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Biomedical subjects

I Sobhani

Publications and source records attributed to I Sobhani.

At least 19 recordsLinked to original sources
PubMed2005

Leptin stimulates the proliferation of human colon cancer cells in vitro but does not promote the growth of colon cancer xenografts in nude mice or intestinal tumorigenesis in Apc(Min/+) mice.

BACKGROUND AND AIMS: Leptin, the product of the ob gene, has been suggested to increase the risk of colon cancer. However, we have shown that although leptin stimulates epithelial cell proliferation it reduces the development of carcinogen induced preneoplastic lesions in the rat colon. Here, we explored the effect of leptin in vitro on proliferation of human colon cancer cells, and in vivo on the growth of HT-29 xenografts in nude mice and the development of intestinal tumours in Apc(Min/+) mice. METHODS: Proliferation of HT-29, LoVo, Caco2, and SW 480 cells was assessed in the absence or presence of leptin (20-500 ng/ml) by 3H-thymidine incorporation and cell count. Leptin (800 microg/kg/day) or its vehicle was delivered for four weeks to nude mice, inoculated with HT-29 cells on day 0, and for six weeks to Apc(Min/+) mice. RESULTS: Leptin dose dependently stimulated cell DNA synthesis and growth in all cell lines. In nude mice, leptin caused a 4.3-fold increase in plasma leptin levels compared with pair fed controls. This hyperleptinaemia, despite leptin receptor expression in tumours, did not induce significant variation in tumour volume or weight. Tumour Ki-67 index was even inhibited. In leptin treated Apc(Min/+) mice, a 2.4-fold increase in plasma leptin levels did not modify the number, size, or distribution of intestinal adenomas compared with pair fed controls. CONCLUSIONS: Leptin acts as a growth factor on colon cancer cells in vitro but does not promote tumour growth in vivo in the two models tested. These findings do not support a pivotal role for hyperleptinaemia in intestinal carcinogenesis.

Adenoma↗
PubMed2001

The H3 receptor is involved in cholecystokinin inhibition of food intake in rats.

We investigated the peripheral effects of an H3-receptor agonist and an H3-receptor antagonist (R)alpha-methylhistamine (Ralpha-MeHA) and thioperamide, respectively, on basal feeding and the CCK8-induced inhibition of food intake in rat. Intraperitoneal injection of thioperamide reduced food intake in a dose-dependent manner with maximal inhibition (35%, P<0.01 vs saline) at 3 mg/kg. (R)alpha-MeHA (0.3-3 mg/kg i.p.), an H3-receptor agonist alone had no effect on feeding but reversed the thioperamide-induced inhibition of food intake in a dose-dependent manner. The maximal feeding inhibitory dose of thioperamide (3 mg.kg i.p) increased by 40% and 22 % (P<0.01 vs saline) brain and stomach histamine contents, respectively. Histamine (0.3 - 6 mg/kg i.p.) and CCK-8 (3 - 30 microg/kg i.p) also inhibited food intake in a dose-dependent manner. Inhibition was 20% to 40% for histamine and 40% to 80% (P<0.01 vs saline) for CCK8. CCK-8 inhibition of feeding was increased by thioperamide and prevented by (R)alpha-MeHA in a dose-dependent way. In addition, CCK-8 did not reduce food intake if rats were pretreated with pyrilamine or ranitidine postsynaptic H1- and H2-receptor antagonists respectively. Our data suggest that the H3-receptor is involved in basal feeding. They also suggest that CCK satiety depends upon the release of histamine which acts on the H2- and H1-receptors, the final mediators of this effect.

Animals↗
PubMed2001

Prevalence of high-grade dysplasia and cancer in the anal canal in human papillomavirus-infected individuals.

