Cirugía de la incontinencia urinaria bajo anestesia general sin ingreso / No disponible

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Grado de utilización de los recursos sanitarios y formas de presentación de los trastornos somatomorfos en atención primaria / Level of use of the sanitary services and forms of appearance o famatoform disorders in primary care

El objetivo de nuestro estudio es conocer el grado de utilización de los recursos sanitarios por parte de los pacientes con diagnóstico de trastorno somatomorfo y las formas de presentación del mismo en nuestro medio. Para ello diseñamos un estudio de casos y controles en el Centro de Salud de La Bañeza (León). Se midió la frecuentación de la consulta de atención primaria, estudios complementarios realizados, derivaciones al segundo nivel asistencial, derivaciones a Salud Mental, prescripciones farmacéuticas realizadas y motivos de consulta, observando que los pacientes con trastorno somatomorfo son más frecuentadores y consumen más recursos que los pacientes sin ese diagnóstico y que los síntomas neurológicos son la forma de presentación más frecuente en nuestro medio

The objective of our study is to know the grade of use of the sanitary services by the patients with the diagnosis of somatoform disorder and their forms of presentation. For this purpose we designed a case-control study in the health center of La Bañeza (León). The frequency these patients go to the health center, the complementary studies made, the enquiries made to other specialists, the enquiries made to the mental health centers, the pharmaceutical prescriptions made and the reasons of consultation were measured, observing that the patients with somatoform disorders go more times to the health center and consume more resources that the patients without that diagnosis and that the neurological symptoms is the more frequent form of appearance of these disorders

MDM2 mediated nuclear exclusion of p53 attenuates etoposide-induced apoptosis in neuroblastoma cells.

The p53 gene in neuroblastoma tumors (NB) is rarely mutated but the protein accumulates in the cytoplasm. Because p53 can mediate the cytotoxic effects of chemotherapeutic agents, it is important to determine whether accumulation of p53 in the cytoplasm impairs p53 function. Data presented here indicate that hyperactive nuclear export of p53 suppresses etoposide-induced apoptosis but does not prevent growth arrest. We compared p53 function in a pair of NB subclones. Our data show etoposide induces complete trans-location of p53 to the nucleus and activation of apoptosis in the neuroblastic NB cell line SH-SY5Y (N-type), which expresses low levels of MDM2. However, in Schwann cell-like SH-EP1 cells (S-type), which have up to 10-fold higher levels of MDM2, p53 accumulates in the cytoplasm and the cells are extremely resistant to etoposide-induced apoptosis. Notably, when MDM2 expression is inhibited in S-type cells, with a phosphorothioated antisense oligonucleotide (AS5), then p53 accumulates in the nucleus and the SH-EP1 cells undergo apoptosis. Surprisingly, induction of p21 and G1-arrest are not attenuated in S-type cells, despite the predominantly cytoplasmic location of p53. Whereas, G1-arrest is attenuated in the SH-SY5Y cells, which have high levels of nuclear p53. Taken together, these findings suggest attenuation of G1-arrest is related to the differentiation status of neuroblastomas and occurs downstream of p53 nuclear accumulation. These results demonstrate for the first time that hyperactive nuclear export of p53 attenuates chemotherapy-induced apoptosis in NB cells, and our findings suggest that inhibitors of MDM2 may enhance the therapeutic efficacy of etoposide by promoting apoptosis rather than trans-differentiation.

Increased apoptosis susceptibility in mesangial cells from spontaneously hypertensive rats.

