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C Alarcón

Publications and source records attributed to C Alarcón.

At least 19 recordsLinked to original sources
PubMed2005

Arbuscular mycorrhizas in coastal sand dunes of the Paraguaná Peninsula, Venezuela.

Arbuscular mycorrhizal colonization was measured in the most abundant plant species of the Paraguaná Peninsula, northwestern Venezuela. These plant species included: Acacia tortuosa, Argusia gnaphalodes, Croton punctatus, Croton rhamnifolius, Egletes prostrata, Melochia tomentosa, Panicum vaginatum, Scaevola plumieri, Sporobolus virginicus, Suriana maritima, Leptothrium rigidum, and Fimbristylis cymosa. Mycorrhizal colonization was assessed using the Trouvelot et al. (1986) method that allows for simultaneous evaluation of frequency of colonization (%F), intensity of colonization (%M), and the proportion of arbuscules (%A) and vesicles (%V) present in the roots. Average frequency of colonization was 69%. The highest frequency of colonization was around 92% in C. rhamnifolius and A. tortuosa; in the other species, it varied from 49 to 86%. L. rigidum and F. cymosa were considered nonmycorrhizal because its colonization was very scarce and at all times appeared without arbuscules. Average intensity of colonization was 7%. The highest intensity of colonization was 18% in C. rhamnifolius. In the other species, it varied from 3 to 15%. Paspalum vaginatum, A. gnaphalodes, M. tomentosa, and S. maritima had their fungal structures tightly packed in modified little ovoid roots. In general, frequency of AM colonization was high and similar to those reported for other tropical ecosystems, whereas the intensity of AM colonization was low and similar to values obtained in analogous studies in disturbed ecosystems.

Environmental Microbiology↗
PubMed2005

Wisconsin and Celsior solutions in renal preservation: a comparative preliminary study.

The aim of this study was to evaluate the efficacy of the Celsior (C) solution for flushing and cold storage of cadaveric renal allografts. Among 177 cadaveric renal allografts harvested and transplanted in our unit, 138 were preserved with the University of Wisconsin (W) solution and 39 with the C solution. The mean age of the recipients was 48.1 +/- 13.5 years, including 107 men and 70 women. The immunosuppressive regimens were tacrolimus-based (n = 118) or cyclosporine-based (n = 59). Grafts perfused with W solution were obtained from older donors than those perfused with C solution (42.3 +/- 16.9 vs 38.1 +/- 12.5 years; P = .017) and had been transplanted to older recipients (49.5 +/- 14.4 vs 43.3 +/- 13.0 years; P = .017). The prevalence of delayed graft function (DGF) was similar in the 2 groups (39.1% in the W group vs 23.7% in the C group; P = .097), as well as the incidence of primary nonfunction grafts (5.8% vs 2.7%; P = .427). The serum creatinine value at 1 month was significantly higher among grafts preserved with W versus solution (1.9 +/- 0.9 vs 1.5 +/- 0.5 mg/dL; P = .000) as well as at 12 months (1.63 +/- 0.5 vs 1.35 +/- 0.4 mg/dL; P = .003). There were no differences in graft survival at 12 months (97% C group vs 88% W group; P = .069). Our results showed that C solution was equivalent to W solution with respect to DGF and primary function of kidneys. The differences in renal function may have been due to differences in donor and recipient ages.

Adenosine↗
PubMed2005

Self-expanding metallic ureteral stents for treatment of ureteral stenosis after kidney transplantation.

The incidence of post-renal transplantation ureteral stenosis ranges from 2%-12%. Because the role of self-expanding ureteral metallic stents for its treatment has been scarcely reported, the aim of this study was to evaluate the efficacy of Nitinol stents. Eleven ureteral stenoses in patients with chronic graft dysfunction (8 cases) or high surgical risk (3 cases) were treated by antegrade percutaneous implantation of Nitinol stents through a nephrostomy tract. The mean follow-up period was 48 +/- 7 months (range, 3-85 months). The patency rate at the moment of return to dialysis, death, or last check-up was 73% (8/11). Three patients (27%) developed stent occlusion. Two patients were treated using a trans-stent double-J catheter and 1 patient using stent removal and pyeloureterostomy using the native ureter. The mean percentage decrease in serum creatinine (Cr) level after stent implantation was 41% (range, 14%-63%). Nitinol ureteral stent implantation is an effective alternative for the treatment of ureteral stenosis in patients with chronic graft dysfunction or high surgical risk.

Creatinine↗
PubMed2004

[Therapy with interferon plus ribavirin in hemodialysis patient with PCR-positive viral hepatitis C].

