Objective To identify the role of autopahgy in the protective mechanism of heme oxygenase 1(HO-1) against hepatic ischemia/reperfusion (I/R) injury.Methods Forty healthy male Sprague-Dawley (SD) rats were randomly (random number table) divided into five groups (n =8 in each group),namely sham group,model group,cobalt protoporphyrin (CoPP) group,zinc protoporphyrin (ZnPP) group and 6-amino-3-methylpurine (3-MA) group.Partial hepatic I/R model was established by clamping the pedicles of left and median lobes for 1 hour and reopening for 6 hours in rats,and the rats in sham group were only received celiotomp without hepatic I/R.In the CoPP group,CoPP (a HO-1 inducer,5 mg/kg) was administered i.p 24 hours before I/R.In the ZnPP or 3-MA group,besides pretreatment with CoPP,the rats were given ZnPP (a HO-1 inhibitor,25 mg/kg) or 3-MA (an autophagy inhibitor,30 mg/kg) i.p 1 hour before I/R.Serum alanine aminotransferase (ALT) was determined with automatic biochemistry analyzer.The hepatic pathological scores (PS) were determined under light microscope using hematoxylin-eosin (HE) staining.The hepatocyte apoptosis index (AI) was assessed with terminal dexynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining.Autophagosomes in liver tissue were counted under electron microscope.The mRNA expressions of HO-1,caspase-3,Beclin-1 and Atg-5 in the liver were determined by reverse transcription-polymerase chain reaction (RT-PCR).The HO-1 activity was also measured by the generation of bilirubin with the method of double-wave spectrophotometry.Results Compared with the sham group,the level of serum ALT significantly increased in the I/R group (U/L:560.3±73.6 vs.49.1 ± 13.8,P ＜ 0.01),HE staining showed a severe hepatic injury (PS:12.0±2.0 vs.1.3±0.9,P ＜ 0.01),TUNEL staining showed a higher hepatocytes apoptosis and the expression of caspase-3 significantly increased [AI:(19.38±3.07)％ vs.(3.25±1.28)％,caspase-3 mRNA (2-△△CT):4.62±0.40 vs.1.05±0.15,both P ＜ 0.01].However,there was no significant difference in the expression of HO-1 and the genes associated with autophagy between the two groups.In the CoPP group,the hepatic injury was blunted compared with that in the I/R group [ALT (U/L):223.3 ± 34.4 vs.560.3 ± 73.6,PS:5.6 ± 2.3 vs.12.0 ± 2.0,AI:(11.38± 2.39)％ vs.(19.38 ± 3.07)％,caspase-3mRNA (2-△△CT):2.42±0.33 vs.4.62±0.40,all P ＜ 0.01].HO-1 was induced in the CoPP group and autophagy was also increased significantly after I/R when compared with those in the I/R group [HO-1 mRNA (2-△△CT):3.01 ±0.71vs.1.14 ± 0.20,HO-1 activity (pmol ·mg-1 · h-1):259 ± 37 vs.113 ± 26,the number of autophagosomes:8.75 ± 0.87 vs.1.25±0.71,Beclin-1 mRNA (2-△△CT):2.85±0.28 vs.1.15±0.11,Atg-5 mRNA (2-△△CT):2.44±0.25 vs.1.14±0.12,all P ＜ 0.01].In the ZnPP group,the activity of HO-1 was much lower than that in the CoPP group,and as a result autophagy was decreased and liver injury was increased.In the 3-MA group,although there was no difference in the activity of HO-1 compared with that in the CoPP group,autophagy was inhibited,and the protective effect of CoPP was eliminated.Conclusion HO-1 could regulate the level of autophagy during liver I/R,and in turn autophagy might mediate the protective effects of HO-1 against liver I/R injury.

Purpose: To report the treatment result of astrocytoma of the brain treated by operation combined radiotherapy. Materials and Methods: 70 patients with brain astrocytoma were treated by radiotherapy after operation from January, 1978 to January, 1989. The radiation dose ranged from 40～64Gy/5～7wks. Results: The 1-,3- and 5-year survival were 91.7%,55.8% and 45.0%,respectively. Conclusion: Radiotherapy is necessary for patients with brain astrocytoma after operation.

