Biomedical subjects

Antonio Osuna

Publications and source records attributed to Antonio Osuna.

31 records · Page 2Linked to original sources

PubMed2003

Development of a dipstick dye immunoassay for diagnosing hydatidosis.

We have developed a kit to diagnose hydatidosis, based on the detection of specific antibodies. This disease, caused by larvae of the cestode Echinococcus granulosus, is a zoonosis commonly found throughout the world. The diagnostic kit discriminates between positive and negative cases in a way that is easily interpreted, i.e., positive cases form a colored band on an inert substrate. The results show test sensitivity to be some 94.87% and specificity 85.71%, which is comparable to those of the ELISA technique. The high sensitivity and specificity of this test affords the great advantage of speed in diagnosing this parasitosis. No other equipment or procedure is required.

Animals↗

PubMed2003

Effects of omapatrilat on blood pressure and renal injury in L-NAME and L-NAME plus DOCA-treated rats.

BACKGROUND: This study investigates the effects of chronic administration of omapatrilat (OMA) on blood pressure (BP), renal injury, and other variables in N(omega)-nitro-L-arginine methyl ester (L-NAME) hypertension and in the low-renin model produced by the simultaneous administration of L-NAME and deoxycorticosterone acetate (DOCA). METHODS: The control, DOCA, L-NAME, L-NAME + DOCA, L-NAME + OMA, and L-NAME + DOCA + OMA groups were used. Tail systolic BP was measured twice a week. After 4 weeks of treatment, mean arterial pressure (MAP), and metabolic, morphologic, and renal variables were measured. RESULTS: The final values of MAP were 109 +/- 5.1 mm Hg for the control group, 113 +/- 3.0 mm Hg for DOCA, 175 +/- 3.7 mm Hg for L-NAME, 193 +/- 3.8 mm Hg for L-NAME + DOCA, 117 +/- 3.9 mm Hg for L-NAME + OMA, and 158 +/- 3.0 mm Hg for L-NAME + DOCA + OMA. The rats treated with L-NAME showed mild and scarce renal lesions, which were prevented by OMA treatment and the L-NAME + DOCA group showed proteinuria and hyaline arteriopathy, which were markedly attenuated in the L-NAME + DOCA + OMA group. Plasma urea and creatinine were significantly increased in the L-NAME + DOCA group, whereas these variables were not significantly greater in the L-NAME + DOCA + OMA group versus controls. The L-NAME + DOCA group showed relative renal and cardiac hypertrophy that was not observed in the L-NAME + DOCA + OMA group. CONCLUSIONS: The simultaneous blockade of neutral endopeptidase (NEP) and angiotensin converting enzyme (ACE) completely prevents L-NAME hypertension. Our results also show that OMA attenuates the increased BP and the renal injury in L-NAME hypertensive rats treated with DOCA. Assuming that this is a low-renin model of hypertension, the protective effect of OMA may be due to an increase in vasodilator peptides produced by both ACE and NEP inhibition.

Animals↗

PubMed2003

Calreticulin-melatonin. An unexpected relationship.

Increasing evidence suggests that melatonin can exert some effect at nuclear level. Previous experiments using binding techniques clearly showed the existence of specific melatonin binding sites in cell nucleus of rat liver. To further identify these sites, nuclear extracts from rat hepatocytes were treated with different percentages of ammonium sulfate and purified by affinity chromatography. Subsequent ligand blot analysis shows the presence of two polypeptides of approximately 60 and approximately 74 kDa that bind specifically to melatonin. N-Terminal sequence analysis showed that the 60 kDa protein shares a high homology with rat calreticulin, whereas the 74 kDa protein shows no homology with any known protein. The binding of melatonin to calreticulin was further characterized incubating 2-[125I]melatonin with recombinant calreticulin. Binding kinetics show a Kd = 1.08 +/- 0.2 nm and Bmax = 290 +/- 34 fmol.mg protein-1, compatible with other binding sites of melatonin in the cell. The presence of calreticulin was further identified by Western blot analysis, and the lack of endoplasmic reticulum contamination in our material was assessed by Western blot and immunostaining with anti-calnexin Ig. The results suggest that calreticulin may represent a new class of high-affinity melatonin binding sites involved in some functions of the indoleamine including genomic regulation.