Traditionally, the treatment of viral hepatitis C (positive Polymerase Chain Reaction -PCR-) was with Interferon. A combination of Interferon plus Ribavirin has been producing better results in last years. Currently, Ribavirin is not indicated for patients with Chronic Kidney Disease because of a high risk of severe anaemia. In a few cases, this treatment is producing good results with previous dose adjustment. We show a case of a 28-year-old man with Chronic Kidney Disease on treatment with periodical hemodialysis and chronic hepatopathy HCV Positive RNA HCV (> 1,000,000 copies/ml) and persistent transaminase elevation. Before kidney transplantation, we decided to use Interferon (3,000,000 IU/48 hours) and Ribavirin (200 mg/24 hours) treatment. After 15 days, we saw normal transaminase values and HCV RNA was negative. The patient required temporary suspension of Ribavirin and two red blood cell transfusions due to severe anaemia. Ribavirin was reintroduced 200 mg/48 h posthemodialysis. The patient did not present any complication again, and could be treated for 14 months. After next 11 months of evolution the patient has normal rates of liver function and negative HCV RNA values.

Adult↗
PubMed2001

[Rheumatoid arthritis among mapuche aborigines. A 16 years experience in the IX Region of the Chile].

BACKGROUND: Mapuche, Chilean natives, represent approximately 9.8% of Chilean population and in the IX region of the country, they account for 18.4% of population over 15 years old. They preserve some socio-cultural characteristics that make them different to the rest of the population. AIM: To describe the epidemiological characteristics rheumatoid arthritis among Mapuche natives. SUBJECTS AND METHODS: Retrospective review of patients of Mapuche origin with rheumatoid arthritis, seen at Temuco Hospital between 1980 and 1996. RESULTS: Among 308 cases gathered, only 106 (93 women, aged 55 +/- 10 years old) complied with 1987 American College of Rheumatology (ACR) criteria for rheumatoid arthritis. The disease began between 29 and 52 years old in 73% of patients and the mean delay in diagnosis was 4.4 years. At diagnosis, 99% had symmetric poliarthritis, 28.3% had either fatigue, fever or weight loss, and 46.9% were in class III or in class IV of ACR-1991. Fifty three percent of patients developed Sicca syndrome, 36% developed nodules, 23% developed Raynaud phenomenon, 11% developed pulmonary involvement, 7% developed vasculitis, 5% developed neurological manifestations and 19% developed ophthalmologic involvement. Rheumatoid factor was positive in 78% and 73% had erosions. HLA DR4 was (+) in 60% of 30 patients. Thirty percent required 3 or more disease modifying drugs and prednisone over 10 mg/day. There was no correlation between functional capacity and several other features of the disease. CONCLUSIONS: Mapuche rheumatoid arthritis patients are detected late and have a poor functional capacity at the time of diagnosis. They also have a higher proportion of extraarticular manifestations, more erosions and require more aggressive treatments.

Adult↗
PubMed1999

Insulin/insulin-like growth factor-I hybrid receptors with high affinity for insulin are developmentally regulated during neurogenesis.

The extensive colocalization of insulin receptor (IR) and insulin-like growth factor-I receptor (IGFR) messenger RNAs during central nervous system development, together with the effects of insulin and IGF-I in neurogenesis, raises the question of how stage- and factor-specific signaling occurs. Thus, it is necessary to characterize the receptor proteins present in vivo to start addressing this issue. Here we have studied the chick embryonic neuroretina at day 6 (E6), when it is predominantly proliferative, and at E12, when neuronal differentiation is advanced. Developmentally regulated high-affinity binding sites for both insulin and IGF-I were detected at E6 and E12. In proliferative neuroretina, typical IGFR with the highest affinity for IGF-I coexisted with separate atypical insulin binding sites, which had similar high affinity for insulin and IGF-I. Immunoprecipitation of ligand-cross-linked receptors with specific antibodies for the IR alpha-subunit, the IR beta-subunit, or the IGFR beta-subunit demonstrated the presence of IR/IGFR hybrids. They were more abundant in E6 than in E12 retina. These hybrid receptors bound most of radiolabeled insulin, but little radiolabeled IGF-I, at tracer concentrations. At E12, the specificity of the insulin binding sites changed, and it was closer to that found with IR in liver, where hybrids were undetectable. The basal autophosphorylation level of these atypical hybrid receptors was high, although insulin and, even more so, IGF-I modestly increased the phosphorylation of two IR beta-subunits of 95 and 105 kDa. The high-affinity/low-discriminative IR/IGFR hybrids predominantly found in a proliferative stage of neurogenesis can mediate the effects of proinsulin and insulin, previously demonstrated in organoculture at this stage. More importantly, this hybrid receptor may be physiologically relevant for the action of the locally produced proinsulin found in early neurogenesis.

