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Biomedical subjects

N Katz

Publications and source records attributed to N Katz.

At least 55 records · Page 3Linked to original sources

Cell adhesion molecule expression in murine lupus-like nephritis induced by lipopolysaccharide.

BACKGROUND: Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule (VCAM) are thought to play important roles in leukocyte recruitment to the kidney. We therefore chose to study mesangial cell adhesion molecule expression in vitro, and the role of these molecules in experimental lupus-like nephritis. METHODS AND RESULTS: When cultured murine mesangial cells were stimulated with interferon-gamma (IFgamma) and tumor necrosis factor-alpha (TNFalpha), mRNA levels for ICAM-1 and VCAM markedly increased. These molecules were detected at the cell surface by flow cytometry. Since lipopolysaccharide (LPS) stimulates TNFalpha and IFgamma production in vivo, we treated mice with Streptococcus minnesota LPS in order to study renal adhesion molecule expression. LPS treatment induced mesangial proliferative glomerulonephritis characterized by leukocyte infiltration, and increases in total glomerular cellularity, volume and matrix area. mRNA levels for ICAM-1 and VCAM were increased in the kidneys of LPS-treated versus control mice. ICAM-1 and VCAM molecules were constitutively expressed in renal vascular endothelium. At 3 and 5 weeks, this vascular staining intensified, and some ICAM-1 and VCAM expression was induced in the glomerular mesangium. ICAM-1 and VCAM induction occurred early and correlated in time with leukocyte infiltration. CONCLUSION: Interactions between cell adhesion molecules expressed by intrinsic glomerular cells and infiltrating leukocytes play a role in the initiation of LPS-induced lupus-like nephritis. These observations are potentially relevant to the understanding and treatment of certain types of human glomerulonephritis.

Animals↗

Environmental influences on perceptual and motor skills of children from immigrant Ethiopian families.

The purpose of this study was to examine environmental influences on perceptual and motor skills of children from immigrant Ethiopian families in Israel in comparison with those of Israeli-born children. The subjects were divided into groups based on age (6- to 8-yr.-olds and 10- to 12-yr.-olds) and length of time in Israel. The results of this study show that the perceptual and motor performance of 6- to 8-yr.-old, less recent Ethiopian immigrants is similar to that of the recent Ethiopian immigrants of the same age. A difference exists between those two groups and the Israeli-born children of the same age. In the 10- to 12-yr.-old age group, there is a marked difference between the performance of the two groups of Ethiopian immigrants. The difference between the less recent immigrants and the Israeli-born children is smaller for most tasks; however, the less recent immigrants' performance is still poorer than that of the Israeli children. These results are compatible with those of other studies describing the difficulties encountered by children who had not studied in formal educational settings and those who have had that experience.

Age Factors↗

Correlation of asbestos fiber burdens in fallopian tubes and ovarian tissue.

Evidence suggests an increased risk of ovarian cancer with asbestos exposure. Ovaries and corresponding fallopian tubes were studied by analytic electron microscopy. There was 71.4% agreement between tube and ovary for presence-type of asbestos. The fallopian tube can provide useful information regarding asbestos exposure when no ovarian tissue is available.

Asbestos↗

Functional disability and rehabilitation outcome in right hemisphere damaged patients with and without unilateral spatial neglect.

