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S A Martin

Publications and source records attributed to S A Martin.

At least 145 records · Page 8Linked to original sources
PubMed1986

Purification and characterization of histidine decarboxylase from mouse kidney.

Histidine decarboxylase was purified 800-fold from the kidneys of thyroxine-treated mice. The purification procedure included precipitation of protein from a crude supernatant after heating it to 55 degrees C at pH 5.5, fractionation with (NH4)2SO4, phosphocellulose column chromatography, chromatofocusing, DEAE-Sepharose column chromatography, gel filtration on Sephacryl S-300 and preparative polyacrylamide-gel electrophoresis. The native enzyme had an estimated Mr of 113 000. The protein was analysed in SDS/10%-polyacrylamide gels and formed a single band corresponding to a subunit Mr of 55 000, indicating that it is a dimer. Three forms of the enzyme were resolved on isoelectrofocusing gels, with pI 5.3, 5.5 and 5.7.

Animals↗
PubMed1986

The influence of age on dorsal hand vein responsiveness to norepinephrine.

The influence of age on the responsiveness of dorsal hand vein alpha-receptors to local infusions of norepinephrine was investigated by the use of a novel technique, the linear variable differential transformer. Studies were conducted in two groups of healthy subjects, 26 elderly individuals (14 men and 12 women) 60 to 78 years old and 32 young individuals (24 men and eight women) 16 to 29 years old. There was wide interindividual variation in responsiveness to norepinephrine within both groups of subjects. The dose of norepinephrine required to produce 50% venoconstriction in the elderly ranged from 1.5 to 300 ng/min (geometric mean 24.0 ng/min). The dose required to produce 50% venoconstriction in younger individuals ranged from 1.6 to 360 ng/min (geometric mean 23.8 ng/min). These results suggest that there is no systematic influence of age on dorsal hand vein alpha-receptor responsiveness. A power calculation demonstrates a very small likelihood of a type II error.

Adolescent↗
PubMed1986

Phosphoenolpyruvate-dependent phosphorylation of hexoses by ruminal bacteria: evidence for the phosphotransferase transport system.

Six species of ruminal bacteria were surveyed for the phosphoenolpyruvate (PEP)-dependent phosphorylation of glucose. Selenomonas ruminantium HD4, Streptococcus bovis JB1, and Megasphaera elsdenii B159 all showed significant activity, but Butyrivibrio fibrisolvens 49, Bacteroides succinogenes S85, and Bacteroides ruminicola B1(4) showed low rates of PEP-dependent phosphorylation and much higher rates in the presence of ATP. S. ruminantium HD4, S. bovis JB1, and M. elsdenii B159 also used PEP to phosphorylate the nonmetabolizable glucose analog 2-deoxy-D-glucose (2-DG). Rates of 2-DG phosphorylation with ATP were negligible for S. bovis JB1 and M. elsdenii B159, but toluene-treated cells of S. ruminantium HD4 phosphorylated 2-DG in the presence of ATP as well as PEP. Cell-free extracts of S. ruminantium HD4 used ATP but not PEP to phosphorylate glucose and 2-DG. Since PEP could serve as a phosphoryl donor in toluene-treated cells but not in cell-free extracts, there was evidence for membrane and hence phosphotransferase system involvement in the PEP-dependent activity. The ATP-dependent phosphorylating enzymes from S. ruminantium HD4 and S. bovis JB1 had molecular weights of approximately 48,000 and were not inhibited by glucose 6-phosphate. Based on these criteria, they were glucokinases rather than hexokinases. The S. ruminantium HD4 glucokinase was competitively inhibited by 2-DG and mannose, sugars that differ from glucose in the C-2 position. Since 2-DG was a competitive inhibitor of glucose, the same enzyme probably phosphorylates both sugars. The S. bovis JB1 glucokinase was not inhibited by either 2-DG or mannose and had a higher Km and Vmax for glucose.

