Robert F Raicht, M.D.

High prevalence of hepatitis C virus infection among immigrants from the former Soviet Union in the New York City metropolitan area: results of a community-based screening program
Batash, Steven; Khaykis, Inessa; Raicht, Robert F; Bini, Edmund J
2008 Apr;103(4):922-927, American journal of gastroenterology
BACKGROUND: Inadequate sterilization and reuse of medical equipment likely contributed to hepatitis C virus (HCV) transmission in the former Soviet Union (FSU). Although New York leads the nation in the number of immigrants from the FSU, the epidemiology of HCV infection has not been evaluated in this population. The aims of this study were to determine the prevalence of and risk factors for HCV infection among immigrants from the FSU in the New York metropolitan area. METHODS: We conducted a 3-day community-based HCV screening program in the two boroughs of the New York metropolitan area with the highest density of FSU immigrants (Brooklyn and Queens). Russian cable television was used to invite subjects to come in for free HCV testing. In the last 2 days of screening, each person also completed an HCV risk factor questionnaire. RESULTS: The overall prevalence of HCV seropositivity among the 283 subjects was 28.3% (95% confidence interval [CI] 23.0-33.5%). The prevalence of HCV infection was similar in men and women (30.3% vs 26.5%, P = 0.48) and was highest in subjects > or = 70 yr old (35.0%). HCV seropositivity was 11.1% in immigrants from Russia, 29.0% from Uzbekistan, 31.0% from the Ukraine, and 36.8% from other regions. Intramuscular injections (odds ratio 9.1, 95% CI 2.0-42.4) and blood transfusions (odds ratio 3.2, 95% CI 1.2-9.0) were the only variables that were significantly associated with HCV infection in the multivariable analysis. CONCLUSIONS: In this community-based screening program we found a high prevalence of HCV infection among immigrants from the FSU, and these infections likely resulted from inadequately sterilized medical equipment and blood transfusions. Universal HCV testing should be strongly considered for all FSU immigrants
— id: 79143, year: 2008, vol: 103, page: 922, stat: Journal Article,

High prevalence of hepatitis C virus infection among Russian immigrants in the New York city metropolitan area: Results of a community-based screening program
Batash, S; Khaykis, I; Raicht, RF; Bini, EJ
2006 ;130(4):A769-A769, Gastroenterology
— id: 108207, year: 2006, vol: 130, page: A769, stat: Journal Article,

High prevalence of HIV and HCV infection among women who are non-injection drug users
Ross, E; Raicht, RF; Dominelli, F; Bini, EJ
2006 OCT ;44(4):290A-291A, Hepatology
— id: 70931, year: 2006, vol: 44, page: 290A, stat: Journal Article,

HCV and HIV infection among non-injecting drug abusers admitted to a residential substance abuse treatment facility in New York City
Ross, E; Raicht, RF; Dominelli, F; Bini, EJ
2004 OCT ;40(4):416A-416A, Hepatology
— id: 47390, year: 2004, vol: 40, page: 416A, stat: Journal Article,

Purification of total RNA from human stool samples
Alexander RJ; Raicht RF
1998 Dec;43(12):2652-2658, Digestive diseases & sciences
While colonoscopy may detect early-stage colon tumors, a less invasive and more cost-effective technique would be beneficial. Stool, which picks up sloughed-off colonic epithelial cells, would be ideal for sampling the mucosa; shed tumor cells may display alterations in gene expression observed in intact tumors. It is first necessary, however, to show that RNA can be isolated from human feces and that this RNA contains human gene transcripts. We have therefore developed a method for the isolation of total RNA from freshly passed human stool, consisting of lysis in chaotropic agents, repeated extraction with phenol and phenol-chloroform, and absorption with an RNA-binding resin. After treatment with RNase-free DNase I, we assayed these preparations for the presence of human RNA by quantitative slot blotting, northern blotting, and reverse transcription-polymerase chain reaction (RT-PCR). We obtained 5-30 microg RNA per gram of stool from cancer patients, and about 5 microg RNA per gram of control stool. Quantitative slot blotting showed that about 10% of this RNA was of human origin. Both northern blotting and RT-PCR demonstrated the presence of human RNA in these samples. To unambiguously demonstrate the isolation of RNA from stool, we incubated a mixture of rat cells and control human stool at 37 degrees C for up to 24 hr. RT-PCR of the RNA isolated from this sample clearly revealed the presence of rat-specific mRNA. These experiments indicate that RNA can be isolated from human stool and that message encoded by human genes can be assayed in these preparations. This procedure may provide a powerful tool to identify patients at risk for colon cancer
— id: 57017, year: 1998, vol: 43, page: 2652, stat: Journal Article,

Expression of protooncogene-encoded mRNA by colonic epithelial cells in inflammatory bowel disease
Alexander RJ; Panja A; Kaplan-Liss E; Mayer L; Raicht RF
1996 Apr;41(4):660-669, Digestive diseases & sciences
Protooncogenes are cell cycle-related genes that are involved in cell growth of proliferation. Alterations in the level of expression of these genes, or expression of aberrant gene productions, have been observed in tumors and precancerous conditions. To determine if expression of these genes is altered in patients with inflammatory bowel disease (IBD) --who are at risk for development of colon cancer--we assayed transcripts of 15 protooncogenes in colonic epithelial cells of IBD patients and controls. Nine of these genes (H-ras, c-myc, c-fos, c-jun, junB, N-myc, c-abl, c-yes, and p53) were expressed in epithelial cells, whereas two (RB1 and N-ras) were not. expression of four other genes (c-src, K-ras, c-raf, and c-myb) was observed, but the intensity of these bands was too low for densitometric analysis. The steady-state levels of transcripts of H-ras and five nuclear protooncogenes (c-myc, c-fos, c-jun, junB, and N-myc) were lower in epithelial cells from involved or uninvolved IBD samples than in normal epithelial cells from either sporadic colon cancer or diverticulitis patients. The level of c-fos mRNA was two- to threefold higher in involved than in uninvolved areas of the colons of two ulcerative colitis (UC) patients, but not in one Crohn's disease (CD) patient. Message abundance of c-abl transcripts was two- to threefold lower in UC epithelial cells than in either the CD or control samples. The steady-state level of c-yes-encoded mRNA was considerably higher in IBD patients resected for colon cancer than in patients resected for active chronic IBD or in controls. The level of p53 message was constant in these samples. Increased levels of c-fos mRNA in involved UC relative to uninvolved UC may be related to the disease process. Decreased expression of c-abl transcript in UC may be a diagnostic marker for UC and may be related to the rate of cell turnover in these diseases. Enhanced expression of c-yes in IBD patients with tumors compared to active chronic IBD and controls suggests that expression of this gene may be a marker for development of colon cancer in IBD
— id: 17777, year: 1996, vol: 41, page: 660, stat: Journal Article,

