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Biomedical subjects

P Martin

Publications and source records attributed to P Martin.

At least 793 records · Page 44Linked to original sources
PubMed1987

Preparation of red-blood-cell-depleted marrow for ABO-incompatible marrow transplantation by density-gradient separation using the IBM 2991 blood cell processor.

Thirty patients who had major ABO blood group incompatibility with their HLA-matched donors underwent allogeneic marrow transplantation after removal of red blood cells (RBC) from donor marrow by Ficoll-Diatrazoate (F-D) separation using the IBM 2991 blood cell processor. We selected the IBM 2991 because we were interested in obtaining information about RBC-depleted mononuclear cells for monoclonal antibody and complement incubation of marrow. The median residual marrow RBC volume was 2.6 ml (1.2% of the original volume) and marrow infusion was well tolerated in every instance. The median doses of nucleated and mononuclear cells were 8.7 X 10(7)/kg and 2.2 X 10(7)/kg recipient weight, respectively, representing median marrow total nucleated and mononuclear cell losses of 63.4% and 52.9%, respectively. The median CFU-GM loss was 52.4%. Four patients died 13-21 days after marrow infusion and were unevaluable for engraftment. One patient failed to achieve engraftment and received a second transplant on day 36 from a second donor. One patient with myelofibrosis had poor engraftment and died on day 177 with low peripheral blood counts. For evaluable patients, no significant differences were observed in the rate of recovery of peripheral blood granulocyte or platelet counts between those receiving RBC-depleted marrow or ABO-matched unprocessed marrow. However, posttransplant red cell transfusion requirements were increased and transfusion independence delayed in patients receiving RBC-depleted marrow as compared to patients receiving unprocessed marrow. We concluded that red cell depletion using the IBM 2991 was effective in removing red cell, but resulted in significant and variable hematopoietic cell losses which may have contributed to graft failure in at least one patient. Such cell losses appear to be inherent in both manual and semiautomated methods for F-D cell separation.

ABO Blood-Group System↗
PubMed1986

Nucleotide sequence of the tetM tetracycline resistance determinant of the streptococcal conjugative shuttle transposon Tn1545.

The nucleotide sequence of the tetracycline resistance gene tetM encoded by streptococcal conjugative shuttle transposon Tn1545 has been determined. The resistance gene was identified as a coding sequence of 1917 base pairs corresponding to a protein with a Mr of 72,500 daltons. This value is in good agreement with that, 68,000 daltons, estimated by SDS-polyacrylamide gel electrophoresis of Escherichia coli minicell extracts. The tetM gene product does not exhibit any sequence homology with either the Gram-negative (tetA, tetB and tetC), or the Bacillus and Staphylococcus tetracycline resistance proteins. The average hydropathy value of the tetM gene product (-0.21) contrasts with those calculated for the other TET proteins which are markedly hydrophobic (0.76 to 0.93). Hybridization experiments performed with an intragenic tetM probe do not support the claim [Taylor, D. (1986), J. Bact. 165, 1037-1039)] that tetracycline resistance in Campylobacter is due to acquisition of tetM.

Amino Acid Sequence↗
PubMed1986

Transformation of quail embryo fibroblasts by a retrovirus carrying a normal human c-myc gene.

We have constructed avian retroviruses expressing the human c-myc oncogene. These viruses morphologically transformed primary quail embryo fibroblasts upon transfection and infection. Transformed cells produced viruses harboring a spliced c-myc gene and contained high levels of p64-67c-myc protein. One of these infectious viruses, vSX-AHM, was molecularly cloned and the nucleotide sequence of the spliced c-myc insert determined. No mutation was found within the c-myc coding sequence of this transforming clone when compared to the normal genomic progenitor. Thus, we concluded that no mutation within the human c-myc gene is required to induce primary avian embryo fibroblast transformation.

Animals↗
PubMed1986

Noradrenergic and opioid mediation of tricyclic-induced reversal of escape deficits caused by inescapable shock pretreatment in rats.

The present study was undertaken to investigate the possible involvement of a noradrenergic and opioid mediation of the reversal by tricyclic antidepressants of escape deficits produced by inescapable shock pretreatment. Rats were first exposed to 60 inescapable shocks (15 s duration, 0.8 mA, every min +/- 15 s) and 48 h later subjected, to daily shuttle-box sessions (30 trials/day, ITI: 30 s) during 3 consecutive days. Twice-daily IP injection of desipramine or clomipramine (total daily dose: 32 mg/kg) prevented escape deficits. Penbutolol (0.125; 0.25; 0.5 mg/kg), prazosin (1; 2 mg/kg) and naloxone (0.5; 1 mg/kg) given once a day dose-dependently attenuated the beneficial effect of tricyclic antidepressants in reducing the number of escape failures in rats exposed to shock pretreatment. In agreement with data obtained in the forced-swimming model, these findings support the notion that activation of noradrenergic and opioid receptors is an important factor in the mediation of the effects of tricyclic antidepressants in animal models of depression.

Animals↗
PubMed1986

Antinociceptive activity of beta-adrenoceptor agonists in the hot plate test in mice.

