Biomedical subjects

M C Chang

Publications and source records attributed to M C Chang.

At least 145 records · Page 8Linked to original sources

PubMed1996

Preload assessment in trauma patients during large-volume shock resuscitation.

OBJECTIVES: To evaluate the utility of the right ventricular end-diastolic volume index (RVEDVI) as a method of preload assessment in trauma patients during large-volume shock resuscitation, and to compare the RVEDVI with the pulmonary artery occlusion pressure (PAOP) as a predictor of preload in this patient population. DESIGN: Retrospective study of a consecutive series of 46 trauma patients, admitted between June 1, 1992, and June 1, 1993, who received a volumetric oximetry pulmonary artery catheter and greater than 10 L of fluid in 24 hours. SETTINGS: University level 1 trauma center. MAIN OUTCOME MEASURES: Correlations of the RVEDVI and PAOP with the cardiac index (CI) during the defined study period. RESULTS: Three hundred fourteen measurements of the RVEDVI, PAOP, CI, and other hemodynamic variables were evaluated. Patients received a mean +/- SD of 22.1 +/- 13.3 L of blood and fluid during the 24 hours. The RVEDVI correlated better (P < .001) with the CI (r = 0.39) than did the PAOP (R = 0.05). Furthermore, there was a better correlation (P < .04) between the RVEDVI and CI when the RVEDVI was 130 mL/m2 or less (r = 0.54) than when it was greater than 130 mL/m2 (r = 0.30). CONCLUSIONS: The RVEDVI is a better predictor of preload than the PAOP in trauma patients during large-volume shock resuscitation. When the RVEDVI is 130 mL/m2 or less, volume administration will likely increase the CI.

Adult↗

PubMed1996

Volumetric assessment of preload in trauma patients: addressing the problem of mathematical coupling.

The availability of the volumetric thermodilution pulmonary artery catheter allows preload assessment based on ventricular volume rather than pressure. This technique has been shown clinically to be a better measure of preload than the pulmonary artery occlusion pressure (PAOP). Critics of the technique argue that the use of thermodilution to measure cardiac output (CO) accounts for the better correlation between right ventricular end-diastolic volume (RVEDV) and CO than PAOP and CO, since stroke volume derived from the CO is a common term to both RVEDV and CO. Previous studies have attempted mathematical corrections for this coupling effect, but direct comparisons using a nonthermodilution measure of CO have not been reported. Our objective was to evaluate the importance of mathematical coupling between RVEDV and CO by assessing the ability of RVEDV to predict CO measured by thermodilution (COTH) compared with CO simultaneously determined by the Fick principle (COFICK). We performed a prospective study of 53 consecutive trauma patients admitted to a Level I trauma center between 10/1/94 and 6/1/95 who received a volumetric pulmonary artery catheter. Using linear regression analysis, RVEDV and PAOP were correlated with simultaneous measurements of both COFICK determined via indirect calorimetry and COTH. Fisher's z-transformation was used to evaluate the correlation coefficients for significant differences (p < .05). The correlation coefficients for RVEDV vs. COTH and RVEDV vs. COFICK were similar (.48 vs. 0.45, p = .76). There was a significant correlation between COTH and COFICK (r = .74, p < .001). RVEDV was significantly better than PAOP at predicting both COTH (p < .001) and COFICK (p = .04). Multivariate regression analysis confirmed that RVEDV was the only estimate of preload which was significantly related to CO. We conclude that mathematical coupling does not have a significant clinical effect on the relationship between RVEDV and CO.

Blood Pressure↗

PubMed1996

Benign parotid tumor with facial nerve paralysis: a case report.

The presence of facial nerve paralysis in the presence of an ipsilateral parotid gland tumor is almost an indication of parotid gland malignancy. Benign parotid gland tumor with facial nerve palsy is very rare. Only three cases have been reported in the literature. The case presented here is a 40 year-old male who had had a right-side parotid tumor for three years, developing a right side facial nerve paralysis within the past three months. After surgical removal of the tumor, the facial nerve function returned to normal. The tumor was a benign tumor, as confirmed by pathological examination.

Adult↗

PubMed1996

Clinical trial of low-dose rHuG-CSF in neutropenic cancer patients following anti-cancer chemotherapy.

