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Biomedical subjects

J Turek

Publications and source records attributed to J Turek.

At least 37 records · Page 2Linked to original sources

Assembly pathway of avian infectious laryngotracheitis virus.

Infectious laryngotracheitis virus (ILTV) is the causative agent of a highly contagious upper respiratory tract infection in chickens. At present, ILTV vaccines are not satisfactory because of development of a latent carrier status in vaccinated birds. Development of recombinant virus vaccines has been hampered by the limited information available on the molecular level and organization of this virus. We isolated 3 assembly intermediates, designated A, B, and C from ILTV-infected cells. Analysis of [3H]thymidine-and [35S]methionine-labeled particles, and electron microscopic studies indicated that particle A was the empty capsid, particle B was the procapsid containing scaffolding protein, and particle C was the DNA-filled capsid. The ILTV procapsids could only be found in the nucleus, which indicated that procapsids could not translocate through the nuclear membrane until they packaged the DNA. The DNA-filled capsids migrated through the nuclear membrane and obtained an envelope from the inner membrane of the nucleus. The enveloped particles then migrated through the lumen of the endoplasmic reticulum into vacuoles in the cytoplasm. Infective virions were isolated from within the infected cells, indicating that budding through the cytoplasmic membrane is not a necessary step in ILTV maturation. Abundant arrays composed of tubules about 45 to 50 nm wide were found in the cytoplasm of chicken embryonic liver cells about 30 to 38 hours after infection. Comparison of the assembly intermediates and the DNA packaging pathway of ILTV with that of bacteriophage pi 29 indicates that similarity exists.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of zearalenone on days 7 to 10 post-mating on blastocyst development and endometrial morphology in sows.

First litter sows in naturally occurring post-weaning estrus were hand mated to proven boars and were fed a diet supplemented with zearalenone, an estrogenic mycotoxin (1 mg zearalenone/kg body weight), or a control diet on days 7 through 10 after mating. Embryos (blastocysts) and endometrial biopsies were collected from control and treated sows on days 9, 11, and 13 after mating. All blastocysts harvested on day 9 were spherical; treatment of sows with zearalenone had no effect on blastocyst development. Blastocysts collected from treated sows on day 11 were in stages of elongation comparable to those of blastocysts from control sows but had mild degenerative changes in the embryonic disks, characterized by slightly retarded development and an increase in the number of necrotic cells. Blastocysts collected from treated sows on day 13 were in an advanced stage of degeneration, characterized by circumferential constrictive division, fragmentation, and degeneration and disorganization of the embryonic disk. Feeding zearalenone to pregnant sows had no effect on the normal decrease in height of the endometrial luminal epithelium on days 9 through 13 after mating and no effect on morphologic appearance of secretory vesicles in the endometrial glandular epithelium. The dosage scheme of zearalenone used in this study did not cause any morphologic changes in the endometrium that could be associated with hyperestrogenism.

Animals↗

Alcohol and drug use in teenagers with diabetes mellitus.

Alcohol and drug use in adolescents with diabetes mellitus was assessed by an anonymous self-administered questionnaire with verification by urine drug screening. Approximately 50% of these adolescents report having tried alcohol and 25% report ongoing use. Almost 25% have tried drugs of abuse and 5% report ongoing use. One of 97 consecutive urine specimens was positive for marijuana. In general, the frequency of alcohol and drug use was less than expected based on other studies of different clinical groups of patients in the same age range. Patients with diabetes who reported drug use or who reported they live in an environment of substance abuse had poorer diabetes control than patients who did not.

Adolescent↗

Readmissions of children with diabetes mellitus to a children's hospital.