We have examined the susceptibility to apoptosis in mesangial cells from spontaneously hypertensive rats (SHR) or from normotensive rats (WKY) and the possible involvement of nitric oxide in this process. Mesangial cells monolayers from either SHR or normal rats were incubated for 12 h in medium with or without fetal calf serum (FCS) and with or without thapsigargin (Tg, 10(-6) M). A series of cultures from rats of both groups was treated with N(G)-nitro-l-arginine methyl ester (l-NAME, 10(-4) M). We assessed apoptosis by propidium iodide staining, by TUNEL nitrite production (Griess reaction), by inducible nitric oxide synthase (iNOS) and Bcl-2 and Bax by Western blot. Incubated with a FCS-free medium, cells from SHR showed a significantly higher apoptotic rate (10.7 +/- 2.0) than with 10% FCS (10% FCS, 4.7 +/- 0.3), while WKY cells did not show this increment (10% FCS, 4.7 +/- 0.3; 0% FCS, 5.9 +/- 0. 3). Apoptosis in cells from WKY increased when incubated with thapsigargin in FCS-free medium (0% FCS+ Tg, 17.7 +/- 2.9%) and increased even more in SHR cells (0% FCS+ Tg, 19.7 +/- 2.9%). Treatment with l-NAME decreased thapsigargin-induced apoptosis in both SHR (8.2 +/- 2.4%) and WKY cells (9.3 +/- 2.4%). An increase in nitrite production and iNOS expression was detected in groups in which the apoptosis rate was elevated. A high rate of apoptosis was also associated with a decrease in the Bcl-2/Bax ratio. Our results indicate that in SHR cells, short-term serum deprivation and the increase in intracellular free calcium concentration with thapsigargin are able to enhance the apoptosis rate in primary cultures and that the expression of iNOS, and hence NO production, is involved in this effect.

Bcl-2 overexpression results in reciprocal downregulation of Bcl-X(L) and sensitizes human testicular germ cell tumours to chemotherapy-induced apoptosis.

Testicular germ cell tumours are hypersentive to chemotherapy and cell lines derived from these tumours are chemosensitive in vitro. We have previously shown that these cell lines express undetectable levels of the suppressor of apoptosis Bcl-2 and relatively high levels of the apoptosis inducer Bax (Chresta et al., 1996). To determine whether the absence of Bcl-2 in these cell lines makes them highly susceptible to drug-induced apoptosis, Bcl-2 was expressed ectopically in the 833K testicular germ cell tumour cell line. Stable overexpressing clones were isolated and three clones were studied further. Surprisingly, Bcl-2 overexpressing cells were sensitized to chemotherapy-induced apoptosis compared to the parental and vector control cells. Analysis of potential mechanisms of sensitization revealed there was a reciprocal downregulation of the endogenously expressed Bcl-X(L) in the Bcl-2 overexpressing clones. Downregulation of Bcl-X(L) to the same extent using antisense oligonucleotides enhanced etoposide-induced apoptosis by twofold. Our results indicate that Bcl-2 and Bcl-X(L) have different abilities to protect against chemotherapy-induced apoptosis in testicular germ cell tumours. In contrast to findings in some tumour cell types, Bcl-2 did not act as a gatekeeper to prevent entry of p53 to the nucleus.

Nitric oxide is involved in apoptosis induced by thapsigargin in rat mesangial cells.

The purpose of this study was to examine the mechanisms of thapsigargin-induced apoptosis in rat glomerular mesangial cells and the possible involvement of nitric oxide (NO) in this process. In mesangial cell monolayers incubated for 12 h in a medium without growth factors and with 10(-6) M thapsigargin, a known specific inhibitor of endoplasmic reticulum Ca(2+)-ATPase, a high percentage of cells showed typical nuclear features of apoptosis, assessed either by staining with propidium iodide (23 vs. 9% in control conditions) or by terminal desoxynucleotidyl transferase-mediated dUTP biotin nick end labelling (TUNEL; 17 vs. 5% in control conditions). When cells were maintained in a medium containing 10% fetal calf serum (FCS) or in a free-calcium medium, the thapsigargin-induced apoptosis rate was very low. In rat mesangial cells treatment with thapsigargin decreased the expression of BCL-2 protein and bcl-2 mRNA, whereas it did not alter the levels of BAX protein or bax mRNA. When mesangial cells were incubated with thapsigargin in the absence of FCS, we detected a significant increase in nitrite production (3.78 +/- 0.96 vs. 1.76 +/- 0.44 micromol/well). Furthermore, the treatment with the NO synthesis inhibitor L-NAME (10(-4) M) induced a significant decrease in the number of apoptotic cells (9%), whereas incubation with the NO donor SIN-1 (10(-5) M) induced a marked increase in the rate of apoptosis (29%). Western and Northern blot analysis of macrophage-type inducible NO synthase (iNOS) demonstrated that thapsigargin treatment induces the expression of the iNOS protein and iNOS mRNA. Treatment with L-NAME prevented the thapsigargin-induced BCL-2 decrease, whereas incubation with SIN-1 potentiated the effect of thapsigargin on BCL-2. Double labelling by immunohistochemistry for iNOS and TUNEL revealed that the same cells that suffered apoptosis were positive for iNOS. In summary, our results indicate that thapsigargin is able to enhance the apoptosis rate of rat mesangial cells by a mechanism that is mediated by an increase in cytosolic free calcium. Increased iNOS expression, and hence increased NO production, seems to be involved in this effect.

