Composición bromatológica de la carne de conejos suplementados con mataratón y cachaza de palma aceitera / Bromatological composition of rabbit meat supplemented with mataraton and palm-press fiber

Objetivo. Evaluar comparativamente el efecto de la suplementación del alimento balanceado comercial (ABC) con follaje de mataratón (Gliricidia sepium) y cachaza de palma aceitera (Elaeis guineensis) en la composición bromatológica de la carne de conejo. Materiales y métodos. Las muestras de carne estudiadas en el presente trabajo, provienen de una investigación previa con un diseño experimental de bloques al azar con tres tratamientos (dietas) y tres repeticiones (bloques) con muestreo de tres réplicas por repetición, donde se utilizaron 27 conejos machos mestizos durante el período postdestete divididos en tres tratamientos: uno control (T0), alimentados sólo con ABC, y dos suplementados con mataratón y cachaza de palma aceitera en proporciones de 30 y 10% (T1), y 10 y 30% (T2), respectivamente, a manera de comparar el efecto de las dietas en el valor nutricional. Resultados. Las muestras de carne provenientes de los diferentes animales en tratamiento, se evaluaron encontrando que la suplementación no afectó significativamente la composición bromatológica (p>0.05) para el contenido de humedad (70.77 a 72.42%), proteínas (19.08 a 20.34%), cenizas (1.53 a 1.68%) y lípidos (6.48 a 7.23%); indicando que indistintamente de la dieta empleada, suplementando el ABC con mataratón/fibra de palma o no, las carnes de conejo obtenidas son nutricionalmente idénticas como alimento. Conclusiones. Con base en los resultados, se sugiere que el follaje de mataratón y la fibra de palma aceitera podrían constituir una alternativa como recursos agronómicos tropicales en la producción de carne de conejo para el consumo humano.

Objective. Comparatively evaluate the effect of supplementing commercial balanced feed (BCF) withmataratón (Gliricidia sepium) foliage and palm-press fiber (Elaeis guineensis) on the bromatologiccomposition of rabbit meat. Materials and methods. The meat samples studied came from a previousresearch which used a randomized block design with three treatments (diets) and three replications(blocks) with three replays by replication sampling where 27 hybrid male rabbits during their postweaning growth period, were used in three treatments: control (T0), animals supplied only with BCF,and two supplemented treatments with mataratón foliage and palm-press fiber at 30 and 10% (T1), and10 and 30% (T2) proportions, respectively, in order to compare the nutritional value of the differentdiets. Results. The evaluation of meat samples from different animals in the treatments showed thatthe bromatological composition of the meat was not significantly affected by the supplementation(p>0.05) for humidity (70.77 to 72.42%), protein (19.08 to 20.34%), ash (1.53 to 1.68%), andlipid (6.48 to 7.23%) contents; indicating that, regardless of the diet used, supplementing CBF withmataraton/palm-press fiber or not, the rabbit meats obtained are nutritionally identical. Conclusions.Based on the results, it is suggested that the foliage of mataraton and palm-press fiber may be analternative, as a tropical agronomic resource, in the rabbit meat production for human consumption.

Posttraumatic growth and social support in individuals with infertility.

BACKGROUND: While research on the psychological experiences of infertility has focused almost exclusively on the negative aspects, clinical experience with individuals and couples facing infertility has demonstrated that personal gain can also arise from the struggle involved. This study examined whether individuals who struggle with infertility report posttraumatic growth (PTG), and if perceived availability of and satisfaction with social support are associated with such growth. Other correlates of PTG are reported as well. METHODS: Using a cross-sectional design, a convenience sample of 121 individuals with infertility completed a background questionnaire, the Posttraumatic Growth Inventory and the Social Support Questionnaire. RESULTS: While individuals reported moderate PTG, moderate availability of, and high satisfaction with social support, there was no significant association between the variables. Infertility-related variables emerged as central to explaining PTG with those with non-female related diagnoses and unexplained diagnoses demonstrating lower PTG than others (t = 2.96, t = 3.6, respectively, P < or = 0.05). Additionally, live birth deliveries was positively associated with PTG (r(2) = 0.22, P < or = 0.02), and those who engaged in clergy counseling had higher PTG than those who did not (t = 2.34, P < or = 0.02). Determinants were unexplained infertility (lower PTG) and number of live birth deliveries (higher PTG). CONCLUSIONS: In spite of limitations related to the convenience sampling, correlational design and subjective self-report nature of the data, findings suggest that individuals who suffer from infertility can experience personal growth. Further research will help identify correlates and provide guidance for mental health practitioners on counseling infertility patients to promote growth.

