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Biomedical subjects

E Morgan

Publications and source records attributed to E Morgan.

At least 73 records · Page 4Linked to original sources
PubMed1991

Craniofacial suture stenosis: morphologic effects.

Craniofacial anomalies, such as Apert's and Crouzon's syndromes, are presumed to be related to premature growth arrest of cranial base growth sites. However, premature growth arrest at cranial vault sutures in animals appears to play a causative role in the development of cranial deformities characteristic of single-suture, or simple, craniosynostosis in humans. To study the possible causative role of cranial vault and other (interface) suture stenoses on the development of craniofacial deformity, a vault suture and an interface suture between the cranial vault and facial skeleton were simultaneously immobilized. Thirty-one New Zealand White rabbits at 9 days of age underwent implantation of dental amalgam growth markers adjacent to cranial vault and facial sutures. In the experimental group (n = 15), methylcyanoacrylate adhesive was applied over the coronal (vault) and frontonasal (interface suture between vault and facial skeleton) sutures to immobilize them. The remaining 16 animals served as sham-treated controls. All animals underwent serial radiographic cephalometry to document growth effects in the cranial vault, cranial base, and facial skeleton. Application of adhesive resulted in statistically significant (p less than 0.05) reduction in growth at the coronal and frontonasal sutures. This was accompanied by an overall significant reduction in neurocranial vault length during the first 30 days of development.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Child sexual abuse sequelae and body-image surgery.

Child sexual abuse is common and damages the body image. Child sexual abuse survivors may request body-image surgery. Seven patients are described in whom child sexual abuse sequelae complicated body-image surgery. Two patients viewed their surgeons as similar to sexual abusers. Yet two patients were clearly, and two possibly, helped by the surgery. Surgeons can detect and manage such patients by (1) having a child sexual abuse therapist on hand for consultation, (2) adding "abuse" to the medical history form, (3) recommending to known or suspected child sexual abuse patients preoperative therapy or a self-help book, (4) obtaining specific permission for any body contact, (5) stating belief in abuse, if revealed, (6) explaining the surgery in unusual detail, (7) recognizing the high-risk child sexual abuse groups, and, (8) declining to operate on the angry child sexual abuse patient.

Adolescent↗
PubMed1988

Variant translocations (9;11): identification of the critical genetic rearrangement.

The t(9;11)(p22;q23) is a recurring abnormality in acute nonlymphocytic leukemia. The analysis of complex 9;11 translocations will aid in the identification of the conserved chromosomal junction or the critical genetic alteration created by the rearrangement; however, variant translocations involving chromosomes #9 and #11 have not been reported. We have identified such variants in two patients who had acute myelomonocytic leukemia and acute monocytic leukemia, characterized by a t(9;11;18)(p22;q23;q12) and a t(9;11;13)(p22;q23;q34), respectively. The conserved junction resulting from these rearrangements is created by the translocation of chromosomal material from 9p to 11q.

Aged↗
PubMed1988

The -ize have it.

Explore the source record for details and available documents.

Terminology as Topic↗
PubMed1988

Chemotherapy-related toxicity in infants treated according to the Second National Wilms' Tumor Study.

Babies under 12 months of age have been included in the National Wilms' Tumor Study (NWTS) series of clinical trials. Undue chemotherapy-related toxicity was encountered early during the course of the second NWTS. The prescribed doses of actinomycin D (AMD), vincristine (VCR), and Adriamycin ([ADR] doxorubicin; Adria Laboratories, Columbus, OH) were therefore halved. The frequency of severe hematologic toxic episodes was reduced (30 of 64 or 47% for babies receiving full doses [FD], and six of 48 or 13% for those given reduced doses [RD]). Similar reductions in pulmonary and hepatic effects were noted, and treatment-related deaths were reduced from 6% to 0 for the FD and RD samples, respectively. These frequencies among RD babies were similar to those encountered in 530 older children administered FD. Reduction of dose did not compromise therapeutic effectiveness.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1988