Increased nitric oxide synthesis and inducible nitric oxide synthase expression in patients with alcoholic and non-alcoholic liver cirrhosis.

1. The synthesis and release of nitric oxide may play a role in the pathogenesis of peripheral vasodilatation and hyperdynamic circulation observed in liver cirrhosis. In this work, we analysed the synthesis of nitric oxide by the lympho-mononuclear cells of peripheral blood from patients with chronic alcoholic and non-alcoholic liver disease and we identified the isoform of nitric oxide synthase involved in the increased nitric oxide synthesis. 2. Patients were classified following clinical and histological criteria in non-alcoholic cirrhotic, alcoholic cirrhotic and non-cirrhotic chronic liver disease. We studied clinical and analytical characteristics, haemodynamic parameters and endotoxin levels in these patients. 3. Cirrhotic patients showed an increase of cardiac output and a decrease of peripheral vascular resistance. These patients had higher levels of plasma endotoxin than those observed in the control group. N omega-Nitro-L-arginine methyl ester (L-NAME)-inhibitable nitrite production from mononuclear lymphocyte cells was higher in patients than in the control group, the highest levels being in non-alcoholic cirrhotic patients, and the lowest levels in patients with non-cirrhotic alcoholic liver disease. 4. Immunocytochemistry studies revealed a positive immunoreactivity for the inducible isoform of nitric oxide synthase in lympho-mononuclear cells that was more evident in non-alcoholic than in alcoholic cirrhotic patients. By Northern blot, inducible nitric oxide synthase mRNA expression was observed only in lymphomononuclear cells from non-alcoholic cirrhotic patients. 5. Our patients show a correlation between nitric oxide synthesis, endotoxin levels and haemodynamic parameters. 6. These findings indicate that lympho-mononuclear cell stimulation may play a role in elevated nitric oxide production in hepatic cirrhosis. Thus, this increased nitric oxide synthesis could be implicated in the pathogenesis of the haemodynamic disturbances frequently found in cirrhotic patients. This increase seems to be induced, at least in part, by activation of an inducible isoform of nitric oxide synthase.

Glomerular cell proliferation and apoptosis in uninephrectomized spontaneously hypertensive rats.

We studied renal function, glomerular cell proliferation and apoptosis for three months after uninephrectomy (UNX) in young, male, spontaneously hypertensive rats (SHR). Apoptosis was assessed by in situ dUTP biotin nick-end labeling method (TUNEL) and by propidium iodide staining. Proliferation rate was determined by immunohistochemistry to proliferating cell nuclear antigen (PCNA). Glomerular bcl-2 expression was assessed by Northern blot analysis. Our results indicate a parallel increase in proliferation and in apoptotic rates in glomerular cells from the first to the second month after UNX. In the third month after UNX, PCNA-labeled cell number continues increasing, whereas TUNEL-labeled cells did not increase. Bcl-2 expression was negative in the first and second months and increased in the third month. Glomerular size and proteinuria increased progressively along the three months of follow-up. Our observations demonstrate a different profile of cell proliferation and apoptosis during the genesis of early glomerular damage in UNX-SHR.

Endogenous angiotensin II and cell hypertrophy in vascular smooth muscle cultures from hypertensive Ren-2 transgenic rats.