OBJECTIVE: To evaluate the impact of unilateral spatial neglect (USN) on the rehabilitation outcome and long-term functioning in activities of daily living (ADL) and instrumental ADL (IADL) of right hemisphere damaged (RHD) stroke patients. DESIGN: Assessments of sensory-motor and cognitive impairment and of functional disability were conducted upon admission to rehabilitation, upon discharge from the rehabilitation hospital, and 6 months after discharge, up to a year postonset. SETTING: The Loewenstein Rehabilitation Hospital, which receives patients from all general hospitals in Israel. PATIENTS: Forty consecutive admissions of adult right-handed patients with a first, single, right hemispheric stroke proven by computed tomography. Based on their total score in the Behavioral Inattention Test for neglect, patients were divided into two groups: 19 with neglect (USN+) and 21 without neglect (USN-). OUTCOME MEASURES: Functional Independence Measure, for ADL; The Rabideau Kitchen Evaluation, for IADL. RESULTS: Impairment and disability levels of RHD patients with and without USN were clearly differentiated. Neglect is associated with lower performance on measures of impairment (sensory-motor and cognitive), as well as on measures of disability in ADL and IADL. Differences were significant in all testing periods. The recovery pattern of USN+ patients is slower and more attenuated. In both groups, most improvement occurs in the first 5 months after onset. USN is the major predictor of rehabilitation outcome from admission to follow-up. CONCLUSIONS: The significance of neglect as a major source of stroke-related long-term disability justifies further research efforts to develop appropriate therapeutic modalities for this complex, multifactorial syndrome.

Activities of Daily Living↗

Angiotensinogen T174M and M235T gene polymorphisms are associated with the extent of coronary atherosclerosis.

BACKGROUND: The relations of the angiotensinogen (AGT) T174M and M235T gene polymorphisms to the risk of coronary heart disease (CHD) have been investigated in only a few studies with conflicting results. RESULTS: Therefore, we analysed the relationship of the AGT gene polymorphisms to the presence and extent of CHD in 2250 male Caucasians whose coronary anatomy was defined by means of coronary angiography. The relative frequencies of the T and M alleles of the T174M and of the M235T gene variation did not significantly differ between patients without or with single-, double- or triple-vessel disease and between subjects without or with myocardial infarction (MI). In contrast the mean CHD score--defined by Gensini--was higher within MM homozygotes of the T174M gene variation than within TT genotypes; TM subjects had intermediate values. In M235T genotypes, mean CHD scores were similar in the total sample and in older individuals (> or = 62 years), whereas in younger individuals (< 62 years) a higher CHD score was found within AGT 235 T allele carriers than within MM homozygotes. In younger individuals with high apoAI plasma levels, the mean CHD score was clearly higher within TT homozygotes of the M235T gene variation than within MM genotypes; MT subjects had intermediate values. An interaction between both angiotensinogen gene polymorphisms on the extent of CHD or on the risk of non-fatal MI were not observed when the M allele of AGT T174M was combined either with the T allele or the TT genotype of M235T. CONCLUSIONS: The present study strengthens the hypothesis of an association of both angiotensinogen gene polymorphisms with the extent of coronary heart disease.

Alleles↗

The p22 phox A640G gene polymorphism but not the C242T gene variation is associated with coronary heart disease in younger individuals.

BACKGROUND: Most recently, evidence has been presented that the NADH/NADPH oxidase p22 phox C242T, but not the A640G gene polymorphism is associated with a reduced risk of coronary artery disease (CAD). METHODS AND RESULTS: We analysed the relationships of both p22 phox gene polymorphisms to CAD in 2205 male Caucasians whose coronary anatomy was defined by means of coronary angiography. In the total population and in high and low risk groups the relative frequencies of the C242T alleles were essentially the same in patients without or with CAD and in individuals without or with myocardial infarction. In contrast, the G allele of the A640G polymorphism was significantly more frequent in subjects without CAD than in patients with CAD (Odds ratio (OR) 0.74 (0.57-0.98); P = 0.038 in multiple logistic regression (MLR)). Correspondingly, the AA genotype of A640G was preferentially found in patients with CAD. These associations did not disappear when the analyses were corrected for multiple comparisons for other gene polymorphisms (ACE I/D gene variation, angiotensinogen T174M and M235T gene polymorphisms, AT1 receptor gene variation, phox C242T gene polymorphism, paraoxonase PON54 and PON191 gene variations) (2p = 0.01 in MLR for the presence of CAD; 2p = 0.039 in multiple regression for the extent of CAD). The association of the A640G gene variation with the presence and extent of CAD was not only identified in the total sample, but was even stronger in various high risk subpopulations of younger individuals (e.g. with hypertension with or without increased apolipoprotein B plasma levels). CONCLUSIONS: Our observations allow the assumption that the p22 phox A640G gene polymorphism is independently associated with the presence and extent of coronary artery disease.