Cloning and pretranslational hormonal regulation of testosterone 16 alpha-hydroxylase (P-45016 alpha) in male rat liver.

cDNA clones for P-45016 alpha were isolated from a male liver lambda gt11 expression library using antibodies against P-45016 alpha. The clones encompassed 1633 and 1791 bp, respectively. The latter clone contained the whole coding sequence. The 20 deduced NH2-terminal amino acids were identical to those of P-450h and the cDNA sequence was in complete agreement with that of P-450 (M-1). Northern blots showed that P-45016 alpha in the rat liver is pretranslationally regulated by the growth hormone secretory pattern. Southern blots indicated that few genes belong to the same P-450 gene family as P-45016 alpha.

Animals↗
PubMed1987

Effects of calcium, calcium channel blockers and Bay K 8644 on contractions induced by muscarinic receptor stimulation of isolated bladder muscle from rabbit and man.

In isolated bladder smooth muscle from both rabbit and man, carbachol-induced contractions were reduced by the calcium channel blocker nifedipine, whereas the calcium channel promotor Bay K 8644 had no effect. In nominally calcium-free medium containing 10(-4) M EGTA, carbachol-induced contractions were reduced by 69% (rabbit) and 87% (man). These contractions were abolished by nifedipine, whereas Bay K 8644 significantly increased their amplitude, in rabbit preparations almost to control level. Electrical field stimulation produced contractions which could be suppressed by scopolamine by about 50% (rabbit) and more than 90% (man). These contractions were abolished by calcium-free medium (10(-4) M EGTA), suppressed by nifedipine, but significantly enhanced by Bay K 8644. The depressant effects of nifedipine, verapamil and diltiazem were reversed by Bay K 8644. The calcium channel blockers relaxed K+-induced contractions to base line, and this action was counteracted by Bay K 8644, less effectively when relaxations were induced by diltiazem. It is concluded that contractions produced by muscarinic receptor stimulation are primarily dependent on calcium bound to the outside of the membrane of the smooth muscle, and/or coming from the extracellular medium. Electrically evoked, scopolamine sensitive contractions seem to be mediated by a mechanism different from that of contractions produced by exogenously added muscarinic receptor agonist. The present data support the view that combined blockade of muscarinic receptors and calcium channels is an effective way of inhibiting bladder contractions in both rabbit and man.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

Interaction between adrenergic and cholinergic nerve terminals in the urinary bladder of rabbit, cat and man.

The influence of muscarinic receptor stimulation (carbachol) and blockade (scopolamine) on the release of 3H-labelled noradrenaline from adrenergic neurons was investigated in isolated detrusor preparations from rabbit, cat and man. A significant influence on the release of 3H from adrenergic nerve terminals was found in the three species with a concentration-dependent decrease and increase induced by carbachol and scopolamine, respectively. Using the alpha 2-adrenoceptor stimulating and blocking agents clonidine and rauwolscine in rabbit and human detrusor preparations, the presence of prejunctionally located inhibitory alpha 2-adrenoceptors could also be demonstrated. The findings indicate the possibility of a functionally important interaction between cholinergic and adrenergic nerves in the urinary bladder mediated via inhibitory muscarinic receptors on adrenergic nerve terminals.

Animals↗
PubMed1987

Effects of acetylethylcholine mustard on [3H]quinuclidinyl benzilate binding and acetylcholine release in rat brain synaptosomes.

