Temperature, Mitochondria, and Reye's Syndrome

PEDIATRICS ◽  
1983 ◽  
Vol 71 (6) ◽  
pp. 985-986
Author(s):  
R. DON BROWN ◽  
JOHN T. WILSON
Keyword(s):  
Mitochondrial Damage ◽  
Reye's Syndrome ◽  
Enhancing Effect ◽  
Control Subjects ◽  
Epidemiologic Data ◽  
Higher Temperature ◽  
And Control

In Reply.— El-Mallakh raises hypothetical questions about an enhancing effect of fever on mitochondrial damage associated with Reye's syndrome. Our article on aspirin and Reye's syndrome1 emphasized the role of prodromal illness in use of aspirin. Fever was only one of several [See table in the PDF] prodormal illness events that were different in patients as compared with control subjects. Results of our analysis of the epidemiologic data from the Ohio study reveal a statistically significant higher temperature in those children which Reye's syndrome as compared with unmatched control subjects (Table) as well as in patients and control subjects matched for record temperatures.1

scholarly journals Lipoprotein(a) in the Nephrotic Syndrome

2000 ◽  
Vol 11 (3) ◽  
pp. 507-513
Author(s):  
CHANTAL DOUCET ◽  
VINCENT MOOSER ◽  
SOPHIE GONBERT ◽  
FRANÇOISE RAYMOND ◽  
JOHN CHAPMAN ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Plasma Concentrations ◽  
Lipoprotein A ◽  
Control Subjects ◽  
Large N ◽  
Catabolic Rate ◽  
Atherogenic Particle ◽  
Normal Urine ◽  
And Control

Abstract. Plasma levels of lipoprotein(a) (Lp(a)), an atherogenic particle, are elevated in kidney disease, which suggests a role of this organ in the metabolism of Lp(a). Additional evidence for a role of the kidney in the clearance of Lp(a) is provided by the fact that circulating N-terminal fragments of apolipoprotein(a) (apo(a)) are processed and eliminated by the renal route. To further understand the mechanism underlying such renal excretion, the levels of apo(a) fragments in plasma and urine relative to plasma Lp(a) levels were determined in patients with nephrotic syndrome (n = 15). In plasma, the absolute (24.7 ± 20.4 versus 2.16 ± 2.99 μg/ml, P < 0.0001) as well as the relative amounts of apo(a) fragments (4.6 ± 3.4% versus 2.1 ± 3.3% of total Lp(a), P < 0.0001) were significantly elevated in nephrotic patients compared with a control, normolipidemic population. In addition, urinary apo(a) excretion in patients with nephrotic syndrome was markedly elevated compared with that in control subjects (578 ± 622 versus 27.7 ± 44 ng/ml per mg creatinine, P < 0.001). However, the fractional catabolic rates of apo(a) fragments were similar in both groups (0.68 ± 0.67% and 0.62 ± 0.47% in nephrotic and control subjects, respectively), suggesting that increased plasma concentrations of apo(a) fragments in nephrotic subjects are more dependent on the rate of synthesis rather than on the catabolic rate. Molecular analysis of apo(a) immunoreactive material in urine revealed that the patterns of apo(a) fragments in nephrotic patients were distinct from those of control subjects. Full-length apo(a), large N-terminal apo(a) fragments similar in size to those present in plasma, as well as C-terminal fragments of apo(a) were detected in urine from nephrotic patients but not in urine from controls. All of these apo(a) forms were in addition to smaller N-terminal apo(a) fragments present in normal urine. This study also demonstrated the presence of Lp(a) in urine from nephrotic patients by ultracentrifugal fractionation. These data suggest that in nephrotic syndrome, Lp(a) and large fragments of apo(a) are passively filtered by the kidney through the glomerulus, whereas smaller apo(a) fragments are secreted into the urine.

Reye's Syndrome and Salicylate Use

PEDIATRICS ◽  
1980 ◽  
Vol 66 (6) ◽  
pp. 859-864
Author(s):  
Karen M. Starko ◽  
C. George Ray ◽  
Lee B. Dominguez ◽  
Warren L. Stromberg ◽  
Dora F. Woodall
Keyword(s):  
Influenza A ◽  
Control Group ◽  
Dependent Manner ◽  
Reye's Syndrome ◽  
Medication Usage ◽  
Cough Headache ◽  
Control Subjects ◽  
Gastrointestinal Complaints ◽  
And Control ◽  
Dose Dependent

