The spectral quality of light is a key driver of photosynthesis and photoadaptation in Stylophora pistillata colonies from different depths in the Red Sea.

Depth zonation on coral reefs is largely driven by the amount of downwelling, photosynthetically active radiation (PAR) that is absorbed by the symbiotic algae (zooxanthellae) of corals. The minimum light requirements of zooxanthellae are related to both the total intensity of downwelling PAR and the spectral quality of the light. Here we used Stylophora pistillata colonies collected from shallow (3 m) and deep (40 m) water; colonies were placed in a respirometer under both ambient PAR irradiance and a filter that only transmits blue light. We found that the colonies exhibited a clear difference in their photosynthetic rates when illuminated under PAR and filtered blue light, with higher photosynthetic performance when deep colonies were exposed to blue light compared with full-spectrum PAR for the same light intensity and duration. By contrast, colonies from shallow water showed the opposite trend, with higher photosynthetic performances under full-spectrum PAR than under filtered blue light. These findings are supported by the absorption spectra of corals, with deeper colonies absorbing higher energy wavelengths than the shallow colonies, with different spectral signatures. Our results indicate that S. pistillata colonies are chromatically adapted to their surrounding light environment, with photoacclimation probably occurring via an increase in photosynthetic pigments rather than algal density. The spectral properties of the downwelling light are clearly a crucial component of photoacclimation that should be considered in future transplantation and photoacclimation studies.

Functional MASP2 single nucleotide polymorphism plays no role in psoriasis.

BACKGROUND: Psoriasis is a heritable disease and genome-wide scans have implicated several loci of susceptibility. The gene for MASP-2, a protease involved in complement activation, is located within one of these loci on chromosome 1p. OBJECTIVES: To assess whether partial or total MASP-2 deficiency is a risk factor for developing psoriasis. METHODS: We screened a cohort of patients affected by plaque psoriasis and their parents by restriction fragment length polymorphism analyses. RESULTS: We detected a single nucleotide polymorphism that leads to an amino acid exchange, which results in dissociation of MASP-2 from a carbohydrate recognition complex. CONCLUSIONS: We show that this mutant allele is not associated with psoriasis. There was no favoured transmission from parents to affected offspring. The calculated allele frequency in this psoriasis group (Scottish and English) was 0.0326, and in the unaffected group 0.0379.

A Crohn's disease-associated insertion polymorphism (3020insC) in the NOD2 gene is not associated with psoriasis vulgaris, palmo-plantar pustular psoriasis or guttate psoriasis.

A C-insertion polymorphism in the NOD2 gene (3020insC) on chromosome 16 is a rare mutation associated with Crohn's disease. Crohn's disease and psoriasis are more commonly observed together than expected by chance. Furthermore a susceptibility locus for psoriasis has been identified on chromosome 16q which overlaps the recently identified susceptibility locus for Crohn's disease. Thus, NOD2 may potentially be important as a candidate susceptibility gene for psoriasis. We tested this hypothesis by genotyping psoriasis patients for the C-insertion polymorphism using the Taqman ABI 7700 sequencing system. No statistically significant differences were observed between psoriasis vulgaris (n = 216), palmo-plantar pustular psoriasis (PPP) (n = 100), guttate psoriasis (n = 118) and the control group (n = 283). In both patient and control groups, no mutant homozygotes were observed and approximately 4% were heterozygotes. This particular insertion mutation in the NOD2 gene does not appear to contribute to the genetic susceptibility of psoriasis vulgaris, PPP or guttate psoriasis. However, other mutations exist in the NOD2 gene, which may potentially have a role in psoriasis susceptibility.

Response of Vibrio parahaemolyticus 03:K6 to a hot water/cold shock pasteurization process.

Vibrio vulnificus and V. parahaemolyticus are natural inhabitants of estuarine environments world wide. Pathogenic strains of these bacteria are often transmitted to humans through consumption of raw oysters, which flourish in the same estuaries. Previous studies reported the effective use of hot water pasteurization followed by cold shock to eliminate from raw oysters naturally and artificially incurred environmental strains of V. vulnificus and V. parahaemolyticus common to the Gulf of Mexico. The present study focused on the use of the same pasteurization method to reduce a highly process resistant Vibrio strain, V. parahaemolyticus O3:K6 to non-detectable levels. Oysters were artificially contaminated with 10(4) and 10(6) V. parahaemolyticus 03:K6 cfu g(-1) oyster meat. Contaminated oysters were pasteurized between 50 and 52 degrees C for up to 22 min. Samples of processed oysters were enumerated for V. parahaemolyticus O3:K6 at 2-min intervals beginning after the 'come-up time' to achieve an oyster internal temperature of at least 50 degrees C. The D value (D(52)deg C) was 1.3-1.6 min. V. parahaemolyticus O3:K6 proved more process resistant than non-pathogenic environmental strains found in Gulf of Mexico waters. A total processing time of at least 22 min at 52 degrees C was recommended to reduce this bacterium to non-detectable levels (< 3 g(-1) oyster meat).

