Making the invisible visible: improving detectability of MRI-invisible residual cervical cancer after conisation by DCE-MRI.

AIM: To determine whether dynamic contrast-enhanced (DCE) magnetic resonance imaging (MRI) quantitative parameters increase the detectability of MRI-invisible residual cervical cancer after conisation. MATERIALS AND METHODS: This retrospective study included 59 patients with MRI-invisible cervical cancer, but positive conisation pathology. Thirty-five patients were confirmed to have residual cervical cancer, and 24 patients showed non-residual cervical cancer. DCE-MRI quantitative parameters were calculated in the anterior or posterior cervix according to the conisation position. Receiver operating characteristic (ROC) analysis was used to find the threshold of DCE-MRI parameters in differentiate residual cervical cancer patients from non-residual cervical cancer patients after conisation. RESULTS: For patients with residual cervical cancer, the Ktrans and Ve values were significantly higher than in their counterparts with non-residual cervical cancer (0.610±0.395 versus 0.366±0.305/min, p=0.013; and 0.703±0.270 versus 0.540±0.280%, p=0.028; respectively). The Ktrans showed the highest area under the ROC curve (AUC) of 0.705 (p=0.004) with a sensitivity of 67.6% and specificity of 68%. CONCLUSION: DCE-MRI quantitative parameters increased the detectability of MRI-invisible residual cervical cancer after conisation.

Diffusion kurtosis imaging in identifying the malignancy of lymph nodes during the primary staging of rectal cancer.

AIM: The aim was to assess the diagnostic value of diffusion kurtosis imaging (DKI) for discriminating between benign and malignant lymph nodes in patients with rectal carcinoma. METHOD: ighty-five patients with rectal adenocarcinoma who underwent total mesorectal excision of the rectum were studied. A total of 273 lymph nodes were harvested and subjected to histological analysis. Quantitative parameters [apparent diffusion parameter Dapp of the Gaussian distribution, apparent kurtosis coefficient Kapp and apparent diffusion coefficient (ADC)] of lymph nodes were derived from DKI. Differences and the diagnostic performance of these parameters were calculated by using the independent-samples t test and receiver operating characteristic curve analyses. RESULTS: The median Dapp and ADC values of metastatic lymph nodes were significantly greater than those of benign lymph nodes, whereas the median Kapp of metastatic lymph nodes was statistically less than that of normal lymph nodes. Dapp had the relatively highest area under the curve of 0.774. When 1126.15 × 10-6  mm2 /s was used as a Dapp threshold value, the sensitivity and specificity were 96.97% and 41.82%, respectively. CONCLUSION: DKI can help differentiate metastatic vs benign lymph nodes during the primary staging of rectal cancer.

[Feasibility of targeted magnetic resonance imaging on visualizing tenascin-C expression in atherosclerosis plaque in high-fat diet fed ApoE(-/-) mice].

OBJECTIVE: To explore the feasibility of targeted magnetic resonance imaging (MRI)on visualizing tenascin-C (TN-C) expression in atherosclerotic plaque in high-fat diet fed ApoE(-/-) mice. METHODS: Aorta artery atherosclerosis was induced in high fat diet fed ApoE(-/-) mice. The atherosclerotic plaques were observed by 7.0T micro-MRI after 14 weeks. Specimens of the samples were obtained randomly and stained with HE and oil red O to observe the pathological changes. The plaques were stained with anti-TN-C antibody to detecting the TN-C. Targeted probe (anti-TN-C-USPIO) was synthesized through chemical coupling methods. The experimental group was injected with targeted probe through tail vein (10 mgFe/kg), and USPIO was used as controls. MRI was performed 8 hours thereafter, intima signal changing in abdominal aorta was observed; specimens of abdominal aorta were taken after scanning, and were stained by Perl's Prussian blue, the deposition of iron particles was observed. RESULTS: Compared with baseline level, MRI evidenced thickened aorta wall; signal was enhanced on T1WI and PDWI, but weakened on T2WI after 14 weeks. HE stained tissue samples demonstrated thicker intima. The plaque was confirmed by the oil red O staining. Immunohistochemistry staining showed significantly upregulated TN-C expression in the plaque. Compared to pre-injection status, MRI signal was lost on T2WI in the atherosclerotic lesions at 8 hours after anti-TNC-USPIO injection (ΔOD =4.78±1.41, t=9.59, P<0.05), while T2WI remained unchanged in control group (ΔOD =1.45±1.01, t=1.93, P>0.05) and matched Perl's Prussian stained section showed enriched blue particles deposition within the plaque while there were only scarce blue particles deposition in the control group. CONCLUSION: Our results show that targeted MRI is feasible to detect TN-C expression in the plaque in vivo, this method might be used to detect in vivo atherosclerotic plaque in large animals or in humans in the future.

