Volume 88  ·   Issue 16  ·  2008

For half a century, kidney transplantation has become an important means to treat uremic patients, and about 700,000 uremic patients have been reborn worldwide. However, acute rejection and chronic rejection after allogeneic kidney transplantation and the toxicity of renal drugs caused by long-term use of immunosuppressive drugs are still the most important reasons for the decline of renal function and eventual loss of renal transplantation [1-3]. Under the current situation of extremely limited donor organs and increasing number of patients to be transplanted, actively preventing and treating rejection after renal transplantation is an important and urgent problem that directly relates to the long-term survival of renal transplantation patients and whether more uremic patients can be effectively treated.

Objective To explore the opportunity of nephrectomy of transplanted kidney. Methods The clinical data of 93 patients who underwent nephrectomy of transplanted kidney out of the 1769 patients who re4ceived kidney implantation between January 1996 and December 2006 were analyzed to discover the best opportunity of the nephrectomy of transplanted kidney. Results Thirty-four transplanted kidneys were resected within the three months after transplant, 25 implanted kidneys underwent resection during the period of 4 to 12 months after transplant, and 34 kidneys were resected one year after transplant. Serum creatinine before nephrectomy was above 115 μmol/L in 83 patients (89.25%). Urine quantity decreased in 62patients. 42 patients showed pain and swelling in the area of the transplanted kidney. Pathology of the reseeted implanted kidneys showed super-acute rejection (n=5) , accelerating-acute rejection (n=8),rupture of transplanted kidney (n=9), thrombus/embolism of transplanted kidney (n=6), aneurism of transplanted kidney (n=3), mycotic infection of transplanted kidney (n=2), CMV infection (n=2),acute necrosis of renal tubulus (n=1), interstitial pyogenesis of transplanted kidney (n=1) , inflammation of renal artery (n=1) , rupture of renal artery (n=1) , bleeding of transplanted kidney (n=1) , and chronic rejection and/or acute rejection (n=53). t5 patients died. 8 of which died due to multiple organ failure, 4 of which due to severe infection, 2 of which due to bleeding in encephala, and 1 due to heart disease. Conclusion Nephreetomy of transplanted kidney is a high risk operation, especially early after transplantation. Once complications occur to the transplanted kidney and/or other organ exploratory operation should be performed to rescue the life of the patients and to stop a vicious circle.

Objective To assess the predictability of individual tacrolimus (FK506) concentrations at different time points for the area under the curve (AUC) and to find the best sampling time for the abbreviated AUC to predict the total body exposure of tacrolimus. Methods 16 primary kidney transplant recipients were treated with methylprednisolone and antilymphocyte globulin for 3 days. The first tacrolimus oral dose, 0.075 mg/kg, was given at day 3 after transplantation. Blood samples were obtained at 0.5,1.0, 1.5, 2.0, 3.0, 5.0, 8.0, and 12.0 hours since taking the first oral dose. The tacrolimus blood concentration was measured by ELISA. Twelve-hour AUC (AUC12) for each patient was calculated using linear trapezoid rule. Associations between blood concentration at each sampling time points and the AUC12were measured by Pearson correlation coefficients. Abbreviated sampling equations were derived by multiple,stepwise regression analyses performed using AUC12 as the dependent variables. The variance in the strength of association between predicted AUC (AUCp) and AUC12 was reflected by the linear regression coefficient the minimum AUC12. The correlation between all the time points concentration, except C1.0, all the drug concentrations at different time points were significantly correlated with AUC ( all P＜0.05 ). Stepwise multiple regression showed that C5.0 might be the best predictor of the total body exposure of tacrolimus (R=0.92, R2=0.85). According to an abbreviated AUC monitoring strategy, the concentrations at hours 5 and 1.5 or hours 5, 1.5, and 3 were well correlated with AUC (R=0.97, R2=0.94 and R=0.99, R2=0.99, respectively). Conclusion Tacrolimus AUC12 shows remarkable interindividual variation after the first oral dose in Chinese renal transplant recipients. C5 may be the best predictor of the first AUC12. Twopoint sampling method using C5 and C1.5 and the three-point sampling method using C5, C1.5, and C3 may be the best abbreviated AUC to cost-effective tacrolimus monitoring strategy.

