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Biomedical subjects

S Daniel

Publications and source records attributed to S Daniel.

At least 73 records · Page 4Linked to original sources
PubMed1996

Quantitative EEG in frontal lobe dementia.

A study on quantitative EEG in 14 patients with frontal lobe dementia (FLD), 14 patients with Alzheimer's disease (AD), and 14 healthy controls was conducted using a complete set of EEG parameters: band power, coherence and fractal dimension. Contrary to earlier studies, we observed higher theta power and sagittal interactions in higher frequency bands in the FLD than in the control group. Lateral interactions of coherence and two indices of fractal dimension were lower in FLD than in controls. There was greater electrophysiological resemblance between the control group and FLD than between any of these groups and AD. This was documented by the results of a discriminant analysis which led to a correct overall classification of 66% of the subjects with misclassifications occurring primarily between control and FLD group.

Analysis of Variance↗
PubMed1996

[Alzheimer dementia and normal aging. Clinical, neuroradiologic, neurophysiologic and molecular biology follow-up data].

A total of 30 patients with clinically diagnosed Alzheimer's disease and 55 healthy, age-approximated controls were followed up over a 2-year period to compare the course of functional and cognitive impairment, quantitative morphological and functional brain changes. No remarkable changes were observed within the control group in any of these modalities. There were significant differences between patients and controls at the first examination: Mini-Mental State Examination (MMSE), 16.1 +/- 7.3 compared with 28.7 +/- 1.4; left lateral ventricle 2.7 +/- 1.1% versus 1.6 +/- 0.7% of the total intracranial volume; right lateral ventricle 2.7 +/- 1.4% versus 1.4 +/- 0.4%; absolute delta-power 1.1 +/- 0.3 versus 0.9 +/- 0.2 microV2; and absolute theta-power 1.1 +/- 0.3 versus 0.8 +/- 0.2 microV2 (means +/- standard deviation). In the patient group, scores on the Blessed dementia rating scale deteriorated from 10.6 +/- 6.1 to 17.9 +/- 9.6; the MMSE decreased by 8.0 +/- 3.7; the left lateral ventricle volume increased by 0.9 +/- 0.7%, the right by 0.9 +/- 0.7% of the total intracranial volume; absolute delta-power increased by 0.2 +/- 0.4 microV2 and theta-power by 0.1 +/- 0.3 microV2. We could not confirm a relationship between age, age at onset or apolipoprotein E4 gene dose and the rate of clinical change. High initial Blessed dementia scores were correlated with more severe ventricular enlargement, and delta-theta increase during the follow-up period. High initial theta-power predicted more severe functional and cognitive deterioration. To our knowledge, this is the first longitudinal study reporting quantitative clinical, morphological and EEG-changes measured in two points in time in patients and non-demented controls.

Aged↗
PubMed1996

Sixteen weeks of hexarelin therapy in aged dogs: effects on the somatotropic axis, muscle morphology, and bone metabolism.

Hexarelin (HEXA; 500 micrograms/kg/die, s.c.) was administered for 16 weeks to six old beagle dogs. The treatment consisted of three on-drug periods spaced by two off-drug periods. During each on period, the growth hormone (GH) peak response to HEXA initially increased and then dropped to pretreatment values. Each time, a wash-out interval restored the same pattern of GH responsiveness. HEXA significantly augmented the indices of spontaneous pulsatility of GH, but plasma insulin-like growth factor I levels did not change during treatment. HEXA apparently reduced bone resorption since it significantly decreased the urinary concentration of lysylpyridinoline, a bone matrix component. Bone formation apparently was not affected since unchanged levels of alkaline phosphatase were recorded. In three of six old dogs, HEXA induced an improvement of some morphological and biochemical muscular indices, evaluated in muscle specimens that, instead, remained unchanged in a group of young untreated controls. These findings indicate that HEXA effectively releases GH and primes the pituitary of old dogs, and strengthen the view that in aging, GH secretion may be restored by pharmacological means. It would also appear that HEXA-induced GH release improves some indices of body composition in old dogs.