Detecting topological currents in graphene superlattices.

Topological materials may exhibit Hall-like currents flowing transversely to the applied electric field even in the absence of a magnetic field. In graphene superlattices, which have broken inversion symmetry, topological currents originating from graphene's two valleys are predicted to flow in opposite directions and combine to produce long-range charge neutral flow. We observed this effect as a nonlocal voltage at zero magnetic field in a narrow energy range near Dirac points at distances as large as several micrometers away from the nominal current path. Locally, topological currents are comparable in strength with the applied current, indicating large valley-Hall angles. The long-range character of topological currents and their transistor-like control by means of gate voltage can be exploited for information processing based on valley degrees of freedom.

Coulomb drag mechanisms in graphene.

Recent measurements revealed an anomalous Coulomb drag in graphene, hinting at new physics at charge neutrality. The anomalous drag is explained by a new mechanism based on energy transport, which involves interlayer energy transfer, coupled to charge flow via lateral heat currents and thermopower. The old and new drag mechanisms are governed by distinct physical effects, resulting in starkly different behavior, in particular for drag magnitude and sign near charge neutrality. The new mechanism explains the giant enhancement of drag near charge neutrality, as well as its sign and anomalous sensitivity to the magnetic field. Under realistic conditions, energy transport dominates in a wide temperature range, giving rise to a universal value of drag which is essentially independent of the electron-electron interaction strength.

Sevoflurane has no adverse effects on renal function in cirrhotic patients: a comparison with propofol.

BACKGROUND: Cirrhotic patients are prone to developing renal dysfunction after anaesthesia and surgery. However, no consensus has been reached whether sevoflurane could have adverse effects on renal function in cirrhotic patients. We hypothesised that the use of sevoflurane for general anaesthesia would lead to post-operative renal dysfunction in cirrhotic patients undergoing liver resection. METHODS: A total of 200 patients undergoing liver resection were randomly assigned to a propofol or sevoflurane group. The influence of sevoflurane or propofol on renal function was evaluated by the maximal change, the difference between the pre-operative baseline and the highest values of serum creatinine and blood urea nitrogen measured at day 1, 3 and 6 post-operatively. RESULTS: The maximal change in serum creatinine after liver resection was -4.52 (5.78) µmol/l and -3.37 (7.34) µmol/l with P = 0.398, and that in blood urea nitrogen was 0.41 (1.49) mmol/l and 0.93 (1.54) mmol/l with P = 0.098 between the sevoflurane group (n = 52) and the propofol group (n = 50), respectively. CONCLUSIONS: Sevoflurane does not seem to impair post-operative renal function in cirrhotic patients undergoing liver resection.

Protective effect of paricalcitol on cyclosporine-induced renal injury in rats.

