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J Levy

Publications and source records attributed to J Levy.

At least 181 records · Page 10Linked to original sources

Sequencing the yeast genome: an international achievement.

The yeast genome is currently being sequenced by a Consortium of European laboratories, in collaboration with a wider international network of researchers. It is expected that within the next two years Saccharomyces cerevisiae will become the first eukaryotic organism to have been completely genetically mapped and sequenced. This article traces the sequencing enterprise from its beginnings, outlining the intentions, the organisation, and the achievements so far. The tasks which remain are discussed, emphasising the follow-on research into the evolution of primitive karyotypes, and, more particularly, into the nature of novel genes revealed during sequencing. The functional analysis of novel genes is attracting an ever wider community of yeast scientists, so that research which began with a decision to sequence a simple genome promises to remain a focus for international cooperation.

Chromosome Mapping↗

Left- and right-handers see people differently: free-vision perceptual asymmetries for chimeric stimuli.

We examined perceptual biases of 72 left-handers on six free-vision chimeric tasks, four entailing judgments of emotion (EP and EC tasks) or femininity (GP and GC tasks) in photographic and cartoon chimeric faces, and two of visuospatial properties in dot-filled rectangles (DN-dots nonface task) and asymmetrical shapes (SN-shapes nonface task), and compared to them to those of 72 right-handers previously described by Luh, Rueckert, and Levy (1991). Neither handedness group had an asymmetric bias on the SN task. Both had left hemispatial biases on all other tasks, which were equal across tasks for left-handers, larger on the EP and EC than other tasks for right-handers, and larger for right- than left-handers only on the EP and EC tasks. Task-specific reliable variance was decreased and variance common to all tasks was increased for left- compared to right-handers, which suggests less differentiation of processes in left- than right-handers.

Analysis of Variance↗

Blood levels of insulin-like growth factors I and II in neonates of non-insulin-dependent diabetic rats.

Circulating levels of insulin like growth factor I (IGF-I) and insulin like growth factor II (IGF-II) were evaluated in plasma samples during the first 72 h of life in neonates of diabetic and control mother rats. Diabetes had been induced in the diabetic dams by streptozotocin at 2 days of age. The rats developed non-insulin dependent diabetes (at 6 weeks of age) and became pregnant at 11 weeks of age. Maternal blood glucose levels were higher in the diabetic mothers (P < 0.05) during the last two-thirds of gestation. Complications occurred at the end of 7.1% of the diabetic pregnancies but none of the controls. Analysis of neonates plasma glucose, IGF-I, and IGF-II concentrations in the first 12, 24, 48, and 72 h after birth revealed higher glucose levels in neonates of diabetic mothers at 72 h compared with controls (118 +/- 7 vs 85 +/- 5 mg/dl, P < 0.05) but there was no difference in IGF-I or IGF-II levels between the groups at any time point. Thus, acquired impaired glucose homeostasis may be seen in neonates of mildly diabetic mothers at early stages of their life but their circulating insulin-like growth factors levels are normal. These data do not support the proposition that fetal IGF-I and -II affect the outcome of pregnancies complicated by mild diabetes in the rodent.

Aging↗

Postnatal regression of glucose transport in a patient with glycogen storage disease type 1b.

Decreased 2-deoxyglucose (2-DOG) uptake is well described in the neutrophils of patients with glycogen storage disease type 1b (GSD 1b). We report a patient with GSD 1b who presented with a normal antenatal and perinatal 2-deoxyglucose uptake that showed a slow regression during the first months of life. These indicate limitations of 2-deoxyglucose uptake in the diagnosis of GSD 1b. While it appears that low uptake rate below 0.25 nmol/min in 10(6) cells is of significance, normal uptake does not rule out the presence of the disease. It seems that antenatal diagnosis of GSD 1b cannot be made by measurement of 2-deoxyglucose uptake in the fetal neutrophils.

Aging↗

Diabetes mellitus: a disease of abnormal cellular calcium metabolism?