Adenosine Triphosphate↗
PubMed1985

The endometrial biopsy as a guide to the management of luteal phase defect.

The endometrial biopsy serves as a useful and valuable tool in the diagnosis and treatment of luteal phase defect (LPD). Eighty patients were diagnosed as having an LPD by endometrial biopsy. The subjects were divided into four equal groups, and different treatment protocols were introduced according to the histologic pattern found in the endometrial biopsy specimen. Patients in group I had glandular stromal asynchrony and were treated with clomiphene citrate therapy. Progesterone suppositories were administered to those patients in group II who showed glandular stromal synchrony. Groups III and IV had the same histologic pattern as groups I and II, but a reversal of the treatment protocol was made. The raw pregnancy rate was 85% and 80% for groups I and II, respectively. Groups III and IV had a raw pregnancy rate of 40% and 30%, respectively. Life-table analysis projected the pregnancy rate based on the protocol of therapy administered. This confirmed our findings and strengthened our belief that the endometrial biopsy is an invaluable guide in the treatment of LPD. This article addresses two distinct endometrial patterns within the framework of LPD and proposes a structured therapeutic regimen to treat this defect.

Actuarial Analysis↗
PubMed1985

Effects of monensin, pyromellitic diimide and 2-bromoethanesulfonic acid on rumen fermentation in vitro.

The effects of monensin, 2-bromoethanesulfonic acid (2-BES) and pyromellitic diimide (diimide) on gas and volatile fatty acid (VFA) production by the rumen microbiota were compared in mixed culture. Oat hay, a hay-concentrate mixture (48% hay, 43% concentrate) and a soluble carbohydrate mixture were used as substrates for microbial growth. The highest concentrations of diimide (10 ppm) and 2-BES (30 microM) decreased methanogenesis by 97 and 76%, respectively, while H2 accumulation was increased 30- and 20-fold, respectively. The effect of monensin on methanogenesis was less dramatic as 10 ppm decreased CH4 accumulation 16% and H2 did not accumulate. Diimide and 2-BES decreased the acetate:propionate ratio with the hay (P less than .05) and soluble carbohydrate mixture (P less than .025). The numbers of saccharolytic, cellulolytic and methanogenic bacteria from sheep fed a diet with diimide (60 ppm) did not differ significantly from sheep fed a control diet. Semicontinuous culture incubations indicated that the mixed rumen microbial population could adapt and degrade diimide after 24 h of incubation.

Alkanesulfonates↗
PubMed1984

Peptidoglycans as promoters of slow-wave sleep. I. Structure of the sleep-promoting factor isolated from human urine.

Fast atom bombardment-mass spectrometry (FABMS) has been used to determine the structure of the urinary sleep-promoting factor (FSu), the nature of whose components had been reported earlier. Less than 1 nmol of the underivatized substance sufficed for the FABMS experiments. The major somnogenic constituent of the purified preparation was a peptidoglycan of Mr = 921 with the structure N-acetylglucosaminyl-N -acetylanhydromuramylalanylglutamyldiaminopimelylalanine. The anhydro linkage is between C-1 and C-6 of the muramyl entity. Two additional substances accompanied the above compound. These were the hydrated form (i.e. in which the muramyl entity had a free reducing end, and a free hydroxyl on C-6), and an anhydro analogue lacking the terminal alanine. The Mr values were 939 and 850, respectively. Methyl esters were prepared, and these were also acetylated. The mass spectra of the methyl ester of Mr = 921 displayed an increase in Mr of 42 (i.e. 3 X 14), indicating the presence, originally, of three free carboxyls. Acetylation increased Mr by a further 168 units (i.e. 4 X 42), indicating 4 hydroxyl or amino groups. These data are consistent with the structure cited above for the main entity of FSu. Similar confirmatory results were obtained for the two minor constituents described above. These operations were worked out on natural muramyl peptides of known structure, obtained from other sources, and the data are given for comparison.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1984

Peptidoglycans as promoters of slow-wave sleep. II. Somnogenic and pyrogenic activities of some naturally occurring muramyl peptides; correlations with mass spectrometric structure determination.