Animals↗
PubMed1998

Synthesis and differentially regulated processing of proinsulin in developing chick pancreas, liver and neuroretina.

Regulated preproinsulin gene expression in nonpancreatic tissues during development has been demonstrated in rodents, Xenopus and chicken. Little is known, however, about the synthesis and processing of the primary protein product, proinsulin, in comparison with these events in pancreas. Using specific antisera and immunocytochemistry, immunoblot and HPLC criteria, we characterize the differential processing of proinsulin in developing neuroretina, liver and pancreas. The chick embryo pancreas expresses the convertase PC2, and largely processes proinsulin to insulin. In contrast, little or no mature PC2 is present in embryonic liver and neuroretina and the (pro)insulin immunoactivity identified is predominantly proinsulin.

Animals↗
PubMed1998

(Pro)insulin and insulin-like growth factor I complementary expression and roles in early development.

Evidence that the insulin-like growth factors play a role in embryonic as well as postnatal growth and central nervous system development has accumulated recently from studies using knock-out mice models. However, no effects of IGF-I and II have been demonstrated prior to organogenesis in these studies. We summarize here results supporting the role of insulin (or its precursor proinsulin) in vertebrate development prior to the expression of IGFs. (Pro)insulin mRNA is expressed in the chick embryo during neurulation and early organogenesis and its inhibition by antisense oligodeoxynucleotides increase apoptosis. In another system, proliferative neuroretina, (pro)insulin expression predominates over IGF-I expression. Modulation of apoptosis by (pro)insulin in retina may be largely responsible for the observed stimulation of DNA synthesis and neuronal differentiation. These effects are elicited as well by IGF-I, expressed later in neuroretina. Thus, these polypeptides have complementary expression in early embryos which suggests coordinated actions during development.

Animals↗
PubMed1997

Role of prepancreatic (pro)insulin and the insulin receptor in prevention of embryonic apoptosis.

The characterization of (pro)insulin as an early embryonic growth factor requires demonstration of its expression and cellular effects in vivo. By in situ hybridization, we found widespread preproinsulin transcripts in the chick embryo throughout gastrulation and neurulation, before the beginning of preproinsulin-like growth factor I expression and pancreatic organogenesis. To analyze the prepancreatic (pro)insulin effect on apoptotic cell death, we treated embryos with antisense oligodeoxynucleotides in ovo and in vitro. The specific effect of two preproinsulin messenger RNA (mRNA) antisense oligodeoxynucleotides was confirmed by the decrease in a biosynthetically labeled protein immunoprecipitated with antiinsulin Igs. Insulin receptor mRNA antisense oligodeoxynucleotide applied in ovo increased by 2.7-fold the level of apoptosis in the 1.5-day embryo (neurulation) compared with that in its random sequence control. In a whole embryo culture, apoptosis increased by 25-35% with the addition of preproinsulin or insulin receptor mRNAs antisense oligodeoxynucleotides, respectively, whereas it decreased by 64% after 10 h in the presence of 10(-8) M chicken insulin. Exogenous insulin also rescued the death induced by preproinsulin antisense oligonucleotides. These findings provide evidence for an autocrine/paracrine role ofpreproinsulin gene products acting through the insulin receptor in the control of cell survival/death during early embryonic development.

Animals↗
PubMed1996

Effects of short-term zinc supplementation on cellular immunity, respiratory symptoms, and growth of malnourished Equadorian children.