Amino Acid Sequence↗

PubMed2003

Localized mucosal leishmaniasis due to Leishmania (Leishmania) infantum: clinical and microbiologic findings in 31 patients.

The clinical and microbiologic characteristics of 31 patients with mucosal leishmaniasis due to Leishmania (Leishmania) infantum are described. Twenty-eight (90%) patients were male. Mean age at presentation was 48 +/- 14 years. Thirteen (42%) patients had no underlying disease, while 18 (58%) patients had several other medical conditions. Fifteen (48%) patients were immunocompromised, 7 patients were infected with human immunodeficiency virus (HIV), and 3 were graft recipients. The primary location of lesions was the larynx in 11 (35%) patients, oral mucosa in 10 (32%) patients, and the nose in 5 (16%) patients. Mucosal lesions were painless in all patients but 2 and consisted of whitish, red, or violaceous nodular swelling or tumorlike masses. Ulceration was reported in 6 patients. Pathologically, the lesions showed a chronic inflammatory infiltrate. Granuloma may be seen. The localization of the lesions determined the symptomatology of the disease. Symptoms included hoarseness, difficulty swallowing, and nasal obstruction. The disease presentation was usually protracted, with a mean time from the onset of symptoms to diagnosis of 13 months (range, 3 wk-4.5 yr), and the clinical diagnosis was usually mistaken for neoplasia of the upper aerodigestive tract. No laboratory abnormalities were found in these patients due to the localized disease, apart from those attributed to underlying diseases. Parasites were easily identified in smears or sections by Giemsa stain or hematoxylin-eosin stain. Leishmania was grown in culture in 12 (60%) patients; culture was negative in 8 (40%) patients. Leishmania (Leishmania) infantum was identified in only 9 instances. The following zymodemes were reported: MON-1 (2 patients), MON-24 (2 patients), MON-27 (1 patient), and MON-34 (1 patient). Serologic test results were known in 25 patients. Serology was usually positive at low titer; 6 (24%) patients had negative serologic test results. Twenty patients were treated with antimonial compounds for between 3 and 36 days. Three patients were given drugs other than antimonial drugs. Five patients were treated only locally, by surgery (3 patients) or topical medical therapy. One patient received no therapy, and treatment was not reported in 2 cases. Patients were cured in 25 (89%) cases, and sequelae were uncommon (14%). Relapse was detected in 2 individuals and 1 patient developed visceral leishmaniasis after treatment. Two HIV-coinfected patients died of causes unrelated to leishmaniasis. The results of the present report stress the clinical importance of searching for the presence of Leishmania in patients with suspected neoplasia of the upper respiratory tract if they have visited or resided in zones endemic for Leishmania (Leishmania) infantum. The treatment of choice for these patients is not established yet, but most patients respond to antimonial compounds given for 28 days or less.

Adult↗

PubMed2003

Chronic blockade of neuronal nitric oxide synthase does not affect long-term control of blood pressure in normal, saline-drinking or deoxycorticosterone-treated rats.

It has been reported that long-term selective inhibition of neuronal nitric oxide synthase (nNOS) produces elevated blood pressure (BP) in normal rats. The present study was designed to analyse the possible influences of the sodium-retaining hormone deoxycorticosterone acetate (DOCA) and of an increased sodium intake on BP effects induced by the chronic blockade of nNOS with 7-nitroindazole (7NI). Two experiments were performed using 7NI at a dose of either 10 mg x kg(-1) x day(-1) (experiment 1) or 30 mg x kg(-1) x day(-1) (experiment 2). The following groups were used in both experiments: control rats, and rats that received either 1 % saline drinking water (Salt), deoxycorticosterone acetate (DOCA), 7NI, 7NI plus 1 % saline (7NI + Salt) or 7NI plus DOCA (7NI + DOCA). The tail systolic BP (SBP) was measured in all rats once a week. At the end of the experimental period, the mean arterial pressure (MAP) and metabolic, morphological and renal variables were measured. There were no significant differences in the tail SBP, final MAP or glomerular filtration rate between the experimental groups and the control group. In both experiments, the plasma renin activity (PRA) was significantly inhibited in the Salt groups and suppressed in the DOCA groups. The PRA significantly increased in the 7NI groups, whereas the 7NI + Salt and 7NI + DOCA groups showed a significant inhibition in PRA, especially compared to the 7NI groups in the two experiments. We conclude that chronic nNOS blockade is unable to increase BP in normal, saline-drinking or DOCA-treated rats. Furthermore, the nNOS blockade does not interfere with the counterbalance between renin and an increased sodium intake or retention.

