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Biomedical subjects

A Morin

Publications and source records attributed to A Morin.

At least 55 records · Page 3Linked to original sources

[Preliminary and multidisciplinary study of three Coptic mummies of the Testut-Latarjet museum at Lyon].

In 1901 Albert Gayet raked up from Antinoe three mummies exhibited to day at the Anatomy Museum of Lyon. The study of the three mummies was made in detail as to their dress, anthropometric and scannographic findings. The clothes were characteristic of coptic civilization. The radiographic date gave a life span of around 40 years. The X-ray imagery shows the remains of cerebral and visceral organs. The sexual criteria are thought to be those of two women and undetermined for the child. Later, several investigations like endoscopic autopsy, tooth microscopy and chromosomic map will be necessary.

Anthropometry↗

Cloning, sequencing, and expression in Escherichia coli of the D-hydantoinase gene from Pseudomonas putida and distribution of homologous genes in other microorganisms.

Pseudomonas putida DSM 84 produces N-carbamyl-D-amino acids from the corresponding D-5-monosubstituted hydantoins. The gene encoding this D-hydantoinase enzyme was cloned and expressed in Escherichia coli. The nucleotide sequence of the 1.8-kb insert of subclone pGES19 was determined. One open reading frame of 1,104 bp was found and was predicted to encode a polypeptide with a molecular size of 40.5 kDa. Local regions of identity between the predicted amino acid sequence and that of other known amidohydrolases (two other D-hydantoinases, allantionase and dihydroorotase) were found. The D-hydantoinase gene was used as a probe to screen DNA isolated from diverse organisms. Within Pseudomonas strains of rRNA group I, the probe was specific. The probe did not detect D-hydantoinase genes in pseudomonads not in rRNA group I, other bacteria, or plants known to express D-hydantoinase activity.

Amidohydrolases↗

Characterization of a single strong tissue-specific enhancer downstream from the three human genes encoding placental lactogen.

The human genes coding for growth hormone (hGH) and placental lactogen (choriosomatomammotropic hormone [hCS]) are clustered on chromosome 17 in the following order: 5' hGH-N hCS-L hCS-A hGH-V hCS-B 3'. So far, a single placenta-specific enhancer has been identified in the locus, 2 kb downstream from the hCS-B gene, and shown to comprise one in vitro binding site for a nuclear protein. We here provide evidence that the hCS-B enhancer is more complex: (i) protection against DNase I digestion in the 3' flanking region of the hCS-B gene reveals four binding sites (DF-1, DF-2, DF-3, and DF-4) for nuclear proteins from either placental or HeLa cells, and (ii) placenta-specific enhancer activity can be fully exerted in transient expression experiments by a 126-bp fragment comprising the DF-3 and DF-4 protein-binding sites. By dissecting this region, we show that enhancer activity is mediated by a synergy between DF-3 and DF-4. Competitions with various oligonucleotides in footprinting and gel retardation experiments indicate that the same protein or set of proteins, different in HeLa and placenta cell nuclei, interacts with sites DF-2, DF-3, and DF-4. We also studied the regions of the hCS-L and hCS-A genes which are highly similar to the hCS-B enhancer. Although they each present the same four protein-binding sites, they exhibit only minor enhancer activity.

Base Sequence↗

Influence of heparin on the chemotactic activity of human thrombin.

Chemoattractant properties of human thrombin have been studied, by polymorphonuclear leucocyte migration under agarose gel, in the presence of various sulphated macromolecules such as standard heparins, low molecular weight heparins, CY216, K2165, PK10169 and pentosane polysulphate. These compounds did not attract polymorphonuclear leucocytes within the range of concentrations used, whilst thrombin alone is a cytotaxin for these cells. Addition of heparins to thrombin led to an increase in the chemoattractant activity of this enzyme for at least one of the doses studied. Augmentation of the chemoattractant activity of thrombin by heparins was shown at concentrations equivalent to those found in-vivo after administration of therapeutic doses of heparin. Pentosane polysulphate, at the studied concentrations, did not lead to a significant rise in the chemoattractant activity of thrombin.

Chemotaxis, Leukocyte↗

Comparative effect of salinomycin and monensin on Streptococcus bovis strain ATCC 9809.