Expression of growth factor receptor-encoded mRNA by colonic epithelial cells is altered in inflammatory bowel disease
Alexander RJ; Panja A; Kaplan-Liss E; Mayer L; Raicht RF
1995 Mar;40(3):485-494, Digestive diseases & sciences
A link between inflammation of the colon in inflammatory bowel disease (IBD) and the increased risk of colon cancer in ulcerative colitis (UC) may be provided by growth factor receptor genes. Their expression may be altered in response to growth factors present in the mucosa, and this, in turn, may induce further genetic changes, linked to carcinogenesis, in the cells of the colonic epithelium. To test this hypothesis, we assayed steady-state levels of eight growth factor receptor mRNAs in colonic epithelial cells of IBD patients and controls. Four of these genes (EGF-R, IGFI-R, CSF1-R, and PDGF-R-beta) were expressed in epithelial cells, whereas four (erbB-2, erbB-3, NGF-R, and met) were not. The level of the former in involved or uninvolved IBD was considerably lower than in normal epithelial cells from either sporadic colon cancer or diverticulitis patients. In contrast, expression was much higher in IBD patients with colon tumors than in active chronic IBD. The level of PDGF-R-beta mRNA was two- to fourfold higher in involved than in uninvolved areas of the colons of two UC patients, but not in one Crohn's disease patient. Message abundance of its ligand, PDGF-beta, however, was the same in paired UC samples. The pattern of expression of PDGF-beta and cripto was identical to that of EGF-R, whereas the level of mRNA of amphiregulin was the same in active chronic IBD and IBD patients with tumors. A fourth growth factor, Kfgf, was not expressed. Increased levels of PDGF-R-beta mRNA in involved UC relative to uninvolved UC may be related to the disease process in UC. Decreased expression of growth factor- and growth factor receptor-encoded mRNA in active chronic IBD may be related to the disease process, or it may be an effect of steroid therapy undergone by these patients. Enhanced expression of these genes in IBD patients with tumors compared to those without tumors suggests that this may be a marker for development of colon cancer in IBD
— id: 17778, year: 1995, vol: 40, page: 485, stat: Journal Article,

OCCULT GASTROINTESTINAL BLOOD-LOSS MAY PREDICT HIGH HEPATIC VENOUS-PRESSURE GRADIENTS IN PATIENTS WITH CIRRHOSIS
ALPERT, DJ; ALEXANDER, RJ; WEINSHEL, EH; RAICHT, RF
1994 OCT ;20(4):A327-A327, Hepatology
— id: 52316, year: 1994, vol: 20, page: A327, stat: Journal Article,

Beta adrenergic stimulation and blockade in cirrhosis: effects on azygos vein blood flow and portal hemodynamics
Weinshel EH; Altszuler HM; Raicht RF; Sedlis SP
1994 Jun;307(6):396-400, American journal of the medical sciences
It is unknown whether beta adrenergic stress has adverse hepatic hemodynamic effects. Therefore, the authors studied the hemodynamic effects of beta adrenergic stimulation and subsequent blockade in 10 patients with cirrhosis (6 Childs A, 3 Childs B, and 1 Childs C) with known or suspected portal hypertension. Free and wedged hepatic vein pressures, hepatic venous pressure gradient, heart rate, mean arterial pressure, cardiac output, and azygos vein blood flow were measured at rest and after isoproterenol infusion (mean dose = 7.3 micrograms/min: target heart rate = 150% to 200% of resting heart rate). Esmolol, an ultra-short-acting beta blocker, was then infused (dose titrated to return heart rate to baseline), and all measurements were repeated. Based on the results, the authors conclude that beta adrenergic stress provoked by isoproterenol infusion significantly increases azygos vein blood flow and hepatic venous pressure gradient. Beta blockade with esmolol reduces azygos vein blood flow and hepatic venous pressure gradient significantly below baseline
— id: 17779, year: 1994, vol: 307, page: 396, stat: Journal Article,

EFFECTS OF PENTOXYFYLLINE ON HEPATIC HEMODYNAMICS
WEINSHEL, EH; LORIN, JD; SEDLIS, SP; RAICHT, RF
1994 APR ;106(4):A1006-A1006, Gastroenterology
— id: 52459, year: 1994, vol: 106, page: A1006, stat: Journal Article,

INTESTINAL PERMEABILITY IS NOT INCREASED IN HIV PLUS PATIENTS
WEINSHEL, EH; SKLAR, BF; RAICHT, RF; MA, TY; HOLLANDER, D
1994 APR ;106(4):A792-A792, Gastroenterology
— id: 52456, year: 1994, vol: 106, page: A792, stat: Journal Article,

Oncogene alterations in rat colon tumors induced by N-methyl-N-nitrosourea
Alexander RJ; Buxbaum JN; Raicht RF
1992 Jan;303(1):16-24, American journal of the medical sciences
The authors assayed oncogene alterations in rat colon tumors induced by the direct-acting chemical carcinogen, N-methyl-N-nitrosourea (MNU). DNA isolated from 34 adenomas and eight carcinomas, as well as adjacent normal colon, of 11 rats was assayed by Southern blotting for restriction fragment length polymorphisms and gene amplifications and deletions in 13 oncogenes known to be involved in human or other animal tumors. In addition to finding apparent point mutations or other small alterations in the fos and abl genes in individual rat colon tumors, the authors observed what appear to be larger alterations (ie, rearrangements, or intragenic insertions or deletions) in the H-ras and myb loci in several tumors. In contrast, no changes in the K-ras, N-ras, myc, N-myc, neu, raf, fms, met, and hst genes were seen in any of these tumors. The frequency of myb gene alterations was higher in carcinomas than in adenomas, suggesting that these changes occurred relatively late during tumorigenesis and were not direct effects of the carcinogen. In addition, the finding of alterations in two or three oncogenes in several MNU-induced rat colon tumors suggests the possibility of more widespread genomic lesions in this model
— id: 17782, year: 1992, vol: 303, page: 16, stat: Journal Article,

