PubMed Health⌕ Search

Biomedical subjects

T Kurtz

Publications and source records attributed to T Kurtz.

At least 19 recordsLinked to original sources
PubMed2001

Defective fatty acid uptake in the spontaneously hypertensive rat is a primary determinant of altered glucose metabolism, hyperinsulinemia, and myocardial hypertrophy.

Genetic linkage studies implicated deficiency of CD36, a membrane fatty acid (FA) transporter, in the hypertriglyceridemia and hyperinsulinemia of the spontaneously hypertensive rat (SHR). In this study we determined whether loss of CD36 function in FA uptake is a primary determinant of the SHR phenotype. In vivo, tissue distribution of iodinated, poorly oxidized beta-methyliodophenyl pentadecanoic acid (BMIPP) was examined 2 h after its intravenous injection. Fatty acid transport was also measured in vitro over 20 to 120 s in isolated adipocytes and cardiomyocytes obtained from SHR and from a congenic line (SHRchr4) that incorporates a piece of chromosome 4 containing wild-type CD36. SHR heart and adipose tissue exhibited defects in FA uptake and in conversion of diglycerides to triglycerides that are similar to those observed in the CD36 null mouse. However, a key difference in SHR tissues is that fatty acid oxidation is much more severely impaired than fatty acid esterification, which may underlie the 4-5-fold accumulation of free BMIPP measured in SHR muscle. Studies with isolated adipocytes and cardiomyocytes directly confirmed both the defect in FA transport and the fact that it is underestimated by BMIPP. Heart, oxidative muscle, and adipose tissue in the SHR exhibited a large increase in glucose uptake measured in vivo using [(18)F]fluorodeoxyglucose. Supplementation of the diet with short-chain fatty acids, which do not require CD36-facilitated transport, eliminated the increase in glucose uptake, the hyperinsulinemia, and the heart hypertrophy in the SHR. This indicated that lack of metabolic energy consequent to deficient FA uptake is the primary defect responsible for these abnormalities. Hypertension was not alleviated by the supplemented diet suggesting it is unrelated to fuel supply and any contribution of CD36 deficiency to this trait may be more complex to determine. It may be worth exploring whether short-chain FA supplementation can reverse some of the deleterious effects of CD36 deficiency in humans, which may include hypertrophic cardiomyopathy.

Adipose Tissue↗
PubMed1999

The impact of nutritional status on the outcome of lung volume reduction surgery: a prospective study.

OBJECTIVES: To study the incidence and clinical significance of nutritional deficiencies in patients with emphysema undergoing lung volume reduction surgery (LVRS). DESIGN: Prospective observational study. SETTING: University-based teaching hospital. PATIENTS: Fifty-one consecutive patients with end-stage emphysema undergoing video-assisted thoracoscopic surgery for LVRS. INTERVENTIONS: All patients had their body mass index (BMI) and serum nutritional indexes (albumin, transferrin, total protein, cholesterol) measured preoperatively and postoperatively. Various clinical parameters were also compared between two groups. RESULTS: The BMI was normal in 24 patients (47%), and 27 patients (53%) had a below normal BMI. A preoperative analysis of the serum nutritional indexes revealed no clinically significant differences between the two groups, but postoperative levels were significantly lower in the low BMI group. Anthropometric measurements supported the designation of nutritional status by BMI. Clinically, 26% of the patients in the low BMI group required prolonged ventilatory support (> 24 h), compared to only 4% of the patients with a normal BMI. The hospital length of stay (LOS) also differed, averaging 15.9 days in the low BMI group, compared to an average of 11.8 days in the normal BMI group. CONCLUSION: Approximately 50% of patients undergoing LVRS for emphysema have a deficient nutritional status identifiable by BMI, but not by standard nutritional indexes. This impaired nutritional status is associated with increased morbidity following LVRS. We suggest that BMI is an accurate determinant of nutritional status in this patient population, and we speculate that preoperative repletion of nutritional deficiencies may decrease hospital morbidity, hospital LOS, and overall costs in the malnourished population undergoing LVRS.

Aged↗
PubMed1995

A genetic linkage map of the laboratory rat, Rattus norvegicus.

We report the construction of the first complete genetic linkage map of the laboratory rat. By testing 1171 simple sequence length polymorphisms (SSLPs), we have identified 432 markers that show polymorphisms between the SHR and BN rat strains and mapped them in a single (SHR x BN) F2 intercross. The loci define 21 large linkage groups corresponding to the 21 rat chromosomes, together with a pair of nearby markers on chromosome 9 that are not linked to the rest of the map. Because 99.5% of the markers fall into one of the 21 large linkage groups, the maps appear to cover the vast majority of the rat genome. The availability of the map should facilitate whole genome scans for genes underlying qualitative and quantitative traits relevant to mammalian physiology and pathobiology.

