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V Gross

Publications and source records attributed to V Gross.

At least 91 records · Page 5Linked to original sources
PubMed1997

Pressure natriuresis in salt-sensitive and salt-resistant Sabra rats.

Salt-resistant (SBN/y) and salt-sensitive (SBH/y) Sabra rats are a useful model of salt-sensitive hypertension with incompletely explored renal mechanisms. We investigated their pressure-natriuresis curves, with and without deoxycorticosterone acetate (DOCA)-salt treatment. To differentiate between extrinsic neural and hormonal mechanisms and intrinsic renal influences, we performed experiments with neural denervation, adrenalectomy, and infusions of vasopressin, norepinephrine, 17-hydroxycorticosterone, and aldosterone as well as without these maneuvers. In untreated SBN/y without controlled neural and circulating hormonal factors, urine flow and sodium excretion increased from 32 to 95 microL/min per gram kidney weight (gkwt) and from 4 to 17 mumol/min per gkwt, respectively, as renal perfusion pressure was increased from 85 to 146 mm Hg. Renal blood flow and glomerular filtration rate were autoregulated and averaged 7.5 and 1.2 mL/min per gkwt. In untreated SBN/y with controlled neural and circulating factors, pressure-diuresis and -natriuresis curves were shifted toward the right, and renal blood flow and glomerular filtration rate ranged between 4.2 and 9.1 or 1 and 1.3 mL/min per gkwt as perfusion pressure was increased from 99 to 164 mm Hg. In both protocols, values in SBH/y did not differ. DOCA-salt increased blood pressure in SBH/y. In SBH/y without controlled neural and hormonal factors, pressure-diuresis and -natriuresis curves were shifted approximately 20 mm Hg toward the right. Fractional sodium and water excretion curves, renal blood flow, and glomerular filtration rate were shifted rightward in parallel. On the other hand, SBH/y with DOCA-salt and controlled neural and hormonal factors had lower sodium and water excretion rates only at the renal perfusion pressure of 150 mm Hg as well as decreased renal blood flow and glomerular filtration rate compared with DOCA-salt SBN/y. These data suggest that both extrinsic and intrinsic factors are responsible for reduced sodium and water excretory capacity in DOCA-salt SBH/y; however, the extrinsic factors may be more important.

Adrenalectomy↗
PubMed1997

Nitric oxide synthase and renin-angiotensin system gene expression in salt-sensitive and salt-resistant Sabra rats.

The molecular mechanisms of salt sensitivity and the contribution of the kidney to salt-induced hypertension in Sabra rats are imperfectly defined. We investigated the expression of the nitric oxide (NO) system (endothelial, inducible, and neural NO synthases) and renin-angiotensin system (renin, angiotensinogen, and angiotensin II type 1A receptor) gene components in the kidneys of SBN/y (salt-resistant) and SBH/y (salt-sensitive) Sabra rat substrains, with and without deoxycorticosterone acetate (DOCA)-salt treatment. We also looked for immunocytochemical evidence of angiotensin II, the effector peptide of the renin-angiotensin system. Inducible and neural NO synthase gene expression values were lower in SBH/y than in SBN/y before and after DOCA-salt treatment. The gene expression level of endothelial NO synthase was not different in SBH/y and SBN/y, either with or without DOCA salt. Renin gene expression was significantly higher in kidneys of SBN/y than in kidneys of SBH/y rats, whereas angiotensinogen gene expression was significantly lower in SBN/y. After DOCA-salt treatment, renin gene expression was strongly suppressed in both strains but more so in SBH/y. Angiotensinogen gene expression, on the other hand, was increased by DOCA salt in SBN/y rats so that the two strains were no longer different. Angiotensin II immunoreactivity was significantly higher in SBN/y than in SBH/y; however, after DOCA salt, immunoreactivity in both strains was no longer detectable. Angiotensin II type 1A receptor gene expression was not different between the two strains, either before or after DOCA-salt administration. We conclude that DOCA salt induced a decrease in the activity of the renin-angiotensin system but did not change NO synthase gene expression in SBH/y and SBN/y. Inducible and neural NO synthase gene expression values were less in SBH/y than in SBN/y, independent of DOCA-salt administration. Thus, the NO system could explain, at least in part, the salt resistance of SBN/y.