During an outbreak of influenza A, seven patients with Reye's syndrome and 16 ill classmate control subjects were evaluated for characteristics of the patients' prodromal illness and the control subjects illness and for medication usage. Patients during the prodrome and control subjects had similar rates of sore throat, coryza, cough, headache, and gastrointestinal complaints except for documented fever which occurred significantly more often in patients than in control subjects (P = .05). While medications which did not contain salicylate were taken as frequently by patients as control subjects, patients took more salicylate-containing medications than did control children (P &lt; .01). All seven patients took salicylate whereas only eight of 16 control subjects did so (P &lt; .05). Patients took larger doses of salicylate than did the entire control group (P &lt; .01). When the eight control subjects who took salicylate were compared with the patients, the patients still tended to take larger doses (P = .08). Patients with fever took salicylate more frequently than control subjects with fever (P &lt; .01). In addition, salicylate consumption was correlated with severity of Reye's syndrome (P &lt; .05). It is postulated that salicylate, operating in a dose-dependent manner, possibly potentiated by fever, represents a primary causative agent of Reye's syndrome.

Aspirin Consumption and Severity of Reye's Syndrome

PEDIATRICS ◽  
1983 ◽  
Vol 71 (2) ◽  
pp. 293-294
Author(s):  
R. DON BROWN ◽  
JOHN T. WILSON
Keyword(s):  
Reye's Syndrome ◽  
Control Subjects ◽  
And Control ◽  
Study Application

To the Editor.— The article by Starko et al1 has been widely quoted, particularly with regard to a possible relationship between salicylate consumption and the severity of Reye's syndrome (RS). Our analysis of their data raises questions about support for their conclusions. It must be emphasized that only seven cases and 16 control subjects were included in their study. Application of the usual X2 tests of equal risk do not show that any variable of the antecedent illness is different between cases and control subjects.

scholarly journals Production of Interferons and β-Chemokines by Placental Trophoblasts of HIV-1-Infected Women

2001 ◽  
Vol 9 (2) ◽  
pp. 95-104 ◽  
Author(s):  
Bang-Ning Lee ◽  
Hunter Hammill ◽  
Edwina J. Popek ◽  
Stanley Cron ◽  
Claudia Kozinetz ◽  
...  
Keyword(s):  
Enzyme Linked Immunosorbent Assay ◽  
Control Subjects ◽  
Trophoblastic Cells ◽  
Inflammatory Protein ◽  
Β Protein ◽  
Immunodeficiency Virus ◽  
Vertical Transmission Of Hiv ◽  
And Control ◽  
Hiv 1

Objective:The mechanism whereby the placental cells of a human immunodeficiency virus (HIV)-1-infected mother protect the fetus from HIV-1 infection is unclear. Interferons (IFNs) inhibit the replication of viruses by acting at various stages of the life cycle and may play a role in protecting against vertical transmission of HIV-1. In addition the β-chemokines RANTES (regulated on activation T cell expressed and secreted), macrophage inflammatory protein-1-α (MIP-1α), and MIP-1β can block HIV-1 entry into cells by preventing the binding of the macrophage-trophic HIV-1 strains to the coreceptorCCR5. In this study the production of IFNs and β-chemokines by placental trophoblasts of HIV-1-infected women who were HIV-1 non-transmitters was examined.Methods:Placental trophoblastic cells were isolated from 29 HIV-1-infected and 10 control subjects. Supernatants of trophoblast cultures were tested for the production of IFNs and β-chemokines by enzyme linked immunosorbent assay (ELISA). Additionally, HIV-1-gag and IFN-β transcripts were determined by a semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) assay.Results:All placental trophoblasts of HIV-1-infected women contained HIV-1-gag transcripts. There were no statistical differences in the median constitutive levels of IFN-α and IFN-γ produced by trophoblasts of HIV-1- infected and control subjects. In contrast, trophoblasts of HIV-1-infected women constitutively produced significantly higher levels of IFN-β protein than trophoblasts of control subjects. Furthermore, the median levels of β-chemokines produced by trophoblasts of HIV-infected and control women were similar.Conclusions:Since there was no correlation between the placental HIV load and the production of interferons or β-chemokines, the role of trophoblast-derived IFNs and β-chemokines in protecting the fetus from infection with HIV-1 is not clear.

The Role of the False Neurotransmitter Octopamine in the Hypotension of Fulminant Hepatic Failure

1977 ◽  
Vol 52 (3) ◽  
pp. 305-310 ◽  
Author(s):  
P. N. Trewby ◽  
R. A. Chase ◽  
M. Davis ◽  
R. Williams
Keyword(s):  
Cardiac Output ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Control Subjects ◽  
Arteriovenous Shunts ◽  
Resting Blood Pressure ◽  
And Control

