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Biomedical subjects

D R Weber

Publications and source records attributed to D R Weber.

15 recordsLinked to original sources
PubMed1991

Hepatosplenic candidiasis: successful treatment with fluconazole.

PURPOSE: To determine if fluconazole is effective treatment for hepatosplenic candidiasis that has not resolved with amphotericin B and flucytosine treatment. PATIENTS AND METHODS: Six patients (ages 3 to 44) with acute leukemia and hepatosplenic candidiasis who did not respond to prior antifungal therapy were treated with fluconazole. RESULTS: All six patients had fever and three had nausea and vomiting; computed tomographic (CT) scan showed lucencies in the liver in six, lucencies in the spleen in five, and lucencies in the kidneys in three. Prior therapy with 1.6 to 4 g of amphotericin B in the five adults and 526 mg of amphotericin B in the child (with the addition of flucytosine in four) failed to improve clinical symptoms or lucencies in the liver, spleen, and kidneys seen on CT scan. Fluconazole was given at a dose of 200 to 400 mg daily (70 to 100 mg in the child) for 2 to 14 months. All patients had resolution of fever and other symptoms in 2 to 8 weeks. Improvement of the lesions noted on CT scan was seen in 4 to 8 weeks in all patients. Total resolution of lesions noted on CT scan occurred by 4 weeks in two patients, but took 4 to 5 months for three patients and 13 months for one patient. Three patients had relapse of their acute leukemia and two died, presumably cured of their candidiasis. Two patients underwent successful bone marrow transplantation without relapse of their candidiasis. CONCLUSION: Fluconazole appears to be useful in the treatment of hepatosplenic candidiasis that has not resolved with amphotericin B and flucytosine therapy.

Acute Disease↗
PubMed1991

Is heparin really necessary in the lock and, if so, how much?

The literature on the issue of whether heparin is necessary in an intermittent peripheral venous access device (lock) is critically reviewed. Issues explored include loss of patency, development of phlebitis, duration of lock placement, type of cannula material, sample size, risk of toxicity with heparin flush solutions, risk of clot embolism, and physical or chemical incompatibilities. Available studies indicate that heparin is not necessary to maintain fluoroethylenepropylene (FEP-Teflon) peripheral venous access devices unless the lock is used to obtain blood specimens. Considering the benefit-to-risk ratio for the use of heparin, it is advisable to maintain FEP-Teflon locks with normal saline alone. When locks are used to obtain blood specimens, as in a pharmacokinetic study, then a dilute heparin flush solution should be used. Whether heparin is necessary for the maintenance of locks composed of other materials is uncertain. Newer, less thrombogenic materials such as ethylene tetrafluoroethylene may also obviate the need for heparin, but comparative trials in a larger number of patients are needed for confirmation. When heparin is used, an effort should be made to avoid systemic toxicities by using the lowest known effective concentration (10 units/mL) pending further studies.

Heparin↗
PubMed1989

DNA sequence of mip, a Legionella pneumophila gene associated with macrophage infectivity.

In a previous study, a 24-kilodalton (kDa) protein surface antigen of Legionella pneumophila was cloned into Escherichia coli and found to be expressed on the host cell surface. Subsequently, a site-directed mutation in this gene (designated mip) in L. pneumophila was found to impair the capacity of this bacterium to initiate intracellular infection in human macrophages. The work presented here indicates that the antigenic gene product is distinct from the 24- to 29-kDa major outer membrane protein of L. pneumophila. In addition, the antigen was identified as a highly basic protein on two-dimensional nonequilibrium polyacrylamide gels and on two-dimensional monoclonal antibody immunoblots. When the DNA fragment encoding this protein was sequenced, a long open reading frame of 699 base pairs was identified within a region to which antigen expression was previously mapped. mip mRNA isolated from both L. pneumophila and transformed E. coli had the same 5' end, as determined by primer extension analysis, indicating that the same promoter sequences are used in both species. A likely factor-independent transcriptional terminator was found 20 residues downstream of the stop codon, suggesting that mip is encoded on a monocistronic message. The inferred polypeptide began with a possible 20- to 24-residue signal sequence, and, as predicted by two-dimensional electrophoresis, had a molecular weight of 24,868 and was a potent polycation with an estimated pI of 9.8.

Amino Acid Sequence↗
PubMed1989

Arachidonate metabolism in cultured fibroblasts derived from normal and infarcted canine heart.

Metabolites of arachidonic acid (eicosanoids) may have an important role in the healing process after myocardial infarction. We examined the ability of cardiac fibroblasts from normal and from healing infarcted ventricle to metabolize arachidonate. We induced myocardial infarction in dogs and then allowed them to recover for 1 week, at which time they were killed, and the heart was removed. Fibroblasts were harvested from normal and from the healing, infarcted areas of the left ventricle. The cells from each source were morphologically indistinguishable. There were 347 +/- 102-fold more fibroblasts cultured from the infarcted area than from the normal area. Interestingly, the infarct-derived cells had a slower doubling time (37.4 +/- 3.7 hours) than the normal cells (22.0 +/- 3.6 hours). The uptake of exogenous arachidonate and its distribution in complex lipids was the same in the cells from each area. When stimulated with the calcium ionophore, free exogenous arachidonate, bradykinin, or histamine the cells produced prostaglandin E2 and prostaglandin I2. In each case the infarct-derived cells produced from twofold to fivefold more prostaglandin than the normal cells. We also found that prostaglandin synthesis was highly dependent on the growth state of the cells with a marked decrease a confluence. Finally, in experiments designed to mimic the early state of infarction, we confirmed that isolated cardiac myocytes release arachidonate and showed that normal fibroblasts can incorporate it. The production of eicosanoids by cardiac fibroblasts may be substantial during the healing of myocardial infarction due to their dramatic proliferation and the increased prostaglandin production per cell.

Animals↗
PubMed1986

Effect of heparin on platelet aggregation inhibited by PGI2, trifluoperazine and verapamil.

The enhancement of platelet aggregation by heparin in the presence of certain inhibitors of aggregation was investigated in an attempt to discern the mechanism through which heparin alters platelet function in plasma. These studies were performed by adding prostaglandin I2 (PGI2), verapamil, or trifluoperazine to platelet-rich plasma (PRP) in the presence or absence of heparin. Adenosine diphosphate (ADP), collagen, or arachidonic acid were used for induction of platelet aggregation. The inhibitory agents reduced platelet aggregation to 5 to 20% of control in the absence of heparin. When present in the reaction mixture along with the inhibitor, heparin restored aggregation to approximately 57 to 92% of control depending on the inhibitor and aggregating agent. This proaggregatory action of heparin was observed when heparin and PGI2 were preincubated together or separately for 20 min prior to the addition of PRP and ADP. Results were similar regardless of the sequence in which PGI2 and heparin were added to PRP, and irrespective of the time of incubation of platelets with PGI2. No suppression of platelet cyclic AMP concentration was observed with heparin alone. Heparin also failed to reduce the magnitude of platelet cyclic AMP accumulation promoted by PGI2, forskolin, or a mixture of PGI2 and forskolin. These observations suggest that heparin promoted platelet aggregation and partially overcame the effect of certain inhibitory agents by mechanism(s) that did not involve a reduction of platelet cyclic AMP.

Blood Platelets↗
PubMed1967

Melioidosis.

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Humans↗