Objective To investigate the Characteristic and clinicopathologic significance of lymphangiogenesis in kidney transplants and their relationship with renaltransplant rejection. Methods Monoclonal podoplanin was used to immunostain the lymphatic microvessels in the 104 paraffin sections of renal transplant biopsies from 67 cases kept in the archives. The morphologic characterization and distribution of lymphatic microvessels, and the lymphatic vessel density (LVD) were compared between normal kidneys and grafts with different pathologic diagnosis. Results (1) No significant proliferation of lymphatic microvessels was observed in normal function renal grafts, and their location and number resembled that of normal kidneys. In the severe acute rejection kidney, lymphatic microvessels were variably larger, and denser confined to the adventitia of small-sized arteries. Numerous podoplanin-expressing lymphatic capillaries and larger caliber vessels are found within and around nodular mononuclear stromal infiltrates in the kidney transplants with chronic/sclerosing allograft nephropathy. (2) The LVD of normal kidney, stable function renal grafts and renal grafts with calciueurin inhibitor toxicity were 1.03±0.31, 1.76±0.52 and 1.87±1.13 respectively, there were not significant differences among this three groups (P＞0.05). The LVD in acute rejection group, C4d+ acute rejection group and chronic/sclerosing allograft nephropathy group were 3.33±0.92, 3.56±1.12 and 18.35±4.79 respectively, all significantly higher than that in stable function group (P＜0.01,0.01,0.01). Conclusions There are varied pathologic characterizations between different grading of rejection. The degree of lymphangiogenesis in renal grafts may be associated with pathologic grading of rejection.

Objective To assess the relationship between the level of serum soluble CD105 and the morphology of plaques examined by intravaseular ultrasound (IVUS) in the patients with stable angina (SA) and unstable angina (UA). Methods 127 patients suspected as having coronary heart disease (CHD) underwent coronary artery angiography (CAG) and then divided into 3 groups according to the CAG results:stable angina (SA) group (n =50), unstable angina (UA) group (n =47), and control group (n =30).Peripheral blood samples were collected and serum soluble CD105 was measured by ELISA. 31 patients from the SA group and 31patients from the UA group underwent IVUS. Results The patients of the SA group mainly had fibrous plaques, while the patients of the UA group mainly had unstable and soft lipid plaques.Calcific plaques were found in the SA group ( 12% ) as well as in the UA group with no statistical difference (18.0%, P=0.08). The eccentric index (EI) of the UA group was 0.82±0.55, significantly higher than that of the SA group (0.54±0.23, P＜0.05 ). The serum soluble CD105 level of the UA group was (4.06±0.19 ) μg/L, significantly higher than that of the control group and SA group [ ( 2.57±0. 54)μg/L and (3.47±0.17) μg/L respectively, both P＜0.05 ], and serum soluble CD105 level of the SA group was significantly higher than that of the control group too ( P＜0.05). The concentration of soluble CD105 in vulnerable plaque group was (4.01±0.18 )μg/L, significantly higher than that of the stable plaque group [ (3.22±0.16 ) μg/L, P＜0.01 ]. Conclusion The serum soluble CD105 level of the UA group is significantly higher than those of the patients with SA and those without CHD. The level of soluble CD105may reflect the instability of CHD as well as the vulnerability of plaques.

Objective To study the blood uric acid levels in the patients with or without coronary artery disease, as well as in the patients with different degrees of coronary artery stenosis, and to investigate the relationship between blood uric acid level and the degree of coronary artery stenosis. Methods 3803 patients who hospitalized frSom January 11999 to December 312006 underwent coronary angiography and uroxisome method to detect the blood uric acid. Results The age of the 2772 patients with coronary artery stenosis was (64±11 ), significantly elder than that of the 1031 patients without coronary artery stenosis [ (58±12), P＜0.01 ]. The percentage of males of the patients with coronary artery stenosis was 69.8%,significantly higher than that of the patients without coronary artery stenosis (50.5%, P＜0.01 ). The proportions of those with history of hypertension, diabetes, cerebral stroke, blood lipid abnormality,smoking, damaged renal function, and use of diuretics (all P＜0.01 ). The blood uric acid level of the patients with coronary artery stenosis was (328±103) μmol/L, not significantly different from that of the patients without coronary artery stenosis (314±98) μmol/L (P = 0. 009). Coronary artery stenosis was significantly correlated to all of the clinical parameters: blood uric acid, hypertension, diabetes, smoking,use of diuretics, blood lipid abnormality, damaged renal function, age and gender (all P＜0.001 ) , and blood uric acid level was significantly correlated with all the clinical parameters too ( all P＜0.05 ) , except age. Multivariable logistic regression showed that blood uric acid level was still independent predictors of coronary artery disease. The more extensive the coronary artery stenosis the higher the blood uric acid level (P＜0.001 ). Conclusion Coronary artery stenosis and blood uric acid level are independently relevant.The more extensive the coronary artery stenosis was, the higher the blood uric acid level was.

