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Biomedical subjects

J M Howell

Publications and source records attributed to J M Howell.

At least 37 records · Page 2Linked to original sources
PubMed1998

Modulation of immune system function by measles virus infection: role of soluble factor and direct infection.

Measles virus infection can result in a variety of immunologic defects. We have begun studies to determine the basis for the lack of immune responsiveness to antigen and mitogen following infection. Here we present data showing that Epstein-Barr virus-transformed B-cell lines infected with measles virus produce a soluble factor that can inhibit antigen-specific T-cell proliferation and inhibit the proliferation of uninfected B cells. The soluble factor was neither interleukin-10, transforming growth factor beta, nor alpha/beta interferon. B cells infected with measles virus or treated with the soluble factor were unable to present antigen to T cells in a manner that supported antigen-specific proliferation. This could represent one mechanism of how measles virus limits T-cell expansion. However, we found that once CD4(+) or CD8(+) T cells were activated, their cytolytic activity was intact whether infected with measles virus or treated with soluble factor. Thus, while slow to be generated these cytoxic cells could participate in viral clearance.

Antigen Presentation↗
PubMed1998

A potential role for glucagon in the treatment of drug-induced symptomatic bradycardia.

Nine cases of symptomatic bradycardia are presented in which treatment with intravenous glucagon was administered when atropine failed to improve the patient's condition significantly. Although the cause often was not obvious at presentation, all nine subjects took oral medications that could have contributed to the development of symptomatic bradycardia. Eight of nine patients demonstrated clinical improvement 5 to 10 min after glucagon administration, which was consistent with its peak clinical action. Beta-blockers, calcium channel blockers, and digoxin were ultimately thought to have contributed to the majority of these presentations. This report suggests that glucagon may have a role in the treatment of symptomatic bradycardia, particularly in the presence of beta-adrenergic blockade and perhaps calcium channel blockade. Furthermore, the results in these cases suggest that future clinical trials should not be limited to drug-induced symptomatic bradycardia.

Adrenergic beta-Antagonists↗
PubMed1997

Glucagon therapy in the treatment of symptomatic bradycardia.

Symptomatic bradycardia is commonly seen in the emergency department. Effective drug therapy for this clinical scenario is limited. Although glucagon has been used in no clinical trial in this setting, its cardiac activity may prove useful, particularly in the setting of beta-adrenergic blockade. We report a case series comprising three patients taking maintenance beta-blocker therapy who presented to the ED with symptomatic bradycardia and hypotension and in whom glucagon therapy obviated the need for further treatment. Further study is warranted to evaluate and define the role of glucagon in the treatment of symptomatic bradycardia.

Adrenergic beta-Antagonists↗
PubMed1997

Wound care.

Soft-tissue injuries remain one of the most common problems encountered in the emergency department. This article discusses techniques to minimize pain during the evaluation and repair process, methods to decrease healing complications, and repair considerations.

Aftercare↗
PubMed1997

Use of the dog model for Duchenne muscular dystrophy in gene therapy trials.

Golden retriever muscular dystrophy (GRMD) is an excellent model for the study of the efficacy of gene therapy in dystrophin deficient myopathies for there are many similarities between affected dogs and Duchenne muscular dystrophy (DMD) in boys. GRMD is not caused by deletion mutation but results from a point mutation in the consensus splice acceptor in intron 6 of the canine dystrophin gene. As a result exon 7 is skipped during processing of the GRMD dystrophin messenger RNA. We have developed a rapid test which makes direct use of exon 7 specific genomic PCR products. We have undertaken preliminary experiments on gene therapy using the mini-gene and the full length gene alone and in combination with lipofectin and/or the bacterial beta-galactosidase reporter gene Lac Z. Following direct injection of the Lac Z plasmid, either alone or with lipofectin, about 50% of the sites showed expression when biopsied some 14 days later. The beta-galactosidase activity was present in muscle and granulation tissue but was never abundant. Pups injected intraperitoneally with Lac Z were found to have positive material in their mesenteric lymph nodes, liver and spleen. Those injected with Lac Z and lipofectin also had positive material in the diaphragm, intercostal muscles and abdominal muscles, but again only a small amount of positive material was present at any of the sites. In animals directly injected into the muscle with the dystrophin mini-gene, half had positive staining for dystrophin in biopsies taken 14 days later. Of the 6 sites in the muscles of animals given the mini-gene and lipofectin only one had fibres positive for dystrophin when examined 14 days later. Six pups were injected directly with full-length gene construct and when biopsies were taken 10 days later two of the animals had strongly stained peripheries to a small number of fibres.

