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Biomedical subjects

M Menon

Publications and source records attributed to M Menon.

At least 37 records · Page 2Linked to original sources
PubMed1989

Prognostic and therapeutic observations of manifestations in the genitourinary tract of adenocarcinoma of the colon and rectum.

To evaluate the significance of involvement of the genitourinary tract in adenocarcinoma of the colon and rectum, we received the records of 178 patients with adenocarcinoma of the colon and rectum admitted to the University of Massachusetts Medical Center from 1980 to 1985. Sixty-eight patients (38 per cent) had urologic manifestations categorized as ureteral obstruction or injury (34 per cent), invasion to the bladder or prostate, or both (10 per cent), isolated gross hematuria (18 per cent), radiation cystitis (6 per cent) and neurogenic bladder (26 per cent). Involvement of the genitourinary tract was more common among patients with recurrent versus primary carcinoma (53 versus 32 per cent) and among patients with high stage (Dukes' C and D) versus low stage (Dukes' A and B) carcinoma (48 versus 21 per cent). The survival rate was worse in patients with high stage compared with low stage disease and no patient with recurrent high stage disease survived beyond three years. Short term survival (less than two years) was not statistically different among patients with or without manifestations in the genitourinary tract: 63 and 45 versus 71 and 66 per cent at one and two years, respectively; however, the five year survival rate was worse among patients with genitourinary involvement (30 versus 54 per cent, p less than 0.05). Surgical and endoscopic intervention of the urinary tract was performed upon 36 patients with Dukes' C and D carcinoma because of life-threatening sepsis or azotemia, or both.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1988

Impairment by cyclosporine of membrane-mediated functions in kidney mitochondria.

This study was performed to evaluate whether cyclosporine penetrates kidney mitochondria and impairs mitochondrial functions, causing nephrotoxicity. Exposure of rat kidney cortical mitochondria in vitro to cyclosporine had little effect on the oxidation of glutamate plus malate. Oxidation of succinate was markedly inhibited by a toxic level of cyclosporine (25 to 50 nmol/mg protein) under resting (State 4) and ADP-stimulated (State 3) conditions. Under uncoupling conditions, induced by the proton ionophore, CCCP or by the calcium ionophore, A23187 plus calcium, mitochondrial respiration was unchanged by cyclosporine. In mitochondria isolated from rats treated with an immunosuppressive dose of cyclosporine (25 mg/kg/day, p.o.), respiration was not significantly impaired. The respiration stimulated by ADP was only diminished in mitochondria from rats treated with 75 mg/kg. The rate of calcium uptake was unchanged by cyclosporine under in vitro and in vivo conditions. Kidney mitochondria of untreated rats maintained in a medium containing respiratory substrates and phosphate released spontaneously accumulated calcium that was accompanied by large amplitude swelling and enhanced respiration. Cyclosporine in vitro inhibited the process of spontaneous calcium discharge at the concentration range of 0.1 to 0.5 nmol/mg protein. Swelling and respiration induced by accumulated calcium was significantly diminished in kidney mitochondria isolated from cyclosporine-treated rats given doses of 25 or 75 mg/kg. The data obtained indicate that cyclosporine interacts with the membrane of kidney mitochondria in virtually the same way under in vitro and in vivo conditions. Cyclosporine at an immunosuppressive level impairs calcium-induced membrane permeability and at a toxic level, the rate of ADP phosphorylation.

Animals↗
PubMed1987

Expression of FMC7 antigen and tartrate-resistant acid phosphatase isoenzyme in cases of B-lymphoproliferative diseases.

A panel of different B-cell malignancies representing various stages of B-cell differentiation were analyzed for the expression of an antigen labeled by the monoclonal antibody FMC7 and of tartrate-resistant acid phosphatase (TracP) activity. The FMC7 antigen and TracP were not found on early immature pre B-cell proliferations, appeared at early and intermediate B-cell stages, reached their peak of expression in terms of both incidence of positivity and staining intensity at the late B cell stage (as represented by hairy cell leukemia) and were lost at the B-cell/plasma cell transition. Although detected at similar stages of B-cell differentiation, FMC7 and TracP appear to be independently expressed and were not related to a particular Ig class. The simultaneous detection of FMC7 and TracP represents a distinguishing parameter for the identification of hairy cell leukemia.

Acid Phosphatase↗
PubMed1987

The effect of streptozotocin-induced diabetes on the neuroendocrine-male reproductive tract axis of the adult rat.