Adenine↗

Detection of myocardial injury during transvenous implantation of automatic cardioverter-defibrillators.

OBJECTIVES: The present study was designed to assess the extent of myocardial injury in patients undergoing transvenous implantation of an automatic implantable cardioverter-defibrillator (ICD) using cardiac troponin I (cTNI), which is a highly specific marker of structural cardiac injury. BACKGROUND: During ICD implantation, repetitive induction and termination of ventricular fibrillation (VF) via endocardial direct current shocks is required to demonstrate the correct function of the device. Transthoracic electrical shocks can cause myocardial cell injury. METHODS: Measurements of total creatine kinase (CK), CK-MB, myoglobin, cardiac troponin T (cTNT) and cTNI were obtained before and after ICD implantation in 49 consecutive patients. Blood samples were drawn before and 2, 4, 8, and 24 h after implantation. RESULTS: Elevations of CK, CK-MB, myoglobin, cTNT and cTNI above cut-off level were found in 25%, 6%, 76%, 37% and 14% of patients, respectively, with peak cTNI concentrations ranging from 1.7 to 5.5 ng/ml. Cumulative defibrillation energy (DFE), mean DFE, cumulative VF time, number of shocks as well as prior myocardial infarction (MI) were found to be significantly related to a rise of cTNI. Mean DFE > or = 18 J and a recent MI were identified as strong risk factors for cTNI rise. CONCLUSIONS: During transvenous ICD implantation myocardial injury as assessed by cTNI rise occurs in about 14% of the patients. Peak cTNI concentrations are only minimally elevated reflecting subtle myocardial cell damage. Patients with a recent MI and a mean DFE > or = 18 J seem to be prone to cTNI rise.

Biomarkers↗

The TT genotype of the methylenetetrahydrofolate reductase C677T gene polymorphism is associated with the extent of coronary atherosclerosis in patients at high risk for coronary artery disease.

BACKGROUND: There are conflicting results on the relationship of N5,N10-methylenetetrahydrofolate reductase C677T gene variation in coronary artery disease and myocardial infarction. METHODS AND RESULTS: We analysed this gene variation in 2453 male Caucasians whose coronary anatomy was defined by coronary angiography. In the total sample, the C677T gene polymorphism was not associated with the presence or the extent of coronary artery disease (defined by the degree of vessel disease or by the coronary heart disease score according to Gensini). However, after excluding individuals with low risk profiles, an association between the C677T TT genotype and the Gensini score was found. This observation applies only to individuals (i) with high glucose levels, (ii) with low apolipoprotein Al/apolipoprotein B ratios, (iii) with low apolipoprotein Al/apolipoprotein B ratios and high lipoprotein (a) levels and (iv) with low apolipoprotein Al/apolipoprotein B ratios and high glucose concentrations. In patients with high glucose levels, the paraoxonase 191 A/B gene variation presupposed whether differences in Gensini scores between C677T C allele carriers and TT homozygotes became apparent, since only in paraoxonase 191 AA homoxygotes, but not in paraoxonase 191 B allele carriers, did C677T TT homozygotes have clearly higher Gensini scores than C allele carriers (two-way interaction; P = 0.013). The MTHFR C677T gene polymorphism was not associated with non-fatal myocardial infarction. CONCLUSION: The present study extends previous observations by the finding that carriers of the N5,N10-methylenetetrahydrofolate reductase C677T TT genotype with various coronary high risk profiles had clearly higher coronary heart disease scores than individuals with at least one C677T C allele.

Adult↗

Accuracy of methemoglobin measurements: comparison of six different commercial devices and one manual method.