Detection of transforming oncogenes in rat colon tumors induced by direct perfusion with N-methyl-N-nitrosourea
Alexander RJ; Garte SJ; Raicht RF; Buxbaum JN
1992 Jan 10;61(2):119-128, Cancer letters
We assayed rat colon tumors induced by N-methyl-N-nitrosourea (MNU) for transforming oncogenes by the NIH 3T3 transfection and nude mouse tumorigenicity assays. Transfection of DNA from 3 of 3 adenomas and 3 of 5 carcinomas induced transformed foci on NIH 3T3 cells. DNA from 2 of 3 primary foci also possessed focus-forming activity, and rat-specific sequences were observed in secondary focus DNAs. Furthermore, NIH 3T3 cells transfected with DNA from a carcinoma and from a primary focus derived from it, both positive in the focus-forming assay, induced tumors in nude mice. We found no evidence for rat H-ras, K-ras, or N-ras sequences in the DNA of any of 16 primary foci derived from 6 rat tumors; thus, in contrast to other animal tumor models induced by MNU, activation of the ras genes does not appear to predominantly occur in MNU-induced rat colon tumors. We also did not observe, in any of these foci, sequences corresponding to the rat neu, raf, fms, met, or hst genes, thus indicating that none of these is the transforming oncogene in our model. These results suggest that an as yet unidentified transforming oncogene may be activated in rat colon tumors induced by MNU
— id: 17780, year: 1992, vol: 61, page: 119, stat: Journal Article,

INTESTINAL PERMEABILITY IN HIV-INFECTION - PROPER CONTROLS ARE NECESSARY
BATASH, S; WEINSHEL, E; FALKENSTEIN, D; RAICHT, R; MA, T; KATZ, K; HOLLANDER, D
1992 MAY ;87(5):680-680, American journal of gastroenterology
— id: 51954, year: 1992, vol: 87, page: 680, stat: Journal Article,

K-ras oncogene mutations in rat colon tumors induced by N-methyl-N-nitrosourea
Jacoby RF; Alexander RJ; Raicht RF; Brasitus TA
1992 Jan;13(1):45-49, Carcinogenesis
We have been studying a rat model of colon cancer in which tumors are induced by direct application of N-methyl-N-nitrosourea (MNU) to discrete areas of the colonic mucosa for a limited period of time. Activation of the ras genes by point mutation has been observed in many experimental tumors, including tumors induced by MNU. To detect potential activating point mutations in the H-ras and K-ras oncogenes in MNU-induced rat colon tumors, DNA samples from 40 adenomas, nine carcinomas, and 14 histologically normal tissue samples from 14 rats--as well as from 16 foci induced on NIH3T3 cells by tumor DNAs--were amplified by the polymerase chain reaction and hybridized with allele-specific oligonucleotide probes. No H-ras point mutations were observed in any of these samples. We did detect K-ras point mutations, however, in four primary tumours--one adenoma (2.5%) and three carcinomas (33%); these mutations were all G----A transitions at the second nucleotide of codons 12 and 13. The absence of detectable ras mutations from the majority of tumors suggests that, in contrast to other animal models utilizing MNU, tumorigenesis in MNU-induced rat colon tumors may predominantly involve activation of genes other than ras
— id: 17781, year: 1992, vol: 13, page: 45, stat: Journal Article,

Enhanced expression of oncogene-encoded mRNA in a rat model of colon cancer
Alexander RJ; Buxbaum JN; Raicht RF
1991 Apr;301(4):238-245, American journal of the medical sciences
We have studied the expression of oncogene-encoded mRNAs in a rat model of colon cancer. In this model, rats are intrarectally administered several low doses of the direct-acting carcinogen, N-methyl-N-nitrosourea (MNU). Tumors, predominantly adenomas, develop 5-7 months following administration of the carcinogen, and many of these progress to carcinomas. Upon assaying the steady-state levels of oncogene-encoded transcripts in normal rat colon, we found that fos and N-myc are highly expressed; H-ras, K-ras, myc, myb, and neu messages are present at lower levels; and N-ras, abl, and raf mRNAs are absent. When we compared transcript levels in rat tumors to those in normal colons from the same animal, we observed a 2-4 fold increase in both myc- and H-ras-encoded mRNAs and a 2-7 fold increase in myb message, but no change in expression of any of the 7 other genes. To test whether this increased expression is related to tumor production or is simply a result of the more rapid cellular turnover observed in tumor tissue, the level of oncogene-encoded transcripts was assayed in colonic mucosae of rats given two treatments known to enhance cell turnover and DNA synthesis in the colon. Neither acute application of MNU nor a diet containing 1% cholic acid caused any change in the level of oncogene-encoded mRNAs in rat colons, thus suggesting that the increased abundance of myc, myb, and H-ras messages in tumors is associated with tumor formation. The enhancement of expression of these genes in adenomas, as well as in carcinomas, further suggests that these alterations occur relatively early during the tumorigenic process
— id: 17783, year: 1991, vol: 301, page: 238, stat: Journal Article,

DETECTION OF TRANSFORMING ONCOGENES IN RAT COLON TUMORS INDUCED BY DIRECT PERFUSION WITH N-METHYL-N-NITROSOUREA
ALEXANDER, RJ; GARTE, SJ; RAICHT, RF; BUXBAUM, JN
1991 APR ;39(2):A278-A278, Clinical research
— id: 51613, year: 1991, vol: 39, page: A278, stat: Journal Article,