Low-dose, subcutaneous recombinant human granulocyte colony-stimulating factor (rHuG-CSF, Lenograstim) was administered to 40 cancer patients (17 men, 23 women) enrolled from two medical centers to verify its clinical effectiveness and safety. The patients' mean age was 50.3 +/- 14.9 years. In this study, there were 20 patients with non-Hodgkin's lymphoma, 10 with breast cancer and 10 with various other solid tumors. The patients first received a course of chemotherapy without rHuG-CSF (control cycle). All patients had at least one episode of neutropenia or leukopenia during the control cycle. rHuG-CSF (2 micrograms/kg/day) was given subcutaneously for 10 days during the study cycle starting on the fourth day of chemotherapy. The nadirs of absolute neutrophil counts (ANC) were 1.8 +/- 0.25 x 10(9)/L and 0.27 +/- 0.05 x 10(9)/L for the rHuG-CSF cycle and pre-rHuG-CSF control cycle, respectively. The number of days of ANC < 1 x 10(9)/L were 1.03 +/- 0.29 and 7.38 +/- 0.58 for rHuG-CSF and control cycles, respectively. The duration from nadir to recovery of ANC (> or = 2 x 10(9)/L) was 9.68 +/- 1.15 days in the rHuG-CSF cycle, vs 22.53 +/- 1.03 days in the control cycle (p < 0.0001). No patient withdrew from the study. Adverse events were mild, with 12.5% to 40% of patients developing myalgia, general malaise, back pain, anorexia or fever. These side-effects were tolerable in all cases. The biochemical abnormalities were subtle and negligible. rHuG-CSF 2 micrograms/kg/day given subcutaneously for 10 days beginning on the fourth day of chemotherapy is very effective (90%), safe and convenient.

Adolescent↗

PubMed1996

Lunate and perilunate dislocation.

BACKGROUND: Perilunate dislocation is an uncommon injury of the wrist due to hyperextension. The factors affecting its prognosis are still controversial. The aim of the present study was to review its fracture types, associated injuries, timing of surgery, different fixation methods and prognostic factors. METHODS: Fourteen patients with perilunate dislocation or fracture dislocation were treated by open reduction and internal fixation, and were followed for at least 12 months. A functional scoring system and X-ray findings were used for follow-up evaluation. RESULTS: Two patients had excellent results, six patients had good results, and four had fair results. Only two patients had poor results. Treatment delayed over one month, transscaphoid perilunar fracture dislocation, or fixation of the transscaphoid fracture with Kirschner wire was associated with poorer results. CONCLUSIONS: Early diagnosis of perilunate dislocation, prompt open reduction and rigid fixation for fracture combined with ligament repair can give more promising results.

Accidents, Traffic↗

PubMed1996

Wraparound injury of posterior interosseous nerve on the unreduced radial head: a case report.

Injury in radial nerve, especially its deep branch, posterior interosseous nerve (PION), is the most common nerve complication associated with Monteggia fracture. According to the reports by Boyd and Spinner, 100% of these injuries recovered spontaneously. Permanent or chronic radial nerve palsy caused by an unreduced radial head is very rare; the optimal treatment is still uncertain. Here a case of chronic PION injury in Monteggia fracture with unreduced radial head is reported.

Adult↗

PubMed1995

Triflavin, an Arg-Gly-Asp-containing peptide, prevents platelet plug formation in in vivo experiments.

Triflavin, an Arg-Gly-Asp-containing peptide from Trimeresurus flavoviridis snake venom (M(r) of 7500 Da) inhibits platelet aggregation through the blockade of fibrinogen binding to activated platelets. The present study demonstrated that the intravenous injection of triflavin (0.1 and 0.25 mg/kg) significantly prolonged the bleeding time about 1.8- to 2.4-fold as compared with control (normal saline) of severed mesenteric arteries in rats, whereas the injection of Gly-Arg-Gly-Asp-Ser (GRGDS) (2-8 mg/kg) failed to increase the bleeding time in this model. Continuous infusion of triflavin (0.08 mg/kg/min) significantly increased the bleeding time about 2.6-fold, and the bleeding time returned to normal within 20 min after the cessation of triflavin infusion. Triflavin (10-20 mg/kg) significantly prolonged the occlusion time of platelet plug formation induced by irradiation of mesenteric venules of fluorescein sodium-pretreated mice. In contrast, trigramin (10-20 mg/kg) and GRGDS (500 and 1000 mg/kg) showed no significant effect. These results suggest that triflavin has an effective antiplatelet effect in vivo and this peptide may be a useful therapeutic agent for arterial thrombosis.