Animals↗
PubMed1994

Frequency of a deletion polymorphism in the gene for angiotensin converting enzyme is increased in African-Americans with hypertension.

In white populations, a deletion polymorphism in the gene for angiotensin converting enzyme (ACE) appears to be associated with increased risk for myocardial infarction but not for hypertension. In a population-association study in African-Americans, we compared the frequency of the ACE deletion polymorphism in subjects with hypertension versus those with normal blood pressure. The frequency of the ACE deletion allele was greater in African-Americans with hypertension than in those with normal blood pressure (P < 0.05). These findings raise the possibility that in some patient subgroups, sequence variation in or near the ACE gene may contribute to the risk for hypertension.

Adult↗
PubMed1992

Assignment of rat linkage group V to chromosome 19 by single-strand conformation polymorphism analysis of somatic cell hybrids.

The rat provides a number of important models of human genetic disease; however, the rat genetic map has not been extensively developed. Although most rat chromosomes carry several gene assignments, some major linkage groups (LG) remain to be mapped. To determine the chromosome location of the largest unmapped linkage group in the rat (LG V containing multiple carboxylesterase loci), we used single-strand conformation polymorphism analysis to identify the rat esterase-10 gene in a panel of rat x mouse somatic cell hybrids. We found that the carboxylesterase gene family and hence LG V are located on rat chromosome 19. We have also confirmed the assignment of the angiotensinogen gene to rat chromosome 19 and have used a large set of recombinant inbred strains to map two anonymous variable number of tandem repeat (VNTR) markers to this chromosome. The current findings bring the total number of genes assigned to rat chromosome 19 from 3 to 19 and provide further evidence of substantial homology between this chromosome and chromosome 8 in the mouse.

Angiotensinogen↗
PubMed1991

The rat renin gene: assignment to chromosome 13 and linkage to the regulation of blood pressure.

It has recently been suggested that in the rat, sequence variation in the renin gene or closely linked genes may have the capacity to affect blood pressure and contribute to the pathogenesis of hypertension. To map the chromosomal location of the rat renin gene and to investigate its relationship to the inheritance of increased blood pressure, we studied a panel of rat x mouse somatic cell hybrids and a large set of recombinant inbred (RI) strains derived from spontaneously hypertensive rats (SHR) and normotensive Brown-Norway (BN) rats. We have found that in the rat, the renin gene is located on chromosome 13 and that it belongs to a conserved synteny group located on chromosome 1 in man and mouse. We have also found the median blood pressure of the RI strains that inherited the renin allele of the SHR to be greater than that of the RI strains that inherited the renin allele of the normotensive BN rat. These findings, together with the results of previous studies, suggest that in the rat, sequence variation in the renin gene, or in genes linked to the renin locus on chromosome 13, may have the capacity to affect blood pressure.

Animals↗
PubMed1990

[Arterial thrombotic complications in Crohn's disease].

In a series of 230 observations of Crohn's disease, the authors describe 4 cases of arterial thrombosis; two of them involving cerebral arteries. These complications occurred in young women without any notable risk factor for atheroma. All patients had highly active Crohn's disease when arterial thrombosis occurred: two of them had several episodes of thrombosis and three, extraintestinal manifestations. As the arterial thromboses are often severe, rarely foreseeable and the venous thromboses frequent, the point is whether to use anticoagulants. When Crohn's disease is highly active, but only if there are no hemorrhagic lesions, anticoagulants at prophylactic doses may be recommended. How to define more exactly a high risk thromboses population deserves further investigation.

Adult↗
PubMed1989

Regulation of hepatic inorganic phosphate and ATP in response to fructose loading: an in vivo 31P-NMR study.