Identification of a novel psoriasis susceptibility locus at 1p and evidence of epistasis between PSORS1 and candidate loci.

The pathogenesis of all forms of psoriasis remains obscure. Segregation analysis and twin studies together with ethnic differences in disease frequency all point to an underlying genetic susceptibility to psoriasis, which is both complex and likely to reflect the action of a number of genes. We performed a genome wide analysis using a total of 271 polymorphic autosomal markers on 284 sib relative pairs identified within 158 independent families. We detected evidence for linkage at 6p21 (PSORS1) with a non-parametric linkage score (NPL)=4.7, p=2 x 10(-6) and at chromosome 1p (NPL=3.6, p=1.9 x 10(-4)) in all families studied. Significant excess (p=0. 004) paternal allele sharing was detected for markers spanning the PSORS1 locus. A further three regions reached NPL scores of 2 or greater, including a region at chromosome 7 (NPL 2.1), for which linkage for a number of autoimmune disorders has been reported. Partitioning of the data set according to allele sharing at 6p21 (PSORS1) favoured linkage to chromosomes 2p (NPL 2.09) and 14q (NPL 2.0), both regions implicated in previous independent genome scans, and suggests evidence for epistasis between PSORS1 and genes at other genomic locations. This study has provided linkage evidence in favour of a novel susceptibility locus for psoriasis and provides evidence of the complex mechanisms underlying the genetic predisposition to this common skin disease.

Clinical challenges that face nurses working in a correctional setting.

The number of people that have been incarcerated into the Australian prison system is increasing. Many of these people come to the system with complicated health needs. Nursing staff provide the first point of contact for their health needs, and it is the responsibility of the nursing staff to be made aware of inmates' needs and how to address these needs. These problems can present an enormous challenge to nurses working in a corrective setting. This essay has been written to demonstrate how nurses at this particular Corrective Centre overcome the problems they encounter in their everyday work environment.

A physical and transcript map based upon refinement of the critical interval for PPH1, a gene for familial primary pulmonary hypertension. The International PPH Consortium.

Primary pulmonary hypertension (PPH), an often fatal disorder, is characterized by sustained elevation of pulmonary artery pressure of unknown cause. In its familial form (FPPH), the disorder segregates as an autosomal dominant and displays markedly reduced penetrance. A gene for FPPH was previously localized to a 25-cM interval on the long arm of chromosome 2 (2q31-q33). We now report a complete yeast artificial chromosome (YAC) and bacterial artificial chromosome (BAC)/P1 artificial chromosome contig (PAC), assembled by STS content mapping, across a newly identified minimum nonrecombinant interval containing the gene designated PPH1. The physical map has served to establish polymorphic marker order unequivocally, enabling the establishment of detailed haplotypes for the region. Together with the identification of novel recombination events in affected individuals from six newly ascertained kindreds, these data have allowed the significant reduction of the minimum PPH1 critical interval to a 4.8-cM region. The region, flanked by the polymorphic markers D2S115 (centromeric) and D2S1384 (telomeric), corresponds to a minimum physical distance of 5.8 Mb at 2q33. Numerous expressed sequence tags and known genes were placed on the YAC/BAC contig spanning the PPH1 gene critical region.

Characterization of the major susceptibility region for psoriasis at chromosome 6p21.3.