Although the pathogenesis of the diabetes mellitus syndrome remains poorly understood, both insulin-dependent diabetes mellitus and non-insulin-dependent diabetes mellitus predispose the individual to a similar spectrum of complications, including hypertension, macrovascular and microvascular disease, cataracts cardiomyopathy, neuropathy, and premature aging, suggesting that these complications develop along a pathway common to both diabetic conditions. Yet not all diabetic persons are affected by all of these complications or to the same degree. What causes this marked variability in the clinical manifestations of the diabetes syndrome remains an enigma. Accumulating data from animal models of diabetes and from studying patients with diabetes reveal that intracellular calcium levels are increased in most tissues. The activities of the membrane, adenosine triphosphatase (ATPase) associated cation pumps, which determine intracellular calcium level (i.e., calcium-ATPase and [sodium + potassium]-ATPase), are also altered. The nature of the alteration is often tissue specific and may depend on the level of blood glucose or insulin, or both. In this review we discuss the potential contribution of these changes in intracellular calcium regulation, whether acquired or genetically determined, to the pathogenesis of the diabetes syndrome, to the abnormalities in insulin secretion and action (mainly in non-insulin-dependent diabetes), and to the complications of both diabetes syndromes. Altered intracellular calcium metabolism may represent a common, underlying abnormality linking the metabolic, cardiovascular, ocular, and neural manifestations of the diabetic disease process.

Animals↗

Human preterm birth is associated with systemic and local changes in progesterone/17 beta-estradiol ratios.

OBJECTIVE: The purpose of this study was to determine whether human preterm birth is associated with changes in 17 beta-estradiol and progesterone concentrations in maternal plasma and amniotic fluid. STUDY DESIGN: Forty healthy women in preterm labor with singleton pregnancies and intact membranes at 32 to 36 weeks of gestation who underwent amniocentesis for evaluation of the microbiologic status of the amniotic cavity were classified into the following two groups: 20 women who were delivered within 1 week from the amniocentesis (preterm delivery group) and 20 who were delivered at term (term delivery group). Maternal plasma and amniotic fluid concentrations of progesterone and 17 beta-estradiol were measured with sensitive and specific commercially available radioimmunoassay kits. RESULTS: The median amniotic fluid concentration of 17 beta-estradiol was significantly higher in women delivered prematurely than in those who were delivered at term (1.5 ng/ml vs 0.9 ng/ml, p = 0.0001). Moreover, the median plasma 17 beta-estradiol concentration was also significantly higher in the preterm delivery group than in the term group (14.1 ng/ml vs 6.9 ng/ml, p = 0.022). In contrast, no significant difference was found in amniotic fluid and plasma concentrations of progesterone between these two groups (24.5 ng/ml vs 27.5 ng/ml and 132.0 ng/ml vs 107.5 ng/ml, respectively). The median amniotic fluid progesterone/17 beta-estradiol ratio was significantly lower in the preterm delivery group than in those delivered at term (18.4 vs 33.6, respectively, p = 0.0017). Moreover, the median plasma progesterone/17 beta-estradiol ratio was also significantly lower in the preterm delivery group than in the term group (9.8 vs 17.0, respectively, p = 0.016). CONCLUSION: Human preterm birth is associated with significantly lower progesterone/17 beta-estradiol ratios than those of women with preterm labor delivered at term.

Adult↗

Decreased activity of (Ca2+ + Mg2+)-adenosine triphosphatase (ATPase) and a hormone-specific defect in insulin regulation of ATPase in kidney basolateral membranes from obese fa/fa rats.

The plasma membrane enzyme (Ca2+ + Mg2+)-adenosine triphosphatase (ATPase) is hormonally regulated and may participate in Ca2+ signaling by removing excess Ca2+ from the cell. Therefore, observations of a hormone-specific loss of insulin stimulation of ATPase in kidney membranes from non-insulin-dependent diabetic (NIDDM) rats may reflect their insulin-resistant state. Consequently, to evaluate whether additional insulin-resistant conditions are associated with impaired function of ATPase and with loss of regulation of the enzyme by insulin, studies were extended to investigate (Ca2+ + Mg2+)-ATPase activities and hormonal regulation of the enzyme in kidney basolateral membranes from obese and lean Zucker rats. (Ca2+ + Mg2+)-ATPase activity was lower in membranes from obese rats compared with lean rats. Maximal velocity (Vmax) of the enzyme activity was 29.2 +/- 2.6 nmol Pi/mg/min in obese rats versus 57.2 +/- 6.5 in lean rats (P < .05). However, the affinity of the enzyme for Ca2+ was similar in obese and lean rats (Km Ca2+, 0.23 +/- 0.025 v 0.23 +/- 0.032 mumol/L Ca2+). Also, the Km for ATP of the enzyme was similar in membranes from obese and lean rats. Insulin, parathyroid hormone (PTH), and cyclic adenosine monophosphate (cAMP) stimulated the ATPase activity in membranes from lean rats in a dose-dependent manner (15% to 28%). Also, the protein kinase C (PKC) stimulator 12-O-tetradecanoyl phorbol-13-acetate (TPA) increased the ATPase activity in membranes from lean rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Hormone-specific defect in insulin regulation of (Ca2+ + Mg2+)-adenosine triphosphatase activity in kidney membranes from streptozocin non-insulin-dependent diabetic rats.