The characteristics of children with diabetes readmitted to Children's Hospital during a 5-year period, 1984 to 1989, were compared with those characteristics of new-onset patients admitted for stabilization and education and to outpatients in the Children's Hospital diabetes program to determine which characteristics were associated with patients who were readmitted. Changes in the frequency of readmissions were examined to determine whether the introduction of a diabetes team and a program that emphasizes the importance of ensuring that patients at risk of readmission consistently received insulin injections resulted in a reduction of readmissions. Readmissions occurred more frequently in patients who were black (71% compared with 38% of new-onset patients and 31% of outpatients) (P less than .001), from one-parent homes (56% compared with 27% of new-onset patients and 24% of outpatients) (P less than .001), and without third-party insurance (45% compared with 18% of new-onset patients and 15% of outpatients) (P less than .001). Readmissions were very common at 14 to 15 years of age (39% of readmissions vs 18% of outpatients) and very uncommon in children younger than age 9 (6% of readmissions vs 27% of outpatients) (P less than .001). Fewer readmissions for ketoacidosis occurred in the summer than in any other season (P less than .05). Readmissions fell by 47% over the 5-year period while new-onset patients increased by 85%. The reduction in frequency of readmissions was due to fewer readmissions for ketoacidosis and fewer readmissions in blacks, in patients from one-parent homes, and in patients without third-party insurance.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

Reviewing diabetes.

Explore the source record for details and available documents.

Diabetes Mellitus↗

Effect of carbon monoxide on the cytochrome P-450-mediated activation of 4-ipomeanol by the isolated perfused rabbit lung.

4-Ipomeanol is a naturally occurring toxin that induces lesions in the lung following its activation to an alkylating metabolite by the pulmonary cytochrome P-450 system. The aim of this study was to determine if an environmentally relevant concentration of carbon monoxide could inhibit the activation of 4-ipomeanol and prevent the associated toxic sequelae in the isolated perfused rabbit lung. The lungs of male New Zealand rabbits were removed and perfused with [14C]-4-ipomeanol for 2 h starting with an initial concentration of 0.1 mM. Lungs were ventilated with either air (control) or 7.5% CO/20% O2. 4-Ipomeanol-derived covalent binding was identical in the control and carbon monoxide treatment groups. Lungs perfused with 4-ipomeanol and ventilated with air or 7.5% CO/20% O2 both displayed alveolar type II cell hyperplasia and alveolar macrophage infiltration. Surprisingly, there was no histological evidence of Clara cell damage in any of the 4-ipomeanol-perfused lungs. These results suggest that the isozymes of pulmonary cytochrome P-450 that act in concert to metabolize 4-ipomeanol are relatively insensitive to inhibition by carbon monoxide.

Animals↗

Simple canine model of arterial thrombosis with endothelial injury suitable for investigation of thrombolytic agents.

Three separate studies were done to evaluate a new canine model of arterial thrombosis with endothelial injury. Endothelial injury was produced by exposing the luminal surface of a 2-cm segment of femoral artery to 100 degrees C saline for 5 min. There was no disruption of proximal or distal blood flow with this model, and thrombolysis was continuously monitored by measuring 125I-labelled fibrin gamma emissions from the thrombus. Study No. 1 showed that complete endothelial denudation was achieved with this model. Study No. 2 demonstrated 1) adherence of the experimentally induced thrombus to subendothelial connective tissue, and 2) endogenous thrombolysis of approximately 9% during the initial 2 h after thrombus formation. Study No. 3 tested the usefulness of the model for evaluating the thrombolytic efficacy of urokinase. Urokinase (30,000 U/Kg, bolus IV injection) caused 38 +/- 5.4% thrombolysis within 90 min of drug administration versus 5.9 +/- 2.4% for a saline-treated control group. We conclude that this model provides a technically simple and reproducible method for the laboratory investigation of thrombosis and thrombolysis in arteries with endothelial injury.

Animals↗

Protection from reperfusion injury in the isolated rat heart by postischaemic deferoxamine and oxypurinol administration.

A Langendorff isolated rat heart preparation was used to determine the effect of oxypurinol, a xanthine oxidase inhibitor, and deferoxamine, an iron binding agent, on the extent of myocardial reperfusion injury after 60 minutes of ischaemia. Thirty rats were divided into three groups of 10, and an isolated heart preparation made from each rat. The isolated hearts were perfused for 15 minutes with a modified Krebs-Henseleit perfusate solution to permit stabilisation of the preparation. Each heart was then subjected to 60 minutes of total ischaemia at 37 degrees C followed by 60 minutes of reperfusion with either saline treated perfusate, oxypurinol treated perfusate (1.3 mmol.litre-1), or deferoxamine treated perfusate (0.61 mmol.litre-1). Reperfusion injury was assessed by the total amount of creatine phosphokinase released into the perfusate, by changes in myocardial vascular resistance, and by morphological examination. The saline treated group released significantly more creatine phosphokinase into the perfusate than either the oxypurinol treated group (p less than 0.05) or the deferoxamine treated group (p less than 0.05). The mean vascular resistance increased for all groups during the 60 minutes of reperfusion compared with that just before ischaemia but was significantly greater in the saline treated group than in the drug treated groups (p less than 0.01). Ultrastructural examination of a randomly selected heart from each group after 60 minutes of reperfusion showed pronounced attenuation of mitochondrial and endoplasmic reticulum swelling, increased maintenance of membrane integrity, and diminished separation of myofilaments in the oxypurinol treated and deferoxamine treated hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Equine endotoxemia: cardiovascular, eicosanoid, hematologic, blood chemical, and plasma enzyme alterations.