We evaluated the protective effect of paricalcitol on cyclosporine (CsA)-induced renal injury using an experimental model of chronic CsA nephropathy. Paricalcitol (50 and 200 ng/kg/d) was concomitantly administered with CsA (15 mg/kg/d) for 28 days in rats. We assessed the effects of paricalcitol by measuring degree of the tubulointerstitial fibrosis (TIF) and inflammation, a profibrotic cytokine (ßig-h3), a proapoptotic gene (caspase-3), apoptotic cell death, and oxidative stress. The CsA-treated rats showed increased TIF and inflammatory cell infiltration, but paricalcitol treatment (200 ng/kg) significantly decreased those compared with the CsA-alone group. The expression of ßig-h3, a biologic marker of transforming growth factor ß1, which was increased in the CsA group, also decreased with paricalcitol treatment. The increased rates of excretion of urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and expression of tissue 8-OHdG produced by CsA treatment were significantly attenuated by paricalcitol treatment. The increased expression of caspase-3 and number of TUNEL-positive cells in the CsA group were decreased with concomitant paricalcitol treatment. The effect of paricalcitol was more evident high among the rather than low-dose cohort. In conclusion, paricalcitol showed antiinflammatory and antifibrotic effects. This finding may provide a rationale for use of paricalcitol in CsA-induced renal injury.

The etomidate requirement is decreased in patients with obstructive jaundice.

BACKGROUND: Patients with obstructive jaundice have increased sensitivity to inhaled anesthetics. In rodent brain, bilirubin can enhance γ-aminobutyric acid A/glycinergic synaptic transmission. Etomidate is a nonbarbiturate hypnotic that induces sedation through γ-aminobutyric acid A receptors in the central nervous system. We tested the hypothesis that patients with obstructive jaundice have an altered sensitivity to etomidate. METHODS: The study design was a comparison of etomidate requirements to reach a Bispectral Index of 50 in patients with obstructive jaundice versus patients with chronic cholelithiasis and normal bilirubin levels. Etomidate was infused at 30 µg/kg/min until this end point was reached. RESULTS: The etomidate requirement in the obstructive jaundice group was lower than that in the control group (150±46 µg/kg vs 206±74 µg/kg, P=0.007). The average decrease in etomidate requirement was 56 µg/kg (95% confidence interval: 16-96 µg/kg). In addition, we found a significant negative correlation between serum total bilirubin and etomidate requirement with Pearson r of -0.545, and 95% confidence interval for r value (-0.791 to -0.148). All subjects were hemodynamically stable during the study. CONCLUSIONS: Etomidate requirements to reach a level of anesthesia defined by a Bispectral Index of 50 are reduced in patients with obstructive jaundice.

Volatile anesthetics might be more beneficial than propofol for postoperative liver function in cirrhotic patients receiving hepatectomy.

Hepatic inflow occlusion during the liver surgery may result in a transient ischemia period followed by reperfusion, and may initiate liver injury and lead to postoperative liver dysfunction. Especially in cirrhotic patients, the tolerance time of ischemia is much shorter and the outcome would be worse. Recently, clinical trials had proved that volatile anesthetics rather than propofol can protect myocardial cells from ischemia reperfusion (IR) injury in cardiac surgery. Meanwhile, animal studies had revealed that volatile anesthetics could induce some endogenous protective molecules in the liver such as hypoxia induced factor-1 (HIF-1), heme oxygenase (HO) enzyme system and inducible nitric oxide synthase (iNOS), which make the volatile anesthetics posing the extraordinary anti-oxidative, anti-inflammatory, anti-apoptotic, and vasodilatory characteristics. However, there is still lack of trials to compare the postoperative outcomes such as liver function in cirrhotic patients undergoing liver surgery with inflow occlusion between volatile anesthetics and propofol anesthesia. Hence we hypothesize that with its anti-IR injury characteristics, volatile anesthetics might be the more appropriate choice in cirrhotic patients undergoing liver surgery with occlusion.

A comparison of liver function after hepatectomy with inflow occlusion between sevoflurane and propofol anesthesia.