Angiotensin II↗
PubMed1997

Effect of ursodeoxycholic acid on the inflammatory activity of indomethacin-induced intestinal inflammation in rats.

The beneficial effects of ursodeoxycholic acid (UDCA) in primary biliary cirrhosis are supposed to be mediated in part by immunological mechanisms. In this study, we have tested whether ursodeoxycholic acid also ameliorates intestinal inflammation induced by indomethacin in rats. Intestinal inflammation was induced in rats by two injections of indomethacin (7.5 mg/kg body weight) 24 h apart. To study its effects on acute inflammation, UDCA (10 mg/kg body weight) was given for three days starting with the first administration of indomethacin; for effects on chronic inflammation, UDCA was given 24 h after the first indomethacin injection for eight days. Rats were sacrificed at days 3 and 9, respectively. In acute inflammation a significant decrease of intestinal injury was observed with UDCA treatment (macroscopic score: 3.00 +/- 0.83 vs. 6.55 +/- 0.53 in controls; p < 0.01; microscopic score: 1.66 +/- 0.28 vs. 2.89 +/- 0.35 in controls; p < 0.05). In chronic inflammation the effects of UDCA treatment were less marked due to a general decline in intestinal injury. Nevertheless a significant decrease in the macroscopic injury score (3.67 +/- 0.62 vs. 1.55 +/- 0.29 in UDCA treated rats; p < 0.01) was observed. Also, there was a significant increase in body weight of UDCA treated rats after nine days compared to controls (28.8% vs. 16% increased body weight in controls; p < 0.01). Thus, ursodeoxycholic acid attenuates the severity of acute damage of small bowel and the development of chronic intestinal inflammation induced by indomethacin in rats.

Acute Disease↗
PubMed1997

Beneficial effect of ursodeoxycholic acid on mucosal damage in trinitrobenzene sulphonic acid-induced colitis.

BACKGROUND: Recently we observed that ursodeoxycholic acid (UDCA) ameliorates an experimental small intestinal inflammation induced by indomethacin in the rat. In this study, we have tested whether ursodeoxycholic acid also reduces mucosal damage in the bile-independent trinitrobenzene sulphonic acid (TNB) model of experimental colitis. METHODS: Intestinal inflammation (colitis) was induced in male Sprague-Dawley rats (250-300 g) by intracolonic administration of TNB (30 mg in 50% ethanol). Rats were treated with UDCA (10 mg/kg) either for 3 days starting with the administration of TNB for an acute inflammation (n = 11) or for 8 days starting one day after induction of colitis related to a more acute/chronic inflammation (n = 11). Rats were sacrificed at day 3 or day 9, respectively. Healing of induced colitis was assessed by macroscopic and blinded microscopic analysis as well as by measurement of bowel wet weight, daily body weight, and myeloperoxidase activity. All examinations were separately performed in three colon segments (S1 3-5 cm, S2 5.5-8 cm and S3 8.5-11 cm from anus). RESULTS: UDCA treatment significantly reduced macroscopically and microscopically detectable injury in acute inflammation in segments 1 and 2. The colitis-rats with acute/chronic inflammation had less marked mucosal damage. Nevertheless, UDCA treatment led to a significant decrease of visible injury parameters which was seen exclusively at the area of maximal ulceration (S2). Furthermore, a significant increase in body weight of UDCA-treated TNB rats compared to controls from day 5 on was found. CONCLUSION: Ursodeoxycholic acid attenuates the severity of acute inflammation and inhibits the development of acute/chronic inflammation predominantly around the area of maximal ulceration in TNB-induced colitis. In addition to our previous studies and results in indomethacin induced enteritis, these data may provide a rationale for studying how UDCA modulates functions of immune cells in the colonic mucosa.

