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Biomedical subjects

T A Miller

Publications and source records attributed to T A Miller.

At least 73 records · Page 4Linked to original sources
PubMed1997

Comparison of adaptations to a 12-month exercise program and late outcome in patients with healed myocardial infarction and ejection fraction <45% and >50%.

To characterize the differences in adaptations to endurance exercise training and prognosis between patients with depressed and normal left ventricular (LV) function, 20 patients with coronary artery disease were studied and followed for 7 years. Patients with normal LV function had enhancement of LV systolic function, but the group with LV dysfunction did not exhibit cardiac adaptations and had more cardiac events than those with normal LV function.

Adaptation, Physiological↗
PubMed1997

Control of circulation in insects.

1. Studies on the physiology of insect circulation have revealed that the insect central nervous system can exert a strong nervous control over certain dorsal vessels and diaphragms. 2. The function of neurohormonal control over the heartbeat of insects, though demonstrated, is less clear. In contrast with studies on the central nervous and skeletal neuromuscular systems, not one neurotransmitter substance has been identified in any of the vessels, pumps or diaphragms responsible for circulation in insects. 3. A coelopulse system was identified and described that suggested a very sophisticated coordination between circulation and respiration in insects. The circulatory systems of cockroach, locust, fly, moth and bee all involve unique specializations. 4. It is suggested that an autonomic nervous system is present in insects and is responsible for coordination and control of both circulation and respiration.

Animals↗
PubMed1997

Protective action of gastrin-17 against alcohol-induced gastric injury in the rat: role in mucosal defense.

Exogenous cholecystokinin (CCK) or exposure of the stomach to the mild irritant 25% ethanol can prevent gastric injury. Ingestion of ethanol also elicits the release of CCK as well as gastrin, which is structurally similar to CCK. This study was undertaken in conscious rats to examine the gastroprotective actions of gastrin and to assess the effect of CCK-gastrin receptor blockade on adaptive cytoprotection with ethanol as the mild irritant. Intravenous (1-25 pmol/kg) administration of gastrin-17 dose dependently increased gastric mucosal blood flow (laser Doppler) and reduced gastric injury caused by 1 ml of orally administered acidified ethanol (150 mM HCl-50% ethanol). Similar gastroprotection was achieved with the gastrin secretagogue 5% peptone (1 ml orogastrically). The gastroprotective capabilities of gastrin-17 were attenuated by the type B CCK (gastrin) receptor antagonist L-365,260 (12.5-25 mg/kg i.p.) and by capsaicin desensitization (125 mg/kg s.c.). CCK octapeptide (5 nmol/kg i.v.)-induced protection was reversed by the type A CCK receptor antagonist MK-329 (1 mg/kg i.p.). Neither receptor antagonist, alone or in combination, reversed the protective effects of the mild irritant 25% ethanol (1 ml orogastrically). Thus, whereas gastrin may play a role in gastric mucosal defense, neither CCK nor gastrin appears to participate in the phenomenon of adaptive cytoprotection.

Acids↗
PubMed1997

Electromechanical microinjection of pink bollworm Pectinophora gossypiella embryos increases survival.

We report and compare methods and apparatus for injection of pink bollworm, Pectinophora gossypiella (Saunders), embryos. Injection with an electromechanical device resulted in 59% survival of embryos. Previous techniques relying on a mechanical manipulator resulted in 8% survival. Pink bollworm (PBW) embryo injection technology is based in part on methods developed for injection and genetic transformation of Caenorhabditis elegans ([Maupas] Dougherty) and Drosophila melanogaster (Meigen) with substantial alterations in both method and apparatus to accommodate special conditions of PBW biology, behavior and morphology. The microinjection methodology described here has direct application to other difficult-to-inject insects and invertebrates.

Animals↗
PubMed1997

Congenital intestinal malrotation causing gestational intestinal obstruction. A case report.

