La presente investigacion trata acerca del manejo odontologico que le brinda a los pacientes geriatricos en el area de estomatologia y cirugia maxilofacial del hospital Rosales y la clinica de consulta externa del Instituto Salvadoreno de rehabilitacion de invalidos. La investigacion inicia con la determinacion de los elementos del diagnostico, donde se justifica el por que de la investigacion, lo que se pretende alcanzar al final de esta, el nivel de generalizacion de los resultados y lo que cubrira el estudio a nivel teorico, tambien se plantean algunas limitaciones que tuvo el grupo investigador en la realizacion de la misma, los sujetos que formaron parte del estudio y el problema en estudio. Luego se establece un marco de referencia, en el cual se plantean los origenes, evolucion y desarrollo del problema, asi como tambien se explican los diferentes puntos de vista que tienen otros autores con respecto al manejo del paciente geriatrico. En la metodologia de la investigacion, se explica el tipo de investigacion que se realizo, la poblacion a quien fue dirigida, metodos, tecnicas e instrumentos que se utilizaron para la realizacion de los dos primeros capitulos y para la recopilacion de los datos, ademas, se plasma la forma como se elaboraron los instrumentos y su descripcion, como se establecio el proceso de recoleccion de los datos y la manera como se tabularon. En el capitulo final se encuentran los cuadros estadisticos que se realizaron a partir de los resultados de la investigacion, cada cuadro presenta su respectiva descripcion, luego se encuentra el analisis que el grupo investigador realizo a partir de los resultados obtenidos en el diagnostico y de su propia experiencia, para luego finalizar con las conclusiones y recomendaciones de la investigacion.
Previously, we found in experimental hypertension (DOCA salt model), that the RhoA/Rho-kinase pathway inhibition by fasudil decreases hypertension (HT), angiotensin (Ang) II levels and vascular remodeling. Besides, in this model fasudil increased ACE2 activity and Ang1-9 plasma levels. These results strongly suggest that in this experimental model, ROCK activity is more dependent on ACE2 and Ang-(1-9) than Ang II levels. There is no current evidence regarding the effect of Ang1-9 on ROCK activity of hypertensive rats. Aim: To determine the effect of the chronic administration of Ang1-9 on blood pressure (BP), vascular damage and activation of RhoA/ROCK pathway in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Methods: The DOCA-salt hypertensive model was used in Sprague-Dawley male rats (age: 5-6 weeks; 150±10 g). DOCA was administered twice a week (60 mg/kg, im) starting immediately after surgery. The animals also received 1% NaCl and 0.4% KCl in the drinking water. Controls (C) were uninephrectomized rats (Sham group, n=12). Hypertensive rats (D) were randomized to receive vehicle (n=10), Ang-(1-9) (600 ng/kg/min, n=12), Ang-(1-9) + the Mas blocker receptor A779 (100 ng kg−1 min−1,n=7) and Ang-(1-9) + the AT2R antagonist PD123319 (PD, 36 ng/Kg min) for 2 weeks. Systolic (S) and diastolic (D) BP, body mass (BM), heart weight (HW), heart mass relative to the length of the tibia (HMR), lumen area (LA), vascular reactivity assays (VRA % dilation at 10-9M AcCh) and ROCK activity by the ratio of phosphorylated vs total MYPT1 (MP/ MT) in the aortic wall were determined. Results: Compared to sham rats, in hypertensive rats VRA was significantly decreased (C: 15 ± 1.8 vs D: 2 ± 0.8), whereas SBP (C: 125 ± 2 vs D: 207 ± 7), AMT/LA (C: 0.32 ± 0.01 vs D: 0.4 ± 0.01) and MP/ MT (C: 1 ± 0.12 vs D: 1.77 ± 0.38) were significantly increased. In DOCA hypertensive rats, Ang1-9 significantly reduced SBP (161 ± 6), AMT/LA (0.37 ± 0.01) and aortic MP/ MT (0.65 ± 0.07) but increased VRA (25 ± 1.1). These beneficial effects of Ang-(1-9) were modified by PD123319 but not by A779. Conclusion: Ang1-9 reduces BP and vascular damage by inhibiting ROCK activity in this model of low renin HT. These effects seem be mediated by the AT2R. Fondecyt 1100874 and 1121060.
In brief: In a pediatric kidney transplant cohort, glucocorticoid treatment was independently associated with FGF23 levels. Using in vivo and in vitro rat model systems, blocking of Fgfr signalling rescued glucocorticoid-induced skeletal manifestations.
