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J L Zimmerman

Publications and source records attributed to J L Zimmerman.

13 recordsLinked to original sources

Does cocaine cause coronary vasospasm in chronic cocaine abusers? A study of coronary and systemic hemodynamics.

The pathogenesis of acute myocardial ischemia or infarction following cocaine abuse is not known. Cocaine causes an increase in circulating catecholamines. Therefore alpha-adrenergic mediated focal or generalized coronary artery spasm has been presumed to be the likely mechanism to induce ischemia. However, coronary vasospasm in chronic cocaine abusers has not been demonstrated angiographically. Moreover, it has been observed that patients commonly manifest ischemic changes hours up to a week after abusing cocaine. In order to evaluate direct effects of cocaine on coronary vasculature, 6 chronic cocaine abusers admitted with prolonged chest pain and electrocardiographic ST- and T-wave changes were studied. Cocaine administered intravenously (maximum 32 mg) produced subjective sensation of central nervous stimulation (the "high") in all patients. However there was no significant change in coronary artery diameter (assessed by computer-assisted quantitative technique), myocardial perfusion (assessed by contrast echocardiography) or left ventricular wall motion (assessed by two-dimensional echocardiography) as compared with the baseline values. Coronary sinus flow (thermodilution) showed an upward trend, a probable reflection of a significant increase in cardiac output (average 62%, p less than 0.007). Despite a significant elevation in heart rate (average 56%, p less than 0.007), mean systemic arterial pressure (average 12%, p less than 0.05) and rate-pressure product (average 69%, p less than 0.005), no symptomatic or acute electrocardiographic changes were observed. It is concluded that recreational doses of cocaine do not cause focal or generalized coronary vasospasm or reduced myocardial perfusion in patients who present with chest pain temporally related to cocaine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Cocaine-associated chest pain.

STUDY OBJECTIVES: To describe the clinical and ECG features of cocaine abusers evaluated in the emergency department and admitted to the medical coronary care unit with chest pain consistent with myocardial ischemia. DESIGN: A four-month retrospective review of all cocaine abusers who presented to the ED with chest pain and a diagnosis of possible myocardial infarction. SETTING: Urban county hospital. TYPE OF PARTICIPANTS: Forty-eight adult cocaine abusers admitted with chest pain. MEASUREMENTS AND MAIN RESULTS: Patients included 34 men and 14 women with a mean age of 29 +/- 7.3 years. The average duration of cocaine abuse in 28 patients for whom it was reported was 5 +/- 4.8 years. Chest pain occurred within one hour of cocaine abuse in 13 admissions (27%), more than one hour after abuse in 13 admissions (27%), and it was not recorded in 23 admissions (47%). Initial ECGs were evaluated in all patients and revealed significant repolarization abnormalities consisting of abnormal ST segment elevations in 18 (37%) and T-wave inversions in 20 (41%) that often persisted on subsequent ECGs. Three patients sustained acute myocardial infarctions. CONCLUSIONS: Our findings confirm a small but significant incidence of myocardial infarction in cocaine abusers presenting to the ED with chest pain. The chronicity of cocaine abuse, the persistence of ECG abnormalities, and the variable temporal relationship of chest pain to cocaine abuse suggest possible chronic myocardial changes as etiologies of ischemia.

Adolescent

Heat shock and thermotolerance in plant and animal embryogenesis.

Although the strategies of early embryogenesis differ greatly among multicellular eukaryotes, there are certain parallels in structure, form, and function that cross even kingdom lines: the extreme heat sensitivity of zygotes and very early embryos, followed by the acquisition of thermotolerance during subsequent development, is one such parallel. The heat sensitivity may be so extreme that even moderate increases in temperature result in lethality (generally associated with the earliest phases of embryogenesis), or the effects may be less severe, resulting in defects in development but not in lethality. Mechanistically, and molecularly, these two forms of thermosensitivity appear to have different origins. On the one hand, outright lethality appears to result from an inability to induce heat shock genes and proteins; on the other hand, heat-induced developmental defects appear to result from an alteration in expression of non-heat shock genes and from a delay in the overall developmental program that generally accompanies the cell's response to heat shock. This review is focused on the developmental regulation of the heat shock response during early embryogenesis and on the impact of this regulation on the development of both animal and plant embryos. The two basic issues that we address here are (i) the expression of heat shock genes in the absence of heat shock during embryogenesis and (ii) the expression (or lack of expression) of heat shock genes after deliberate exposure of the embryos to heat shock and the consequences of this expression on its subsequent survival and development.