Studies in the streptozotocin rat model for diabetes mellitus suggest that sexual dysfunction in these animals may result from diabetes-induced alterations of the neuroendocrine-reproductive tract axis. Our investigation was performed to better define the effects of diabetes on the neuroendocrine sex accessory organ axis in the male rat. Rats were rendered diabetic, and were either left untreated or treated with insulin, testosterone or both. Diabetes resulted in decreased body and reproductive organ weights, as well as diminished sperm counts and motility and prostatic acid phosphatase. Seminal fructose was increased. A significant decrease in serum LH, FSH and testosterone was noted. Insulin treatment of the diabetic rats restored serum gonadotropins, reproductive organ weight, sperm counts and motility, and seminal fructose to control levels. Prostatic weight and prostatic acid phosphatase levels remained abnormal. Testosterone restored the above mentioned parameters to control levels, with the exception of LH. Treatment with insulin and testosterone had a synergistic effect on spermatogenesis. A GnRH stimulation test demonstrated that pituitaries of diabetic animals had a blunted response, with diminished LH and FSH secretion. In the diabetic animal, there are both pituitary and testicular abnormalities which may be responsible for reproductive dysfunction.

Animals↗
PubMed1987

Effect of cyclosporine A on male reproduction in rats.

We examined the effects of the immunosuppressive drug cyclosporine A on male reproduction in sexually mature rats. The drug was administered subcutaneously in 3 doses (10, 20 and 40 mg. per kg. daily) for 14 days. Cyclosporine A administration resulted in a dose-dependent decline in body and reproductive organ weights, histology of the testis showed definite degenerative changes, and sperm counts and motility decreased. Spermatozoa from treated rats retained the cytoplasmic droplet and they were decapitated. Consequently, sterility occurred in rats treated with high doses of cyclosporine A. A reduction in circulating testosterone and an increase in gonadotropins were noted. The possibility existed that the cyclosporine A-induced alterations in the male reproductive system were secondary to the hepatic or nephrotoxic effects of the drug. Therefore, we assessed liver and kidney function by assay of the serum levels of bilirubin, alkaline phosphatase, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase and creatinine. Except for an increase in bilirubin, none of the other liver function studies was altered, thereby eliminating hepatocellular damage as the etiology of impaired reproductive function in cyclosporine A-treated rats. We observed an increase in creatinine levels in animals treated with higher doses of cyclosporine A, consistent with mild renal failure. However, the fact that a decline in reproductive function was seen even in the group treated with 10 mg. per kg. cyclosporine A daily, which had normal serum creatinine levels, suggests that the alterations in male reproduction seen with this therapy are not entirely the result of nephrotoxicity.

Animals↗
PubMed1986

The uptake of oxalate by rat liver and kidney mitochondria.

Oxalate, a metabolic end product, forms calcium oxalate deposits in the tissues under a variety of pathological conditions. In order to determine whether oxalate is able to penetrate the mitochondrial matrix, the uptake of oxalate by rat liver and kidney cortical mitochondria was characterized. Mitochondria did not swell in an iso-osmotic medium of ammonium oxalate unless a small amount of phosphate was provided. This phosphate-induced swelling was prevented by N-ethylmaleimide. The uptake of [14C]oxalate by liver and kidney mitochondria followed first order kinetics and was inhibited by mersalyl an inhibitor of the phosphate and dicarboxylate carriers. Accumulation of [14C]oxalate at equilibrium was significantly higher by mitochondria energized with succinate than by rotenone-inhibited mitochondria due to higher matrix pH as determined by the [14C]5,5'-dimethyloxazolidine-2, 4-dione distribution ratio. The velocity of oxalate accumulation by mitochondria was temperature dependent. The activation energy was 81.5 and 86.5 J/mol for liver and kidney mitochondria, respectively. In both types of mitochondria, the rate of oxalate uptake was hyperbolic with respect to the concentration of oxalate. The apparent Km was 28.8 +/- 0.6 and 13.4 +/- 1.2 mM and the Vmax 87.1 +/- 1.1 and 66.1 +/- 3.1 nmol X mg-1 X min-1 at 12 degrees C for liver and kidney mitochondria, respectively. Phenylsuccinate exhibited mixed inhibition of the rate of oxalate uptake. Oxalate exhibited also a mixed inhibition of the uptake and oxidation of malate by mitochondria. The data obtained provide evidence that oxalate is transported across the mitochondrial membrane by a phosphate-linked, carrier-mediated system similar to or identical to the dicarboxylate transporter.

Animals↗
PubMed1986

Reactivity patterns of monoclonal antibodies positive on myelomonocytic leukemia cells as defined by esterase isoenzyme analysis.

