Adolescent ; Humans ; Leukemia, Myeloid, Acute ; etiology ; pathology ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; complications ; pathology

Biomedical Research ; Drugs, Chinese Herbal ; therapeutic use ; Evidence-Based Medicine ; Medicine, Chinese Traditional ; methods ; Phytotherapy ; methods

Objective To investigate the effect of sufentanil preconditioning on the expression of Toll-like receptor 4 (TLR4) in myocardium during myocardial ischemia-reperfusion (I/R) in rats.Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each):sham operation group (group S),I/R group and sufentanil preconditioning group (group SPC).Myocardial ischemia was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 2 h of reperfusion.In group SPC,the rats were subjected to 3 consecutive cycles of 5 min sufentanil infusion at 0.2 μg· kg-1 ·min-1 via the femoral vein at 5 min interval before ischemia.In groups S and I/R,the rats were subjected to the equal volume of normal saline instead.HR and mean arterial pressure (MAP) were recorded at 30 min before ischemia (T0),immediately before ischemia (T1),at 30 min of ischemia (T2),and at 30 and 120 min of reperfusion (T3-4).At the end of reperfusion,blood samples were obtained to determine the serum concentration of TNF-α.The rats were then sacrificed and hearts were removed for measurement of myocardial infarct size and expression of TLR4 and NF-κB p65 in myocardium (using Western blot).Results There was no significant difference in HR among the three groups (P ＞ 0.05).Compared with group S,MAP was significantly decreased at T2-4,the serum concentration of TNF-α was increased,and the expression of TLR4 and NF-kB p65 protein in myocardium was upregulated in groups I/R and SPC (P ＜ 0.01).Compared with group I/R,no significant difference was found in MAP at all time points (P ＞ 0.05),and myocardial infarct size was significantly decreased,serum concentrations of TNF-α were decreased,and the expression of TLR4 and NF-κB p65 protein in myocardium was down-regulated in group SPC (P ＜ 0.01).Conclusion The mechanism by which sufentanil preconditioning alleviates myocardial I/R injury may be related to down-regulation of TLR4 expression in rat myocardium.

Objective To observe the security and efficacy of sevoflurane inhalation in combination with remifentanil controlled hypotension in patients undergoing functional endoscopic sinus surgery.Methods Forty pa tients undergoing elective functional endoscopic sinus surgery were randomly divided into propofol group (group P)and sevoflurane group(group S).In group P,patients received remifentanil 0.2μg · kg-1 · min-1 and propofol 4 ～6mg · kg-1 · min-1 intravenously,those in group S received remifentanil 0.2pg · kg-1 · min-1 and continuous inhalation of sevoflurane 2 ～ 3％,the end-tidal concentration was 1.1 ～ 1.7MAC.MAP was retained at 65 ～ 75 mmHg in the two groups.MAP and HR were recorded before controlled hypotension (T1),5min after controlled hypotension (T2),30min after controlled hypotension(T3),the termination of surgery(T4) and 5min after the termination of surgery(T5).Record the patient opening eyes time,wake extubation time,duration of surgery,blood loss.Also observed with or without respiratory depression,drowsiness,restlessness,nausea,vomiting and other adverse reactions.The same surgery fell surgical field quality rating according to Fromme operative field score table.Results Compared with T1,MAP(F =73.68) and HR(F =24.60) decreased significantly(P ＜ 0.05) at the other time points.There was no statistically significant difference in MAP(t =0.90) and HR(t =1.00) at the same time points between the two groups (P ＞ 0.05).Extubation time (t =0.44),duration of operation (t =1.23),operative field score (t =0:43) and blood loss (t =0.58) has no significant differences (P ＞ 0.05).Conclusion Inhalation hypotension by sevoflurane is feasible and safe in the functional endoscopic sinus surgery.It shows good quality of surgical field and less adverse reactions.

Aim To investigate the effects of Aplysin on the inhibition of gastric cancer cell in vitro .Methods MTT assay was used to examine the inhibition of gastric cancer cell 1ine SGC-7901 by Aplysin in different concentrations and at different times.The morphologic changes and the apoptosis of SGC-7901 was observed by inverted microscope and Hematoxylin-Eosin(HE)staining.Reverse transcriptase polymerase chain reaction(RT-PCR)assay was used to detect the changes of COX-2 mRNA expressions.Results Aplysin could decrease the proliferation significantly in a dose-dependent manner in SGC-7901 cells.When treating SGC-7901 with Aplysin in concentration of 120, 240 mg·L~(-1) for 24 h, the growth of the cell was obviously inhibited observing by inverted microscope.Aiso, when treating with the same concentration for 18 h, its chromatin became crimpled and breakdown, as well as cell shrinkage and apoptotic bodies formation when using HE staining.The apoptotic rates(%)of SGC-7901 was(15.0±2.12)%, (18.4±2.3)%, respectively, which was significantly higher than(1.4±0.55)% that in control group(P <0.01).60、120、240 mg·L~(-1) Aplysin could not effectively inhibited the mRNA expressions of COX-2(P ＞0.05).Conclusions Aplysin can inhibit the proliferation and induces apoptosis of SGC-7901 cells.

