Publications by authors named "Canessa M"

Over the past thirty years, the red gorgonian in the Mediterranean Sea has faced increasing threats, including heat waves and human activities such as artisanal and recreational fishing. Epibiosis on damaged gorgonian colonies is generally used as an indirect indication of stressed conditions. The density and height of and the percentage of colonies affected by epibiosis and entangled in lost fishing gear were monitored to investigate the phenomenon and its trend over time in the Ligurian Sea.

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  • The golden coral Savalia savaglia acts as an ecosystem engineer in Mediterranean waters, affecting the growth and health of nearby gorgonians and black corals while thriving in unique conditions near underwater freshwater springs in Boka Kotorska Bay, Montenegro.
  • A population of over 1000 colonies was found, demonstrating high abundance and significant size, which suggests active asexual reproduction and non-parasitic growth on available coral skeletons.
  • Given its ecological significance, the establishment of a permanent Marine Protected Area is recommended to ensure the ongoing health of this unique animal forest and its surrounding biodiversity.
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  • Congenital hydrocephalus (CH) is a diverse set of birth defects with varying prevalence, and this study aimed to analyze the early neonatal case fatality rate (CFR) and total birth prevalence (BPR) among newborns with CH using data from 25 international registries from 2000 to 2014.
  • The study found that the early neonatal CFR was 5.9 per 100 liveborn CH cases, with syndromic cases having a significantly higher CFR than non-syndromic cases (10.4% vs. 4.4%).
  • Although there were substantial differences in CFR and BPR across registries, higher CFR often correlated with higher BPR; however, most
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The timing for surgical treatment in patients with primary organic severe mitral valve regurgitation and preserved left ventricular ejection fraction (LVEF) systolic is a challenge since it depends upon LV end systolic dimension and LVEF which may be late markers of LV dysfunction. Echocardiography is the most important tool in the diagnosis of mechanisms, etiology, severity, and hemodynamic consequences of mitral regurgitation. The global longitudinal strain (GLS), a new and sensitive method for the detection of LV dysfunction, might be a useful method for the evaluation of preclinical systolic dysfunction.

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Background: Hypospadias is a common male birth defect that has shown widespread variation in reported prevalence estimates. Many countries have reported increasing trends over recent decades.

Objective: To analyze the prevalence and trends of hypospadias for 27 international programs over a 31-yr period.

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Marine caves are unique and vulnerable habitats exhibiting high biodiversity and heterogeneity, but threatened by multiple global and local disturbances. Marine caves, although widely distributed along the Mediterranean coast, suffer for the lack of quantitative data on their structure and function, which hinder their conservation status assessment. Thanks to the availability of a nearly 30-year-long series of data (1986-2013), we evaluated ecosystem change in the Bergeggi marine cave (Ligurian Sea, NW Mediterranean), a cave with a complex shape and high habitat heterogeneity.

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Introduction: Heavy menstrual bleeding (HMB) occurs in 37% of adolescents and compromise their quality of life.

Objective: To measure the magnitude of the impact of the SME on the quality of life in adolescents.

Patients And Method: We interviewed adolescents diagnosed with HMB between 10 and 18 years old and one of their guardians.

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Our objective was to evaluate the frequency and type of malformations associated with gastroschisis in a large pool of international data, to identify malformation patterns, and to evaluate the role of maternal age in non-isolated cases. Case-by-case information from 24 registries, all members of the International Clearinghouse for Birth Defects Surveillance and Research (ICBDSR), were evaluated. After the exclusion of other abdominal wall defects cases were classified as: (a) isolated; (b) recognizable syndrome, chromosomal or not; (c) multiple congenital anomalies (MCA).

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Adrenal zona glomerulosa (ZG) cells produce aldosterone in response to angiotensin II and extracellular potassium through different mechanisms which involve changes in cytosolic free calcium (Cai). Protein kinase C (PKC) activation is part of the angiotensin II signalling cascade but its effects on Cai are unknown. PKC activation with 1 microM phorbol 12-myristate 13-acetate (PMA) and 8 mM Ko significantly increased the rate of calcium influx (P < 0.

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Indirect evidence has suggested that K-Cl cotransport in human and sheep erythrocytes is activated physiologically by a serine-threonine phosphatase. It is activated experimentally by H2O2 and by staurosporine, a kinase inhibitor. Activation by H2O2 and staurosporine is inhibited by serine-threonine phosphatase inhibitors, suggesting that the activators stimulate the phosphatase.

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We measured erythrocyte Na+/Li+ and Na+/H+ countertransport (CT) activity (millimoles per liter per cell per hour) in 10 healthy control subjects (age, 38 +/- 4 years; body mass index, 25 +/- 1 kg/m2) and in 25 hypertensive patients with non-insulin-dependent diabetes mellitus ([NIDDM] age, 49 +/- 3 years; body mass index, 29 +/- 1 kg/m2; fasting plasma glucose, 157 +/- 12 mg/dL) 4 weeks after discontinuation of previous antihypertensive treatment. Na+/Li+ CT was significantly increased in hypertensive NIDDM patients compared with controls (0.56 +/- 0.

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We have previously shown that a pretreatment with phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC), reduced deoxygenation-induced K+ loss and Ca2+ uptake and prevented cell dehydration in sickle anemia red blood cells (SS cells) (H. Fathallah, E. Coezy, R.

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Deoxy-stimulated cation fluxes have been implicated in the generation of the dense and irreversibly sickled red blood cells (RBCs) in patients homozygous for hemoglobin S (SS). We now report on the effect of short term deoxygenation on K+ and Na+ transport in RBCs from control mice (C57Bl/6J) and a transgenic (alphaHbetaS[betaMDD]) mouse line that expresses high levels of human alphaH and betaS-chains and has a small percent dense cells but does not exhibit anemia. In transgenic mouse RBCs (n = 5) under oxygenated conditions, K+ efflux was 0.