The effect of salinomycin (2.5 mg/l) on the in vitro growth of Streptococcus bovis strain ATCC 9809, on its catabolism of glucose and on its anabolism of lactic acid was compared with that of monensin (5.0 mg/l). In control cultures containing no ionophore, glucose consumption and lactic acid production were completed concomitantly with maximal growth which was reached after 2 h of incubation at 37 degrees C. No further growth of S. bovis was observed within 2 h after the addition of one or the other ionophore to exponentially growing cultures. Glucose consumption and lactic acid production continued for 6 h after the addition of monensin and for 8 h after the addition of salinomycin. As observed in cultures without ionophore, glucose was totally consumed and lactic acid was stoichiometrically produced in cultures grown in the presence of one or the other ionophore. Thus, salinomycin and monensin inhibited bacterial growth but not fermentation of glucose by S. bovis.

Anti-Bacterial Agents↗

Polyadenylic: polyuridylic acid-induced determinants of host resistance to cytomegalovirus and their potentiation by hyperthermia.

The ability of spleen cells from poly A:poly U-treated mice to inhibit murine cytomegalovirus (MCMV) replication in confluent monolayer cells of secondary mouse embryo fibroblasts (MEFs) cultured at 37 and 40 degrees C was investigated. When spleen cells from BALB/c mice injected 48 h earlier with poly A:poly U were added to MEFs infected 2 h previously with MCMV, 37% less plaques were observed than in cultures containing control cells. Of interest, the poly A:poly U-induced antiviral activity at the elevated temperature (40 degrees C) resulted in a further drop to 61% in MCMV-induced plaques compared to those of the normothermic (37 degrees C) cultures. The antiviral function of spleen cells induced by poly A:poly U was evident in the supernatant fluid when cultured for 48 h at 37 degrees C. MCMV-induced plaques were reduced to 52 and 5% of controls in the plaque assays performed at 37 and 40 degrees C, respectively. Supernatant fluids generated at 40 degrees C, however, inhibited MCMV replication only when incubated at 40 degrees C. No direct inhibitory effect of the supernatant fluids on MCMV was evident; rather, inhibition was effected directly on the MEFs. The NK cell fraction of spleen cells from poly A:poly U-treated mice alone showed only a slight inhibitory effect at 40 degrees C. However, in the presence of the supernatant fluid from poly A:poly U-exposed spleen cells, the antiviral activity of NK cells was significantly increased both at 37 and 40 degrees C. The cellular source of the culture fluid showing poly A:poly U-induced antiviral activity appeared to be in the T-cell population. It was completely neutralized by monoclonal anti-IFN gamma antibody but not by anti-IFN beta, anti-IL4, anti-transforming growth factor, or anti-prostaglandin E2. In conclusion, these data document the ability of spleen cells from poly A:poly U-treated mice to inhibit MCMV replication and this activity is potentiated by hyperthermic conditions. The antiviral function of poly A:poly U-treated spleen cells appeared to be due mainly to the action of IFN gamma produced by T cells. The enhanced antiviral activity by hyperthermia appeared to be related to the action of IFN gamma rather than its production.

Animals↗

Polyadenylic:polyuridylic acid-induced protection of BALB/c mice against acute murine cytomegalovirus infection.

Treatment of BALB/c mice with poly(A):poly(U) 18 h prior to infection with a lethal dose of murine cytomegalovirus (MCMV) increased survival. In parallel with increased survival, a 10- to 100-fold reduction of plaque-forming MCMV was found in the liver and spleen of mice 4 days post-infection with a sublethal dose of MCMV. Poly(A):poly(U) did not significantly increase natural killer cell activity or prolong the duration of elevated cytotoxic activity in infected animals. The possible role of interferon in the poly(A):poly(U)-induced protection of BALB/c mice is discussed.

Animals↗

[The role of gastrin releasing peptide as a lung growth factor].