BACKGROUND & AIMS: The incidence of anal cancer is higher in patients with anal canal condyloma, a sexually transmitted disease, than in the general population. We determined the prevalence of anal dysplasia and cancer in patients with anal canal condyloma with respect to human immunodeficiency virus (HIV) status, immunity status, and human papillomavirus types. METHODS: In 174 consecutive patients (114 HIV positive, 60 HIV negative) with anal canal condyloma, lesions were cured, and the patients were then followed up prospectively. Langerhans cells (LCs) in normal anal mucosa were quantified, and viruses (Epstein-Barr virus, cytomegalovirus, human simplex virus 1, and various human papillomavirus [HPV] types) were characterized on inclusion. During follow-up (median 26 months), relapsed condylomas were resected and examined histologically. HIV load and CD4 T-lymphocyte counts in serum were determined at each visit. RESULTS: Several factors differed significantly between HIV-positive and HIV-negative patients: LCs/mm anal tissue (15 vs. 30), oncogenic HPV (27% vs. 13%), other current anal infections (44% vs. 0%), and sex ratio (93% vs. 73% male). During follow-up, condylomas relapsed in 75% of the HIV-positive patients, with 19 high-grade dysplasias (HGDs) and 1 invasive carcinoma, but in only 6% of HIV-negative patients, with 1 HGD. Male sex, HIV positivity, and <15 LCs/mm tissue were independent risk factors for condyloma relapse. HIV positivity, HGD before inclusion, and condyloma relapse were independent risk factors for HGD and cancer. Serum HIV load was associated with relapse, whereas CD4 T-lymphocyte counts were not. CONCLUSIONS: The prevalence of HGD and carcinoma is higher in HIV-positive than in HIV-negative patients, probably because of HPV activity. HIV-positive patients with high serum HIV load and/or a history of anal dysplasia should be examined by anoscopy, and condylomas should be analyzed histologically.

Adult↗
PubMed2000

[Helicobacter pylori and gastric neoplasms: adenocarcinoma and lymphoma].

Helicobacter pylori is a risk factor for gastric carcinoma and an established carcinogenic bacterium. The relative risk to induce a gastric cancer is estimated to be 3 to 6 compared to that of individuals without H. pylori. Gastric atrophy and intestinal metaplasia in gastric mucosa are 2 well recognized precancerous lesions. Their occurrence and evolution are multifactorial depending on age at first infection, duration of infection and host's genetic characteristics. Prevention using H. pylori eradication is recommended only in individuals with high risk of cancer. Gastric lymphoma, although less frequent, may be due to H. pylori infection. Only in low grade lymphoma H. pylori eradication and periodic surveillance are recommended.

Adenocarcinoma↗
PubMed2000

Are sphincter defects the cause of anal incontinence after vaginal delivery? Results of a prospective study.

PURPOSE: Anal incontinence affects approximately 10 percent of adult females. Damage to the anal sphincters has been considered as the cause of anal incontinence after childbirth in the sole prospective study so far available. The aims of the present study were to determine prospectively the incidence of anal incontinence and anal sphincter damage after childbirth and their relationship with obstetric parameters. METHODS: We studied 259 consecutive females six weeks before and eight weeks after delivery. They were asked to fill in a questionnaire assessing fecal incontinence. Anal endosonography (7-10 MHz) was then performed. Two independent observers analyzed internal and external anal sphincters. RESULTS: A total of 233 patients (90 percent) were assessed, of whom 31 had cesarean section. De novo sphincter defects were observed in 16.7 percent (14 percent external, 1.7 percent internal, and 1 percent both) in the postpartum period only after vaginal delivery. These disruptions occurred with the same incidence after the first and the second childbirth. Independent risk factors (odds ratio; 95 percent confidence interval) for sphincter defect were forceps (12; 4-20), perineal tears (16; 9-25), episiotomy (6.6; 5-17), and parity (8.8; 4-19) as revealed by multivariate analyses. The overall rate of anal incontinence was 9 percent and independent risk factors (odds ratio; 95 percent confidence interval) involved forceps (4.5; 1.5-13), perineal tears (3.9; 1.4-10.9), sphincter defect (5.5; 5-15), and prolonged labor (3.4; 1-11). Among these patients only 45 percent had sphincter defects. CONCLUSION: Anal incontinence after delivery is multifactorial, and anal sphincter defects account for only 45 percent of them. Primiparous and secundiparous patients have the same risk factors for sphincter disruption and anal incontinence. Because external anal sphincter disruptions are more frequent than internal anal sphincter damage, surgical repair should be discussed in symptomatic patients.

Adolescent↗
PubMed2000

Leptin secretion and leptin receptor in the human stomach.