The plasma membrane enzyme (Ca2+ + Mg2+)-adenosine triphosphatase [(Ca2+ + Mg2+)-ATPase] is hormonally regulated, and may participate in Ca2+ signaling by removing excess Ca2+ from the cell. Insulin increases ATPase activity in kidney cortical basolateral membranes (BLM) from normal rats, but fails to do so in membranes from insulin-resistant non-insulin-dependent diabetic (NIDDM) rats. To investigate mechanisms of insulin regulation of ATPase and to evaluate whether the loss of this regulation in diabetes is hormone-specific and depends on blood glucose levels, (Ca2+ + Mg2+)-ATPase function and its hormonal regulation were studied in kidney BLM from rats with mild and severe NIDDM. Km values for ATP and Ca2+ affinity of the ATPase were similar in diabetic and control rats, but the maximal velocity (Vmax) of the enzyme was higher in diabetic groups. Insulin, the protein kinase C (PKC) stimulator 12-0-tetradecanoylphorbol 13-acetate (TPA), parathyroid hormone (PTH), and cyclic adenosine monophosphate (cAMP) all increased the ATPase activity in BLM from controls by increasing the enzyme's affinity for Ca2+. A protein kinase A (PKA) inhibitor (H8 in low concentrations) abolished cAMP and PTH effects, but not those of insulin, whereas the PKC inhibitors (sphingosine and high concentrations of H8) did abolish the effects of insulin. Stimulations of ATPase activity by insulin and by PTH and cAMP were additive. Insulin and TPA lost their stimulatory effects on ATPase in BLM from rats with either mild or severe NIDDM, but PTH and cAMP maintained their stimulatory effects in these membranes. The data show [1] (Ca2+ + Mg2+)-ATPase activity is increased in NIDDM, and a hormone-specific loss of insulin stimulation of ATPase occurs; (2) these defects are not dependent on the level of glycemia; and (3) the stimulatory effects of insulin on the ATPase may be mediated in part via PKC. We suggest that the hormone-specific defect in insulin regulation of ATPase seen in the NIDDM rats may contribute to their insulin resistance.

Animals↗

Callosal efficiency is related to sustained attention.

The purpose of this study was to determine whether there is a relationship between the efficiency of interhemispheric communication (IHC) and the ability to sustain attention. Children were tested on a vigilance task in which the amount of time between target presentations (interstimulus intervals; ISI) was varied. IHC was assessed by comparing within-field and between-field matches on a tachistoscopic task. Subjects who showed better IHC had faster RTs on the long ISI trials of the vigilance task, suggesting callosal involvement in the ability to sustain attention over a long period of time in the absence of sensory input.

Arousal↗

Direct growth inhibition of human endometrial cancer cells by the gonadotropin-releasing hormone antagonist SB-75: role of apoptosis.

OBJECTIVE: Our objective was to study the direct action of the gonadotropin-releasing hormone antagonist SB-75 and the agonist buserelin on the proliferation of endometrial cancer cells. STUDY DESIGN: Two human endometrial cell lines that differ in histologic subtype and estrogen receptor content were treated with gonadotropin-releasing hormone analog. We measured the number of viable cells, cell cycle parameters, and apoptotic processes. RESULTS: Growth of the Ishikawa cells was inhibited by SB-75 in a dose-dependent manner. 17 beta-Estradiol partially abolished the inhibitory effect of SB-75. The growth of the HEC-1A cells was not affected by the antagonist. Neither endometrial cancer cell line showed significant sensitivity to the agonist buserelin. Tenfold concentration of the gonadotropin-releasing hormone agonist did not abolish the inhibitory effect of the antagonist on cell growth. The growth inhibition was not associated with any change in cell cycle parameters but was associated with an induction of apoptosis. CONCLUSION: The gonadotropin-releasing hormone antagonist SB-75 directly inhibits the growth of some human endometrial cancer cells and thus may be suitable for the treatment of endometrial tumors.