Animals↗
PubMed1996

[Endosonographic demonstration of extrapancreatic and extraintestinal gastrinoma].

HISTORY AND CLINICAL FINDINGS: No cause had been found for chronic diarrhoea in a 57-year-old man. Up to 15 watery stools daily had been without relation to food intake and without blood admixture. But muscular cramps had developed, especially in the legs. The patient had a history of recurrent peptic ulcers for which a selective proximal vagotomy had been performed 13 years ago. Physical examination was unremarkable. INVESTIGATIONS: Alkaline phosphatase activity (182 U/l) and C-reactive protein (9.3 mg/l) were slightly raised; serum iron was 42 micrograms/dl, while all other routine laboratory tests, including protein electrophoresis, blood picture and differential count were within normal limits. Gastroscopy revealed ulcerative duodenitis, gastritis with erosions and numerous ulcers and reflux oesophagitis, grade III-IV. Endosonography showed enlarged gastric mucosal relief as sign of foveolar hyperplasia and a ca. 4 x 3 cm tumour next to the duodenal bulb. Gastrin level was 7537 pg/ml (normal < 150 pg/ml). Computed tomography and somatostatin receptor scintigraphy confirmed the site and size of the gastrinoma. TREATMENT AND COURSE: Treatment with omeprazole (40 mg three times daily) slightly improved the symptoms. The tumour was excised a week after diagnosis. The patient has been symptom-free since then. CONCLUSION: Chronic diarrhoea of unknown aetiology can be caused by an endocrine tumour; endosonography can often provide information on the diagnosis and location of such a tumour.

Chronic Disease↗
PubMed1996

Impact of oxidative stress on human cytomegalovirus replication and on cytokine-mediated stimulation of endothelial cells.

Transplantation-related pathogenic factors such as ischemia or allograft-directed inflammation are associated with oxidative changes that might lead to cellular oxidative stress. The aim of this study was to investigate the impact of oxidative stress on: (1) CMV replication in cultured human endothelial cells and (2) the stimulation of endothelial cells by proinfiammatory cytokines. Both pathomechanisms are known to contribute to graft rejection crises in vivo. Oxidative stress was induced in endothelial cell cultures with 10-200 microM buthionine sulfoximine. Western blotting showed a significant increase in the production of CMV-specific immediate early and late proteins in buthionine sulfoximine-treated cultures. Immunocytochemical staining suggested that this effect was caused by increased numbers of CMV antigen expressing cells (66% immediate early; 78%, late). Quantitative polymerase chain reaction for CMV-specific DNA and virus titration revealed that enhanced viral replication levels correlated with increased virion production. As a measure for the endothelial cell activation status, the surface expression of HLA-ABC and HLA-DR and adhesion molecules (ICAM-1, ELAM-1, VCAM-1) was quantified by fluorometric methods. Whereas oxidative stress alone did not modulate any surface molecule expression, the IFN-gamma-mediated expression of HLA-ABC and HLA-DR and the IL-1-mediated expression of ICAM-1, but not of ELAM-1 and VCAM-1 (IL-1 + TNF-alpha), was amplified. Interestingly, the amplification of HLA molecule expression was even higher in CMV-infected endothelial cells. This study provides evidence that oxidative stress contributes to the regulation of CMV replication, virus shedding, and the activation of endothelial cells by proinflammatory cytokines as it is observed in transplant recipients.

Base Sequence↗
PubMed1996

Antisense oligonucleotides for ICAM-1 attenuate reperfusion injury and renal failure in the rat.

