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C C Teixeira

Publications and source records attributed to C C Teixeira.

15 recordsLinked to original sources

The efficacy of folk medicines in the management of type 2 diabetes mellitus: results of a randomized controlled trial of Syzygium cumini (L.) Skeels.

OBJECTIVE: To investigate whether a tea prepared from leaves of jambolan, Syzygium cumini (L.) Skeels, has an antihyperglycaemic effect in patients with type 2 diabetes mellitus. RESEARCH DESIGN AND METHODS: Patients with type 2 diabetes mellitus were enrolled in a double-blind, double-dummy, randomized clinical trial. The three experimental groups received a tea prepared from leaves of S. cumini plus placebo tablets, placebo tea plus glyburide tablets or placebo tea plus placebo tablets. RESULTS: In total, 27 patients were allocated to one of the treatment groups and followed for 28 days. Fasting blood glucose levels decreased significantly with glyburide and did not change with S. cumini tea or placebo. Body mass index, creatinine, gamma-glutamyl transferase, alkaline phosphatase, aspartate aminotransferase (SGOT), alanine aminotransferase (SGPT), 24-h glicosuria, 24-h proteinuria, triglycerides, total, low-density lipoprotein and high-density lipoprotein cholesterol did not vary significantly between the different groups. CONCLUSIONS: Tea prepared from leaves of S. cumini has no hypoglycaemic effect.

Adult↗

Phosphate ions mediate chondrocyte apoptosis through a plasma membrane transporter mechanism.

In a previous investigation we showed that phosphate ions (Pi) induced apoptosis of terminally differentiated hypertrophic chondrocytes. To explore the mechanism by which Pi induces cell death, we asked the following two questions. First, can we prevent Pi-induced apoptosis by inhibiting plasma membrane Na-Pi cotransport? Second, which specific Na-Pi transporters are expressed in chondrocytes and are they developmentally regulated? Terminally differentiated hypertrophic chondrocytes were isolated from chick tibial cartilage and cell death was measured in the presence of 3-7 mmol/L Pi. To ascertain whether apoptosis was linked to a rise in cellular Pi loading, we examined the effect of phosphonoformic acid (PFA), a competitive inhibitor of Na-Pi cotransport on Pi-induced apoptosis in chondrocytes. We found that 1 mmol/L PFA blocked anion-induced cell death and prevented an increase in the cell Pi content. In a parallel study, we determined that the bisphosphonate, alendronate, also protected chondrocytes from death, albeit at a lower concentration than PFA. Using a DNA end-labeling procedure, we showed that the Pi-treated cells were apoptotic and, as might be predicted, the presence of PFA blocked induction of the death sequence. Next, we examined the expression of two Pi transporters in relation to chondrocyte maturation and anion treatment. We noted that there was expression of the constitutive transporter, Glvr-1, and a type II cotransporter in chick growth plate cells. Although these transport systems are active in terminally differentiated cells, it is probable that the initiation of apoptosis may require the induction of other Pi-transport systems. It is concluded that, at the mineralization front, cell death is linked directly to the elevation in environmental anion concentration and the concomitant rise in intracellular Pi levels.

Alendronate↗

Phosphate-induced chondrocyte apoptosis is linked to nitric oxide generation.

An elevation in inorganic phosphate (P(i)) concentration activates epiphyseal chondrocyte apoptosis. To determine the mechanism of apoptosis, tibial chondrocytes were treated with P(i), and nitrate/nitrite (NO/NO) levels were determined. P(i) induced a threefold increase in the NO/NO concentration; inhibitors of nitric oxide (NO) synthase activity and P(i) transport significantly reduced NO/NO levels and prevented cell death. Furthermore, a dose-dependent increase in cell death was observed after exposure of chondrocytes to S-nitrosoglutathione. P(i) increased caspase 3 activity 2.7-fold. Both caspase 1 and caspase 3 inhibitors protected chondrocytes from P(i)-induced apoptosis. P(i) caused a significant decrease in the mitochondrial membrane potential, while NO synthase inhibitors maintained mitochondrial function. While P(i) caused thiol depletion, inhibition of P(i) uptake or NO generation served to maintain glutathione levels. The results suggest that NO serves to mediate key metabolic events linked to P(i)-dependent chondrocyte apoptosis.