Angiotensin I↗

PubMed2002

Role of endothelium-derived relaxing factors in adrenomedullin-induced vasodilation in the rat kidney.

The present study aimed to evaluate the contributions of endothelium-derived hyperpolarizing factor (EDHF), the nitric oxide (NO)-cGMP pathway, and prostaglandins to adrenomedullin-induced vasodilation in isolated rat kidney. Inhibition of the NO-cGMP pathway with N(omega)-nitro-L-arginine methyl ester (L-NAME) or 1H-[1,2,4]oxadiazolo-[4,3a]quinoxalin-1-one (ODQ) reduced the maximal vasodilator response to adrenomedullin by approximately 50%. Pretreatment of the vessels with the potassium channel inhibitor, tetraethylammonium or increased extracellular K(+), also decreased the maximal response to adrenomedullin by approximately 50%. The simultaneous administration of blockers of both endothelium-derived relaxing factors had a combined effect that almost suppressed adrenomedullin-induced vasodilation. The administration of indomethacin did not modify the renal response to adrenomedullin. Our results suggest that the vasodilator response to adrenomedullin in the isolated perfused kidney of rats is mediated by EDHF and NO to a similar extent. Our data also provide evidence that prostaglandins play no role in the vasodilator response to adrenomedullin in the renal vasculature.

Acetylcholine↗

PubMed2002

Pre- and postsurgical detection of IgG, IgM, and IgA specific to hydatidosis by ELISA with purified antigen enriched with the 5/B antigen complex.

An enzyme-linked immunoassay (ELISA) using purified 5/B Echinococcus enriched antigen was used to follow IgG, IgM, and IgA antibody levels pre- and posttreatment or surgical removal of hydatid cysts. The sensitivity was 97%, 37.5%, and 54.5%, respectively, and the specificity was 95.7%, 100%, and 98.9%, respectively. All isotypes could be detected 3 years after surgical removal of cysts in patients showing no remaining cyst evidence. This was especially true for IgG, which persisted in 85.2% of the patients. The data indicate that antigen purification improves specificity without affecting sensitivity, although this new antigen offers no advantages in the postsurgical monitoring of the patients.

Adolescent↗

PubMed2002

Dietary fiber down-regulates colonic tumor necrosis factor alpha and nitric oxide production in trinitrobenzenesulfonic acid-induced colitic rats.

Previous studies have revealed the beneficial effects exerted by dietary fiber in human inflammatory bowel disease, which were associated with an increased production of SCFA in distal colon. The aim of the present study was to elucidate the probable mechanisms involved in the beneficial effects of a fiber-supplemented diet (5% Plantago ovata seeds) in the trinitrobenzenesulfonic acid (TNBS) model of rat colitis, with special attention to its effects on the production of some of the mediators involved in the inflammatory response, such as tumor necrosis factor alpha (TNFalpha) and nitric oxide (NO). Rats were fed the fiber-supplemented diet for 2 wk before TNBS colitis induction and thereafter until colonic evaluation 1 wk later. The results obtained showed that dietary fiber supplementation facilitated recovery from intestinal insult as evidenced both histologically, by a preservation of intestinal cytoarchitecture, and biochemically, by a significant reduction in colonic myeloperoxidase activity and by restoration of colonic glutathione levels. This intestinal anti-inflammatory effect was associated with lower TNFalpha levels and lower NO synthase activity in the inflamed colon, showing significant differences when compared with nontreated colitic rats. Moreover, the intestinal contents from fiber-treated colitic rats showed a significantly higher production of SCFA, mainly butyrate and propionate. We conclude that the increased production of these SCFA may contribute to recovery of damaged colonic mucosa because they constitute substrates for the colonocyte and, additionally, that they can inhibit the production of proinflammatory mediators, such as TNFalpha and NO.

Adenocarcinoma↗

PubMed2002

Incidence of diabetes mellitus requiring insulin treatment after renal transplantation in patients with hepatitis C.

