11C-choline positron emission tomography in bladder cancer: Report of four cases

Little work has been done with positive emission tomography (PET) in bladder tumors because high urinary excretion of (18)F-FDG makes visualization of the bladder tumor difficult. (11)C-choline has recently been reported as a new tracer which lacks urinary radioactivity. We report the result of (11)C-choline PET in four patients with invasive bladder tumors. In one case, (11)C-choline PET could detect bladder tumor effectively without urinary activity and bone metastasis despite negative bone scintigraphy. On the other hand, an intense accumulation of the tracer in the bladder hampered the interpretation on PET scanning in three patients. The mechanisms of the (11)C-choline accumulation in the bladder were reported to be due to inflammatory and proliferative changes in the mucosa of the bladder from previous catheterization or other factors. Further study is necessary to prove the value of (11)C-choline PET for detecting primary bladder cancer and bone metastasis.     

卡介苗对体外培养膀胱癌细胞株的直接作用和形态学观察

我们用卡介苗（ＢＣＧ）直接作用于体外培养膀胱癌细胞株，用扫描电镜和相差显微镜观察，癌细胞形态学发生明显变化，癌细胞表面结构损伤严重，微绒毛和长突起消失，残存畸变，小球密集成片，肿瘤表面结构与胞体分离，癌细胞生长抑制曲线表明，癌细胞的生长抑制率随着时间延长和ＢＣＧ浓度增大而增高。实验证明，ＢＣＧ对膀胱细胞有直接损伤作用。     

膀胱前间隙炎性假瘤临床病理观察及文献复习

目的 探讨膀胱前间隙炎性假瘤的临床病理特征及发病因素，以提高对本病的认识。方法 复习3例膀胱前间隙炎性假瘤的临床特征、组织病理学、免疫表型及相关文献。结果 3例患者均为女性，均为输卵管结扎术后1～2年发现膀胱前间隙炎性假瘤，CT及B超提示膀胱前壁肿块，但膀胱黏膜光滑。术中发现肿块位于膀胱前间隙并累及膀胱前壁。病理检查：眼观为灰白色质韧的结节状肿块，镜下见炎性假瘤的病理特征及不同程度炎症背景，有组织疏松区、黏液样区、部分区域梭形细胞和纤维母细胞排列杂乱，细胞较大，光镜检查时易误诊为肉瘤，但缺乏核异型。3例均成功行肿块连同部分膀胱壁切除术，随访3～5年无复发。结论 膀胱前间隙炎性假瘤形态上需与软组织肉瘤、结节性筋膜炎、术后梭形细胞结节、间质性膀胱炎等疾病相鉴别，既往输卵管结扎术和感染可能是其重要的致病因素。     

特殊型前列腺增生症的诊治

收治特殊型前列腺增生症１１０例，分别伴有逼尿肌无力、不稳定性膀胱、前列腺结石、膀胱结石、前列腺炎或糖尿病。认为：治疗前认真检查发现特殊前列腺增生症，是提高治愈率、减少并发症的关键步骤之一。     

Genetically determined N-acetylation and oxidation capacities in Japanese patients with non-occupational urinary bladder cancer

Summary Genetically determined polymorphisms of N-acetylation and oxidative capacity have been studied using dapsone and metoprolol in 51 Japanese patients with spontaneous bladder cancer and 203 healthy control subjects.The results for N-acetylation pharmacogenetics were against the initial expectation that there would be a preponderance of slow acetylators in the cancer group, as 3 such patients (5.9%) were found as compared to 13 (6.4%) in the healthy group. There was no poor metabolizer (PM) of metoprolol in the cancer group, whereas in the healthy group one (0.5%) was a PM. There were no significant differences between the groups in the frequency of slow acetylator and poor oxidiser phenotypes, or in the frequency distribution profiles of acetylation (monoacetyldapsone/dapsone) and oxidative metabolic ratio (log metoprolol/-hydroxymetoprolol).The results indicate that neither N-acetylation nor the debrisoquine/sparteine-type oxidative phenotype and/or capacity represent a genetic predisposition to spontaneous bladder carcinogenesis in Japanese patients. In the normal Japanese population there is a great predominance of rapid acetylators and extensive oxidisers.     