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.

Comparison of antibody and aptamer receptors for the specific detection of thrombin with a nanometer gap-sized impedance biosensor.

Nanogap-impedance biosensors with electrode separations of 75 nm have been fabricated by means of standard optical lithography and a sacrificial layer technique. Due to a large surface-to-volume ratio and high sensitivity, these sensors are superior compared to open interdigitated electrode structures. As a model, the blood coagulation factor thrombin was detected. As specific receptors, either an antibody or a RNA-aptamer have been used. The microwave frequency impedance measurements showed that both ligands were equally suitable for the specific detection of thrombin.

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.

Nitric oxide synthases and cyclophosphamide-induced cystitis in rats.

The role of inducible (iNOS) and neuronal nitric oxide (nNOS) synthases and of tachykinin NK1 receptors on the pathogenesis of cyclophosphamide (CYP)-induced cystitis was investigated, in rats. CYP-induced cystitis was characterized by large increases in bladder-protein plasma extravasation (PPE), increases in the urinary excretion of nitric oxide (NO) metabolites and histological evidences of urothelial damage, edema, extensive white blood cell infiltrates and vascular congestion of the bladder. The specific iNOS inhibitor, S-methylthiourea (MITU), produced marked inhibition (>90%) of CYP-induced increases in PPE associated with amelioration of tissue inflammatory changes. Treatment with 7-nitroindazole (7-NI; 20, 40 and 80 mg/kg), a selective nNOS inhibitor, did not significantly reduce CYP-induced increases in PPE and failed to produce histological improvement. In addition, treatment with MITU, but not with 7-NI, inhibited the increases in the urinary excretion of NO metabolites induced by CYP treatment. WIN 51,708 (17-beta-hydroxy-17-alpha-ethynyl-androstano[3,2-b]pyrimido[1,2-a]benzimidazole; WIN), a selective NK1-receptor antagonist, reduced the increases in EPP and ameliorated the inflammatory changes in the bladder induced by CYP. However, the maximal degree of protection achieved with WIN was significantly less than that produced by MITU. Combined treatment with the iNOS inhibitor and the NK1 antagonist produced no greater effect than that produced by the iNOS inhibitor alone. Our results suggest that NO plays a fundamental role in the production of the cystitis associated with CYP treatment. The iNOS, and not nNOS, seems responsible for the inflammatory changes. Part of the increases in NO may due to activation of NK1 receptors by neuropeptides such as substance P possibly released from primary afferent fibers.

Expression of inducible nitric oxide synthase in primary culture of rat bladder smooth muscle cells by plasma from cyclophosphamide-treated rats.

Intraperitoneal administration of cyclophosphamide (50-150 mg/kg) for 6 or 12 h induced edema and hemorrhagic changes in rat bladder, which were both dose and time-dependent. Pretreatment with nitric oxide synthase (NOS) inhibitors N(G)-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg) or with s-methylisothiourea (40 mg/kg) ameliorated the cyclophosphamide-induced cystitis. Cyclophosphamide administration also produced increases in NO-metabolite levels (nitrate+nitrite) in the urine and plasma of rats. Greater increases in NO metabolites were observed with 150 than with 50 mg/kg of cyclophosphamide, and at 12 than at 6 h after cyclophosphamide injection. Pretreatment with L-NAME and s-methylisothiourea significantly reduced cyclophosphamide-induced increases in urine and plasma NO-metabolite levels. To explore the mechanism by which cyclophosphamide increases the expression of inducible NOS (iNOS), primary cultures of rat bladder smooth muscle were developed. Exposure to tumor necrosis factor alpha (TNF-alpha) plus interferon gamma, produced a marked increase in the expression of iNOS and in NO production in the culture medium. However, exposure to cyclophosphamide or to its metabolite acrolein (10(-6)-10(-4) M for 24 h) did not increase iNOS or NO-metabolite levels. On the other hand, incubation of primary cell cultures with plasma from rats treated with cyclophosphamide (150 mg/kg, 12 h) produced a marked increase in iNOS expression and NO production. Taken together, our results indicate that NO plays an important role in the pathogenesis of cyclophosphamide-induced cystitis in rats, and some factors may be released in cyclophosphamide-treated rat plasma which stimulate iNOS expression in primary culture of rat bladder smooth muscle cells.