Animals↗
PubMed1996

First-time suicide attempters, repeat attempters, and previous attempters on an adolescent inpatient psychiatry unit.

OBJECTIVE: To compare clinical characteristics of hospitalized adolescents who (1) have recently made their first suicide attempt, (2) have recently made a second or subsequent attempt, (3) have made previous but no recent attempts, or (4) have never made an attempt. METHOD: Semistructured psychiatric diagnostic interviews were used to determine history of recent and previous suicidal behavior among 225 consecutively admitted adolescents to an inpatient psychiatric facility. Twenty-seven first-time attempters, 32 repeat attempters, and 40 previously suicidal youths were compared with 126 nonsuicidal youths in terms of severity of self-reported depressive symptoms, state anxiety, trait anxiety, state anger, and trait anger. RESULTS: Repeat attempters and previous attempters both reported more depressive symptomatology and trait anxiety than did nonsuicidal youths. In addition, youths with a previous history of suicide attempts, but no recent attempts, evidenced more trait anger than all other groups. First-time suicide attempters reported levels of distress that were intermediate to the other groups. CONCLUSIONS: Repeat attempters and previous attempters in hospital settings both report more distress than do nonsuicidal youths. Interventions should focus not only on resolution of immediate crises, but also on youths' ability to cope with ongoing difficulties that engender depression and chronic anxiety.

Adaptation, Psychological↗
PubMed1996

Linkage disequilibrium between HLA class II (DR, DQ, DP) and antigen processing (LMP, TAP, DM) genes of the major histocompatibility complex.

TAP, LMP and DM genes map within the major histocompatibility complex (MHC) class II region between the DQB1 and DPB1 loci, and are involved in the processing of peptides bound to HLA class I or class II molecules. In order to determine the various linkage disequilibria existing between these genes and HLA class II genes, we have analyzed TAP1, TAP2, LMP2, DMA, DMB, DRB1, DQA1, DQB1 and DPB1 polymorphisms in 162 unrelated healthy Caucasian individuals. Many positive or negative associations were observed between alleles at these loci, such as between DR/DQ and TAP2, DM or LMP, between DP and DMB, and between TAP2 and DM, TAP2 and LMP. Conversely, no linkage disequilibrium was detected between some closely related genes (DR/DQ and TAP1, TAP1 and TAP2, LMP2 and DM), in agreement with the existence of recombination hot spots in this region. Other weak linkage disequilibria are likely to exist in this region. These data allow to define some conserved MHC class II haplotypes including HLA class II and TAP, LMP and DM alleles. Furthermore, the knowledge of such linkage disequilibria is of outstanding importance in order to avoid misinterpretation of the data when studying MHC class II associations with autoimmune diseases.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1996

Review on the multifactorial aspects of bioincompatibility in CPB.

Over the last few years, a great emphasis has been placed on the bioincompatibility of foreign, nonphysiological materials used during CPB. It is only recently that bioincompatibility has objectively been recognized to be multifactorial, with the dominant implicated sources being cardiotomy blood suction, shear stresses or flow dynamics and, to a lesser degree, the blood/artificial surface interactions, the heparin/protamine complex and the various forms of emboli or debris. In summary, in CPB, the reduction of postoperative complications, such as whole body inflammatory reactions, bleeding and organ dysfunctions, can only be impacted if the primary, dominant sources of bioincompatibility are reduced or eliminated.

Biocompatible Materials↗
PubMed1996

Longitudinal cognitive, electroencephalographic and morphological brain changes in ageing and Alzheimer's disease.