BACKGROUND: In this study, we compared liver function tests after hepatectomy with inflow occlusion as a function of propofol versus sevoflurane anesthesia. METHODS: One hundred patients undergoing elective liver resection with inflow occlusion were randomized into a sevoflurane group or a propofol group. General anesthesia was induced with 3 µg/kg fentanyl, 0.2 mg/kg cisatracurium, and target-controlled infusion of propofol, set at a plasma target concentration of 4 to 6 µg/mL, or sevoflurane initially started at 8%. Anesthesia was maintained with target-controlled infusion of propofol (2-4 µg/mL) or sevoflurane (1.5%-2.5%). The primary end point was postoperative liver injury assessed by peak values of liver transaminases. RESULTS: Transaminase levels peaked between the first and the third postoperative day. Peak alanine aminotransferase was 504 and 571 U/L in the sevoflurane group and the propofol group, respectively. Peak aspartate aminotransferase was 435 U/L after sevoflurane and 581 U/L in the propofol group. There were no significant differences in peak alanine aminotransferase or peak aspartate aminotransferase between groups. Other liver function tests including bilirubin and alkaline phosphatase, and peak values of white blood cell counts and creatinine, were also not different between groups. CONCLUSIONS: Sevoflurane and propofol anesthetics resulted in similar patterns of liver function tests after hepatectomy with inflow occlusion. These data suggest that the 2 anesthetics are equivalent in this clinical context.

A clinical prospective comparison of anesthetics sensitivity and hemodynamic effect among patients with or without obstructive jaundice.

BACKGROUND: To compare isoflurane anesthesia in patients with or without hyperbilirubinemia undergoing hepatobiliary surgery. METHODS: Forty-two patients with obstructive jaundice and 40 control patients with normal liver function scheduled for hepatobiliary surgery under isoflurane anesthesia were studied. Anesthesia was induced with propofol (1.5-2 mg/kg) and remifentanil (2 microg/kg). After tracheal intubation, anesthesia was titrated using isoflurane in oxygen-enriched air, adjusted to maintain a bispectral index (BIS) value of 46-54. Ephedrine, atropine and remifentanil were used to maintain hemodynamic parameters within 30% of the baseline. The mean arterial blood pressure (MAP), heart rate (HR), drug doses and the time taken to recover from anesthesia were recorded. RESULTS: Demographic data, duration and BIS values were similar in both groups. Anesthesia induction and maintenance were associated with more hemodynamic instability in the patients with jaundice and they received more ephedrine and atropine and less remifentanil and isoflurane (51.1+/-24.2 vs. 84.6+/-20.3 mg/min; P for all <0.05) than control patients. Despite less anesthetic use, the time to recovery and extubation was significantly longer than that in control. CONCLUSION: Patients with obstructive jaundice have an increased sensitivity to isoflurane, more hypotension and bradycardia during anesthesia induction and maintenance and a prolonged recovery time compared with controls.

The effects of obstructive jaundice on the pharmacodynamics of propofol: does the sensitivity of intravenous anesthetics change among icteric patients?

BACKGROUND: Some studies suggest that certain clinical symptoms of cholestasis, such as fatigue and pruritus, result from altered neurotransmission. Patients with obstructive jaundice also have labile blood pressure and heart rate. In the present study, the authors investigated whether obstructive jaundice affects a patient's sensitivity to hypnotics and the haemodynamic profile of propofol. METHODS: Thirty-six ASA physical status I/II/III patients with serum total bilirubin (TBL) from 7.8 to 362.7 micromol/l scheduled for bile duct surgery were recruited. A computer-controlled propofol infusion programmed for effect site target was used to rapidly attain and maintain sequential increase of the compartment concentration (from 1 to 3 microg/ml). Each target-controlled concentration was maintained for about 12 min, and arterial blood samples were drawn for propofol concentration determination. The bispectral index (BIS) and mean arterial pressures (MAP) were used as indices of the propofol effect. The relation between the concentration and the effects was described by the Hill equation. The pharmacodynamic parameters were optimized using a nonlinear mixed-effect model. RESULTS: TBL was not a significant covariate of EC(50) for the pharmacodynamic model. For BIS and MAP, the parameters of the pharmacodynamic model were E(max)=75.77%, EC(50)=2.34 microg/ml, and gamma=1.82, and E(max)=47.83%, EC(50)=1.49 microg/ml, and gamma=1.88, respectively. CONCLUSIONS: We demonstrated that obstructive jaundice with serum TBL from 7.8 to 362.7 micromol/l had no effect on propofol pharmacodynamics observed by BIS and MAP.

