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I Levels (i + level)

Distribution by Scientific Domains

Medical Sciences	72%
Life Sciences	18%

Selected Abstracts

The Endogenous Amine 1-Methyl-1,2,3,4- Tetrahydroisoquinoline Prevents the Inhibition of Complex I of the Respiratory Chain Produced by MPP+

JOURNAL OF NEUROCHEMISTRY, Issue 1 2000
Juan Parrado
Abstract : The endogenous monoamine 1-methyl-1,2,3,4-tetrahydroisoquinoline has been shown to prevent the neurotoxic effect of MPP+ and other endogenous neurotoxins, which produce a parkinsonian-like syndrome in humans. We have tested its potential protective effect in vivo by measuring the protection of 1-methyl-1,2,3,4-tetrahydroisoquinoline in the neurotoxicity elicited by MPP+ in rat striatum by tyrosine hydroxylase immunocytochemistry. Because we know that cellular damage caused by MPP+ is primarily the result of mitochondrial respiratory inhibition at the complex I level, we have extended the study further to understand this protective mechanism. We found that the inhibitory effect on the mitochondrial respiration rate induced by MPP+ in isolated rat liver mitochondria and striatal synaptosomes was prevented by addition of 1-methyl-1,2,3,4-tetrahydroisoquinoline. This compound has no antioxidant capacity ; therefore, this property is not involved in its protective effect. Thus, we postulate that the preventive effect that 1-methyl-1,2,3,4-tetrahydroisoquinoline has on mitochondrial inhibition for MPP+ could be due to a "shielding effect," protecting the energetic machinery, thus preventing energetic failure. These results suggest that this endogenous amine may protect against the effect of several parkinsonism-inducing compounds that are associated with progressive impairment of the mitochondrial function. [source]

Frequency of Acute Coronary Syndrome in Patients with Normal Electrocardiogram Performed during Presence or Absence of Chest Pain

ACADEMIC EMERGENCY MEDICINE, Issue 6 2009
Samuel D. Turnipseed MD
Abstract Objectives:, The authors hypothesized that patients with active chest pain at the time of a normal electrocardiogram (ECG) have a lower frequency of acute coronary syndrome (ACS) than patients being evaluated for chest pain but with no active chest pain at the time of a normal ECG. The study objective was to describe the association between chest pain in patients with a normal ECG and the diagnosis of ACS. Methods:, This was a prospective observational study of emergency department (ED) patients with a chief complaint of chest pain and an initial normal ECG admitted to the hospital for chest pain evaluation over a 1-year period. Two groups were identified: patients with chest pain during the ECG and patients without chest pain during the ECG. Normal ECG criteria were as follow: 1) normal sinus rhythm with heart rate of 55,105 beats/min, 2) normal QRS interval and ST segment, and 3) normal T-wave morphology or T-wave flattening. "Normal" excludes pathologic Q waves, left ventricular hypertrophy, nonspecific ST-T wave abnormalities, any ST depression, and discrepancies in the axis between the T wave and the QRS. Patients' initial ED ECGs were interpreted as normal or abnormal by two emergency physicians (EPs); differences in interpretation were resolved by a cardiologist. ACS was defined as follows: 1) elevation and characteristic evolution of troponin I level, 2) coronary angiography demonstrating >70% stenosis in a major coronary artery, or 3) positive noninvasive cardiac stress test. Chi-square analysis was performed and odds ratios (ORs) are presented. Results:, A total of 1,741 patients were admitted with cardiopulmonary symptoms; 387 met study criteria. The study group comprised 199 males (51%) and 188 females (49%), mean age was 56 years (range, 25,90 years), and 106 (27%) had known coronary artery disease (CAD). A total of 261 (67%) patients experienced chest pain during ECG; 126 (33%) patients experienced no chest pain during ECG. There was no difference between the two groups in age, sex, cardiac risk factors, or known CAD. The frequency of ACS for the total study group was 17% (67/387). There was no difference in prevalence of ACS based on the presence or absence of chest pain (16% or 42/261 vs. 20% or 25/126; OR = 0.77, 95% confidence interval = 0.45 to 1.33, p = 0.4). Conclusions:, Contrary to our hypothesis concerning patients who presented to the ED with a chief complaint of chest pain, our study demonstrated no difference in the frequency of acute coronary syndrome between patients with chest pain at the time of acquisition of a normal electrocardiogram and those without chest pain during acquisition of a normal electrocardiogram. [source]