Liquid chromatographic method with electrochemical detection for determination of cisapride in serum.

A sensitive liquid chromatographic (LC) method using electrochemical detection was developed for the identification and quantitation of cisapride in serum. The serum samples were deproteinized by a simple acetonitrile precipitation technique followed by n-hexane extraction. Cisapride in the deproteinized serum was separated by an isocratic elution with an ODS Hypersil LC column (150 x 4.6 mm) using a mobile phase consisting of 0.05M Na2HPO4-acetonitrile (60 + 40), pH 8.4. Cisapride eluted from the column was detected by a Coulochem II electrochemical detector. The precision of this assay method was determined by intra- and inter-day analyses of cisapride-free fetal bovine serum samples that were spiked with 25, 50, and 100 ng/mL cisapride. For the intra-day assay, recoveries were 94.3 +/- 1.4, 90.1 +/- 2.9, and 103.2 +/- 9.2%, respectively. This electrochemical detection LC method could be very useful in monitoring plasma levels of cisapride.

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.

P38 MAPK, but not p42/p44 MAPK mediated inducible nitric oxide synthase expression in C6 glioma cells.

Recently mitogen-activated protein kinase (MAPK) has been reported to play an important role in phosphorylation cascades governing cell growth and protein expression in numerous cell types. In order to explore the signaling mechanism by which inducible nitric oxide synthase (iNOS) is regulated in C6 glioma cells, we investigated the role of MAPK in iNOS expression by using the specific MAPK inhibitors. First the induction of nitric oxide by lipopolysaccharide (LPS), tumor necrosis factor alpha (TNFalpha), interferon gamma (IFNgamma), alone or their combination, was studied in C6 glioma cells. Administration of LPS, TNFalpha, or IFNgamma alone had no detectable stimulatory effect on the production of nitric oxide (NO). However, combination of the three factors elicited a significant elevation of NO level in C6 cell culture medium. Subsequently pretreatment of C6 cells with a specific inhibitor of p38 MAPK, SB202190, resulted in a dose-dependent inhibition of NO production and iNOS expression, but PD98059, an inhibitor of p42/p44 MAPK activation, had no effect. These data suggest that p38 MAPK mediates iNOS expression in C6 glioma cells, but p42/p44 MAPK is not involved in this process.

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.

Reactive oxygen species generated by cyanide mediate toxicity in rat pheochromocytoma cells.

Peroxide formation has been implicated in impairment of motor function by cyanide which occurs in both animals and man. The present study employs the neuronal model, rat pheochromocytoma (PC12) cells to evaluate peroxidation as a toxic mechanism of cyanide. Confocal imaging shows that peroxides form within a few seconds in cell cytoplasm after cyanide exposure and continue to accumulate over a period of several minutes. Peroxide generation by cyanide is decreased to about 50% by phospholipase A2 inhibitors indicating involvement of arachidonic acid in the oxidative process. Also antioxidant defense enzymes (CuZn superoxide dismutase and especially catalase) in PC12 cells are inhibited by cyanide. It appears that peroxide accumulation after cyanide treatment involves both inhibition of breakdown and increased production. Furthermore, both peroxide accumulation and cell death induced by cyanide in PC12 cells are blocked by an antioxidant (ascorbate). These data support the hypothesis that the cytotoxic action of cyanide is related in part to an oxidative process.