The structures of components of the sleep-promoting material purified from human urine were established by fast atom bombardment-mass spectrometry, as reported in the accompanying paper (Martin, S. A., Karnovsky, M. L., Krueger, J. M., Pappenheimer, J. R., and Biemann, K. (1984) J. Biol. Chem. 259, 12652-12658). We report here that two substances isolated from that preparation, viz. N-acetylglucosaminyl-1,6 -anhydro-N-acetylmuramyl-Ala-gamma-Glu-diaminopimelyl-Ala) and that compound lacking the terminal alanine, are active as somnogens. Cerebro-intraventricular administration of 1 pmol of the glycotetrapeptide was sufficient to induce prolonged excess sleep in rabbits. A similar substance obtained from Brevibacterium divaricatum in which the free carboxyls of the glutamic and diaminopimelic moieties, indicated above, were amidated (N-acetylglucosaminyl-1,6-anhydro-N-anhydromura-myl-Ala-iso- Gln- epsilon-amido-diaminopimelyl -Ala-Ala) was not active as a promoter of slow-wave sleep. Deamidation of this peptide to a mixture of the free dicarboxylic forms produced a somnogenic substance. Our findings show that in addition to the muramyl form of peptidoglycan monomers, the anhydro muramyl form, with no reducing end, is compatible with somnogenic activity. Furthermore, the data obtained with a natural product amplify our earlier observations with smaller synthetic molecules of the importance of amidation/deamidation in the structure-activity relationships of muramyl peptides.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1984

Histidine decarboxylase phenotypes of inbred mouse strains: a regulatory locus (Hdc) determines kidney enzyme concentration.

Mouse kidney histidine decarboxylase (HDC) provides a model system to study genetic control of a hormone-regulated enzyme (inducible by estrogen and thyroxine; repressible by testosterone). Five major HDC phenotypes scored on the basis of (i) enzyme activity and (ii) the difference in activity between the sexes (females usually higher than males) have been discovered by screening 38 strains of mice. One genetic difference between high-activity strains (DBA/2 and C3H/He) and low-activity strains (C57BL/6 and C57BL/10) has been examined in detail. The phenotypic difference segregates as a single gene in both conventional crosses and between recombinant inbred (RI) strains. Immunoprecipitation has shown that the activity difference is due to an alteration in the number of enzyme molecules. The phenotypic difference between high and low strains can therefore be attributed to different alleles of a single regulatory locus, Hdc; the allele Hdcb determines low HDC concentration, and the allele Hdcd high concentration. Hdc has been mapped to chromosome 2 using data from both comparisons of strain distribution patterns of previously mapped loci within RI strains and a conventional three-point cross. The probable gene order is B2m-pa-Hdc, with map distances of 3.1 +/- 1.7 and 2.0 +/- 1.4 cM, respectively.

Alleles↗
PubMed1984

A structural gene (Hdc-s) for mouse kidney histidine decarboxylase.

The concentration of mouse kidney histidine decarboxylase (HDC) is modulated by estrogen, testosterone, and thyroxine in a tissue-specific manner. Variation in HDC levels between strains of mice can be used to investigate the genetic regulation of enzyme structure, tissue specific expression, and induction and repression by hormones. Variation in the structure of HDC between different inbred strains of mice affecting its Km for the cofactor pyridoxal-5'-phosphate (PLP) and its heat stability has been discovered. The alternative phenotypes are additively inherited in crosses and the heat stability difference is due to alleles of a single structural gene, Hdc-s, which segregate among the BXD and BXH recombinant inbred strains. The allele Hdc-sb determines the heat-stable phenotype (C57BL substrains), and the allele Hdc-sd the heat-labile phenotype (DBA/2 and C3H/He strains). The alleles of the structural gene cosegregate with alleles of a regulatory gene previously named Hdc (determining kidney enzyme concentration); there were no recombinants among 38 RI strains. Therefore the two loci are less than 0.685 cM apart and comprise part of the HDC gene complex, [Hdc], on chromosome 2 of the mouse.