BACKGROUND: Hepatitis C virus (HCV) infection has been associated with an increased incidence of diabetes mellitus, both in the general population and among transplant patients. METHODS: To test this hypothesis, we reviewed the records of 1614 patients who had undergone renal transplant at six Spanish centres between 1992 and 1998. We established the rate of onset of diabetes mellitus requiring >1 month of treatment with insulin (insulin-treated diabetes mellitus, I-TDM) among the 177 patients showing HCV antibody seropositivity at the time of transplant (HCV+ group). As controls, 177 HCV patients were selected who had received a kidney allograft immediately before or after the study patients at the same centre. RESULTS: The HCV+ patients were well matched with controls in terms of characteristics (except a longer time on dialysis) and immunosuppressive treatment. After a mean follow-up of 44 months, 28 cases of I-TDM were diagnosed (9.6% in HCV+ and 6.2% HCV-, not significant (NS); odds ratio 1.6; 95% confidence interval 0.75-3.50). The onset of I-TDM was somewhat later in HCV+ patients (467 days vs. 292 days in HCV- patients, NS). Multivariate analysis identified the following prognostic factors for I-TDM onset: age and BMI at the time of transplant, and polycystic kidney disease as the underlying cause of chronic renal insufficiency. No correlation was found with HCV positivity or time on dialysis. CONCLUSIONS: We were unable to confirm a greater incidence of post-renal transplant insulin-requiring diabetes in association with HCV infection. However, the observed tendency towards such an association suggests that the follow-up period would need to be extended.

Adult↗

PubMed2002

In vitro and in vivo activities of three acridine thioethers against Leishmania donovani.

The lack of definitive chemotherapeutic agents to fight against visceral leishmaniasis has lead to the testing of numerous compounds. In the present work, we carry out an in-depth study of the activity against Leishmania donovani of three acridine derivatives both in vitro and in vivo. These compounds have proven to be highly effective at medium and high concentrations of 10 microg/ml, against both flagellate and nonflagellate forms of the parasite, which, though obtained in vitro, closely resemble natural intracellular amastigotes. The in vivo assays showed a significant reduction in the percentage of parasitation versus control, for all the compounds tested. In addition, we have studied the possible mechanism by which these acridine derivatives act: they displayed a greater inhibitory effect against macromolecule synthesis in treated flagellates, yet alterations are also caused in the production of end metabolites and in the activity of different enzymes. The data obtained indicate that the acridine derivatives had several targets, one of them is the synthesis of nucleic acids and proteins, while the second one might be interaction with the carbohydrate and energy-production processes in the parasite. This conclusion is consistent with our observations concerning the ultrastructural changes induced in the parasite by these compounds principally at the mitochondrial level.

Acetates↗

PubMed2002

Nitric oxide synthase activity in hyperthyroid and hypothyroid rats.

OBJECTIVE: Thyroid disorders are accompanied by important changes in haemodynamic and cardiac functions and renal sodium handling. Since nitric oxide (NO) plays a crucial role in regulating vascular tone and renal sodium excretion, the present paper was designed to determine whether changes in the activity of NO synthase (NOS) participate in the cardiovascular and renal manifestations of thyroid disorders. METHODS: We measured NOS activity in the heart (left and right ventricles), vessels (aorta and cava) and kidney (cortex and medulla) of euthyroid, hyperthyroid and hypothyroid rats after 6 weeks of treatment. NOS activity was determined by measuring the conversion of L-[(3)H]-arginine to L-[(3)H]-citruline. RESULTS: NOS activity was higher in all tissues from hyperthyroid rats when compared with controls, except in the right ventricle. In the hypothyroid group, NOS activity showed a more heterogeneous pattern, with significant increases in both ventricles but significant reduction in the aorta, while in the vena cava, renal cortex and medulla the enzyme activity also tended to be higher, but significance was not reached. CONCLUSIONS: These data indicated that NOS activity was upregulated in tissues primarily related to blood pressure control in hyperthyroid rats, suggesting that an increased NO production may contribute to the hyperdynamic circulation in hyperthyroidism and may have a protective homeostatic effect in the target organs of the hypertension that accompanies this endocrine disease. The aortic and renal findings in hypothyroid rats suggested a possible role for NOS in the increased peripheral resistance and the normal pressure-diuresis-natriuresis response of these hypotensive animals, although hypothyroidism produced a heterogeneous tissue response in NOS activity.

