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Biomedical subjects

S A Abbas

Publications and source records attributed to S A Abbas.

At least 19 recordsLinked to original sources
PubMed2006

Effect of captopril in the presence of kinin B2 receptor antagonist on duration of survival after prolonged coronary artery ligation in hypertensive rats.

In the present investigation, we evaluated the potential effects of captopril, an angiotensin-converting enzyme inhibitor, in the absence and presence of kinin B(2) receptor antagonist (D-Arg-[Hyp3-D-Phe7]-BK) on the duration of survival after prolonged coronary artery ligation in spontaneously hypertensive rats (SHR). The captopril treatment (16 and 32 microg/kg; i.v.) resulted in a significant (p < 0.05) increase in survival time of SHR when compared with that of saline-treated control SHR. Kinin B(2) receptor antagonist (4 microg/kg; i.v.) pretreatment abolished (p > 0.05) the beneficial effect of captopril on the survival time when compared with that in saline-treated control SHR. Both the ligation of coronary artery and captopril treatment resulted in a significant (p < 0.001) fall in systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) of SHR when compared with those of the saline-treated control SHR. In addition, captopril administration caused a significant (p < 0.05) fall in SBP, DBP, and HR of SHR before ligation of the coronary artery (preligation). However, there was no significant change (p > 0.05) in SBP, DBP, and HR between saline- and kinin B(2) receptor antagonist plus captopril-treated SHR during preligation. These finding might indicate that captopril possesses a cardioprotective property as demonstrated by an increase in the survival time of SHR. This beneficial effect of captopril is mediated via the kinin B(2) receptor pathway because kinin B(2) receptor antagonist pretreatment blocked the captopril-induced increase in the survival time of SHR.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

The effect of bradykinin and its antagonist on survival time after coronary artery occlusion in hypertensive rats.

It is known that BK does play a role in the cardioprotective effect of angiotensin converting enzyme (ACE) inhibitors. The present study therefore was conducted to examine the effects of bradykinin (BK) and its antagonist on survival time in spontaneously hypertensive rats (SHR) with coronary artery ligation for 15 min and continuously. We also evaluated the heart rate and blood pressure (BP) in the presence and absence of BK and BK2 receptor antagonist, D-Arg-[Hyp-D-Phe7]BK. Coronary artery was ligated in anaesthetized rats and they were artificially ventilated with room air (stroke volume, 4 ml; 48 strokes/min) as described by the previous investigators. Lead II elecrocardiogram (ECG) was recorded from subcutaneous steel needle electrodes. Results of this investigation indicated that BK treatment 4 microg/kg (i.v.) and 8 microg/kg (i.v.) caused significant (P < 0.05) increase in survival time in SHR with coronary artery ligation for 15 min and continuously as compare to their respective saline-treated controls. However, BK antagonist treatment 4 microg/kg (i.v.) abolished the increase in survival time caused by BK treatment. The mean values of survival time between the saline-treated and BK antagonist plus BK-treated rats did not differ significantly (P > 0.05). The heart rate and BP responses were greatly reduced (P < 0.001) in the presence of coronary artery ligation. These findings suggest that BK might have cardioprotective effect to increase the survival time in rats by activating BK2 receptors after coronary artery ligation.

Animals↗
PubMed1997

Local urokinase delivery with the Channel balloon: device safety, pharmacokinetics of intracoronary drug delivery, and efficacy of thrombolysis.

