Adolescent ; Adult ; Aged ; Bone Marrow ; pathology ; Child ; Female ; Humans ; Lymphoma, Non-Hodgkin ; diagnosis ; pathology ; Male ; Middle Aged ; Spleen ; pathology ; Young Adult

Objective To evaluate the efficacy of nalmefene antagonizing postoperative respiratory depression induced by opioids.Methods Two hundred and forty ASA Ⅰ orⅡpatients aged 18-64 yr with body weight fluctuating within 20% of the standard body weight were included in this multicenter,randomized,double-blind,positive drug-controlled study.Anesthesia was induced with etomidate 0.3 mg/kg and TCI of sufentanil(effect-site concentration 0.4.ng/ml).Tracheal intubation was facilitated with vecuronium 0.1 mg/kg or rocuronium 0.6mg/kg.The patients were mechanically ventilated.PETCO2 was maintained at 35-45 mm Hg.Anesthesia was maintained with sevoflurane+ sufentanil TCI(Ce=0.1-0.4 ng/ml).Patients undergoing neurosurgery and liver or kidney operation were excluded.The operation time was within 3 h.The residual effects of muscle relaxants were reversed after operation.The patients were randomly divided into 2 groups(n=120 each):group Ⅰneloxone andgroup Ⅱ nalmefene.Naloxone 0.1 mg or nalmefene 0.25 μg/kg was injected iv over 30 s and was repeated 5 min later if necessary until the respiratory rate＞10 bpm,PETCO2＜45 mm Hg and apnea time＜15 s.The total amount of naloxone was≤0.4 mg while that of nalmefene≤1 μg/kg.BP,HR,SpO2,PETCO2,respiratory rate and apnea time were recorded immediately before and at 2 and 5 min after haloxone/nalmefene administration and then every 5 min until 5 min after extubation.The recovery of spontaneous breathing within 30 min after naloxone/nalmefene administration,extubation time and Ramsay sedation score at 5 min after extubation were recorded.The patients were also observed for adverse reactions.Results Spontaneous breathing recovered within 30 min after naloxone/nalmefene administration in all patients in both groups.The extubation time was significantly shorter in nalmefene group than in naloxone group.There was no significant difference in Ramsay sedation score,BP,HR,SpO2 and incidence of adverse reactions between the 2 groups.Conclusion Nalmefene is better than naloxone in antagonizing opioid-induced postoperative respiratory depression.

Objective To study the clinical features and to improve the treatment on the elderly patients with brain tumor.Methods Retrospective analysis of 163 cases with brain tumor which had been confirmed by CT,MRA or pathology.Results Of all the 163 cases,121 were located in supratentorium,most of which were meningiomas and gliomas.Most patients(129 cases)had comorbidity.After operation,symptoms disappeared or obviously improved in 126 cases,moderately improved in 19 cases,and did not changed in 6 patients.Twelve cases died after operation in a month, in which 9 patients were over 75 years old.The death rate of operation was 6.1%.Conclusions It is important to know the atypical manifestation of brain tumor in the elderly,which may prevent clinical misdiagnosis and mistherapy.The perioperative management is indispensable to the prognosis of the patients.The choice of operation and medication should be in individualized.

The purpose of the present study was to investigate the effect of meperidine on rat ventricular muscle. Cardiac function was assessed in Langendorff-perfused rat hearts and intracellular calcium level was recorded in enzymatically isolated rat ventricular myocytes using spectrofluorometric techniques. To explore the underlying mechanism, whole-cell configuration of patch-clamp technique was used to record L-type Ca(2+) current. The results showed that meperidine decreased the product of heart rate and left ventricular developed pressure (LVDP HR), maximal rate of the left ventricular pressure increase (LV +dP/dt(max)) and decrease (LV -dP/dt(max)), but increased left ventricular end-diastolic pressure in a dose-dependent manner (0-1000 micromol/L). Meperidine also produced a dose-dependent reduction in electrically induced [Ca(2+)](i) transient amplitude and an increase in diastolic [Ca(2+)](i) baseline level, but did not alter the caffeine (20 mmol/L) induced Ca(2+) release from intracellular ryanodine-sensitive Ca(2+) stores. Meperidine at 100 micromol/L inhibited L-type Ca(2+) current to 67.4 10.1% of control but did not affect the voltage dependency of activation and inactivation. The inhibitory effect of meperidine on Ca(2+) current could not be prevented by pretreatment with the opioid receptor antagonist naloxone. These data suggest that meperidine exerts a negative inotropic effect by inhibiting L-type Ca(2+) current. The lack of effect of naloxone implies that the action is independent of the opioid receptor.
Animals ; Calcium Channels, L-Type ; drug effects ; Depression, Chemical ; Dose-Response Relationship, Drug ; Heart Rate ; drug effects ; Male ; Meperidine ; pharmacology ; Myocardial Contraction ; drug effects ; Myocytes, Cardiac ; metabolism ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Ventricular Function, Left ; drug effects

OBJECTIVETo investigate the effects of pethidine on electrophysiological properties of the isolated ventricular myocytes and the underlying mechanism.

