Tuning porosity in macroscopic monolithic metal-organic frameworks for exceptional natural gas storage.

Widespread access to greener energy is required in order to mitigate the effects of climate change. A significant barrier to cleaner natural gas usage lies in the safety/efficiency limitations of storage technology. Despite highly porous metal-organic frameworks (MOFs) demonstrating record-breaking gas-storage capacities, their conventionally powdered morphology renders them non-viable. Traditional powder shaping utilising high pressure or chemical binders collapses porosity or creates low-density structures with reduced volumetric adsorption capacity. Here, we report the engineering of one of the most stable MOFs, Zr-UiO-66, without applying pressure or binders. The process yields centimetre-sized monoliths, displaying high microporosity and bulk density. We report the inclusion of variable, narrow mesopore volumes to the monoliths' macrostructure and use this to optimise the pore-size distribution for gas uptake. The optimised mixed meso/microporous monoliths demonstrate Type II adsorption isotherms to achieve benchmark volumetric working capacities for methane and carbon dioxide. This represents a critical advance in the design of air-stable, conformed MOFs for commercial gas storage.

Granivory of invasive, naturalized, and native plants in communities differentially susceptible to invasion.

Seed predation is an important biotic filter that can influence abundance and spatial distributions of native species through differential effects on recruitment. This filter may also influence the relative abundance of nonnative plants within habitats and the communities' susceptibility to invasion via differences in granivore identity, abundance, and food preference. We evaluated the effect of postdispersal seed predators on the establishment of invasive, naturalized, and native species within and between adjacent forest and steppe communities of eastern Washington, USA that differ in severity of plant invasion. Seed removal from trays placed within guild-specific exclosures revealed that small mammals were the dominant seed predators in both forest and steppe. Seeds of invasive species (Bromus tectorum, Cirsium arvense) were removed significantly less than the seeds of native (Pseudoroegneria spicata, Balsamorhiza sagittata) and naturalized (Secale cereale, Centaurea cyanus) species. Seed predation limited seedling emergence and establishment in both communities in the absence of competition in a pattern reflecting natural plant abundance: S. cereale was most suppressed, B. tectorum was least suppressed, and P. spicata was suppressed at an intermediate level. Furthermore, seed predation reduced the residual seed bank for all species. Seed mass correlated with seed removal rates in the forest and their subsequent effects on plant recruitment; larger seeds were removed at higher rates than smaller seeds. Our vegetation surveys indicate higher densities and canopy cover of nonnative species occur in the steppe compared with the forest understory, suggesting the steppe may be more susceptible to invasion. Seed predation alone, however, did not result in significant differences in establishment for any species between these communities, presumably due to similar total small-mammal abundance between communities. Consequently, preferential seed predation by small mammals predicts plant establishment for our test species within these communities but not between them. Accumulating evidence suggests that seed predation can be an important biotic filter affecting plant establishment via differences in consumer preferences and abundance with important ramifications for plant invasions and in situ community assembly.

Identification of genes differentially expressed in benign prostatic hyperplasia.

Differences between benign prostatic hyperplasia (BPH) and normal prostate tissue at the level of mRNA expression provide an opportunity to identify candidate genes for this disease. A cDNA subtraction procedure was used to isolate differentially expressed genes in BPH. The subtraction was done by solution hybridization of BPH cDNA against excess normal prostate cDNA. We identified known, EST, and novel genes by sequence and database analysis of the subtracted cDNAs. Several of these cDNAs were used as probes in Northern blotting analysis to confirm over-expression of their corresponding mRNAs in BPH tissues. One highly upregulated sequence of interest shared identity with a known mRNA encoding human NELL2, a protein containing epidermal growth factor-like domains. NELL2 was not previously reported to be expressed in prostate and may code for a novel prostatic growth factor. In situ hybridization analysis of hyperplastic prostate specimens demonstrated that NELL2 mRNA expression is predominantly localized in basal cells of the epithelium. Disease-related changes in the levels of NELL2 may contribute to alterations in epithelial-stromal homeostasis in BPH. (J Histochem Cytochem 49:669-670, 2001)

Characterization of the human cysteinyl leukotriene CysLT1 receptor.

The cysteinyl leukotrienes-leukotriene C4(LTC4), leukotriene D4(LTD4) and leukotriene E4(LTE4)-are important mediators of human bronchial asthma. Pharmacological studies have determined that cysteinyl leukotrienes activate at least two receptors, designated CysLT1 and CysLT2. The CysLT1-selective antagonists, such as montelukast (Singulair), zafirlukast (Accolate) and pranlukast (Onon), are important in the treatment of asthma. Previous biochemical characterization of CysLT1 antagonists and the CysLT1 receptor has been in membrane preparations from tissues enriched for this receptor. Here we report the molecular and pharmacological characterization of the cloned human CysLT1 receptor. We describe the functional activation (calcium mobilization) of this receptor by LTD4 and LTC4, and competition for radiolabelled LTD4 binding to this receptor by the cysteinyl leukotrienes and three structurally distinct classes of CysLT1-receptor antagonists. We detected CysLT1-receptor messenger RNA in spleen, peripheral blood leukocytes and lung. In normal human lung, expression of the CysLT1-receptor mRNA was confined to smooth muscle cells and tissue macrophages. Finally, we mapped the human CysLT1-receptor gene to the X chromosome.

