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Dive into the research topics where Joseph L. Kinzie is active.

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Featured researches published by Joseph L. Kinzie.


The American Journal of Gastroenterology | 2001

Prevalence of hepatitis A virus and hepatitis B virus immunity in patients with polymerase chain reaction-confirmed hepatitis C: Implications for vaccination strategy

Firdous Siddiqui; Milton G. Mutchnick; Joseph L. Kinzie; Rene Peleman; Paul Naylor; Murray N. Ehrinpreis

OBJECTIVES:Administration of vaccine for hepatitis A virus (HAV) and hepatitis B virus (HBV) is recommended for patients with chronic hepatitis C (CHC) because of the potential for increased severity of acute hepatitis superimposed on existing liver disease. The aim of this study is to determine the prevalence of antibodies directed against HAV and HBV in patients with CHC, analyze demographic and risk factors associated with this prevalence, and develop a cost-effective vaccination strategy.METHODS:We reviewed records from 1092 CHC patients. Demographics and information regarding risk factors were obtained by history and questionnaire administered to all patients. The costs of vaccination and antibody testing were determined, based on standard laboratory and clinic charges at our institution. HAV and HBV markers were correlated to race, age, and risk factors.RESULTS:Of the total population studied (n = 1092), 72% were African-Americans, 27% white, and 1% others. Of 671 CHC patients tested for anti-HAV IgG, 252 (38%) were positive. Of 743 CHC patients tested for HBV antibodies (anti-hepatitis B core IgG or anti-hepatitis B surface), 494 (67%) were positive. African-Americans are more likely to have antibodies to HAV and HBV (67% and 75%, respectively) compared to whites (27% and 20%). The prevalence of anti-HAV was 76% in patients >60 yr, 34% in the 40- to 60-yr-old age group, and 21% in patients <40 yr. The highest prevalence of HBV antibodies was found in patients between the ages of 40–60 yr. No HCV risk factors were associated with increased HAV risk. In CHC patients with HBV antibodies, however, illicit injection drug use was the predominant risk factor.CONCLUSIONS:The prevalence of anti-HAV in patients with CHC was found to be similar to that of the general population in the United States (33% according to recent Centers for Disease Control data), consistent with the hypothesis that the two infections do not share risk factors. Because the prevalence of HAV immunity is low in CHC patients <40 yr, empiric HAV vaccination is cost effective. If two doses of vaccine are to be given, however, antibody testing of all HCV patients is indicated. In the subset of patients >60 yr of age or who are African-American, where the prevalence of HAV exposure is considerably higher, it would be cost effective to check the antibody (


American Journal of Physiology-cell Physiology | 1999

Folic acid inhibition of EGFR-mediated proliferation in human colon cancer cell lines

Richard Jaszewski; A. Khan; Fazlul H. Sarkar; Omer Kucuk; Martin Tobi; Abbas Zagnoon; Ravi Dhar; Joseph L. Kinzie; Adhip P.N. Majumdar

36.00), before vaccination (


Antiviral Research | 1994

Prospectives on the treatment of chronic hepatitis B and chronic hepatitis C with thymic peptides and antiviral agents

Milton G. Mutchnick; Murray N. Ehrinpreis; Joseph L. Kinzie; Rene Peleman

97.00). The prevalence of HBV antibodies, however, is significantly increased in patients with CHC compared with the general population (5.3% per the Centers for Disease Control), likely as a result of exposure to similar parenteral risk factors. HBV antibody testing (


Life Sciences | 1997

Endogenous codeine and morphine in anorexia and bulimia nervosa

Mary Ann Marrazzi; Elliot D. Luby; Joseph L. Kinzie; Inam D. Munjal; Sydney Spector

26.00 per test) should, therefore, be undertaken in all CHC patients who are hepatitis B surface antigen negative, as this approach is cost-effective compared to empiric HBV vaccination (


Journal of Clinical Gastroenterology | 1997

Zollinger-Ellison syndrome, acromegaly, and colorectal neoplasia

Martin Tobi; Annemieke Cats; Benedict Maliakkal; Joseph L. Kinzie; Roy Maliakkal; Robin P. F. Dullaart; Gordon D. Luk

438.00 for a three injection course).