Amino Acid Sequence↗

PubMed1995

The morphologic change of endothelial cells by ancrod-generated fibrin is triggered by alpha v beta 3 integrin binding and the subsequent activation of a G-protein coupled phospholipase C.

The mechanism of morphologic change of human cultured umbilical vein endothelial cells (HUVECs) caused by fibrin was investigated. Ancrod, a thrombin-like enzyme, did not cause morphologic alteration of HUVEC by itself at concentrations ranging from 0.01 to 10 U/ml. However, when 0.02 U/ml of ancrod was added to cultured HUVEC monolayers in the presence of citrated plasma, it caused pronounced morphologic change of HUVEC after 6-10 h incubation period. Gly-Pro-Arg-Pro (4 mg/ml), an inhibitor of fibrin polymerization, prevented the morphologic alteration, indicating that the morphologic alteration was caused by the polymerized fibrin. The morphologic change of HUVEC caused by ancrod-generated fibrin was not observed in the presence of an intracellular calcium mobilization inhibitor TMB-8 (50 microM), and the morphologic alteration was also less pronounced with BAPTA(15 microM)-loaded HUVECs and HUVECs pretreated with EGTA (1.2 mM). Ancrod (in Medium 199) itself did not stimulate phosphoinositide breakdown of HUVEC. However, when ancrod was present in plasma, it caused an increase of [3H]IP1 of HUVECs preloaded with [3H]myoinositol. This IP1 increment was inhibited by Gly-Pro-Arg-Pro. The increase of IP1 was significantly inhibited by the pretreatment of monoclonal antibodies 23C6 and 7E3 directed against alpha v beta 3 integrin. Neomycin (1 mM) and pertussis toxin (100 ng/ml), but not aspirin or mepacrine, blocked this enhanced phosphoinositide breakdown. The morphologic change was also prevented by the monoclonal antibodies, 23C6 and 7E3. These results suggest that both intra- and extra-cellular calcium participate in the event of morphologic change of HUVEC caused by ancrod-generated fibrin, and the morphologic change is mediated, at least in part, by fibrin binding to integrin alpha v beta 3 on HUVECs, causing the subsequent activation of the endogenous G-protein coupled phospholipase C.

Ancrod↗

PubMed1995

Characterization of a thrombin-like enzyme, grambin, from the venom of Trimeresurus gramineus and its in vivo antithrombotic effect.

A thrombin-like enzyme, grambin, was purified to homogeneity by gel filtration, affinity and ion-exchange chromatography from the venom of Trimeresurus gramineus. Its mol. wt was estimated to be 45,400 by SDS-PAGE under reduced conditions. The mass of neutral sugars in grambin is estimated to be 20.7% of total mass. Grambin's NH2-terminal ten amino acid residues show a high homology to other venom thrombin-like enzymes. It clots human fibrinogen with a specific activity of 220-250 NIH thrombin-equivalent units/mg protein. It preferentially releases fibrinopeptide A accompanied by a slow release of trace amounts of fibrinopeptide B as monitored by HPLC following enzyme treatment of fibrinogen. EDTA, aprotinin, hirudin and heparin did not affect the fibrinogen-clotting activity of grambin in purified human fibrinogen solution. Diisopropyl fluorophosphate, phenylmethylsulfonyl fluoride and leupeptin inhibited the clotting activity of grambin whereas iodoacetamide did not affect its activity, indicating that grambin is a serine protease rather than a cysteine protease. In addition, it caused defibrinogenation and showed a marked antiplatelet effect when administered intravenously to mice. It also significantly prolonged the time lapse of platelet-rich thrombus formation in the irradiated mesenteric venules of fluorescein sodium-treated mice. Therefore, grambin may be used as a therapeutic agent not only in treatment of venous thrombosis but also in prevention of arterial thrombosis.