Propofol pharmacokinetics in patients with obstructive jaundice.

The effect of obstructive jaundice on the distribution and elimination of propofol was studied in 15 patients with obstructive jaundice (total serum bilirubin, TBL >/= 17.1micromol.l(-1)) and in 15 control patients (TBL < 17.1micromol.l(-1)). Following an i.v. bolus dose of propofol (2-2.5 mg.kg(-1)) multiple arterial samples were obtained at timed intervals for 4 h and blood concentrations of propofol were measured by high pressure liquid chromatography. Compartmental analysis of propofol concentrations revealed a three-compartment model with elimination from a central compartment in all patients. Pharmacokinelic parameters: volumes of distribution at steady state (V(SS)), volumes of distribution at equilibrium (V(r)), volumes of the central compartment (V) and total body clearance (Cl) were similar in patients with obstructive jaundice (mean 12.3 (SD 6.0) litre.kg(-1), 32.99(21.42) litre.kg(-1), 0.241(0.131) litre.kg(-1), and 28.8(8.2) ml.min(-1).kg(-1) respectively) compared with contro1 group (11.9 (5.4) litre.kg(-1), 28.30(13.70) litre.kg(-1), 0.297(0.112) litre.kg(-1), and 33.9(7.6) ml.min(-1).kg(-1) respectively) (P>0.05). Half-times of the three phases (T(1/2)(alpha),T(1/2)(beta),T(1/2)(gamma)) were also similar between both groups.We conclude that in patients with obstructive jaundice the pharmacokinetics of propofol are similar to those of patients without obstructive jaundice.

Protein kinase epsilon dampens the secretory response of model intestinal epithelia during ischemia.

BACKGROUND: Luminal fluid sequestration and diarrhea are early manifestations of mesenteric ischemia. This can be modeled in vitro with the use of T84 intestinal epithelia, where ischemia induces Cl(-) secretion with adenosine-mediated autocrine feedback. Protein kinase C (PKC) regulates epithelial transport and, in some organ systems, is involved in the response to ischemic stress. The purpose of this study was to define the role of PKC on epithelial transport during ischemia. METHODS: By voltage-current clamp, short-circuit current (Isc) equals Cl(-) secretion. Ischemic conditions were simulated with the use of a well-established chemical hypoxia protocol. RESULTS: Chemical hypoxia briskly activated Isc. Gö6850, an antagonist of novel and conventional PKC isoforms, markedly enhanced the ischemia-induced Isc response, although Gö6976 (which inhibits only conventional isoforms) had no effect. Rottlerin, a specific inhibitor of PKC delta, did not attenuate ischemic Isc. Both phorbol 12-myristate, 13-acetate and bryostatin-1, which selectively activate PKC epsilon in T84 cells, markedly attenuated the Isc response to ischemia. Both agents also inhibited the Isc response to exogenous adenosine. CONCLUSIONS: PKC (likely the novel epsilon isoform) in intestinal epithelia modulates ischemia-induced alterations in ion transport. Inhibition of PKC epsilon exaggerates the secretory response that is induced by ischemia and by authentic adenosine; conversely, augmented activation of PKC epsilon inhibits secretion. Manipulation of PKC epsilon could limit luminal fluid sequestration during mesenteric ischemia.

Regulation of epithelial transport and barrier function by distinct protein kinase C isoforms.