BACKGROUND AND AIM: The circulating peptide leptin produced by fat cells acts on central receptors to control food intake and body weight homeostasis. Contrary to initial reports, leptin expression has also been detected in the human placenta, muscles, and recently, in rat gastric chief cells. Here we investigate the possible presence of leptin and leptin receptor in the human stomach. METHODS: Leptin and leptin receptor expression were assessed by immunohistochemistry, reverse transcriptase-polymerase chain reaction (RT-PCR), and western blot analysis on biopsy samples from 24 normal individuals. Fourteen (10 healthy volunteers and four patients with non-ulcer dyspepsia and normal gastric mucosa histology) were analysed for gastric secretions. Plasma and fundic mucosa leptin content was determined by radioimmunoassay. RESULTS: In fundic biopsies from normal individuals, immunoreactive leptin cells were found in the lower half of the fundic glands. mRNA encoding ob protein was detected in the corpus of the human stomach. The amount of fundic leptin was 10.4 (3.7) ng leptin/g mucosa, as determined by radioimmunoassay. Intravenous infusions of pentagastrin or secretin caused an increase in circulating leptin levels and leptin release into the gastric juice. The leptin receptor was present in the basolateral membranes of fundic and antral gastric cells. mRNA encoding Ob-RL was detected in both the corpus and antrum, consistent with a protein of approximately 120 kDa detected by immunoblotting. CONCLUSION: These data provide the first evidence of the presence of leptin and leptin receptor proteins in the human stomach and suggest that gastric epithelial cells may be direct targets for leptin. Therefore, we conclude that leptin may have a physiological role in the human stomach, although much work is required to establish this.

Adult↗
PubMed2000

[Postpartum sphincter rupture and anal incontinence: prospective study with 259 patients].

AIMS: Damage to the anal sphincter has been considered as the cause of anal incontinence after childbirth. The aims of the present study were to determine prospectively the incidence of anal incontinence and anal sphincter damage after childbirth, and their relationship with obstetric parameters in France. PATIENTS AND METHODS: We studied 259 consecutive women six weeks before and eight weeks after delivery. They were asked to fill out a questionnaire dealing with faecal and urinary incontinence. Anal endosonography (B&K 7-10 MHz) was then performed. Two independent observers analyzed internal and external anal sphincters. RESULTS: Two hundred and thirty-three women (90%) were assessed, among whom 31 had had a caesarean section. De novo sphincter defects were observed in 19.3% (39 patients) in the postpartum period only after vaginal delivery (202 patients). These disruptions occurred with the same incidence after the first and second childbirth. Independent risk factors (odds ratio; 95% confidence interval) for sphincter defect were forceps (odds ratio 11.9; 4.8-33.3), perineal tears (odds ratio 16.1; 4.4-83.9), episiotomy (odds ratio 6.6; 1.7-34.2), and pauciparity < or = 2 (odds ratio 8.8; 1-78.3), as revealed by multivariate analyses. The overall rate of de novo anal incontinence was 9% (20 patients), and independent risk factors involved forceps (odds ratio 4.5; 1.5-13), perineal tears (odds ratio 3.9; 1.4-10.9), de novo sphincter defect (odds ratio 5.5; 5-15) and prolonged labor (odds ratio 3.4; 1-11). Among the 20 women who had de novo anal incontinence, only 45% (9 patients) had sphincter defects. CONCLUSION: De novo anal incontinence after delivery is multifactorial and anal sphincter defects account only for 50% of them. Primiparous and secundiparous women have the same high-risk factor for sphincter disruption and anal incontinence. Since external anal sphincter disruptions are more frequent than internal anal sphincter damage, surgical repair should be discussed.

Adolescent↗
PubMed1998

[Chronic inflammatory bowel disease: new insight from genetics].

The cause of chronic inflammatory bowel disease remains unknown. A genetic origin has been suggested by studies in twins. The gene or genes involved in Crohn's disease is probably situated on chromosome 16 and the genes involved in ulcerative colitis on chromosomes 2 and 7. It will undoubtedly take some time before the exact loci are precisely identified, but current research suggests that clinical applications are not far off.