Amino Acid Sequence↗

PubMed1995

Inhibition of tumor promotion in benzo[a]pyrene-initiated CD-1 mouse skin by crocetin.

The effects of topical application of crocetin on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced promotion of skin tumors, hyperplasia, hydrogen peroxide, ornithine decarboxylase (ODC) and inflammation were evaluated in female CD-1 mice. Topical application of crocetin (0.2 or 1.0 mumol) with TPA (15 nmol) twice weekly for 20 weeks to mice previously initiated with benzo[a]pyrene (B[a]P) inhibited the number of TPA-induced tumors per mouse by 69 and 81% respectively. Pre-application of the same amount of crocetin also afforded significant protection against TPA-induced hyperplasia in the ear skin. Topical application of crocetin inhibited tumor promoter-caused induction of epidermal ODC activity by TPA (5 nmol). The topical application of crocetin (0.2 or 1.0 mumol) inhibited TPA-induced edema of mouse ears by 76 and 87% respectively. Pretreatment of mouse skin with various amounts of crocetin caused inhibition of hydrogen peroxide and myeloperoxidase production by TPA. These results indicate that crocetin possesses potential as a cancer chemopreventive agent against tumor promotion.

Animals↗

PubMed1995

The antiplatelet activity of ancrod on administration to rabbits.

Ancrod, a thrombin-like enzyme purified from the venom of Calloselasma rhodostoma, was administered to rabbits intravenously, and blood samples were obtained at 1, 3, 6, 10, and 24 hours after infusion. Ancrod caused a rapid and sustained defibrinogenation within the first 6 hours, with production of fibrinogen degradation products (FDPs) peaking at 1 hour and declining to background level at 6 hours. No significant changes in platelet count, white cell count, or hematocrit was observed. Citrated PRP prepared 1, 3, and 6 hours after ancrod infusion showed diminished aggregation, adenosine triphosphate (ATP) release, and thromboxane B2 formation on the addition of collagen. Although platelet suspension prepared from defibrinogenated platelet-rich plasma (PRP) at 3 hours showed no significant change in aggregation and ATP-releasing activity, the latent period of platelet aggregation was prolonged. When the remaining platelet-poor plasma obtained from defibrinogenated PRP at 3 hours was used to suspend the normal washed platelets prepared from PRP before ancrod infusion, the platelets showed a similar defect in aggregation and release action. Addition of fibrinogen (200 micrograms/ml to 2 mg/ml) to the above preparation partially restored aggregation but not capacity for secretion and thromboxane formation. When normal washed platelets were suspended with the defibrinogenated plasma, prepared by mixing ancrod with normal plasma in vitro and removing the formed fibrin, the platelet suspension showed impaired platelet aggregability, and the aggregability could be restored to the normal level by the addition of exogenous fibrinogen to this preparation.(ABSTRACT TRUNCATED AT 250 WORDS)

Ancrod↗

PubMed1995

Incorporation of [1-carbon-11]palmitate in monkey brain using PET.

UNLABELLED: We determined regional incorporation coefficients (k*) of plasma [1-11C]palmitate into stable brain lipids of anesthetized monkeys with PET. METHODS: Carbon-11-palmitate was injected intravenously in untreated animals and in animals pretreated with methyl palmoxirate (MEP), an inhibitor of beta-oxidation of palmitate in the brain and periphery. Plasma radioactivity was followed, and brain radioactivity was determined at various times using PET. A least-squares method was used to fit the data to an operational equation to obtain regional values of k* and of cerebral blood volume (Vb) in individual experiments. RESULTS: MEP significantly decreased the integral of plasma [11C]CO2 following 11C-palmitate infusion. Mean values of k* in monkeys not given MEP were 4.9, 4.2, 4.9, 4.0 and 2.9 x 10(-5) ml/sec.g for the temporal, frontal, parietal and occipital cortices and white matter, respectively. With the exception of k* in white matter, which was increased by MEP, k* in the other brain regions was not significantly changed by MEP. The Vb ranged from 0.035 ml/g to 0.048 ml/g in gray matter regions and equaled 0.022 ml/g in white matter. CONCLUSION: PET can be used to determine regional incorporation coefficients of 11C-palmitate into the primate brain in vivo. Combined with MEP, 11C-palmitate could be used with PET to examine regional brain phospholipid metabolism in humans in normal and pathological conditions.