EFFECTS OF BETA-ADRENERGIC STIMULATION AND BLOCKADE ON AZYGOUS VEIN BLOOD-FLOW AND PORTAL HEMODYNAMICS IN CIRRHOSIS
Weinshel, EH; Altszuler, HM; Raicht, RF; Sedlis, SP
1990 Oct;12(4):874-874, Hepatology
— id: 32038, year: 1990, vol: 12, page: 874, stat: Journal Article,

Direct cholangiography
Falkenstein DB; Raicht RF
1989 Feb;9(1):63-76, Seminars in liver disease
The role of direct cholangiographic methods has evolved significantly over the last two decades as other high-resolution imaging modalities have become available. Most of the time, careful clinical evaluation of a patient combined with ultrasonography or CT will enable a physician to arrive at a correct diagnosis with a high level of precision. In this article we have attempted to indicate situations in which direct cholangiographic methods are necessary to diagnose and treat certain hepatobiliary problems. Considerable controversy exists concerning the application of these methods for treatment of biliary problems. However, in circumstances in which the issues are openly discussed, application of these techniques can be agreed on. Direct cholangiography, like coronary angiography, is a technology that provides considerable valuable information that at present cannot be obtained by other techniques, and, in well-defined circumstances, is necessary for precise diagnosis and therapy
— id: 17784, year: 1989, vol: 9, page: 63, stat: Journal Article,

EGD IS ESSENTIAL IN THE EVALUATION OF ESOPHAGEAL SYMPTOMS IN HIV + PATIENTS
PEARLMAN, K; WEINSHEL, E; FALKENSTEIN, D; RAICHT, R
1988 SEP ;83(9):1023-1023, American journal of gastroenterology
— id: 41761, year: 1988, vol: 83, page: 1023, stat: Journal Article,

LIVER-BIOPSY IN AIDS PATIENTS
PEARLMAN, K; WEINSHEL, E; FALKENSTEIN, D; RAICHT, R
1988 MAY ;94(5):A347-A347, Gastroenterology
— id: 41782, year: 1988, vol: 94, page: A347, stat: Journal Article,

Persistent pneumoperitoneum after percutaneous endoscopic gastrostomy
Schnall HA; Falkenstein DB; Raicht RF
1987 Jun;33(3):248-250, Gastrointestinal endoscopy
— id: 17785, year: 1987, vol: 33, page: 248, stat: Journal Article,

Oncogene alterations in primary human colon tumors
Alexander RJ; Buxbaum JN; Raicht RF
1986 Dec;91(6):1503-1510, Gastroenterology
We have examined alterations in six oncogenes--H-ras, K-ras, N-ras, myc, fos, and N-myc--in nine primary human colon tumors. Tumors were obtained within an hour of resection; as a control for each tumor, adjacent normal colon tissue was also obtained. Deoxyribonucleic acid extracted from each tissue sample was assayed by digesting with appropriate restriction endonucleases and, after gel electrophoresis and transfer to nitrocellulose, hybridizing with radiolabeled oncogene probes. Amplification of the myc locus, relative to adjacent normal colon tissue, was observed in two of these tumors; by dot-blotting, it was estimated that myc was amplified twofold to fivefold in each tumor. No rearrangements of myc, however, were observed in any of these tumors. Examination of the H-ras alleles of these nine tumors revealed that eight possess only 'common' alleles of this gene, and that each was identical to its control. Normal colon DNA of the ninth patient, however, was found to possess both a 'common' and a 'rare' allele, and the 'common' allele of H-ras appeared to be deleted in the tumor DNA of this patient. A restriction polymorphism indicative of a mutation in the 12th codon of K-ras was not found in any of these tumors, and we observed no evidence of rearrangement of amplification of the N-ras, K-ras, fos, or N-myc genes
— id: 17786, year: 1986, vol: 91, page: 1503, stat: Journal Article,

ONCOGENE ALTERATIONS IN PRIMARY HUMAN-COLON TUMORS
Alexander, RJ; Buxbaum, JN; Raicht, RF
1986 Apr;34(2):A436-A436, Clinical research
— id: 31033, year: 1986, vol: 34, page: A436, stat: Journal Article,

Hemorrhoids or rectal varices: defining the cause of massive rectal hemorrhage in patients with portal hypertension
Weinshel E; Chen W; Falkenstein DB; Kessler R; Raicht RF
1986 Mar;90(3):744-747, Gastroenterology
Identifying the source of lower gastrointestinal hemorrhage in patients with chronic liver disease and portal hypertension can be challenging. We present 2 cases of hemorrhage from rectal varices and a discussion on the differences between simple hemorrhoids and rectal varices. Evaluation of rectal bleeding in patients with portal hypertension is discussed and possible therapeutic options are described
— id: 17787, year: 1986, vol: 90, page: 744, stat: Journal Article,

Alcohol-induced liver disease
Frank D; Raicht RF
1985 Jan-Feb;9(1):66-82, Alcoholism: clinical & experimental research
— id: 17789, year: 1985, vol: 9, page: 66, stat: Journal Article,

Postgastrectomy polyps--a cause of bleeding
Weinshel E; Falkenstein DB; Raicht RF
1985 Jun;31(3):202-204, Gastrointestinal endoscopy
— id: 17788, year: 1985, vol: 31, page: 202, stat: Journal Article,

INTESTINAL PERFORATION ASSOCIATED WITH CYTOMEGALOVIRUS-INFECTION IN PATIENTS WITH ACQUIRED IMMUNE-DEFICIENCY SYNDROME
FRANK, D; RAICHT, RF
1984 ;79(3):201-205, American journal of gastroenterology
— id: 41096, year: 1984, vol: 79, page: 201, stat: Journal Article,

Reduction of N-methyl-N-nitrosourea-induced colon tumors in the rat by cholesterol
Cohen BI; Raicht RF; Fazzini E
1982 Dec;42(12):5050-5052, Cancer research
Patient populations with a propensity to develop colon cancer have increased amounts of fecal cholesterol (and/or cholesterol metabolites). In this study, we report the effect of increased colonic concentrations of cholesterol and its metabolites on colon tumor promotion. The chemical carcinogen N-methyl-N-nitrosourea was instilled intrarectally into rats to initiate colon tumor formation. Following initiation, a cholesterol-supplemented diet was given. Despite a 2-fold elevation of fecal cholesterol, the number of colon tumors found was significantly reduced. These studies suggest that under certain conditions cholesterol may inhibit colon carcinogenesis
— id: 17790, year: 1982, vol: 42, page: 5050, stat: Journal Article,