Animals↗

PubMed2002

Chronic alpha1-adrenergic blockade improves hypertension and renal injury in L-NAME and low-renin L-NAME-DOCA hypertensive rats.

BACKGROUND: The present study investigated the contribution of alpha1-adrenergic blockade to hypertension induced by long-term blockade of nitric oxide and chronic treatment with deoxycorticosterone acetate (DOCA), which produced a low renin model of hypertension. We studied the effects of chronic administration of prazosin, an alpha1-receptor antagonist, on blood pressure (BP), renal injury, and other variables in N(omega)-nitro-L-arginine methyl ester (L-NAME) and L-NAME+DOCA hypertensive rats. MATERIAL/METHODS: The rats were divided into 6 groups: Control, DOCA, L-NAME, L-NAME+DOCA, L-NAME+ prazosin, and L-NAME+DOCA+prazosin. Tail systolic BP was measured twice a week. After a 6-week evolution, mean arterial pressure (MAP) was measured, along with selected metabolic, morphological and renal variables. RESULTS: The final MAP values were 105+/-1 for Control, 107+/-0.6 for DOCA, 153+/-3 for L-NAME, 175+/-2 for L-NAME+DOCA, 126+/-2 for L-NAME+prazosin and 127+/-5 for L-NAME+DOCA+prazosin. Proteinuria and hyaline arteriopathy were prevented in L-NAME+prazosin rats and markedly attenuated in the L-NAME+DOCA+prazosin group. Plasma urea and creatinine were significantly increased in the L-NAME+DOCA group, but not in the L-NAME+ DOCA+prazosin group as against controls. The DOCA and DOCA+L-NAME groups showed relative renal and cardiac hypertrophy, which was not observed in the DOCA+L-NAME+prazosin group. CONCLUSIONS: Alpha1-adrenergic tone plays an important role in the increased BP and renal injury of L-NAME hypertension. Our results also indicate that when PRA is suppressed by DOCA in L-NAME hypertension, the increased BP and renal injury are largely dependent on the alpha1-adrenergic tone.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed2000

Deoxycorticosterone suppresses the effects of losartan in nitric oxide-deficient hypertensive rats.

Chronic inhibition of the renin angiotensin system prevents increased BP and renal injury in N(G)-nitro-L-arginine methyl ester (L-NAME) hypertension. However, a relationship between plasma renin activity and the protective effect of chronic angiotensin II (Ang II) blockade has not been established. With this background, this study was undertaken to evaluate how the chronic administration of deoxycortisone acetate (DOCA) modifies the effects of losartan on BP, renal injury, and other variables in L-NAME hypertensive rats. The following groups were used: Control, DOCA, L-NAME, L-NAME + losartan, L-NAME + DOCA, and L-NAME + DOCA + losartan. Tail systolic BP was measured twice a week. After 4-wk evolution, mean arterial pressure and metabolic, morphologic, and renal variables were measured. The final mean arterial pressure values were 116 +/- 6 mmHg for control, 107 +/- 2 mmHg for DOCA, 151 +/- 5 mmHg for L-NAME, 123 +/- 2 mmHg for L-NAME + losartan, 170 +/- 3 mmHg for L-NAME + DOCA, and 171 +/- 5.5 mmHg for L-NAME + DOCA + losartan. Losartan prevented microalbuminuria, hyaline arteriopathy, and glomerulosclerosis of L-NAME hypertension but was ineffective in L-NAME + DOCA-treated rats. Plasma protein was significantly reduced in the L-NAME + DOCA group when compared with control and L-NAME groups, whereas no significant differences were observed in the other groups. Plasma renin activity was suppressed in the DOCA (0.55 +/- 0.2) and L-NAME + DOCA (0.60 +/- 10.2) groups but unsuppressed in the L-NAME + DOCA + losartan group (5.8 +/- 1). The conclusion is that DOCA blocks the preventive effect of losartan on the increased BP and renal injury of L-NAME hypertension, which suggests that DOCA transforms L-NAME hypertension into an Ang II-independent model of hypertension. These data also suggest that losartan prevents L-NAME hypertension by blocking the activity of systemic Ang II.

Albuminuria↗