Effect of Smoking on Serum Pepsinogen I Level Depends on Serological Status of Helicobacter pylori

CANCER SCIENCE, Issue 3 2001
Masayuki Tatemichi
Serum pepsinogen (sPG) levels are used in gastric cancer screening programs. However, modification of sPG levels by smoking habit, according to the status of Helicobacter pylori (H. pylori) infection has been little investigated. This study investigated the effects of smoking on serum levels of pepsinogen I (PG I), pepsinogen II (PG II), and gastrin by IgG titer of antibody against H. pylori (Hp-IgG titer) using the data from 356 current-smokers and 262 non-smokers (133 never-smokers and 129 ex-smokers) in a cross-sectional study of 618 men aged 40 to 49 years. PG I, PG II, PG I/PG II ratio and gastrin were significantly associated with Hp-IgG titer in never-smokers [Spearman's correlation coefficient (95% confidence interval): 0.23 (0.07, 0.39), 0.52 (0.41, 0.63), -0.40 (-0.54, -0.27), and 0.25 (0.10, 0.41), respectively]. However, the correlation coefficients of PG I and PG H decreased in current-smokers, 0.02 (-0.1, 0.13) and 0.32 (0.22, 0.42), respectively. In H. pylori seronegative and low titer cases, the mean PG I level was significantly (P<0.01) higher in current-smokers, compared with non-smokers. However, in high titer cases, the mean PG I level was lower in current-smokers. Mean PG II and gastrin levels, and PG I/PG II ratio did not differ according to smoking habits by Hp-IgG titer. The gastrin level was significantly correlated with PG H, but not PG I. These data indicate that current smoking influences the serum PG I level depending on Hp-IgG titer and the associations between sPGs and Hp-IgG titer. Gastrin is not involved in the modification of PG I levels by smoking. [source]

Prospective Study of the Clinical Features and Outcomes of Emergency Department Patients with Delayed Diagnosis of Pulmonary Embolism

ACADEMIC EMERGENCY MEDICINE, Issue 7 2007
Jeffrey A. Kline MD
Objectives:The authors hypothesized that emergency department (ED) patients with a delayed diagnosis of pulmonary embolism (PE) will have a higher frequency of altered mental status, older age, comorbidity, and worsened outcomes compared with patients who have PE diagnosed by tests ordered in the ED. Methods:For 144 weeks, all patients with PE diagnosed by computed tomographic angiography were prospectively screened to identify ED diagnosis (testing ordered from the ED) versus delayed diagnosis (less than 48 hours postadmission). Serum troponin I level, right ventricular hypokinesis on echocardiography, and percentage pulmonary vascular occlusion were measured at diagnosis; patients were prospectively followed up for adverse events (death, intubation, or circulatory shock). Results:Among 161 patients with PE, 141 (88%) were ED diagnosed and 20 (12%) had a delayed diagnosis. Patients with a delayed diagnosis were older than ED-diagnosed patients (61 [±15] vs. 51 [±17] years; p < 0.001), had a longer median time to heparin administration (33 vs. 8 hours; p < 0.001), and had a higher frequency of altered mental status (30% vs. 8%; p = 0.01) but did not have a higher frequency of prior cardiopulmonary disease (25% vs. 23%). Patients with a delayed diagnosis had equal or worse measures of PE severity (right ventricular hypokinesis on echocardiography, 60% vs. 58%; abnormal troponin I level, 55% vs. 24%); on computed tomographic angiography, ten of 20 patients with a delayed diagnosis had PE in lobar or larger arteries and >50% vascular obstruction. Patients with a delayed diagnosis had a higher rate of in-hospital adverse events (9% vs. 30%; p = 0.01). Conclusions:In this single-center study, the diagnosis of PE was frequently delayed and outcomes of patients with delayed diagnosis were worse than those of patients with PE diagnosed in the ED. [source]

Lack of PSD-95 drives hippocampal neuronal cell death through activation of an ,CaMKII transduction pathway

