Structural-metabolic changes in the ventricular myocardium in massive experimental pulmonary embolism]

A comparative study of hemodynamic and structural-metabolic changes in myocardium of right (RV) and left (LV) ventricles by compensative massive pulmonary embolism (MPE) and decompensated MPE was made in 29 mongrel dogs. By decompensated MPE the histoenzymological and ultrastructural methods reveal changes in RV which are not adequate to its high hemodynamic load: the catabolic enzymes activity decreases, the numeral density of mitochondrial profiles decreases too, the fraction of damaged mitochondria increases. By decompensated MPE the myocardial metabolism shifts from catabolic to biosynthetic processes, the activity of NADP.H-D and G-6-PDG increase in both ventricles.     

The bioemulsifier alasan: role of protein in maintaining structure and activity

Alasan, the bioemulsifier of Acinetobacter radioresistens KA53, is a high-molecular-mass complex of polysaccharide and protein. Enrichment culture was used to isolate a bacterial strain that grew on alasan as the sole source of carbon and energy, causing the loss of the protein portion of alasan, as well as the emulsifying activity. The degradation was mediated by extracellular proteinases/alasanases. One of these enzymes, referred to as alasanase II, was purified to homogeneity. Alasanase II, as well as pronase, inactivated alasan, whereas a polysaccharide-degrading enzyme mixture, snail juice, had no effect on emulsifying activity. Deproteinization of alasan with phenol yielded a viscous polysaccharide with no emulsifying activity. Heating alasan to 50 °C led to a 2.5-fold irreversible increase in viscosity with no change in emulsifying activity. Heating to 60°–90 °C caused a drop in viscosity and a 5.8-fold increase in emulsifying activity. The deproteinized alasan showed no increase in emulsifying activity and only small changes in viscosity when heated. Received: 31 October 1997 / Accepted: 29 November 1997     

Mutations in ARL2BP,Encoding ADP-Ribosylation-Factor-Like 2 Binding Protein,Cause Autosomal-Recessive Retinitis Pigmentosa

Retinitis pigmentosa (RP) is a genetically heterogeneous retinal degeneration characterized by photoreceptor death, which results in visual failure. Here, we used a combination of homozygosity mapping and exome sequencing to identify mutations in ARL2BP, which encodes an effector protein of the small GTPases ARL2 and ARL3, as causative for autosomal-recessive RP (RP66). In a family affected by RP and situs inversus, a homozygous, splice-acceptor mutation, c.101−1G>C, which alters pre-mRNA splicing of ARLBP2 in blood RNA, was identified. In another family, a homozygous c.134T>G (p.Met45Arg) mutation was identified. In the mouse retina, ARL2BP localized to the basal body and cilium-associated centriole of photoreceptors and the periciliary extension of the inner segment. Depletion of ARL2BP caused cilia shortening. Moreover, depletion of ARL2, but not ARL3, caused displacement of ARL2BP from the basal body, suggesting that ARL2 is vital for recruiting or anchoring ARL2BP at the base of the cilium. This hypothesis is supported by the finding that the p.Met45Arg amino acid substitution reduced binding to ARL2 and caused the loss of ARL2BP localization at the basal body in ciliated nasal epithelial cells. These data demonstrate a role for ARL2BP and ARL2 in primary cilia function and that this role is essential for normal photoreceptor maintenance and function.     

Trunk implanted zinc-bentonite as a source of zinc for apple trees

Summary The feasibility of zinc supply to apples (Malus spp. var. Golden Delicious) by various Zn-bentonite preparations implanted in the trunk was studied. A preliminary experiment included four preparations and was conducted in one plantation in 1980. A larger scale experiment in 1981, tested Zn-bentonite (ZnB) and Zn-bentonite + ZnEDTA (ZnBEA) in four plantations in the south, center and north of Israel. Clay tablets were implanted in holes drilled in the tree trunk in April. The youngest, fully developed leaves on the new growth were sampled periodically and Zn content was determined.ZnB and ZnBEA implanted at the rate of 15 mg Zn/cm trunk circumference significantly increased Zn content above that of the control trees until mid-September. The ZnBEA preparation supported significantly higher leaf concentrations than the ZnB preparation. Peak concentrations in trees treated with the ZnBEA preparation were 75.8, 47.4, 38.4, and 23.7 ppm in the four plantations and occurred in May. The Zn concentration in the youngest leaves decreased during the season but there was evidence that in some cases Zn behaved as a phloem mobile element. Soil, climate and previous zinc treatments affected considerably the Zn concentration found in leaves in the four plantations making it impossible to identify a single critical concentration level.No damage to the trees was observed as a result of the drilling and implantation of the clay tablets. Clay analysis at the end of the season showed that about two-thirds of the Zn added to the trees was used. The amount of Zn supplied per tree in the implantation procedure was 80–90% lower than that supplied in the routine spraying operations.     

Zinc-desferrioxamine attenuates retinal degeneration in the rd10 mouse model of retinitis pigmentosa

Iron-associated oxidative injury plays a role in retinal degeneration such as age-related macular degeneration and retinitis pigmentosa. The metallo-complex zinc-desferrioxamine (Zn/DFO) may ameliorate such injury by chelation of labile iron in combination with release of zinc. We explored whether Zn/DFO can affect the course of retinal degeneration in the rd10 mouse model of retinitis pigmentosa. Zn/DFO-treated animals showed significantly higher electroretinographic responses at 3 and 4.5 weeks of age compared with saline-injected controls. Corresponding retinal (photoreceptor) structural rescue was observed by quantitative histological and immunohistochemical techniques. When administered alone, the components of the complex, Zn and DFO, showed a lesser, partial effect. TBARS, a marker of lipid peroxidation, and levels of oxidative DNA damage as quantified by 8-OHdG immunostaining were significantly lower in Zn/DFO-treated retinas compared with saline-injected controls. Reduced levels of retinal ferritin as well as reduced iron content within ferritin molecules were measured in Zn/DFO-treated retinas. The data, taken together, suggest that the protective effects of the Zn/DFO complex are mediated through modulation of iron bioavailability, leading to attenuation of oxidative injury. Reducing iron-associated oxidative stress using complexes such as Zn/DFO may serve as a “common pathway” therapeutic approach to attenuate injury in retinal degeneration.     