1. An investigation was carried out into the mechanism of unexplained hypotension in patients with fulminant hepatic failure. The cardiac output and peripheral resistance were compared in normotensive and hypotensive patients. In addition, the serum concentration of the false neurotransmitter octopamine and the pressor response to noradrenaline, and to the indirectly acting sympathomimetic agent tyramine, were measured in hypotensive and normotensive patients with fulminant hepatic failure and in healthy subjects. 2. The cardiac output and the peripheral resistance were decreased in the hypotensive patients, and their mean heart rate was slower than in the normotensive patients. Although the serum octopamine concentration was significantly elevated in the patients compared with the control subjects, the highest octopamine concentrations were unexpectedly found in the normotensive patients and a significant positive correlation could be demonstrated between the resting blood pressure and the serum octopamine concentration. The pressor response to tyramine and noradrenaline were similar in the hypotensive patients, the normotensive patients and control subjects. 3. These results suggest that neither increased serum concentrations of the false neurotransmitter octopamine, nor end-organ insensitivity to released noradrenaline are responsible for the hypotension. A more likely explanation is toxic depression of the vasomotor centre. The opening of peripheral arteriovenous shunts, possibly as a result of endotoxaemia, might be an additional factor.

Liver Coenzyme a Ester Content: Comparison between Reye's Syndrome and Control Subjects

1982 ◽  
Vol 63 (5) ◽  
pp. 455-460 ◽  
Author(s):  
Ellen S. Kang ◽  
Mary T. Capaci ◽  
David N. Korones ◽  
Nilima Tekade
Keyword(s):  
Fatty Acids ◽  
Coenzyme A ◽  
Relative Increase ◽  
Reye's Syndrome ◽  
Postmortem Change ◽  
Mean Values ◽  
Control Subjects ◽  
The Mean ◽  
And Control ◽  
Control Samples

1. The concentrations of the acid soluble and insoluble coenzyme A (CoA) esters were measured in samples of liver obtained at autopsy from Reye's syndrome and control subjects because the long chain fatty CoA compounds which make up the bulk of the acid insoluble CoA esters are known to inhibit a number of mitochondrially located enzymes, several of which may be affected in Reye's syndrome. 2. Concentrations of the acid insoluble esters varied widely in both control and Reye's liver samples. The difference between the mean values was not statistically significant (1·06 ± sem 0·33 nmol/g wet weight in Reye's samples vs 0·88 ± 0·21 in control samples). 3. Concentrations of the acid soluble CoA esters, which include the short chain fatty CoA compounds, were higher in Reye's liver samples than in samples from controls. The mean value for Reye's samples was 104·8 ± sem 29·4 nmol/g of liver compared with 26·4 ± 10·1 nmol/g for control samples (P < 0·05). 4. Studies with rats designed to assess postmortem change indicate that the liver concentration of the acid insoluble CoA compounds does not change during a 4 h period at 4°C. This finding suggests that the observations made in Reye's liver was probably due to a premorbid abnormality. 5. These findings implicate a block in the β-oxidation of fatty acids and could account for the reported relative increase in the concentrations of the short to medium chain fatty acids in the plasma of Reye's syndrome patients.

An approach to conducting epidemiologic research within cooperative clinical trials groups.

1984 ◽  
Vol 2 (6) ◽  
pp. 670-675 ◽  
Author(s):  
S Grufferman ◽  
E Delzell ◽  
E R Delong
Keyword(s):  
Clinical Trials ◽  
Epidemiologic Studies ◽  
Birth Certificates ◽  
Epidemiologic Research ◽  
Control Subjects ◽  
Short Period ◽  
Childhood Rhabdomyosarcoma ◽  
And Control ◽  
Control Study

Cooperative clinical trials groups offer exciting opportunities for conducting epidemiologic research for several reasons: they facilitate accrual of sufficient numbers of subjects in a short period of time, even for studies of rare diseases; they provide uniform pathologic review and uniform collection of subjects' entry data; and they provide a more representative sample of cases than a single-institution study. Despite these advantages, few epidemiologic studies of etiologic factors have been done through these groups because methods for selecting appropriate control subjects and for obtaining information from geographically scattered subjects have not been available. An approach that can serve as a model for this type of research has been developed. A collaborative case-control study of childhood rhabdomyosarcoma (RMS) with the Intergroup Rhabdomyosarcoma Study (IRS) was recently begun. The study, which is independently funded, evaluates the role of environmental factors in the etiology of RMS. Parents of subjects were interviewed by telephone and control subjects were selected from the same communities as patients by random digit dialing . Interview data are supplemented by information from birth certificates and, for patients, by IRS data. This new methodology permits a large study of a rare tumor in a relatively short period of time.

