Biomedical subjects

E M Messing

Publications and source records attributed to E M Messing.

77 records · Page 5Linked to original sources

PubMed1976

Hypertension and post-traumatic renal arteriovenous fistula: demonstration of unilaterally elevated renin secretion.

Ipsilateral elevation and contralateral suppression of renin secretion have been established in a patient with a post-traumatic renal arteriovenous fistula associated with diastolic hypertension. This finding is rare because of the dilutional effect of arterial blood shunted in the renal vein. Increased renin secretion in this instance supports the proposed mechanism of diastolic hypertension with renal arteriovenous fistula.

Adult↗

PubMedDate not supplied

Bladder cancer: natural history, tumor markers, and early detection strategies.

Transitional cell bladder carcinoma is characterized by a dichotomous, multichronotopic natural history. Low and moderate grade Ta lesions frequently recur, yet rarely invade, and carry an excellent prognosis with currently available treatments. High grade Ta lesions, tumors with lamina propria invasion (T1), and carcinoma in situ often progress to invasive disease, at which time overall prognosis is significantly decreased, despite various treatment alternatives. Although early detection of bladder tumors, prior to muscle invasion, should vastly improve our ability to save both bladders and lives, current methods of detection are neither sufficiently sensitive nor specific. Tumor marker analysis is an exciting new frontier in bladder cancer evaluation, and may have important applications to early detection strategies, in combination with simple hematuria testing and other selected noninvasive screening methods.

Biomarkers, Tumor↗

PubMedDate not supplied

Growth factors and bladder cancer: clinical implications of the interactions between growth factors and their urothelial receptors.

Growth factors (GFs) are a class of proteins that bind to specific cell surface receptors (GF-Rs), inducing a variety of responses including mitosis, in susceptible target cells. Abnormal production, expression, and/or function of GFs or GF-Rs can result in unregulated growth, the hallmark of malignant transformation. This chapter reviews those GFs/GF-Rs that have been linked to human bladder cancer. It focuses particularly on one [epidermal growth factor (EGF), which is excreted in urine in high concentrations] and its possible role in the development and growth of urothelial malignancy. Potential clinical applications in diagnosis, staging, prevention, and treatment are discussed.

Epidermal Growth Factor↗

PubMedDate not supplied

Correlation between N-acetyltransferase activities in uroepithelia and in vivo acetylator phenotype.

The relationship between in vivo acetylator phenotype of individuals and N-acetyltransferase (NAT) activity in the cytosol of their cultured uroepithelia was examined in four urology patients. In vivo acetylator phenotypes were assigned by determining the ratio of N-acetyl vs. total [N-acetyl+free] sulfamethazine in urine and blood following a single oral dose (1 gm) of sulfamethazine. From the same patients, a surgical specimen of the ureter was obtained, uroepithelial cells were cultured in vitro, and the cytosols prepared. NAT activities were determined by measuring the amount of 4-acetylaminobiphenyl formed from incubation of uroepithelial cytosol with the substrate, 4-aminobiphenyl, and the cofactor [14C]acetyl coenzyme A. The two individuals phenotyped as "slow acetylators" by the in vivo method had NAT activities of 8.3 and 16.2 pmol 4-acetylaminobiphenyl/mg protein/min. In contrast, the two individuals phenotyped as "rapid acetylators" showed activities of 50.9 and 109.5 pmol 4-acetylaminobiphenyl/mg protein/min. The rapid acetylators exhibit about 6-fold greater uroepithelial NAT activities than slow acetylators, thus showing a direct correlation between the NAT activity in the uroepithelium, the target tissue of the human bladder carcinogen 4-aminobiphenyl, and the in vivo acetylator phenotype. These results imply that susceptibility of individuals to arylamine-induced bladder cancer might be associated with NAT activities in their target cells and that in vivo acetylator phenotyping could serve as a useful and relevant biochemical screening marker to assess the risk of developing bladder cancer.

Acetylation↗

PubMedDate not supplied

Relationship between in vivo acetylator phenotypes and cytosolic N-acetyltransferase and O-acetyltransferase activities in human uroepithelial cells.

The in vivo acetylator phenotype as well as N-acetyltransferase (NAT) and O-acetyltransferase (OAT) activities in cytosols from cultured uroepithelia were determined in 25 urological patients. In vivo acetylator phenotypes were categorized by determining the amounts of 5-acetylamino-6-formylamino-3-methyluracil (AFMU) and 1-methylxanthine in urine after the administration of a 200 mg dose of caffeine. Subjects were grouped according to the AFMU/AFMU + 1-methylxanthine ratio as "slow" (< 0.41) or "rapid" (> or = 0.41) acetylators. The uroepithelia were obtained from these subjects, cultured in vitro, and the cytosols were prepared. NAT and OAT activities were determined using 4-aminobiphenyl (ABP) and [3H]N-hydroxy-4-aminobiphenyl (N-OH-ABP) as substrates, respectively. In vivo phenotyping resulted in 18 patients being slow acetylators and seven rapid. The mean NAT and OAT activities for these different subsets were: 3.58 nmol/mg protein/min and 409 pmol/mg tRNA/mg protein for the slow; and 3.38 nmol/mg protein/min and 428 pmol/mg tRNA/mg protein for the rapid, respectively. Furthermore, in individual samples, NAT and OAT activities tended to parallel each other, implying that the same enzyme might catalyze both NAT and OAT activities in uroepithelia. The N-acetylation of ABP was inhibited by N-OH-ABP and also by p-aminobenzoic acid, a substrate which is preferred by the monomorphic NAT enzyme. Similarly, OAT-mediated binding of [3H]N-OH-ABP to tRNA was inhibited in a dose-dependent manner by ABP and p-aminobenzoic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylation↗