The proliferation of the bronchial epithelium and tumors associated with this tissue is controlled by various growth factors. The main factor is Gastrin Releasing Peptide (GRP), the human counterpart of the amphibian bombesin. These neuropeptides also act as neuromediators and gut hormones. All peptides of this family share a conserved C terminal sequence which is required for biological activity. The determination of this sequence has provided the basis for the design of specific agonist and antagonist peptides and for the generation of monoclonal antibodies (Mab). GRP interacts with a receptor coupled to a G protein and the signalling process leads to the activation of phospholipase C and kinases, and the mobilization of calcium. GRP promotes the proliferation of foetal and adult bronchial epithelium and of small cell lung cancer (SCLC) cells. GRP is also an autocrine growth factor for some SCLC cell lines. The growth of these lines is reduced in vitro and in vivo by MAb and specific antagonists. Hyperplasia of GRP producing cells has been shown in various lung diseases in adults and children. Pharmacological data on GRP suggest that its antagonists could be used in the treatment of SCLC (in addition to chemotherapy) and of interstitial lung disease. The cloning of the GRP receptor should facilitate the design of specific and potent antagonists of the peptide.

Adult↗

Daily variations in concentration of vasoactive intestinal polypeptide immunoreactivity in discrete brain areas of the rat.

The concentration of VIP-like immunoreactivity (VIP-LI) was determined by radioimmunoassay at various times of the day in 11 discrete brain areas and in the antehypophysis of rats maintained on a regular 12 h/12 h light-dark cycle. In the suprachiasmatic and periventricular nuclei the VIP-LI increased during the dark period and decreased during the subsequent light period. In addition, the VIP-LI exhibited complex variations in the locus coeruleus, the periaqueductal gray matter and the paraventricular nucleus, but did not change in the other areas investigated.

Analysis of Variance↗

Visceral perception in health and functional dyspepsia. Crossover study of gastric distension with placebo and domperidone.

The symptoms of functional dyspepsia are still unexplained. To evaluate the possible role of abnormal visceral perception, we studied the symptomatic responses and the pressure variations during progressive gastric distension in 10 female healthy control subjects (mean age 33.6 years) and in 10 female patients with functional dyspepsia (mean age 35.2 years). A rubber balloon was positioned 4 cm below the lower esophageal sphincter (LES) and inflated with progressively larger volumes of air by steps of 50 ml; pressures at the gastric fundus and at the LES were continuously recorded by perfused manometric catheters. Each subject was studied on two separate occasions after randomized double-blind administration of either placebo or 20 mg of domperidone. Symptomatic responses and the manometric data were analyzed at the time of the initial recognition of distension (bloating step) and at the time of reporting pain or up to a maximum of 700 ml of balloon inflation (pain or 700-ml step). On placebo, the volumes of gastric distension were more than two times lower in patients than in control subjects at the bloating step (185 +/- 32 ml vs 470 +/- 40 ml, P = 0.001) and at the pain or 700-ml step (265 +/- 54 ml vs 600 +/- 34 ml, P less than 0.005), while the pressure gradients (pressure at inflation steps minus baseline pressure before beginning inflation) were not statistically different between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Secretogranin I (chromogranin B) mRNA accumulation is hormonally regulated in GH3B6 rat pituitary tumor cells.

Secretogranin I (SgI; chromogranin B) belongs to a class of acidic tyrosine-sulfated secretory proteins believed to play a role in the secretory process of endocrine cells. Our aim here was to compare the levels of SgI mRNA to that of prolactin (PRL) and growth hormone (GH), using rat pituitary cell lines. As far as the constitutive expression is concerned, we found a positive correlation between SgI mRNA and PRL mRNA levels. However, the neuropeptide TRH (50 nM) inhibited the accumulation of SgI mRNA in GH3B6 cells whereas, as expected, it induced a rapid and sustained increase in PRL mRNA accumulation. By contrast, 17 beta-estradiol (1 nM) stimulated the accumulation of both SgI and PRL mRNAs, with the same EC50 (18-59 pM). Reciprocally, treatment with dexamethasone (100 nM) reduced the level of SgI and PRL mRNAs to 23% and 29% of control, respectively, but led to a 2.1-fold increase in the GH mRNA level. Altogether, the present work shows that SgI gene expression is subject to multiple hormonal regulations and occasionally parallels the regulation of the PRL gene but never that of the GH gene, under the conditions tested.

Animals↗

Effect of hirudin on the chemotactic properties of alpha-thrombin.