Objective To evaluate the features and value of magnetic resonance (MR) perfusion imaging (PI) of avascular necrosis of the femoral head (ANFH). Methods MR, gadolinium (Gd)enhanced MR and MRPI were performed in 21 patients with a probable diagnosis of ANFH. Results MRI showed that 10 of the 21 patients were with ANFH,5 in bilateral femoral heads, and 5 in unilateral femoral head, totally in 15 femoral head, 2 at the Froberg stage Ⅰ , 4 at the stage Ⅱ, 2 at the stage Ⅲs, and 7 at the stage Ⅳ. Gd-enhanced MR showed that 2 femoral heads were not enhanced, 10 were slightly enhanced,reduction) was decreased with or without prolonged TrP(time to peak), the MTT (mean transit time) was declined, and then slowly increased (n=2). Conclusion MRPI reflects the blood perfusion of the femoral head. The type of the MRPI cure reflects the pathological progression of ANFH, evaluates the activity of the femoral head, and is useful to the clinical physicians to estimate the stage of ANFH and choose treatment for the patients. MRPI is a method in diagnose ANFH at the initial microcirculatory injury stage.

Objective To test whether the germline mutation plays a role in the prognosis of decortication surgery for autosomal dominant polycystic kidney disease (ADPKD) patients. Methods 175PKD patients, 153 of which had family history, underwent decortication surgery and collection of peripheral blood samples to detect the PKD1 mutation. The correlation between PKD1 mutation and clinical features was analyzed. Results 61 of 175 patients were found to be with PKD1 mutations, i.e. they suffered from ADPKD. The pain relief time of the patients with mutations at the 3'end (≥7812) [ (53±4) months] was significantly longer than that of the patients with mutations at 5'end (＜7812) [ (39±5 ) months, X2 =7.677,P=0.006].The time with normal renal function of the patients with mutations at the 3'end was (52.7±3.1) months, significantly longer than that of the patients with mutations at the 5'end [ (40.2±2.6) months, x2=7.963,P=0.005]. The mutation type was associated with renal survival time after surgery only (P=0.021). The renal survival time of patients with in-frame mutation was (38.1±3.2) months,significantly shorter than those of the patients with truncating and missense mutations [ (49.5±4.0) months and (54.0±3.9) months respectively, P＜0.05 ]. Conclusion The position and type of PKD1 mutation are significantly associated with the prognosis of decortication surgery. The PKD1 mutation can be an indicator for the choice of the surgery in ADPKD patients.

Objective To investigate the clinical features and to evaluate the visual and anatomical outcomes in a series of vitreous surgeries for retinal detachment associated with macular hole in high myopic eyes. Methods The clinical data of 40 patients (40 eyes) , 8 males and 32 females, aged 33 -76, who received vitreous surgery for retinal detachment due to macular hole in high myopic eyes with the previous refractive error≥-6.00 D without peripheral retinal hole from January 2001 to January 2007 were retrospectively analyzed. The patients were followed up for 12.3 months. Results Overall anatomical success was achieved in 36 eyes (90.0%). 30 eyes ( 75.0% ) had visual improvement. Vision remained unchanged in 5 eyes (12.5%) and decreased in 5 eyes. Postoperative visual acuity improved much more than preoperative visual acuity (P=0.000). Predictors of poor visual outcome were: posterior staphyloma (P=0.023) and atrophy of retinal pigment epithelium (P=0.001 ). Internal limiting membrane (ILM)peeling (ILM-peeled group) was performed on 17 eyes, and the ILM was not removed on 23 eyes (ILM-preserved group). The anatomic reattachment rate after the initial surgery in the ILM-peeled group was 94.1%. and in the ILM-preserved group was 78.3%. There was not significant difference in the improvement of postoperative visual acuity between these two groups (P = 0.240). Conclusion Vitreous surgery achieves retinal reattachment and improves or preserves the visual acuity in the eyes with retinal detachment due to macular hole in high myopic eyes.