The kinetics of the protective effect of beta-sitosterol against MNU-induced colonic neoplasia
Deschner EE; Cohen BI; Raicht RF
1982 ;103(1):49-54, Journal of cancer research & clinical oncology
The effect of dietary supplementation with beta-sitosterol (0.2% of diet) was followed in Fischer rats after both acute and chronic feeding. Compared to controls after 3 and 7 days, the number of epithelial cells per crypt column in both plant sterol fed groups was shifted to lower values; moreover, fewer cells above cell position 12 were engaged in DNA synthesis. Continued feeding of beta-sitosterol for 28 weeks revealed the number and position of 3HTdR-labeled cells per crypt column after 1 pulse labeling to be similar to that seen in the acute phase. However, differences were more marked after 24 h showing the maximum number of labeled cells per column to be at least 25% less than the untreated group and the leading edge of labeled cells moving more slowly up the crypt wall. Rats treated with N-methyl-N-nitrosourea (MNU) intrarectally (8 mg/animal) while simultaneously consuming beta-sitosterol demonstrated a reduction in the size of the proliferative compartment as well as the number of labeled cells per crypt column as compared to rodents receiving just the carcinogen (3.3 and 5.4 mean labeled cells per column, respectively). At this time, MNU-treated rats fed beta-sitosterol had a significantly decreased colonic tumor incidence (Raicht et al. 1980). This plant sterol which passes through the digestive tract relatively unabsorbed appears to slow colonic epithelial cell proliferation resulting in a reduced expression of neoplastic transformation
— id: 17791, year: 1982, vol: 103, page: 49, stat: Journal Article,

Effects of bile acids on colon carcinogenesis in rats treated with carcinogens
Cohen BI; Raicht RF
1981 Sep;41(9 Pt 2):3759-3760, Cancer research
Primary bile acids were studied as possible colon tumor promoters or inhibitors in a rat model of chemically induced colon cancer. Cholic acid feeding increased the number of animals with tumors, the number of tumors per animal, and the number of tumors per tumor-bearing animal. Tumor enhancement was attributed to deoxycholic acid, the bacterial metabolite of cholic acid. When chenodeoxycholic acid was fed to the rats in our model, tumor incidence was increased, but the number of tumors per animal and the number of tumors per tumor-bearing animal were similar to controls. The different fecal bile acid pattern obtained with chenodeoxycholic acid may be responsible for the differences in tumor incidence. The methodology to characterize and identify all steroidal components of the feces requires extraction, thin-layer chromatography, gas-liquid chromatography, and gas-liquid chromatography-mass spectrometry. Newer techniques include LH-20 chromatography (for sulfated steroids) and high-pressure liquid chromatography
— id: 17793, year: 1981, vol: 41, page: 3759, stat: Journal Article,

Sterol metabolism in the rat: effect of alcohol on sterol metabolism in two strains of rats
Cohen BI; Raicht RF
1981 Spring;5(2):225-229, Alcoholism: clinical & experimental research
Sterol metabolism studies using a combination of isotopic and chromatographic procedures were carried out in two strains of rats fed 5% ethanol (36% of calories) in the diet. Feeding ethanol to the Fisher rat over 17 days produced no significant changes in body weight. Cholesterol levels in various tissues were elevated in the ethanol-fed group: plasma cholesterol, +61%; liver cholesterol, +47%; and bile cholesterol, +57%. The alcohol-fed Fisher rat showed several changes in sterol metabolism over controls: fecal acidic steroid output, +13%; fecal neutral sterol output, +51%; endogenous neutral sterol output, +107%; cholesterol turnover, +54%; and cholesterol balance, +18%. Ethanol feeding to the Sprague Dawley rat showed similar differences between ethanol-fed vs. control rats. Cholesterol levels were significantly elevated in plasma (+35%) and in the liver (+81%). Sterol metabolism data showed the following differences (alcohol vs. control): fecal acidic steroid output, +9%; fecal neutral sterol output, +17%; endogenous neutral sterol output, +72%; cholesterol turnover, +33%; and cholesterol balance +13%. The Fisher rat maintained almost constant weight throughout the experimental period and is a preferable strain for sterol balance studies using liquid diets. A major finding of these experiments was the increased concentration of cholesterol in liver, plasma, and bile in both strains of rats. The sterol balance measurements indicated that this tissue accumulation of cholesterol was due to enhanced cholesterol synthesis as well as inhibition of bile acid syntheses
— id: 17797, year: 1981, vol: 5, page: 225, stat: Journal Article,

EFFECT OF CHOLESTEROL-FEEDING AND ALCOHOL ON STEROL-METABOLISM IN THE RAT
COHEN, BI; RAICHT, RF
1981 JAN 20 ;1(1):71-71, Arteriosclerosis
— id: 98633, year: 1981, vol: 1, page: 71, stat: Journal Article,

EFFECTS OF ETHANOL ON CHOLESTEROL LEVELS AND STEROL-METABOLISM IN RATS
Cohen, BI; Raicht, RF; Islam, MA
1981 ;5(1):145-145, Alcoholism: clinical & experimental research
— id: 30254, year: 1981, vol: 5, page: 145, stat: Journal Article,

Acute and chronic effect of dietary cholic acid on colonic epithelial cell proliferation
Deschner EE; Cohen BI; Raicht RF
1981 ;21(6):290-296, Digestion
Administration of cholic acid (1.0% of the diet) to male Fisher rats for 3 days resulted in increased numbers of DNA synthesizing epithelial cells per colonic crypt column as compared to those found in either control or 0.2% cholic acid-fed rats. The middle third of the crypt was the area stimulated to contribute the additional proliferating cells. The maximum number of 3H-TdR-labeled cells was doubled by 24 h and migration had processed further up the colonic crypt of the 1% cholic acid-fed rats than the 0.2% cholic acid or control animals. Compared with cholic acid-deprived rats, long-term dietary intake of 0.2% cholic acid (26 weeks) was found to heighten the numbers of labeled cells per column and expand the proliferative compartment. The enhanced manifestation of colonic neoplasia in MNU-induced rats consuming cholic acid (previously reported by us) appears related to the elevated levels of cell proliferation brought about in response to the deleterious action of the bile acid on the mucosa. Increased numbers of epithelial cells undergoing DNA synthesis in cholic acid-treated animals would allow the earlier expression of malignant transformation in the large intestine
— id: 17796, year: 1981, vol: 21, page: 290, stat: Journal Article,

