Biomedical subjects

W Mahapokai

Publications and source records attributed to W Mahapokai.

4 recordsLinked to original sources

PubMed2001

Immune response in hormonally-induced prostatic hyperplasia in the dog.

We induced prostatic enlargement in castrated dogs using either androgen alone or androgen combined with estrogen. In addition to previously reported hyperplastic changes, marked infiltration with immune effector cells was observed. This mononuclear cell infiltrate was phenotypically characterized using CD3 as pan T-lymphocyte marker, CD79 for B-lymphocytes, MAC378 for macrophages, and antibodies against kappa- and lambda-immunoglobulin (Ig) light chains for plasma cells. The majority of inflammatory cells (>80%) in the mononuclear infiltrates were T-lymphocytes and the numbers correlated with the degree of inflammation. The B-lymphocytes were found particularly in areas with marked follicular formation and diffuse infiltration, whereas there were only a few positive cells (<10%) in areas with a moderate or slight inflammation. Macrophages were found primarily in areas with atrophic and cystic changes with and without inflammation. The expression of lambda-Ig-positive cells depended on the degree of inflammation (5-10%), whereas immunoreactivity of kappa-Ig did not correlate with the extent of inflammatory reaction. Our present findings together with the evaluation of longitudinal biopsies of hormonally-induced BPH indicate that hyperplasia preceded cell-mediated and humoral immune response.

Androstane-3,17-diol↗

PubMed2000

Cell kinetics and differentiation after hormonal-induced prostatic hyperplasia in the dog.

BACKGROUND: Our aim was to characterize the immunophenotypical changes in canine prostate epithelium after hormonal-induced benign prostatic hyperplasia (BPH). METHODS: Castrated dogs (aged 1-2 and 9-12 years) were treated with vehicle (group C), androstanediol (group A), or androstanediol plus estradiol (group AE). Surgical prostate biopsies were obtained before and after castration and after hormonal treatment. Tissue sections were stained using antibodies specific for basal cells (34betaE12), transiently proliferating (TP)/amplifying cells (RCK103), and luminal exocrine cells (RGE53). RESULTS: Castration resulted in a marked reduction in specific immunoreactivity associated with luminal secretory cells and basal cells in young dogs. In older dogs the number of basal cells remained constant. Hormonal treatment (AE) resulted in an increased number of cells with an immunophenotype that was associated with the TP/amplifying cell compartment and hyperplastic luminal epithelium. CONCLUSIONS: The relative increase in TP/amplifying cells in hormonally induced BPH in the dog is in line with a stem-cell-derived proliferation. Moreover, the finding of androgen-independent basal cells in the prostate of older dogs may contribute to the enhanced risk of development of BPH with increasing age.

Age Factors↗

PubMed2000

Models for studying benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is one of the most common diseases affecting aging man. Attempts have been made to clarify the etiology and pathogenesis and, to that end, experimental models have been developed. To date, in vitro and in vivo models have been used, depending on the concept of the study. Spontaneous animal models are limited to the chimpanzee and the dog. Ethical and financial factors restrict the applicability of these models. The hormonal-induced canine BPH model is a good alternative that closely resembles human BPH in many aspects. The experimental models currently used for studying BPH are reviewed. Prostate Cancer and Prostatic Diseases (2000) 3, 28-33

Journal Article↗

PubMed2000

Gauged attenuation of congenital portosystemic shunts: results in 160 dogs and 15 cats.

Portosystemic shunts were ligated over a gauged stainless steel rod in 160 dogs and 15 cats, using a midline celiotomy. The diameter of the rod varied with the size of the shunt and the diameter of the portal vein cranial to the shunt. Shunts were narrowed to the smallest diameter that did not cause signs of portal hypertension such as cyanosis of the stomach, pancreas, and small intestine. A slight discoloration was accepted only if the heart rate, end-expiratory CO2%, or arterial blood pressure (if available) did not deviate more than 15% from the values that were recorded at the beginning of the surgical procedure. The perioperative mortality (0-30 days) was 29%. The most common cause of death was euthanasia because of hypoplasia of the portal vein cranial to the shunt. Animals with intrahepatic shunts had a significantly lower probability of survival than animals with extrahepatic portocaval or portoazygos shunts. In dogs, large breed and a high body weight were also significant risk factors for non-survival. Age had a significant effect on risk of non-survival, with an increased risk for older dogs, irrespective of the breed of the dog (large breed vs. small breed). The probability of survival without recurrence of hepatoencephalopathy (HE) after 1 and 4 years was 61.3% and 55.7%, respectively. The only variable that was significantly associated with non-recurrence of HE was the breed of the dog, there being a lower probability for large breeds. Among the animals that survived surgery for more than 30 days, there was a significant higher probability of recurrence of HE in cats than in dogs.

Abdomen↗