Clenbuterol, isoproterenol and salbutamol increased the latency in the licking response of mice on the hot plate at 56.5 degrees C. This effect was dose-related and obtained after IP administration. Clenbuterol was active at lower doses than isoproterenol and salbutamol, a result which is consistent with its better penetration in the central nervous system. Moreover, the effect of clenbuterol was stereospecific, the (-)-isomer being the active form. Our results suggest the implication of central beta-adrenoceptors in the modulation of the response to a painful stimulation.

Albuterol↗
PubMed1986

Dose pipecolic acid interact with the central GABA-ergic system?

Several previous studies have suggested a strong GABA-mimetic action of the endogenous brain imino acid, L-pipecolic acid (L-PA). In the present study, these observations were evaluated using electrophysiological and neurochemical methods. In contrast to published data our electrophysiological studies on rat cortical neurones in situ showed only a weak, but bicuculline-sensitive depressant action of L-PA on cortical neurones. Furthermore, L-PA proved to have no affinity for any of the three components of the GABA-benzodiazepine-chloride channel receptor complex. However, using a modification of published methods a weak affinity for the GABA-B receptor site was demonstrated (IC50 = 1.8 X 10(-3) M). L-PA showed no anticonvulsive activity in several tests; in particular, it did not protect mice from seizures induced by inhibition of L-glutamate-1-decarboxylase (EC 4.1.1.15: GAD). L-PA had a very weak action on brain GABA levels of mice, and did not modify the rate of GABA synthesis. In conclusion, these results are not compatible with a strong in vivo interaction between L-PA and GABA-mediated inhibitory transmission.

Animals↗
PubMed1986

The antigastrinic effect of a phenothiazine (LM 24056) prevents gastric secretory activity of histamine.

Gastric antisecretory phenothiazine LM 24056 inhibited acid and pepsin responses to feeding in dogs. Administered perorally two hours before feeding, LM 24056 reduced significantly the secretory responses to combinations of feeding either with antramine, a natural histamine derivate, or with synthetic histamine. LM 24056 reduced circulating gastrin levels (p less than 0.01 and p less than 0.001) and gastrin responses to feeding (p less than 0.01) without modifying neither circulating histamine concentrations nor histamine responses to feeding. The residual acid and pepsin secretions were closely related to gastrin reduction and endogenous or exogenous histamine, by themselves, seemed to be unable to recover the levels of secretory responses observed in response to feeding alone or in combination with antramine or histamine. These data favour a new scheme of gastric secretion regulation where gastrin would be the last step for stimulating parietal and chief cells. LM 24056 by reducing circulating gastrin prevents stimulatory effect of exogenous or feeding-released endogenous histamine. Histamine would not be thus the final common mediator for gastric secretion.

Animals↗
PubMed1986

Normal development of the skeleton in chick limb buds devoid of dorsal ectoderm.

It has been suggested that the ectoderm on the dorsal and ventral faces of the limb bud plays a part in controlling the pattern of cartilage differentiation. To test this, the dorsal wing bud ectoderm in the chick embryo was destroyed by irradiation with ultraviolet light at stage 17-19, at the very beginning of limb bud development, but the apical ectodermal ridge was spared. The irradiated ectoderm disappeared within 24 hr (by stage 23-24) and did not regenerate thereafter; thus the dorsal surface of the limb bud was kept denuded throughout most of the period of skeletal pattern formation. By 6 or 7 days after the irradiation (stage 35), when the rudiments of all the adult skeletal elements are normally present in recognizable form, the irradiated wings could be placed into two categories, those that were approximately normal in shape and those that had curled dorsally. All of these limbs were reduced in size, to varying degrees, when compared to their controls and lacked dorsal soft tissues. The limbs that were normal in shape, however, even though sometimes denuded over practically the whole extent of their dorsal surface, almost always had a complete and normally proportioned cartilage pattern, suggesting that ectoderm (other than the apical ectodermal ridge) does not exert any direct control over the development of the limb cartilage pattern. However, many of those limbs that had curled as a result of the irradiation did have major pattern deformities, suggesting that the topology of cartilage differentiation does depend on the shape of the limb bud.

Animals↗
PubMed1986

A transient expression assay for tissue-specific gene expression of alcohol dehydrogenase in Drosophila.

The regulation of expression of the alcohol dehydrogenase gene of Drosophila was examined by injecting plasmids containing the gene directly into preblastoderm embryos and subsequently staining for alcohol dehydrogenase activity in somatic cells of larvae and adults. The alcohol dehydrogenase genes introduced in this manner were expressed normally in both adults and larvae; i.e., alcohol dehydrogenase activity was found exclusively in tissues where it would normally be expressed. Activity was found in some cells in more than 90% of all surviving third instar larvae, but not all cells which would normally express the enzyme were positive, presumably due to the random distribution of the injected DNA to the cells of the embryo. Regulated expression was not dependent on the vector used: tissue-specific expression was obtained from alcohol dehydrogenase genes inserted in the P-element vector, Carnegie-4; in pBR322; in pUC18; or in bacteriophage lambda. The bulk of the injected DNA was not integrated into the chromosome and appeared to persist throughout development as supercoiled and nicked circles. Using the procedure and in vitro mutagenesis, we were able to show that the alcohol dehydrogenase gene was expressed in a normal tissue-specific manner in larvae if there were 777 nucleotides of upstream information present.