Digestive Diseases and Sciences | 2006

Peutz-Jeghers Syndrome Diagnosed in a Schizophrenic Patient with a Large Deletion in the STK11 Gene

Michael Kam; Jorge Massare; Steven Gallinger; Joseph L. Kinzie; Donald W. Weaver; John D. Dingell; Susmita Esufali; Bharati Bapat; Martin Tobi

Although accumulating evidence suggests a chemopreventive role for folic acid in colon cancer, the regulation of this process in unknown. We hypothesize that supplemental folic acid exerts its chemopreventive role by inhibiting mucosal hyperproliferation, an event considered to be central to the initiation of carcinogenesis in the gastrointestinal tract. The present investigation examines the effect of supplemental folic acid on proliferation of Caco-2 and HCT-116 colon cancer cell lines. Furthermore, because certain tyrosine kinases, particularly epidermal growth factor receptor (EGFR), play a role in regulating cell proliferation, we also examined the folic acid-induced changes in tyrosine kinase activity and expression of EGFR. In Caco-2 and HCT-116 cells, maintained in RPMI 1640 medium containing 1 microg/ml folic acid, we observed that the supplemental folic acid inhibited proliferation in a dose-dependent manner. Pretreatment of HCT-116 and Caco-2 cell lines with supplemental folic acid (1.25 microg/ml) completely abrogated transforming growth factor-alpha (TGF-alpha)-induced proliferation in both cell lines. Tyrosine kinase activity and the relative concentration of EGFR were markedly diminished in both cell lines following a 24-h exposure to supplemental folic acid. The folic acid-induced inhibition of EGFR tyrosine kinase activity in colon cancer cell lines was also associated with a concomitant reduction in the relative concentration of the 14-kDa membrane-bound precursor form of TGF-alpha. In conclusion, our data suggest that supplemental folic acid is effective in reducing proliferation in two unrelated colon cancer cell lines and that EGFR tyrosine kinase appears to be involved in regulating this process.Although accumulating evidence suggests a chemopreventive role for folic acid in colon cancer, the regulation of this process in unknown. We hypothesize that supplemental folic acid exerts its chemopreventive role by inhibiting mucosal hyperproliferation, an event considered to be central to the initiation of carcinogenesis in the gastrointestinal tract. The present investigation examines the effect of supplemental folic acid on proliferation of Caco-2 and HCT-116 colon cancer cell lines. Furthermore, because certain tyrosine kinases, particularly epidermal growth factor receptor (EGFR), play a role in regulating cell proliferation, we also examined the folic acid-induced changes in tyrosine kinase activity and expression of EGFR. In Caco-2 and HCT-116 cells, maintained in RPMI 1640 medium containing 1 μg/ml folic acid, we observed that the supplemental folic acid inhibited proliferation in a dose-dependent manner. Pretreatment of HCT-116 and Caco-2 cell lines with supplemental folic acid (1.25 μg/ml) completely abrogated transforming growth factor-α (TGF-α)-induced proliferation in both cell lines. Tyrosine kinase activity and the relative concentration of EGFR were markedly diminished in both cell lines following a 24-h exposure to supplemental folic acid. The folic acid-induced inhibition of EGFR tyrosine kinase activity in colon cancer cell lines was also associated with a concomitant reduction in the relative concentration of the 14-kDa membrane-bound precursor form of TGF-α. In conclusion, our data suggest that supplemental folic acid is effective in reducing proliferation in two unrelated colon cancer cell lines and that EGFR tyrosine kinase appears to be involved in regulating this process.