The Channel balloon is a new local drug-delivery catheter that has the dual capability of high-pressure lesion dilation and low-pressure drug infusion. The purpose of this study was to assess the safety and efficacy of this device in the local delivery of urokinase in the porcine model. Three in vivo protocols were performed in 57 anesthetized swine to assess the safety of Channel balloon use in the coronary vasculature, the pharmacokinetics of local urokinase delivery, and the ability of the catheter to lyse intraluminal thrombus. First, safety studies were performed in 18 coronary vessels in 13 pigs to compare angiographic and histologic changes following use of the Channel balloon with conventional balloon angioplasty. Second, intramural deposition of 123I-labeled urokinase was measured in 24 coronary arteries in 20 pigs to assess the efficiency and technical determinants of urokinase delivery and the time course of intramural drug retention. Finally, an in vivo thrombus model was used in 24 pigs to compare the thrombolytic capacity of local urokinase delivery with the Channel balloon in comparison with conventional urokinase infusion techniques. All balloon inflations and drug infusions with the Channel balloon were well tolerated in all animals without adverse angiographic, hemodynamic, or electrical sequelae. Comparative histologic studies with the Channel balloon demonstrated no additional vessel trauma beyond that seen with conventional balloon angioplasty. Between 0.09 and 0.35% of infused urokinase was intramurally deposited, with intracoronary persistence for at least 5 h. Drug infusion pressure did not significantly affect drug deposition, although larger amounts of urokinase were deposited with larger balloon:artery ratios and higher urokinase concentrations. In comparison to conventional systemic and guiding catheter infusions, local delivery of urokinase with the Channel balloon resulted in higher levels of clot dissolution. These studies have demonstrated safe intracoronary use of the Channel balloon in the porcine model. Local infusion of urokinase with this device results in significant intramural drug deposition that persists for at least 5 h. In comparison with conventional thrombolytic techniques, local urokinase delivery with the Channel balloon may result in enhanced intravascular thrombolysis.

Angioplasty, Balloon, Coronary↗
PubMed1997

Disposition of aerosolized liposomal amphotericin B.

Amphotericin B (AmB) is an important drug for the treatment of fungal infection, but toxicity limits the lung tissue doses which may be achieved through intravenous administration. Although incorporation of AmB in liposomes reduces these effects and increases the therapeutic index for intravenous administration, targeted delivery to lung tissues via inhaled liposomal AmB aerosol may be a more effective approach. Aerosolization of liposomal amphotericin B targets the lungs, the organs first infested by many fungi. Development of optimal aerosolized liposomal AmB therapies requires a better understanding of the effect that liposome surface charge has on lung clearance kinetics. In this work we evaluated the clearance kinetics and organ distribution of inhaled liposomal AmB in male Balb/C mice. Mice were exposed via nose only to AmB-containing liposomal aerosols having positive, negative, or neutral surface charge characteristics. The formulations were aerosolized using a Collison nebulizer. Groups of animals were euthanized at predetermined times and the lungs and other organs were analyzed for AmB. AmB was not detected in serum and other organs such as kidneys, liver, and brain. The disposition of neutral and positive liposomal amphotericin B in lungs followed biexponential kinetics. The alpha and beta phase half-lives for positive liposomes were 1.3 and 15.1 days, respectively, and 2.3 and 22 days for neutral liposomes. AmB delivered via negative liposomes exhibited monoexponential clearance with a half-life of 4.5 days. These results suggest that toxic side effects in nontarget tissues are minimal and may indicate a potential for long term protection against fungal infections.

Aerosols↗
PubMed1996

New high-performance liquid chromatographic method for amphotericin B analysis using an internal standard.

A simple and reproducible HPLC method for the analysis of amphotericin B (AmB) in serum, lung and liver using natamycin as the internal standard was developed. AmB and natamycin were extracted from serum, lung and liver and were separated using an isocratic elution from C18 reversed-phase column. The mobile phase consisted of acetonitrile-10 mM acetate buffer pH 4.0 (37:63, v/v). The HPLC system had two detectors in series. One was set at 303 nm and the other at 383 nm for the detection of natamycin and AmB, respectively. The retention times of AmB and natamycin were 15 and 6 min, respectively. The recovery efficiency was 96%-70%. The limit of quantification was 0.1 microgram/ml. The assay was reproducible, the within-day coefficient of variation (n = 6) was < 8% for serum, lungs and liver. The between-day variability (n = 6) was < 7.7% for serum, liver and lungs at 1 microgram/ml or 1 microgram/g tissue concentration. The assay was linear within the range 1-40 micrograms/ml (r2 = 0.99).

Amphotericin B↗
PubMed1996

Factors associated with the release of cardiac troponin T following percutaneous transluminal coronary angioplasty.