OBJECTIVE: To assess the effect of zinc supplementation on respiratory tract disease, immunity and growth in malnourished children. DESIGN: A randomized double-blind placebo-controlled trial. SETTING: A day-care center in Quito, Ecuador. SUBJECTS: Fifty children (12-59 months old) recruited by height-for-age and weight-for-age deficit. INTERVENTIONS: Twenty-five children (supplemented, S group) received 10 mg/day of zinc as zinc sulfate, and 25 (nonsupplemented, NS group) received a placebo during 60 days. All were also observed during a 60-day postsupplementation period. Two children of the S group dropped out. Daily the clinical presence of cough, respiratory tract secretions, and fever, was recorded. On days 0,60 and 120, the cutaneous delayed-type hypersensitivity (DTH) to multiple antigens, and anthropometric parameters were assessed. On days 0 and 60 serum zinc levels were also measured. RESULTS: On day 60, DTH was significantly larger (20.8 +/- 7.1 vs 16.1 +/- 9.7 mm), and serum zinc levels were significantly higher (118.6 +/- 47.1 vs 83.1 +/- 24.5 micrograms/dl) in the S group than in the NS group (P <0.05 for each). The incidence of fever [relative risk (RR): 0.30, c.i. = 0.08- 0.95, P =0.02], cough (RR): 0.52, c.i. = 0.32-0.84, P = 0.004) and upper respiratory tract secretions (RR):0.72, c.i. = 0.59-0.88, P = 0.001) was lower in the S group than in the NS group at day 60. At the end of the postsupplementation observation period (day 120), the incidence of fever and upper respiratory tract secretions was the same in both the S and NS groups. The incidence of cough was higher at day 120 in the S group than in the NS group (RR): 2.28, c.i. = 1.37-3.83, P = 0.001). CONCLUSIONS: This study supports a role for zinc in immunity, and immunity to respiratory infections, while pointing out the need for larger studies.

Adjuvants, Immunologic↗
PubMed1995

Autocrine/paracrine role of insulin-related growth factors in neurogenesis: local expression and effects on cell proliferation and differentiation in retina.

Early neurogenesis progresses by an initial massive proliferation of neuroepithelial cells followed by a sequential differentiation of the various mature neural cell types. The regulation of these processes by growth factors is poorly understood. We intend to understand, in a well-defined biological system, the embryonic chicken retina, the role of the insulin-related growth factors in neurogenesis. We demonstrate the local presence of signaling elements together with a biological response to the factors. Neuroretina at days 6-8 of embryonic development (E6-E8) expressed proinsulin/insulin and insulin-like growth factor I (IGF-I) mRNAs as well as insulin receptor and IGF type I receptor mRNAs. In parallel with this in vivo gene expression, E5 cultured neuroretinas synthesized and released to the medium a metabolically radiolabeled immunoprecipitable insulin-related peptide. Furthermore, insulin-related immunoreactive material with a HPLC mobility close to that of proinsulin was found in the E6-E8 vitreous humor. Exogenous chicken IGF-I, human insulin, and human proinsulin added to E6 cultured neuroretinas showed relatively close potencies stimulating proliferation, as determined by [methyl-3H]thymidine incorporation, with a plateau reached at 10(-8) M. These factors also stimulated neuronal differentiation, indicated by the expression of the neuron-specific antigen G4. Thus, insulin-related growth factors, interestingly including proinsulin, are present in the developing chicken retina and appear to play an autocrine/paracrine stimulatory role in the progression of neurogenesis.

Animals↗
PubMed1995

Increased secretory demand rather than a defect in the proinsulin conversion mechanism causes hyperproinsulinemia in a glucose-infusion rat model of non-insulin-dependent diabetes mellitus.

Hyperproinsulinemia in non-insulin-dependent diabetes mellitus (NIDDM) is due to an increased release of proinsulin from pancreatic beta cells. This could reside in increased secretory demand placed on the beta cell by hyperglycemia or in the proinsulin conversion mechanism. In this study, biosynthesis of the proinsulin conversion enzymes (PC2, PC3, and carboxypeptidase-H [CP-H]) and proinsulin, were examined in islets isolated from 48-h infused rats with 50% (wt/vol) glucose (hyperglycemic, hyperinsulinemic, and increased pancreatic proinsulin to insulin ratio), 20% (wt/vol) glucose (normoglycemic but hyperinsulinemic), and 0.45% (wt/vol) saline (controls). A decrease in the islet content of PC2, PC3, and CP-H from hyperglycemic rats was observed. This reduction did not correlate with any deficiency in mRNA levels or biosynthesis of PC2, PC3, CP-H, or proinsulin. Furthermore, proinsulin conversion rate was comparable in islets from hyperglycemic and control rats. However, in islets from hyperglycemic rats an abnormal increased proportion of proinsulin was secreted, that was accompanied by an augmented release of PC2, PC3 and CP-H. Stimulation of the beta cell's secretory pathway by hyperglycemia, resulted in proinsulin being prematurely secreted from islets before its conversion could be completed. Thus, hyperproinsulinemia induced by chronic hyperglycemia likely results from increased beta cell secretory demand, rather than a defect in the proinsulin processing enzymes per se.

Animals↗
PubMed1994

A Kex2-related endopeptidase activity present in rat liver specifically processes the insulin proreceptor.

