion of T-cells and enhance the proliferation and activation of T-cells.

CONCLUSIONSThe anti-PD-1/PD-L1 pathway shows promise as a new target for sepsis treatment. This review provides a basis for clinical trials and future studies aimed at revaluating the efficacy and safety of this targeted approach.

Animals ; B7-H1 Antigen ; metabolism ; Disease Models, Animal ; Humans ; Immunosuppression ; Programmed Cell Death 1 Receptor ; metabolism ; Sepsis ; metabolism

Objective: To discuss the etiology, pathogenesis, clinical manifestation, diagnosis and therapy of sphenoid wing dysplasia(SWD) associated with neurofibromatosis type Ⅰ(NF-Ⅰ). Methods: We retrospectively reviewed its clinical manifestations, imaging, surgical treatment, complications and postoperative outcome of one NF-Ⅰ patient with SWD. Results: A 14 years-old girl presented with pulsating exophthalmos, loss of vision and café au lait spots. Radiological studies showed right-side orbital enlargement and complete absence of the greater wing of the sphenoid. Titanium mesh was tailored intraoperatively to close the defect as a barrier between the orbital cavity and the cranium and then covered by periosteum.The patient developed postoperative infectious which was controlled by after antibiotic treatment and proper drainage. Proptosis improved significantly after surgery within a month. Ocular pulsation subsided and clinical symptoms improved at 28-month follow-up. Conclusions Sphenoid greater wing dysplasia associated with neurofibromatosis type Ⅰ is a rare inherited autosomal dominant disorders. The treatment should be customized to each patient. Titanium mesh reconstruction is patients with symptomatic sphenoid dysplasia. It can correct the proptosis and pulsating exophthalmos without the risk of bone resorption and recurrence.However, high risk of infection is associated with the procedure.