130,581 research outputs found
Different pathways of degradation of SP-A and saturated phosphatidylcholine by alveolar macrophages
No full textAlveolar macrophages degrade surfactant protein (SP) A and saturated phosphatidycholine [dipalmitoylphosphatidylcholine (DPPC)]. To clarify this process, using rabbit alveolar macrophages, we analyzed the effect of drugs known to affect phagocytosis, pinocytosis, clathrin-mediated uptake, caveolae, the cytoskeleton, lysosomal pH, protein kinase C, and phosphatidylinositol 3-kinase (PI3K) on the degradation of SP-A and DPPC. We found the following: 1) SP-A binds to the plasma membrane, is rapidly internalized, and then moves toward degradative compartments. Uptake could be clathrin mediated, whereas phagocytosis, pinocytosis, or the use of caveolae are less likely. An intact cytoskeleton and an acidic milieu are necessary for the degradation of SP-A. 2) Stimulation of protein kinase C increases the degradation of SP-A. 3) PI3K influences the degradation of SP-A by regulating both the speed of internalization and subsequent intracellular steps, but its inhibition does not prevent SP-A from reaching the lysosomal compartment. 4) The degradation of DPPC is unaffected by most of the treatments able to influence the degradation of SP-A. Thus it appears that DPPC is degraded by alveolar macrophages through mechanisms very different from those utilized for the degradation of SP-A
Growth hormone and insulin-like growth factor I in a Sydney Olympic gold medallist
No full textAn Italian athlete who won a gold medal at the Sydney Olympic Games was studied. She was accused of doping after the finding of high levels of plasma growth hormone (GH) before the Games. She was studied firstly under stressed and then under unstressed conditions. In the first study, GH was measured every 20 minutes for one hour; it was above the normal range in all blood samples, whereas insulin-like growth factor I (IGF-I) was normal. In the second study, GH progressively returned to accepted normal levels; IGF-I was again normal. It was concluded that the normal range for GH in athletes must be reconsidered for doping purposes, because athletes are subject to stress and thus to wide variations in GH levels
Quadro sinottico delle informazioni disponibili in letteratura sugli Efemerotteri europei (Hexapoda: Ephemeroptera).
No full textEffect of glycyrrhetinic acid on membrane band 3 in human erythrocytes.
No full textAbstract: Glycyrrhetinic acid (GA) is a hydrolytic product of the triterpene glycoside of glycyrrhizic acid, one of the main constituents of licorice root, which has long been studied, due to its several biological and endocrine properties. In this paper, GA was tested on human erythrocytes, and GA-induced alterations were compared with those Caused by diamide, a mild oxidant inducing well-characterized cell/membrane alterations, and n-ethylmaleimide (NEM), as alkylating agent. In order to verify the biochemical steps underlying the action of GA, band 3 Tyr-phosphorylation level, enzyme recruitment and hand 3 clustering in cells pre-incubated with GA before diamide treatment were all examined. Results show that GA, in a close-dependent manner, prevents both diamide and NEM-induced band 3 Tyr-phosphorylation, but not GSH decrease caused by both compounds. In addition, diamide-induced band 3 clustering and IgG binding to altered cells were also completely reversed by GA pre-treatment. Also, when membrane sensitivity toward proteolytic digestion was tested, GA-treated cells showed high resistance to proteolysis. In conclusion, ill human erythrocytes, GA is proposed to Strengthen membrane integrity against both oxidative and proteolytic damage
Different pathways of degradation of SP-A and saturated phosphatidylcholine by alveolar macrophages.
No full textAlveolar macrophages degrade surfactant protein (SP) A and saturated phosphatidycholine [dipalmitoylphosphatidylcholine (DPPC)]. To clarify this process, using rabbit alveolar macrophages, we analyzed the effect of drugs known to affect phagocytosis, pinocytosis, clathrin-mediated uptake, caveolae, the cytoskeleton, lysosomal pH, protein kinase C, and phosphatidylinositol 3-kinase (PI3K) on the degradation of SP-A and DPPC. We found the following: 1) SP-A binds to the plasma membrane, is rapidly internalized, and then moves toward degradative compartments. Uptake could be clathrin mediated, whereas phagocytosis, pinocytosis, or the use of caveolae are less likely. An intact cytoskeleton and an acidic milieu are necessary for the degradation of SP-A. 2) Stimulation of protein kinase C increases the degradation of SP-A. 3) PI3K influences the degradation of SP-A by regulating both the speed of internalization and subsequent intracellular steps, but its inhibition does not prevent SP-A from reaching the lysosomal compartment. 4) The degradation of DPPC is unaffected by most of the treatments able to influence the degradation of SP-A. Thus it appears that DPPC is degraded by alveolar macrophages through mechanisms very different from those utilized for the degradation of SP-A
MeSH term explosion and author rank improve expert recommendations
No full textInformation overload is an often-cited phenomenon that reduces the productivity, efficiency and efficacy of scientists. One challenge for scientists is to find appropriate collaborators in their research. The literature describes various solutions to the problem of expertise location, but most current approaches do not appear to be very suitable for expert recommendations in biomedical research. In this study, we present the development and initial evaluation of a vector space model-based algorithm to calculate researcher similarity using four inputs: 1) MeSH terms of publications; 2) MeSH terms and author rank; 3) exploded MeSH terms; and 4) exploded MeSH terms and author rank. We developed and evaluated the algorithm using a data set of 17,525 authors and their 22,542 papers. On average, our algorithms correctly predicted 2.5 of the top 5/10 coauthors of individual scientists. Exploded MeSH and author rank outperformed all other algorithms in accuracy, followed closely by MeSH and author rank. Our results show that the accuracy of MeSH term-based matching can be enhanced with other metadata such as author rank
Polycystic ovary syndrome: implications of corticotropin in the regulation of blood pressure, aldosterone, and androgen secretion.