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2002
Fabrizio Gardoni
Abstract The PSD-95 protein family organizes the glutamatergic postsynaptic density and it is involved in the regulation of the excitatory signal at central nervous system synapses. We show here that PSD-95 deficiency by means of antisense oligonucleotides induces significant neuronal cell death within 24 h both in primary hippocampal cultures and in organotypic hippocampal slices. On the other hand, cultured cortical neurons are spared by PSD-95 antisense toxicity until they reach a NR2A detectable protein level (24 days in vitro). The neurotoxic event is characterized by increased ,CaMKII association to NR2 regulatory subunits of NMDA receptor complex. As a direct consequence of ,CaMKII association, we found increased GluR1 delivery to cell surface in cultured hippocampal neurons paralleled by AMPA-dependent increase in [Na+]I levels. In addition, both CaMKII specific inhibitor KN-93 and AMPA receptor antagonists CNQX and NBQX rescued neuronal survival to control values. On the other hand, both the NMDA channel blocker MK-801 and Dantrolene, an inhibitor of calcium release from ryanodine-sensitive endoplasmic reticulum stores, failed to have any effect on neuronal survival in PSD-95 deficient neurons. Thus, our data provide clues that PSD-95 reduced expression in neurons is responsible for neuronal vulnerability mediated by direct activation of ,CaMKII transduction pathway in the postsynaptic compartment. [source]

Serum Levels of Leptin As Marker For Patients At High Risk of Gastric Cancer

HELICOBACTER, Issue 6 2009
Lisette G. Capelle
Abstract Background:, Serological screening for gastric cancer (GC) may reduce mortality. However, optimal serum markers for advanced gastric precursor lesions are lacking. Aim:, To evaluate in a case,control study whether serum leptin levels correlate with intestinal metaplasia (IM) and can serve as a tool to identify patients at high risk for GC. Materials and Methods:, Cases were patients with a previous diagnosis of IM or dysplasia, controls were patients without such a diagnosis. All patients underwent endoscopy. Fasting serum was collected for the measurement of leptin, pepsinogens I/II, gastrin, and Helicobacter pylori. Receiver operating characteristic (ROC) curves and their area under the curve (AUC) were provided to compare serum leptin levels with other serological markers. Results:, One hundred nineteen cases and 98 controls were included. In cases, the median leptin levels were 116.6 pg/mL versus 81.9 pg/mL in controls (p = .01). After adjustment for age, sex and BMI, leptin levels remained higher in cases than in controls (p < .005). In multivariate analysis, male sex (p = .002), age (<0.001), low pepsinogen levels (p = .004) and high leptin levels (p = .04) were independent markers for the presence of IM. In addition, a ROC curve including age, sex and pepsinogen I levels had an AUC of 0.79 (95% CI (0.73,0.85)). Adding serum leptin levels increased the AUC to 0.81 (95% CI (0.75,0.86)). Conclusions:, High leptin levels are associated with an increased risk of IM. Moreover, serum leptin levels are a significant independent marker for the presence of IM. However, in combination with the serological test for pepsinogen I the additional value of serum leptin levels is rather limited. [source]

Helicobacter pylori Infection is Associated with Reduced Circulating Ghrelin Levels Independent of Body Mass Index

HELICOBACTER, Issue 5 2005
Akiko Shiotani
ABSTRACT Background., Ghrelin stimulates growth hormone and has orexigenic and adipogenic effects. Plasma ghrelin levels are reduced in obesity and possibly in Helicobacter pylori infection. Aim., To investigate whether there was a relation between H. pylori infection, body mass index (BMI) and serum ghrelin or leptin levels. Methods., University students undergoing an annual health check-up were invited to participate. H. pylori status was based on the presence of specific IgG H. pylori antibodies in urine. Fasting serum ghrelin, leptin levels, and pepsinogen I and II levels were measured by enzyme immunoassay (EIA). Results., Eight hundred and one students volunteered. There was no significant difference in the height and BMI between those with and without H. pylori infection. The population of ghrelin study consisted of 132 (66 H. pylori -positive and 66 H. pylori -negative) students matched for age, sex, and BMI. The ghrelin level in the H. pylori -positive group was significantly lower (median 55 pmol/l) compared to the H. pylori- negative group (103 pmol/l) (p < .00001). Leptin, triglyceride, total cholesterol, and HDL-cholesterol were not different between the two groups, whereas LDL-cholesterol levels were significantly higher (106 versus 100 mg/dl) (p = .03) in the H. pylori -positive group. Leptin levels correlated with the BMI (r = 0.53) (p < .00001). Among H. pylori -positive subjects, ghrelin correlated only with pepsinogen I levels (r = 0.26, p = .04). Conclusions.,H. pylori infection was associated with a reduction in circulating ghrelin levels independent of sex and BMI. [source]