Objective To assay the serum omentin level in obese and newly diagnosed type 2 diabetes mellitus (T2DM) patients and investigate the relations hip between serum omentin level and body fat parameters, glucose and lipid metabolism and insulin resistance index (IR) etc. Methods 143 Shanghainese, 74 males and 69 females, aged 20-69, underwent evaluation of body mass index (BMI),waist circumference (W), hip circumference (H), and waist hip ratio (WHR). 69 patients with T2DM were divided into 2 subgroups: normal weight (T2DM-NW) subgroup (n=36, with BMI＜25 kg/m2) and overweight/obese (T2DM-OW/OB) subgroup (n=8, with BMI≥25 kg/m2). 74 patients with normal glucose regulation (NGR) were subdivided into 2 subgroups : normal weight (NGR-NW) subgroup (n=36,with BMI＜25 kg/m2) and overweight/obese (NGR-OW) subgroup (n=38, with BMI≥25 kg/m2). The level of fasting serum omentin was measured by ELISA. Blood glucose, HbAle, lipids, and insulin levels were also measured. Insulin sensitivity was assessed by HOMA-IR. Results After age and sex adjusted,the serum omentin level of the T2DM group was (17.5±5.8)μg/L , siguificandy lower than that of the NGR group [ (20.0±7.6)μg,/L, P＜0.05 ] ; the serum omentin level of the overweight/obese subjects was ( 16.8±6.0)μg/L, significantly lower than that of the NW subjects [ (20.7±7.2 μg/L, P＜0.01 ]. The serum omentin level of the T2DM -OW/OB subgroup was significantly lower than that of the NGR-OW/OB group (P＜0.05). Partial correlation analysis showed that the serum omentin was negatively correlated to waist W, WHR, natural logarithm of HOMA-insulin resistance indexes [In(HOMA-IR)], triglycerides (TG), BMI,fasting serum insulin (FINS), and 2 hour OGTT glucose (2 hPG) (r=-0.329, -0.313,-0.301, -0.299, -0.298, -0. 240, and -0.166 respectively,P＜0.01 or P＜0.05), and positively correlated to high density lipoprotein- cholesterol (HDL-C) (r=0.400, P＜0.01). Multiple linear regression showed that HDL-C, W and in (HOMA-IR) were independent variables of omentin. Conelusion The serum omentin level is low in the obese and type 2 diabetes mellitus subjects, and is correlated with obese indexes, insulin resistance and lipid metabolism. Serum omentin may directly contribute to the underlying pathophysiology of insulin resistance syndrome.

Objective To observe the effects of irbesartan, an angiotensin Ⅱ receptor blocker, on the protein expression of janus kinases-signal transducers and activators of transcription (JAKs-STATs) in kidneys in hypertension and to evaluate the role of the JAKs-STATs pathway in hypertension with renal injury. Methods Twelve spontaneously hypertension rats (SHRs) were randomly divided into 2 equal group, treated with gastric perfusion of normal saline for 8 weeks. Six Wistar-Kyoto (WKY) rats were treated with normal saline as control group. Blood pressure was measured every week from the caudal vein.Eight weeks later the kidneys were taken out. Renal angiotensin Ⅱ (Ang Ⅱ ) concentration was measured by radioimmunoassay. Reverse transcriptase-polymerase chain reaction was used to detect the mRNA expression of JAK1, 2 and STAT1, 3 in the renal tissue. Western blotting was used to detect the protein expression of JAK1,2 and STAT1, 3 in the renal tissue. Results The blood pressure levels 1, 2, 4, 6,and 8 weeks after the treatment of irbesartan of the SHR- Ⅰ, group were all significandy lower than that before treatment and those of the SHR group at the corresponding days. Since 2 weeks after the treatment the blood pressure levels of the SHR- Ⅰ group were all nit significantly different from those of the WKY group (all P＞0.05 ). The degrees of glomerular hypertrophy and renal fibrosis of the SHR-Ⅰ group were significantly lower than those of the SHR group. The mRNA expression levels of Ang Ⅱ in renal cortical homogenate of the SHR-Ⅰand SHR groups were (79.4±14.8 ) pg/mg tissue and ( 83.4±8.2 ) pg/mg tissue respectively, both significantly higher than that of the WKY group (43.2±13.6) pg/mg tissue, both P＜0.01 ), and there was no significant difference in the Ang Ⅱ mRNA expression between the SHR-Ⅰ and SHR groups (P＞0.05 ). The mRNA expression levels of JAK1 and 2 and STAT1 and 3 in the renal tissues of the SHR-Ⅰ group were significantly lower than those of the SHR group (all P＜0.01 ) , and there were no significant differences between the SHR-Ⅰ group and WKY group ( all P＞0.05 ). The protein expression levels of JAK1 and 2 and STAT1 and 3 in kidneys of the SHR-Ⅰ group were significantly lower than those of the SHR group (all P＜0.01 ), and were not significantly different from those of the WKY group (all P＞0.05 ). Conclusion The JAKs-STATs pathway may be involved in the renal pathological changes in hypertension. Irbesartan attenuates the renal pathological changes by decreasing the gene expression of JAK1 and 2 and STAT1 and 3 in the renal tissues.

