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T Chajek

Publications and source records attributed to T Chajek.

At least 19 recordsLinked to original sources
PubMed1998

An in vivo study of the chlorhexidine release profile of the PerioChip in the gingival crevicular fluid, plasma and urine.

The release profile of chlorhexidine from the PerioChip (Chip), a biodegradable local delivery system that contains 2.5 mg of chlorhexidine gluconate (CHX) in a cross-linked hydrolyzed gelatin matrix, into the gingival crevice, was evaluated in an in vivo, open label, single-center, 10-day pharmacokinetic study conducted on 19 volunteers with chronic adult periodontitis. Each volunteer had a single chip inserted into each of 4 selected pockets, with probing pocket depths of between 5-8 mm, at time 0. Gingival crevicular fluid (GCF) samples were collected using filter paper strips prior to Chip placement and at 2 h, 4 h, 24 h and 2, 3, 4, 5, 6, 8, and 9 days post-Chip placement. The GCF volume was measured using a calibrated Periotron 6000. Blood samples were collected at times 0, 1, 4, 8, 12 h and 5 days post-dosing. Urine was collected as a total 24-h specimen immediately post-dosing and 2 single samples at time 0, prior to dosing, and 5 days. The CHX was eluted from the paper strips and the CHX levels in GCF, blood and urine quantified using HPLC. The results indicate an initial peak concentration of CHX in the GCF at 2 h post-Chip insertion (2007 microg/ml) with slightly lower concentrations of between 1300-1900 microg/ml being maintained over the next 96 h. The CHX concentration then progressively decreased until study conclusion with significant CHX concentrations (mean=57 microg/ml) still being detectable at study termination. CHX was not detectable in any of the plasma or urine samples at any time point during the study. These results indicate that the PerioChip can maintain clinically effective levels of CHX in the GCF of periodontal pockets for over 1 week with no detectable systemic absorption.

Adult↗
PubMed1988

The effect of cyclosporin A (CsA) treatment on gingival tissue of patients with Behçet's disease.

Gingival biopsies were obtained at various intervals for a period of two years from 12 patients suffering from Behçet's disease who were under a clinical trial of cyclosporin A (CsA) treatment. The levels of nondialyzable hydroxyproline (Hypro) were determined in the medium of the cultured tissues. Histologic examinations were also performed every three months. Correlations between the CsA blood levels and the levels of nondialyzable Hypro indicated a reciprocal relationship, especially at blood levels of CsA higher than 600 ng/ml. Histologic examination of gingival sections from CsA-treated patients showed swelling of the epithelial cells, formation of perinuclear clear zones, widening of intercellular gaps and formation of several basal cell layers. In addition, foci of PAS-positive material were found in both the epithelium and stroma. It is assumed that the gingival enlargement observed in the CsA-treated patients was not due to an increase in tissue collagen but rather to an increase in epithelium combined with an accumulation of noncollagenous extracellular matrix material.

Behcet Syndrome↗
PubMed1988

Treatment of endogenous uveitis with cyclosporine A.

Thirty patients suffering from severe sight-threatening bilateral chronic endogenous uveitis were treated with initial dosages of 10 mg/kg/d of CsA. After 1 month of therapy, all patients but one demonstrated a rapid decrease of the intraocular inflammatory processes along with an arrest of the deterioration of vision. After 1 year (or more) of treatment, most patients still show the same visual acuity achieved after 1 month. During the 3-year span of this study, attempts at tapering off the CsA dosage to less than 5 mg/kg/d induced a temporary flare-up in 20 of the 24 patients followed without interruption for more than 6 months. Nonetheless, control of the intraocular inflammation was finally achieved by 5 mg CsA/kg/d or less in 14 of the 25 patients. In six of these 14 patients the CsA dosage was further tapered to total discontinuation. Two of the six patients showed a rapid reactivation of the intraocular inflammatory processes with a profound decrease in vision within 1 and 3 weeks, respectively. In four patients, control of the intraocular inflammation and preservation of good visual acuity have been observed for a period of up to 18 months.

Behcet Syndrome↗
PubMed1988

Evaluation of conventional therapy versus cyclosporine A in Behçet's syndrome.