Psoriasis is a common inflammatory skin condition caused by genetic and environmental factors. Recent genome-wide linkage analyses have identified a locus encoding susceptibility to psoriasis and placed this gene in the 12 cM interval between markers D6S426 and D6S276 on chromosome 6p21.3. This is a broad region and encompasses the human major histocompatibility complex. We have sought to localize the susceptibility gene more precisely by exploiting the linkage, haplotype, and linkage disequilibrium information available through genotyping 118 affected sib pairs, their parents and other affected family members. A total of 14 highly polymorphic markers were genotyped, combining anonymous loci with the class I genes HLA-B and -C distributed across a genetic interval of approximately 14 cM including the entire major histocompatibility complex. Through the application of higher density mapping within the major histocompatibility complex, we identified those regions most commonly shared identical by descent in patients with psoriasis. Using the transmission-disequilibrium test, we found significant evidence of linkage and allelic association across an interval defined by the markers tn62 (p = 1.0 x 10(-7)), HLA-B (p = 4.0 x 10(-7)), and HLA-C (p = 2.7 x 10(-9)), a region encompassed within a 285 kb genomic DNA fragment. Hence these studies contribute to the refinement of the localization of a major psoriasis susceptibility gene and place the critical region near to HLA-C.

A defect in the regional deposition of adipose tissue (partial lipodystrophy) is encoded by a gene at chromosome 1q.

Partial lipodystrophy (PLD), also known as "Dunnigan-Kobberling syndrome," is transmitted as a highly penetrant autosomal dominant disorder that is characterized by a dramatic absence of adipose tissue in the limbs and trunk, more evident in females than in males. In contrast, fat is retained on the face, in retro-orbital space, and at periserous sites. Associated metabolic abnormalities, including insulin resistance, hyperinsulinemia, and dyslipidemia, are referred to as "metabolic syndrome X" (Reaven 1988). Despite the intense interest in the genetic determinants underlying fat deposition, the genes involved in the lipodystrophic syndromes have not been identified. We ascertained two multigeneration families, with a combined total of 18 individuals with PLD, and performed a genomewide search. We obtained conclusive evidence for linkage of the PLD locus to microsatellite markers on chromosome 1q21 (D1S498, maximum LOD score 6.89 at recombination fraction .00), with no evidence of heterogeneity. Haplotype and multipoint analysis support the location of the PLD locus within a 21.2-cM chromosomal region that is flanked by the markers D1S2881 and D1S484. These data represent an important step in the effort to isolate and characterize the PLD gene. The identification of the gene will have important implications for the understanding of both developmental and metabolic aspects of the adipocyte and may prove useful as a single-gene model for the common metabolic disorder known as "syndrome X."

Hyperoxia stimulates interleukin-8 release from alveolar macrophages and U937 cells: attenuation by dexamethasone.

Pulmonary oxygen toxicity is associated with histological evidence of polymorphonuclear neutrophil (PMN) infiltration into lung parenchyma. What guides infiltration of these cells is unknown. A number of chemoattractants for PMN have been documented including interleukin-8 (IL-8), a cytokine released by alveolar macrophages (AM) and other cell types. The purposes of this study were to 1) determine whether human AM and the histiocytic U937 cell line release IL-8 in response to hyperoxia, 2) assess whether hyperoxia results in increased IL-8 steady-state mRNA levels in U937 cells and 3) establish whether dexamethasone could attenuate noted effects of hyperoxia. Our study shows that hyperoxia stimulates human AM and U937 cell release of IL-8. Hyperoxia also increases IL-8 mRNA levels in U937 cells. IL-8 released in response to hyperoxia by AM was biologically active as evidenced by ability to induce PMN chemotaxis. A polyclonal antibody to IL-8 partially attenuated this chemotactic activity. Finally, dexamethasone at concentrations of 10 microM, 1 microM, and 100 nM markedly reduced hyperoxia-induced IL-8 release and mRNA synthesis by U937 cells. We conclude that IL-8 may be important in the pathogenesis of pulmonary oxygen toxicity and that therapeutic concentrations of dexamethasone can suppress production of this cytokine.

Endogenous and exogenous catalase in reoxygenation lung injury.