Animals↗

Absence of antihyperglycemic effect of jambolan in experimental and clinical models.

The use of alternative therapies to treat diabetes, including teas prepared with different vegetables, is widespread in Brazil. In Porto Alegre, a southern city of Brazil, the tea prepared from leaves of Syzygium cumini (L.) Skeels or S. jambos (L.) Alst has been report to be used frequently by diabetic patients. We investigated the postulated antihyperglycemic effect of the S. cumini (L.) Skeels in three experiments. In the first, a randomized, parallel, placebo controlled trial, tea prepared from leaves of S. cumini did not present any antihyperglycernic effect in 30 non-diabetic young volunteers submitted to a glucose blood tolerance test. In the animal experiments, we tested the effect of increasing doses of the crude extract prepared from leaves of S. cumini administrated for 2 weeks, on the post-prandial blood glucose level of normal rats and rats with streptozotocin-induced diabetes mellitus. The treatment did not produce any antihyperglycernic effect in both models. These results do not rule out hypoglycemic effects in patients with type 2 diabetes mellitus, but strongly suggest that, for a while, the jambolan can not be recommended as an antihyperglycemic treatment.

Adolescent↗

New horizons in understanding early tooth development.

Information on the mechanism that governs tooth shape, size, and location in the developing jaw is sparse. One hypothesis holds that exogenous signals from the ectomesenchyme and epithelium of the embryonic jaw induce a specific pattern of cellular development that leads to tooth formation. A second hypothesis is that a specific tooth type develops from select clones of cells. The objective of this review is to consider these ideas in light of recent studies on genes that regulate embryonic patterning. Special attention is directed at the notion that there is restricted expression of specialized genes. These genes are expressed in overlapping domains along the jaw axis. Genes expressed within a region provide a unique homeobox code that serves to specify a tooth type and ultimately determines tooth form and position in the developing jaw. Expression of this genetic 'bar code' is carefully controlled by the dental epithelium, neural crest-derived cells, and growth factors. The latter agents also probably serve as epithelial signals that activate events that lead to odontogenic differentiation and morphogenesis.

Animals↗

The effect of Syzygium cumini (L.) skeels on post-prandial blood glucose levels in non-diabetic rats and rats with streptozotocin-induced diabetes mellitus.

This study was undertaken to investigate whether a tea prepared from Syzygium cumini, reported to be used by diabetics in Porto Alegre, Brazil, might have an antihyperglycemic effect in experimental models. Teas prepared from leaves and seeds of S. cumini, in concentrations ranging from 2-64 g/l, were administered, as water substitute for 14-95 days, to 16 groups with 8-9 normal albino rats and to four groups with 10-12 rats with streptozotocin-induced diabetes mellitus. Post-prandial blood glucose levels were determined by the glucose oxidase method on blood samples obtained by decapitation. None of the tea concentration had any detectable antihyperglycemic effect either in normal or in diabetic rats, suggesting that this plant, prepared in a manner similar to that employed by humans, is destitute of an antihyperglycemic effect.

Animals↗

Retinoic acid modulation of glutathione and cysteine metabolism in chondrocytes.