When ocular structures are affected in Behçet's syndrome, a rapid loss of vision has been the rule regardless of the type of treatment--corticosteroids, Leukeran, Imuran, colchicine. The objectives of the present study were to compare, in a masked manner, conventional treatment (corticosteroids/Leukeran) to treatment with CsA. Forty patients suffering from Behçet's syndrome with active ocular inflammatory reactions were included in the study. These were randomly assigned to conventional or CsA regimens and were regularly examined by a multidisciplinary group of physicians. The unmasked internist modulated the treatment and recorded systemic manifestations. The masked ophthalmologists recorded the ocular findings without knowledge of the assigned type of treatment. An analysis of the results 3 years after initiation of the study shows that CsA is more effective than conventional therapy in decreasing the active ocular inflammatory processes and arresting the deterioration of visual acuity. Regarding the extraocular symptoms, however, conventional therapy is superior to CsA, especially for the control of skin lesions and arthritis. Side effects were recorded in a much higher incidence among patients receiving CsA. However, tight and constant control of the CsA dosage as performed in this study has, so far, prevented clinical and biochemical nephrotoxic manifestations in patients assigned to this treatment.

Adrenal Cortex Hormones↗
PubMed1980

Interaction of lecithin:cholesterol acyltransferase and cholesteryl ester transfer protein in the transport of cholesteryl ester into sphingomyelin liposomes.

When isolated lecithin:cholesterol acyltransferase was incubated with cholesterol-lecithin liposomes in the presence of apolipoprotein A-1, cholesteryl ester accumulated until a maximal ester/lecithin weight ratio of 0.03 was reached. This was independent of the amount of enzyme present or the proportion of cholesterol relative to lecithin. The inhibition of transferase associated with accumulation of cholesteryl ester was relieved by additional lecithin-cholesterol liposomes but not by addition of sphingomyelin liposomes containing the same proportion of substrate unesterified cholesterol. These results indicate that it is the accumulation of cholesteryl ester product which directly inhibits transferase activity. When isolated cholesteryl ester transfer protein from human plasma was included in the reaction mixture, cholesteryl ester was transported to sphingomyelin-cholesterol liposomes, with associated release of transferase from product inhibition. Cholesteryl ester incorporated directly into the liposomes or synthesized from free cholesterol via the transferase reaction was equally transferred to sphingomyelin acceptor liposomes, indicating that the cholesteryl ester in these particles formed a single miscible pool for transfer.

Apolipoproteins↗
PubMed1978

Lipoprotein lipase of cultured mesenchymal rat heart cells. I. Synthesis, secretion and releasability by heparin.

Cell suspensions prepared from rat hearts were separated by replating into F1, F2 and M cultures, and cultured for 3--11 days. Lipoprotein lipase activity was highest in the F1 cultures which consisted mainly of non-beating, mesenchymal cells. The enzyme activity was released into the medium only after addition of heparin. The release occurred by an initial rapid phase and a continuous slow phase. Both the rapid and the slow release of enzyme activity by heparin were inhibited by about 70% after a 4 h pretreatment with colchicine. Thus, it seems that the vesicular transport is responsible for the translocation of lipoprotein lipase to the cell surface also during the slow process of release. The residual activity in the colchicine treated cultures was higher than in the controls indicating that no inhibition of enzyme synthesis occurred. The slow phase of enzyme release continued also after removal of heparin from the medium but was reduced markedly when protein synthesis was inhibited by cycloheximide. Thus the increase in total enzyme activity encountered after exposure to heparin resulted from stimulation of new enzyme synthesis. The half-time of lipoprotein lipase in the F1 cultures was 35 min and full restoration of enzyme activity was found 60 min after complete removal of cycloheximide from the system. These data indicate that the culture system can be used to study regulation of new enzyme synthesis and its turnover.

Animals↗
PubMed1978

Isolation and characterization of a human serum cholesteryl ester transfer protein.

Human plasma has been shown to contain an apolipoprotein that mediates the transport of cholesteryl ester from high density lipoprotein (HDL) to very low density lipoprotein (VLDL) or low density lipoprotein (LDL). This activity, confined to the density greater than 1.063 g/ml interval, has been isolated from HDL and appears as a single migrating species by anionic or sodium dodecyl sulfate/polyacrylamide gel electrophoresis. It is unreactive to antibodies to the major HDL apolipoproteins. Antibodies prepared against this factor and immobilized on Sepharose remove the capacity of HDL and density greater than 1.21 g/ml fractions as well as whole plasma to transport cholesteryl ester from HDL. The system shows saturation kinetics with respect to plasma LDL and VLDL concentrations, and transport of cholesteryl ester was associated with reciprocal and equimolar back-transport of triglyceride from VLDL and LDL to the HDL fraction. The possible relationship of this apoprotein to apoprotein D is discussed.