Objective To investigate the effects of α-arbutin and β-arbntin on tyrosinase activity and melanin content in murine melanocytes (MCs) cocultured with murine keratinocytes (KCs) and to define whether the difference in configuration of glucosidic linkage (s) of hydroquinone glucosides is correlated with their inhibitory activities against tyrosinase. Methods Mouse MCs of the line melan-a and mouse KCs of the line SP-1 were cocuhured at a ratio of 1:5. The ceils were treated for 4 days with the compound [α-arbutin or β-arbutin 0.04, 0.2, or 1 mg/ml, nicotinamide 0.04, 0.2, or 1 mg/ml, and 8-methoxypsoralen (S-MOP) 10, 50, 100 μmol/L respectively]. Phenotypic alterations of MCs cocuhured with KCs were examined and photographed by phase-contrast microscopy. The viability/proliferation of the treated ceils was measured by methylthiazol tetrazolium (MTT) assay. The tyrosinase (monophenolase and o-diphenolase) activities were determined by incorporation of radioactive L-[14C] tyrosine substrate into the melanin, and the melanin content was determined by spectrophotometric assay. Results 1 mg/ml nicotinamide slightly increased the melanin in dendrites and cytoplasm of the MCs. The dendrites of the MCs treated by 1 mg/ml α-arbutin and β-arbutin were long and thin and melanin was less compared with the control group. 8-MOP significantly promoted the proliferation of the melan-a and SP-1 cells, especially of the melan-a cells. Nicotinamide, α-arbutin, and β-arbutin did not significantly influence the proliferation of the MCs and KCs. The tyrosinase activity and melanin content were increased by 8-MOP dose-dependently and dramatically inhibited by α-arbutin, and β-arbntin dose-dependently. The inhibitory effect of α-arbutin on tyrosinase was stronger than that of β-arbutin at a dose of 1 mg/ml (the tyrosinase activity:37%±4% vs 54%±9%, P=0.034).Conclusion α-arbutin is an effective and safe ingredient for skin-whitening purpose in vitro experiment. Clinical implication remains to be further evaluated by in vivo studies.

Objective To investigate the dynamical procession of proliferation and apoptosis of ceils in vascular wall after vascular stent implantation. Methods The femoral arteries of 16 rabbits were punctured. Balloon was inserted into the bilateral carotid arteries to cause injury of the tuniea intima. A stent was implanted in unilateral carotid artery through the femoral artery and the opposite carotid artery was used as control. Four rabbits were sacrificed immediately, and 7, 14, and 28 days after operation respectively.Then the section of carotid artery where the tunica intima was injured and the stent was placed was resected and divided into 3 parts to undergo electron microscopy to observe cell proliferation and apoptosis, HE staining and imrnunohistochemistry to detect proliferating cell nuclear antigen (PCNA), and Western blotting to detect the protein expression of the p53 and bel-2, 2 apoptosis-related genes. Results HE staining showed irregular thickening of the vascular walls in both the injured and implanted carotid arteries. PCNA expression was negative immediately after operation, positive 7 days after operations, and strongly positive 14days after operations, and then became negative 28 days after operation; PCNA expression was negative in the normal vascular walls. Electric microscopy showed that the injured intima and tissues where the stents were placed had much more extra matrix, collagenous fibers and lots of cells, some of the cells were rich in secretary granules, few phagocytes were seen, and apoptotie cells were seen in the samples 28 days after operations. Western blotting showed that protein expression of p53 was seen in the normal carotid tissues ; in the tissues of the stenting groups at a very low degree immediately after operation and then at a gradually increased degrees 14 and 28 days later; and the intimal injury group only showed a weak expression immediately and 7 days after operation, and a strong expression 14 days later. Bcl-2 expression was negative at any time points in the normal carotid tissues, and was negative in the tissues of the stenting group immediately after operation, however, was slightly positive 7 days after operation, negative again 14 and 28 days after operation in the stenting group; while was negative immediately after operation, highly positive 7 days later, slightly positive 14 days later, and negative again 28 days after operations in the intimal injury group. Conclusion Abnormal apoptosis occurs in the vascular tissues implanted with stem. The cell proliferation is active in the early and mid period after stent implantation, followed by cell apoptosis which inhibits proliferation in the late period.