Adenocarcinoma, Papillary↗

Killing of meningococci by neutrophils: effect of vaccination on patients with complement deficiency.

To evaluate the in vitro effect of meningococcal vaccination, 3 C7-deficient (C7-D) siblings and 2 normal controls were studied before and 6 weeks after vaccination with treatment meningococcal vaccine (serogroups A, C, Y, and W). Serobactericidal activity was not detected in the C7-D subjects and was low in the controls. Neither group was affected by vaccination. However, opsonized phagocytic killing increased significantly following vaccination in C7-D subjects and normal controls, despite only a modest increase in antimeningococcal titers. Heat inactivation of sera added to neutrophils resulted in low killing activity, which did not increase after vaccination. Thus, tetravalent meningococcal vaccine appears to enhance the phagocytic killing of meningococci in both normal and C7-deficient persons and should be given to all persons with C7 deficiencies.

Adult↗

Management of the axilla in patients with breast cancers one centimeter or smaller.

Very small breast cancers are being diagnosed with increased frequency, and, until recently, little information regarding the incidence of axillary lymph node metastases in these most favorable tumors was available. Moreover, scarce data exist regarding axillary failure in this cohort as a function of initial treatment, be it surgery, radiation, or simply observation. In the present study, limited to women with invasive cancers measuring no more than 10 mm, the incidence of pathologically positive axillary nodes was 12.3%. The incidence of nodal metastases was influenced by tumor size (albeit not quite significantly, p = .08); not one patient with a tumor < or = 5 mm had axillary node metastases, compared to 14.7% in those with cancers 6 to 10 mm. The histologic grade and tumor location were also important in predicting nodal positivity. The incidence of positive nodes was 38% in those with poorly differentiated cancers, compared to 8% and 7% in women with well and moderately differentiated cancers, respectively, p = .03. Axillary nodal positivity was seen in 17% of outer quadrant vs 3% of central and inner quadrant primaries, p < .01. The axilla was managed with surgery alone (76%), radiation alone (6%), surgery and radiation (6%), or simply observation (10%). With a median follow-up of 55 months, not one patient has suffered a nodal recurrence, and in our experience, survival free of distant relapse was not adversely affected by the omission of axillary surgery.

Axilla↗

Quantitation of HIV-1 in whole blood of infected children.

OBJECTIVE: To validate the technique of HIV-1 culture from whole blood for the quantitation of viral load in infected children. PATIENTS: Forty-three HIV-1-infected children were followed in two paediatric centres. METHODS: Quantitative HIV-1 cultures from unfractionated whole blood using an end-point dilution technique were compared with simultaneous quantitative cultures of peripheral blood mononuclear cells (PBMC) and plasma. RESULTS: Good sensitivity (93%) of the methods used was confirmed. A close correlation (r = 0.80) was observed between HIV-1 titres measured directly from whole blood and those expected from PBMC and plasma titres. The mean whole blood viral load was higher in patients with more severe signs of disease, but the difference did not reach statistical significance. The whole blood viral titres measured sequentially at monthly intervals remained within one dilution of each other in 16 of the 22 patients studied. CONCLUSION: In this study, the quantitation of HIV-1 in unfractionated blood allowed for a reliable and sensitive measurement of the whole blood viral load in infected children.

Adolescent↗

The prevalence of Helicobacter pylori positivity in human immunodeficiency virus-infected children.

To investigate the prevalence of Helicobacter pylori infection in pediatric patients infected with the human immunodeficiency virus, we sought to detect the presence of antibodies against this organism in 23 human immunodeficiency virus-infected children of central African ethnic origin by means of a second-generation enzyme-linked immunoassay (ELISA) test for the detection of immunoglobulin G (IgG) antibodies to Helicobacter pylori (Malakit Helicobacter pylori, Biolab, Limal, Belgium). They were compared to an asymptomatic control population matched for age and ethnic origin. Blood samples were taken during routine blood analysis before the monthly administration of intravenous gamma-globulins in the human immunodeficiency virus-infected patients and during preoperative blood analysis in the control population. Despite the fact that most human immunodeficiency virus-infected patients had IgG antibodies against other frequently encountered pathogens, none of them had a positive serology for Helicobacter pylori, compared to 10 of 52 patients (19.2%) in the control population. This difference is statistically significant (p = 0.01).

Adolescent↗