Apolipoproteins↗
PubMed1978

A genetic study of Behçet disease in Israel.

The frequency of HLA-B5 in 24 Israeli Behçet disease (BD) patients from various subpopulations was significantly greater than in 615 control individuals (P less than 0.003). The relative risk for a B5 carrier to develop BD was calculated to be 5.0. Six patients were offspring of consanguineous marriages, which is not unexpected in the populations studied. Five of the patients had only one HLA-B antigen, which in four cases was B5. Two of the latter were B5 homozygotes, indicating a possible greater susceptibility. This study confirms the reported association between BD and HLA-B5 in a populationnot previously investigated. Furthermore, these data support the suggestion that B5 is associated with BD in populations deriving from the Mediterranean Basin, the Middle East and Far East.

Adolescent↗
PubMed1978

Very low density lipoprotein. Metabolism of phospholipids, cholesterol, and apolipoprotein C in the isolated perfused rat heart.

The fate of rat plasma very low density lipoprotein (VLDL) constituents was determined in the isolated perfused rat heart. VLDL was labeled with [(14)C]palmitate, (32)P-phospholipids, [(3)H] cholesterol, and (125)I-apolipoprotein C (apoC). Perfusions were performed with an albumin-containing buffer and without plasma. Radioactivity was followed in fractions of d < 1.019, d 1.019-1.04, d 1.04-1.21, and d > 1.21 g/ml, prepared by ultracentrifugation.VLDL triglycerides were progressively hydrolyzed to fatty acids (10-120-min perfusions). Concomitantly, phospholipids, cholesterol (predominantly unesterified), and apoC were removed from the VLDL to all other fractions. About 30-35% of the phosphatidylcholine was hydrolized to lysophosphatidylcholine and was recovered at d > 1.21 g/ml. The phosphatidylcholine-and triglyceride-hydrolyzing activities were confined to membrane supported enzyme(s). The other 60-65% of the phosphatidylcholine was removed unhydrolyzed and was found in fractions of d 1.019-1.04 (10-15%), d 1.04-1.21 (25-30%), and d > 1.21 g/ml (15-20%). [(32)P]Sphingomyelin accumulated at the fraction of d 1.04-1.21 g/ml. Unesterified cholesterol was found in the fraction of d 1.04-1.21 g/ml. ApoC was recovered predominantly in fractions of d 1.04-1.21 (50-60%) and d > 1.21 g/ml (30-40%). Cholesteryl esters were associated with VLDL during the hydrolysis of 50-70% of the triglycerides, but with advanced lipolysis, appeared in higher densities, mainly d 1.019-1.04 g/ml. The fraction of d 1.04-1.21 g/ml, (containing phosphatidylcholine, sphingomyelin, unesterified cholesterol, and apoC) contained by negative staining, many disk-like structures. The study demonstrated that removal of surface constituents (phospholipids, unesterified cholesterol, and apoC) during lipolysis of VLDL is an intrinsic feature of the lipolytic process, and is independent of the presence of plasma. It also indicated that surface constituents may be removed in a particulated form.

Animals↗
PubMed1977

Rat heart in culture as a tool to elucidate the cellular origin of lipoprotein lipase.

Lipoprotein lipase was determined in 5-day old cell cultures derived from hearts of newborn rats. With the help of the preplating method the cells were subdivided into cultures containing predominantly cardiac myocytes and into those composed mainly of mesenchymal cells. Lipoprotein lipase activity, associated with the mesenchymal cells was ten times higher than the activity found in the cultures containing mainly the myogenic cells. It is suggested that the mesenchymal cells are the progenitors of lipoprotein lipase in rat heart.

Animals↗
PubMed1977

Pre- and post-natal development of lipoprotein lipase and hepatic triglyceride hydrolase activity in rat tissues.