Fructose loading results in hepatic accumulation of fructose 1-phosphate (Fru1 P). The goals of the present experiments were: first, to distinguish between ATP, intracellular inorganic phosphate (Pi), and extracellular Pi as sources of phosphate for the phosphorylation of fructose, and second, to examine the influence of ATP and Fru1 P on movement of phosphate into and out of these three pools. To achieve these goals, 31P-NMR was used to monitor the response of hepatic ATP, Pi and Fru1 P to two consecutive injections of fructose. The first was administered with ATP at the control level, and the second, 1 h after the first, with ATP at 65% of the control level. Changes in intra- and extracellular Pi were distinguished by correlating measurements of total NMR-detectable phosphorus and NMR-detectable Pi with measurements of plasma Pi. The initial fructose injection resulted in rapid accumulation of Fru1 P, small decreases in plasma and NMR-detectable Pi and a dramatic decrease in ATP. Total NMR-detectable phosphorus did not change, suggesting that phosphate did not enter or leave the liver. Therefore, accumulation of Fru1 P was initially balanced by an equivalent decrease in ATP, without large changes in Pi. Following the second injection, when ATP was at 65% of control. Fru1 P accumulated at approximately the same rate and to the same level as achieved following the first injection. There was little further change in ATP and a marked decrease in NMR-detectable Pi, while plasma Pi was higher than after the first injection. Therefore the greater decrease in NMR-detectable Pi following the second injection represented a significant decrease in intracellular Pi. Return of Fru1 P to control coincided with a dramatic increase in plasma Pi, and a decrease in total NMR-detectable phosphate. This suggests that phosphate released from Fru1 P entered the extracellular space. These data suggest the mechanisms by which intracellular Pi is regulated. When sufficient ATP is available, ATP hydrolysis supplies phosphate for the synthesis of Fru1 P, and prevents a significant decrease in intracellular Pi. When ATP is reduced, accumulation of Fru1 P depletes intracellular Pi. Therefore, decreased availability of ATP correlates with increased utilization of intracellular Pi. When Fru1 P returns to control, the increase in intracellular Pi is limited by release of Pi into the plasma.

Adenosine Triphosphate↗
PubMed1988

Prolonged continuous versus intermittent oral acyclovir treatment in normal adults with frequently recurring genital herpes simplex virus infection.

In Year 1 of this two-year trial, patients with six or more genital herpes recurrences in the past year received suppressive treatment with either acyclovir, 400 mg, or placebo, orally twice daily for one year, and physician-documented recurrences were treated with open-labeled acyclovir, 200 mg, orally five times per day for five days (acute treatment). In Year 2, patients received open-labeled acyclovir treatment either with daily suppressive therapy or intermittent acute therapy. Among 683 patients who completed two years of treatment, 348 received continuous suppressive treatment for two years, 276 received acute treatment in Year 1 and suppressive treatment in Year 2, 24 received suppressive treatment in Year 1 and acute treatment in Year 2, and 35 received acute treatment for two years. Patient groups receiving intermittent acute acyclovir treatment experienced means of 7.0 to 12.6 recurrences/year during treatment as compared with 1.4 to 1.9 recurrences/year among groups receiving continuous suppressive treatment. No patients who received acute treatment remained recurrence-free for two years as compared with 29 percent of patients receiving continuous acyclovir suppression for two years. There was no evidence of cumulative toxicity detected by clinical, hematologic, or blood chemistry evaluations performed monthly in Year 1 and quarterly in Year 2. Suppressive oral acyclovir therapy remained effective and well-tolerated in this two-year trial.

Acyclovir↗
PubMed1986

[Long-term course of syphilitic aortic insufficiency with ostial stenosis following surgical treatment].

Syphilitic aortic insufficiency and coronary ostial stenosis is a rare condition. It was diagnosed in 8 patients referred for surgery. The infection, acknowledged in 3 cases, was contracted over 15 years prior to admission! The operative indication was aortic valve replacement in 6 cases (Stage II to IV dyspnoea) and coronary insufficiency in 2 cases (Stage III angina pectoris). Two cases of ostial stenosis were not identified at coronary angiography, illustrating the potential diagnostic pitfall of a disease which is often unrecognised nowadays. Preoperative echocardiography of the left main coronary artery, especially its intra-aortic segment, may be of value but was not performed in these old cases. Surgery consisted in aortic valve replacement and coronary revascularisation by decortication of the ostia or coronary bypass (1 case). The evolution was excellent in the 6 survivors, especially with respect to the anginal syndrome which was completely cured without associated treatment. A protocol of echocardiographic surveillance of the left main coronary artery has been instituted in these patients to detect any late postoperative changes after ostial decortication.

Aged↗
PubMed1985

[Emboligenic abscess of the aortic ring disclosing gonococcal endocarditis. Value of echocardiography].

Echocardiography has become a valuable diagnostic modality in bacterial endocarditis and of even more importance in following the subsequent course of the infection while on medical therapy. It can play an extremely important role in certain clinical circumstances, even before blood culture results are available or hemodynamic or auscultatory abnormalities appear. Nevertheless, in spite of this usefulness, the limitations of echocardiography should be recognized. The examination lacks absolute specificity and sensitivity which could result in inaccurate or delayed information in diagnosing a lesion or in recognizing local or regional complications. These advantages and limitations are well illustrated in an unusual case due to Neisseria gonorrhoeae, a causative agent whose incidence may increase over the years to come.

Abscess↗