The white spot syndrome virus DNA genome sequence

AbstractWhite spot syndrome virus (WSSV) is at present a major scourge to worldwide shrimp cultivation. We have determined the entire sequence of the double-stranded, circular DNA genome of WSSV, which contains 292,967 nucleotides encompassing 184 major open reading frames (ORFs). Only 6% of the WSSV ORFs have putative homologues in databases, mainly representing genes encoding enzymes for nucleotide metabolism, DNA replication, and protein modification. The remaining ORFs are mostly unassigned, except for five, which encode structural virion proteins. Unique features of WSSV are the presence of a very long ORF of 18,234 nucleotides, with unknown function, a collagen-like ORF, and nine regions, dispersed along the genome, each containing a variable number of 250-bp tandem repeats. The collective information on WSSV and the phylogenetic analysis on the viral DNA polymerase suggest that WSSV differs profoundly from all presently known viruses and that it is a representative of a new virus family

Los Pirineos en el contexto de las montañas del mundo: rasgos generales y peculiaridades

29 páginas.Este trabajo introductorio intenta presentar la cordillera de los Pirineos, y especialmente sus características naturales dominantes, señalando en particular aquellas que comparte con otras cordilleras del globo, y aquellas que son peculiares de esta cadena, o compartidas con pocos sistemas montañosos similares. Veamos pues, en primer lugar, algunos rasgos generales de la mayor parte de las cordilleras.Peer reviewe

Protection of the Ovine Fetal Gut against Ureaplasma-Induced Chorioamnionitis: A Potential Role for Plant Sterols

Chorioamnionitis, clinically most frequently associated with Ureaplasma, is linked to intestinal inflammation and subsequent gut injury. No treatment is available to prevent chorioamnionitis-driven adverse intestinal outcomes. Evidence is increasing that plant sterols possess immune-modulatory properties. Therefore, we investigated the potential therapeutic effects of plant sterols in lambs intra-amniotically (IA) exposed to Ureaplasma. Fetal lambs were IA exposed to Ureaplasma parvum (U. parvum, UP) for six days from 127 d–133 d of gestational age (GA). The plant sterols β-sitosterol and campesterol, dissolved with β-cyclodextrin (carrier), were given IA every two days from 122 d–131 d GA. Fetal circulatory cytokine levels, gut inflammation, intestinal injury, enterocyte maturation, and mucosal phospholipid and bile acid profiles were measured at 133 d GA (term 150 d). IA plant sterol administration blocked a fetal inflammatory response syndrome. Plant sterols reduced intestinal accumulation of proinflammatory phospholipids and tended to prevent mucosal myeloperoxidase-positive (MPO) cell influx, indicating an inhibition of gut inflammation. IA administration of plant sterols and carrier diminished intestinal mucosal damage, stimulated maturation of the immature epithelium, and partially prevented U. parvum-driven reduction of mucosal bile acids. In conclusion, we show that β-sitosterol and campesterol administration protected the fetus against adverse gut outcomes following UP-driven chorioamnionitis by preventing intestinal and systemic inflammation

Dissociation of transforming growth factors beta 1 and beta 2 from surfactant protein A (SP-A) by deglycosylation or deoxycholate treatment

We were able to demonstrate the presence of transforming growth factor beta 1 and transforming growth factor beta 2 (TGF-beta 1,2) in human as well as porcine pulmonary surfactants and SP-A purified from these surfactants. Human SP-A contained 480 +/- 74 pg TGF-beta 1 and 61 +/- 16 pg TGF-beta 2 per mg SP-A and human pulmonary surfactant contained 140 +/- 28 pg TGF-beta 1 and 67 +/- 13 TGF-beta 2 per mg protein. Porcine SP-A contained 306 +/- 46 pg TGF-beta 1 and 43 +/- 12 pg TGF-beta 2 per mg SP-A and porcine pulmonary surfactant contained 75 +/- 18 pg TGF-beta 1 and 22 +/- 13 TGF-beta 2 per mg protein. Size-exclusion chromatography indicated binding of TGF-beta 1,2 to SP-A Deglycosylation of SP-A released TGF-beta 1,2 from SP-A indicating a role for the carbohydrate moieties of SP-A in binding of TGF-beta 1,2. TGF-beta-free SP-A was obtained by incubating SP-A with 5 mM deoxycholate at pH 9.2 followed by size-exclusion chromatography, a protocol which can be used to study the biological activities of SP-A and TGF-beta 1,2 separately. In addition, we demonstrated that after incubation of SP-A with TGF-beta 1,2, only a part of the added TGF-beta 1,2 can be measured, whereas after acid treatment almost all added TGF-beta 1,2 was determined, suggesting that complex formation between SP-A and TGF-beta 1,2 influences the measurements of TGF-beta 1,2 in biological samples

Dissociation of transforming growth factors beta 1 and beta 2 from surfactant protein A (SP-A) by deglycosylation or deoxycholate treatment