Electrophoresis, Capillary ; methods ; Humans ; Micelles ; Paraquat ; blood

Child ; Female ; Hemoptysis ; etiology ; Humans ; Lupus Erythematosus, Systemic ; complications ; diagnosis

AIM:To study the effect of remifentanil on monophasic action potential and transmural dispersion of repolarization (TDR) in the 3-layer myocardium of isolated rabbit hearts .METHODS:Adult rabbits (n=18, 2.0 ~2.5 kg) were used to isolate the hearts for preparing Langendorff perfusion model .The hearts were randomly divided into 3 groups after perfusion with K-H solution for 15 min: the perfusion in control group ( C group ) continued for 60 min; the hearts in remifentanil group ( R group ) were perfused with 12 μg/L remifentanil K-H solution for 60 min; the hearts in remifentanil+aminophylline group ( RA group ) were given 60-min perfusion of 12 μg/L K-H remifentanil +30 mg/L aminophylline .The HR and 3 layers of myocardial monophasic action potential ( MAP) in the left ventricular anterior wall were recorded at time points after balanced infusion for 15 min ( T0 ) , and continued perfusion for 15 min ( T1 ) , 30 min ( T2 ) and 60 min ( T3 ) .The monophasic action potential duration of repolarization at 90%( MAPD90 ) and the transmural dispersion of repolarization (TDR) were calculated.The early afterdepolarization, delay afterdepolarization and arrhythmia were also observed.RESULTS:In R group, slower HR and prolonger MAPD90 and TDR at T1 ~T3 were observed as com-pared with those at T0(P<0.05).R group showed slower HR and longer MAPD 90 and TDR than C group and RA group (P<0.05).CONCLUSION:Remifentanil slows the HR, extends the MAPD90 and increases the TDR, thus being prone to induce reentry.Aminophylline makes HR faster and MAPD90 shorter, thereby reducing the TDR.

Objective To evaluate the effect of aminophylline on monophasic action potential (MAP) during remifentanil-induced negative chronotropic effect in the isolated rabbit hearts.Methods Eighteen healthy adult rabbits,weighing 2.0-2.5 kg,wereused in the study.Their hearts were excised and retrogradely perfused in a Langendorff apparatus.After 15 min of stabilization with K-H solution,the isolated hearts were randomly divided into 3 groups (n =6 each) using a random number table:control group (group C),remifentanil group (R group),and remifentanil + aminophylline group (RA group).Group C was perfused with 37 ℃ K-H solution for 60 min.Group R was perfused with K-H solution containing remifentanil 12 ng/ml for 60 min.Group RA was perfused with K-H solution containing remifentanil 12 ng/ml and aminophylline 30 μg/ml for 60 min.At 15 min of stabilization and 15,30 and 60 min of perfusion,HR and MAP in the myardium of left ventricle were recorded:MAP duration at 90％ and 50％ repolarization (MAPD90,MAPD50) was calculated.The early after depolarization,delay after depolarization and arrhythmia were recorded.Results Compared with group C,HR was significantly decreased at 15,30 and 60 min of perfusion,and MAPD50 and MAPD90 were prolonged in goup R,and HR was increased in group RA.HR was significantly higher,and MAPD50 and MAPD90 were shorter in RA group than in group R.No early after depolarization,delay after depolarization or arrhythmia developed in each group.Conclusion Aminophylline antagonizes remifentanil-induced negative chronotropic effect through shortening monophasic action potential duration in the myocardium of left ventricle of the isolated rabbit hearts.

Objective To explore the expression of transcriptional regulation factor FHL 1 in pancreatic fibrosis of chronic pancreatitis (CP) and clinical significance.Methods Serum samples from 20 CP patients treated in the Department of Gastroenterology , Nanjing General Hospital and 20 healthy controls in the corresponding period were collected .The level of FHL1 in the serum was detected by ELISA .Twenty male Wistar rats were randomly divided into control group and CP group according to the body weight .The CP rat model was established by injecting dibutyltin dichloride ( DBTC) through tail vein .All the rats were killed at 28 days after injection and the pancreas was collected , which was observed using hematoxylin and eosin ( HE) staining to investigate pathological changes . The expression of FHL1 in pancreas was measured by immunohistochemistry (IHC) and Western blotting (WB).Results The average of serum FHL1 level in two groups were (0.86 ±0.22)g/L and (1.18 ±0.22)g/L, respectively.The level of FHL1 in serum of CP patients was significantly lower than that of healthy cases , and the difference was statistically significant (t=10.54, P=0.001).Damaged pancreatic lobular structure , acinar atrophy and the obvious fibrous hyperplasia were observed in CP rats .The pathological score of abnormal structure , acinar atrophy, fibrosis, and inflammatory cell infiltration in the pancreas of the CP group was (2.2 ±0.4),(2.0 ±0.7),(2.4 ±0.3) and (2.8 ±0.6), respectively, but was all 0 in control group.The difference between two group was statistically significant ( t value =17.24, 9.01, 25.22 and 14.75, respectively, all P<0.001).The expression of FHL1 in the pancreatic tissue of CP group were less than that of normal group , and the difference was statistically significant (IHC:15 798 ±3 247 vs 37 570 ±9 254, t=2.438,P=0.016;WB:0.44 ±0.11 vs 0.89 ±0.03, t=4.289, P=0.002).Conclusions The protein of FHL1 was in low expression in the pancreas of CPs , indicating that FHL1 may participate in the formation of pancreatic fibrosis .