BACKGROUND: The natural course of cognitive performance, electrophysiological alterations and brain atrophy in ageing and Alzheimer's disease (AD) has been investigated in numerous studies, but only few attempts have been made to examine the relationship between clinical, electroencephalographic (EEG) and morphological changes with quantitative methods prospectively over longer periods of time. METHOD: Fifty-five patients with clinically diagnosed AD and 66 healthy elderly controls were examined biannually using a cognitive test (CAMCOG), EEG band power and volumetric estimates of brain atrophy. RESULTS: On average cognitive performance deteriorated by 28 points on the CAMCOG in the AD group, the alpha/theta ratio decreased by 0.2, and the proportion of intracranial cerebrospinal fluid volume increased by 3.5% during a 2-year period. Similar changes were observed after a second 2-year interval. A multiple regression model demonstrated a significant influence of age on cognition and atrophy and a significant influence of the estimated duration of symptoms on cognition, alpha/theta ratio and brain atrophy at the initial examination. Cognitive performance at the first examination exerted significant effects on the performance and also on brain atrophy at re-examination after 2 or 4 years, whereas the EEG and neuroimaging findings at the previous examination were exclusively related to the corresponding findings at the follow-up examinations. In the control group no significant cognitive, EEG and morphological changes were observed after 2 and 4 years. CONCLUSION: After 2 consecutive follow-up periods, we were able to verify significant deteriorations of cognition accompanied by neurophysiological and neuroradiological changes in AD, but not in normal ageing. In clinically diagnosed AD, cognitive performance at the followup examination could not be predicted by the previous alpha/theta ratio or by the previous degree of global brain atrophy, whereas the cognitive test score determined not only performance, but also structural findings at follow-up. Performance on cognitive tests appears to be a more sensitive indicator of the degenerative process than EEG band-power and morphological changes in manifest AD. Neuroimaging, neurophysiology and genetic risk markers may be more important for the early differential diagnosis than for the prediction of the course of illness.

Age of Onset↗
PubMed1995

CD66b, CD66c and carcinoembryonic antigen (CEA) are independently regulated markers in sera of tumor patients.

Non-specific cross-reacting antigens (NCA-95 = CD66b and NCA-50/90 = CD66c) are members of the CEA (carcinoembryonic antigen = CD66e) family. Analysis of mRNA levels of CD66c in colon tumors suggests that this antigen is strongly up-regulated compared to its normal counterpart and could, therefore, be of clinical interest. CD66c is also expressed in normal lung and spleen tissues and, above all, on granulocytes. The appearance of CD66b in serum, the only strictly granulocyte-specific antigen, could point to the involvement of granulocytes in disease. Specific sandwich ELISAs have been established to determine CEA, CD66b and CD66c levels in serum. Controls have been carried out by testing sera from patients with benign tumors or inflammatory diseases and from healthy individuals. In sera of most patients suffering from solid tumors, sensitivities for CD66c are comparable to or lower than those for CEA. CD66c showed a much higher sensitivity in early colon tumor stages. Sensitivities over 40% have been determined for CD66b in sera of patients with uterine and kidney carcinomas. CML patients revealed sensitivities of 84% for CD66c and 47% for CD66b. Investigations of sera from patients with inflammatory colon diseases which are negative for CEA showed high sensitivity for CD66c but not for the granulocyte-specific CD66b. Patients with mastopathy revealed sensitivities of over 40% for both CD66c and CD66b. CD66b, CD66c and CEA are independently regulated proteins in a high percentage of patients. The simultaneous determination of CEA and CD66b/c can increase the sensitivities for malignant tumors but high sensitivities of CD66b/c for benign diseases limit their usefulness as tumor markers. CD66b may be interesting as a marker for kidney and corpus carcinomas, for which good markers are not yet available.

Adult↗
PubMed1995

Family study of linkage disequilibrium between TAP2 transporter and HLA class II genes. Absence of TAP2 contribution to association with insulin-dependent diabetes mellitus.