Pathogenesis of experimental Ebola virus infection in guinea pigs.

The subtype Zaire of Ebola (EBO) virus (Mayinga strain) was adapted to produce lethal infections in guinea pigs. In many ways, the disease was similar to EBO infections in nonhuman primates and humans. The guinea pig model was used to investigate the pathologic events in EBO infection that lead to death. Analytical methods included immunohistochemistry, in situ hybridization, and electron microscopy. Cells of the mononuclear phagocyte system, primarily macrophages, were identified as the early and sustained targets of EBO virus. During later stages of infection, interstitial fibroblasts in various tissues were infected, and there was evidence of endothelial cell infection and fibrin deposition. The distribution of lesions, hematologic profiles, and increases in serum biochemical enzymes associated with EBO virus infection in guinea pigs was similar to reported findings in experimentally infected nonhuman primates and naturally infected humans.

Pathology of experimental Ebola virus infection in African green monkeys. Involvement of fibroblastic reticular cells.

BACKGROUND: Ebola virus has been responsible for explosive lethal outbreaks of hemorrhagic fever in both humans and nonhuman primates. Previous studies showed a predilection of Ebola virus for cells of the mononuclear phagocyte system and endothelial cells. OBJECTIVE: To examine the distribution of lesions and Ebola virus antigen in the tissues of six adult male African green monkeys (Cercopithecus aethiops) that died 6 to 7 days after intraperitoneal inoculation of Ebola-Zaire (Mayinga) virus. METHODS: Tissues were examined histologically, immunohistochemically, and ultrastructurally. RESULTS: A major novel finding of this study was that fibroblastic reticular cells were immunohistochemically and ultrastructurally identified as targets of Ebola virus infection. CONCLUSIONS: The role of Ebola virus-infected fibroblastic reticular cells in the pathogenesis of Ebola hemorrhagic fever warrants further investigation. This is especially important because of recent observations indicating that fibroblastic reticular cells, along with the reticular fibers they produce, maximize the efficiency of the immune response.

Experimental reproduction of a spiking mortality syndrome of turkeys.

Two-day-old turkey poults were inoculated with either a chicken embryo homogenate used previously to produce spiking mortality syndrome in chickens (the "Oakwood Agent") or an intestine-pancreas homogenate collected from field turkeys with the syndrome known as spiking mortality of turkeys. Twelve days postinoculation, the mean plasma insulinlike growth factor-1 (IGF-1) level and mean body weights were significantly depressed, and the mean plasma growth hormone level was significantly elevated, in the poults receiving the turkey-derived homogenate (P < or = 0.0003), as was previously reported in chickens with spiking mortality syndrome. The depression in plasma IGF-1 levels may explain the runting seen in poults that survive spiking mortality of turkeys in the field. Following a 4-hr fast and a brief cool water spraying, poults exhibited clinical signs indistinguishable from those of chicks with spiking mortality syndrome. However, plasma glucose levels in the affected poults were within the normal range, unlike chickens with spiking mortality syndrome. Immunohistochemistry on formalin-fixed intestines, ceca, and bursae produced positive staining using an arenavirus antibody in epithelial cells of poults inoculated with the turkey homogenate and those inoculated with the Oakwood Agent. Tissues of uninoculated controls were negative. Poults inoculated with the Oakwood Agent did not show noticeable disease.

Experimental reproduction of hypoglycemia-spiking mortality syndrome in broiler chickens with the use of homogenized brains containing arenaviruslike particles.

Severe hypoglycemia-spiking mortality syndrome was experimentally reproduced in broiler chicks. Inoculum was homogenized brains from 28-day-old commercial broiler chicks with central nervous system signs (50% [v/v] in phosphate-buffered saline with 2% fetal calf serum). Oral inoculations of 1.2 ml of the homogenate were given at 1 day of age to broiler chicks (n = 15). Fourteen days later, chicks were fasted and stressed with a 2-sec cool water spray. Six chicks (40%) developed clinical signs of spiking mortality syndrome and were severely hypoglycemic. Uninoculated control chicks (n = 15) from the same hatch, also fasted and stressed simultaneously, were unaffected. Examination of a banded fraction produced from the inoculum with the use of transmission electron microscopy with negative staining revealed viruslike particles indistinguishable from arenavirus particles stained and examined simultaneously. Avian encephalomyelitis virus was isolated by one of three laboratories attempting virus isolation with the use of embryonating chicken eggs.

Pathology and immunohistochemistry of callitrichid hepatitis, an emerging disease of captive New World primates caused by lymphocytic choriomeningitis virus.