Objective To investigate the protective effect of meglumine adenosine cyclosphosp (MAC) on the cerebral ischemia-reperfusion (I/R) injury in rabbits.Methods Twenty four healthy rabbits were randomly divided into control group (n =6),I/R group (n =6),MAC pretreated group (n =6),and MAC treated group (n =6).Cerebral ischemia-reperfusion injury model was made by separating and electrocoagulating vertebral arteries and clipping common carotid arteries in the latter 3 groups after anesthesia.The sham-operated group underwent vessel separation without clipping.L/R group was administered with nothing,while MAC pretreated group with MAC before ischemia,and MAC treated group with MAC just after ischemia.Blood was gathered from jugular vein before ischemia,and 30 min,1 h,and 2 h after reperfusion for testing IL-8,superoxide dismutase (SOD) and malondialdehyde (MDA).The brain tissue slice was observed by optical microscope.Results Compared to control group and before ischemia,the levels of IL-8 and SOD in serum were significantly increased and decreased,and the levels of MDA was significantly increased at 30 min after reperfusion in I/R group; the levels of IL-8 and MDA in serum were significantly increased,and the levels of SOD in serum was significantly decreased at 1 h and 2 h after reperfusion in I/R group.The levels of IL-8 in serum was less at 30 min and 1 h and 2 h after reperfusion in MAC pretreated group than in I/R group.At 1 h and 2 h after reperfusion,the levels of MDA in serum was less and the levels of SOD in serum was higher in MAC pretreated group than in I/R group.At 1 h and 2 h after reperfusion,the levels of IL-8 in serum were less and the levels of SOD in serum were higher in MAC treated group than in I/R group.The levels of MDA in serum were less at 2 h after reperfusion in MAC treated group than in I/R group.Compared to I/R group,pathological change was lighter in the MAC pretreated and MAC treated group.Conclusions MAC has a fine cerebral-protective effect and has no side effect.

The thoracic aorlae of 39 goats and the inferior venae cavae of 9 goats were anastomosed experimentally with the Large Blood Vessel Anastomat. The pathological changes of these vessels were observed dynamically within one year after the operation. It was found that the Large Blood Vessel Anastomat was rather effective. The vessels anastomosed with this instrument showed a better result than those anastomosed with manual suture.

Objective To investigate the management of severe haemorrhage following minimally invasive percutaneous nephrolithotomy.Methods A retrospective study was accomplished on 3857 patients of minimally invasive percutaneous nephrolithotomy from Jan 1995 to Feb 2004.Fourteen patients,11 males and 3 females with a mean age of 45 years,developed severe haemorrhage requiring a haemostasis procedure(0.4%).Results Three cases of nephrectomies for haemostasis were performed at the beginning of our experience.Renal arteriography was performed in 11 patients,and the results showed that 5 patients were suffered with arteriovenous fistulas,4 cases with false aneurysms,1 case with arteriovenous fistulas and false aneurysms,and 1 case with arteriolar injury.All the patients with vascular abnormalities were successfully treated by highly selective embolization.Conclusion The severe haemorrhage following minimally invasive percutaneous nephrolithotomy is a rare complication,but impossible to be predicted.Renal arteriography and selective embolization is a safe and effective procedure for the management of severe haemorrage following minimally invasive percutaneous nephrolithotomy.

Objective　To analyze the clinical indications,efficacy and safety of Chinese minimally invasive percutaneous nephrolithotomy (MPCNL) in treating upper urinary calculi based on our experience.Methods　From June 1992 to September 2010,a total of 10,452 patients (6060 males and 4392 females)with a mean age of (47.6 ± 13.7) years (7 months-93 years) received MPCNL in our center.The mean stone burden was (777.4 ± 740.3) mm2 (20 - 4 080 mm2 ).The data of stone burden,operative techniques,operating time,stone-free rate,major complication,hospital stay and stone composition were investigated.　Results　Of the 10 452 cases,11 801 procedures were performed on 10 876 (5493 left and 5383right) renal units,including 10 102 first stage procedures,1604 secondary procedures,86 third procedures and 9 fourth procedures.There were 11 830 tracts established,including 373 (3.15％ ) tracts of 14 F,7867 (66.50％) tracts of 16 F and 3590 (30.35％) tracts of 18 F.There were 1207 (10.20％),9174(77.55％) and 1449 (12.25％) punctures located in upper,middle and lower pole,respectively.956(8.79％) renal units were managed with multiple tracts,which including 2 tracts in 846 (7.78％) units,3tracts in 85 (0.78％) units,4 tracts in 18 (0.17％) units and 5 tracts in 7 (0.06％) units.Pneumatic lithotripsy was used in 8563 (72.56％) procedures,Holmium:YAG laser lithotripsy was used in 2981(25.26％)　procedures and Pneumatic lithotripsy + Holmium: YAG laser lithotripsy was used in 257(2.18％) procedures.762 (7.29％) cases needed ESWL to clean the stone after MPCNL.The average operating time was ( 101.3 ± 44.2) min ( 10 -240 min).The stone-free rate of MPCNL was 89.9％,which increased to 93％ by adjunctive ESWL.And the mean hospital stay was ( 13.2 ± 6.4) days (2 - 72 days).The major complications happened on 321 (3.07％) cases,including 294 (2.81％ ) cases of blood transfusion,12 (0.11％ ) cases of sepsis,2 (0.02％) cases of renal abscess,9 (0.09％) cases of pleura injury,2 (0.02％) cases of colon injury and 2 (0.02％) cases of death.53 (0.51％) cases needed selective renal arterial embolization to achieve hemostasis.The main stone compositions were analyzed in 4345 cases.Calcium oxalate,calcium phosphate,magnesium ammonium phosphate,uric acid,ammonium urate,carbapatite and cystin were 91.74％,90.33％,14.91％,17.77％,4.83％,8.47％ and 0.51％,respectively. Conclusions　MPCNL is an effective and safe treatment option for all kinds of upper urinary calculi in patients at all ages with a high stone free rate and low major complication rate.