No full textn a recent issue of Hypertension, Chen et al1 have described a correlation between androgen levels and blood pressure in young women with polycystic ovary syndrome (PCOS), and this correlation was independent from age, insulin resistance, obesity, and dyslipidemia. We would like to discuss other factors involved in the interpretation of these data.
High adrenal androgen levels in women with PCOS can also be related to an increase of corticotropin (ACTH). The major question is why ACTH could be responsible for an increase of adrenal androgens in PCOS. Previous reports have documented that patients with PCOS have reduced activity of 11β-hydroxysteroid dehydrogenase type 1, the enzyme that activates cortisone to cortisol.2 11β-Hydroxysteroid dehydrogenase type 1 may enhance the metabolic clearance rate of cortisol, thereby reducing negative feedback and increasing ACTH-dependent adrenal androgen production. It is interesting, at this point, that an extremely high increase of cortisone metabolites and of androgen concentrations are reported in some patients with PCOS and cortisone reductase deficiency.3
In a recent paper by Cascella et al,4 a positive correlation was found between aldosterone and mean blood pressure in patients with PCOS and, more interestingly, between aldosterone and C- reactive protein, metabolic patterns, and intima-media thickness. Both androgens1 and aldosterone4 correlate with blood pressure, and these findings are consistent with chronic ACTH drive in adrenals of patients with PCOS.
In fact, whereas administration of high amounts of ACTH for several days or 11-hydroxylase deficiency is associated with suppression of aldosterone and increase of deoxycorticosterone, a chronic ACTH drive because of a partial defect of 11β-hydroxysteroid dehydrogenase type 1 could activate aldosterone synthase at the level of adrenal glomerulosa and androgen secretion by the adrenal reticularis. We, therefore, suggest that a relative chronic increase of ACTH related to a slight deficiency of 11β-hydroxysteroid dehydrogenase type 1 can explain the reported hormonal pattern of these subjects.
The correlation among aldosterone, oxidative stress, metabolism abnormalities, and blood pressure is consistent with a primary involvement of aldosterone and not of androgens in the increase of blood pressure. These data also support the possibility of therapy with spironolactone in patients with PCOS. The drug blocks both the proinflammatory status because of aldosterone binding to mineralocorticoid receptors and the clinical picture of hyperandrogenism because of the binding of androgens to androgen receptors. We have recently stressed these concepts in a study of women with PCOS.
Pseudohypoaldosteronism in eight families: different forms of inheritance are evidence for various genetic defects.
No full textPseudohypoaldosteronism is a rare hereditary disorder presenting in early infancy with renal salt loss leading to hyponatremia and hyperkalemia despite high levels of plasma aldosterone. The patients are insensitive to mineralocorticoids; however, sodium supplementation is able to correct electrolyte abnormalities. Absent or greatly diminished type I aldosterone receptors in peripheral mononuclear leucocytes have been recently demonstrated and explain the lack of response to mineralocorticoids. We have studied the mode of inheritance in eight families with a total of nine patients. There was evidence for an autosomal recessive form of inheritance in four families, while the other four families appeared to have an autosomal dominant mode of transmission. In three families the autosomal recessive form was characterized by normal receptor as well as hormone data in both parents, while in one family receptor levels in both parents were greatly reduced, but hormone levels were normal. In the four families with an autosomal dominant mode of transmission there was always one parent with reduced receptor binding in peripheral mononuclear leucocytes and elevated serum hormone levels. These parents were entirely asymptomatic. In an extended family we were able to study an aunt and her newborn daughter, who were both also biochemically affected but clinically asymptomatic. It, therefore, appears that this dual pattern of genetic transmission may indicate differing genetic defects which cause the same clinical picture of pseudohypoaldosteronism
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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