The major objective of this investigation was to determine the thiol status of chondrocytes and to relate changes in the level of glutathione and cysteine to maturation of the cells as they undergo terminal differentiation. Chondrocytes were isolated from the cephalic portion of chick embryo sterna and treated with all-trans retinoic acid for one week. We found that the addition of 100 nM retinoic acid to the cultures decreased the intracellular levels of glutathione and cysteine from 6.1 to 1.6 and 0.07 to 0.01 nmol/microgram DNA respectively; retinoic acid also caused a decrease in the extracellular concentration of cysteine. The decrease in chondrocyte thiols was dose and time dependent. To characterize other antioxidant systems of the sternal cell culture, the activities of catalase, glutathione reductase and superoxide dismutase were determined. Activities of all of those enzymes were high in the retinoic acid-treated cells; the conditioned medium also contained these enzymes and the cytosolic isoenzyme of superoxide dismutase. We probed the specificity of the thiol response by using immature caudal chondrocytes. Unlike the cephalic cells, retinoic acid did not change intracellular glutathione and extracellular cysteine levels, although the retinoid caused a reduction in the intracellular cysteine concentration. Finally, we explored the effect of medium components on chondrocyte thiol status. We noted that while ascorbate alone did not change cell thiol levels, it did cause a 4-fold decrease in the extracellular cysteine concentration. When retinoic acid and ascorbic acid were both present in the medium, there was a marked decrease in the level of glutathione. In contrast, the phosphate concentration of the culture medium served as a powerful modulator of both glutathione and cysteine. Results of the study clearly showed that there is a profound decrease in intracellular levels of both cysteine and glutathione and that thiol levels are responsive to ascorbic acid and the medium phosphate concentration. These findings point to a critical role for thiols in modulating events linked to chondrocyte maturation and cartilage matrix synthesis and mineralization.

Animals↗

End labeling studies of fragmented DNA in the avian growth plate: evidence of apoptosis in terminally differentiated chondrocytes.

The chondro-osseous junction has been the subject of considerable scrutiny, especially in terms of the fate and role of the terminally differentiated chondrocyte. Although it has been proposed that these cells change their phenotype and survive in the epiphysis, possibly as osteoblasts, evidence from a number of other studies suggests that chondrocytes may undergo apoptosis or programmed cell death. A useful test for programmed cell death is to end label DNA in cryosections using the commercial reagent ApopTag and detect antibody binding to fragmented DNA by epifluorescence; more direct assessments include examination of the nucleus for condensation of chromatin evaluating fragmentation through alkaline and pulsed field agarose gel electrophoresis of DNA, and measuring apoptosis by flow cytometry. We found that we could label cells in the proliferative and the hypertrophic region of the proximal tibial growth plate of the chick with ApopTag. Most of the chondrocytes in the hypertrophic region were labeled by the reagent; in contrast, few proliferative chondrocytes were stained by the end-labeling procedure. Both agarose and pulsed field electrophoresis were used to confirm that there was fragmentation of chondrocyte DNA. Alkaline gel electrophoresis indicated that there was more fragmentation of DNA from hypertrophic cells than from proliferative chondrocytes. Further evidence in support of apoptosis was provided by electron microscopic observation of cells in the hypertrophic region of the growth plate. We noted that many of the cells in this region of the growth plate appeared to be undergoing programmed cell death since their nuclei contained condensed chromatin. Finally, we used flow cytometry to analyze chondrocytes isolated from the proliferating and hypertrophic regions of the growth plate for apoptosis. Dual parameteric flow cytometric contour plots of Hoechst and 7-amino-actinomycin D fluorescence showed that abut 8% of cells in the plate were apoptotic. Most of these cells were in hypertrophic cartilage. In summary, the results of this investigation indicate that chondrocytes terminate their life history by apoptosis. While it is possible that the terminal labeling studies may overestimate the number of cells undergoing this event, the data lend credence to the view that cells are removed from the epiphysis through apoptosis. If this is the case, then chondrocytes probably enter the terminal phase of their life as fully functioning cells and genomic, and/or local environmental conditions provide termination signals that initiate events that lead to programmed cell death.

Animals↗

Adenine nucleotide metabolism by chondrocytes in vitro: role of ATP in chondrocyte maturation and matrix mineralization.