We investigated the possible role of a tissular renin-angiotensin system in promoting the growth of vascular smooth muscle cells (VSMCs) from hypertensive transgenic rats (TGRs) with the mouse renin gene Ren-2. Mean arterial pressure values were 99.4 +/- 2.8 and 186.7 +/- 5.0 mm Hg for control Sprague-Dawley rats (SDs) and TGRs, respectively (p < 0.05). The tunica media of femoral arteries obtained from hypertensive TGRs was found to be thickened compared to that of age-matched normotensive SDs. Angiotensin II could be detected by dot blot and immunocytochemistry and quantified by radioimmunoassay in transgenic VSMCs, but not in control SD ones. Under serum-free conditions, VSMCs derived from TGRs showed a higher protein content than those derived from SDs (337 +/- 19 vs. 269 +/- 14 pg/cell, p < 0.05, n = 3). Under the same basal conditions, the mean planar cell surface area was significantly higher in TGR VSMCs than in SD ones (4,764 +/- 204 vs. 4,074 +/- 238 micron 2, p < 0.05). In addition, TGR VSMCs showed an enhanced [14C]-leucine uptake but SD VSMCs did not (13,188 +/- 663 vs. 7,633 +/- 713 dpm/well, p < 0.05). VSMCs showed a concentration-dependent proliferative response to fetal calf serum (FCS) that was more marked in TGRs than in SDs. In the absence of FCS, c-fos and c-jun mRNAs were expressed only in transgenic cultures. From the present results, we can hypothesize that cultured TGR VSMCs are able to synthesize angiotensin II that, being almost exclusive into the cells, contributes to produce VSMC growth in the absence of FCS stimulation.

Elevated glomerular and blood mononuclear lymphocyte nitric oxide production in rats with chronic bile duct ligation: role of inducible nitric oxide synthase activation.

Recent work indicates that nitric oxide (NO) plays an important role in the systemic and renal alterations of cirrhosis. In the present study, we have evaluated whether the inducible NO synthase (iNOS) isoform participates in the enhanced renal and systemic NO production of a rat model of cirrhosis. In vitro and in vivo experiments were performed in rats subjected to chronic bile duct ligation (BDL) and in sham-operated (SO) animals. Plasma nitrite (3.1 +/- 0.1 micromol/L in SO and 6.6 +/- 0.2 micromol/L in BDL), glomerular nitrite production (6.4 +/- 0.1 vs. 9.8 +/- 0.1 nmol/24h/7,000 glomeruli, respectively), and mononuclear lymphocyte cells nitrite production (0.3 +/- 0.04 vs. 0.6 +/- 0.12 nmol/10(6) cells, respectively) were all significantly higher in BDL than in SO. Moreover, mononuclear lymphocytes and glomeruli from BDL rats showed an increased expression of macrophage-type iNOS, detected by Western blot. Kidneys from BDL animals also showed an increased calcium-independent NO synthase activity, compared with those from SO rats. Constitutive endothelial-type NO synthase expression in glomeruli or the activity of calcium-dependent NO synthase in whole kidney did not show differences between BDL and SO rats. In cultured mesangial cells from normal rats, the addition of plasma from BDL but not of plasma from SO significantly stimulated (35%) nitrite production and increased the expression of macrophage-type iNOS. In addition, administration of aminoguanidine (AG), a preferential iNOS inhibitor, elevated dose-dependently mean arterial pressure in both groups, but this increase was greater in BDL (26.5 +/- 4.4 mm hg) than in SO (13.6 +/- 2.6). In BDL, AG also increased sodium and water excretion and glomerular filtration rate. In contrast, there were only small nonsignificant changes in SO animals. Therefore, these results indicate that the expression, activity and production of NO in kidneys, glomeruli, and mononuclear lymphocyte cells is elevated in BDL rats, and this is partly because of a plasma-derived substance(s), which stimulates iNOS formation. The amelioration of the arterial hypotension and the associated reduced excretory levels of these cirrhotic animals by aminoguanidine further support the involvement of the inducible NO synthase isoform in the renal alterations observed in BDL animals.

Gentamicin treatment increases mesangial cell nitric oxide production.