Kinetic and morphologic alterations in the colon of a patient with multiple polyposis
Deschner EE; Raicht RF
1981 May 15;47(10):2440-2445, Cancer
The histologic and proliferative characteristics of 16 colonic biopsies taken from an operative specimen of a 38-year-old female patient with multiple polyposis are presented. Kinetic measurements are based on 3HTdR incorporation accomplished in vitro, using both single and double labelling techniques. Epithelial cells in adenomatous tissue were more actively engaged in DNA synthesis than those normal-appearing mucosa (L.I.13.0 +/- 6.9 versus 9.3 +/- 1.6); however, because of extreme variability between biopsies, the difference was not significant. No difference in S phase duration was found, but a faster turnover time (Tg) than that in the normal appearing colonic mucosa was estimated (Tg 52.6 hours versus 74.2 hours). Only two of ten biopsies containing normal-appearing mucosa had a completely normal incorporation pattern with proliferative cells located only in the lower two thirds of crypts. Eight biopsies showed extension of the proliferative compartment to the luminal surface. One of these eight also expressed an additional proliferative defect, namely, a shift of the major zone of DNA synthesis to the middle and upper regions of the crypts. This specimen had been located adjacent to an area of microscopic adenoma. Subpopulations of labelled epithelial cells showing transition from normal to hyperplastic or to adenomatous appearance were in the otherwise normal-appearing crypts. The majority of labelled hyperplastic-appearing cells occupied the lower thirds of the crypts, whereas 68% of labelled adenomatous-appearing cells were located in the middle and upper zones of the glands. Based on these observations, the development of an adenoma is believed forecast by the redistribution of the proliferative compartment toward the surface. A further stage in tumorogenesis before the appearance of a focus of neoplasia is the emergence of actively proliferating cells transforming to a more adenomatous appearance primarily in that same location, that is, the middle and upper third of the colonic crypts
— id: 17794, year: 1981, vol: 47, page: 2440, stat: Journal Article,

Isolation and quantitation of sulfated and unsulfated steroids in human feces
Islam MA; Raicht RF; Cohen BI
1981 Apr;112(2):371-377, Analytical biochemistry
— id: 17795, year: 1981, vol: 112, page: 371, stat: Journal Article,

Sterol metabolism in the rat. Effect of cholesterol and cholesterol-alpha-epoxide on sterol metabolism in rats fed liquid diets
Raicht RF; Cohen BI
1981 Dec 23;666(3):455-461, Biochimica & biophysica acta
Certain oxygenated derivatives of cholesterol have dramatic effects on cholesterol synthesis. The present study compared the effects of cholesterol and an oxygenated metabolite, cholesterol-alpha-epoxide, on sterol metabolism in rats. Sterol balance measurements using isotopic and chromatographic techniques were carried out in rats fed liquid control diets, control diets + cholesterol (1 mg/ml), and control diets + cholesterol-alpha-epoxide (1 mg/ml). Sterol metabolism was affected by both cholesterol and cholesterol-alpha-epoxide. Cholesterol feeding decreased cholesterol synthesis (-9.57 +/- 7.23 mg/day), increased endogenous bile acid synthesis (7.71 +/- 1.18 mg/day), and increased cholesterol turnover (7.78 +/- 2.33 mg/day) compared to controls. Cholesterol-alpha-epoxide had no effect on cholesterol synthesis, endogenous bile acid synthesis and cholesterol turnover compared to controls. However, animals fed cholesterol-alpha-epoxide had large increases in total acidic steroid output (determined by chromatographic analysis, 12.33 +/- 4.05 mg/day). This finding suggests that cholesterol-alpha-epoxide is absorbed and converted to bile acids. Apparently, the epoxide enters the bile acid biosynthetic pathway distal to the rate-limiting step of 7 alpha-hydroxylation. As a result, large amounts of bile acids are formed from the epoxide without affecting endogenous cholesterol or bile acid synthesis. This was confirmed in a separate experiment by feeding [4-14C]cholesterol-alpha-epoxide and recovering labeled bile acids (hyodeoxycholic acid and lithyocholic acid) as well as the starting radioactively labeled epoxide in the feces
— id: 17792, year: 1981, vol: 666, page: 455, stat: Journal Article,

Effect of cholic acid feeding on N-methyl-N-nitrosourea-induced colon tumors and cell kinetics in rats
Cohen BI; Raicht RF; Deschner EE; Takahashi M; Sarwal AN; Fazzini E
1980 Mar;64(3):573-578, Journal of the National Cancer Institute
— id: 17799, year: 1980, vol: 64, page: 573, stat: Journal Article,

Protective effect of plant sterols against chemically induced colon tumors in rats
Raicht RF; Cohen BI; Fazzini EP; Sarwal AN; Takahashi M
1980 Feb;40(2):403-405, Cancer research
Diets rich in vegetables are associated with a low incidence of colon cancer. Since plant sterols are plentiful in vegetarian diets, we studied the effect of beta-sitosterol on colon tumor formation in rats treated with the carcinogen N-methyl-N-nitrosourea. We demonstrated that beta-sitosterol nullified in part the effect of this direct-acting carcinogen on the colon. We suggest that plant sterols may have a protective dietary action action to retard colon tumor formation. The beneficial effects of vegetarian diets may be enhanced because of the presence of these compounds
— id: 17800, year: 1980, vol: 40, page: 403, stat: Journal Article,