Adenoviridae↗
PubMed1997

Characterization of fatal beta blocker ingestion: a review of the American Association of Poison Control Centers data from 1985 to 1995.

OBJECTIVE: To characterize beta blocker-related deaths. METHODS: This is a retrospective review of beta blocker-related exposure data and fatality case abstracts reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System during the 11 year period, 1985 to 1995. Historical and laboratory data were used to determine those fatalities which resulted primarily from beta blocker intoxication. RESULTS: Of 52,156 reported beta blocker exposures, 164 were fatal. In 38 cases, beta blockers were implicated as the primary cause of death. Propranolol was responsible for the greatest number of exposures (44%) and implicated as the cause of death in a disproportionately high percentage of fatalities (71%). Patients were generally young women; 63% were female and 92% were less than 50 years old. The dysrhythmias most often noted in fatal cases were bradycardia and asystole. Cardiopulmonary arrest did not develop until patients were in the care of health care personnel in 59% of cases. Though glucagon was initiated more often than any other intervention in fatal intoxications (83%), optimal dosing and maintenance infusions appear to have been underutilized. CONCLUSIONS: The predominance of fatalities associated with propranolol compared to other beta blockers reflects both its greater frequency of use over the time period studied and its greater toxicity. Since 59% developed. cardiac arrest after reaching health care personnel, further study should focus on identifying medical intervention that can reduce mortality in this group.

Administration, Oral↗
PubMed1996

Hemodynamic effects of calcium chloride in a canine model of acute propranolol intoxication.

STUDY OBJECTIVE: To evaluate the hemodynamic effects of calcium chloride in a canine model of acute propranolol toxicity. METHODS: Two minutes after the completion of a propranolol infusion (10 mg/kg), a bolus of .125 mL/kg 10% CaCl solution followed by an infusion of .375 mL/kg over the next 30 minutes or a bolus and subsequent infusion of an equivalent volume of normal saline solution was administered to each dog. RESULTS: CaCl yielded significant improvements in propranolol-induced decreases in cardiac index and stroke volume compared with saline solution-treated control animals (overall alpha = .05). Furthermore, CaCl administration resulted in earlier improvement in propranolol-induced alterations in mean arterial pressure, maximal left ventricular pressure change over time, and peripheral vascular resistance compared with saline solution (overall alpha = .05). We observed no difference between treatment groups in response to propranolol-induced bradycardia or QRS-interval prolongation. CONCLUSION: In this model of acute propranolol toxicity, CaCl therapy improved depressed hemodynamic status, mainly by a positive inotropic action.

Acute Disease↗
PubMed1996

Acute myocardial infarction and congestive heart failure.

The effective treatment of patients with acute myocardial infarction (AMI) and acute congestive heart failure (CHF) requires quick triage, accurate identification, and appropriate pharmacologic management. This article describes the initial assessment and management of adult patients with AMI and CHF, beginning with the first interaction of such patients with the emergency department staff.

Acute Disease↗
PubMed1996

Level I trauma certification and emergency medicine resident major trauma experience.