OBJECTIVE: During nitric oxide inhalation, methemoglobinemia needs to be monitored. We compared six commercially available instruments and one manual method for methemoglobin measurements. In addition, we studied whether and to what degree methylene blue interferes with methemoglobin measurements. DESIGN: In vitro methodologic study. SETTING: Research laboratory in a university hospital. PATIENTS: Five healthy volunteers from whom red blood cells were obtained. INTERVENTIONS: Methemoglobinemia was generated in a red blood cell suspension by nitric oxide; methemoglobin was measured with six commercial instruments and one manual photometric method to calculate variation coefficients and to determine the differences between the devices. Methemoglobin was measured with and without the addition of methylene blue with two instruments. Measurements were performed immediately after the addition of methylene blue. MEASUREMENTS AND MAIN RESULTS: All six commercially available instruments had variation coefficients of <0.1 at methemoglobin concentrations of 5%, whereas the manual photometric method did not reach a variation coefficient of <0.1 at 8% of methemoglobin. Apart from two devices that measured slightly but significantly higher methemoglobin levels, all instruments measured similar values of methemoglobin when the same samples were determined simultaneously. Higher concentrations of methylene blue (10, 40, 100 microM) reduced substantially the apparent concentrations of methemoglobin. Interference by methylene blue was most pronounced at low methemoglobin levels. CONCLUSIONS: With some limitations, all commercial instruments that were tested performed adequately for the monitoring of methemoglobinemia. Methylene blue interferes with the methemoglobin measurements in a dose-dependent manner.

Adult↗

Intramuscular flunitrazepam versus intramuscular haloperidol in the emergency treatment of aggressive psychotic behavior.

OBJECTIVE: The authors examined the efficacy of intramuscular flunitrazepam compared with intramuscular haloperidol for the immediate control of agitated or aggressive behavior in acutely psychotic patients. METHOD: Twenty-eight actively psychotic inpatients, aged 20-60 years, who were under treatment with neuroleptic agents were selected for the study. Each was randomly assigned on a double-blind basis to receive either 5 mg i.m. of haloperidol (N=13) or 1 mg i.m. of flunitrazepam (N=15) during an aggressive event. Verbal and physical aggression was measured over time with the Overt Aggression Scale. Patients were also rated with the Brief Psychiatric Rating Scale and the Clinical Global Impression scale. RESULTS: Both flunitrazepam and haloperidol exhibited acute antiaggressive activity. This beneficial effect, as assessed by the Overt Aggression Scale, was obtained within 30 minutes. CONCLUSIONS: Intramuscular flunitrazepam may serve as a convenient, rapid, safe, and effective adjunct to neuroleptics in reducing aggressive behavior in emergency psychiatric settings.

Acute Disease↗

The factor II G20210A and factor V G1691A gene transitions and coronary heart disease.

BACKGROUND: G to A transitions at nucleotide position 20210 of the factor II (Fll) gene and at 1691 of the factor V (FV) gene have been shown to be associated with an increased risk of venous thrombosis. Since it is still unclear whether both gene variations are also related to an increased risk of coronary heart disease (CHD), we studied the relation of both gene variations to coronary artery disease (CAD) and myocardial infarction (MI) in a sample of 2210 male individuals whose coronary anatomy were defined by coronary angiography. RESULTS: In the total sample, the FII G20210A gene variation was not associated with the presence or the extent of CAD, the latter defined either by the degree of vessel disease or by a CHD score according to Gensini. However, individuals with unfavourable lipid profiles showed pronounced differences in CHD scores between GA heterozygotes and GG homozygotes: this observation applied in particular to younger patients (<62 years; mean age of total sample) who simultaneously had low apoAI/apoB ratios (< 1.19, mean value) and high Lp(a) plasma levels (>28 mg/dl; mean value). In addition, in subjects without acetylsalicylic acid treatment GA heterozygotes had clearly higher CHD scores than AA genotypes. Further restriction to smokers, to subjects with high fibrinogen plasma levels (>3.47 g/l; mean value) or to patients with high glucose concentrations (>112 mg/dl; mean value) tended to increase the difference in CHD score between FII G20210A genotypes. An association of the FII G20210A gene variation with non-fatal MI was not observed. In the total sample and in high and low risk subpopulations, an association of the FV G1691A gene variation was not detected neither with presence and extent of CAD or with nonfatal MI. CONCLUSION: The importance of the factor II G20210A gene variation for CHD may be restricted to individuals with major cardiovascular risk factors. In addition, the present study did not strengthen the hypothesis of the factor V G 1691 A transition as a risk factor of coronary heart disease neither in the total sample nor in subgroups of individuals who were at high or low risk of CHD.

