Adenolymphoma ; enzymology ; metabolism ; Humans ; Lymphoma, T-Cell ; enzymology ; metabolism ; Lymphoma, T-Cell, Peripheral ; enzymology ; metabolism ; Male ; Middle Aged ; Nitric Oxide Synthase Type I ; metabolism ; Up-Regulation

Objective To study the effects of 3,5-diiodotyrosine (DIT) and potassium iodide (KI) on myocardial ATPase activity in hyperthyroidism Wistar rats induced by thyroid tablets.Methods Seventy-two Wistar rats were divided into 8 groups according to body weight by the random number table method (9 rats in each group),respectively,which were control group,hyperthyroidism model group,low,medium and high doses groups (both DIT and KI contents were 25.0,166.7,500.1 μg/kg).Physiological saline was intragastrically administrated to the control group;the hyperthyroidism model group was given thyroid tablet suspension (200.0 mg/kg);DIT and KI groups were given thyroid tablet suspension with corresponding doses of iodine simultaneously.The medicine was given once a day for a mouth,all the rats were sacrificed and heart tissue was collected.The colorimetric method was used to examine the activity of ATPases (Na+-K+-ATPase,Mg2+-ATPase,Ca2+-ATPase).Results The activities of Na+-K+-ATPase,Mg2+-ATPase,Ca2+-ATPase were significantly different statistically between groups (F =2.99,3.03,6.18,all P ＜ 0.01).Compared with the control group [(4.01 ± 0.22),(4.28 ± 0.28),(4.46 ± 0.35) μmol/mg·h],the activities of ATPases (Na+-K+-ATPase,Mg2+-ATPase,Ca2+-ATPase included) were reduced significantly in hyperthyroidism model group [(3.60 ± 0.25),(3.42 ± 0.31),(3.85 ± 0.17)μ mol/mg·h,all P ＜ 0.01];the activities of Mg2+-ATPase in DIT medium dose group [(3.89 ± 0.35)μmol/mg ·h],Ca2+-ATPase in DIT medium and high doses groups [(4.12 ± 0.20),(4.09 ± 0.21)μ mol/mg·h] were reduced significantly (all P ＜ 0.05);the activities of Na+-K+-ATPases,Ca2+-ATPase were decreased significantly in three KI groups [(3.64 ± 0.32),(3.60 ± 0.32),(3.53 ± 0.33),(3.93 ± 0.22),(3.90 ± 0.23),(3.85 ± 0.26)μmol/mg·h],Mg2+-ATPase in KI high dose group [(3.65 ± 0.49)μmol/mg·h] was decreased significantly (P ＜ 0.05or ＜ 0.01).Compared with the hyperthyroidism model group,the activities of ATPase were increased in most of the DIT groups [Mg2+-ATPase in low,medium doses groups:(4.06 ± 0.51),(3.89 ± 0.35)μmol/mg·h;Ca2+-ATPase in low,medium,high doses groups (4.15 ± 0.26),(4.12 ± 0.20),(4.09 ± 0.21)μmol/mg·h,all P ＜ 0.05].Conclusion Supplementation of thyroid tablets in the process of hyperthyroidism formation in Wistar rats will reduce myocardial damage by DTT compared with the same dose of KI.

Ethylene carbodiimide (ECDI) is a chemical coupling agent,more and more studies have focused on the immune tolerance induced by administration of ethylene carbodiimide (ECDI)-fixed syngeneic splenocytes (Ag-SPs) coupled to peptides or to whole myelin proteins,in order to establish a novel and effective tolerance therapy for autoimmune diseases.The mechanisms and applications of immune tolerance induced by Ag-SPs in several kinds of common autoimmune diseases were summarized,and were compared with their counterparts in the traditional treatment.