We were able to demonstrate the presence of transforming growth factor beta 1 and transforming growth factor beta 2 (TGF-beta 1,2) in human as well as porcine pulmonary surfactants and SP-A purified from these surfactants. Human SP-A contained 480 +/- 74 pg TGF-beta 1 and 61 +/- 16 pg TGF-beta 2 per mg SP-A and human pulmonary surfactant contained 140 +/- 28 pg TGF-beta 1 and 67 +/- 13 TGF-beta 2 per mg protein. Porcine SP-A contained 306 +/- 46 pg TGF-beta 1 and 43 +/- 12 pg TGF-beta 2 per mg SP-A and porcine pulmonary surfactant contained 75 +/- 18 pg TGF-beta 1 and 22 +/- 13 TGF-beta 2 per mg protein. Size-exclusion chromatography indicated binding of TGF-beta 1,2 to SP-A Deglycosylation of SP-A released TGF-beta 1,2 from SP-A indicating a role for the carbohydrate moieties of SP-A in binding of TGF-beta 1,2. TGF-beta-free SP-A was obtained by incubating SP-A with 5 mM deoxycholate at pH 9.2 followed by size-exclusion chromatography, a protocol which can be used to study the biological activities of SP-A and TGF-beta 1,2 separately. In addition, we demonstrated that after incubation of SP-A with TGF-beta 1,2, only a part of the added TGF-beta 1,2 can be measured, whereas after acid treatment almost all added TGF-beta 1,2 was determined, suggesting that complex formation between SP-A and TGF-beta 1,2 influences the measurements of TGF-beta 1,2 in biological samples

Pulmonary Vascular Endothelial Growth Factor Expression and Disaturated Phospholipid Content in a Chicken Model of Hypoxia-Induced Fetal Growth Restriction

Background: Prenatal hypoxia is an important cause of intrauterine growth retardation that affects fetal lung maturation, although previous studies have rendered conflicting results. The fetal chicken model allows the study of the isolated effects of hypoxia during development. Objectives: We hypothesized that prenatal hypoxia would differentially affect surfactant synthesis, depending on timing and duration of hypoxia. Pulmonary vascular endothelial growth factor (VEGF) expression was analyzed as a possible link between oxygen sensing and surfactant production. Methods: Fertilized White Leghorn eggs were incubated in normoxia, hyperoxia (60% O-2) from day 15 or hypoxia (15% O-2) from either day 6 or day 15 of incubation. Whole lung disaturated phospholipids (DSPL) and mRNA expression of VEGF isoforms were quantified at day 16 and 19. Results: Lung DSPL content increased approximately threefold between day 16 and 19 in control animals. Both hypoxia and hyperoxia from day 15 significantly increased DSPL content at day 19 versus control (103 +/- 22 and 116 +/- 18 vs. 81 +/- 15 mu g/mg protein, p <0.01 and p <0.001, respectively), while long-term hypoxia tended to decrease DSPL content (65 +/- 17 mu g/mg protein, p = 0.056). No differences in DSPL content were observed at day 16. Short-term hypoxia transiently up-regulated VEGF146 1.5-fold at day 16 (p <0.05). A similar trend was observed for VEGF122 (p = 0.058) and VEGF190 (p = 0.08), while no differences were present at day 19. Conclusions: Both prenatal hypoxia and hyperoxia induced during critical windows of lung development differentially modulate surfactant synthesis. Our data support the concept that fetal oxygen tension is a key signal in the regulation of the surfactant system

A comparison of four different models of acute respiratory distress syndrome in sheep

BACKGROUND: Acute respiratory distress syndrome (ARDS) can have various causes. The study objective was to investigate whether different pathophysiologic models of ARDS would show different respiratory, cardiovascular and inflammatory outcomes. METHODS: We performed a prospective, randomized study in 27 ventilated ewes inducing ARDS using three different techniques to mimic the pulmonary causes of ARDS (ARDSp): warm saline lavage (n = 6), intratracheal hydrochloric acid (HCl; n = 6), intratracheal albumin (n = 10), and one technique to mimic an extrapulmonary cause of ARDS (ARDSexp): intravenous lipopolysaccharide (LPS iv; n = 5). ARDS was defined when PaO2 was &lt; 15 kPa (112 mmHg) when ventilated with PEEP 10 cm H2O and FiO2 = 1.0. The effects on gas exchange were investigated by calculating the oxygenation index (OI) and the ventilation efficacy index (VEI) every 30 min for a period of 4 h. Post mortem lung lavage was performed to obtain broncho-alveolar lavage fluid (BALF) to assess lung injury and inflammation. Lung injury and inflammation were assessed by measuring the total number and differentiation of leukocytes, the concentration of protein and disaturated phospholipids, and interleukine-6 and -8 in the BALF. Histology of the lung was evaluated by measuring the mean alveolar size, alveolar wall thickness and the lung injury score system by Matute-Bello et al., as markers of lung injury. The concentration of interleukin-6 was determined in plasma, as a marker of systematic inflammation. RESULTS: The OI and VEI were most affected in the LPS iv group and thereafter the HCl group, after meeting the ARDS criteria. Diastolic blood pressure was lowest in the LPS iv group. There were no significant differences found in the total number and differentiation of leukocytes, the concentration of protein and disaturated phospholipids, or interleukin-8 in the BALF, histology of the lung and the lung injury score. IL-6 in BALF and plasma was highest in the LPS iv group, but no significant differences were found between the other groups. It took a significantly longer period of time to meet the ARDS criteria in the LPS iv group. CONCLUSION: The LPS model caused the most severe pulmonary and cardiovascular insufficiency. Surprisingly, there were limited significant differences in lung injury and inflammatory markers, despite the different pathophysiological models, when the clinical definition of ARDS was applied