1,720,990 research outputs found
Testosterone Disorders and Male Hypogonadism in Kidney Disease
No full textChronic kidney disease (CKD) causes substantial alterations in the male endocrine system, which affect puberty, libido, and sexual function. A major effect of CKD is a reduction in testosterone levels because of both primary and hypogonadotrophic hypogonadism. In addition to impairment of pubertal growth and sexual maturation in children with CKD, clinical evidence suggests that uremic hypogonadism strongly contributes to several CKD complications, including erectile dysfunction, muscle wasting and frailty, anemia, decreased bone mineralization, depression, and cognitive impairment. This review focuses on a reappraisal of the physiologic role of testosterone, with an emphasis on the hypogonadal condition linked to CKD and its complications
Alterazioni del metabolismo dell'acqua e del sodio
No full textCapitolo nel Manuale di Nefrologia 201
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe 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
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Effects of chronic metabolic acidosis on splanchnic protein turnover and oxygen consumption in human beings.
No full textBACKGROUND & AIMS: Although metabolic acidosis stimulates protein catabolism, its effects on splanchnic protein turnover and energy expenditure have not been measured in human beings. We investigated the effects of chronic metabolic acidosis (CMA) on splanchnic protein dynamics and oxygen consumption in human beings by using a leucine tracer and mass-balance techniques.
METHODS: Five subjects were studied after 6 days of HCl-, CaCl(2)-, and NH(4)Cl-induced acidosis; 8 subjects served as controls. Blood samples were collected from the radial artery and the hepatic veins. Measurements were performed on plasma and whole-blood samples.
RESULTS: Based on plasma measurements, subjects who had undergone CMA had lower rates of splanchnic proteolysis (-35%) and protein synthesis (-50%; P < .05) than controls, as well as a negative leucine kinetic balance (-6.81 +/- 2.48 micromol/kg/min/1.73 m(2) body surface [BS](-1)), compared with the neutral balance in control plasma samples (0.76 +/- 2.11 micromol/kg/min/1.73; P < .05 between groups). Based on measurements from whole blood, splanchnic proteolysis and protein synthesis did not differ significantly between CMA and control samples, and the net leucine kinetic balance was neutral in both groups (CMA, -0.69 +/- 1.57; controls, -0.74 +/- 3.45 micromol/kg/min/1.73). In CMA whole-blood measurements, splanchnic oxygen consumption (44.8 +/- 4.3 mL/min/1.73 m(2) BS) was slightly lower than in controls (57.5 +/- 8.4 mL/min/1.73 m(2) BS; P = NS). Splanchnic protein synthesis correlated with oxygen consumption (r = 0.82; P < .001).
CONCLUSIONS: CMA reduces splanchnic protein turnover and results in a negative leucine balance--an effect that apparently is offset by the contribution of blood cells to organ leucine (and protein) dynamics. Protein synthesis is a major contributor (about 67%) to energy expenditure in splanchnic organ
Uric acid and angiotensin II additively promote inflammation and oxidative stress in human proximal tubule cells by activation of toll-like receptor 4.
No full textRenal proximal tubular cells (PTECs) participate in several mechanisms of innate
immunity, express toll‐like receptors (TLRs), and proinflammatory cytokines.
Hyperuricemia may be a promoter of inflammation and renal damage.
Angiotensin II (Ang II) modulate immune and inflammatory responses in renal
tubular cells. With the aim to evaluate the effect of uric acid (UA) and Ang II on
oxidative stress and inflammation mediated by toll‐like receptor 4 (TLR4)
activation in human PTECs, human kidney 2 (HK2) were incubated for 24 hr with
UA (12 mg/dl) and Ang II (10−7 M). HK2 were pretreated with an antagonist of
TLR4 (TAK 242), valsartan or losartan. The genic expression of TLR4, monocyte
chemoattractant protein‐1 (MCP1), and Nox4 was quantified with reverse
transcription polymerase chain reaction, proteins were evaluated with Western
blot. The incubation of HK2 either with UA or with Ang II determines an
increased expression of TLR4, production of proinflammatory cytokines as MCP1
and pro‐oxidants as Nox4 (p < 0.05). TAK 242 attenuates the expression of MCP1
induced both by UA and Ang II. Valsartan attenuated all the effects we described
after exposure to Ang II but not those observed after UA exposure. At variance,
pretreatment with losartan, which inhibits UA internalization, attenuates the
expression of TLR4, MCP1, and Nox4 in cells previously treated with UA, Ang II,
and UA plus Ang II. Proinflammatory pathways are induced in an additive manner
by UA and Ang II (p < 0.05) and might be mediated by TLR4 in PTECs. Renin–
angiotensin–aldosterone system (RAAS) activation, hyperuricemia, and innate
immunity interplay in the development of chronic tubular damage and the
interaction of several nephrotoxic mechanisms blunt the protective effect of
RAAS inhibition
The role of uric acid in renal damage: A history of inflammatory pathways and vascular remodeling
No full textIncreased serum uric acid levels are associated to renal arteriolopathy and predict poor outcome in IgA nephropathy
No full textBackground and aims: IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide and a leading cause of end stage renal disease (ESRD). In addition to classical progression factors, other atherosclerosis-related factors, including hyperuricemia (HU), have been associated to the renal progression of IgAN. Increased serum uric acid (SUA) levels are well known to be concomitant of cardiovascular and kidney diseases, and have been proposed to be implicated in the development of arteriolar damage (AD). The aim of the present study was to explore the correlation between SUA levels, renal damage and its implication for outcome in IgAN patients. Methods and results: Clinical, laboratory and histologic data of 145 patients with biopsy proven IgAN were collected and retrospectively analyzed to determine the correlation between SUA levels, renal damage and the primary outcome (death or ESRD). Biopsy-proven AD was defined by the presence of arteriolar hyalinosis and/or intimal thickening. HU, defined as the highest SUA gender-specific tertile, was >7.7 mg/dl for males and >6.2 mg/dl for females. The prevalence of AD increased with the increase in the SUA level tertiles (p = 0.02). At logistic regression analysis SUA was independently related to the presence of AD (OR 1.75 [95%CI 1.10–2.93], p = 0.03). HU and AD had a synergic impact on progression of IgAN. Patients having both AD and HU, showed a reduced survival free from the primary outcome as compared to those having only one risk factor or neither (p = 0.01). Conclusions: SUA levels are independently associated with AD and poor prognosis in patients with IgAN
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