BACKGROUND: Intestinal obstruction in pregnancy is rare. The mortality rate is higher during pregnancy than in the general population and applies to fetal as well as maternal survival. Major causes of intestinal obstruction in the pregnant women include adhesions, volvulus and intussusception. CASE: A 27-year-old woman, gravida 2, para 1, estimated gestational age approximately 26 weeks, with a high-level, complete small bowel obstruction. The patient failed a trial of conservative management and required laparotomy, at which time a congenital malrotation was found. She was treated successfully with a modified Ladd's procedure. There was no maternal or fetal morbidity. CONCLUSION: This case represents an extremely rare cause of bowel obstruction in pregnancy; a paucity of such cases have been reported.

Adult↗
PubMed1996

Transforming growth factor-beta, osteogenin, and bone morphogenetic protein-2 inhibit intercellular communication and alter cell proliferation in MC3T3-E1 cells.

Intercellular communication by gap junctions has been implicated to function in the control of cell growth and differentiation in osseous tissues-processes which are regulated, in part, by peptide growth factors, including transforming growth factor-beta (TGF-beta) and the bone morphogenetic proteins (BMPs). Using the osteoblastic cell line MC3T3-E1, we tested the hypothesis that the effects of TGF-beta and BMPs on cell proliferation may be correlated to changes in intercellular communication. In a series of proliferation assays, MC3T3-E1 cells were cultured in the presence of bone morphogenetic protein-2 (BMP-2) or TGF-beta for up to 48 hr. Proliferation of cells during the linear log phase (days 2 to 4) was assessed by 3H-thymidine (3H-TdR) incorporation. After times ranging from 6 to 48 hr, BMP-2 significantly inhibited uptake of 3H-TdR at doses of 50-800 ng/ml. Similarly, TGF-beta inhibited uptake of 3H-TdR at doses of 2-32 ng/ml. In a separate group of experiments, intercellular communication through gap junctions was demonstrated by cell-cell transfer of the fluorescent tracer, lucifer yellow, after microinjection. One series of experiments showed that the gap junctional intercellular communication (GJIC) of cells, incubated for 48 hr in the presence of the higher dose of osteogenin (OG) (5.0 vs. 0.5 microgram/ml) or higher dose of TGF-beta (2.0 vs. 0.2 ng/ml), was significantly inhibited compared to control. In another series of experiments, time and dose dependent effects of BMP-2 and TGF-beta on GJIC were investigated. In the time course experiments (3, 6, 12, 24, and 48 hr), TGF-beta (2.0 ng/ml) demonstrated a statistically significant effect in inhibiting GJIC as early as 6 hr, while BMP-2 (50 ng/ml) inhibited GJIC after 24 and 48 hr of treatment. The dose-dependent effects of BMP-2 and TGF-beta on cell couplings, determined at 48 hr, showed significant inhibitory effects with BMP-2 at 25 and 50 ng/ml and with TGF-beta at 2 and 4 ng/ml. The cell count results and injection study performed at 12 hr, at a fixed cell density, confirmed that the inhibitory effect was not due to differences in cell density. The 50% effective inhibitory concentrations (EC50) calculated for BMP-2 and TGF-beta at 48 hr, showed no dose correlation between proliferation and GJIC, suggesting that these two events are independent occurrences. Additionally, marked morphological change was observed in the cells treated with TGF-beta. The observation may suggest that TGF-beta may have effects upon cytoskeletal elements in osseous tissues.

3T3 Cells↗
PubMed1996

Gastric injury and protection against alcohol and acid: influence of perturbations in glutathione metabolism.