The leukocyte adhesion molecule ICAM-1 is implicated in ischemic renal reperfusion injury. We tested the utility of an ICAM-1 antisense oligodeoxyribonucleotide (ODN) with lipofectin, six hours prior to 30 minutes of bilateral renal ischemia in the rat. We measured ICAM-1 expression by immunohistochemistry and Western blot. Our antisense ODN showed a specific ICAM-1 surface expression inhibition in vitro. We then assessed ICAM-1 expression, leukocyte infiltration, serum creatinine, serum urea concentration, and renal histology in rats subjected to renal ischemia and controls. Serum creatinine and urea concentrations 12 and 24 hours post-ischemia were increased in saline treated and reverse ODN treated rats, compared to antisense ODN treated or sham operated rats (P < 0.05). Western blotting showed decreased ICAM-1 protein in antisense ODN-treated kidneys, compared to reverse ODN treated and saline treated ischemic controls (P < 0.05). Antisense ODN also ameliorated the ischemia-induced infiltration of granulocytes and macrophages (P < 0.05), and resulted in less cortical renal damage as assessed by a quantitative pathological grading scale (P < 0.05), compared to reverse ODN or saline treatment. Thus, antisense ODN for ICAM-1 protected the kidney against ischemic renal failure. The clinical applicability of these findings extends beyond ischemic acute renal failure.

Acute Kidney Injury↗
PubMed1996

Biochemical study of individual zonae from human oocytes that failed to undergo fertilization in intracytoplasmic sperm injection.

Successful intracytoplasmic sperm injection (ICSI) is dependent upon the competence of the oocyte to respond to the injection of a spermatozoon in the presence of calcium. This study determined if oocytes that failed to become fertilized (absence of any pronuclei) failed to undergo cytoplasmic activation, as ascertained by an electrophoretic shift in the zona pellucida (zona) protein, huZP2. Of 48 zonae individually analysed, 58% did not have a detectable huZP2 shift. Three patterns were observed. In seven patients, none of the unfertilized oocyte huZP2 shifted (16 out of 48); in two, all zonae exhibited a huZP2 shift (five out of 48); in eight, there was a mixture of shifted and unshifted (27 out of 48) in each case. There was no clear relationship between the presence of the huZP2 shift and maternal age, pregnancy outcome, male-factor infertility, or fertilization rate. However, in six couples diagnosed as having no detectable male-factor infertility, 73% (11 out of 15) of the zonae had unshifted huZP2, suggesting that an oocyte defect is involved in some cases of failed fertilization after ICSI. One likely cause for the absence of the huZP2 shift is a failure of cytoplasmic activation. Since oocytes were injected at metaphase II, we hypothesize that some oocytes that failed to fertilize have completed nuclear (meiotic) without cytoplasmic maturation.

Adult↗
PubMed1996

Expression of proliferating cell nuclear antigen (PCNA) and Ki-67 in dysplasia in inflammatory bowel disease.

OBJECTIVE: Previous studies have revealed large variations in the interobserver agreement of dysplasia grading in inflammatory bowel disease. Therefore, we investigated the diagnostic value of two novel monoclonal antibodies (MIB 1 against Ki-67 and PC 10 against PCNA) in the detection of dysplasia. METHODS: A total of 62 biopsies were investigated and histologically classified as follows: 13 probably positive for dysplasia; 15 low-grade dysplasia; five high-grade dysplasia; and 15 inflammation without dysplasia and 14 normal controls. The percentage of positive Ki-67- or PCNA-stained nuclei (= labelling index) was determined in relation to the distribution throughout the mucosa. RESULTS: In all biopsies PCNA-labelling index exceeded that of Ki-67-labelling index. In the superficial half of the crypt PCNA- and Ki-67-labelling indices in the biopsies with 'indefinite for dysplasia, probably positive' or low-grade dysplasia exceeded that of normal tissue (P < 0.001). However, an unequivocal discrimination between biopsies with 'indefinite for dysplasia, probably positive' or low-grade dysplasia and inflammation was not possible. PCNA- and Ki-67-labelling indices were significantly higher in high-grade than in low-grade dysplasia (PCNA 81.4% vs. 44.3%, Ki-67 54.8% vs 30.9%, P < 0.001). Most interestingly, labelling indices of both markers were significantly (P < 0.0001) higher in biopsies with high-grade dysplasia than with active inflammation in the superficial half of the crypt. CONCLUSION: PCNA and Ki-67 are useful adjuncts in the diagnosis of high-grade dysplasia, because high-grade dysplasia can easily be distinguished from low-grade dysplasia or active inflammation if the distribution of the positive-stained cells within the mucosa is taken into account. Lower unspecific binding and lower influence on proliferation activity by inflammation prompts us to prefer Ki-67 (MIB 1).