The phorbol ester phorbol 12-myristate 13-acetate (PMA) inhibits Cl(-) secretion (short-circuit current, I(sc)) and decreases barrier function (transepithelial resistance, TER) in T84 epithelia. To elucidate the role of specific protein kinase C (PKC) isoenzymes in this response, we compared PMA with two non-phorbol activators of PKC (bryostatin-1 and carbachol) and utilized three PKC inhibitors (Gö-6850, Gö-6976, and rottlerin) with different isozyme selectivity profiles. PMA sequentially inhibited cAMP-stimulated I(sc) and decreased TER, as measured by voltage-current clamp. By subcellular fractionation and Western blot, PMA (100 nM) induced sequential membrane translocation of the novel PKC epsilon followed by the conventional PKC alpha and activated both isozymes by in vitro kinase assay. PKC delta was activated by PMA but did not translocate. By immunofluorescence, PKC epsilon redistributed to the basolateral domain in response to PMA, whereas PKC alpha moved apically. Inhibition of I(sc) by PMA was prevented by the conventional and novel PKC inhibitor Gö-6850 (5 microM) but not the conventional isoform inhibitor Gö-6976 (5 microM) or the PKC delta inhibitor rottlerin (10 microM), implicating PKC epsilon in inhibition of Cl(-) secretion. In contrast, both Gö-6976 and Gö-6850 prevented the decline of TER, suggesting involvement of PKC alpha. Bryostatin-1 (100 nM) translocated PKC epsilon and PKC alpha and inhibited cAMP-elicited I(sc). However, unlike PMA, bryostatin-1 downregulated PKC alpha protein, and the decrease in TER was only transient. Carbachol (100 microM) translocated only PKC epsilon and inhibited I(sc) with no effect on TER. Gö-6850 but not Gö-6976 or rottlerin blocked bryostatin-1 and carbachol inhibition of I(sc). We conclude that basolateral translocation of PKC epsilon inhibits Cl(-) secretion, while apical translocation of PKC alpha decreases TER. These data suggest that epithelial transport and barrier function can be modulated by distinct PKC isoforms.

Pharmacokinetic comparison of omeprazole capsules and a simplified omeprazole suspension.

The pharmacokinetics of omeprazole delayed-release capsules and a simplified omeprazole suspension (SOS) were studied. Seven healthy volunteers randomly received either one 20-mg omeprazole delayed-release capsule or SOS (omeprazole 20 mg in 10 mL) for seven days before being crossed over to the opposite treatment for seven more days after a two-week washout period. On days 1 and 7, blood samples were drawn at intervals up to 360 minutes after drug administration. Plasma omeprazole concentrations were determined by a validated high-performance liquid chromatographic method, and pharmacokinetic values were determined. Area under the concentration-versus-time curve (AUC) from zero to six hours, AUC from time zero to infinity (AUC0-infinity), and maximum plasma concentration (Cmax) increased by 102%, 113%, and 85%, respectively, after seven days of treatment with the capsule. AUC0-infinity for SOS on day 1 was 58% of that for the capsule (p = 0.0141), and on day 7 it was 49% of that for the capsule (p = 0.0044). AUC0-infinity for SOS increased by 85% from day 1 to 7, but the difference was not significant. Cmax for SOS on day 1 was twice that for the capsule (p = 0.0014), but by day 7 the difference between the two formulations was negligible. Time to Cmax (tmax) for SOS on days 1 and 7 was shorter than for the capsule by 82% (p < 0.0001) and 70% (p < 0.0006), respectively. After one week of therapy, omeprazole absorption was faster and tmax was 70% shorter for SOS than for the capsule formulation, but AUC0-infinity was 49% lower for SOS.

Evaluation of electrocardiographic and hemodynamic effects of caffeine with acute dosing in healthy volunteers.