Adolescent↗
PubMed1998

Regression of rectal stenosis secondary to neoplasm in an HIV1-positive patient with gancyclovir antiviral therapy: report of a case.

PURPOSE: The case of a human immunodeficiency virus-positive patient with rectal stenosis caused by a tumor that completely regressed in response to gancyclovir is presented. METHODS: Several biopsies from the tumoral mass failed to show any stigmata of non-Hodgkin's lymphoma, adenocarcinoma, or Kaposi sarcoma. No parasites could be detected in rectal biopsies. Viral inclusions showing both Epstein-Barr virus and cytomegalovirus on immunostained sections suggested an unusual form of viral infection. RESULTS: Antiviral therapy (gancyclovir 10 mg/kg/day) had a dramatic effect on pain and discharge of blood, and suppressed rectal difficulties within three days of therapy. The antiviral treatment was stopped at Day 10 because of leukopenia. Endoscopic and histologic examinations revealed normal rectal mucosa after 3, 6, 9, 12, and 18 months of follow-up. CONCLUSION: This is the first case of complete and long-term regression of a rectal stenosis secondary to a tumoral mass in response to antiviral therapy in patients with human immunodeficiency virus.

Antiviral Agents↗
PubMed1998

A diffuse T lymphocytic gastrointestinal mucosal infiltration associated with Sjögren's syndrome resulting in a watery diarrhea syndrome and responsive to immunosuppressive therapy.

We report the case of a 45-yr-old white man, investigated for chronic diarrhea, malabsorption and weight loss associated with sicca syndrome. Endoscopic and x-ray examinations showed normal macroscopic mucosa in gastrointestinal tract (GIT). Immunohistochemistry showed diffuse polyclonal T cell lymphocytes infiltrating either epithelium and lamina propria in GIT. There was no villous atrophy in the jejunum and ileum. Corticosteroids, azathioprine, and cyclosporine failed to improve symptoms. Monthly intravenous cyclophosphamide administered over 1 yr, stopped the diarrhea and weight loss. The patient is free of symptoms up to a 5-yr follow-up.

Cell Movement↗
PubMed1996

Regulation of platelet-activating factor production in gastric epithelial cells.

The authors have previously reported that platelet-activating factor (PAF), a phospholipid mediator with potent proinflammatory activities, is produced in the gastric mucosa and stimulates gastric acid secretion in humans and animals. In the present study they used the human gastric tumour cells HGT1 (clone 6) to examine whether PAF production is regulated by neuromediators. PAF was extracted by ethanol and assayed by the washed platelet aggregation test. HGT1 cells produced PAF spontaneously (110 +/- 20 pg 10(6) cells). The addition of vasoactive intestinal peptide (VIP; 10(-9) to 10(-7) mol L(-1)) or of histamine (10(-5) to 10(-3) mol L(-1)) increased PAF production by three- to fivefold, while the addition of carbachol (10(-7) to 10(-4) mol L(-1)) increased PAF production up to sevenfold. PAF production was also increased up to 10- to 13-fold, in a dose- and time-dependent manner, by the addition of calcium and two- to threefold by the addition of phorbol myristate acetate (PMA; 10(-7) to 10(-5) mol L(-1)). However, the addition of dibutyryl cyclic AMP (dBcAMP; 10(-6) to 10(-4) mol L(-1) was without any effect. This is the first report showing PAF production by gastric epithelial cells in response to histamine, VIP and carbachol. Furthermore, the findings are consistent with a central role of calcium in this production. The results of this study, together with those of previous studies from the authors' laboratory, support the hypothesis that PAF is a physiological mediator of gastric acid secretion.

Animals↗
PubMed1996

Lanreotide inhibits human jejunal secretion induced by prostaglandin E1 in healthy volunteers.