The American Journal of Gastroenterology | 2000

Symptomatic gastric sarcoidosis and the role of steroids

Ahmad Khalifa; Joseph L. Kinzie; Firdous Siddiqui

At the present time, interferon is considered the only effective therapeutic approach in the treatment of both chronic hepatitis B and chronic hepatitis C. It is clear that the disappointing response rates in both chronic hepatitis B and C place added emphasis on efforts to identify alternative forms of therapy. In addition to the development of other antiviral agents including the nucleoside analogs which might prove more effective and have fewer associated side-effects, other agents currently under investigation include thymic peptides such as thymosin alpha 1. In the future, the therapeutic approach to the treatment of chronic hepatitis B and C may consist of combination therapy using perhaps an immune modulator and an antiviral agent or, several antiviral drugs. Alternatively, there is indication that cellular targeting systems with delivery of the toxic material to the specific cell containing the virus may be more effective, while minimizing side-effects. Finally, there are agents such as ursodeoxycholic acid which perhaps, makes bile less toxic and can be used as adjunctive therapy with improvement in liver chemistry values. The treatment of chronic hepatitis B and chronic hepatitis C has shifted in emphasis form the concept of treating liver disease towards that of treating viral infections which happen to effect primarily the liver.


The American Journal of Gastroenterology | 2000

Argon plasma coagulator treatment in the management of hematochezia secondary to chronic radiation proctopathy

Prasad M. Kulkarni; Joseph L. Kinzie; Murray N. Ehrinpreis

The endogenous plasma alkaloids codeine and morphine were shown to be elevated in patients with anorexia nervosa and bulimia nervosa compared to control subjects. The role of these opioids in the pathophysiology of these eating disorders is discussed in relation to an auto-addiction opioid model. This model proposes that endogenous opioids are released during an initial period of dieting and reinforce a state of starvation dependence [1,2].


The American Journal of Clinical Nutrition | 1992

Taurine deficiency after intensive chemotherapy and/or radiation.

Tusar K. Desai; Joseph Maliakkal; Joseph L. Kinzie; Murray N. Ehrinpreis; Gordon D. Luk; Jan Cejka

Zollinger-Ellison syndrome (ZES) and acromegaly are two hypersecretory states in which colorectal neoplasia has been described, but the incidence in the former condition may not be increased. We describe four patients with colorectal neoplasia associated with the ZES and review other published cases. Tissue ELISA with Adnab-9 antibody, a putative colorectal cancer risk marker, from a patient with ZES and from seven patients with acromegaly was compared to 13 controls at average risk for colorectal neoplasia. The patient with ZES without detectable colonic neoplasia and seven patients with acromegaly had increased binding of Adnab-9 in the colonic mucosa by ELISA. The difference was significant for the acromegaly patients compared to the controls (p < 0.05). The accumulated 34 instances of colorectal neoplasia in ZES patients suggests that this association may not be rare. Adnab-9 expression, detectable in both ZES and acromegaly, may reflect predisposition to colorectal neoplasia in both hyper-secretory states. Therefore, while a basis for association of colorectal neoplasia and hypergastrinemia exists, the clinical data are not compelling enough to warrant surveillance of patients with ZES. To resolve this problem, more definitive case control studies should be conducted.


Gastroenterology Clinics of North America | 1988

Management of the malignant polyp

Ehrinpreis Mn; Joseph L. Kinzie; Richard Jaszewski; Peleman Rl

Since the unraveling of the human genome through chromosomal analysis, unique associations have been found between diseases. In this vein, interesting findings in a patient with schizophrenia and Peutz-Jeghers syndrome (PJS) prompted us to perform germline genetic analysis. Schizophrenia, a common psychiatric disorder affecting about 1% of the population [1], is a severe and persistent debilitating psychiatric disorder believed to be polygenic in origin, having associations with many different chromosomes [2]. The exact causes of schizophrenia are not known. There is a tenfold increased risk for schizophrenia when a first-degree family member is affected, suggesting strong genetic correlations [2]. The hallmark symptoms of schizophrenia are hallucinations, often auditory, and delusions.

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Martin Tobi

Wayne State University

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Desai Tk

Harper University Hospital

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Gordon D. Luk

University of Texas Southwestern Medical Center

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Luk Gd

Harper University Hospital

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Silverman Al

Harper University Hospital

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