BACKGROUND: Recent studies have suggested that immunoassay of cardiac troponin T (cTnT) provides a more sensitive measurement of myocardial necrosis than creatine kinase MB (CK-MB) mass concentration. HYPOTHESIS: The purpose of this study was to compare the release of cTnT and CK-MB isoenzyme in patients undergoing percutaneous coronary angioplasty, and to investigate the clinical, procedural, and angiographic correlates of abnormal elevations of both of these markers. METHODS: Total creatine kinase (total CK), CK-MB, and cTnT levels were measured immediately before and 12 h following intervention in 110 patients, including 100 consecutive patients undergoing coronary angioplasty and 10 control patients undergoing diagnostic cardiac catheterization. All patients had normal levels of all three markers at baseline. A postintervention total CK level > 225 U/l, an increase in CK-MB > 5.0 ng/ml, and/or an increase in cTnT > 0.04 ng/ml were considered indicative of myocardial injury. RESULTS: Coronary angioplasty was successfully performed in all 100 patients without emergency bypass surgery or death, although six patients required emergent placement of an intracoronary stent for threatened closure. Eight patients demonstrated an abnormal increase in total CK, including six who were undergoing primary angioplasty for an acute myocardial infarction. One of these patients sustained a Q-wave infarction. Post angioplasty, 18 patients had elevations of both CK-MB and cTnT, 23 had elevations of only cTnT, and the remaining 59 patients had elevations of neither. All patients with CK-MB elevation also had cTnT elevation. Neither serologic marker increased in the diagnostic catheterization control patients. In comparison with patients without postintervention cTnT rise, patients with abnormal cTnT levels had a higher incidence of complex lesion morphology (p < 0.01) and intracoronary thrombus (p < or = 0.0001) prior to coronary angioplasty, and a higher incidence of coronary dissection (p < or = 0.01), abrupt closure (p < or = 0.05), and side-branch occlusion (p < or = 0.01) during angioplasty. In patients with elevation of both cTnT and CK-MB, postintervention CK-MB levels were 12-fold higher and cTnT levels were 21-fold higher than in patients with isolated elevation of only cTnT (p < 0.01). CONCLUSIONS: These data indicate that > 40% of patients undergoing coronary angioplasty have evidence of minor degrees of myocardial damage, as evidenced by cTnT release. High-risk coronary lesions and both minor and major complications of angioplasty are associated with cTnT release. cTnT appears to be a more sensitive marker of myocardial injury than CK-MB under these circumstances. In comparison with isolated cTnT rise, elevation of both CK-MB and cTnT may be indicative of greater levels of myocardial injury.

Aged↗
PubMed1995

Enzyme inhibitors: new and known polybrominated phenols and diphenyl ethers from four Indo-Pacific Dysidea sponges.

Extracts and pure compounds isolated from four samples of Dysidea sp. sponges collected from two geographically distinct regions of the Indo-Pacific (Chuuk Atoll and Fiji) were assayed against five different enzyme assays, four of which are relevant to anticancer drug discovery and one of which (15-lipoxygenase) may detect compounds significant in modulating the development of atherosclerotic plaque. The pure compounds that inhibited various enzymes were polybrominated phenols and polybrominated phenoxyphenols. Fourteen of these phenols were isolated, six of which were new compounds. A variety of the phenols inhibited inosine monophosphate dehydrogenase (IMPDH), guanosine monophosphate synthetase, and 15-lipoxygenase. No activity was observed with protein tyrosine kinase pp60v-src or matrix metalloprotease.

Animals↗
PubMed1990

Synthesis of some monodeoxyfluorinated methyl and 4-nitrophenyl alpha-D-mannobiosides and a related 4-nitrophenyl alpha-D-mannotrioside.