Alcohol Dehydrogenase↗
PubMed1986

Phencyclidine (PCP) abuse. A close-up look at a growing problem.

PCP or "angel dust" is a dissociative anesthetic agent with notoriety as an abuse substance. Numerous members of many subcultures are frequent users of this drug. It is well known in California's psychedelia, along the East Coast, and in the middle- and working-class suburbs of the Midwest. It is important that practitioners become acquainted with the drug and its effects. Persons intoxicated with PCP have murdered their own children and have even jumped out of high-rise apartment buildings. States of florid psychosis lasting for days can follow a brief encounter with PCP. Inadvertent administration of narcotics and barbiturates to patients with acute PCP intoxication can lead to a crisis that could prove to be fatal.

Adult↗
PubMed1986

Characterization of a MH2 mutant lacking the v-myc oncogene.

We have previously reported that a virus, MH2-PA200, lacking the ability to transform quail embryo cells, could be isolated from wild type (wt) MH2 stocks passaged on chicken neuroretina cells. We report here the molecular cloning and extensive characterization of this MH2-PA200 provirus. Molecularly cloned MH2-PA200 DNA was found to stimulate the growth of neuroretina cells by transfection assays and our results indicate that this recombinant virus was derived from the RAV-1 helper virus, in which v-mil and a small part of v-myc of MH2 were acquired at the expense of helper (delta gag-pol-delta env) sequences. In order to assess the precise boundary between the myc and env genes we determined the nucleotide sequence of the junction fragment and showed that 11 of 13 nucleotides of the env gene were identical to the myc sequence at the recombination point. The nucleotide sequence of the myc-env junction fragment of another similar and independently generated MH2 mutant showed similarly 9 nucleotides of homology between the env and myc sequences at the recombination point that took place at another site, suggesting that a homologous recombination occurred between MH2 and RAV-1 viruses to generate MH2-PA200 and similar mutants.

Animals↗
PubMed1986

The lesion of serotonergic neurons does not prevent antidepressant-induced reversal of escape failures produced by inescapable shocks in rats.

The present study was aimed at testing the hypothesis (based mainly on biochemical evidence) of the implication of brain serotonergic neurons in the induction of learned helplessness (escape deficit) and its reversal by antidepressants in rats. After desipramine (25 mg/kg IP)-pretreatment rats were either sham-operated or infused with 5,7-dihydroxytryptamine (5,7-DHT, 3 micrograms of free base in 0.4 microliter saline containing 0.02% ascorbic acid) into the midbrain raphe area. Three weeks later, experimental animals were exposed to 60 randomized inescapable shocks (0.8 mA; 15 sec duration), control rats being not shocked, and 48 hr later, they were subjected to daily shuttle-box sessions (30 trials/day; ITI = 30 sec) on 3 consecutive days in order to assess escape deficits. After inescapable shock pretreatment separate groups of rats were given twice daily injections of clomipramine (total daily dose: 32 mg/kg), desipramine (24 mg/kg), imipramine (32 mg/kg), nialamide (32 mg/kg) or saline. After behavioral testing, animals were sacrificed, and tryptophan hydroxylase activity was assayed in the cerebral cortex, the hippocampus and the striatum. We found that damage to serotonergic neurons associated with a 70% loss of tryptophan hydroxylase activity altered neither escape deficits produced by prior exposure to inescapable shock, nor the ability of either antidepressant studied to reverse escape failures in the shuttle-box paradigm. These findings cast some doubts on the hypothesized crucial role of serotonergic neurons in helpless behavior and its reversal by antidepressants.

Animals↗
PubMed1986

Shuttle-box deficits induced by inescapable shocks in rats: reversal by the beta-adrenoreceptor stimulants clenbuterol and salbutamol.

Beta-adrenoreceptor stimulants such as salbutamol and clenbuterol have been reported to be effective in depressive states and to share many actions with classical antidepressants in animals. To further explore the antidepressant activity of these drugs, we investigated their effects in rats subjected to helplessness training. Rats were first exposed to inescapable shock pre-treatment (60 shocks, 15 sec duration, 1 mA every minute +/- 15 sec) and 48 hr later, shuttle-box training (30 trials/day, ITI: 30 sec) was initiated in order to evaluate escape and avoidance deficits. Rats pretreated with inescapable shocks exhibited escape and avoidance deficits when tested for subsequent responding in a shuttle-box. The deficits are particularly marked at the third training session. Daily IP injections of clenbuterol (total daily dose: 0.5 and 0.75 mg/kg) and salbutamol (16 and 24 mg/kg) prevented escape deficits as did daily injections of classical antidepressants such as desipramine (16 and 24 mg/kg/day) and clomipramine (16 and 24 mg/kg/day). These data extend previous results bearing on the similarity of action of beta receptor stimulants and tricyclic antidepressants and further support the notion of a close relationship between noradrenergic function, more especially beta-adrenoreceptors, and "helpless" behavior.

Adrenergic beta-Agonists↗