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K:Cl cotransport is involved in generating dense red blood cells (RBCs) in homozygotes for HbS (SS). We report on the properties of this transport system in RBCs from control and transgenic mice expressing high levels of human alpha(H) and beta(S) chains. Unlike human SS RBCs, mouse RBCs incubated in isotonic media exhibited a Cl(-)-dependent K+ efflux and therefore have a different set-point for activation.

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Insulin activation of red blood cell (RBC) Na+/H+ (NHE) and Na+/Li+ (NLiE) exchanges is mimicked by okadaic acid, thus suggesting that it may change the state of phosphorylation of serine/threonine NHE residues. To investigate the role of the serine/threonine protein kinase C (PKC) in insulin regulation, we evaluated the effect of phorbol 12-myristate 13-acetate (PMA; 1 microM) and insulin on PKC activity, membrane protein phosphorylation, and the activation kinetics of both exchangers. Our studies revealed that PMA decreased cytosolic PKC activity (4.

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Increased activity of the sodium transporter, sodium-lithium countertransport (SLC), is reported in hypertensive white patients with evidence of cardiac and renal injury. The purpose of this study was to determine whether increased SLC activity detects risk for nephropathy or vascular disease in nondiabetic, young adult African-Americans. We examined 85 African-Americans aged 25 to 33 years with measurement of blood pressure, an oral glucose tolerance test to measure insulin response to glucose challenge, and an insulin clamp for insulin sensitivity (M).

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Abnormalities of intracellular calcium homeostasis and sodium-proton exchange have been implicated in the pathophysiology of essential hypertension. To further define the nature of cytosolic calcium abnormalities and whether they relate to increased sodium-proton exchange in hypertension, we have studied peripheral lymphocytes from normotensive and hypertensive subjects. Lymphocyte cytosolic calcium was significantly increased (P < .

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In the present study we investigated the effect of a selective alpha 1-adrenergic blocker (doxazosin), an angiotensin-converting enzyme (ACE) inhibitor (captopril), and a calcium channel antagonist (nifedipine) on renal function in hypertensive non-insulin-dependent diabetic patients. 30 NIDD hypertensive patients (age = 50 +/- 3 years; BMI = 30 +/- 1 kg/m2) (mean +/- SEM) were studied before and after a 12-week period of antihypertensive treatment. Ten patients were treated with doxazosin (Cardura) (2-8 mg once daily or 8 mg b.

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Establishing whether high ambient glucose affects the plasma membrane Na+/H+ exchanger is relevant to understanding the adverse effects of high glucose on cell replication and the mechanisms of the increased exchanger activity encountered in diabetic patients with nephropathy. In 8 primary and 15 first-passage isolates of human endothelial cells cultured in 30 mmol/l glucose for 8.7 +/- 2.

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We compared the effects of captopril, nifedipine, and doxazosin on glucose and lipid metabolism in 30 hypertensive non-insulin-dependent diabetes mellitus (NIDDM) patients (age = 50 +/- 3 years; body mass index = 30 +/- 1 kg/m2). Of these patients, 9 were treated with captopril, 11 with nifedipine, and 10 with doxazosin for 12 weeks. Blood pressure, fasting plasma glucose (FPG) concentration, HbA1c, oral glucose tolerance test (OGTT), euglycemic insulin clamp, and plasma lipids were measured before and after a 3-month period.

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The purpose of this study was to determine whether early nephropathy, evidenced by urinary albumin excretion, can be detected in young African American subjects with only borderline hypertension, and whether there is a relationship of albuminuria with insulin resistance and with sodium-lithium countertransport activity. Clinically well young African American men and women including normotensive (blood pressure < 135/85 mm Hg, n = 41) and borderline hypertensive (blood pressure > or = 135/85 mm Hg, n = 26) individuals were studied. Each subject underwent an oral glucose tolerance test and euglycemic hyperinsulinemic clamp study.

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Human red blood cells possess a Na (+)H (+) antiporter in the plasma membrane that can exchange external Na(+) for intracellular H(+) when the intracellular pH falls below 7.0. The antiporter can also exchange Na(+) for Li(+) and that is named Na (+)Li (+) countertransport (SLC).

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We recently reported that incubation of red blood cells with insulin markedly decreases the affinity for external Na+ and increases the maximal transport rate (Vmax) of Na(+)-Li+ countertransport. The association of hypertension with insulin resistance and its compensatory hyperinsulinemia led us to investigate the relationship between insulin levels in vivo and the Na+ activation kinetics of this antiporter. We studied normotensive (n = 28) and hypertensive (n = 25) subjects after they had fasted overnight and determined their plasma glucose and insulin concentrations.

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The purpose of this study was to determine whether antihypertensive therapy with the angiotensin converting enzyme inhibitor lisinopril would alter cell Na+ transport kinetics, metabolic parameters associated with insulin resistance, or both in young adults with mild hypertension. Sixteen young adults (mean age 29 +/- 4 years) were treated with placebo for 8 weeks, then with lisinopril for 12 weeks. Metabolic risk factors examined included plasma lipid levels, plasma insulin concentration during an oral glucose tolerance test, and insulin sensitivity determined by an euglycemic hyperinsulinemic clamp procedure.

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Red blood cells (RBC) of subjects homozygous for hemoglobin A (AA), C (CC) and S (SS) exhibit different cell volumes which might be related to differences in cell volume regulation. We have investigated how rapidly K:Cl cotransport is activated and deactivated to regulate the cell volume in these cells. We measured the time course of net K+ efflux after step changes in cell volume and determined two delay times: one for activation by cell swelling and a second for deactivation by cell shrinkage.

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