The insulin proreceptor is cleaved by limited proteolysis post-translationally at an Arg-Lys-Arg-Arg site to generate its mature alpha- and beta-subunit form. An 35S-labelled insulin proreceptor substrate preparation and a 15-mer peptide substrate that mimics the amino acid sequence around and including the insulin proreceptor processing site (IRP-peptide) has revealed an endopeptidase activity that catalyses insulin proreceptor cleavage in a rat liver subcellular fraction. Under optimal conditions, normal 35S-labelled insulin proreceptor substrate processing by this fraction was quantitative. This fraction was not able to process an 35S-labelled insulin proreceptor variant substrate (where the Arg-1 of the tetrabasic cleavage site had been replaced by Ala-1), similarly to previous in vivo observations, suggesting that this endopeptidase activity has physiological relevance. Biochemical characterization of the insulin proreceptor/IRP-peptide processing revealed this rat liver endopeptidase activity to have a broad pH range (> 70% maximal activity between pH 5.5 and 10.0) and a pH optimum of pH 8-10. It was Ca(2+)-dependent activity, maximally active between 0.5 and 5 mM Ca2+ and half-maximally activated between 50 and 90 microM Ca2+. Endoproteolytic activity was not inhibited by group-specific inhibitors of serine-, cysteinyl or aspartyl proteinases or by 1,10-phenanthroline; however, EDTA and 1,2-cyclohexanediaminetetraacetic acid did inhibit the activity, but this was accounted for by Ca2+ chelation. The IRP-peptide substrate assay enabled measurement of an apparent Km of 22 microM and a Vmax of 18.6 pmol/min for this endopeptidase activity. These biochemical characteristics suggest that insulin proreceptor processing endopeptidase activity to be a legitimate member of the Kex2-related proprotein convertase family. Immunoblotting detected furin and PACE4 proteins (both members of this family) to be present in the rat liver subcellular fraction containing insulin proreceptor processing activity. Since the biochemical characteristics of the insulin proreceptor processing endopeptidase activity mostly resembled those of furin activity, it is likely that insulin proreceptor proteolytic maturation can be catalysed by furin in the liver.

3T3 Cells↗
PubMed1994

What beta-cell defect could lead to hyperproinsulinemia in NIDDM? Some clues from recent advances made in understanding the proinsulin-processing mechanism.

Pancreatic beta-cell dysfunction is a characteristic of non-insulin-dependent diabetes mellitus (NIDDM). An aspect of this dysfunction is that an increased proportion of proinsulin is secreted, but an actual beta-cell defect that leads to hyperproinsulinemia is unknown. Nevertheless, an impairment in beta-cell proinsulin conversion mechanism has been suggested as the most likely cause. Insulin is produced from its precursor molecule, proinsulin, by limited proteolytic cleavage at two dibasic sequences (Arg31, Arg32 and Lys64, Arg65). Two endopeptidase activities catalyze this cleavage: PC2 and PC3. PC2 endopeptidase cleaves predominately at Lys64, Arg65, and PC3 endopeptidase cleaves at Arg31, Arg32. The recent identification and characterization of these endopeptidases has enabled a better understanding of the human proinsulin-processing mechanism. In particular, experimental evidence suggests that the majority of human proinsulin processing is sequential. PC3 cleaves proinsulin first to generate a proinsulin conversion intermediate that is the preferred substrate of PC2. Both PC2 and PC3 activities are influenced by Ca2+ and pH, but the more stringent Ca2+ and pH requirements of PC3 suggest it as the most likely enzyme to regulate proinsulin conversion, as well as initiate it. When an increased demand is placed on the proinsulin-processing mechanism by a glucose-stimulated increase in proinsulin biosynthesis, there is a coordinate increase in PC3 biosynthesis (but not in PC2). This supports PC3 as the key endopeptidase that regulates proinsulin processing. In this perspective, the current concepts of the enzymology and regulation of proinsulin conversion at a molecular level are reviewed.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

[Acquired hemoglobin H disease associated with a myelodysplastic syndrome].

Some patients found to have clonal panmyelopathies develop an acquired defect of haemoglobin synthesis clinically similar to haemoglobin H disease. A 58 year-old male diagnosed of simple refractory anaemia developed microcytosis and hypochromia. At the same time, his myelodysplastic syndrome became a refractory anaemia with excess of blasts. 33% of the red blood cells had "golf ball" inclusions after incubation with brilliant cresyl blue. Cellulose acetate electrophoresis revealed an haemoglobin H band. The globin chain synthesis alpha/beta ratio was 0.69. The molecular analysis demonstrated the integrity of both alpha genes in each chromosome. There were no familiar antecedent of haemoglobinopathy.

Anemia, Refractory, with Excess of Blasts↗