METHODSLangendorff was applied to perfuse rat heart model and whole-cell current clamp and voltage clamp techniques were used.

RESULTSPethidine decreased heart rate (HR) in a concentration dependent manner and caused severe atrioventricular block (AVB) at >or=250 micromol/L. Pethidine reduced action potential amplitude and maximal rate of depolarization, prolonged action potential duration. Pethidine at 100 micromol/L decreased sodium currents (I(Na)), transient outward potassium currents (I(to)), delayed rectifier potassium currents (I(k)) and L-type calcium currents (I(Ca.L)) to (60.7+/-6.9)%, (55.4+/-5.6)%, (65.1+/-8.0)% and (67.4+/-10.1)% of control levels,respectively. These effects could be recovered by washout. Naloxone, an opioid receptor antagonist, could not abolish the effects of pethidine on ionic currents.

CONCLUSIONPethidine decreased HR and induced AVB, which may be related to the inhibition of I(Na), I(to), I(k) and I(Ca-L) of heart. The depression of cardiac currents is not mediated by opioid receptor.

Action Potentials ; drug effects ; Animals ; Heart ; drug effects ; physiology ; Heart Block ; chemically induced ; Heart Rate ; drug effects ; In Vitro Techniques ; Ion Channels ; antagonists & inhibitors ; Male ; Meperidine ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid ; physiology

A(p.G888S)were detected in POLG1 gene.Sequence analysis of parental blood DNA revealed that her father carried L83P and her mother carried G888S.Conclusions The characteristics of clinical manifestation,electrophysiology,pathology and POLG1 gene mutation of the patient were highly consistent with Alpers syndrome.The prominent white matter change and increased immunological factors in CSF were first reported in Alpers syndrome.Alpers syndrome should be considered for those patients whose liver function were severely impaired after exposure to valproic acid.

Chromatography, High Pressure Liquid ; methods ; Flavonoids ; analysis ; Flowers ; chemistry ; Lonicera ; chemistry ; classification ; Luteolin ; analysis ; Plants, Medicinal ; chemistry ; Quercetin ; analogs & derivatives ; analysis ; Reproducibility of Results ; Rutin ; analysis ; Sensitivity and Specificity

OBJECTIVETo investigate the expression of programmed cell death 5 (PDCD5) in tissues of normal human prostate (NP), benign prostatic hyperplasia (BPH), and prostate cancer (PCa) in order to assess the clinical role of PDCD5 in PCa.

METHODSPDCD5 expression was determined by EnVision immunohistochemical staining in formalin-fixed and paraffin-embedded specimens obtained from 12 subjects with NP, 22 with BPH, and 22 with PCa. In addition, PCa cases were classified as low/middle-risk (Gleason sum < or = 7) and high-risk (Gleason sum >7) on the basis of Gleason grade. Positive expression rates and intensity of PDCD5 protein were observed under light microscope and analyzed with computer imaging technique. Expression of PDCD5 was compared among different prostatic tissues.

RESULTSThe expression of PDCD5 was significantly lower in tissue of PCa than in tissues of NP and BPH (P<0.01). However, there was no significant difference in PDCD5 expression between tissues of NP and BPH. In addition, the expression of PDCD5 was further downregulated with the increase of Gleason sum in PCa.

CONCLUSIONSBy downregulating apoptosis, low PDCD5 expression may play an important role in the occurrence and development of PCa. PDCD5 is supposed to have a potential clinical value to be a new predictor of progression and target of gene therapy in PCa.

Aged ; Apoptosis ; Apoptosis Regulatory Proteins ; analysis ; physiology ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Neoplasm Proteins ; analysis ; physiology ; Prostate ; chemistry ; Prostatic Neoplasms ; chemistry ; etiology ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; analysis