The polymorphic TAP1 and TAP2 genes encode a transporter protein required for delivery of cytosolic peptides to class I molecules in the endoplasmic reticulum. Associations have been observed between TAP2 alleles and predisposition to autoimmune diseases such as IDDM but their interpretation has been complicated by the existence of LD between TAP2 and HLA class II loci, and conclusions are still contradictory. In order to precisely define LD on class II haplotypes, we performed an extensive familial analysis. A total of 466 individuals from 55 normal families and 49 IDDM multiplex families was studied, providing information on 420 independent haplotypes. The IDDM-predisposing DRB1*03 and DRB1*04 alleles were in strong negative LD with TAP2-B (delta = -0.035 and -0.034, respectively), and positive LD with TAP2-A (delta = + 0.055 and + 0.012). Positive LD was also found between TAP2-B and DRB1*01 and TAP2-C and DRB1*11 alleles. We then addressed the question of whether TAP2 is an independent additional IDDM-protective or predisposing genetic factor. No TAP2 effect was evidenced when considering DRB1*03 and/or 04 patients. A decreased TAP2-B phenotype frequency was observed in DRB1*03- and DRB1*04-negative IDDM patients compared with DRB1*03- and DRB1*04-negative normal controls (38.6% vs 63%, pc < 0.05), but was probably related to a combination of different weak LD between DRB1 and TAP2 alleles. It thus appears that there is no primary association between TAP2 alleles and IDDM. However, TAP polymorphism may allow us to define particular extended HLA haplotypes involved in susceptibility to autoimmune diseases.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1995

Local and systemic effects of endotoxin in contracting skeletal muscle.

PURPOSE: This study was performed to determine the direct effect of endotoxin on force generation, O2 consumption and vascular resistance in contracting skeletal muscle. MATERIALS AND METHODS: We vascularly isolated the gastrocnemius muscle of dogs anesthetized with sodium pentobarbital and mechanically ventilated. The muscle was perfused from a proximal vessel or by a pump that withdrew blood from the contralateral leg. The nerve to the muscle was stimulated with supramaximal voltage 12 tr/min, 15-Hz impulses and a duty cycle of 0.4. Blood flow was measured with an electromagnetic flow probe, and oxygen consumption (VO2) was calculated from the flow and arterial-venous O2 content. In Protocol 1 (local infusion), contractions were stimulated for 30 minutes and endotoxin (n = 6) or saline (n = 6) was infused into the vasculature of the isolated gastrocnemius muscle after 10 minutes of contraction and continued for another 20 minutes of contraction. In Protocol 2 (systemic infusion), The normal tension and flow to the gastrocnemius were established and endotoxin (n = 5) or saline (n = 5) infused systemically. One hour later, the flow was set at the control level of contracting muscle, and contractions were stimulated for 30 minutes. RESULTS: In both groups, endotoxin did not alter the tension VO2, arterial venous oxygen difference, or vascular resistance at the end of the stimulation period. CONCLUSION: Endotoxin must affect muscle force production by acting through intermediates such as cytokines, and the effect is not apparent in the first 60 minutes.

Animals↗
PubMed1995

Cumulative pregnancy rates and pregnancy outcome after in-vitro fertilization: > 5000 cycles at one centre.

Cumulative pregnancy rates and pregnancy outcome analysis are useful methods for advising an infertile couple of the probability of in-vitro fertilization (IVF) success. All 5209 IVF cycles in 2391 couples at University Hospital, London, Ontario, Canada, over 10 years were studied. Cumulative pregnancy rates were estimated using life table analysis. The Cox proportional hazards model was used to estimate the influence of covariates. Oocyte retrieval and embryo transfer were achieved in 84 and 64% of cycles initiated respectively. There were 644 intra-uterine and 24 ectopic pregnancies (13%/cycle initiated, 15%/oocyte retrieval and 20%/embryo transfer). Cumulative pregnancy rates following six cycles were: tubal 55%, idiopathic 65%, endometriosis 60%, multifactorial 63% and male 40%. There were 68 spontaneous abortions (10.6%) and three induced abortions for congenital anomalies. The multiple gestation rate was 22%. Caesarean section and preterm delivery rates were 35 and 20% respectively, due in part to the high proportion of multiple gestations. Of 15 deliveries which resulted in stillbirths and/or neonatal deaths, 12 were multiple gestations; 18 pregnancies (3.3%) were complicated by congenital malformations. No increases in congenital malformations or spontaneous abortions were identified. Cumulative pregnancy rates were lower in cases of male infertility. Success rates did not decline with successive IVF cycles. IVF is an evolving infertility treatment.