Biopsy↗
PubMed1996

Distinct patterns of immunoglobulin classes and IgG subclasses of autoantibodies in patients with inflammatory bowel disease.

OBJECTIVE: The pathophysiological significance of autoantibodies in inflammatory bowel diseases (IBD) is still unclear. To assess specific immunological abnormalities we examined the distribution and restriction of immunoglobulin classes and subclasses of anti-neutrophil cytoplasmic antibodies (ANCAs) in ulcerative colitis and of antibodies to pancreatic juice (APJs) in Crohn's disease. METHODS: We tested 62 sera of patients with ulcerative colitis and 184 sera of patients with Crohn's disease for their immunoglobulin class and IgG subclass distribution of ANCAs (in ulcerative colitis patients) and APJs (in Crohn's disease patients) by fluorescence isothiocyanate (FITC)-labelled anti-human antibodies in an immunofluorescence assay with human granulocytes or pancreas as substrate. Twenty-five patients with Wegener's granulomatosis were used for comparison. RESULTS: In ulcerative colitis ANCAs were found in 74% of the patients. They were predominantly of the IgG (96%) and IgA class (37%). In Crohn's disease APJs (present in 28% of the cases) were of the IgG (98%) and IgA class (71%). ANCAs in ulcerative colitis were of the IgG1 (73%) and IgG3 (5%) subclasses, APJs in Crohn's disease of the IgG1 (94%), IgG2 (20%) and IgG3 (2%) subclasses. The immunoglobulin class and IgG subclass distributions of ANCAs and APJs resembled the changes in total immunoglobulin classes and IgG subclasses in ulcerative colitis or Crohn's disease. CONCLUSION: The immunoglobulin classes and IgG subclasses of autoantibodies in ulcerative colitis and Crohn's disease differ from each other and from the distribution of autoantibodies in vasculitic diseases (Wegener's granulomatosis, microscopic vasculitis, systemic lupus erythematosus). These alterations reflect specific pathophysiological features of ulcerative colitis and Crohn's disease.

Adolescent↗
PubMed1996

Increased interleukin 8 expression in the colon mucosa of patients with inflammatory bowel disease.

To test whether there is a difference in the expression of interleukin 8 (IL8) between Crohn's disease and ulcerative colitis and to determine the main site of its synthesis this study analysed IL8 in mucosal biopsy specimens of patients with Crohn's disease and ulcerative colitis by enzyme linked immunosorbent assay (ELISA) and by in situ hybridisation. IL8 was measured by ELISA in 38 normal control patients, eight inflammatory control patients, 55 Crohn's disease biopsy specimens (26 patients), and 67 ulcerative colitis biopsy specimens (35 patients). IL8 mRNA was determined in samples by in situ hybridisation using a specific IL8 RNA probe. IL8 protein was significantly increased in macroscopically inflamed specimens of Crohn's disease (median 118 pg/specimen, p < 0.0001), ulcerative colitis (median 140 pg/specimen, p < 0.001), and inflammatory controls (median 30 pg/specimen, p = 0.010) compared with normal controls (median 4 pg/specimen). IL8 was also increased in uninflamed specimens of Crohn's disease (median 46 pg/specimen, p < 0.001) but not of ulcerative colitis patients (median 9 pg/specimen, p = 0.3). IL8 protein in the mucosa correlated significantly with macroscopic inflammation in Crohn's disease (r = 0.47, p < 0.001) and in ulcerative colitis (r = 0.60, p < 0.001). IL8 mRNA was detected by in situ hybridisation in 31 of 55 biopsy specimens (56%) of Crohn's disease patients, in 38 of 67 specimens of ulcerative colitis patients (57%), in five of eight inflammatory controls (63%) and in five of 38 normal controls (13%). Mucosal IL8 mRNA expression correlated with mucosal IL8 protein (r = 0.46, p < 0.001). IL8 mRNA was only detected in inflammatory cells of the interstitium but not in mucosal epithelial cells. IL8 is produced mainly in the lamina propria of the colon in inflammatory bowel disease and correlates with mucosal inflammation.