Objective To summarize the imaging features of intracranial solitary fibrous tumors (ISFT).Methods Ten patients with ISFT proven histopathologically were collected.Four cases had CT data and all cases had MR data.The imaging features and pathological results were retrospectively analyzed.Results All cases were misdiagnosed as meningioma at pre-operation.All lesions arose from intracranial meninges including 5 lesions above the tentorium,4 lesions beneath the tentorium and 1lesion growing around the tentorium.The margins of all the masses were well defined,and 8 lesions presented multilobular shape.CT demonstrated hyerattenuated masses in all 4 lesions,smooth erosion of the basicranial skull in 1lesion,and punctiform calcification of the capsule in 1lesion.T1WI showed most lesions with isointense or slight hyperintense signals including homogeneous in 4 lesions and heterogeneous in 6 lesions.T2WI demonstrated isointense or slight hyperintense in 2 lesions,mixed hypointense and hyperintense signals in 4,cystic portion in 2,and two distinct portion of hyperintense and hypointense signal,so called “yin-yang”pattern,in 2.Strong enhanced was found in all lesions,especially in 8 lesion with heterogeneous with the low T2 signal.“Dural tail” was found in 4 lesions.Conclusions ISFI has some specific CT and MR features including heterogeneous signal intensity on T2WI,strong enhancement of areas with low T2 signal intensity,slight or no “dural tail”,without skull thickening,and the typical “yin-yang” pattern.

ObjectiveTo evaluate the role of p38MAPK signaling pathway in the up-regulation of heme oxygenase-1 (HO-1) expression in the lung tissue in rats with acute lung injury (AL1) induced by endotoxic shock.MethodsForty-eight male SD rats,aged 8 weeks,weighing 180-200 g,were randomly divided into 4 groups ( n =12 each):control group ( group C ) ; endotoxic shock group ( group LS );endotoxic shock +SB203580 (a specific p38MAPK inhibitor) group (group LSS) and SB203580 group (group SB).Normal saline 0.5ml was injected via the femoral vein in groups C and SB,while LPS 10 mg/kg (in 0.5 ml normal saline) was injected via the femoral vein in groups LS and LSS.When MAP was decreased to 75％ of baseline value,10％ dimethyl sulfoxide (DMSO) 0.1 ml was infused via the femoral vein in groups C and LS,while SB203580 5 mol/kg (in 10％ DMSO 0.1 ml) was infused via the femoral vein at a rate of 0.01 ml/min in groups LSS and SB.Arterial blood samples were obtained at 6 h after LPS or normal saline was given for blood gas analysis and oxygenation index (PaO2/FiO2) was calculated.Then the rats were sacrificed and the lungs were removed for microscopic examination.The pathological changes of the lung were scored.The lung water content was calculated.The MDA content,SOD activity,and expression of HO-1 mRNA and protein,p38MAPK protein and phospharylated p38MAPK (p-p38MAPK) protein were determined.ResultsCompared with group C,the oxygenation index and SOD activity were significantly decreased,the pathological score,lung water content and MDA content were significantly increased,and the expression of HO-1 mRNA and protein and p-p38MAPK protein was significantly up-regulated ( P＜0.05),while no significant change was found in p38MAPK protein expression in groups LS and LSS,and no significant change was found in the indexes mentioned above in group SB (P＞0.05).Compared with group LS,the oxygenation index and SOD activity were significantly increased,the pathological score,lung water content and MDA content were significantly decreased,the expression of HO-1 mRNA and protein was significantly up-regulated,and p-p38MAPK protein expression was down-regulated ( P＜0.05),and no significant change was found in p38MAPK protein expression in group LSS ( P＞0.05).ConclusionThe inhibition of p38MAPK signaling pathway can lead to the up-regulation of HO-1 expression in lung tissues in rats with ALI induced by endotoxic shock.

Objective To evaluate the myocardial protective effect of dexmedetomidine during non-cardiac surgery in patients with coronary heart disease.Methods Eighty ASAⅡor Ⅲ patients with coronary heat disease (NYHA Ⅱ or Ⅲ)aged 43-76 yr weighing 52-80 kg scheduled for elective upper abdominal surgery were randomly divided into 2 groups(n=40 each)：control group(group C)and dexmedetomidine group(group D).Anesthesia was induced with etomidate 0.25 mg／kg，sufentanil 0.5 μg／kg and vecuronium 0.1 mg／kg.The patients were tracheal intubated and mechanically ventilated.A loading dose of dexmedetomidine 1μg/kg was injected intravenously 10 min before induction followed by infusion at 0.4 μg·kg-1·h-1 until the end of operation in group D.While equal volume of normal saline was given in group C.BIS was maintained at 40-49.Blood samples were taken before induction and at the end of operation for determination of serum concenlrations of IL-6，TNF-α，cardiac troponin Ⅰ(cTnI)and glycogen phosphorylase BB(GP-BB).The adverse cardiovascular events were recorded during operation.Results The serum concentrations of IL-6，TNF-α，cTnI and GP-BB and incidences of tachycardia and myocardial ischemia were significantly lower，while the incidences of bradycardia highcr in group D than in group C (P<0.05).Conclusion Dexmedetomidine Can exert the myocardial protective effect during non-cardiac surgery in patients with coronary heart disease and the mechanism may be related to the inhibition of the release of pro-inflammatory cytokines.