High-performance liquid chromatography using electrochemical detection for the determination of prazosin in biological samples.

For the quantitation of prazosin a sensitive high-performance liquid chromatographic (HPLC) method was developed. This HPLC analysis method uses an electrochemical detection technique for the identification and quantitation of prazosin. In this assay the serum samples were deproteinized by using a simple acetonitrile precipitation technique that was followed by n-hexane extraction. Prazosin in the deproteinized serum sample was separated by an isocratic elution with an ODS Hypersil HPLC column (150 x 4.6 mm) using a mobile phase consisting of 0.05 M Na2HPO4-acetonitrile (60:40), pH 8.4. Prazosin that was eluted from the column was detected using a Coulochem II electrochemical detector. The precision of this assay method was assessed by performing inter- and intra-assay analyses by spiking prazosin free fetal bovine serum samples with 20 and 40 ng/ml concentrations of prazosin. In the intra-assay the recovery was 95.40 +/- 4.82% and 97.80 +/- 3.40%, respectively, for 20 and 40 ng/ml concentrations of prazosin that were used to spike the serum samples. This electrochemical detection HPLC assay method could be very useful in monitoring plasma levels of prazosin.

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.

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

Effects of chronic morphine on biliary tract responses to cholecystokinin-octapeptide in female guinea pigs.

Acute and chronic opiates impairs the emptying of bile from the gallbladder of male guinea pigs. In view of the higher incidence of gallstone attacks in women, the aim of this study was to determine if this impairment would extend to female guinea pigs. Implantation of morphine pellets (400mg) in female guinea pigs did depress CCK-induced emptying of gallbladder bile. Likewise, gallbladder muscle strips isolated from the morphine treated animals showed depressed responses to CCK. The morphine treatment also antagonized CCK-induced cessation of bile flow present in female guinea pigs. In addition, the morphine treatment blocked both CCK-induced phasic contractions of the isolated isolated Sphincter of Oddi and the secondary cessation of bile flow observed following iv CCK. Thus this study demonstrates that opiate antagonism of CCK does extend to the biliary tract of female guinea pigs, and suggests that resultant biliary stasis could facilitate gallstone formation.

Enhanced lithogenicity of bile following chronic morphine administration to female guinea pigs.

Acute and chronic opiate exposure impairs the emptying of bile from the gallbladder. In this study, the effects of a 4-day morphine regimen on bile composition were examined. Bile acids and phospholipids concentration of bile obtained from the gallbladder of female morphine-treated (MT) guinea pigs were reduced by 60% and 80% respectively, resulting in a highly lithogenic bile. Concentrations of bile acids and phospholipids of spontaneously secreted bile were not reduced. However, the lithogenicity of the hepatic bile in MT animals was still increased because of a 10 fold elevation in cholesterol concentration. Ratios of solute concentrations of stored and freshly secreted bile indicated that morphine also impaired the ability of the gallbladder to concentrate bile. Thus chronic morphine exposure increased bile lithogenicity by increasing cholesterol content and also by diluting the bile in the gallbladder. These alterations and the previously described biliary stasis indicates that chronic opiate and endogenous opioid exposure should facilitate gallstone formation.

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.

Effects of chronic morphine on biliary tract responses to cholecystokinin-octapeptide in male guinea pigs.

Opioid peptides share the spasmogenic action of acutely administered morphine on the sphincter of Oddi. In this study, gallbladder function was assessed following chronic opioid administration. Implantation of morphine pellets (400 mg) in male guinea pigs depressed cholecystokinin-octapeptide(CCK)-induced emptying of gallbladder bile (monitored via a duodenal cannula). Gallbladder muscle strips, isolated from the morphine treated animals, showed depressed contractile responses to CCK. This antagonism was non-specific and indirectly mediated, as ACh contractions were also depressed, whereas CCK-induced contractions of gallbladder strips from untreated animals were unaffected by direct exposure to morphine (3 x 10(-6)M). The depression of CCK stimulation of bile flow by chronic morphine administration in male guinea pigs suggests that chronic exposure to opioids can impede gallbladder emptying.

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.