Adult↗

The 4G4G genotype of the plasminogen activator inhibitor 4G/5G gene polymorphism is associated with coronary atherosclerosis in patients at high risk for this disease.

BACKGROUND: Disturbances in fibrinolytic activity, such as increase in plasminogen activator inhibitor (PAI) activity, have been linked with an increased risk for coronary artery disease (CAD) and myocardial infarction (MI). Since 4G4G homozygotes of an insertion/deletion (4G/5G) gene variation in the promoter of PAI-I have been shown to have increased levels of PAI-I, we analysed the relation of this gene polymorphism to CAD and MI in a population of 2565 participants who underwent coronary angiography for diagnostic purposes. RESULTS: In the total sample, the PAI-I 4G/4G genotype was associated with the presence, but not with the extent of CAD. However, in a subgroup of former and present smokers (n = 1782) or of individuals with a BMI above the mean value of 26.9 kg x m(-2) (n = 1269), the PAI-I 4G4G genotype was not only associated with the presence, but also with the extent of CAD, defined either by the number of diseased vessels or by the CHD score according to Gensini. This observation also applied to other high-risk groups of individuals with high BMI and hypertension (n = 869), of subjects with high fibrinogen plasma levels (>3.53 g x l(-1), mean value) and hypertension (n = 599) and of former and present smokers with high fibrinogen and hypertension (n = 452). An association of the gene variation with MI was not detected. CONCLUSIONS: The present data indicate that the 4G/4G genotype of the PAI-I gene polymorphism is an independent risk factor for coronary artery disease and that the additional presence of major cardiovascular risk factors accelerates the risk for this disease.

Aged↗

Elevated awaking thresholds during sleep: characteristics of chronic war-related posttraumatic stress disorder patients.

BACKGROUND: Sleep disturbances are one of the hallmarks of posttraumatic stress disorder (PTSD); however, sleep laboratory studies have provided inconsistent evidence of the existence of objective sleep disturbances in PTSD patients. Reports that awaking thresholds from sleep in war-related PTSD patients were significantly elevated compared to normals are discordant with complaints of insomnia. The present study investigated the relationship between awaking threshold from REM sleep in war-related PTSD patients and their dream recall, dream content, and clinical condition. METHODS: After informed consent was obtained from 12 PTSD patients and 12 controls, they were investigated by polysomnographic recordings for 4 nights. Awaking thresholds to clicks were determined during 1 night, and dreams were collected during 2 nights. Patients' symptoms were assessed by the Zung and Beck depression scales, Impact of Events Scale, State and Trait Anxiety, and Symptom Check List questionnaires. RESULTS: Although there were no significant differences between sleep data of patients and controls, PTSD patients had significantly higher awaking thresholds. Awaking thresholds were significantly positively related to depression and anxiety scores. Patients' dreams were significantly more aggressive and hostile, and in 6 patients they included explicit war-related contents. The severity of the clinical picture was significantly related to the dreams' scores of aggression-hostility, and to sleep quality variables. CONCLUSIONS: Elevated awaking thresholds from sleep are a characteristic finding in chronic war-related PTSD patients, which may help to explain the diverse sleep laboratory findings in this syndrome.