The effects of acetylethylcholine mustard and its aziridinium derivative (AMMA) on acetylcholine (ACh) release and [3H]quinuclidinyl benzilate (QNB) binding were studied in rat cortical synaptosomes. After incubation for 5 min at 37 degrees C, AMMA reduced [3H]QNB binding with an IC50 of 9 microM. Following incubation for 5 min with 50 microM AMMA and washing, there was a 62% reduction in the [3H]QNB binding capacity with no change in the KD value for the remaining receptors, a result indicating the irreversibility of the AMMA binding. AMMA and oxotremorine both reduced the basal and 30 mM K+-induced release of newly synthesized [3H]ACh in dose-dependent manners over a 2.5-min period. At identical 50 microM concentrations, AMMA produced a much longer inhibition of basal [3H]ACh release than oxotremorine did. The inhibition of basal and 30 mM K+-induced [3H]ACh release by AMMA (10-250 microM) was blocked by 2 microM atropine during a 2.5-min release incubation, but not during a 30-min release incubation. After synaptosomes were treated with 50 microM AMMA for 5 min and the unbound drug was washed out from the tissue, [3H]ACh release (basal and K+-induced) was reduced. AMMA (50 microM) reduced high-affinity choline uptake and ACh synthesis by greater than 90% in this tissue, but these effects did not account for the [3H]ACh release inhibition, because they were not atropine sensitive and hemicholinium-3 had no effect on [3H]ACh release under the conditions used in these studies, i.e., after extracellular [3H]choline was washed out. Taken together, these results suggest that AMMA may be an irreversible agonist at presynaptic muscarinic autoreceptors.

Acetylcholine↗
PubMed1987

Initial clinical studies of piritrexim.

Piritrexim (PTX) is a second-generation, lipid-soluble inhibitor of dihydrofolate reductase (DHFR). Metabolic inhibition occurs within seconds after rapid diffusion into human cancer cells. We describe the initial phase I studies with iv and oral forms of this drug given on a daily basis for 5 days to patients with cancer. The dose-limiting toxicity is primarily hematologic (leukopenia, granulocytopenia, thrombocytopenia), but phlebitis is also encountered with iv administration and gastrointestinal problems (nausea, vomiting) with oral administration. Oral toxicity can be reduced by giving the daily dose in 2 divided doses. The maximum tolerated dose (MTD) for the iv route is 170 mg/m2 per day for 5 days; for the oral route it is 480 mg/m2 per day for 5 days. Unlike an earlier lipid-soluble folate antagonist, piritrexim did not cause neurologic or histamine-like disorders.

Administration, Oral↗
PubMed1987

Rapid microwave fixation of rat mast cells. I. Localization of granule chymase with an ultrastructural postembedding immunogold technique.

We defined the ultrastructural localization of chymase in rat peritoneal mast cells using standard aldehyde fixation and a newly described microwave fixation method (Login GR, Dvorak AM: Microwave energy fixation for electron microscopy. Am J Pathol 120: 230, 1985; Login GR, Stavinoha WB, Dvorak AM: Ultrafast microwave energy fixation for electron microscopy. J Histochem Cytochem 34:381, 1986) and postembedding immunogold labeling. Thin sections were exposed first to goat IgG anti-rat chymase and second to gold-conjugated rabbit Ig directed against goat IgG. By transmission electron microscopy, gold particles were localized to the matrix of cytoplasmic granules. Control sections treated with nonimmune sera did not exhibit labeling of mast cells. Thin sections treated simultaneously with purified rat mast cell chymase and anti-chymase antibody in competition studies, showed a marked reduction in granule staining. These findings demonstrate that a microwave fixation method can be used to rapidly fix cell suspensions for postembedding immunocytochemical studies.

Animals↗
PubMed1986

Effects of AF64A on [3H]acetylcholine synthesis in neuron-enriched primary brain cell cultures.

[3H]Acetylcholine (ACh) synthesis was measured in primary neuronal cultures from neonatal rat brains. Neuronal [3H]ACh synthesis was blocked by hemicholinium-3 and depended on the age of the cultures, increasing for ca. 10 days, and eventually declining. The irreversible inhibitor AF64A (10 or 30 microM) inhibited [3H]ACh synthesis from [3H]choline at concentrations (10 or 30 microM) with affecting choline acetyltransferase activity. Nine-day-old cultures recovered 90% of their [3H]ACh synthesis within 7 days after AF64A, while 13-day-old cultures never recovered. These results suggest that the turnover of neuronal choline transporters is age-related.

Acetylcholine↗