Objective To evaluate the effect of electro-acupuncture (EA) at Zusanli and Feishu on endotoxin shock-induced acute lung injury in rabbits.Methods Sixty healthy male New Zealand white rabbits aged 2 months weighing 1.5-2.0 kg were randomly divided into 6 groups (n =10 each):group sham operation (group S); group zinc protoporphyrin-Ⅸ (ZnPP-Ⅸ) (group Z); group lipopolysaccharide (LPS) (group L); group LPS + EA (group EL) ; group LPS + sham EA (group SEL) and group LPS + EA + ZnPP-Ⅸ (group ELZ).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 400 mg/kg and tracheostomized.The animals kept spontaneous breathing.Right internal carotid artery was cannulated for BP monitoring.Ear vein was cannulated for drug administration.LPS 5 mg/kg was injected iv in groups L,EL,SEL,ELZ.Endotoxin shock was confirmed by decrease in BP by 20 ％ of the baseline value and PaO2/FiO2 ≤ 300.ZnPP-Ⅸ (heme oxygenase (HO-1 ) inhibitor)10μmol/kg was injected intraperitoneal at 2 h after LPS injection in groups Z and ELZ.Bilateral 15 min EA stimulation of Zusanli and Feishu ( according to atlas of animal acu-points) was performed once a day for 5 days before LPS administration in groups EL and ELZ.The animals were sacrificed by blood-letting at 6 h after LPS administration.The lungs were removed for microscopic examination (0 =no injury,4 =most severe injury),detection of alveolar epithelial cell apoptosis (by TUNEL) and determination of HO-1 protein and mRNA expression.Results LPS significantly increased lung injury scores,alveolar epithelial cell apoptosis index (the number of apoptotic cells/total cells) and HO-1 protein and mRNA expression.EA significantly attenuated lung injury and alveolar epithelial cell apoptosis induced by LPS and further increased the expression of HO-1 protein and mRNA in group EL as compared with group L.The protective effects of EA was counteracted by ZnPP- Ⅸ in group ELZ.Conclusion EA at Zusanli and Feishu can attenuate endotoxin shock-induced lung injury by up-regulation of HO-1 expression and inhibiting alveolar epithelial cell apoptosis in the lung.

Objective To evaluate the role of activator protein-1 (AP-1) in the up-regulation of heme oxygenase-1 (HO-1) expression during lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats.Methods Forty-eight healthy male Sprague-Dawley rats,weighing 200-220 g,aged 2.5-3.0 months,were randomly divided into 4 groups (n=12 each): normal control group (group C),ALI group,curcumin + ALI group (group Cur+ ALI),and curcumin group (group Cur).In groups C and ALI,normal saline 0.5 ml and LPS 10 mg/kg (0.5 ml) were injected intravenously,respectively,30 min after 0.1％ dimethyl sulfoxide (the vehicle for curcumin) 0.5 ml was injected intraperitoneally.In groups Cur+ ALl and Cur,curcumin 20 mg/kg (0.5 ml) was injected intraperitoneally,and 30 min later LPS 10 mg/kg and normal saline 0.5 ml were injected,respectively.The rats were then sacrificed at 6 h after injection of LPS.The lungs were removed for microscopic examination.The pathological changes of the lung were scored.The malondialdehyde (MDA) content,superoxide dismutase (SOD)activity and expression of HO-1,AP-1 and HO-1 mRNA in lung tissues were determined.Results Compared with group C,the pathological score and MDA content were significantly increased,the SOD activity was significantly decreased,and the expression of HO-1,AP-1 and HO-1 mRNA was up-regulated in groups ALl and Cur +AL(l) (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group Cur (P ＞ 0.05).The pathological score and MDA content were significantly higher,and the SOD activity and expression of HO-1,AP-1 and HO-1 mRNA were significantly lower in group Cur + ALl than in group ALI(P ＜ 0.05).Conclusion Transcription factor AP-1 activation is involved in the up-regulation of HO-1 expression during LPS-induced ALI in rats.