Reexpansion pulmonary edema parallels reperfusion (reoxygenation) injuries in other organs in that hypoxic and hypoperfused lung tissue develops increased vascular permeability and neutrophil infiltration after reexpansion. This study investigated endogenous lung catalase activity and H2O2 production during hypoxia (produced by lung collapse) and after reoxygenation (resulting from reexpansion), in addition to assessing the effects of exogenous catalase infusion on the development of unilateral pulmonary edema after reexpansion. Lung collapse resulted in a progressive increase in endogenous catalase activity after 3 (14%) and 7 days (23%), while activities in contralateral left lungs did not change (normal left lungs averaged 180 +/- 11 units/mg DNA). Tissue from control left lungs released H2O2 into the extracellular medium at a rate calculated to be 242 +/- 34 nmol.h-1.lung-1. No significant change in extracellular release of H2O2 occurred after 7 days of right lung collapse. However, after reexpansion of the previously collapsed right lungs for 2 h, H2O2 release from both reexpanded right and contralateral left lungs significantly increased (88 and 60%, respectively) compared with controls. Infusion of exogenous catalase significantly increased plasma and lung catalase activities. Exogenous catalase infusion prevented neither the increase in lung permeability nor the infiltration with neutrophils that typically occurs in reexpanded lungs. These data indicate that lung hypoxia/reoxygenation, induced by sequential collapse and reexpansion, has specific effects on endogenous lung catalase activity and H2O2 release. However, exogenous catalase does not prevent reexpansion pulmonary edema, eliminating extracellular (but not intracellular) H2O2 as an important mediator of unilateral lung injury in this model.

Apical Pneumocystis carinii pneumonia in AIDS patients not receiving inhaled pentamidine prophylaxis.

Isolated apical Pneumocystis carinii pneumonia might develop in AIDS patients receiving aerosolized pentamidine prophylaxis. Demonstrated here are two cases of apical P carinii pneumonia occurring in patients not receiving inhaled pentamidine prophylaxis. Such isolated apical localization of P carinii should be differentiated from tuberculosis and fungal infection.

Effects of hypoxia and reoxygenation on lung glutathione system.

Reexpansion pulmonary edema (RPE) parallels reperfusion (reoxygenation) injuries in other organs in that hypoxic and hypoperfused lung tissue develops increased vascular permeability and neutrophil infiltration after reexpansion. This study investigated the lung cellular glutathione system during hypoxia (produced by lung collapse) and after reoxygenation (produced by reexpansion). Two separate groups of rabbits were studied to determine effects of lung hypoxia-reoxygenation on 1) lung glutathione peroxidase and reductase enzyme activities and 2) lung tissue, plasma, and alveolar lavage fluid total (reduced glutathione plus glutathione disulfide) and oxidized glutathione. Neither lung collapse for 3-7 days nor reexpansion for 2 h after 7 days of collapse affected glutathione peroxidase [controls, 0.36 +/- 0.04 (left), 0.38 +/- 0.03 U/mg DNA (right)] or reductase [controls, 0.12 +/- 0.01 (left), 0.14 +/- 0.01 U/mg DNA (right)] activities. The concentration of glutathione disulfide increased markedly in right alveolar lavage fluid, but not in plasma, after right lung reexpansion. Right lung total glutathione decreased significantly (-19%) after 7 days of collapse. After right lung reexpansion, both left (-65%) and right (-68%) lung total glutathione decreased significantly. The percent of total glutathione present in the oxidized form increased significantly in both left (to 15.5 +/- 4.0% of total) and right (to 18.7 +/- 6.3% of total) lungs after reexpansion of the right lung. These data indicate that lung tissue hypoxia, produced by unilateral lung collapse, was associated with a unilateral decrease in lung total glutathione content. Right lung reoxygenation, due to rapid reexpansion, caused a bilateral decrease in lung total glutathione content and an increase in right lung and alveolar lavage fluid glutathione disulfide concentration.

Polyethylene glycol-conjugated superoxide dismutase in unilateral lung injury due to re-expansion (re-oxygenation).

This study evaluated the effects of polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) in re-expansion pulmonary edema, a unilateral lung injury due in part to re-oxygenation of hypoxic, collapsed lung tissue. The hypothesis underlying this investigation was that extracellular superoxide contributed to the lung inflammation in this model, and that PEG-SOD could be used to test for extra-cellular superoxide involvement. The right lungs of 2-3 kg rabbits were collapsed for seven days by intrapleural air injections. Immediately prior to lung re-expansion, rabbits received intravenously 10,000 units/kg PEG-SOD (n = 6) or an equal volume of H2O2-inactivated PEG-SOD (n = 6). Inactive PEG-SOD pretreated rabbits had a marked increase in re-expanded lungs' lavage albumin concentration (right 1653 +/- 230 micrograms/ml, left 404 +/- 160 micrograms/ml; p less than .01). Active PEG-SOD did not inhibit this permeability increase (right 1744 +/- 242 micrograms/ml, left 180 +/- 53 micrograms/ml; p less than .01). However, active PEG-SOD significantly decreased both total number and percent neutrophils in alveolar lavage (right 24.8 +/- 9.4%, left 4.2 +/- 0.8%; p less than .05) compared to inactive PEG-SOD pretreated rabbits (right 52.8 +/- 5.8%, left 8.7 +/- 2.4%; p less than .01). Pretreatment with active PEG-SOD significantly increased lung tissue (20.4 +/- 1.5 units/mg DNA), blood (400 +/- 8 units/ml) and right lung lavage (30.0 +/- 3.1 units/ml) SOD activities compared to those from inactive PEG-SOD pretreated rabbits (respectively: 16.0 +/- 1.0 units/mg DNA, 335 +/- 14 units/ml and 10.8 +/- 1.3 units/ml; p less than .05 for each comparison).(ABSTRACT TRUNCATED AT 250 WORDS)