Adult↗

Bone age in adolescents with schizophrenia and obsessive-compulsive disorder.

The bone age (BA), height and weight of 20 adolescents with schizophrenia and 21 matched adolescents with obsessive-compulsive disorder (COD) were measured. The BA of the schizophrenic patients was significantly higher than their chronological age (CA)(p < 0.05), while the OCD subjects' BA was non-significantly lower than their CA. In addition, the difference between CA and BA (delta ages) in the schizophrenic adolescents was significantly different from the delta ages of the OCD adolescents (p , 0.05). Gender did not significantly affect BA or delta ages. A positive correlation (r = 0.5, p < 0.01) was obtained between CA and delta ages in the schizophrenic patients but not in the OCD patients. Both groups were within the normal range of weight and height percentiles.

Adolescent↗

Transcriptional activation of the haem oxygenase-1 gene by cGMP via a cAMP response element/activator protein-1 element in primary cultures of rat hepatocytes.

The expression of the rate-limiting enzyme of haem degradation, haem oxygenase-1 (HO-1), can be induced by various stimuli, including lipopolysaccharide, tumour necrosis factor alpha and NO. The NO signal can be transmitted by cGMP, therefore this study was aimed at testing the activation of the HO-1 gene by cGMP. In primary cultures of rat hepatocytes, both HO-1 mRNA and protein were induced by the NO donor sodium nitroprusside and 8-bromo-cGMP. The HO-1 mRNA induction by cGMP was prevented by the specific protein kinase G inhibitor KT5823. The cGMP-dependent HO-1 mRNA induction was dose-dependent and transcriptionally regulated, as determined by studies with actinomycin D and a nuclear run-on assay. Cycloheximide lowered the cGMP-dependent induction of HO-1 mRNA to about one half. Luciferase reporter constructs driven by about 800 bp of the 5'-flanking region of the rat HO-1 gene were transiently transfected into primary rat hepatocytes; 8-bromo-cGMP caused a 6-fold induction, which was obliterated by deletion and mutation of the cAMP response element/activator protein-1 (CRE/AP-1) (-665/-654) site. Thus HO-1 induction by cGMP appears to be stimulated by the protein kinase G pathway and may be mediated mainly via a CRE/AP-1 element in the rat HO-1 promoter.

Alkaloids↗

[Cytogenetic study of thyroid patients treated with external irradiation or radioiodine].

Where clinically permitted, either external irradiation or radioiodine therapy is usually recommended for the treatment of differentiated thyroid cancer patients. This paper describes an attempt to clarify the radiation burden and the distribution of radiation doses on the lymphocytes in consequence of these two therapeutic modalities, and the circumstances of the applicability of biological dosimetry. Thyrotoxic patients with intact thyroid glands underwent 131I therapy were also analysed for this purpose. An analysis was made of the extent to which exposure to local neck irradiation (50 Gy) or radioiodine therapy (1734-2600 MBq) causes chromosomal aberrations in the lymphocytes of thyroid disease patients after total or subtotal thyroidectomy, or thyrotoxic patients with intact thyroid glands (185-595 MBq). The irradiated volume of lymphatic tissues played the most important role in the formation of chromosomal aberrations. External irradiation caused 10-times more aberrant cells than 131I therapy did in cancer patients. In thyrotoxic patients the lower therapy doses of radioiodine caused a significantly higher frequency of aberrations than that observed in thyroid cancer patients. Selective radiosensitivity of lymphocytes was supported by the analysis of the Poisson distribution of aberrations, which suggested a homogeneous dose distribution only in 131I-treated and thyroidectomized cancer patients. In conclusion, we suggest that the results of studies of the genetic alterations in the lymphocytes exposed to radioiodine, under well-defined circumstances should not be ignored before the mode of radiation treatment is chosen. On the other hand, in the modelling of accidental environmental radioiodine exposure, only thyrotoxic patients with an intact thyroid gland and heterogeneous dose-distribution are a suitable group.

Adult↗