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Biomedical subjects

N Marin

Publications and source records attributed to N Marin.

7 recordsLinked to original sources
PubMed2002

Lack of relationship between infection by Helicobacter pylori and vomiting that usually occurs during pregnancy, although possible relationship with severe forms of emesis.

OBJECTIVE: It has been reported that infection by Helicobacter pylori may cause severe vomiting during pregnancy (hyperemesis gravidarum). Two studies were carried out in order to examine the relationship between this infection and less severe vomiting. DESIGN AND METHODS: The first study was a retrospective study involving 3438 women who required admission to the hospital during pregnancy. In 178 women, vomiting was recorded as one of the diagnoses at the time of discharge. In 162 of these women, a serum specimen was available to study the presence of anti-Helicobacter pylori antibodies (anti-HP Ab). The second study examined the presence of vomiting and anti-HP Ab in an additional 250 pregnant women who were admitted to the Maternity Ward for childbirth. In this study, the duration and intensity of emesis during the previous months was recorded. RESULTS: In the first study, no significant difference was found between the prevalence of anti-HP Ab in the 162 women in the study and a control group of women without emesis (43.2 vs 42.9%, p = NS). In the second study, there was no significant difference in seroprevalence between the women with emesis and the control group without vomiting, with the exception of the more severe cases (anti-HP Ab 77.8%, p < 0.05). CONCLUSION: The results of this study do not show that there is a relationship between infection by Helicobacter pylori and less severe vomiting during pregnancy. Nevertheless, we believe that additional studies should carried out in order to determine the relationship between the more severe cases of emesis during pregnancy and this treatable infection.

Adult↗
PubMed2001

Hepatic response to sepsis: interaction between coagulation and inflammatory processes.

OBJECTIVES: a) To review the hepatic response to sepsis and to establish how this response contributes to coagulation and inflammatory processes; b) to review the physiologic and biochemical mechanisms that suggest hepatic dysfunction may occur during sepsis, enhance procoagulant and proinflammatory activities, and participate in the potential evolution to multiple organ dysfunction syndrome. DATA SOURCES: A summary of published medical literature from MEDLINE search files and published reviews on liver function in experimental and human sepsis. DATA SUMMARY: In sepsis, the liver plays a major role in host defense mechanisms. Kupffer cells are responsible for bacterial scavenging, bacterial products inactivation, and inflammatory mediators clearance and production. Hepatocytes, via receptors for many proinflammatory cytokines, modify their metabolic pathway toward gluconeogenesis, amino-acid uptake, and increased synthesis of coagulant and complement factors and protease inhibitors. The acute-phase protein (APP) response also contributes to the procoagulant state, especially by enhancing the inhibition of protein C (alpha1-antitrypsin and alpha2-macroglobulin) and by decreasing liver synthesis of protein C and antithrombin (negative APPs). Elevated C-reactive protein levels (positive APPs) promote the expression of tissue factor by mononuclear cells. Increased liver production of thrombin-activatable fibrinolytic inhibitor (positive APPs) enhances fibrinolysis inhibition. Conversely, such hepatic inflammatory and coagulation processes in sepsis may alter the function of this organ. Indeed, the liver can be injured by activated Kupffer cells that release chemokines, attract blood neutrophils into the liver, and activate them. Neutrophils up-regulate their surface adhesion molecules, tissue factor, and Kupffer cells, whereas tissue factor pathway inhibitor and thrombomodulin are almost undetectable in endothelial cells. This may lead to microcirculatory disturbances, fibrin deposition, hepatocyte injury, endotoxin and bacteria spillover, and multiple organ failure. CONCLUSIONS: In sepsis, the liver participates in host defense and tissue repair through hepatic cell cross-talk that controls most of the coagulation and inflammatory processes. When this control is not adequate, a secondary hepatic dysfunction may occur and may sometimes lead to bacterial products spillover, enhanced procoagulant and inflammatory processes, and in turn, multiple organ failure and death.

Acute-Phase Proteins↗
PubMed1998

Rigiscan evaluation of specific nervous impairment in patients with diabetes and erectile disorders.

OBJECTIVE: A proposed new, minimally invasive, and painless method for studying impairment of the autonomic system of the penile region in type 2 diabetes patients. RESEARCH DESIGN AND METHODS: Thirteen subjects were selected from 150 patients with type 2 diabetes and erectile dysfunction who were studied in accordance with the National Institutes of Health consensus. The 13 subjects (group A), aged 55 +/- 8 years, had acceptable metabolic control (HbA1c, < 8%); no arterial or venous diseases or initial Peyronie's disease, as evaluated by penile Doppler ultrasonography and intracavernous prostaglandin E1 injection; and penile tumescence at the base (PTB) < 30 mm. Group B consisted of 13 control subjects with the same characteristics, including mean age (53.1 +/- 9 years), metabolic control (HbA1c, 7.3 +/- 0.7%), and duration of disease (8.3 +/- 0.7 years), but PTB was > 30 mm. Student's t test was used to evaluate differences in the results of autonomic cardiovascular tests, somatic tests (vibration perception threshold [VPT]), and diabetic neuropathy score (DNS) in both groups. The coefficient of variation of PTB was evaluated using the Rigiscan device (Dacomed, Minneapolis, MN), and Bayes' test was used to test sensitivity, specificity, and positive predictive values of the cardiovascular tests. RESULTS: Patients with PTB < 30 mm had significant (P < 0.05) impairment of parasympathetic tests (lying to standing, P < 0.02; standing to lying, P < 0.04; squat test, P < 0.03) compared with subjects with higher PTB values. No difference in DNS and VPT at the base and tip of the penis was found between the two groups. The variability of the test is 10% in normal subjects and 15% in both groups of patients. PTB sensitivity was 54%, specificity 89%, and positive predictive value 79%. CONCLUSIONS: In patients with diabetes and without vascular diseases, the PTB evaluated by Rigiscan is related to impairment of the autonomic nervous system. A PTB value < 30 mm may be considered a useful, noninvasive marker in studying parasympathetic damage of the penile region.