Ponies with electromagnetic blood flow transducers implanted around the main pulmonary and left main coronary arteries, were used to evaluate effects of chronic sublethal endotoxin on cardiac output (CO), stroke volume, and left coronary blood flow (LCBF). Plasma thromboxane (TX), as indicated by TXB2, prostacyclin as indicated by 6-keto-prostaglandin (PG) F1 alpha, and hematologic and blood chemical values also were evaluated. Over 24 hours, 2 groups of ponies were given progressively increasing IV and intraperitoneal doses of Escherichia coli lipopolysaccharide (LPS) at 0, 6, 12, and 18 hours. Group 1 was not treated and group 2 was treated with flunixin meglumine, before each LPS insult. Initial LPS inoculation in group 1 led to 10-fold increases in TXB2 and 6-keto-PGF1 alpha values by 30 and 90 minutes, respectively. These eicosanoid values returned to base line by 6 hours after each insult. Although repeated LPS injections stimulated recurring high plasma concentrations of 6-keto-PGF1 alpha, TXB2 production became less with each successive LPS insult. Cardiac output decreased to 55% to 60% of base-line values in association with increased 6-keto-PGF1 alpha values. Left coronary blood flow could not be evaluated accurately. Severe lactic acidosis developed in group 1. Group-2 ponies remained clinically normal, indicating protection of cardiovascular function and peripheral perfusion with flunixin meglumine. Seemingly, flunixin meglumine helped to maintain acceptable cardiovascular function and tissue perfusion during endotoxemia. Flunixin meglumine given to healthy ponies had no effect on cardiovascular function.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

Release of eicosanoids from white blood cells, platelets, smooth muscle cells, and endothelial cells in response to endotoxin and A23187.

Endotoxin produces numerous pathophysiologic changes in animals, including vascular endothelial cell damage and hematologic changes. Direct effects of endotoxin on arachidonic acid metabolism and the release of eicosanoids from endothelial cells and neutrophils have been reported. A rapid release of these autocoids occurs when cells are incubated with endotoxin, and this appears to be one of the earliest endotoxin-induced changes. Some of these eicosanoids may result in beneficial effects, and others may result in detrimental effects. This study was to determine the release of eicosanoids from white blood cells, platelets, smooth muscle cells, and endothelial cells in response to varying amounts of endotoxin and the calcium ionophore A23187. The results indicate that endotoxin has a major direct effect on vascular endothelial cells and smooth muscle cells as indicated by its ability to increase the synthesis of predominately i6-keto-PGF1 alpha by these cells. These effects were seen within a dose range of endotoxin that is lethal in horses. Very high concentrations of endotoxin (100 micrograms/ml) were required to stimulate a small increase in the production of i6-keto-PGF1 alpha and iLTC4 by freshly isolated neutrophils. Stimulation of cells with A23187 revealed that, of the eicosanoids measured, the one produced predominately by endothelial cells and smooth muscle cells was 6-keto-PGF1 alpha, by platelets was TxB2, and by neutrophils was LTC4 (LTB4 was not measured). A mixture of all white blood cells including platelets when incubated with A23187 produced large amounts of TxB2, LTB4, and LTC4 with smaller amounts of 6-keto-PGF1 alpha. The results indicate that endotoxin directly affects cells and stimulates them to produce thromboxane and prostacyclin, but very high concentrations of endotoxin were required to stimulate neutrophils to produce rather small increases in iLTC4.

6-Ketoprostaglandin F1 alpha↗