Gentamicin-induced decreases in glomerular filtration rate have been associated with a marked decline in the glomerular capillary ultrafiltration coefficient which could be mediated by mesangial cell contraction. We have assessed a possible role of endogenous nitric oxide (NO) as a modulator of the proliferative and contractile effects of gentamicin on mesangial cells. NO synthesis and release, measured as nitrite production, were increased in the presence of gentamicin; this increase was blocked by coincubation with L-NAME. Mesangial cells treated with gentamicin, but not cells under control conditions, expressed mac-iNOS mRNA and presented positive immunoreactivity for mac-iNOS. Gentamicin induced a reduction of the planar surface area of cultured rat mesangial cells; cell treatment with gentamicin plus L-arginine significantly decreased the contractile effect of gentamicin. Gentamicin increased both [3H]thymidine incorporation into DNA and viable cell number; when L-arginine was added together with gentamicin, this abolished the effect of gentamicin on mesangial cell proliferation. The present studies demonstrate that gentamicin induces the expression of mac-iNOS and produces contraction and proliferation in mesangial cells. These actions seem to be modulated by mesangial NO synthesis and release.

Effect of hypothalamic-hypophysary inhibitory factor on mesangial cell activation.

We examined the effect of a sodium pump inhibitor isolated from bovine hypothalamus and pituitary tissues on contraction, proliferation, and calcium mobilization in primary cultures of rat mesangial cells. Hypothalamic-hypophysary inhibitory factor (HHIF) inhibited rubidium uptake in a concentration-dependent manner (0.2 U/mL: 56.8 +/- 6.3% inhibition). It also induced a concentration- and time-dependent decrease in planar cell surface area. Maximal contraction (25 +/- 5% reduction in cell size) was reached at 60 minutes with a concentration of 0.2 U/mL. This effect was inhibited by both verapamil and TMB-8 (10(-5) mol/L). HHIF was also observed to increase DNA synthesis (0.2 U/mL: 4361 +/- 168 versus 2129 +/- 162 cpm per well under control conditions) and cell proliferation (0.2 U/mL: 52,290 +/- 1931 versus 10,512 +/- 121 cells per well under control conditions). Both effects were also inhibited by verapamil and TMB-8. Moreover, HHIF induced the expression of immediate early genes c-fos and c-jun mRNA. HHIF-induced effects were accompanied by an increase in cytosolic free calcium (203 +/- 58 versus 101 +/- 2 nmol/L under control conditions), which was inhibited by verapamil and TMB-8. In summary, HHIF induces mesangial cell contraction and proliferation; these effects seem to be mediated by an increase in cytosolic free calcium levels.

Gentamicin activates rat mesangial cells. A role for platelet activating factor.

Gentamicin-induced decreases in glomerular filtration rate have been associated with a marked decline in the glomerular capillary ultrafiltration coefficient which could be mediated by mesangial cell contraction or release of vasoactive hormones. We studied the effect of gentamicin on mesangial cells proliferation, contraction and Ca2+ mobilization. Moreover, we attempted to assess a possible role of platelet activating factor (PAF) as a mediator of the observed effects of gentamicin on mesangial cells. Gentamicin induced a reduction of planar surface area of cultured rat mesangial cells that was blunted by the PAF-antagonist, BN-52021. Gentamicin induced an increase in [Ca2+]i that was inhibited by BN-52021. Gentamicin also stimulated [3H]thymidine incorporation into DNA, an effect that was also reduced by BN-52021, and by other two structurally different PAF receptor antagonists: alprazolam and BB-823. Gentamicin induced c-fos mRNA expression in quiescent mesangial cells. Gentamicin stimulated the synthesis and release of PAF in cultured rat mesangial cells. The present studies demonstrate that gentamicin activates mesangial cell function. These actions seem to be mediated, at least in part, by PAF synthesis and release.

Dose-response effects of VIP on the rabbit exocrine pancreatic secretion. Comparison with PACAP-27 actions.