OBJECTIVE: American College of Surgeons (ACS) and Residency Review Committee for Emergency Medicine (RRC-EM) guidelines conflict regarding the role of emergency physicians in directing major trauma resuscitations. This article describes the impact of ACS level I trauma certification on emergency medicine (EM) resident trauma experience. METHODS: A written survey and a follow-up letter were sent to all 101 EM program directors as of August 16, 1994. The survey addressed demographics and trauma experience at hospitals designated by the RRC-EM as primary training sites. RESULTS: There were 95 (94%) survey respondents. Estimates of the percentage of trauma resuscitations directed by EM residents were significantly lower at level I centers (52% +/- 27%, 95% CI 45-59%) than they were at non-level I centers (70% +/- 30%, 95% CI 58-82%) (p < 0.01). There was no significant difference in trauma census between level I and non-level I centers. Of 14 respondents who said they were cited by the RRC-EM for inadequate trauma experience, ten (71%) were in ACS level I trauma centers (p = 1.0). Twelve of the 14 respondents cited for inadequate trauma experience were in either the Northeast or the Midwest. CONCLUSIONS: EM residents direct a smaller percentage of major trauma resuscitations at ACS level I hospitals than they do at non-level I facilities. This finding is not offset by an increased trauma census at level I facilities and may be more pronounced in the Northeast and the Midwest.

Certification↗
PubMed1996

Mutation segregation and rapid carrier detection of X-linked muscular dystrophy in dogs.

OBJECTIVES: To use exon 7-specific genomic polymerase chain reaction (PCR) products to identify the genotypes of normal, affected, and carrier female dogs in pedigrees segregating Golden Retriever muscular dystrophy (GRMD), and to confirm the concordant segregation of the mutation in all carrier and affected dogs presently available. DESIGN: The GRMD mutation is found in the consensus splice acceptor site in intron 6 of the canine dystrophin gene. PCR cycle-sequencing and restriction fragment length polymorphism/PCR were used for determination of the pattern of segregation of the point mutation which causes GRMD. ANIMALS: Normal, clinically affected, and obligate carrier dogs in pedigrees of GRMD. PROCEDURE: DNA from blood was amplified, using PCR and primers that bracket all of exon 7 of the canine dystrophin gene as well as 100 base pairs of intron on either side. PCR products were either cycle-sequenced directly or submitted to a second round of PCR, using 1 of the original primers coupled with a mutagenic restriction fragment length polymorphism-primer, which thus creates an artificial restriction site. Digestion with Stu I detected the normal allele. To detect the affected allele, Sau96 I was used to digest the 310-base pair exon 7 genomic fragment directly. CONCLUSIONS: Simple, clear diagnosis of carrier status was possible using these methods. This mutation is passed through all carrier and affected dogs in both United States GRMD colonies and the colony in Australia. CLINICAL RELEVANCE: Rapid, accurate diagnosis of carrier and affected dogs will enhance study of this homologue of Duchenne muscular dystrophy.

Alleles↗
PubMed1995

Infrared emission detection tympanic thermometry may be useful in diagnosing acute otitis media.

To determine the utility of infrared emission detection (IRED) tympanic thermometry in diagnosing acute suppurative otitis media (ASOM), a prospective, nonblinded sampling of ear temperatures was performed. Children between the ages of 6 months and 6 years presenting to an urban emergency department were included in the study. Tympanic temperatures were determined in all subjects. Clinical data, tympanic audiometry, and telephone follow-up were used to define ASOM. Temperature differences were determined for children with unilateral ASOM and those without ear infection. Data from 48 patients were analyzed. The mean temperature difference in the control group, 0.23 degrees +/- 0.15 degrees C (95% confidence interval [CI], 0.17 degree to 0.29 degree C) differed from those with ASOM: 0.39 degree +/- 0.29 degree C (95% CI, 0.25 degree to 0.53 degree C, P = .047). Logistic regression was used to describe the predictive relationship between temperature difference and probability of ASOM. We conclude that IRED tympanic thermometry may be useful in diagnosing ASOM when used with other clinical data.

Acute Disease↗