Objective To analyze the injury mechanism of hyperlipidemia-associated acute pancreatitis utilizing proteomics. Methods Ten SD rats were fed with high fat feed to establish hyperlipidemic models, and 10 SD rats were fed with normal feed to be used as control group. Six weeks later 5 rats from each group were intraperitoneally injected with caendin to establish acute edematous pancreatitis models, and 5 rats from each group were injected with bile acid taurocholate into pancreatic duct to cause acute necrotizing pancreatitis. Nine hours after the establishment of models the rats were killed with their pancreases taken out. Differential protein analysis was performed using two-dimensional differential ingel electrophoresis (2D-DIGE) and tandem mass spectrometry (MALDI-TOF/TOF). Immunohistochemical method was adopted to confirm the significantly changed proteins. Results Rat models of hyperlidemiaassociated acute edematous pancreatitis and rat models of hyperlidemia-associated acute necrotic pancreatitis were well established. Fifty-nine spots were detected by DeCyder Analysis Software between acute necrotic pancreatitis with and without hyperlipidemia samples and 39 markedly changed protein spots were identified by MALDI-TOF-TOF. Twelve spots were detected between the samples of acute edematous pancreatitis with and without hyperlipidemia and 7 of them were identified. Differentially expressed proteins in hyperlipidemiaassociated pancreatitis included pancreatic enzymes, such as lipase, amylase, and alpha-l-antiproteinase,ER stress and calcium influx related proteins including GRP78, HSP60 and protein disulfide isomerase.Other proteins associated with DNA replication and damage repair, apoptosis, cell metabolism, circulatory dysfunction, and signal transduction were identified in hyperlipidemia-associated acute pancreatitis.Conclusion Some proteins related to ER stress, apoptosis, circulatory dysfunction and signal transduction show differential expression in acute pancreatitis with hyperlipidemia. Hyperlipidemia intensifies acute pancreatitis through various ways. ER stress-related proteins such as GRP78, HSP60, protein disulfide isomerase, and calreticulin can be regarded as biomarkers of early diagnosis and target of further treatment in severe acute pancreatitis.

Objective To evaluate the physical properties, biocompatibility, and pharmacokinetics of the China-made sirolimus-heparin elnting stent (SHES) as well as its inhibition effect on the in-stent restenosis in vitro and in vivo. Methods Polylactide coglycotide (PLGA)-heparin complex was sprayed to the surface of sirolimus-coated nitinol stent to make the sirolimus-heparin eluting stent (SHES). The physical and degrading efficiency, blood compatibility, and pharmacokinetics of this stent were studied in vitro.Fifteen dogs were implanted with SHES + bare-metal stent (BMS) into the bilateral iliac arteries (n=4),sirolimus-eluting stentt (SES) + BMS into the bilateral iliac arteries (n=4), SHES+SES into the bilateral iliac arteries (n=4), and with 2 SHESs into the bilateral iliac arteries (n=2), and 2 SHESs into the abdominal aorta (n=1). Based on the condition of strict anticoagulation, 30, 60, and 240 days after the implantation angiography of the peripheral arteries where the stents were placed was performed in 7, 7, and 1 dog respectively. Then all of the dogs were killed. The compliance, radial force, and visibility of stentt,in-stent thrombosis, in-stent diameter, reference segment diameter, late loss of diameter, and restenosis rate were observed. Results The SHES had even surface coating, and good compliance and radial extension.Blood compatibility test showed only few platelets adhered to the stent surface without deformity or obvious aggregation, and the clotting time was prolonged because of the blood coagulation factors to be activated in a low level. Degrading test and pharmacokinetics in vitro showed that sirolimus could be continuously released in a period of 3 months and heparin in a period of 50 day. The whole 30 stents were successfully implanted into the dog peripheral arteries without complication. The SHES showed satisfactory compliance and good visibility , and its blood concentration of sirolimus was 1.79-2.22 ng/ml immediately after stent implantation, 0.4 ng/ml 7 d later, and its release could be continuous about 3 months. Angiography 30 days after the implantation showed no thrombosis and intimal hyperplasia. Angiography 60 days after the implantation showed 2 cases of SES obstruction due to in-stent thrombosis, 1 case of SHES stricture and 3 cases of BMS stricture resulted from intimal hyperplasia, and 1 case of mild sinking of the arterial lumen proximate to the SHES. There were significant differences in the in-stent diameter and its late loss value between the SHES, SES, and bare stent (F:0.049, P＜0.05 ; F: 0.047, P＜0.05 ). 240 days after the implantation two SHESs placed in bilateral iliac arteries of a dog were un-obstructed. Concluslon The China-made peripheral arterial SHES not only has good physical properties and biocompatibility, but also reduces the restenosis rate resulted thanks to its effective anticoagulation and the inhibitory effect on the intimal hyperplasia simultaneously.