The reactivity with monoclonal antibodies (MoAbs) specific for myelomonocytic cells and the expression of a particular esterase isoenzyme were analyzed in 159 cases of acute myeloid leukemias. The incidence of positivity of 16 MoAbs (MCS-2, MCS-1, OKM1, My-1, Leu-M1, Leu-M3, CA-2-38, MY4, MY7, MY8, MY9, VIM-D2, VIM-D5, Mo1, Mo2, 63D3) was studied using the indirect immunofluorescence technique. A carboxylic esterase isoenzyme which can be inhibited completely and selectively by sodium fluoride (NaF) was demonstrated by isoelectric focusing on horizontal polyacrylamide gels. This NaF-sensitive isoenzyme indicated the monocytic origin of the blast cells as it is specific for this cell lineage. Prior to the immunological-isoenzymatic analysis all cases were categorized into two subtypes according to morphological criteria of the FAB classification system: 147 cases of AML (FAB M1-3) and 12 cases of AMMoL/AMoL (FAB M4/5). However, 15 out of 147 cases of AML expressed the NaF-sensitive isoenzyme and were therefore assigned to the group AMMoL/AMoL. Likewise, 1 case, diagnosed morphologically as AMMoL, was negative for this marker isoenzyme and was assigned to the other leukemia subtype. The incidence of reactivity varied widely for the MoAbs tested regarding the overall results on all cases and the positivity of cases of either AML or AM-MoL/AMoL. The MoAbs were grouped into four classes depending on the pattern of reactivity with myeloblastic or monoblastic or both subtypes of acute myeloid leukemia. The MoAbs MCS-2, MY7, Leu-M1, and MY9 detected the vast majority of cases with either myelocytic or monocytic involvement (group-I: "pan-myelomonocytic" reactivity). The MoAbs MCS-1, OKM1, VIM-D5, and Mo1 showed a predominance in their staining pattern for monocytic variants, but were also positive on a substantial percentage of nonmonocytic cases (group-II: predominantly reactive with monocytic, but also myelocytic cases). The MoAbs Leu-M3, MY4, VIM-D2, Mo2, and MY8 reacted with the large majority of AMMoL/AMoL cases and with a small number of AML cases (group-III: monocyte-"specific" reactivity). The MoAbs of group-I are useful in differentiating acute lymphoid from acute myeloid leukemias. The MoAbs of group-III, and to a lower extent those of group-II, will be of considerable value in the subtyping of acute myeloid leukemias. The results show that accuracy of leukemia classification might not always be achieved by morphology alone, but that immunological and biochemical aspects should be included as well, and several MoAbs are very useful tools for classification and subtyping of acute myeloid leukemias.

Antibodies, Monoclonal↗
PubMed1986

Phenotyping of malignant hematopoietic cells. Analysis of 1200 cases of leukemia-lymphoma.

1255 cases of leukemia-lymphoma were tested between 1972 and 1984 by multiple marker analysis. Routine leukemia phenotyping was performed using standard morphological and cytochemical techniques in combination with clinical and histo-pathological information; the main emphasis was put on immunological surface marker analysis using erythrocyte rosette assays, TdT and a large panel of poly- and monoclonal antibody tests. The 1255 cases were divided into these major types and subtypes: 349 cases of ALL and related immature T- and Burkitt-lymphomas (cALL, pre B-ALL, B-ALL and Burkitt-lymphomas, T-ALL and immature, mostly leukemic T-lymphomas, Null-ALL), 454 cases of mature T- and B-cell malignancies (T-CLL, mycosis fungoides, Sezary-syndrome, T-lymphomas, B-CLL, hairy cell leukemia, multiple myeloma, B-lymphomas), 263 cases of acute myeloid leukemias (AML, AMMoL/AMoL), 182 cases of chronic myeloid leukemias (CML in chronic phase, CMoL, CML in blast crisis), 6 cases of erythroleukemia and 1 case of megakaryoblastic leukemia. A simplified classification scheme which has been used in our laboratories is presented. Phenotyping is of diagnostic, prognostic and therapeutic relevance, most evidently for patients with ALL. Routine leukemia phenotyping should be performed with highly standardized techniques and reagents and by combining information from several fields in the multiple marker analysis. New areas of leukemia research might become very useful for the routine procedure of phenotyping.

Adult↗
PubMed1986

Inhibition of gonadotropin-releasing hormone receptors in rat anterior pituitary monolayer cell cultures by danazol.

To study possible cellular antigonadotropic effects of danazol, monolayer cultures of anterior pituitary cells from immature female rats were treated with danazol. Measurements of luteinizing hormone release in response to 10(-8) mol/L gonadotropin-releasing hormone challenge and iodine 125-labeled gonadotropin-releasing hormone binding activity were done after exposure to increasing concentrations of danazol and for increasing lengths of time. It was found that luteinizing hormone secreted by pituitary cells in response to gonadotropin-releasing hormone was inhibited after danazol treatment in a dose- and time-dependent manner when compared to controls. Also, a 45% decrease in gonadotropin-releasing hormone receptor binding capacity was observed in pituitary cells cultured in the presence of increasing concentrations of danazol in the range of 10(-8) to 10(-4) mol/L when compared to controls. Furthermore, exposure to danazol for 25 to 96 hours caused a marked decrease in gonadotropin-releasing hormone binding activity (p less than 0.005). Under these experimental conditions danazol treatment decreased the pituitary receptors for gonadotropin-releasing hormone in a dose- and time-dependent manner. Scatchard analysis of saturation curves for the binding of gonadotropin-releasing hormone to cellular gonadotropin-releasing hormone receptors indicated that the observed decrease in gonadotropin-releasing hormone binding in the danazol-treated group was due to a change in the number of gonadotropin-releasing hormone binding sites rather than a change in the affinity. It is therefore concluded that the antigonadotropic activity of danazol appears to be related to a decrease in gonadotropin-releasing hormone receptors in the pituitary.

Animals↗