The ontogenic development of lipoprotein lipase and liver triglyceride hydrolase was studied in the rat. The enzyme activity measured in extrahepatic tissues fulfilled the criteria of lipoprotein lipase from the onset of measurable activity, i.e. it was inhibited by protamine and 1 M NaCl and showed requirement for serum and heparin for optimal activity. In the liver, measurable amounts of triglyceride hydrolase, active at pH 8.6 were detected 6 days prior to birth. However, till the fourth postnatal day about 50% of this activity was inhibited by NaCl and its sensitivity towards protamine was also higher than that of the enzyme in adult liver. Three patterns of development of enzymic activity were observed in extrahepatic tissues. In the lung, the lipoprotein activity reached the adult values one day prior to birth, while in the kidney only 30% of adult activity were found at birth. A linear increase of enzyme activity was observed in the heart; only 25% of adult activity were detected at birth and 100% were reached only 20 days after birth. The increase in lipoprotein lipase activity in the heart was accompanied by morphological differentiation of cardiocytes and by a progressive development of the capillary bed, which might be related to the pattern of development of enzyme activity in this organ. Adipose tissue lipoprotein lipase activity in inguinal fat fell from values 15 times than adult values between the 4th and 40th postnatal days. The enzyme activity in epididymal fat increased steeply between day 10 and 40, at which time it exceeded the adult values very considerably. These findings indicate that the regulation of the development of lipoprotein lipase activity in extrahepatic tissues is governed by local factors, which can differ even in the same type of tissue, as exemplified by the difference between inguinal and epididymal fat.

Adipose Tissue↗
PubMed1977

Treatment of acute hepatic encephalopathy with L-dopa.

A clinical report of a 30-year-old woman who developed acute hepatic failure in the fifth month of pregnancy is presented. L-dopa administration resulted in a marked improvement in both level of consciousness and electroencephalogram. The literature dealing with L-dopa therapy in hepatic encephalopathy is reviewed.

Adult↗
PubMed1976

Interaction of concanavalin A with membrane-bound and solubilized lipoprotein lipase of rat heart.

Concanavalin A was used to study the configuration of lipoprotein lipase at the surface of capillary endothelium. Incubation of heart homogenates with increasing concentrations of concanavalin A for 5-60 min resulted in inhibition of up to 50% of enzyme activity. The inhibition was related to the concentration of lectin and the time of incubation and was fully reversible by postincubation with alpha-methyl-D-mannoside. Rat hearts were perfused for 5-60 min and lipoprotein lipase activity determined in postheparin perfusates and in the perfused heart. When the lectin was introduced into the perfusate a significant reduction of heparin-releasable enzyme was found after 30 min of perfusion. The missing enzyme could be recovered by postperfusion with alpha-methyl-D-mannoside, but not by addition of the sugar to the perfusate withdrawn from the apparatus. These results suggested binding of lectin to the surface-located enzyme and support for such a binding was obtained by the finding of release of labeled lectin into the perfusate by heparin. Perfusion of hearts with concanavalin A for 60 min resulted also in a fall in nonreleasable lipoprotein lipase. The mechanism of this fall is not due to impairment of enzyme synthesis, as leucine incorporation into protein was not reduced. Since neither perfusion nor postincubation with alpha-methyl-D-mannoside restored enzyme activity, the fall was most probably due to irreversible inhibition. It is concluded that mannose residues of lipoprotein lipase in heart homogenates and at the endothelial surface of heart capillaries are available to interact with a specific lectin. Such an interaction renders the enzyme less releasable by heparin during perfusion and causes a significant inhibition of enzyme activity in homogenates.

Animals↗
PubMed1976

Non-invasive quantitation of corneal copper in hepatolenticular degeneration (Wilson's disease).

The corneal copper content was measured by X-ray excitation spectrometry in two controls and in seven patients with Wilson's disease. Patients who were treated irregularly or not treated at all showed a high corneal copper content. Those who were adequately treated had low levels, comparable to the controls. In one case the corneal copper content declined 45%, after a course of dimercaprol. The corneal copper measured showed no correlation with the slit-lamp appearance of the Kayser-Fleischer ring. It is suggested that non-invasive X-ray excitation spectrometry can provide a fast and reliable method for the early diagnosis of Wilson's disease and for the objective evaluation of the efficacy of the treatment of this disease.

Adolescent↗