The objective of the investigation was to explore the notion that chondrocytes in the growth plate secrete nucleotides and that these compounds are used to regulate cell maturation and matrix mineralization. Chondrocytes were isolated from the cephalic region of chick embryo sterna and maintained in culture until confluent. To promote expression of the mature phenotype, cultures were then treated with retinoic acid. During the culture period, medium was removed and analyzed for nucleotides using a modified reverse-phase high-performance liquid chromatography (HPLC) procedure. We found that culture medium, conditioned by the chondrocytes, contained significant quantities of nucleotides. Moreover, the nucleotide concentrations were similar in magnitude to levels reported for media conditioned by other cell types. In terms of species, adenosine diphosphate (ADP) was the major nucleotide present in the conditioned medium; adenosine monophosphate (AMP) was present, but at a lower concentration than ADP. To examine the possibility that adenosine triphosphate (ATP) was released by the cultured chondrocytes, but was rapidly degraded into ADP and AMP, we examined the kinetics of ATP breakdown by chondrocytes. We found that chondrocytes degraded over 70% of exogenous ATP within 15 minutes. Similar experiments performed with ADP and AMP indicated that these nucleotides were also degraded by the cells, but at a slower rate than ATP. To determine whether the extracellular nucleotides modulate cartilage development, we examined the effect of exogenous ATP on four major determinants of chondrocyte function: alkaline phosphatase activity, cell proliferation rate, anaerobic metabolism, and mineral deposition. We found that ATP caused only minimum alterations in cell number and alkaline phosphatase activity; however, it increased the lactate content of the medium probably by stimulating anaerobic glycolysis. We noted that ATP had a significant effect on the amount and type of mineral deposited into chondrocyte cultures. Compared with untreated controls, ATP stimulated formation of a small amount of poorly crystallized calcium phosphate. The results of the study show for the first time that chondrocytes release nucleotides into the extracellular milieu. Although they are rapidly degraded, they serve to regulate both mineral formation and energy metabolism.

Adenosine Triphosphate↗

A rapid and ultrasensitive method for measurement of DNA, calcium and protein content, and alkaline phosphatase activity of chondrocyte cultures.

Most investigators are cognizant of the problems inherent in counting cells embedded in a complex and abundant extracellular matrix. To overcome these obstacles, we developed a new method of isolating nucleic acids from chondrocytes which facilitates measurement of cell number by DNA analysis. Chondrocytes were isolated from chick embryo sterna and grown continuously without subculturing for 2-3 weeks in monolayer. The cells were treated with triton X-100 and the nucleic acid content of the extract was determined by measuring DNA fluorescence in the presence of Hoechst dye 33258. To minimize background fluorescence due to the triton, we precipitated the DNA with alcohol and then solubilized the nucleic acids in EDTA. This simple procedure removed the detergent and substantially increased the sensitivity of the method. Thus, we could measure with high precision and high recovery, the DNA content of cultures of 10,000-50,000 cells. In a single well containing 0.5-1.0 million cells, sufficient material remained for subsequent measurements of alkaline phosphatase activity and protein and calcium content. As the mineral present in the triton-treated samples was soluble in EDTA, we experienced no problems in measuring the calcium content of the culture. In addition, as triton X-100 is a nonionic detergent, we were able to measure cell and matrix proteins; moreover, the presence of the triton maintained the catalytic state of alkaline phosphatase. We conclude that this procedure provides a simple and rapid approach to measuring major indicators of chondrocyte maturation and function.

Alkaline Phosphatase↗

Effects of deferoximine on chondrocyte alkaline phosphatase activity: proxidant role of deferoximine in thalassemia.