Renal sodium reabsorption depends on the activity of the Na+,K+-ATPase α/β heterodimer. Four α (α1-4) and 3 β (β1-3) subunit isoforms have been described. It is accepted that renal tubule cells express α1/β1 dimers. Aldosterone stimulates Na+,K+-ATPase activity and may modulate α1/β1 expression. However, some studies suggest the presence of β3 in the kidney. We hypothesized that the β3 isoform of the Na+,K+-ATPase is expressed in tubular cells of the distal nephron, and modulated by mineralocorticoids. We found that β3 is highly expressed in collecting duct of rodents, and that mineralocorticoids decreased the expression of β3. Thus, we describe a novel molecular mechanism of sodium pump modulation that may contribute to the effects of mineralocorticoids on sodium reabsorption.
In the acrosome reaction, the spermatozoon plasma membrane fuses with the outer acrosomal membrane, resulting in the release of the acrosomal content. Several compounds, such as sex steroids, are known to modulate the acrosomal exocytosis. Testosterone regulates various functions in male reproductive physiology; however, little is known about the relationship between testosterone and the acrosome reaction. Thus, our objective was to study the effect of testosterone on the acrosome reaction of human spermatozoa. To evaluate the acrosomal exocytosis, spermatozoa were incubated with testosterone (0.2, 2.0 and 20 nmol l−1), progesterone and control medium for 60, 120, 240 and 1440 min. The acrosome reaction was assessed by staining with Hoechst 33258 and fluorescein isothiocyanate–conjugated P. sativum agglutinin lectin. In general, spermatozoa incubated with progesterone had the highest percentage of acrosomal exocytosis. The percentage of acrosome reaction obtained in the three treatments with testosterone differed from that observed for progesterone at 120, 240 and 1440 min (24 h). Additionally, significant differences were found between testosterone (2.0 and 20 nmol l−1) and progesterone after 60 min. Differences between control and the three testosterone treatments studied were obtained only at 1440 min. In general terms, these results show that testosterone exerts no inductor effects on the acrosome reaction of human spermatozoa.
Background: Recently, we proposed that Angiotensin (Ang)-[1-9] prevents the hypertension (HT) and exerts cardioprotective effect in the heart probably by antagonizing AngII actions. We hypothesized here that Ang-(1-9) rather than Ang-(1-7), reduces HT and vascular remodeling through AT2 receptor blocker (AT2R) and eNOS. Objective: To determine the antihypertensive and vascular effects of Ang-(1-9) in hypertensives rats and the signaling pathways involved in Ang-(1-9) effects. Methods: Male Lewis rats were made hypertensive by Goldblatt procedure (GB, 2K-1 clip, n = 38). As controls we used sham operated rats (S, n = 12). Four weeks after surgery, hypertensive rats were randomized to receive vehicle (n = 11), Ang-(1-9) (602 ng/kg/min, n = 12), Ang-(1-9)+Mas blocker receptor A779 (100 ng kg−1min−1,n = 8) and Ang-(1-9)+AT2R blocker PD123319 (36 ng kg−1min−1, n = 7). Six weeks after surgery, systolic blood pressure (SBP, mmHg), aortic media thickness (AMT, μm), TGF-β1 and collagen I aortic (CA) levels (fold vs S), vascular reactivity assays (VRA, % dilation at 10−9M AcCh), eNOS mRNA levels (fold) and plasma nitrate concentrations (PNC, μМ) were determined. Results: Compared to sham, GB rats had a significant (p < 0.05) increase of SBP (50%), AMT (35%), TGFβ1 (2 fold), CA (4 fold), VRA (5%) and decrease of PNC (40%). The Ang-(1-9) decreased SBP (18%), AMT (10 %), TGFβ1 (1.9 fold), CA (2 fold), increased VRA (20%), and PNC (1.6 fold). These effects were reduced by PD123319 but not by A779. Conclusion: The current study provides strong evidence for antihypertensive and antiremodeling effects of Ang-(1-9) that are mediated both by the AT2R and eNOS. Fondecyt 1100874
Summary The acrosome reaction (AR) is influenced by the action of several molecules such as GABA, P 4 , and E 2 . Objective: to determine the interaction between GABA / E 2 , and GABA / P 4 in the AR. Methods: Washed human spermatozoa capacitated for 2 h were incubated in the following conditions: BWW medium alone (control) or BWW plus: P 4, E 2, GABA, GABA+ P 4 or GABA+ E 2. The % of AR was determined by FITC-PSA. Results: Spermatozoa incubated with GABA or P 4 showed higher % of AR; additionally, separate and simultaneous P 4 and GABA incubations showed no significant difference in the % of AR. GABA plus E 2 incubation showed lower % of AR than GABA only incubated spermatozoa. Conclusions: The AR would be modulated by inductors such as GABA and P 4 ; there is not synergistic interaction between these molecules on AR induction; besides, there are inhibitory hormones such as E 2 , whose effect prevails in a combined GABA/E 2 incubation. The localisation of these compounds would determine timely AR occurrence.
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