Effect of colestipol on sterol metabolism in the rat
Takahashi M; Sarwal AN; Raicht RF; Cohen BI
1980 Jun;15(6):434-438, Lipids
Sterol metabolism studies using isotopic and chromatographic techniques were performed on rats fed diets supplemented with colestipol (Upjohn). Compared to controls, colestipol altered sterol metabolism dramatically. Bile acid output increased from 7.0 mg/day to 12.2 mg/day (0.42% colestipol) and 39.6 mg/day (1.67% colestipol). Daily fecal neutral sterol output and daily endogenous neutral sterol output increased 36% and 55%, respectively, on the 1.67% colestipol diet. Cholesterol absorption was reduced by colestipol feeding. Cholesterol balance increased dramatically with 1.67% colestipol administration (43.5 mg/day vs -1.0 mg/day in controls). Colestipol exerts its effect by binding bile acids and by bile acid depletion interfering with cholesterol absorption
— id: 17798, year: 1980, vol: 15, page: 434, stat: Journal Article,

Influence of bile on kinetic behavior of colonic epithelial cells of the rat
Deschner EE; Raicht RF
1979 ;19(5):322-327, Digestion
The acute effect of bile deprivation on colonic epithelial cell proliferation in Sprague-Dawley rats was investigated and compared with its effect on jejunum and ileum. 2. days after the creation of bile fistula, tritiated thymidine was injected and animals sacrificed 1 and 24 h later. Compared with control untreated animals, sham-operated restrained rats had a reduced labeling and mitotic index of the colonic epithelial cell population as well as a slower migration of cells to the lumen. Colonic cell proliferation in animals deprived of bile flow was reduced a further 50%. Moreover, no evidence of cell migration or appreciable decline in grain density was seen over 24 h in bile fistula rats. Alterations in cell proliferation in both sham and bile fistula treated rats became less marked as one proceeded proximally to the small bowel. Therefore, significant alterations in cell kinetics result when normal bile flow is interrupted, suggesting its importance in the regulatory control of colonic cell proliferation
— id: 17802, year: 1979, vol: 19, page: 322, stat: Journal Article,

PLANT STEROLS - ROLE IN LARGE BOWEL-CANCER
Raicht, RF; Cohen, BI; Sarwal, A; Takahashi, M; Fazzini, E
1979 ;76(5):1296-1296, Gastroenterology
— id: 30024, year: 1979, vol: 76, page: 1296, stat: Journal Article,

Effects of dietary administration of chenodeoxycholic acid on N-methyl-N-nitrosourea-induced colon cancer in rats
Sarwal AN; Cohen BI; Raicht RF; Takahashi M; Fazzini E
1979 Sep 28;574(3):423-432, Biochimica & biophysica acta
— id: 17801, year: 1979, vol: 574, page: 423, stat: Journal Article,

EFFECTS OF DIETARY ADMINISTRATION OF CHENODEOXYCHOLIC ACID ON INDUCED COLON CANCER IN RATS
Sarwal, AN; Raicht, RF; Cohen, BI; Takahashi, M; Fazzini, E
1979 ;38(3):864-864, Federation Proceedings (Federation of American Societies for Experimental Biology)
— id: 30158, year: 1979, vol: 38, page: 864, stat: Journal Article,

Sterol metabolism studies in rats: effects of taurodeoxycholic acid feeding on sterol metabolism
Raicht RF; Cohen BI; Eliav B; Mosbach EH
1978 Sep;13(9):605-609, Lipids
— id: 17804, year: 1978, vol: 13, page: 605, stat: Journal Article,

Ursodeoxycholic acid. Effects on sterol metabolism in rats
Raicht RF; Cohen BI; Sarwal A; Takahashi M
1978 Oct 25;531(1):1-8, Biochimica & biophysica acta
Sterol balance studies using isotopic and chromatographic techniques were performed in rats fed diets supplemented with ursodeoxycholic acid. Compared to controls, ursodeoxycholic acid dramatically altered sterol metabolism. Ursodeoxycholic acid was absorbed and circulated in the enterohepatic circulation. The biliary bile acid composition was significantly altered with ursodeoxycholic acid the predominant biliary bile acid (67%). Cholesterol absorption was depressed by 34%; bile acid synthesis was depressed by 30%; however, cholesterol balance was significantly increased. It is apparent that the effects of ursodeoxycholic acid on sterol metabolism are different in several respects from chenodeoxycholic acid
— id: 17803, year: 1978, vol: 531, page: 1, stat: Journal Article,

EFFECTS OF BILE-ACIDS ON INDUCED COLON CANCER IN RATS
Raicht, RF; Cohen, BI; Fazzini, E; Sarwal, A; Takahashi, M
1978 ;75(5):981-981, Gastroenterology
— id: 29867, year: 1978, vol: 75, page: 981, stat: Journal Article,

URSODEOXYCHOLIC ACID - EFFECTS ON STEROL-METABOLISM IN RATS
Raicht, RF; Cohen, BI; Sarwal, AN; Takahashi, M
1978 ;26(3):A324-A324, Clinical research
— id: 29920, year: 1978, vol: 26, page: A324, stat: Journal Article,

An improved method for the identification and quantitation of secondary bile acids in biological samples
Takahashi M; Raicht RF; Sarwal AN; Mosbach E; Cohen BI
1978 Jul 1;87(2):594-603, Analytical biochemistry
— id: 17805, year: 1978, vol: 87, page: 594, stat: Journal Article,

Sterol metabolism studies in the rat. Effects of dietary plant sterols and bile acids on sterol metabolism
Cohen BI; Raicht RF; Mosbach EH
1977 May 25;487(2):287-296, Biochimica & biophysica acta
— id: 17806, year: 1977, vol: 487, page: 287, stat: Journal Article,