Whole-exome sequencing identifies mutations in GPR179 leading to autosomal-recessive complete congenital stationary night blindness

Congenital stationary night blindness (CSNB) is a heterogeneous retinal disorder characterized by visual impairment under low light conditions. This disorder is due to a signal transmission defect from rod photoreceptors to adjacent bipolar cells in the retina. Two forms can be distinguished clinically, complete CSNB (cCSNB) or incomplete CSNB; the two forms are distinguished on the basis of the affected signaling pathway. Mutations in NYX, GRM6, and TRPM1, expressed in the outer plexiform layer (OPL) lead to disruption of the ON-bipolar cell response and have been seen in patients with cCSNB. Whole-exome sequencing in cCSNB patients lacking mutations in the known genes led to the identification of a homozygous missense mutation (c.1807C>T [p.His603Tyr]) in one consanguineous autosomal-recessive cCSNB family and a homozygous frameshift mutation in GPR179 (c.278delC [p.Pro93Glnfs^∗57]) in a simplex male cCSNB patient. Additional screening with Sanger sequencing of 40 patients identified three other cCSNB patients harboring additional allelic mutations in GPR179. Although, immunhistological studies revealed Gpr179 in the OPL in wild-type mouse retina, Gpr179 did not colocalize with specific ON-bipolar markers. Interestingly, Gpr179 was highly concentrated in horizontal cells and Müller cell endfeet. The involvement of these cells in cCSNB and the specific function of GPR179 remain to be elucidated.     

An integrated pan‐tropical biomass map using multiple reference datasets

We combined two existing datasets of vegetation aboveground biomass (AGB) (Proceedings of the National Academy of Sciences of the United States of America, 108 , 2011, 9899; Nature Climate Change, 2 , 2012, 182) into a pan‐tropical AGB map at 1‐km resolution using an independent reference dataset of field observations and locally calibrated high‐resolution biomass maps, harmonized and upscaled to 14 477 1‐km AGB estimates. Our data fusion approach uses bias removal and weighted linear averaging that incorporates and spatializes the biomass patterns indicated by the reference data. The method was applied independently in areas (strata) with homogeneous error patterns of the input (Saatchi and Baccini) maps, which were estimated from the reference data and additional covariates. Based on the fused map, we estimated AGB stock for the tropics (23.4 N–23.4 S) of 375 Pg dry mass, 9–18% lower than the Saatchi and Baccini estimates. The fused map also showed differing spatial patterns of AGB over large areas, with higher AGB density in the dense forest areas in the Congo basin, Eastern Amazon and South‐East Asia, and lower values in Central America and in most dry vegetation areas of Africa than either of the input maps. The validation exercise, based on 2118 estimates from the reference dataset not used in the fusion process, showed that the fused map had a RMSE 15–21% lower than that of the input maps and, most importantly, nearly unbiased estimates (mean bias 5 Mg dry mass ha^?1 vs. 21 and 28 Mg ha^?1 for the input maps). The fusion method can be applied at any scale including the policy‐relevant national level, where it can provide improved biomass estimates by integrating existing regional biomass maps as input maps and additional, country‐specific reference datasets.     

Role of Flagella in Virulence of the Coral Pathogen Vibrio coralliilyticus

A recently available transposition system was utilized to isolate a nonmotile mutant of the coral-bleaching pathogen Vibrio coralliilyticus. The mutation was localized to the fhlA gene, and the mutant lacked flagella. The flhA mutant was unable to exhibit chemotaxis toward coral mucus or to adhere to corals and subsequently cause infection.Coral reefs have been described as the rain forests of the sea due to their enormous biodiversity. Unfortunately, during the past few decades nearly 30% of the worldwide coral population has been severely damaged by various diseases (9). Coral bleaching is a disruption of the Symbiodinium-coral symbiosis and results in “whitening” of the coral due to the loss of the Symbiodinium symbiont or its pigment. On a global scale, bleaching is one of the major coral diseases (5) and tends to correlate with increased seawater temperatures (10). Thermal stress is the generally accepted hypothesis to explain the mechanism of the disease. In the last several years, bacterial bleaching of corals has been suggested as an alternative hypothesis to explain some coral bleaching episodes (21, 22). Vibrio shiloi was the first bacterium shown to be a causative agent of coral bleaching in the Mediterranean coral Oculina patagonica (13, 14). More recently, Vibrio coralliilyticus has been reported to be the causative agent of temperature-induced bleaching of Pocillopora damicornis (3, 4) and white syndrome in Indo-Pacific corals (25). Thus, infections by V. coralliilyticus could have an impact on global coral health.Chemotaxis and flagellum-mediated motility allow bacteria to pursue nutrients and to reach and maintain their preferred niches for colonization (7, 8). Several Vibrio species (both pathogens and symbionts) require functional flagellum-mediated motility to invade their hosts and establish successful colonization (17, 18, 27, 28).In this study, we utilized a recently available Tn5-based transposition system to isolate a nonmotile mutant of the coral-bleaching pathogen V. coralliilyticus. The mutation was localized to the gene flhA. Here we demonstrate that the flagellum is critical for chemotaxis toward coral mucus, adhesion to the corals, and infection by V. coralliilyticus.