Objective:To investigate the effects and mechanisms of Wnt pathway inhibitor IWR-1-endo on the biological behaviors of human hepatocarcinoma cell Huh7.Methods:Human hepatocellular carcinoma cell Huh7 was cultured in vitro, and Huh7 cells were treated with IWR-1-endo at different concentrations (0, 20, 40, 80, 160, 320 μmol/L). Scratch test was used to detect changes in cell migration ability at diffe-rent drug concentrations, plate cloning was used to detect changes in cell proliferation, Western blotting was used to detect changes in the expression of Wnt pathway related protein β-catenin, and immunofluorescence staining was used to detect the expression of β-catenin in cytoplasm and nucleus. Results:The results of the scratch test showed that the 24 h scratch healing rates of Huh7 cells treated with 0, 20, 40, 80, 160, 320 μmol/L IWR-1-endo were (20.55±0.05)%, (12.10±0.08)%, (9.36±0.10)%, (3.62±0.09)%, (0.62±0.04)% and (0.23±0.02)%, respectively, and there was a statistically significant difference ( F=230.87, P<0.001). Further pair comparison showed that there were statistically significant differences in 24 h scratch healing rates among different concentrations (all P<0.001). The 48 h scratch healing rates were (34.77±0.08)%, (17.69±0.05)%, (11.60±0.04)%, (5.68±0.07)%, (2.66±0.04)% and (1.75±0.02)%, respectively, and there was a statistically significant difference ( F=589.68, P<0.001). Further pair comparison showed that there were statistically significant differences in 48 h scratch healing rates among different concentrations (all P<0.001). After treatment with IWR-1-endo at the concentration of 0, 20, 40, 80, 160, 320 μmol/L, the clone formation rates of Huh7 cells were (61.67±0.21)%, (57.33±0.11)%, (50.00±0.25)%, (36.67±0.28)%, (23.33±0.12)% and (15.00±0.08)%, respectively, and there was a statistically significant difference ( F=403.56, P<0.001). Further pair comparison showed that there were statistically significant differences in clone formation rates among different concentrations (all P<0.001). After treatment with 0, 20, 40, 80, and 160 μmol/L IWR-1-endo for 24 h, the relative expression levels of β-catenin in Huh7 cells were 0.30±0.08, 0.25±0.07, 0.22±0.05, 0.15±0.01 and 0.06±0.02, respectively, and there was a statistically significant difference ( F=247.00, P<0.001). Compared with 0 μmol/L, the relative expression levels of β-catenin treated with 80 and 160 μmol/L had statistical significance ( P=0.014; P=0.008). Compared with 0 mol/L, immunofluorescence showed that the expressions of β-catenin in cytoplasm and nucleus were reduced after 80 μmol/L IWR-1-endo treatment. Conclusion:Wnt pathway inhibitor IWR-1-endo can inhibit the migration and proliferation of hepatocarcinoma cells Huh7 by inhibiting the activity of Wnt pathway. The above inhibitory effects are dose-dependent.

BACKGROUNDVascular hyporeactivity, which occurs in the terminal stage of hemorrhagic shock, is believed to be critical for treating hemorrhagic shock. The present study was designed to examine whether the CB1 cannabinoid receptor (CB1R) was involved in the development of vascular hyporeactivity in rats suffering from hemorrhagic shock.

METHODSSixteen animals were randomly divided into two groups (n = 8 in each group): sham-operated (Sham) and hemorrhagic shock (HS) groups. Hemorrhagic shock was induced by bleeding. The mean arterial pressure (MAP) was reduced to and stabilized at (25 +/- 5) mmHg for 2 hours. The vascular reactivity was determined by the response of MAP to norepinephrine (NE). In later experiments another twelve animals were used in which the changes of CB1R mRNA and protein in aorta and superior mesenteric artery (SMA) were analyzed by RT-PCR and Western blotting. In addition, we investigated the effects of a CB1R antagonist on the vascular hyporeactivity and survival rates in rats with hemorrhagic shock. Survival rates were analyzed by the Fisher's exact probability test. The MAP response was analyzed by one-way analysis of variance (ANOVA).

RESULTSVascular hyporeactivity developed in all animals suffering from hemorrhagic shock. The expression of CB1R mRNA and protein in aorta and 2 - 3 branches of the SMA were significantly increased in the HS group after the development of vascular hyporeactivity when compared to those in Sham group. When SR141716A or AM251 was administered, the MAP response to NE was (41.75 +/- 4.08) mmHg or (44.78 +/- 1.80) mmHg respectively, which was higher than that in saline groups with (4.31 +/- 0.36) mmHg (P < 0.01). We also showed an increased 4-hour survival rate in the SR141716A or AM251-treated group with 20% or 30%, but with a statistically significant difference present between the AM251-treated and saline groups (P < 0.05).

CONCLUSIONSCB1R is involved in vascular hyporeactivity resulting from hemorrhagic shock in rats, and CB1R antagonist may be useful in treating patients with traumatic, hemorrhagic shock who need field-rescue or initial treatment.

Animals ; Blotting, Western ; Gene Expression Regulation ; drug effects ; Hypotension ; metabolism ; Male ; Piperidines ; pharmacology ; Pyrazoles ; pharmacology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1 ; antagonists & inhibitors ; genetics ; metabolism ; physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Shock, Hemorrhagic ; metabolism ; mortality ; Survival Rate