Birth Rate↗
PubMed1994

Characterization of a fluorescent substance P analog.

We describe the development and characterization of substance P labeled at Lys3 with fluorescein ([fluorescein Lys3]SP) as a fluorescent probe for the neurokinin 1 (NK1) receptor. [fluorescein Lys3]SP is an agonist at the human NK1 receptor, with an affinity for both the high-affinity and low-affinity binding states of the receptor approximately 6-fold lower than that of substance P. Binding of the probe to the human NK1 receptor expressed in Sf9 insect cells was observed directly by monitoring either a decrease in fluorescence intensity or an increase in anisotropy of the [fluorescein Lys3]SP. Detection by anisotropy gave the larger signal and thus was used to characterize the interaction of [fluorescein Lys3]SP with the receptor. The anisotropy of the bound ligand was 0.17, compared to 0.04 for the free ligand. The fluorescence was quenched by about 15% upon binding to the receptor. Bound [fluorescein Lys3]SP was displaced by unlabeled SP and by the quinuclidine antagonist L-703,606. As expected for an agonist, binding was also reduced by the addition of the nonhydrolyzable guanine nucleotide analog GppNHp. [fluorescein Lys3]SP should provide a useful structural and kinetic probe for the NK1 receptor.

Amino Acid Sequence↗
PubMed1994

Critical phosphorylation sites for acetyl-CoA carboxylase activity.

Acetyl-CoA carboxylase (ACC) is rapidly regulated by reversible phosphorylation; phosphorylation inactivates ACC, whereas dephosphorylation activates the enzyme. Among protein kinases only cAMP-dependent protein kinase and 5'-AMP-dependent protein kinase can inactivate ACC; cAMP-dependent protein kinase phosphorylates Ser-77 and -1200; 5'-AMP-dependent protein kinase phosphorylates Ser-79, -1200, and -1215. In this report, the construction and expression of ACC cDNA containing the entire coding region (7.2 kilobase pairs) is described. In order to identify the critical phosphorylation site(s) for each protein kinase, we introduced site-specific mutations at Ser-77, -79, -1200, and -1215 of ACC cDNA and a series of mutated ACCs containing various combinations of these four mutated sites was expressed. By examination of the various mutant ACCs, we provided evidence that the effect of cAMP-dependent protein kinase is entirely mediated by the phosphorylation of Ser-1200 and that Ser-79 is important for 5'-AMP-dependent protein kinase action in vitro.

Acetyl-CoA Carboxylase↗
PubMed1994

Trophic exchanges between parent and young during development of Glossiphonia complanata (Annelida, Hirudinea).

Glossiphoniids are iteroparous hirudineans that brood their offspring. The young are attached by the posterior sucker to the parent's ventral side until development is complete. The weight loss of the brooding adults is commonly attributed to their reduced possibility of feeding and to the increased metabolic expense for movements needed to ventilate the offspring. The present study showed that there is a passage of nutritive substrates between the parental body wall and the young's sucker. A possible correlation between this passage and the reabsorption of some muscle fibers that occurs in the adult's body wall is also analyzed.

3-O-Methylglucose↗
PubMed1994

Cloning of human acetyl-CoA carboxylase cDNA.