An ecological risk assessment for spinosad use on cotton

PEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 1 2002
Cheryl B Cleveland
Abstract Spinosad is a reduced-risk insecticide with a novel mode of action that provides an alternative to older classes of insecticides such as organophosphates, carbamates and pyrethroids. A comprehensive ecological risk assessment for spinosad use in US cotton crops is presented within a framework of tiered levels of refinement following the guidelines of the US EPA for ecological risk assessments. Toxicity information for a variety of species is documented and utilized, environmental concentrations estimated, and risk characterizations in the form of risk quotients are quantified. Results indicate that spinosad use in cotton does not exceed the most conservative Tier I levels of concern (LOC) values for groundwater, mammals and birds or acute risk to aquatic organisms. Use of very conservative Tier I screening methods resulted in exceeding LOC values for chronic exposure for some aquatic organisms, thus prompting further refinement. When the exposure prediction was refined using less conservative, Tier II mechanistic environmental fate transport models to predict off-site transport and environmental concentrations, chronic risk was not predicted for these species. Spinosad is acutely toxic to bees under laboratory conditions, but toxicity of residue studies and field studies indicate that under actual use conditions the impact on bees is minimal. © 2001 Society of Chemical Industry [source]

Effect of Smoking on Serum Pepsinogen I Level Depends on Serological Status of Helicobacter pylori

IGF-I, leptin and active ghrelin levels in very low birth weight infants during the first 8 weeks of life

ACTA PAEDIATRICA, Issue 1 2010
N Ohkawa
Abstract Aim:, We investigated the relationship between plasma insulin-like growth factor I (IGF-I), leptin, active ghrelin levels, and postnatal growth in very low birth weight (VLBW) infants. Method:, Plasma IGF-I, leptin, and active ghrelin levels were measured at birth and at 2, 4, 6 and 8 weeks after birth in 61 VLBW infants, including 31 appropriate-for-gestational-age (AGA) and 30 small-for-gestational-age (SGA) infants. Results:, Insulin-like growth factor I levels were the lowest at birth, but increased gradually over the first 8 weeks of life. IGF-I was positively correlated with body weight, body length and body mass index at all time points. Leptin levels did not change over the study period. Ghrelin levels were significantly lower at birth; however, there were no significant differences between the levels after 2 weeks of age. Leptin and ghrelin levels were not correlated with anthropometrical measures. IGF-I levels at birth were significantly lower in SGA than in AGA infants, but the leptin and ghrelin levels were not significantly different between the two groups. Conclusion:, Insulin-like growth factor I is related to length and weight gain in the prenatal and the early postnatal periods in VLBW infants, but this does not appear to be the case for leptin and ghrelin. [source]

Serial analysis of troponin I levels in patients with ischemic and nonischemic dilated cardiomyopathy

CLINICAL CARDIOLOGY, Issue 5 2006
Ulrich Nellessen M.D.
Abstract Background: Ongoing myocardial cell damage forms the basis for progression of chronic heart failure. Evidence is accumulating that progressive loss of cardiac myocytes is associated with the release of cardiac troponin I (cTnI). Hypothesis: This study sought to determine whether levels of cTnI are of prognostic value for risk stratification of patients with chronic heart failure. Methods: Release of cTnI was measured by conventional enzyme immunoassay following serum ultrafiltration in 58 consecutive patients hospitalized for chronic heart failure and 31 healthy volunteers serving as control group. Determination of serum levels was performed every 2 weeks over a time interval of 3 months. According to the results of coronary angiography, patients were divided into Group D showing normal coronary arteries (n = 33, ejection fraction 27 ± 6.1%) and Group I showing severe coronary heart disease (n = 25, ejection fraction 28.8 ± 7.8%). Survival of patients was evaluated after a mean time interval of 3 years. Results: The mean cTnI serum level over all measurements was 0.66 ± 1.8 ng/ml in patients versus 0.11 ± 0.48 ng/ml in volunteers. At all six points of analysis, the mean cTnI serum level was significantly different (p < 0.001) between patients and volunteers. There was no significant difference between patients with and without coronary heart disease following hospital discharge, however, troponin release was significantly different between survivors and nonsurvivors (n = 27) (0.56 ng/ml vs. 0.84 ng/ml; p < 0.05). Conclusion: Permanent cTnI release is a common finding in patients with chronic heart failure and a strong prognosticator. In this setting, coronary morphology seems to play a minor role for disease progression. [source]