STUDY OBJECTIVE: To evaluate the effects of moderate, single-dose caffeine consumption on electrocardiographic variables: PR, QRS, QT, QTc, and RR intervals, and QT and QTc interval dispersion. Effects of caffeine on blood pressure and heart rate also were evaluated. DESIGN: Randomized, double-blind, placebo-controlled, crossover study. SETTING: University school of pharmacy. PATIENTS: Ten healthy volunteers aged 17 years or older. INTERVENTION: Participants abstained from caffeinated products for at least 2 days before the study began and were randomly designated to receive placebo or caffeine 400 mg on various days. For each of the study phases, a baseline 12-lead electrocardiogram (ECG) was performed and a subsequent 12-lead ECG performed 3 hours after ingesting the study drug. Blood pressure readings were taken with each ECG. MEASUREMENTS AND MAIN RESULTS: No significant changes in any intragroup or intergroup electrocardiographic variables occurred. Caffeine increased blood pressure (systolic blood pressure [SBP]/diastolic blood pressure [DBP]) from 118+/-5/75+/-6 mm Hg to 128+/-8/77+/-7 mm Hg versus baseline (p=0.0022 and p=0.0368 for SBP and DBP, respectively). After drug dosing, SBP in the caffeine group was significantly higher than in the placebo group (128+/-8 mm Hg versus 119+/-7 mm Hg, p=0.0174). CONCLUSION: Moderate caffeine consumption by healthy young adults does not acutely affect PR, QRS, QT, QTc, and RR intervals, or QT and QTc interval dispersion. Caffeine-naive subjects experienced persistent elevations in SBP and DBP 3 hours after caffeine ingestion, indicating that longer caffeine abstinence than that which is recommended is necessary for blood pressure determination in the clinical setting.

Do HMG-CoA reductase inhibitors affect fibrinogen?

OBJECTIVE: To review commonly used fibrinogen assay methods and the evidence demonstrating an association between fibrinogen and increased risk of coronary artery disease and to review the current literature to determine and assess the impact of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors on fibrinogen. DATA SOURCES: Primary and review articles identified from a MEDLINE search (1966-December 1999); references obtained from these publications were subsequently reviewed for additional relevant articles. STUDY SELECTION AND DATA EXTRACTION: All articles were evaluated, and all relevant information was included in this review. DATA SYNTHESIS: The Clauss method is currently the preferred method for determining plasma fibrinogen concentrations, due to its high degree of accuracy and precision. Furthermore, unlike immunologic methods, its reliability is unaffected by change in triglycerides. The effects of four HMG-CoA reductase inhibitors (atorvastatin, lovastatin, simvastatin, pravastatin) on fibrinogen have been evaluated. Atorvastatin has been shown to induce significant increases in fibrinogen (22% increase; p <0.05) by using the immunonephelometric method. This method also demonstrated that lovastatin use was associated with a 24.4% increase (p < 0.0001) in plasma fibrinogen concentration. Simvastatin has been shown in multiple studies using the Clauss method to have a neutral effect on fibrinogen. The majority of studies have revealed significant decreases (7-19%) in fibrinogen following treatment with pravastatin. CONCLUSIONS: Future studies need to be performed evaluating the effects of HMG-CoA reductase inhibitors on fibrinogen, but using direct comparisons and clotting assay methodology.

[Using chengqi prescription to prevent hepatic ischemia/reperfusion injury after liver transplantation in rats].

OBJECTIVE: To study the effect of Chengqi prescription in preventing hepatic ischemia/reperfusion injury after liver transplantation in rats. METHODS: Rat in situ liver transplantation model was used, donor liver was preserved in Ringer's solution for 4 hrs under 4 degrees C, then divided randomly into Chinese medicine group (Chengqi prescription), polymyxin B group, mannitol group, normal saline group and sham operation control group, each group further subdivided into two subgroups: 1 hr group and 4 hrs group after transplantation. The serum ALT and liver injury index was determined. RESULTS: In preventing hepatic ischemia/reperfusion injury after liver transplantation, the Chengqi prescription was polymyxin B showed more effective than that of mannitol and normal saline, and the effect of Chengqi prescription was higher than that of polymyxin B (P < 0.05). CONCLUSION: Chengqi prescription was effective in preventing hepatic ischemia/reperfusion injury after liver transplantation in rat.