Animals↗

PubMed1995

Characterization of endothelial cell differential attachment to fibrin and fibrinogen and its inhibition by Arg-Gly-Asp-containing peptides.

We investigated the adhesion of human umbilical vein endothelial cells (HUVECs) to fibrin(ogen) molecule of varying structure for identifying sites that mediate cell attachment. Fibrin was prepared either with ancrod which liberates only FPA from fibrinogen, or with thrombin, which liberates both FPA and FPB. Both fibrin preparations equally supported HUVEC attachment. GRGDS, RGD-containing peptides of snake venoms, and monoclonal antibodies against alpha v beta 3 (23C6 and 7E3) inhibited the attachment of HUVECs to fibrin by 65-75%. In contrast, the attachment of HUVECs to fibrinogen was less effective and was almost completely inhibited by both RGD-containing peptides and by antibodies against integrin alpha v beta 3 (85-95% inhibition). The C-terminal dodecapeptide of fibrinogen gamma chain (residues 400-411) inhibited minimally the attachment of HUVECs to fibrin. Additionally, the binding of RGD-containing snake venom peptides to HUVECs was both RGD- and divalent-cation-dependent. The IC50S for inhibition of HUVEC attachment to fibrin were 0.09 microM (rhodostomin), 1.54 microM (trigramin) and 1.64 microM (halysin). These results indicate that fibrin mediated support of cell attachment is independent of the cleavage of FPB from fibrinogen. HUVEC attachment to fibrinogen was almost completely inhibited by RGD-containing peptides and by antibodies against alpha v beta 3. In contrast, the attachment to fibrin was partially resistant to RGD-containing peptides and to the monoclonal antibodies against integrin alpha v beta 3. However, alpha v beta 3 is the major receptor mediating HUVEC attachment to fibrin.

Amino Acid Sequence↗

PubMed1994

Ancrod-formed fibrin stimulates prostacyclin production of human umbilical vein endothelial cells via de novo synthesis of cyclooxygenase.

Ancrod, a thrombin-like enzyme, has been used as defibrinogenating agent in prevention of venous thrombosis. This study showed ancrod in citrated plasma elevated 6-keto PGF1 alpha production of human umbilical vein endothelial cells; this increment of 6-keto PGF1 alpha was completely inhibited by Gly-Pro-Arg-Pro, an inhibitor of fibrin polymerization. The enhanced prostacyclin production, but not basal level of prostacyclin, was inhibited by actinomycin D and cycloheximide. In washed aspirin-pretreated cells, ancrod-formed fibrin induced restoration of prostacyclin production by a cycloheximide- and actinomycin D-sensitive process. Ancrod-formed fibrin stimulated synthesis of cyclooxygenase as probed by Western blotting and this enhancement was blocked by actinomycin D and cycloheximide. In conclusion, we first report that ancrod-formed fibrin stimulates prostacyclin production of human endothelial cells and this event is dependent on de novo synthesis of cyclooxygenase.

6-Ketoprostaglandin F1 alpha↗

PubMed1994

In vivo effect of a thrombin-like enzyme on platelet plug formation induced in mesenteric microvessels of mice.

Ancrod caused defibrinogenation and exhibited ex vivo antiplatelet activity in experimental rabbits. In this study, platelet thrombus was induced by irradiation of the mesenteric microvessels with filtered light in mice pretreated with fluorescein sodium intravenously. Ancrod (0.5-2 U/kg) dose-dependently, significantly prolonged the time lapse of inducing platelet plug formation in mesenteric venules when it was intravenously infused. At these doses, ancrod depleted plasma fibrinogen and displayed ex vivo antiplatelet aggregation induced by collagen. Ancrod (1 U/kg) prolonged the occlusion time about 2.1 folds (from control 103.2 +/- 17.0 to 211.2 +/- 26.3 seconds) with a duration longer than 60 min. On the other hand, PGI2 briefly prolonged the occlusion time about 1.5 folds when it was given by continuous infusion (250-500 ng/kg/min). Heparin (100-250 U/kg) had no significant effect in this model. Therefore, ancrod may be used as a therapeutic agent not only in treatment of venous thrombosis and possibly in prevention of arterial thrombosis.