The Role of Trace Strength in Recency and Frequency Judgements by Amnesic and Control Subjects

1978 ◽  
Vol 30 (2) ◽  
pp. 347-354 ◽  
Author(s):  
Felicia A. Huppert ◽  
Malcolm Piercy
Keyword(s):  
Specific Information ◽  
Repeated Presentation ◽  
Control Subjects ◽  
Trace Strength ◽  
And Control

Amnesic and control subjects were required to judge the recency and frequency of presentation of complex pictures. The pictures were shown either once or three times 10 min or 24 h before testing. In both groups recency judgements were influenced by frequency of presentation, and frequency judgements by recency of presentation. Because the amnesic patients were unable to discriminate between the effects of repeated presentation and recent presentation, it was concluded that their judgements were determined solely by trace strength. Because controls showed some ability to make this discrimination, it was concluded that their judgements were determined jointly by trace strength and specific information about time and frequency of presentation.

Abstract 14318: Long Noncoding RNA Differentiation Antagonizing Non-protein Coding RNA 201 Ameliorates Endothelial Dysfunction via Sponging MicroRNA-216a

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
rongxia li ◽  
Shujun Yang ◽  
Yu Chen ◽  
Weili Zhang
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Noncoding Rna ◽  
Protective Factor ◽  
Luciferase Assay ◽  
Protein Coding ◽  
Control Subjects ◽  
Vulnerable Plaques ◽  
And Control

Background: Endothelial dysfunction contributes to the initiation of atherosclerosis, which has been associated with the long noncoding RNAs (lncRNAs). However, the role of lncRNAs in endothelial function remains largely unknown. This study aimed to investigate whether the differentiation antagonizing non-protein coding RNA 201 (DANCR201) regulated the endothelial function. Methods and Results: The whole transcriptome sequencing was conducted to identify differentially expressed lncRNAs in the peripheral blood from patients with coronary artery diseases who had coronary calcified plaques (n=10), vulnerable plaques (n=5), and control subjects without coronary plaques (n=10). The characteristics of plaques were determined by the coronary computed tomography angiography. The results showed that DANCR201 was significantly downregulated in patients with vulnerable plaques compared to those with calcified plaques and control subjects. The RNA fluorescence in situ hybridization showed that DANCR201 was localized in both cytoplasm and nuclei. Next, we assessed the role of DANCR201 in endothelial function. In the replicative aging model of human umbilical vein endothelial cells (HUVECs), DANCR201 was found to decrease in senescent passage 20 cells compared with young passage 3 cells. Furthermore, DANCR201 overexpression in HUVECs significantly repressed monocytes adhesion to endothelium, inhibited the expression of pro-inflammatory cytokines interleukin 1β, intercellular cell adhesion molecule 1, tumor necrosis factor α, and promoted the abilities of endothelial proliferation and migration, indicating that DANCR201 was a protective factor for endothelial function. Bioinformatics analysis of miRNA-lncRNA interactions indicated that DANCR201 contained a candidate binding sequence of miR-216a which had been reported to promote the endothelial dysfunction through NF-κB pathway. The luciferase assay further showed that DANCR201 specifically combined with miR-216a. Conclusions: Our data indicated that DANCR201 can improve endothelial function via sponging miR-216a, ultimately maintaining vascular normalization. DANCR201 maybe a potential therapeutic target for atherosclerotic plaque progression and instability.

scholarly journals Role of Cortisol and Growth Hormone in the Development of Ketosis Resistance in Malnutrition Related Diabetic Mellitus

1970 ◽  
Vol 18 (1) ◽  
pp. 5-9
Author(s):  
MA Rayhan Khandakar ◽  
M Suhrab Ali ◽  
M Obaidullah ◽  
Liaquat Ali
Keyword(s):  
Diabetes Mellitus ◽  
Growth Hormone ◽  
Serum Cortisol ◽  
Diabetic Control ◽  
Serum Growth Hormone ◽  
Cross Sectional ◽  
Control Subjects ◽  
And Control ◽  
Niddm Patients

Malnutrition Related Diabetes Mellitus (MRDM), a separate clinical class of diabetes mellitus recognized by WHO Study Group on Diabetes Mellitus in 1985 exhibits peculiar metabolic characteristic of ketosis resistance. To explore the role of cortisol and growth hormone in the development of ketosis resistance, a cross sectional study was carried out involving 21 newly diagnosed MRDM patients, 19 NIDDM patients, and 16 age matched non-diabetic control at BIRDEM, Dhaka. MRDM patients presented with significantly lower Body Mass Index (P<0.001) and significantly higher level of serum glucose (P<0.001) in comparison to NIDDM and control subjects. The mean serum cortisol was significantly higher in MRDM and NIDDM subjects compared to that of control (P<0.05). Therefore, regarding cortisol, MRDM patients behave exactly like NIDDM patients The serum growth hormone levels were similar in MRDM, NIDDM and control subjects. So it can be suggested from the study that cortisol and growth hormone may not play any significant role in the development of ketosis resistance in MRDM patients.    doi: 10.3329/taj.v18i1.3295 TAJ 2005; 18(1): 5-9

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