The homozygous form of beta-thalassemia, the most common single gene disorder, is treated by red cell transfusion therapy. Following transfusion, the chelator, deferoximine, is administered to patients to remove excess iron. However, when this drug is given to young children, metaphyseal dysplasia and abnormalities of linear growth are frequently observed. To explore the notion that deferoximine interferes with endochondral growth by chelating zinc, we examined the effect of the drug on chondrocytes maintained in long-term culture. We found that deferoximine caused a dose-dependent inhibition of a wide range of functions including cell proliferation, protein synthesis (and possibly under-hydroxylation of type X collagen), and mineral deposition. Directly relevant to the mineralization process was the observation that the drug dramatically lowered the activity of alkaline phosphatase, a zinc-requiring enzyme. To test the hypothesis that enzyme inhibition was due to chelation of zinc by deferoximine, the cell culture medium was supplemented with excess zinc. However, this treatment did not overcome the deferoximine-dependent change in enzyme activity. We next examined the possibility that deferoximine, in the presence of ascorbate, could form a free radical system that would serve to inactivate the enzyme. Using alkaline phosphatase extracted from chick cartilage, we noted that the activity of the phosphatase was markedly reduced in the presence of deferoximine and ascorbate. These effects were consistant with the notion that deferoximine and ascorbate can act as a prooxidant couple. This conclusion was confirmed when we measured the oxidative activities of the system using nitrobule tetrazolium and cytochrome c. Indeed, we noted that deferoximine markedly activates the autocatalytic oxidation of ascorbate.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗

A simple simulated public speaking test for evaluating anxiolytic drugs.

1. We evaluated the feasibility of using a simulated public speaking (SPS) test to assess the activity of anxiolytic drugs. SPS was achieved by requesting subjects to present a speech to an audiocassette recorder. Thirty volunteers were randomly assigned to one of three groups treated with 10 mg diazepam, 10 mg buspirone or placebo, under double-blind conditions. One h after drug administration, subjective states were measured by the Visual Analogue Mood Scale (VAMS), the State-Trait Anxiety Inventory (STAI) and by a Bodily Symptoms Scale (BSS). Heart rate and blood pressure were also recorded. 2. SPS induced both physiological and subjective changes characteristic of anxiety. Moreover, diazepam attenuated experimentally induced increases in excitement (as measured by VAMS) and agitation (as measured by BSS). Therefore, SPS using an audiocassette recorder is sensitive to a prototypical anxiolytic and may thus be a useful test for evaluating putative anxiolytics. 3. No effect was observed with the new anxiolytic drug buspirone. However, the present negative result may be explained by clinical data indicating that patients may experience a longer lag period before the onset of the anxiolytic effect of buspirone.

Adult↗

Hepatic regeneration following partial hepatectomy in mice infected with Schistosoma mansoni.

Signs of hepatic regenerative activity were detected by radioactive thymidine incorporation and cariometry in hepatic parenchymal cells of mice infected with 30 cercariae of Schistosoma mansoni for 10 weeks and then submitted to partial (30%) hepatectomy. The same methods failed to detect regeneration in mice submitted to partial hepatectomy, to S. mansoni infection or to sham operation, as well as in normal control mice. The stimulus required for hepatic regeneration in the mouse apparently needs to be strong, as was the case when the effects of partial hepatectomy were added to those of S. mansoni-induced lesions. These data show that extensive schistosomal lesions do not impede hepatic cell regeneration by the mouse.

Animals↗

Congenital dacryocystocele with intranasal extension.

PURPOSE: Congenital dacryocystocele is a rare anomaly in the newborn child. The swelling of lachrymal sac is observed by birth and it is associated with obstruction of lachrymal system either above or below lachrymal sac. METHODS: Diagnosis was made by clinical observation. Some ancillary examinations, such as ultrasonography, tomography, and rhinoscopy, were useful. RESULTS: The authors describe the clinical case of a newborn with a unilateral congenital dacryocystocele. This anomaly was successfully treated with probing and marsupialization of the nasal cyst. CONCLUSIONS: Treatment of this congenital anomaly is by light compressive massage, probing with silicone intubation of lachrymal system to assure prolonged permeability of the system, or with marsupialization of the nasal cyst. In some cases with intranasal extension of dacryocystocele, collaboration with an otolaryngologist may be necessary.

Cysts↗