Callitrichid hepatitis is an arenavirus infection that recently emerged as a highly fatal disease of New World primates in the Callitrichidae family. As we previously reported, these primates develop hepatitis after contact with mice that are infected with variants of LCMV (LVMCCH), recently determined to have 86% identity with GC-P gene of the Armstrong and Western strains of LCMV. Here, we describe the histopathological lesions and tissue localization of viral antigens in confirmed cases of callitrichid hepatitis from recent outbreaks in two U.S. zoos. The liver in marmosets and tamarins with fatal infections consistently showed degeneration, necrosis, and inflammation, with variable involvement of the spleen, lymph nodes, adrenal glands, intestine, pancreas, and central nervous system. Lymphocytic choriomeningitis virus antigens were identified immunohistochemically in necrotic foci in these organs as well as in nondegenerating areas in lungs, kidney, urinary bladder, brain, and testes. The multi-organ tropism and histological pattern of LCMV infection in marmosets and tamarins are similar to those reported for the highly virulent arenavirus that causes Lassa fever in humans. Comparative studies of callitrichid hepatitis and Lassa fever would therefore be mutually beneficial for human and nonhuman primate medicine.

Pathogenesis of Pichinde virus infection in strain 13 guinea pigs: an immunocytochemical, virologic, and clinical chemistry study.

Pichinde virus has been adapted to produce lethal infection of Strain 13 guinea pigs. Viral replication and presence of viral antigen in frozen tissues stained by immunofluorescence has been previously described. Further investigation into the pathogenesis of this disease has been hampered by the lack of a light microscopic method for correlating histologic lesions and the presence of Pichinde viral antigens. For this purpose, we developed a sensitive immunocytochemical technique for staining Pichinde viral antigens in formalin-fixed, paraffin-embedded tissue. Enhancement of the immunocytochemical staining with nickel chloride markedly improved detection of viral antigens. We examined frozen and formalin-fixed tissues from Strain 13 guinea pigs for viral antigens by light microscopy and immunocytochemistry at various intervals after infection with Pichinde virus. Progressive involvement of different tissues correlated with organ injury measured by serum biochemical abnormalities. Pichinde viral antigen was first detected in splenic macrophages five days after infection and their subsequent destruction facilitated persistent viremia. The inability to clear virus led to multiple organ infection and vascular involvement. Ensuing infections involved particularly the liver, spleen, adrenal glands, lungs, and intestines. Gastroenteritis developed, with extensive involvement of the muscularis mucosa throughout the gastrointestinal tract. Water and food intake decreased rapidly after day 8, leading to marked weight loss. Fatty changes of the liver suggested metabolic derangement that was further exacerbated terminally by adrenal infection and pulmonary impairment.

Mating factor dependence of G1 cell cycle mutants of Saccharomyces cerevisiae.

Mutants in four G1 cdc strains of Saccharomyces cerevisiae were isolated which failed to show division arrest in the presence of α-factor. The cell cycle properties, terminal arrest morphology and mating competence of these mutants at the restrictive temperature were examined. The G1 specific arrest of the cdc 36 and cdc39 mutants is dependent upon the availability of an intact mating factor response system in Mat a cells. Cdc28 and cdc37 mutants exert their cell cycle blocks independently of the mating factor pathway. It is likely that the nature of the primary growth defect in cdc36 and cdc39 mutants is such that the α-factor pathway is activated in the absence of the pheromone at the restrictive temperature and that G1 arrest is a secondary consequence of a non-cycle specific event in such mutants.

Taurine transport in epilepsy.

Previous studies of plasma taurine concentrations in epileptics have yielded equivocal results. We measured plasma and urinary taurine in 41 epileptic and 68 control subjects and found plasma concentrations among epileptics to be comparable in general to those of controls, but that two or three classes of plasma taurine concentrations, possibly genetically regulated, occur in both epileptic and control subjects. Our previous studies and data from the present study on taurine excretion revealed three excretion classes under genetic control. The principal finding is that epileptics include disproportionate numbers of low excretors (high reabsorbers), who are presumptive homozygotes for the allele effecting higher reabsorption. If confirmed, these findings suggest that the transport of taurine, rather than absolute taurine concentration, may explain the efficacy of taurine administration in some epileptics but not in others. The locus involved may be one component in the polygenic diathesis to the idiopathic epilepsies.

Potential sources of errors in cation-exchange chromatographic measurement of plasma taurine.

We examined the potential sources of error in automated cation-exchange chromatographic quantitation of plasma taurine, both in sample preparation and in the analysis. Principal sources of error include: use of serum instead of plasma, which produces gross overestimates; use of tripotassium ethylenediaminetetraacetate (EDTA) as anticoagulant in systems involving ninhydrin detection (a ninhydrin-positive contaminant of EDTA emerges coincident with taurine); contamination with platelets; and placing volumes exceeding 20 microL on the cartridge used in the Technicon TSM Amino Acid Analyzer. We arrived at a simple technique in which we use EDTA as anticoagulant, micropore filtration to produce platelet-free plasma, and o-phthalaldehyde as the detection reagent for the sensitivity required to measure accurately the low concentration of taurine in plasma.