This study assessed the role that inhibition of glutathione (GSH) synthesis and decreased GSH peroxidase (GPX) activity in the rat played in modulating gastric injury induced by ethanol and acid and its prevention by 16,16-dimethyl PGE2 (dmPGE2) and the mild irritant, 25% ethanol. Although numerous studies have proposed that GSH may be important in maintaining gastric mucosal defense, the exact role of this antioxidant in protecting the stomach from injury remains undefined. The present study addressed this consideration by blocking the synthesis of GSH and altering the major pathway by which it exhibits its antioxidant activity and determining the effect of these perturbations on gastric injury and protection. Four to six rats were used for each experimental group. GSH synthesis was blocked by the potent and specific inhibitor L-buthionine sulfoximine (BSO), 2 or 6 mmole/kg intraperitoneally. The activity of the major form of GPX, which is selenium dependent and utilizes GSH as a substrate to detoxify hydrogen peroxide and other hydroperoxides, was inhibited by placing animals on a selenium-deficient diet for 6 weeks. Gastric damage was induced by 100% ethanol, 50% ethanol in 150 mM HCl, and 0.75 M HCl. Prevention of such injury was accomplished with oral pretreatment using 25% ethanol or dmPGE2 (5 microgram/kg). The damaging effects of 100% ethanol, 50% ethanol/150 mM HCl, or 0.75% M HCl were not adversely affected by BSO pretreatment even though GSH synthesis was inhibited by as much as 80%. Similarly, inhibition of GPX activity by 58% in adult rats and 98% in weanling rats failed to potentiate the damaging effect of 100% ethanol. Furthermore, with both perturbations in GSH metabolism, the protective action of dmPGE2 and 25% ethanol was maintained. Our results indicate that profound alterations in gastric GSH metabolism by themselves do not aggrevate the injurious effects of ethanol or acid, nor do they prevent the protective action of a prostaglandin or mild irritant.

Animals↗
PubMed1996

Gastric injury induced by ethanol and ischemia-reperfusion in the rat. Differing roles for lipid peroxidation and oxygen radicals.

This study determined the role that oxygen-derived free radicals played in the production of gastric injury in rats challenged orally with concentrated ethanol or subjected to vascular compromise. In the ethanol study, rats were pretreated with a variety of free radical scavengers or enzyme inhibitors prior to exposing the stomach to 100% ethanol. At sacrifice, the degree of macroscopic damage to the glandular gastric mucosa was quantified. In separate studies, the effects of ethanol on gastric mucosal levels of enaldehydes (malondialdehyde and 4-hydroxynonenal) were examined as an index of lipid peroxidation. Superoxide dismutase and catalase pretreatment were without benefit in reducing injury in our ethanol model, excluding potential contributory roles for the superoxide anion or hydrogen peroxide, respectively. Dimethyl sulfoxide and desferoxamine were likewise without protective capabilities, eliminating a role for the hydroxyl radical. Allopurinol, a xanthine oxidase inhibitor, provided no protection under acute conditions, even though partial protection was noted when administered chronically. Further, enaldehyde levels were not increased over control levels in alcohol-exposed mucosa, indicating no enhanced lipid peroxide formation. In contrast, in animals in which ischemia to the stomach was induced followed by reperfusion, marked gastric injury was observed in combination with enhanced enaldehyde levels. Prevention of enaldehyde formation by a 21-aminosteroid concomitantly prevented injury induced by ischemia-reperfusion. These findings support the conclusion that ischemia-reperfusion injury to the stomach is an oxygen-derived free radical process whereas ethanol-induced injury clearly involved some other process. Although allopurinal was partially protective against ethanol damage when administered chronically, observations in other models of injury suggest that this action is independent of its inhibitory effect on xanthine oxidase.

Allopurinol↗
PubMed1996

Activity-dependent changes in impulse conduction in a focal nerve lesion.