1. Somatostatin inhibits hormonal secretions in the gastrointestinal tract. Somatostatin analogues are used in the treatment of VIPome-related watery diarrhoea. In addition, more than 10% of patients with AIDS suffer from diarrhoea likely due to the increased intestinal secretion of water and ions. However, the direct effect of somatostatin on the flux of water and ions in the intestine has not been, so far, analyzed in vivo. The aim of the present study was to evaluate the effect of lanreotide, a somatostatin analogue, on the movements of water and ions in the jejunum in man. 2. Accordingly, 10 healthy volunteers (age 18-35 years, mean 27) and two patients with AIDS (26 and 33 years) suffering from water diarrhoea (> 800 ml day-1) underwent intestinal perfusion using a four lumen tube with proximal occluding balloon. The segment tested was 25 cm long. The jejunum was infused by an isotonic control saline solution containing polyethylene glycol (PEG) as nonabsorbable marker. Basal jejunal secretions were measured in all subjects. Prostaglandin E1 (PGE1) was administered intraluminally to stimulate jejunal secretion in healthy volunteers. The effect of intravenous lanreotide on the jejunal PGE1-induced secretions of water and electrolytes was analysed in healthy subjects and on the basal secretions in AIDS patients. Each period was analyzed on the basis of three (10 min) successive intestinal juice collections after 20-30 min equilibration time. The antisecretory effect of lanreotide was evaluated in each subject as the difference between fluxes compared to the control period. 3. In healthy volunteers, PGE1 induced secretion of H2O, Na+, K+ and Cl- in the jejunum and lanreotide reduced significantly PGE1-induced response. In both AIDS patients basal fluxes of water and ions were reduced by lanreotide in a dose-dependent manner. 4. Somatostatin can reduce stimulated-jejunal secretion of ions and water in normal subjects and may improve water diarrhoea in AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed1996

[Laxative effect and tolerance of lactulose administrated in one or two intakes in the treatment of chronic idiopathic constipation. Groupe d'Investigateurs O'Ile-de-France (GIIF)].

OBJECTIVES: The aim of this study was to compare the tolerance and effects of lactulose taken at a daily dose of 20 mg in one or two intakes, in the treatment of idiopathic chronic constipation. METHODS: A total of 121 outpatients (30 men, 91 women, mean age 55) was included in a prospective double blind crossover multicentric study. Patients took lactulose according to two different ways of administration and for two successive 3-week periods. Each period consisted in 2 weeks of adaptation and one week of evaluation. At the end of each period, a global visual satisfactory scale was evaluated as a global index. Patients collected every day the frequency and the aspects of the stools, the quality of exoneration and the existence of digestive symptoms. RESULTS: Number of stools per week (7.29 +/- 3.20 vs 7.08 +/- 3.03), consistency, quality of exoneration, were equivalent whatever the number of intakes and the period of treatment. With one or two intakes, the satisfactory index was the same but significantly better at the end of the second period. With one or two intakes, frequency and intensity of side effects were low and identical. They mostly occurred during the first period. CONCLUSION: Effects and tolerance with one single intake of lactulose (20 g) in the evening and with two intakes, were found to be equivalent. Effect on exoneration persists during the six weeks of administration and then tolerance improves.

Adolescent↗
PubMed1996

[Proctitis of diversion on an excluded rectum in patients with hemorrhagic rectocolitis].

OBJECTIVES: Diversion colitis is characterized by inflammatory lesions affecting colon or rectum excluded from the fecal stream for varied etiologies. These lesions may mimic both ulcerative colitis and Crohn's disease. The aim of our study was to examine the excluded rectum in patients with ulcerative colitis, and to study the evolution of the pathological lesions after ileo-rectal anastomosis. METHODS: Eighteen patients with ulcerative colitis treated by total colectomy before ileo-rectal anastomosis were studied. The pathological features i.e. glandular alteration, inflammatory infiltrate and mucosal ulceration or fissure, were studied during 3 periods: initial colectomy, excluded rectum at surgery for anastomosis and rectal biopsies after anastomosis. RESULTS: We observed on the excluded rectum a follicular lymphoid hyperplasia (18 cases), granulomas with giant cells (9 cases), mucosal fissures (9 cases). The inflammation extended to the submucosa in all cases and was occasionaly transmural. These lesions disappeared after the anastomosis and then seemed to be connected with the rectal diversion. CONCLUSIONS: The pathological changes of diversion proctitis that includes mucosal fissures, granulomas with giants cells or transmural inflammation, may lead to an erroneous diagnosis of Crohn's disease. The review of the previous colectomy is then mandatory to confirm the initial diagnosis of ulcerative colitis. These lesions disappear after anastomosis.

Adolescent↗