Objective To investigate the expression of αVβ3 integrin and platelet endothelial cell adhesion molecule-1 (CD31) in progressive liver fibrosis of rats. Methods Sixty-four SD rats were randomly divided into 4 equal groups: TAA group, undergoing peritoneal injection of 10% thioacetamine (TAA) 175 mg/kg twice a week to induce liver fibrosis, TAA control group undergoing peritoneal injection of normal saline (NS), BDL group undergoing ligation and resection of common bile duct to induce liver fibrosis, and BDL control group undergoing sham operation. Three and 9 weeks later 2 rats from the 2 TAA groups and 1 and 4 weeks later 2 rats from the 2 BDL groups were killed with their liver taken out to undergo sirius red staining and computer image analysis to observe the area of fibrosis. Immuuohistochemistry was used to detect the expression of αVβ3 integrin and CD31. The co-location of αVβ3 integrin and α-smooth muscle antibody (SMA) in the liver tissues was observed by immunohistochemical and double immunofluorescence staining. Real-time PCR and Western blotting were used to examine the mRNA and protein expression of αVβ3 integrin and CD31. Results The sirius red stained areas 3 and 9 weeks later of the TAA group were 5.8%±1.2% and 16.5%±3.6% respectively, and the sirius red stained areas 1 and 4 weeks later of the BDL group were 6.6% ±1.6% and 18.5% ±4.5% respectively. Immunohistochemical and double immunofluorescence staining showed that there was an overlapping of αVβ3 and α-SMA expression. Expression of CD31 was extended in the endothelial ceils and portal area of both models, and new blood vessels were seen in the fibrotic septum and among the hyperplastic bile ducts. The levels of αVβ3 and CD31 mRNA expression of the TAA and BDL groups were both upregulated (F = 28.66, P＜0.01,F=19.62, P＜0.01 and F=32.60, P＜0.01, F=42.36, P＜0.01 respectively) and were increased along with the degree of fibrosis. The levels of protein expression of αVβ3 and CD31 showed the similar trend of their mRNA expression. Conclusion The levels of αVβ3 integrin and CD31 expression are upregulated in liver fibrotic tissue. Such overexpression is involved in the activation of hepatic stellate cells and angiogenesis that correspond with fibrotic remodeling.

Objective To investigate the effects and mechanism of retinoid X receptor (RXR) activation on macrophages proliferation induced by lightly oxidized low-density lipoprotein (LoxLDL).Methods Serum-starved mouse macrophages of the line RAW264. 7 were stimulated with 20 μg/mLLoxLDL for 24 h to induce proliferation in the absence or presence of varying doses of RXR special agonist 9-cis retinoid acid (RA). The cell viability was assayed by MTT method. The DNA synthesis was assayed by BrdU ELISA. The apoptotic percentage of cells was measured by flow cytometry using propidium iodide (PI) staining. Nur77 and RARβ protein expressions were detected by Western blotting. Results After treated by LoxLDL for 24 h, the cell viability and DNA synthesis ( A value) of the RAW264.7 ceils were increased by 0.79±0.12 and 1.81±0.31 respectively. Co-incubated with LoxLDL and 10-s mol/L and 10-7 mol/L 9-cisRA the ceil viability decreased to 0.43±0.10 and 0.26±0.07 respectively( both P＜0. 05 ), and the DNA synthesis decreased to 1.14±0.43 and 0.72±0.06 respectively(both P＜0.05 ) The apoptotic rate of the ceils treated with LoxLDL was (3.08±0.30) %, not significantly different from those of the cells cocultured with LoxLDL and 10-9-10-7 mol/L 9-cisRA (2.74±0.13 ) % , (2.94±0.24) % , and (2.48±0.42) % respectively, all P＞0.05. The orphan nuclear receptor Nur77 protein expression was up-regulated by more than 5 times after LoxLDL treatment. 9-cisRA down-regulates the Nut77 expression and increased the expression of the downstream gene RARβ. Condnsion RXR activation significantly inhibits the macrophage proliferation induced by LoxLDL. The mechanism may be related to the regulation of RXR/Nur77 heterodimer and its downstream gene RARβ.