Treatment of methyl 3,4,6-tri-O-benzyl-2-O-(2,3,4-tri-O-acetyl-alpha-D-mannopyranosyl)-alpha -D- mannopyranoside with N,N-diethylaminosulfur trifluoride (Et2NSF3), followed by O-deacetylation and catalytic hydrogenolysis, afforded methyl 2-O-(6-deoxy-6-fluoro-alpha-D-mannopyranosyl)-alpha-D-mannopyranoside (8). Methyl 6-deoxy-6-fluoro-2-O-alpha-D-mannopyranosyl-alpha-D-mannopyranoside (11) was similarly obtained from methyl 3-O-benzyl-2-O-(2,3,4,6-tetra-O-acetyl-alpha-D-mannopyranosyl-alpha-D- mannopyranoside. 1,2,3,4-Tetra-O-acetyl-6-deoxy-6-fluoro-beta-D-mannopyranose (13), used for the synthesis of the 4-nitrophenyl analogs of 8 and 11, as well as their 3-O-linked isomers, was obtained by treatment of 1,2,3,4-tetra-O-acetyl-beta-D-mannopyranose with Et2NSF3. Treatment of 13 with 4-nitrophenol in the presence of tin(IV) chloride, followed by sequential O-deacetylation, isopropylidenation, acetylation, and cleavage of the acetal group, afforded 4-nitrophenyl 4-O-acetyl-6-deoxy-6-fluoro-alpha-D-mannopyranoside (18). Treatment of 13 with HBr in glacial acetic acid furnished the 6-deoxy-6-fluoro bromide 19. Glycosylation of diol 18 with 20 gave 4-nitrophenyl 4-O-acetyl-6-deoxy-6-fluoro-3-O- (21) and -2-O-(2,3,4,6-tetra-O-acetyl-alpha-D-mannopyranosyl)-alpha-D- mannopyranoside (23) in the ratio of approximately 2:1, together with a small proportion of a branched trisaccharide. 4-Nitrophenyl 4,6-di-O-acetyl-alpha-D-mannopyranoside was similarly glycosylated with bromide 19 to give 4-nitrophenyl 4,6-di-O-acetyl-3-O- and -2-O-(2,3,4-tri- O-acetyl-6-deoxy-6-fluoro-alpha-D-mannopyranosyl)-alpha-D-mannopyranosid e. The various di- and tri-saccharides were O-deacetylated by Zemplén transesterification.

Carbohydrate Sequence↗
PubMed1989

Serum alpha(1----3)-L-fucosyltransferase, carcinoembryonic antigen, and sialyl Lewis X-i antigen levels in lung cancer.

Serum alpha(1----3)-L-fucosyltransferase activity was measured in 58 patients with lung cancer, 27 benign diseases, and in 100 healthy controls. The levels of enzyme activity were significantly higher in the sera of patients with cancer when compared to those in benign diseases and healthy controls. The elevation of the enzyme activity correlated with the clinical stages and to the size of the primary tumors. Follow-up studies with various stages showed that the enzyme activity was useful in tracking the clinical course of disease after surgery. To evaluate the usefulness of this enzyme as a diagnostic marker, carcinoembryonic antigen (CEA) and sialyl Lewis X-i antigen levels were also measured. The results indicate that alpha(1----3)-L-fucosyltransferase could be a more specific tumor marker than such tumor-associated antigens in lung cancer.

Carcinoembryonic Antigen↗
PubMed1989

Synthesis of some oligosaccharides containing the O-(2-acetamido-2-deoxy- beta-D-glucopyranosyl)-(1----2)-O-alpha-D-mannopyranosyl unit. Potential substrates for UDP-GlcNAc:alpha-D-mannopyranosyl-(1----6)-N-acetyl-beta-D- glucosaminyltransferase (GnT-V).