Sterol metabolism studies in the rat. Effects of primary bile acids (sodium taurochenodeoxycholate and sodium taurocholate) on sterol metabolism
Cohen BI; Raicht RF; Mosbach EH
1977 Mar;18(2):223-231, Journal of lipid research
Sterol metabolism studies using a combination of isotopic and chromatographic procedures were carried out in rats fed either a low-cholesterol stock diet or a stock diet containing 0.1% cholesterol. The primary bile acids, sodium taurochenodeoxycholate and sodium taurocholate, were added to the stock diets at a level of 0.5%, as required. Feeding sodium taurochenodeoxycholate and sodium taurocholate led to a decrease in acidic steroid synthesis, cholesterol turnover, and cholesterol balance, compared to controls. Sodium taurochenodeoxycholate feeding did not influence cholesterol absorption, but rats fed sodium taurocholate showed a twofold increase in cholesterol absorption as well as an accumulation of cholesterol in the liver. Rats receiving diets containing sodium taurochenodeoxycholate or sodium taurocholate plus cholesterol (0.1%) showed decreased acidic steroid synthesis, cholesterol turnover, and cholesterol balance, compared to the corresponding controls (Group 2, high cholesterol diet). Significantly larger amounts of cholesterol were absorbed in the taurocholate group (34.1 mg/day); these animals increased their concentrations of cholesterol in liver and plasma. The rats fed taurocholate plus 0.1% cholesterol differed from those fed taurochenodeoxycholate plus 0.1% cholesterol in the following respects: a) increased cholesterol absorption (35%), and b) accumulation of cholesterol in liver and plasma
— id: 17807, year: 1977, vol: 18, page: 223, stat: Journal Article,

Effect of a hydrocholeretic agent (Zanchol) on sterol metabolism in rats
Raicht RF; Cohen BI; Eliav BB; Mosbach EH; Zimmon DS
1977 Mar;72(3):507-509, Gastroenterology
The keto acid, gamma-oxo-gamma-(8-fluoranthene)butyric acid (Zanchol) markedly alters sterol metabolism in rats. It stimulates cholesterol and bile acid synthesis and decreases cholesterol absorption
— id: 17808, year: 1977, vol: 72, page: 507, stat: Journal Article,

EFFECTS OF ZANCHOL ON STEROL-METABOLISM IN RATS
RAICHT, RF; COHEN, BI; MOSBACH, E; ZIMMON, DS
1976 ;24(3):A290-A290, Clinical research
— id: 49724, year: 1976, vol: 24, page: A290, stat: Journal Article,

EFFECTS OF ZANCHOL ON STEROL-METABOLISM IN RATS
Raicht, RF; Cohen, BI; Mosbach, EH; Zimmon, DS
1976 ;71(5):924-924, Gastroenterology
— id: 29442, year: 1976, vol: 71, page: 924, stat: Journal Article,

The effect of a hydrocholeretic agent (Zanchol) on biliary lipids in post cholecystectomy patients
Zimmon DS; Kerner MB; Aaron MB; Raicht RF; Mosbach EH; Kessler RE
1976 Apr;70(4):640-643, Gastroenterology
— id: 17809, year: 1976, vol: 70, page: 640, stat: Journal Article,

An improved method for the isolation, quantitation, and identification of bile acids in rats feces
Cohen BI; Raicht RF; Salen G; Mosbach EH
1975 Apr;64(2):567-577, Analytical biochemistry
— id: 17811, year: 1975, vol: 64, page: 567, stat: Journal Article,

ZANCHOL, A POTENTIAL LITHOLYTIC AGENT IN MAN
Kerner, M; Raicht, RF; Mosbach, EH; Zimmon, DS
1975 ;69(3):836-836, Gastroenterology
— id: 28639, year: 1975, vol: 69, page: 836, stat: Journal Article,

Sterol balance studies in the rat. Effects of dietary cholesterol and beta-sitosterol on sterol balance and rate-limiting enzymes of sterol metabolism
Raicht RF; Cohen BI; Shefer S; Mosbach EH
1975 Jun 23;388(3):374-384, Biochimica & biophysica acta
Sterol balance measurements using isotopic and chromatographic techniques were carried out in rats fed diets containing beta-sitosterol (0.8%) and cholesterol (1.2%). The activities of the rate-limiting enzymes of cholesterol synthesis (beta-hydroxy-beta-methylglutaryl-CoA reductase, EC 1.1.1.34) and bile acid synthesis (cholesterol 7 alpha-hydroxylase) were determined in the same animals. Cholesterol feeding increased cholesterol absorption from 1.2 to 70 mg/day. The increased absorption was compensated for by inhibition of hepatic cholesterol synthesis, enhanced conversion of cholesterol to bile acids (from 13.7 to 27.3 mg/day) and a slight increase in the excretion of endogenous neutral steroids (from 7.7 to 11.2 mg/day). Despite the adaptation there was accumulation of cholesterol in the liver (from 2.2 to 9.2 mg/g). Beta-Sitosterol feeding inhibited cholesterol absorption (calculated absorption was zero). In these rats there was enhanced cholesterol synthesis (from 20.0 to 28.8 mg/day, but no change in the rates of bile acid formation. Measurements of the activities of the rate-limiting enzymes showed fair correlation with cholesterol-bile acid balance. In cholesterol fed animals, beta-hydroxy-beta-methylglutaryl-CoA reductase was inhibited 80% and cholesterol 7 alpha-hydroxylase was enhanced 61%. In beta-sitosterol-fed animals, the reductase was increased 2-fold and cholesterol 7 alpha-hydroxylase was not significantly different from controls
— id: 17810, year: 1975, vol: 388, page: 374, stat: Journal Article,

Effect of dietary bile acids, cholesterol, and beta-sitosterol upon formation of coprostanol and 7-dehydroxylation of bile acids by rat
Cohen BI; Mosbach EH; Raicht RF
1974 Dec;9(12):1024-1029, Lipids
— id: 17812, year: 1974, vol: 9, page: 1024, stat: Journal Article,

Effects of clofibrate on sterol metabolism in the rat
Cohen BI; Raicht RF; Shefer S; Mosbach EH
1974 Oct 16;369(1):79-85, Biochimica & biophysica acta
— id: 17814, year: 1974, vol: 369, page: 79, stat: Journal Article,

Effects of sodium taurochenodeoxycholate and sodium taurocholate on cholesterol absorption in the rat
Raicht RF; Cohen BI; Mosbach EH
1974 Dec;67(6):1155-1161, Gastroenterology
— id: 17813, year: 1974, vol: 67, page: 1155, stat: Journal Article,