The present study was undertaken to determine whether, in patients with a focal nerve lesion, the axonal hyperpolarization produced by conduction of brief trains of impulses would result in conduction block in cutaneous afferents, thus indicating a site of impaired safety margin for impulse transmission. In 25 patients with focal conduction slowing across the carpal tunnel segment of the median nerve, a conditioning train of 10 supramaximal stimuli at 200 Hz resulted in a reduction in amplitude and an increase in latency of the test volley set up by a supramaximal stimulus. These changes exceeded those seen in control subjects, but followed a similar time course, with full recovery within 150 ms. There was a significant correlation between these changes and the severity of the compression neuropathy as indicated by the degree of focal conduction slowing in routine nerve conduction studies. Control data suggested that the measured changes in amplitude could be explained by temporal dispersion of the compound sensory volley. This view was supported by measurements of the changes in amplitude (and latency) in normal subjects during acute compression before conduction block had developed. In addition, there were similar linear relationships between the activity-dependent amplitude reduction and the corresponding change in latency for both the patients and the control subjects, indicating that there was no need to invoke factors additional to those operating in the control subjects to explain the greater amplitude depression in the patients. It is concluded that, although the depression in amplitude was greater in patients than in healthy subjects, the magnitude of this change can be explained by temporal dispersion of the abnormal compound sensory action potential associated with greater conduction slowing. Activity-dependent conduction block may play little role in the pathophysiology of carpal tunnel syndrome.

Action Potentials↗
PubMed1996

Excision of neck redundancy with single Z-plasty closure.

In selected patients, particularly males, redundancy of skin of the neck can be treated effectively by direct excision and a single large Z-plasty closure so that the horizontal portion corresponds to the neck crease. Reduction of the thyroid cartilage can be performed simultaneously. The relative advantages and disadvantages between this approach and the more commonly performed facelift are discussed.

Aged↗
PubMed1996

Growth factors in surgery.

Surgical reconstruction of functional and aesthetic defects is often compromised by donor-tissue limitations and wound-healing constraints--problems that can potentially be overcome by peptide growth factor therapy. The effectiveness of growth factor therapy in animal models and in limited human clinical trials has been realized. Epidermal growth factor (EGF), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), platelet-derived wound-healing formula (PDWHF), transforming growth factor (TGF), the bone morphogenetic proteins (BMPs), and general considerations of growth factor therapy are reviewed.

Growth Substances↗
PubMed1996

Evaluation of a novel osteogenic factor, bone cell stimulating substance, in a rabbit cranial defect model.

A novel osteogenic factor, bone cell stimulating substance (BCSS), was recently isolated from bovine bone. Unlike the bone morphogenetic proteins, which are generally 20- to 40-kDa glycoproteins belonging to the transforming growth factor-beta superfamily, BCSS is a 2.5-kDa, water-soluble polypeptide. This study evaluated the osteogenic potential of BCSS in combination with coralline-derived porous hydroxyapatite to reconstruct a large, nonhealing cranial defect in the rabbit. Twenty-four rabbits underwent a 16 x 20 mm full-thickness (extradural) excision of the parietal bones and were divided into six groups of four rabbits each. Group 1 through 5 were reconstructed with 16 x 20 x 1.5 mm hydroxyapatite implants treated with: (1) 20 osteogenic units (424 micrograms) BCSS, (2) 8 osteogenic units (170 micrograms) BCSS, (3) 4 osteogenic units (85 micrograms) BCSS, (4) 0 osteogenic units (424 micrograms) inactive BCSS analog, or (5) left untreated. Group 6 was left unreconstructed. Implants were harvested at 12 weeks and analyzed for percentage of lamellar bone formation by a computerized microscope video image analysis system. Groups reconstructed with BCSS-treated hydroxyapatite implants demonstrated more bone ingrowth than did the control hydroxyapatite groups not treated with BCSS (inactive BCSS analog or untreated). Linear regression dose-response analysis indicated an average 3.2 percent increase in bone ingrowth for a 10-U increase in BCSS (p = 0.043). The unreconstructed control group demonstrated no healing. With a molecular mass of only 2.5 kDa and its identity not completely known, BCSS is a novel factor that seems to possess osteogenic potential similar to that of previously investigated osteogenic proteins.

Animals↗