Biomedical subjects

A Malavé

Publications and source records attributed to A Malavé.

9 recordsLinked to original sources

PubMed2006

Detection of Rev peptides with impedance-sensors--comparison of device-geometries.

Two different impedance-sensor geometries have been compared for the detection of Rev peptides with a molecular weight of 2.4 kDa. Planar, two-dimensional interdigitated capacitor (IDC) sensors with electrode separations of 1.1 microm as well as three-dimensional nanogap-sensors with an electrode separation of 75 nm have been used. Both sensors have been operated at a fixed frequency of 980 MHz. We discuss the specific interaction of the Rev peptide to an immobilized RNA anti-Rev aptamer (9.2 kDa) for peptide concentrations in the range of 100 nM-2 microM. For the IDC sensor, only peptide concentrations above 500 nM gave detectable signals. For the nanogap sensor, the binding process was clearly visible for all concentrations applied. The higher sensitivity of the nanogap compared to the IDC is ascribed to the improved surface-to-volume ratio.

Biosensing Techniques↗

PubMed2001

Protective effect of berberine on cyclophosphamide-induced haemorrhagic cystitis in rats.

The urotoxicity of cyclophosphamide and the protective effect of the herb berberine were investigated in this study. Administration of 150 mg/kg cyclophosphamide intraperitoneally caused a serious haemorrhagic cystitis in rats after 12 hr, including bladder oedema, haemorrhage, and dramatic elevation of nitric oxide metabolites (nitrite+nitrate) in urine and in plasma. To explore whether cyclophosphamide-induced cystitis could be prevented by berberine, rats were pretreated with a single dose or two doses of berberine at 50, 100, or 200 mg/kg intraperitoneally then challenged with cyclophosphamide (150 mg/kg, intraperitoneally). The results indicated that pretreatment of rats with berberine could reduce cyclophosphamide-induced cystitis in a dose-dependent manner. Furthermore, we found that two doses of berberine showed greater protection against cyclophosphamide urotoxicity than when given a single dose. In addition, our data shows that a single dose of 200 mg/kg berberine, or two doses of 100, and 200 mg/kg berberine could completely block cyclophosphamide-induced bladder oedema and haemorrhage, as well as nitric oxide metabolites increase in rat urine and plasma. In conclusion, our findings suggest that berberine could be a potential effective drug in the treatment of cyclophosphamide-induced cystitis, and provides us with the bright hope in the prevention and treatment of cyclophosphamide urotoxicity.

Animals↗

PubMed2000

Expression of vascular endothelial growth factor mRNA in GI-101A and HL-60 cell lines.

Vascular endothelial growth factor (VEGF) is a potent angiogenic factor that has a strong association with growth and metastasis of various cancers. We analyzed the expression of VEGF mRNA levels in human breast-tumor derived GI-101A cells and in human promyelocytic leukemia derived HL-60 cells using RT-PCR technique. During our RT-PCR analysis we detected the expression of three splice variants of VEGF mRNA at 400, 520 and, 650 bp lengths, which were amplified by a single set of VEGF specific forward and reverse primers. The three RT-PCR products detected by us in these cells correspond to the mRNA splice variants coding for the three isoforms of VEGF respectively, VEGF(121), VEGF(165), and VEGF(189). Treatment of GI-101A and HL-60 cells with phorbol 12, 13-dibutyrate (PDB) or diethylstilbestrol (DES) resulted in a significant increase of VEGF mRNA levels in a dose dependent manner. Both treatments increased the levels of all three splice variants of VEGF mRNA and a maximum increase was detected with 10 microM concentrations of PDB or DES treatments after 2 h. Interestingly, both PDB and DES mediated stimulation of VEGF mRNA expression was completely blocked by the PKC inhibitor chelerythrine. Quantitation of VEGF levels by ELISA technique confirmed that changes seen in mRNA levels following different treatments altered the release of VEGF. Our results suggest that PDB and DES mediated effects on VEGF expression in GI-101A and HL-60 cells occur at the gene transcription level.

Alkaloids↗

PubMed1999

Expression of mdm-2 oncoprotein in the primary and metastatic sites of mammary tumor (GI-101) implanted athymic nude mice.

The expression of mdm-2 oncoprotein (p90) was determined in a human breast tumor xenograft line (GI-101) that was derived from a 57 year old female cancer patient with recurrent, infiltrating ductal adenocarcinoma (Stage IIIa, T3N2MX). Immunoprecipitation coupled western blot analysis of the primary tumors that have been obtained from xenograft implanted athymic nude mice, using mdm-2 (Ab-1) mouse monoclonal antibody, primarily revealed high level expression of a 90 kD full length mdm-2 protein. In the GI-101 tumor the level of full length mdm-2 (p90) protein expression increased with the increase in the size of the tumor (100 to 2,000 mm(3)) and a maximum expression was detected in 2,000 mm(3) size tumors. In addition to the expression in the primary site, a significantly high level expression of mdm-2 protein (p90) was detected in the lung and liver tissues also, which are the known metastatic sites for GI-101 xenograft tumors. However, the level of mdm-2 protein expression was undetectable in the lung and liver tissues obtained from control mice. A cell line (GI-101A) derived from the GI-101 xenograft tumor also showed a high level expression of mdm-2 protein after several generations of cell passage. When the GI-101A cells were treated with DES (Diethylstilbestrol) the mdm-2 protein expression increased after 10 min treatment and reached a peak level at 40 min. Interestingly, DES (10 and 20 microM) treatment increased the total cell number also after 96 hr treatment compared to the non-treated cells. It appears that mdm-2 (p90) may have a significant role in supporting the tumor cell growth as well as the metastatic process of the GI-101A cells.