Acetyl-CoA carboxylase is the rate-limiting enzyme in the biogenesis of long-chain fatty acids. In order to understand the mechanisms that regulate human acetyl-CoA carboxylase at the gene level, and the relationship between its structure and function, cDNA clones for human acetyl-CoA carboxylase have been isolated and sequenced. Human acetyl-CoA-carboxylase cDNA contains 7020 nucleotides encoding a protein of 2340 amino acids with a calculated relative molecular mass of 264575. The human enzyme shows approximately 85% identity in nucleotide sequence with previously cloned rat acetyl-CoA carboxylase, and shows 90% identity in the amino acid sequence. Two human acetyl-CoA-carboxylase mRNA species, which differ in the 5' untranslated region with the same coding sequence, have been identified. The sequence analysis reveals that type I and type II acetyl-CoA-carboxylase mRNA contain 313- and 173-base-long 5' untranslated regions, respectively. The first 240 nucleotides in the 5' untranslated region of type I acetyl-CoA-carboxylase mRNA replace the first 100 nucleotides of the (G + C)-rich region of the 5' untranslated region of the type II mRNA. These two species of mRNAs are the only species of human ACC mRNA which have been detected compared to at least five species in rat tissues, and they are expressed in a tissue-specific manner.

Acetyl-CoA Carboxylase↗
PubMed1994

Alterations in glutathione levels in Parkinson's disease and other neurodegenerative disorders affecting basal ganglia.

Reduced glutathione (GSH) and oxidized glutathione (GSSG) levels were measured in various brain areas (substantia nigra, putamen, caudate nucleus, globus pallidus, and cerebral cortex) from patients dying with Parkinson's disease, progressive supranuclear palsy, multiple-system atrophy, and Huntington's disease and from control subjects with no neuropathological changes in substantia nigra. GSH levels were reduced in substantia nigra in Parkinson's disease patients (40% compared to control subjects) and GSSG levels were marginally (29%) but insignificantly elevated; there were no changes in other brain areas. The only significant change in multiple-system atrophy was an increase of GSH (196%) coupled with a reduction of GSSG (60%) in the globus pallidus. The only change in progressive supranuclear palsy was a reduced level of GSH in the caudate nucleus (51%). The only change in Huntington's disease was a reduction of GSSG in the caudate nucleus (50%). Despite profound nigral cell loss in the substantia nigra in Parkinson's disease, multiple-system atrophy, and progressive supranuclear palsy, the level of GSH in the substantia nigra was significantly reduced only in Parkinson's disease. This suggests that the change in GSH in Parkinson's disease is not solely due to nigral cell death, or entirely explained by drug therapy, for multiple-system atrophy patients were also treated with levodopa. The altered GSH/GSSG ratio in the substantia nigra in Parkinson's disease is consistent with the concept of oxidative stress as a major component in the pathogenesis of nigral cell death in Parkinson's disease.

Aged↗
PubMed1994

Glutathione-related enzymes in brain in Parkinson's disease.

The activities of enzymes related to glutathione synthesis, degradation, and function were analyzed in various brain regions (cerebral cortex, caudate nucleus, putamen, globus pallidus, and substantia nigra) from patients dying with pathologically proven Parkinson's disease (PD) and multiple system atrophy (MSA), and from matched controls with no neurological disorder. The activity of the glutathione degradative enzyme, gamma-glutamyltranspeptidase, was selectively elevated in substantia nigra (SN) in PD. In contrast, the activity of the synthetic enzyme, gamma-glutamylcysteine synthetase, was unaltered in SN and other brain areas in PD. Similarly, glutathione peroxidase and glutathione transferase activities were unaltered in SN or in other brain regions in PD. gamma-Glutamylcysteine synthetase, gamma-glutamyltranspeptidase, glutathione peroxidase, and glutathione transferase activities were normal in SN and most other brain areas in MSA. However, glutathione peroxidase activity was increased in the lateral globus pallidus and caudate nucleus in MSA. The depletion of reduced glutathione (GSH) in the SN in PD, with no change in oxidized glutathione (GSSG), may be due to efflux of GSH mainly out of glia promoted by gamma-glutamyltranspeptidase, perhaps with additional increased conversion of GSH to GSSG (which itself is transported out of cells by gamma-glutamyltranspeptidase), in response to increased hydrogen peroxide formation.

Aged↗