Background Doxycycline is a broad spectrum antibiotic,and it is frequently used in the treatment of ocular surface diseases.Objective The purpose of the present study was to investigate the effect of doxycycline on the inhibition of cell proliferation in bovine corneal myofibroblasts in vitro and assess its contribution to ocular surface repairing mechanism.Methods Six fresh bovine corneas were collected.The corneal stromal layer was isolated by two-step method of 1.0 g/L and 2.0 g/L collegenase-1.Isolated cells were plated at mantaryay culture flask in 10％ FBS of RPMI-1640.Vimentin and alpha-smooth muscle actin (α-SMA) organization were evaluated by immunocytochemistry,and the cells with influoresccence staining for vimentin and α-SMA were identified as the corneal myofibroblasts.Doxycycline at the concentrations of 10,20,40,60,80 mg/L was added to the medium,respectively,in different concentrations of doxycycline groups.Dexamethasone (120 mg/L)was used in the same way in the positive control group,and no drug was used in the negative control group.Cell proliferation was evaluated by MTT and the cell cycle was analyzed by BD FACScan flow cytometer assay 24 hours and 48 hours after addition of any drug.Results The cells grew well and showed the positive response for vimentin and α-SMA.MTT assay showed that the A570values of bovine corneal myofibroblasts were gradually declined with the increase of the concentration of doxycycline and lapse of active time,showing statistically significant difference (Fconcentration =1233.778,P＜0.001 ; Ftime =227.564,P ＜ 0.001).And the difference between the two factors was also statistically significant (Ftime*concentration =51.656,P＜0.001).Flow cytometry cell cycle analysis showed that 24 hours after 10,20,40,60,80 mg/L doxycycline treated,the perentage of of corneal myofibroblast cell in G0-G1 phase was 82.85％,84.36％,85.18％,87.12 ％ and 89.31％,showing significant increase in comparison with 63.89％ of the negative control group (all P＜0.05),and that of 40 mg/L doxycycline group was near the positive control group.Forty-eight hours after 10,20,40,60,80 mg/L doxycycline treated,the perentage of of corneal myofibroblast cell in G0-G1 phase was 82.78％,86.15％,88.23％,89.57％,93.00％,with significant increase in comparison with 70.17％ of the negative control group (all P ＜ 0.01),and that of 40 mg/L doxycycline group was near the positive control group.Conclusions The growth of the bovine corneal myofibroblasts is inhibited by doxycycline in time-and dosedependent manner in the range from 10 mg/L to 80 mg/L,and 40 mg/L of doxycycline has an obviously inhibitory action as 120 mg/L dexamethasone.

Objective To investigate the development of ultrastructure in grafts from a xenograft model of human hemangioma on nude mice.Methods Human infantile hemangioma tissue was obtained in surgery and planted into subcutaneous layer of nude mice in small pieces.The grafts were harvested on the 2~(nd),5~(th),15~(th),30~(th),45~(th) day and then at 2~(nd),3~(rd),4~(th),6~(th) month for transmission electron microscopic view.Results In early stage after transplantation,signs of degeneration and necrosis were more evident.On the 30~(th) day,the number of endothelial cells increased and some of the endothelial cells were larger in size with high nuclear to plasm ratio.At the 2~(nd) month,the number of endothelial cells increased,while some of these cells turned flat.Later,high endothelial cells decreased in number and collapse and pyknosis of plasm,formation of secondary lysosome,margination of chromatin,fragmentation of nucleus were evident with surrounding deposition of adipose and collagen.Conclusions With xenotransplantation of human infantile hemangioma tissue onto nude mice,the grafts may survive ischemia and proliferate,and then gradually involute.The development resembles a natural course of human infantile hemangioma.