Objective To evaluate the effects of diaphragm biofeedback training on gastroesophageal reflux disease (GERD). Methods Nineteen GERD patients underwent diaphragm biofeedback training combined with acid suppression by proton pump inhibitor (PPI). The patients exercised abdominal deep breathing under the guidance of biofeedback device about 15 min once a week in hospital and 20 min twice daily at home in fasting state. The symptoms, endoscopic findings, and esophageal motility were re-evaluated at the end of the 8th week. Results ( 1 ) Fourteen patients completed 8-week training course. Eleven of the 14 patients discontinued the acid inhibitor and 2 of the 14 patients continued the acid suppression on-demand at the end of the course, and one patient made no response. (2) Esophageal remanometry in 10 of the 14 patients showed that the crural tension at resting state was (12±4) mm Hg,significantly higher than the baseline value [ (8±3) mm Hg, P＜0.05 ], however, there were not significant differences in the lower esophageal sphincter (LES) pressure, esophagogastric junction (EGJ) pressure,and peristaltic amphtude of the distal esophagus ( all P＞0.05 ). (3) Six of the 7 patients with reflux esophagitis (RE) who underwent follow-up endoscopy presented normal findings and the grading of 1 patient was changed from RE LA-C to RE LA-A. (4) Two of the 14 patients who were followed up for 4 weeks intermittently used antacids and relapse occurred in 1 of the 9 patients who were followed up for 8 weeks.Conclusion Diaphragm biofeedback improves reflux symptoms significantly and discontinues or reduces the dosage of acid inhibiter in a part of patients. Biofeedback training may provide a new way to enhance antireflux barrier at the EGJ in GERD patients.

A 63-year-old female was admitted to the hospital on July 11, 2007 due to anorexia, stomach distension and discomfort accompanied by nausea and vomiting for 1 month, and was in trance for 2 days. One month before admission, she had no obvious trigger for loss of appetite, stomach distension and discomfort accompanied by nausea and vomiting, without abdominal pain and diarrhea. The symptoms gradually worsened in the past week, so she came to the emergency department of Qilu Hospital of Shandong University and was given symptomatic treatment such as antiemetic. Two days ago, she developed trance. Blood biochemistry: Ca2+4.44 mmol/L, K +3.00 mmol/L, Na +133 mmol/L, Cl-89 mmol/L, blood routine: platelet 55×109/L, all the rest were normal. Liver and kidney function: alanine aminotransferase (ALT) 61 IU/L, aspartate aminotransferase (AST) 63 IU/L, alkaline phosphatase (AKP) 120 IU/L, blood urea nitrogen (BUN) 10.86 mmol/L, creatinine (Cr) 111 μ mol/L. Thyroid function: free triiodothyronic acid (FT3) 1.85 pg/ml (normal 1.8~4.6), thyroxine (FT4) 12.02 pmol

Positive end-expiratory pressure (PEEP) is a key element in the treatment of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), but its optimal level is still unknown.To compare the prognostic effects of two PEEP protocols, one aimed at increasing alveolar recruitment and limiting lung hyperinflation, and the other aimed at minimizing alveolar surface tension, on ALI patients, Alain Mercat and colleagues from France conducted a multicenter randomized controlled trial in 767 adults with ALI [mean (SD) age, 59.9 (15.4) years] in 37 intensive care units in France from September 2002 to December 2005, the results of which were published recently in the journal JAMA (JAMA, 2008, 299:646-655).

acute renal failure (ARF) is increasingly common, which is not only expensive to treat, but also poor clinical prognosis. Patients often have high mortality, long hospital stay, and need long-term dialysis treatment. At present, there are many methods for renal replacement therapy, including intermittent, continuous, long-term hemodialysis, hemofiltration or both. Although dialysis technology has made great progress, many questions about the best treatment plan for ARF patients are still unresolved.