Functional cognitive disorder (FCD) refers to complaints of persistent problematic cognitive decline, which is inconsistent between self-reported symptoms and daily function and/or neuropsychological test results, and the symptoms lasted for at least six months without obvious progress. Poor ability to reflect on and monitor cognitive processes has been suggested as a key mechanism underlying the disorder. In this review, the concept, research status, clinical manifestations and diagnosis of FCD were systematically examined, which is helpful to identify the subjective cognitive decline caused by non-degenerative diseases and conduct individualized intervention treatment.

The results of studies on the association between tea consumption and Parkinson’s disease (PD) have been inconsistent. Therefore, the aim of this study was to perform an updated meta-analysis to better resolve any association between tea consumption and PD. We searched PubMed, Embase, and the Cochrane Library– from their commencement to November 2016 – for qualified studies that evaluated the associations between tea drinking and risk of PD. A total of nine case–control studies and three prospective cohort studies were included. The meta-analysis showed that tea consumption was associated with a reduced risk of developing PD(OR, 0.82; 95% CI, 0.69–0.98) when case–control studies and prospective cohort trials were considered together. Subgroup analysis on the category of tea consumption and risk of PD showed that black tea was not associated with PD (OR: 0.89; 95% CI, 0.64–1.24; I2 =0.0%), but other kinds of tea was associated with a reduced risk of developing PD (OR: 0.67; 95% CI, 0.48–0.95; I2 =0.0%). Subgroup analysis on the dose of tea consumption and PD risk showed that drinking more than one cup of tea daily was associated with a reduced risk of developing PD in case–control studies (OR: 0.38; 95% CI, 0.22–0.66; I2 =0.0%). No indication of publication bias was found. In conclusion, the current evidence showed that tea consumption was associated with a reduced risk of developing PD. The results of our subgroup analysis suggested that people who drinking more than one cup of non-black tea daily might have a reduced risk of developing PD

BACKGROUND: Previous studies have examined the bulk transcriptome of peripheral blood immune cells in acquired immunodeficiency syndrome patients experiencing immunological non-responsiveness. This study aimed to investigate the characteristics of specific immune cell subtypes in acquired immunodeficiency syndrome patients who exhibit immunological non-responsiveness. METHODS: A single-cell transcriptome sequencing of peripheral blood mononuclear cells obtained from both immunological responders (IRs) (CD4 + T-cell count >500) and immunological non-responders (INRs) (CD4 + T-cell count <300) was conducted. The transcriptomic profiles were used to identify distinct cell subpopulations, marker genes, and differentially expressed genes aiming to uncover potential genetic factors associated with immunological non-responsiveness. RESULTS: Among the cellular subpopulations analyzed, the ratios of monocytes, CD16 + monocytes, and exhausted B cells demonstrated the most substantial differences between INRs and IRs, with fold changes of 39.79, 11.08, and 2.71, respectively. In contrast, the CD4 + T cell ratio was significantly decreased (0.39-fold change) in INRs compared with that in IRs. Similarly, the ratios of natural killer cells and terminal effector CD8 + T cells were also lower (0.37-fold and 0.27-fold, respectively) in the INRs group. In addition to several well-characterized immune cell-specific markers, we identified a set of 181 marker genes that were enriched in biological pathways associated with human immunodeficiency virus (HIV) replication. Notably, ISG15 , IFITM3 , PLSCR1 , HLA-DQB1 , CCL3L1 , and DDX5 , which have been demonstrated to influence HIV replication through their interaction with viral proteins, emerged as significant monocyte marker genes. Furthermore, the differentially expressed genes in natural killer cells were also enriched in biological pathways associated with HIV replication. CONCLUSIONS We generated an atlas of immune cell transcriptomes in HIV-infected IRs and INRs. Host genes associated with HIV replication were identified as markers of, and were found to be differentially expressed in, different types of immune cells.
Humans ; Acquired Immunodeficiency Syndrome ; Transcriptome/genetics* ; HIV ; HIV Infections/genetics* ; Leukocytes, Mononuclear/metabolism* ; CD4-Positive T-Lymphocytes/metabolism* ; Virus Replication ; Membrane Proteins/metabolism* ; RNA-Binding Proteins/metabolism*