Alprostadil↗
PubMed1993

Alcohol intake impairs glucose counterregulation during acute insulin-induced hypoglycemia in IDDM patients. Evidence for a critical role of free fatty acids.

In this study, we assessed the effects of alcohol intake on glucose counterregulation in response to acute insulin-induced hypoglycemia in IDDM patients and in normal control subjects. Nine euglycemic IDDM patients and 9 normal control subjects were studied. After a baseline period, insulin (0.15 U/kg) was administered subcutaneously to induce hypoglycemia. Each IDDM patient was studied 3 times. In the first study, alcohol was orally administered as wine. In the second (control) study, water was administered instead of wine. In the third study, wine was given; however, a continuous infusion of heparin plus intralipid was administered to prevent the fall in plasma free fatty acid. Normal control subjects underwent only the alcohol and the control studies. In IDDM patients alcohol intake impairs, whereas in normal subjects it supports glucose counterregulation. Alcohol intake is associated with normal catecholamine responses in both IDDM diabetic patients and normal subjects. In both IDDM patients and normal subjects, hepatic glucose production in the recovery phase of the alcohol study was normal. Plasma glucose rate of disappearance was significantly increased by alcohol intake in IDDM (13.72 +/- 0.82 vs. 11.84 +/- 0.53 mumol.kg-1 x min-1; P < 0.05). Alcohol intake in both normal subjects and IDDM patients decreased plasma free fatty acid (267 +/- 22 vs. 156 +/- 20 microM; P < 0.01 and 356 +/- 29 vs. 96 +/- 12 microM; P < 0.01). We hypothesized that in IDDM patients, deficient glucose recovery during alcohol intake is the result of the ability of alcohol to depress lipolysis.

Acute Disease↗
PubMed1991

Human GATA-3: a lineage-restricted transcription factor that regulates the expression of the T cell receptor alpha gene.

In addition to its role in the recognition of foreign antigens, the T cell receptor (TCR) alpha gene serves as a model system for studies of developmentally-regulated, lineage-specific gene expression in T cells. TCR alpha gene expression is restricted to cells of the TCR alpha/beta+ lineage, and is controlled by a T cell-specific transcriptional enhancer located 4.5 kb 3' to the C alpha gene segment. The TCR alpha enhancer contains four nuclear protein binding sites called T alpha 1-T alpha 4. In this report we describe the identification and characterization of a novel human cDNA, hGATA-3 that binds to the T alpha 3 element of the human TCR alpha enhancer. hGATA-3 contains a zinc finger domain that is highly related to the DNA-binding domain of the erythroid-specific transcription factor, GATA-1, and binds to a region of T alpha 3 that contains a consensus GATA binding site (AGATAG). Northern blot analyses of hematopoietic cell lines demonstrate that hGATA-3 is expressed exclusively in T cells. Overexpression of hGATA-3 in HeLa cells or human B cells specifically activated transcription from a co-transfected reporter plasmid containing two copies of the T alpha 3 binding site located upstream of the minimal SV40 promoter. Taken together these results demonstrate that hGATA-3 is a novel lineage-specific hematopoietic transcription factor that appears to play an important role in regulating the T cell-specific expression of the TCR alpha gene.

Amino Acid Sequence↗
PubMed1990

Effect of a chronic infusion of atrial natriuretic peptide on vascular reactivity in normotensive and renal hypertensive rats.

In a previous study, we found that a long-term infusion of atrial natriuretic peptide (ANP) produced a sustained reduction of mean arterial pressure and peripheral vascular resistance in two-kidney, one-clip (2K-1C) hypertensive rats, whereas in control rats it had only a transient effect on cardiac output. However, plasma levels of ANP were actually 3-fold higher in normotensive than in hypertensive rats. Previous studies suggested that plasma ANP levels might modulate the vascular reactivity to the peptide. The present study examined whether the lack of chronic hemodynamic effects of ANP in control rats was due to changes in vascular reactivity to the peptide. In control rats, vascular reactivity to ANP was reduced 50% by a chronic infusion of ANP. However, in 2K-1C hypertensive rats, a long-term infusion of ANP had no effect on the vascular reactivity to ANP. The results of the present study indicate that the lack of persistent hemodynamic effects of a chronic infusion of ANP in control rats may be due to a decrease in the vascular reactivity to the peptide. The sustained hypotensive and vasodilatory effects of a long-term infusion of ANP in 2K-1C hypertensive rats are associated with no changes in the vascular reactivity to ANP.

Animals↗