Diffuse pneumonia and acute respiratory failure due to infectious mononucleosis in a middle-aged adult.

This report describes a 48-yr-old patient who developed bilateral hilar adenopathy, diffuse pulmonary infiltrates, and respiratory failure in association with infectious mononucleosis. Lung and paratracheal lymph node biopsies suggested the diagnosis, and an acute Epstein-Barr virus infection was confirmed serologically. Pulmonary involvement in infectious mononucleosis is reviewed, and atypical features, which may lead to diagnostic difficulty, particularly in the older adult, are discussed.

Lodoxamide tromethamine prevents neutrophil accumulation in reexpansion pulmonary edema.

Reexpansion pulmonary edema (RPE) is an acute, unilateral lung injury initiated by cytotoxic oxygen metabolites and temporally associated with an influx of polymorphonuclear neutrophils (PMNs); these toxic oxygen products appear to result from reoxygenation of chronically collapsed lung. Lodoxamide tromethamine (U-42585E) reduces infarct size after reperfusion of ischemic myocardium. The possible protective effects of lodoxamide in RPE were examined. Right lungs of rabbits were collapsed for 7 days by injection of air into the pleural space. Reexpansion was accomplished by chest tube with negative pressure in spontaneously ventilating rabbits. Twelve pairs of animals received either lodoxamide (20 mg/kg/h intravenously (i.v.) from 30 min before reexpansion until they were killed) or an equivalent volume of sterile saline. After 2 h, animals were killed by i.v. pentobarbital. Right and left lungs of six pairs of animals were lavaged with 25 ml saline each; the remaining six pairs of animals were studied by measurement of lung wet/dry weight ratio. Albumin concentrations in lavage fluid (BAL) of lodoxamide-treated animals were 243 +/- 165 micrograms/ml in right lung and 29 +/- 15 micrograms/ml in left lung (p less than 0.03); albumin concentration in right lung BAL of untreated animals was 1,180 +/- 319 micrograms/ml (p less than 0.02 vs. lodoxamide-treated animals). PMN percentages in right BAL (3.8 +/- 3.1) and left BAL (2.9 +/- 2.2) did not differ in lodoxamide-treated animals (p greater than 0.65); PMN percentage in right BAL of untreated animals was 18.7 +/- 2.9 (p less than 0.001 vs. lodoxamide-treated animals).(ABSTRACT TRUNCATED AT 250 WORDS)

Re-expansion, re-oxygenation, and rethinking.

In a 1902 American Journal of the Medical Sciences case report, Riesman described "albuminous expectoration" following thoracentesis, a phenomenon that is now recognized as re-expansion pulmonary edema (RPE). Both cellular and biochemical mechanisms that produce lung injury in RPE have been described recently. Pathophysiologically, this unilateral edematous lung injury resembles the adult respiratory distress syndrome (ARDS) because both are characterized by intra-alveolar-activated neutrophils and markedly increased lung capillary permeability. Biochemical mechanisms that operate in RPE are analogous to those in diverse re-oxygenation (reperfusion) injuries that have been described recently in the heart, kidney, brain, and intestine. Re-oxygenated lung tissue appears to produce excess superoxide and other cytotoxic oxygen metabolites, although lung xanthine oxidase, the commonly recognized source of these oxidants, is exceedingly low. Riesman's critical analyses of the re-expansion edema fluid in his case provided an impetus for others to hypothesize that increased permeability pulmonary edema in RPE represented re-oxygenation injury of the lung microvasculature.