A dose-response study of the effects of vasoactive intestinal peptide (VIP) on the exocrine pancreatic secretion of the rabbit has been made. Furthermore, the actions of VIP and pituitary adenylate cyclase activating peptide (PACAP) on the exocrine pancreatic secretion were compared at a similar molar dose. After the infusion of VIP a linear dose-response relationship for pancreatic flow rate and bicarbonate output, up to the dose of 4 micrograms/kg, was observed. VIP acts as a partial agonist of secretin, the rabbit pancreas being less sensitive to VIP compared with other mammals. Moreover, VIP did not significantly stimulate the pancreatic protein output. PACAP stimulated the hydroelectrolyte fraction of the exocrine pancreatic secretion in a similar manner to that of VIP. Unlike what was observed with VIP, PACAP, on the same molar basis, significantly stimulated the protein and amylase outputs. Furthermore, PACAP releases VIP, so that the action of PACAP on the hydroelectrolyte fraction may be partially mediated by VIP; on the other hand, VIP is not involved in the effect of PACAP on the pancreatic enzyme secretion of this species.

[Kawasaki disease in Mexican children]. / Enfermedad de Kawasaki en niños mexicanos.

The records of 16 cases seen at Mexico Children's Hospital with a diagnosis of KD were reviewed. Mean age was three years; eight were infants, and males were dominant with a ratio of 4.3:1. Two cases occurred in sibling. Evidence of myocarditis was recognized in six, and 12 had coronary anomalies, including five with aneurysms. Two infants with severe coronary disease died, one suddenly with myocardial ischemia, and one with a ruptured aortic aneurysm. Another infant developed severe stenosis of the right coronary artery but remains asymptomatic. Two cases have persistent coronary ectasia and seven are asymptomatic with a normal echocardiogram. Predictors of coronary risk were correlated with clinical outcome. All six cases with 6 or more points had coronary anomalies, two developed giant aneurysms, two died and one has severe coronary stenosis. Of 10 cases with less than 6 points, four did not have coronary involvement, none developed giant aneurysms and none died nor developed severe coronary sequelae. Although KD has been sporadically reported in this country, the present series, the largest from a single institution, firmly establishes the presence of the disease in Mexico.

[Atlas of bidimensional subdiaphragmatic echocardiography. Technics, anatomical planes and its interpretation]. / Atlas de ecocardiografía bidimensional subdiafragmática. Técnica, planos anatómicos y su interpretación.

The interpretation of the standard echocardiogram is difficult in patients with chest deformities or lung pathology. In these instances the sub-diaphragmatic approach yields better resolution of some structures. We discuss the techniques and the advantages of such approach.

[2-dimensional echocardiography in fixed fibrous subaortic stenosis. Correlation with hemodynamics and M-mode echocardiography]. / Ecocardiografía bidimensional en la estenosis subaórtica fibrosa fija. Correlación con hemodinámica y ecocardiografía modo M.

Comparative diagnostic capacity is analyzed between two dimensional echocardiography (E-BD), hemodynamics, surgery and the M-Mode, to accurately establish the diagnosis, variety and severity of fixed fibrous subaortic stenosis, in 29 patients, whose previous diagnosis were made by two dimensional images, using paraesternal, apical and subxiphoid long axis. Group I is made up of 17 patients who had two dimensional echocardiography, M-Mode, and catheterization; Group II is composed of 12 patients who only had two-dimensional echocardiography and M-Mode. Within Group I, hemodynamics showed subaortic gradient in 81%, transvalvular in 13% and no gradient in 6%; the ventriculography showed subaortic obstruction only in 59% of the patients and was normal in 41%. The M-Mode echocardiography registered protosystolic aortic closure (CPSAo) in 50%; the subaortic obstruction was seen as a band, in 44%, non-specific echoes in the outflow tract in 12% and this was normal in 44%. The two cases with transvalvular gradient, the M-Mode registered the subaortic band, and in the case without gradient, the ventriculography showed the subvalvular obstruction. In Group II, the diagnostic signs of M-Mode were: CPSAo in 58%, band in 17%, non specific echoes in the outflow tract in 8%, and this was normal in 75%. The results support other data in that two-dimensional Echocardiography is more sensitive and more specific than M-Mode, intraventricular pressure curves and ventriculography.(ABSTRACT TRUNCATED AT 250 WORDS)