Animals↗

PubMed1993

Physicochemical characterization of acetaminophen-ethylcellulose solid dispersion.

In this study, ethylcellulose was evaluated as a carrier for the preparation of sustained release of acetaminophen via solid dispersion technique. Physical mixture at the same level of acetaminophen and ethylcellulose was prepared. Differential scanning calorimetry and scanning electron microscope were used to characterize the physical properties of the various systems and to determine if there is possible interaction between acetaminophen and ethylcellulose.

Acetaminophen↗

PubMed1992

Ethylcellulose as a carrier for controlled-release acetaminophen tablets.

In this study ethylcellulose was evaluated as a carrier for preparation of prolonged release acetaminophen tablets. Solid dispersions containing three levels of ethylcellulose and acetaminophen (1:3; 1:1; 3:1) were prepared by the solvent method. Also physical mixtures at the same level of ethylcellulose and acetaminophen were prepared. Systems composed of solid dispersion or physical mixture containing the equivalent weight of 50 mg acetaminophen, Emcompress as diluent and 1% magnesium stearate as lubricant were compressed into tablets and tested for dissolution. The dissolution data showed that the drug release decreased as the level of ethylcellulose increased in the solid dispersion formulations. The drug release from tablets prepared with solid dispersion followed the diffusion controlled model for inert porous matrix, while the drug release from tablets prepared with physical mixture followed the first-order kinetic model.

Acetaminophen↗

PubMed1986

Lack of tolerance of morphine-induced spasm of guinea pig sphincter of Oddi.

To determine whether guinea pigs chronically exposed to morphine would develop tolerance to the morphine-induced contraction of the sphincter of Oddi (SO), adult male guinea pigs were implanted with morphine pellets (100 mg morphine). The effect of increasing IV doses of morphine on the SO was assessed by determining the duration of which saline perfusate stopped flowing into the duodenum of morphine-treated guinea pigs (MTGP) vs nonimplanted animals (non-MTGP). Isolated bovine and guinea pigs SO were also challenged with morphine. In the in vivo experiments the spasmogenic response of the SO from MTGP to morphine was greater than that of SO from non-MTGP. However, morphine had no effect on isolated SO. These results indicate that chronic morphine exposure does not result in tolerance of the SO to the spasmogenic effects of morphine. On the contrary, chronic morphine even sensitized the SO to morphine, in addition, the in vitro data indicated that morphine does not act directly on the smooth muscle of SO to cause its spasmogenic effect.

Ampulla of Vater↗

PubMed1983

Block by phencyclidine of acetylcholine and barium induced adrenal catecholamine secretion.

Activation of the sympathetic system by phencyclidine (PCP) should result in catecholamine release from the adrenals. However, adrenalectomy does not reduce PCP-induced hypertension. In an attempt to rectify this inconsistency, the direct effects of PCP on the bovine adrenal medulla were examined. At (3 X 10(-6) M), PCP reduced the acetylcholine-(ACh)-induced catecholamine release by 50%. Surprisingly, barium-induced secretion of catecholamines was also reduced by PCP. ACh-induced catecholamine release was not altered by 10(-3)M 4-aminopyridine (4 AP), the potassium channel blocker. Thus, calcium antagonist actions of PCP and consequent block of catecholamine secretion from adrenal medulla may explain the lack of effect of adrenalectomy on PCP-induced hypertension. Possible contributions of calcium and/or potassium channel blockade to other manifestations of PCP overdosage are discussed.

4-Aminopyridine↗

PubMed1983

Local anesthetic activity and disopyramide toxicity.

In the isolated frog sciatic nerve preparation, IC50 concentrations for nerve block were 0.34 +/- 0.9 mM for lidocaine (LIDO), 0.62 +/- 0.11 mM for procaine, 11.9 +/- 6.1 mM for disopyramide (DIP), and 52.8 +/- 24 mM for MIP (the mono-demethylated metabolite of DIP). In contrast to the LIDO block, DIP-induced nerve block was irreversible. DIP-induced depression of the electrically stimulated rat ventricular strip was completely reversed by washing the drug-free Tyrode's solution. In mice receiving 250 mg/kg DIP, neither convulsions nor death could be prevented by diazepam or other anticonvulsants. These results suggest that DIP has a very weak local anesthetic action which does not contribute significantly to disopyramide toxicity.

Action Potentials↗