A study by an agarose technique of the chemotactic power of human alpha-thrombin on polymorphonuclear leukocytes reveals that this enzyme has a chemotactic activity. Hirudin, which inhibits the coagulant properties of thrombin, suppresses these chemotactic properties. This effect could be explained by the binding of hirudin to the structural domain of alpha-thrombin involved in its chemotactic activity.

Binding Sites↗

Localization of the structural domain responsible for the chemotactic properties of thrombin on polymorphonuclear leukocytes.

Human alpha thrombin at 1.1.10(-5) M is chemotactic for human polymorphonuclear leukocytes. This thrombin property disappears when the alpha thrombin (1.1.10(-5) M) hirudin (1.32.10(-5) M) mixture is realized. The same result is obtained when the thrombin at 1.1. 10(-5) M is inhibited by antithrombin III in a ratio of 1 mol of thrombin for 4.5 mol of antithrombin III. The hirudin and the antithrombin III appear therefore to mask, by their binding the structural domain responsible for the chemotactic properties of thrombin on polymorphonuclear leukocytes.

Antithrombin III↗

Coagulation impact on chemotactic activity generation for polymorphonuclear leukocytes.

Chemotactic technique in agarose gel has exposed the attractive properties of human alpha thrombin with respect to human polymorphonuclear leukocytes. The observed chemotaxis is maximal between 1.4.10-5 M and 1.6.10-5 M but extends from 2.8.10-6 M to 2.2.10-5 M. Human prothrombin, in an identical concentration zone as that studied for thrombin shows no chemotactic activity on the polymorphonuclear leukocytes. During coagulation the formed alpha thrombin attracts the polymorphonuclear leukocytes to it's formation site.

Chemotactic Factors↗

Triiodothyronine inhibits transcription from the human growth hormone promoter.

Three DNA constructs, the natural human growth hormone gene (hGH-hGH) its 500 bp promoter linked to the chloramphenicol acetyl transferase reporter gene (hGH-CAT), and its structural part linked to the herpes virus thymidine kinase promoter (TK-hGH) were introduced into rat pituitary GC cells by DEAE-dextran transfection. Transient expression was followed as a function of triiodothyronine (T3) concentration. The hGH-CAT expression was specifically inhibited by T3 following a typical dose-response curve while hGH-GH gene expression was not significantly modified. The transient expression of TK-hGH increased as a function of T3 concentration. These results indicate that T3 exerts two opposite effects on hGH gene expression. First, it down-regulates expression by acting on the promoter; second, it up-regulates expression by acting on the structural part of the gene. These action could be due to regulation of transcription and mRNA stabilization, respectively.

Animals↗

[Pygomelus. A single monster or a double monster?].

With an anatomical case and a clinical case, the authors describe the pygomelus, a very rare monstruosity. Legend and reality are often mixed in the description of literature. It is difficult to classify this monstruosity either in the simple monster or in the twin monsters.

Abnormalities, Severe Teratoid↗

Preferential role of calcium in the regulation of prolactin gene transcription by thyrotropin-releasing hormone in GH3 pituitary cells.

TRH induces two separate events in pituitary PRL cells. It increases the release of stored PRL and enhances the rate of PRL gene transcription, which results in an increased steady state concentration of PRL messenger RNA (mRNA) and a concomitant augmentation of PRL production. The mechanisms underlying the release process involve the activation of phosphatidylinositol turnover which generates inositol 1,4,5-trisphosphate and 1,2-diacylglycerol. In order to determine whether these intracellular messengers also mediate the stimulation of PRL gene expression by TRH, we have correlated the level of receptor occupancy with the rate of gene transcription and investigated the action of drugs which increase cytosolic calcium or activate protein kinase C. We have determined that sustained stimulation of transcription requires the persistent occupancy of a limited number of TRH receptor sites and that the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), calcium ionophores (A23187, ionomycin), and the calcium channel agonist BAY K 8644 enhance PRL gene transcription. However, TPA is less potent and ionomycin requires a low concentration of TPA to fully mimic TRH action, whereas BAY K 8644 alone displays the same potency as TRH. The effects of BAY K 8644 and TRH are not additive and thus suggest that the influx of calcium plays a predominant role in the regulation of PRL gene transcription by TRH.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