Animals↗
PubMed1984

A regulatory locus, Hdc-e, determines the response of mouse kidney histidine decarboxylase to estrogen.

Levels of histidine decarboxylase (HDC; EC 4.1.1.22) activity in female mouse kidney are modulated by estrogen (administered as implanted pellets). In some inbred strains HDC activity is induced by estrogen, while in others the enzyme is repressed. Immunoprecipitation with an anti-fetal rat HDC antiserum has shown that induction and repression of HDC levels are due to changes in enzyme concentration. Segregation analysis has identified a single additively inherited regulatory locus, Hdc-e, which determines the response to estrogen. The allele Hdc-eb (C57BL/10) determines induction, and the allele Hdc-ed (DBA/2) determines repression. Preliminary evidence indicates cosegregation of Hdc-e alleles with alleles of another regulatory locus, Hdc-c (determining kidney HDC concentration), and therefore putative linkage of Hdc-e with the HDC gene complex on chromosome 2. This is the first report of a mammalian regulatory gene controlling two opposite mechanisms, induction and repression in response to a single effector.

Animals↗
PubMed1984

Giant cell tumor of major salivary glands: report of three cases, one occurring in association with a malignant mixed tumor.

Three cases of a heterofore undescribed neoplasm of major salivary glands morphologically similar to giant cell tumor of bone are presented. All tumors were located in the parotid gland of adult individuals, and all patients are alive and well following surgical excision. One of the three cases was associated intimately with a malignant mixed tumor (carcinoma in pleomorphic adenoma). Ultrastructural and immunohistochemical studies failed to provide conclusive evidence about the specific nature of the tumor cells. The major salivary glands should be added to the long list of organs in which extraskeletal giant cell tumors have been observed, whether alone or in association with an epithelial malignancy.

Adenoma, Pleomorphic↗
PubMed1983

Prostaglandin production by the pregnant and non-pregnant rabbit uterus.

We have studied the prostaglandin synthesis of the pregnant and non-pregnant rabbit uterus in a microsomal membrane preparation, and in an ex vivo perfused uterus preparation which retains agonist stimulated prostaglandin production. In both the microsomal and isolated perfused system, prostacyclin was the major arachidonic acid metabolite produced; PGE2 was also produced in substantial quantities while TxB2 and PGF2 alpha were not detectable. Moreover, oxytocin was a specific stimulus of PGE2 release. The steroid hormone milieu influenced the level of agonist stimulated prostaglandin release; in general, ovariectomized, estrogen treated animals were more responsive to agonist stimulation than those treated with estrogen followed by progesterone. The microsomal studies indicated that the pregnant animal had a greatly enhanced capacity to metabolize arachidonic acid when compared with the non-pregnant animal. However, this was not reflected in the ability of agonists to stimulate prostaglandin release in the ex vivo perfused preparation.

Animals↗
PubMed1983

Cholecystokinin inhibits pancreatic and hepatic carcinogenesis.

Cholecystokinin (CCK) has trophic actions on abdominal viscera. To determine whether CCK enhances malignant growth in a similar fashion, we gave hamsters CCK together with di-isopropanol nitrosamine (DIPN), a known pancreatic and hepatic carcinogen. After 40 weeks of injections, those animals receiving both DIPN and CCK developed no cancers, while the control animals receiving DIPN alone developed pancreatic and hepatic carcinomas. This suggests that CCK inhibits carcinogenesis in this model. Although the mechanism of this effect is unknown, some implications for human carcinogenesis are testable by currently available methods.

Animals↗