Four different oligosaccharides containing the 2-acetamido-2-deoxy-beta-D-glucopyranosyl-(1----2)-alpha-D-mannopyran osy l sequence as a terminal disaccharide unit were synthesized, namely: 4-nitrophenyl O-(2-acetamido-2-deoxy-beta-D- glucopyranosyl)-(1----2)-O-alpha-D-mannopyranosyl-(1----6)-beta-D- mannopyranoside (27), 4-nitrophenyl O-(2-acetamido-2-deoxy-beta-D-glucopyranosyl)-(1----2)-O-alpha-D-mann opy ranosyl - (1----6)-beta-D-glucopyranoside (29), allyl O-(2-acetamido-2-deoxy-beta-D-glucopyranosyl-(1----2)-alpha-D- mannopyranosyl-(1----6)-beta-D-glucopyranoside (31), and allyl O-(2-acetamido-2-deoxy-beta-D-glucopyranosyl)-(1----2)-O-alpha-D- mannopyranosyl-(1----6)-O-beta-D-glucopyranosyl-(1----4)-beta-D-gluco pyr anoside (33). A common glycosyl donor, namely, 2-O-(2-acetamido-3,4,6-tri-O-acetyl-2-deoxy-beta-D- glucopyranosyl)-3,4,6-tri-O-acetyl-alpha-D-mannopyranosyl bromide was employed for the synthesis of 27, 29, 31, and 33, the structures of which were all established by 13C-n.m.r. spectroscopy.

Carbohydrate Sequence↗
PubMed1989

Separation by liquid chromatography (under elevated pressure) of benzyl and nitrophenyl glycosides of oligosaccharides.

Liquid chromatography under elevated pressure (l.c.) was employed for the separation of some benzyl and nitrophenyl glycosides of a variety of mono-, di-, tri-, and tetra-saccharides. The separation was conducted on a Waters Carbohydrate Analysis column by use of a mixture of acetonitrile-water as the mobile phase. In general, monosaccharides emerged first from the column, followed sequentially by di-, tri-, and tetra-saccharides. It was observed that the pattern of substitution imparts a noticeable effect on the elution profiles of isomeric oligosaccharides. Also, substitution of a hydroxyl group with a methyl group, or its replacement with a fluorine atom, led to a substantial decrease in retention times of some oligosaccharides. Moreover, resolution was clearly enhanced, and retention times were congruently increased by decreasing the water content of the mobile phase.

Benzyl Compounds↗
PubMed1989

Synthetic mucin fragments. Benzyl O-beta-D-galactopyranosyl-(1----3)-O-(2-acetamido-2-deoxy-beta-D- glucopyranosyl)-(1----6)-2-acetamido-2-deoxy-alpha-D-galactopyranoside and O-alpha-L-fucopyranosyl-(1----3)-O-(2-acetamido-2-deoxy-beta-D- glucopyranosyl)-(1----6)-2-acetamido-2-deoxy-D-galactopyranose.

Benzyl 2-acetamido-6-O-(2-acetamido-2-deoxy-4,6-O-isopropylidene-beta-D- glucopyranosyl)-2-deoxy-3,4-O-isopropylidene-alpha-D-galactopyranoside (2) was obtained by acetalation of its parent disaccharide with 2,2-dimethoxypropane in hot N,N-dimethylformamide and in the presence of 4-toluenesulfonic acid. Glycosylation of 2 with 2,3,4,6-tetra-O-acetyl-alpha-D-galactopyranosyl bromide (catalyzed by mercuric cyanide), followed by removal of the protecting groups afforded the title trisaccharide 7. A second product was also isolated, which was identified as a derivative of 7 having a 2-cyanopropyl group. Glycosylation of diacetal 2 with 2,3,4-tri-O-benzyl-alpha-L-fucopyranosyl bromide (under catalysis by bromide ion), followed by systematic removal of the protecting groups furnished the title trisaccharide 13. The structures of both 7 and 13 were established by 13C-n.m.r. spectroscopy.

Magnetic Resonance Spectroscopy↗
PubMed1989

Tumor-related elevation of serum (alpha 1----3)-L-fucosyltransferase activity in gastric cancer.

(alpha 1----3)-L-Fucosyltransferase activity was measured in serum samples from 90 gastric cancer patients, 10 patients with benign diseases and 100 healthy controls. The enzyme activity was significantly elevated in the serum samples of patients with cancer compared to those from patients with benign diseases (P less than 0.01) and healthy controls (P less than 0.001). The elevation of the enzyme activity was found to correlate strongly with the clinical stage of disease. The sensitivity of (alpha 1----3)-L-fucosyltransferase was also demonstrated to be high in comparison with the tumor-associated antigens, such as carcinoembryonic antigen and sialylated Lewis X-i. Follow-up studies of (alpha 1----3)-L-fucosyltransferase in 11 cancer patients with disease at different stages showed that the enzyme activity could be useful for monitoring the post-surgical course of the disease. These results suggest that (alpha 1----3)-L-fucosyltransferase activity has a clinically important potential as a tumor marker in gastric cancer.