Adolescent↗
PubMed1996

Lifelong angiotensin-converting enzyme inhibition, pressure natriuresis, and renin-angiotensin system gene expression in transgenic (mRen-2)27 rats.

The transgenic rat (TGR) (mRen-2)27 is said to have low circulating active renin values in plasma and little or no renin gene expression in the kidney. Nevertheless, intrarenal angiotensin II-related effects appear to be responsible for the rightward shift in pressure-natriuresis curves of TGR. To clarify the role of the intrarenal renin-angiotensin system in modulating TGR pressure-natriuresis, TGR were given lifelong lisinopril by treating TGR and their mothers before conception. Rat and mouse renin, AT1 receptor, and angiotensinogen gene expression in the kidneys were studied with in situ hybridization. Neural and endocrine regulatory differences between TGR and Sprague-Dawley Hannover (SDH) rats were eliminated by renal denervation and infusion of vasopressin, aldosterone, 17-OH corticosterone, and norepinephrine. TGR with lisinopril had blood pressures similar to SDH. In TGR with lisinopril, the pressure-natriuresis curve was shifted leftward but not quite to the values observed in SDH given lisinopril. The histology of lisinopril-treated TGR was indistinguishable from normal SDH. Lisinopril increased rat renin and angiotensinogen gene expression both in SDH and TGR, but it did not influence mouse renin gene expression in TGR. Discontinuing lisinopril increased blood pressure in TGR and shifted the pressure-natriuresis relationship rightward. Thus, the components of the endogenous renin-angiotensin system and the mouse renin transgene were present and expressed in kidneys of TGR. The rat gene components responded to lisinopril as expected, but the mouse renin transgene expression was not influenced. Lisinopril normalized TGR blood pressure; however, a detectable leftward shift in pressure-natriuresis remained. These studies underscore the role of angiotensin-mediated effects of the mouse renin transgene in terms of shifting pressure-natriuresis in TGR.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Nisoldipine and pressure-natriuresis curves in transgenic (mRen2)27 rats.

OBJECTIVES: The mechanism by which antihypertensive drugs influence pressure natriuresis gives insight into their mode of action. We tested the effects of nisoldipine on pressure natriuresis, glomerular filtration rate, and renal blood flow in transgenic (mRen2)27 rats and Sprague-Dawley Hannover control rats. METHODS: The rats were anaesthetized, uninephrectomized with denervation of the remaining kidney, administered noradrenaline, 17-hydroxycorticosterone, vasopressin, and aldosterone to 'clamp' these regulatory systems and nisoldipine (0.5 mg/kg bolus plus 0.017 mg/kg per min). The glomerular filtration rate and renal plasma flow were measured with inulin and PAH. Renal perfusion pressure was varied from approximately 100 to approximately 200 mmHg with clamps above and below the kidney. RESULTS: Nisoldipine shifted not only the pressure-diuresis and pressure-natriuresis curves but also the fractional sodium and water curves leftwards in transgenic (mRen2)27 rats, but not in Sprague-Dawley Hannover rats. Nisoldipine increased the glomerular filtration rate and renal blood flow in transgenic (mRen2)27 rats but not in Sprague-Dawley Hannover rats. CONCLUSIONS: Nisoldipine shifts the pressure-natriuresis curve in transgenic (mRen2)27 rats leftwards; sodium and water excretion is increased for any given perfusion pressure. This effect is intrinsic to the kidney and is associated with inhibition of tubular sodium and water reabsorption and with an increase in renal perfusion.

Animals↗
PubMed1996

Oral pH-modified release budesonide versus 6-methylprednisolone in active Crohn's disease. German/Austrian Budesonide Study Group.

