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J L Lynch

Publications and source records attributed to J L Lynch.

6 recordsLinked to original sources
PubMed2001

Radiographic resolution of lymphocytic interstitial pneumonitis (LIP) in children with human immunodeficiency virus (HIV): not a sign of clinical deterioration.

BACKGROUND: The literature and anecdotal evidence associate the resolution of radiographic findings of lymphocytic interstitial pneumonitis (LIP) with a decline in immune and clinical status of human immunodeficiency virus (HIV) infected children. OBJECTIVE: As our clinical impression was the opposite, we sought to elucidate this contradiction. MATERIALS AND METHODS: Of 52 pediatric patients infected with the HIV currently being followed at our institution, 20 (38.5%) carried the diagnosis of LIP and 13 (65%) of these have had complete resolution of radiographic findings of LIP. We retrospectively reviewed the chest radiographs, CD4 counts, and clinical history of these 13 patients. RESULTS: Of the 13 patients who had resolution of radiographic findings, 11 (84.6%) had no significant change in CD4 count at the time of resolution and remained clinically stable during a mean follow-up period of 32 months. Two patients (15.3%) developed severe CD4 lymphocytopenia at the time of resolution of LIP, but clinically remained stable. None of these 13 patients had a recurrence of LIP, even with subsequent increases in CD4 count. CONCLUSION: We suggest that in contradiction to previously published data, resolution of LIP on chest radiographs is not an indicator for poor prognosis for the HIV-infected pediatric patient.

CD4 Lymphocyte Count↗
PubMed1995

Effect of inhibitors of factor Xa or platelet adhesion, heparin, and aspirin on platelet deposition in an atherosclerotic rabbit model of angioplasty injury.

Acute thrombotic reocclusion and restenosis after successful coronary angioplasty are limitations of the procedure. Although the restenotic process is not completely understood, acute platelet deposition and thrombosis are considered important initiating mechanisms. The effort to identify pharmacologic agents capable of modifying acute platelet action following mechanical injury requires an animal model mimicking the clinical pathophysiology as closely as possible. We developed a model of angioplasty-induced injury in atherosclerotic rabbit femoral arteries. Acute 111indium-labelled platelet deposition and thrombosis were assessed four hours after balloon-injury in arteries subjected to prior endothelial damage (air desiccation) and cholesterol supplementation (one month). The effects of recombinant tick anticoagulant peptide (rTAP), a blood coagulation factor Xa (fXa) inhibitor and of recombinant leech antiplatelet protein (rLAPP), a platelet adhesion inhibitor, were compared to heparin (HEP) and aspirin (ASA). Recombinant TAP and HEP, but not rLAPP or ASA, successfully prevented thrombus formation and reduced platelet deposition in balloon-injured vessel segments to levels not significantly different from those observed in the contralateral atherosclerotic non-balloon-injured vessels. Therefore, this model, incorporating balloon catheter dilation of arteries exhibiting neointimal growth and atherosclerotic plaque formation, may be useful for evaluation of possible adjunctive therapies during angioplasty.

Angioplasty, Balloon, Coronary↗
PubMed1966

On the mechanism of action of the antibiotic O-carbamyld-serine in Streptococcus faecalis.

Lynch, Judith L. (Northwestern University, Evanston, Ill.), and Francis C. Neuhaus. On the mechanism of action of the antibiotic O-carbamyl-d-serine in Streptococcus faecalis. J. Bacteriol. 91:449-460. 1966.-The antibiotic O-carbamyl-d-serine, an analogue of d-alanine, is an inhibitor of bacterial cell-wall biosynthesis. Growth of Streptococcus faecalis R in the presence of O-carbamyl-d-serine resulted in the accumulation of the cell-wall precursor uridine diphosphate-NAc-muramyl-l-alanyl-d-glutamyl-l- lysine (UDP-NAc-muramyl-l-ala-d-glu-l-lys). The incorporation of d-alanine from l-alanine into peptidoglycan is catalyzed by the sequential action of the following enzymes: (i) alanine racemase; (ii) d-alanine: d-alanine ligase [adenosine diphosphate (ADP)]; (iii) UDP-NAc-muramyl-l-ala-d-glu-l-lys: d-ala-d-ala ligase (ADP); (iv) phospho-NAc-muramyl-pentapeptide translocase [uridine monophosphate (UMP)]. O-carbamyl-d-serine is an effective inhibitor of the alanine recemase (K(i)= 4.8 x 10(-4)m, K(m) of l-alanine = 6.8 x 10(-3)m). In addition, d-ala-O-carbamyl-d-ser was formed when d-alanine and O-carbamyl-d-serine were incubated with d-alanine: d-alanine ligase (ADP). This dipeptide was utilized by the UDP-NAc-muramyl-l-ala-d-glu-l-lys: d-ala-d-ala ligase (ADP) with the formation of UDP-NAc-muramyl-l-ala-d-glu-l-lys-d-ala- O-carbamyl-d-ser. From a consideration of the following results, i.e., (i) accumulation of UDP-NAc-muramyl-l-ala-d-glu-l-lys; (ii) absence of d-ala-O-carbamyl-d-ser accumulation in bacterial cultures grown in the presence of O-carbamyl-d-serine; and (iii) effective inhibition of the racemase, it was concluded that the first enzyme, the racemase, is the primary site of antibiotic action.

Alanine↗