Biomarkers, Tumor↗
PubMed1988

Synthesis of uridine 5'-(2-acetamido-2,4-dideoxy-4-fluoro-alpha-D-galactopyranosyl) diphosphate and uridine 5'-(2-acetamido-2,6-dideoxy-6-fluoro-alpha-D-glucopyranosyl) diphosphate.

Benzyl 2-acetamido-3,6-di-O-benzyl-2-deoxy-alpha-D-glucopyranoside was converted into its 4-O-(methylsulfonyl) derivative (2) by treatment with methanesulfonyl chloride in pyridine. Displacement of the methylsulfonyloxy group of 2 with fluoride ion afforded benzyl 2-acetamido-3,6-di-O-benzyl-2,4-dideoxy-4-fluoro-alpha-D-galactopyranosi de, which on hydrogenolysis, followed by acetylation, furnished 2-acetamido-1,3,6-tri-O-acetyl-2,4-dideoxy-4-fluoro-D-galactopyranose. Treatment of this and of 2-acetamido-1,3,4-tri-O-acetyl-2,6-dideoxy-6-fluoro-D-glucopyranose with trimethylsilyl trifluoromethanesulfonate in 1,2-dichloroethane at approximately 50 degrees afforded the 4-deoxy-4-fluoro- or the 6-deoxy-6-fluoro-oxazolines (5) and (11), respectively. Reaction of 5 and 11 with dibenzyl phosphate in 1,2-dichloroethane produced the alpha-linked dibenzyl phosphate derivatives 6 and 12, respectively. Catalytic hydrogenation of 6 provided 2-acetamido-3,6-di-O-acetyl-2,4-dideoxy-4-fluoro-alpha-D-galactopyranosy l phosphate (7), and that of 12 gave 2-acetamido-3,4-di-O-acetyl-2,6-dideoxy-6-fluoro-alpha-D-glucopyranosyl phosphate (13). Coupling of 7 and 13 with uridine 5'-monophosphomorpholidate in dry pyridine at approximately 37 degrees, followed by O-deacetylation, furnished the title compounds, respectively, isolated and characterized as their respective dilithium salts.

Carbohydrate Conformation↗
PubMed1988

Synthesis of O-alpha-L-fucopyranosyl-(1----3)-O-beta-D-galactopyranosyl-(1----4)-2- acetamido-2-deoxy-D-glucopyranose (N-acetyl-3'-O-alpha-L-fucopyranosyllactosamine).

Methyl 2-O-benzyl-beta-D-galactopyranoside (6) was obtained in five, good yielding steps from methyl beta-D-galactopyranoside (1). Treatment of 1 with tert-butylchlorodiphenylsilane in N,N-dimethylformamide in the presence of imidazole afforded a 6-(tert-butyldiphenylsilyl) ether, which was converted into its 3,4-O-isopropylidene derivative (3). Benzylation of 3 with benzyl bromide-silver oxide in N,N-dimethylformamide, and subsequent cleavage of its acetal and ether groups then afforded 6. On similar benzylation, followed by the same sequence of deprotection, benzyl 2-acetamido-3,6-di-O-benzyl-4-O-[6-O-(tert-butyldiphenylsilyl)-3,4 -O- isopropylidene-beta-D-galactopyranosyl]-2-deoxy-alpha-D-glucopyranoside gave the 2-O-benzyl derivative (10). Compound 10 was converted into its 4,6-O-benzylidene acetal (11). Glycosylation (catalyzed by halide-ion) of 11 with 2,3,4-tri-O-benzyl-alpha-L-fucopyranosyl bromide afforded the fully protected trisaccharide derivative (13). Cleavage of the benzylidene and then the benzyl groups of 13 furnished the title trisaccharide (16). The structure of 16 was established by 13C-n.m.r. spectroscopy.

Benzyl Compounds↗