OBJECTIVE: Corticosteroids are effective in acute Crohn's disease (CD). The present study assessed the effectiveness and safety of oral pH-modified release budesonide (BUD) in patients with active CD in comparison with 6-methylprednisolone (MPred). DESIGN: This was a prospective multicentre, randomized, double-blind, double-dummy study. METHODS: A total of 67 patients with active CD (CDAI > 150) were included. Patients were treated with 3 x 3 mg BUD (n = 34) or MPred (n = 33) according to a weekly tapering schedule (48-32-24-20-16-12-8 mg). The primary aim was remission of CD (CDAI < 150 and decrease by at least 60 points from baseline) after eight weeks. RESULTS: Baseline demographics, disease activity and localization of CD in the small bowel and the colon were similar in both treatment groups. On an intention-to-treat basis 19/34 patients in the BUD group (55.9%) and 24/33 patients in the MPred group (72.7%) were in remission after eight weeks (P = 0.237). Therapy failed in 15/34 patients (44.1%) of the BUD group and in 9/33 patients (27.3%) of the MPred group. The mean CDAI decreased from 262 +/- 50 to 118 +/- 69 in the BUD-group and from 262 +/- 81 to 95 +/- 61 in the Mored group (P = 0.183, final CDAI BUD vs. MPred). Steroid-related side effects appeared in 28.6% of the patients in the BUD group and in 69.7% of the patients in the Mored group (P = 0.0015). CONCLUSIONS: Oral pH-modified release budesonide (3 x 3 mg/day) is almost as effective as a conventional corticosteroid in patients with active CD but causes significantly less corticosteroid-related side effects.

Administration, Oral↗
PubMed1996

[Ambulatory education of patient with Crohn disease/ulcerative colitis].

BACKGROUND: Patient education has been accepted widely over the past years as a valid component of disease management in patients with chronic diseases. The aim of our study was to evaluate the effects of patient education in patients with inflammatory bowel disease. Participation in a patient education program should increase the patient's disease-related knowledge and positively influence the patient's quality of life, depression, beliefs of internal control and social activity. METHODS: We studied 36 patients with Crohn's disease and ulcerative colitis: 18 were educated in four sessions, 18 were not educated (control-group). The following topics were presented: diagnosis, causes and course of disease; medication and surgery; nutrition and social benefits and stress management and coping with the disease. RESULTS: The effects of the program were evaluated before, immediately and three months after the intervention using questionnaires. Participants in the program showed a significant increase in knowledge after three months compared with the non-participants. There were positive, although not significant effects on psychosocial variables. CONCLUSION: Patient education is a valuable means to increase knowledge of disease and treatment in patient's with Crohn's disease and ulcerative colitis. Effects on psychosocial variables need to be examined on a long term basis in larger patient groups.

Adaptation, Psychological↗
PubMed1996

The renin-angiotensin system and renal function in transgenic (mRen2)27 rats.

The transgenic rat (TGR)(mRen2)27 was the first hypertensive transgenic rat model developed. The model is unique in that it allows studying the effects of a single gene, namely the mouse salivary gland renin gene (mRen2), in the rat. The transgene is expressed in various rat tissues, including the central nervous system, adrenal gland, and the kidney. TGR exhibit a rightward shifted pressure-natriuresis curve that is overwhelmingly angiotensin II (Ang II) dependent. The mRen2 transgene, the rat's own renin gene, angiotensinogen, and the type 1 Ang II receptor, AT1, are all expressed in the kidneys of TGR. The rat's own renin gene is regulated normally in renal tissue, while the mRen2 transgene operates independently of blood pressure. These results, coupled with findings that the mRen2 transgene product converts rat angiotensinogen more effectively than endogenous rat renin, that the TGR may have high circulating mouse renin levels which increase with age, and the fact that high circulating prorenin concentrations are present in these TGR, shed light on the kidney's role in the blood-pressure-elevating mechanisms of TGR. The viewpoint that the kidneys are not mechanistically important in this TGR model must be revised.

Angiotensin II↗