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  1. Home
  2. Browse by Author

Browsing by Author "Hubbard, Gene B."

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    Nonhuman Primates as Models for Studies of Prostate Specific Antigen and Prostatic Diseases
    (The Prostate, 2008) Mubiru, James N.; Hubbard, Gene B.; Dick, Edward J.; Furman, Jaime; Troyer, Dean A.; Rogers, Jeffrey
    Because prostate specific antigen (PSA) is released at increased levels into the blood early in the development of prostate cancer, benign prostatic hyperplasia (BPH) and prostatitis, it is widely used as a marker for these diseases. However, PSAhas clinical limitations as a screen for prostatic diseases due to its low sensitivity and specificity. There is a strong need to better understand the biology of PSA and factors affecting its serum levels. METHODS. Weevaluated cynomolgus macaques, rhesus macaques, baboons, and marmosets for their suitability as models for the study of PSA biology and prostatic diseases. RESULTS. Prostates of several nonhuman primates are anatomically similar to the human counterpart. Anti-human PSA antibody detected PSA antigens in all the Old World monkeys (cynomolgus macaques, rhesus macaques, and baboons) but not in marmosets. Of the Old World monkeys, cynomolgus macaques have the highest serum PSA levels; baboons have the lowest. Serum PSA levels from macaques includes a number of outlier samples with unusually high values. We also report two cases of abnormal pathologies in macaques accompanied by high serum PSA levels. One case consisted of prostatic hyperplasia involving both glandular and basal cells in a cynomolgus macaque and another of glandular hyperplasia and atrophy in a rhesus macaque. The finding that pathological changes in the prostate of macaques may lead to increases in serum PSA is worthy of further exploration. CONCLUSION. Cynomolgus macaques and rhesus macaques are promising animal models for PSA biology studies.
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    Polymerase Chain Reaction Detection of Trypanosoma cruzi in Macaca fascicularis Using Archived Tissues
    (The American journal of tropical medicine and hygiene, 2009) Williams, Jeff T.; Mubiru, James N.; Schlabritz-Loutsevitch, Natalia E.; Rubicz, Rohina C.; VandeBerg, John L.; Dick Jr, Edward J.; Hubbard, Gene B.
    This study describes conventional and real-time polymerase chain reaction (PCR) methods developed to detect and quantify Trypanosoma cruzi DNA in cynomolgus monkeys (Macaca fascicularis) using formalin-fixed paraffin-embedded blocks archived for periods of up to 6 years. The highest concentration of T. cruzi DNA was found in the myocardium, urinary bladder, stomach, lymph node, adrenal gland, and colon. The concentration of T. cruzi DNA detected in cardiac tissues was 10–100- fold greater than found elsewhere; the mean concentrations of T. cruzi DNA in non-cardiac tissues were otherwise comparable. Trypanosoma cruzi DNA was amplified from cerebrum but not cerebellum or kidney. Successful use of DNA from formalin-fixed, paraffin-embedded blocks is important because most pathology laboratories routinely archive wax blocks. This archived resource can be used for further studies on the prevalence of this disease.
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    A Preliminary Study of the Baboon Prostate Pathophysiology
    (The Prostate, 2007) Mubiru, James N.; Hubbard, Gene B.; Dick Jr., Edward J.; Butler, Stephanie D.; Valente, Anthony J.; Troyer, Dean A.; Rogers, Jeffrey
    Prostate cancer, benign prostatic hyperplasia, and prostatitis frequently affect men worldwide. At present there are no suitable animal models for these diseases. This study explores the potential use of the baboon as a model for prostatic diseases. METHODS. Prostates of 48 baboons of different ages were studied. Prostate specific antigen (PSA) and alpha-methyl-acyl-CoA racemase (AMACR) were localized in the different lobes of the prostate by Western blotting and immunohistochemistry. PSA in baboon serum was demonstrated by radioimmunoassay and western blotting. BaboonAMACRcDNA was cloned and its expression assayed in baboon tissues. RESULTS. The baboon prostate is anatomically and histologically similar to its human counterpart, with cranial and caudal lobes corresponding to central and peripheral zones of the human prostate. We found lymphocytic infiltration (91%), and sclerosing/atrophic lesions (34%). PSA tissue immunostaining intensity and alpha-methyl-acyl-CoA racemase (AMACR) gene expression levels differed between the cranial and caudal lobes of the prostate. The cloned baboon AMACR cDNA showed 96% homology with its human counterpart. Anti-human AMACR, PSA and basal keratin antibodies stained intracellular and basement membrane structures in the baboon prostate. The sclerosing/atrophic lesions were comparable to their human counterparts. CONCLUSIONS. The similarity of baboon prostate to its human counterpart and the fact that human antibodies (AMACR, PSA, basal keratin) are reactive to baboon prostatic proteins indicates that the baboon is a promising model for human prostatic diseases.
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    Spontaneous heart disease in the adult chimpanzee (Pan troglodytes)
    (Journal of medical primatology, 2009) Seiler, Brittany M.; Seiler, Brittany M.; Dick Jr, Edward J.; Guardado-Mendoza, Rodolfo; VandeBerg, John L.; Williams, Jeff T.; Mubiru2, James N.; Hubbard, Gene B.
    A high incidence of heart disease, especially idiopathic cardio- myopathy (IC), is seen in chimpanzees (Pan troglodytes). Methods We reviewed clinical records and necropsy reports of 87 adult chimpanzees for possible causes of heart disease/IC. We examined age, sex, cause of death, weight, diet, environment, infectious diseases, experimental uses and clinical pathology. Results The overall prevalence of heart disease in chimpanzees was 67.81%; the prevalence of IC was 51.72%. The prevalence of IC was signifi- cantly higher in males (60.32%) than that in females (29.17%, P = 0.009). The prevalence of other heart disease was higher in females (25%) than that in males (12.70%, P = 0.165). Heart failure occurred in 47.13% of chimpanzees. Heart disease was the primary cause of death in 34.49% of chimpanzees; 29.88% died of unknown causes. Conclusions We found no evidence that diet, environment, viral agents, experimental use or disease exposure contributed to the deaths resulting from IC in chimpanzees.

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