Simultaneous detection of fluorescent in situ hybridization and in vivo incorporated BrdU in a human bladder tumour

We have used fluorescent in situ hybridization and simultaneous in vivo bromodeoxyuridine labelling of a solid bladder cancer to examine tumour cell subsets for possible proliferative growth differences. In this dual-labelled preparation, most tumour cell nuclei exhibited monosomy 9, consistent with reported karyotypes of bladder cancer. Incorporated bromodeoxyuridine was visualized with a fluoresceinated antibody in 5-6 per cent of the tumour cells, concordant with S-phase estimates by cell cycle analysis of the flow cytometric DNA histogram. A majority of the bromodeoxyuridine-positive cells also carried the monosomy 9 chromosome abnormality. This is the first report to demonstrate the feasibility of combined in situ hybridization and detection of bromodeoxyuridine incorporated in vivo in human tumour cells in order to provide information on the growth rate of specific subsets of tumour cells identified by chromosomal constitution.     

Urofacial (Ochoa) syndrome

Between 1965 and 1986 we saw 36 children with enuresis and urinary tract infection in association with “inversion” of facial expression when laughing. Urologic work-up of these patients disclosed characteristic findings of mild neuropathic bladder in all cases, with severe urinary tract damage in most of them. The clear association of distortion in facial expression and neuropathic bladder with resultant damage to the genitourinary tract should prompt urological evaluation of individuals with “inversion” of facial expression. About two thirds of the patients also had moderate to severe constipation. We suggest the term urofacial syndrome for this disorder. The occurrence of the disorder in multiple sibs, normal parents, increased parental consanguinity, and equal sex ratio indicate autosomal recessive inheritance.     

Lactate dehydrogenase activity and isoform distribution in normal and hypertrophic smooth muscle tissue from the rat

The lactate dehydrogenase (LDH) activity and isoform distribution of LDH were investigated in tissue samples from the rat portal vein, aorta and urinary bladder. In addition, samples were obtained from hypertrophic urinary bladder. The total LDH activity per unit smooth muscle volume was higher in the urinary bladder compared to that in portal vein and aorta. Five LDH isoforms, reflecting different combinations of the two polypeptide chains denoted H and M, could be separated by agarose gel electrophoresis. The aorta contained more of the H form compared to the portal vein and urinary bladder. This difference suggests that the aorta, which is a slow smooth muscle, is more adapted for aerobic metabolism than the faster muscles of portal vein and urinary bladder. In the hypertrophic urinary bladder a shift in LDH isoform pattern towards less of the H form was found, which correlates with a better maintenance of contraction in anoxia in this type of hypertrophic smooth muscle.     

Effect of hydrostatic pressure on ADH induced osmotic water flow in toad bladder

The effect of hydrostatic pressure (HP) on antidiuretic hormone (ADH) stimulated osmotic water flow (Jv) across the toad urinary bladder was evaluated. Jv for ADH-stimulated bladders was significantly reduced by an elevation of the serosal HP gradient to 1 cm H₂O. Subsequent elimination of the HP gradient resulted in a recovery of Jv. Serosal HP also caused a reversible increase in sucrose permeability (P sucrose). For ADH-treated bladders fixed with glutaraldehyde during serosal HP exposure, subsequent exposure to a mucosal or serosal HP gradient caused acceleration or inhibition of Jv, respectively. The reduction in ADH-associated Jv with serosal HP was apparently caused by a back-flux of water through a paracellular pathway. Jv and P sucrose were not affected by mucosal HP during ADH stimulation. The results suggest a specific sensitivity of a paracellular pathway to a small serosal HP gradient in bladders with ADH-stimulated water flow. The reversibility of this effect on P sucrose suggests that the elements comprising the apical junctions are dynamic structures capable of recovering at least some of their permeability properties.