Animals

Molecular evolution of two actin genes from carrot.

We have isolated and sequenced two full-length cDNA clones encoding actin from carrot. The two carrot clones are almost identical at the nucleotide level, and are quite homologous to each other and to other plant actins at the amino acid level. In those regions where amino acid variation exists between the two genes from carrot, the differences have arisen from very simple changes at the nucleotide level. The most common changes are nucleotide insertion(s) coupled to the deletion of a different nucleotide(s) nearby in the DNA sequence, resulting in the restoration of the proper reading frame for the protein; thus, these changes can be viewed as multiple or coupled frameshift mutations. There are almost no base substitutions between the two carrot genes. In contrast to this, when the carrot actin nucleotide sequences are compared to those of a soybean actin gene or a maize actin gene, many base substitutions are observed (ca, 21.8% and 23.5%), more than half of which are third base changes which do not alter the protein sequence. At the amino acid level, both carrot genes show greater similarity to maize actin than they do to soybean actin, thus reinforcing the idea that plant actin genes diverged from a single common ancestral actin gene prior to the divergence of monocots and dicots.

Actins

Novel regulation of heat shock genes during carrot somatic embryo development.

We have determined that somatic embryos of carrot exhibit a number of interesting and unusual properties when exposed to heat shock at different times in their development. Specifically, we have seen that mid-globular embryos can be arrested irreversibly in their development when heat-shocked, whereas all other stages of embryogenesis, both before and after this stage, are fully capable of normal development after the stress. In investigating the molecular basis of this developmental sensitivity to heat shock, using a cloned heat shock gene encoding a small heat shock protein, we have determined that globular embryos both synthesize and accumulate significantly less heat shock mRNA when compared with embryos of any other stage or to callus suspension cells. In fact, there appears to be no transcriptional induction of heat shock gene expression in response to heat shock during this time period; the gene is expressed at the same relatively low level both before and after heat shock. However, in spite of the low level of heat shock mRNA available, globular embryos synthesize the full complement of heat shock proteins in response to heat treatment. The globular embryos appear to accomplish this by translating the existing heat shock mRNAs at an elevated rate, which compensates for the low level of available mRNA. Once the embryos have progressed beyond the globular stage of development, regulation at the transcriptional level resumes, and the embryos again exhibit normal development after heat shock.

Animals

The effect of etodolac on type II collagen-induced arthritis in mice.

Type II collagen-induced arthritis (CIA) and mice was used as a model to evaluate the effect of etodolac on the arthritic and immunological parameters of the experimental disease. In a preventative protocol, a significant reduction was observed in the number of joints progressing to ankylosis. At high doses (16 mg/kg/day) a significant delay in the onset of arthritis was also observed. No significant effect was seen on the progression of the disease when etodolac was administered in established CIA. No consistent variations were observed in the anti-type II collagen response or other immunological parameters of the experimental arthritis.

Acetates

Porcine toxoplasmosis in Indiana.

Toxoplasmosis was diagnosed at necropsy in a 4-week-old pig from a litter of 16 born to a clinically normal sow. Multifocal acute necrosis of blood vessels and parenchyma was found in the small intestine, mesenteric lymph nodes, liver, lungs, and brain. Numerous tachyzoites, ultrastructurally indistinguishable from Toxoplasma gondii, were found in lesions. The affected pig and seven other littermates died after diarrhea had developed within 1 to 2 weeks of birth. The most likely source of infection was oocysts from cats on the farm.

Animals

Orf.

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Adult