Ancrod↗

PubMed1994

The effect of methyl palmoxirate on incorporation of [U-14C]palmitate into rat brain.

We examined the dose response, time course and reversibility of the effect of methyl 2-tetradecylglycidate (McN-3716, methyl palmoxirate or MEP), an inhibitor of beta-oxidation of fatty acids, on incorporation of radiolabeled palmitic acid ([U-14C]PA) from plasma into brain lipids of awake rats. MEP (0.1, 1 and 10 mg/kg) or vehicle was administered intravenously from 10 min to 72 hr prior to infusion of [U-14C]PA. Two hr pretreatment with MEP (0.1 to 10 mg/kg) increased brain organic radioactivity 1.2 to 1.8 fold and decreased brain aqueous radioactivity by 1.2 to 3.0 fold when compared to control values. At 10 mg/kg, MEP significantly increased brain organic fraction from 40% in controls to 85%, 30 min to 6 hr pretreatment, and resulted in a redistribution of the radiolabeled fatty acid toward triacylglycerol. MEP changed the lipid/aqueous brain ratio of incorporated [U-14C]PA from 0.67 to 5.7. The incorporation rate coefficient, k*, was significantly increased by MEP (10 mg/kg) at 2 hr (31%), 4 hr (59%) and 6 hr (34%). All effects were reversed by 72 hr, consistent with a half-life of approximately 2 days for carnitine palmitoyl transferase I. These results indicate that intravenous MEP may be used with [1-11C]palmitic acid for studying brain lipid metabolism in vivo by positron emission tomography, as it significantly reduces the large unincorporated aqueous fraction that would result in high background radioactivity.

Animals↗

PubMed1994

Cerebral microvessel phospholipase A2 activity in senescent mouse.

Phospholipase A2 activity was measured in cerebral microvessels isolated from 5 to 6 month (young adult) and 21 to 24 month (aged adult) old mice. Radiolabeled 1-stearoyl-2-[1-14C]arachidonyl choline phosphoglyceride was used as the enzyme substrate, and enzyme activity determined at pH 8 and pH 9. Activity in older animals was significantly less than in younger animals at both pH's. With choline phosphoglyceride as a substrate, phospholipase A2 activity was predominantly Ca(2+)-dependent, although a small, but measurable Ca(2+)-independent component was present. Negligible production of diacylglycerol indicated little or no phospholipase C activity. These findings indicate that activity of a phospholipase A2, which utilizes choline phosphoglyceride as a substrate, is affected by the aging process. Moreover, a change in PLA2 activity would result in altered metabolism of specific phosphoglycerides and turnover of fatty acids at the sn-2 position in cerebral microvessels.

Aging↗

PubMed1994

Dietary tannins from cowpeas and tea transiently alter apparent calcium absorption but not absorption and utilization of protein in rats.

Tannins reportedly alter absorption and utilization of protein and minerals. The present study investigated the effect of tannins extracted from 'Mississippi Silver' cowpeas and black tea when incorporated into nutritionally balanced diets. Condensed tannins were incorporated into the diet of weanling male Sprague-Dawley rats at 0.0, 0.0057, 0.0171 and 0.057 g/100 g diet for 28 d. Ingestion of tannin from cowpeas or tea did not change significantly growth rate, protein efficiency ratio, apparent protein digestibility, nitrogen excretion, relative liver weight, or nitrogen concentration of liver. During d 11-18, apparent calcium absorption was lower in rats fed the medium and high levels of cowpea tannin and in those fed all levels of tea tannin compared with the control group. By wk 4, no differences were observed in apparent calcium absorption among treatment groups. Apparent magnesium absorption was not affected by dietary treatment, nor was femur content of calcium or magnesium. We conclude that at the levels of condensed tannins fed, a short-term reduction of apparent calcium absorption occurred; however, by wk 4 calcium absorption was comparable to that of the control group. The acute change that occurred in apparent calcium absorption did not influence bone calcium content.

Absorption↗