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J Luk

Publications and source records attributed to J Luk.

5 recordsLinked to original sources

Protein misfolding and misprocessing in complex disease.

Scientists from over 20 major research centers recently convened to discuss advances and new discoveries in "Protein MisFolding and MisProcessing in Disease." Understanding protein mechanisms the underlying etiology of complex diseases lies in analyzing the associated biochemical mechanisms, which include folding patterns, processing patterns, chaperone regulators, stress pathways, and signal transduction.

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Observations on mortality during the 1918 influenza pandemic.

The original purpose of our study was to examine the unusual W-shaped mortality curve associated with the 1918 influenza pandemic and possibly explain the peak in mortality among individuals aged 20-40 years. We plotted age-specific excess mortality instead of total mortality for the 1918 pandemic using a 5-year baseline. For comparison, we also graphed excess mortality curves for the 1957 and 1968 pandemics using 5-year baselines. The 1957 and 1968 curves exhibited the usual U-shaped curve, with high excess mortality among infants and the elderly population relative to young adults. The 1918 curve, however, presented unexpected results. A peak in excess mortality among infants and young adults was seen, but the expected W shape did not result. We instead found negative excess mortality among elderly individuals, suggesting that this group was exposed, at an earlier date, to an influenza strain similar to the so-called Spanish influenza (H1N1) strain.

Adolescent↗

Detection of enterobacterial lipopolysaccharides and experimental endotoxemia by means of an immunolimulus assay using both serotype-specific and cross-reactive antibodies.

The immunolimulus (IML) assay system uses solid-phase endotoxin antibodies to capture lipopolysaccharide (LPS), which is then quantified by a modification of the chromogenic limulus amebocyte lysate (CLAL) method. Monoclonal antibodies (MAbs) reactive with selected O antigen serotypes of Escherichia coli (O18) and Salmonella typhimurium (O9, 12), when used in the IML, were shown to be highly specific in detecting their respective endotoxins in purified form and in plasma samples from experimentally infected animals. A murine MAb that was broadly cross-reactive with E. coli, Salmonella, and Shigella endotoxins also proved to be highly effective in the IML assay for capturing LPS molecules from both E. coli and S. typhimurium strains. These results indicate that IML assays can detect smooth-type enterobacterial endotoxins in plasma and suggest that such assays have potential for use in the rapid diagnosis of sepsis and endotoxemia caused by different enterobacterial species.

Animals↗

Role of V1 receptors in the action of vasopressin on the baroreflex control of heart rate.

Arginine vasopressin (AVP) elicits a larger decrease in heart rate for a given increase in arterial pressure than do other vasoconstrictors, but there is disagreement as to whether this results from an increase in baroreflex gain or a resetting of the baroreflex to a lower blood pressure. It is also unclear which type of vasopressin receptor mediates the action of vasopressin on the baroreflex. In the present study, the effects of vasopressin, selective vasopressin V1 and V2 receptor agonists, oxytocin, and a vasopressin V1 receptor antagonist on the baroreflex control of heart rate were investigated in conscious, chronically prepared rabbits. Baroreflex curves were generated with intravenous infusions of phenylephrine and nitroprusside and analyzed using a four-parameter logistic model. Intravenous infusion of vasopressin at 5 ng.kg-1.min-1 increased mean arterial pressure by 9 mmHg and decreased heart rate by 31 beats/min. The arterial pressure at the midrange of the baroreflex curve (BP50) decreased from 75.9 +/- 4.8 to 57.6 +/- 1.7 mmHg (P < 0.01), indicating a shift of the baroreflex curve to a lower pressure, but the gain did not change significantly. The actions of vasopressin on blood pressure, heart rate, and BP50 were completely blocked by pretreatment with d(CH2)5[Tyr(Me)2]AVP, a selective V1 receptor antagonist. Infusion of [Phe2,Ile3,Orn8]AVP, a selective V1 receptor agonist, produced cardiovascular effects similar to those of vasopressin and decreased the BP50 of the baroreflex from 73.0 +/- 2.2 to 63.8 +/- 2.2 mmHg (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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