人蛔虫和猪蛔虫同域种群DNA多态性研究

在我国蛔虫感染遍布各地,受染人数达5亿多.而在多数农村流行区,生猪饲养十分普遍,人群和猪群的蛔虫感染往往并存,且人、猪接触密切.据作者在江西省新建县蔓湖村进行的一年纵向调查,当地人群蛔虫感染率和猪群蛔虫感染率比较接近(约60%-70%),土壤蛔虫卵污染普遍而严重,并长年稳定 ( Peng, W.D. et al. 1996 Ascaris, people and pigs in rural Jiangxi, China. Parasitology 113:547～557.). 因此这些地区人蛔虫和猪蛔虫交叉感染的机会是大量存在的.     

Autoimmune lymphoproliferative syndrome with defective Fas: genotype influences penetrance

Autoimmune lymphoproliferative syndrome (ALPS) is a disorder of lymphocyte homeostasis and immunological tolerance. Most patients have a heterozygous mutation in the APT1 gene, which encodes Fas (CD95, APO-1), mediator of an apoptotic pathway crucial to lymphocyte homeostasis. Of 17 unique APT1 mutations in unrelated ALPS probands, 12 (71%) occurred in exons 7-9, which encode the intracellular portion of Fas. In vitro, activated lymphocytes from all 17 patients showed apoptotic defects when exposed to an anti-Fas agonist monoclonal antibody. Similar defects were found in a Fas-negative cell line transfected with cDNAs bearing each of the mutations. In cotransfection experiments, Fas constructs with either intra- or extracellular mutations caused dominant inhibition of apoptosis mediated by wild-type Fas. Two missense Fas variants, not restricted to patients with ALPS, were identified. Variant A(-1)T at the Fas signal-sequence cleavage site, which mediates apoptosis less well than wild-type Fas and is partially inhibitory, was present in 13% of African American alleles. Among the ALPS-associated Fas mutants, dominant inhibition of apoptosis was much more pronounced in mutants affecting the intracellular, versus extracellular, portion of the Fas receptor. Mutations causing disruption of the intracellular Fas death domain also showed a higher penetrance of ALPS phenotype features in mutation-bearing relatives. Significant ALPS-related morbidity occurred in 44% of relatives with intracellular mutations, versus 0% of relatives with extracellular mutations. Thus, the location of mutations within APT1 strongly influences the development and the severity of ALPS.     

Identification of caveolin-1 as a fatty acid binding protein

In an attempt to identify high affinity, fatty acid binding proteins present in 3T3-L1 adipocytes plasma membranes, we labeled proteins in purified plasma membranes with the photoreactive fatty acid analogue, 11-m-diazirinophenoxy[11-3H]undecanoate. A single membrane protein of 22 kDa was covalently labeled after photolysis. This protein fractionated with caveolin-1 containing caveolae and was immunoprecipitated by an anti-caveolin-1 monoclonal antibody. Furthermore, 2D-PAGE analysis revealed that both the alpha and beta isoforms of caveolin-1 could be labeled by the photoreactive fatty acid upon photolysis, indicating that both bind fatty acids. The saturable binding of the photoreactive fatty acid suggests caveolin-1 has a lipid binding site that may either operate during intracellular lipid traffic or regulate caveolin-1 function.     

The flattened face of type II beta phosphatidylinositol phosphate kinase binds acidic phospholipid membranes

Type II beta phosphatidylinositol phosphate kinase is a representative phosphatidylinositol phosphate kinase that is active against membrane-bound substrates. The structure of the enzyme contains a flattened basic face that spans the crystallographic dimer interface and is adjacent to the active site. Analytical ultracentrifugation shows that phosphatidylinositol phosphate kinase is a dimer in solution. Modeling suggested that the flattened face binds to acidic phospholipids by electrostatic interactions. The enzyme binds to acidic vesicles containing phosphatidylserine, phosphatidic acid, or phosphoinositides mixed with phosphatidylcholine, but not to neutral phosphatidylcholine vesicles. Binding to acidic vesicles is abolished in the presence of 1.0 M NaCl, consistent with an essential electrostatic contribution to the free energy of binding. The +14 charge on the flattened face of the dimer was reduced to +2 in the triple mutant Lys72Glu/Lys76Glu/Lys78Glu. The mutation has no effect on dimerization, but reduces the apparent KA for 25% phosphatidylserine/75% phosphatidylcholine mixed vesicles by 16-fold. The reduction in the level of binding can be ascribed to a loss of electrostatic interactions based on the finite difference solution to the Poisson-Boltzmann equation. The mutant reduces catalytic activity toward phosphatidylinositol 5-phosphate by approximately 50-fold. The wild-type enzyme binds half-maximally to phosphatidylinositol 4,5-bisphosphate-containing vesicles at a mole fraction of 0.3% in a phosphatidylcholine background, as compared to a 22% mole fraction in phosphatidylserine. The binding to phosphatidylinositol 4,5-bisphosphate-containing membranes is less sensitive to salt and to the triple mutation than binding to phosphatidylserine-containing membranes, suggesting that at least part of phosphatidylinositol 4,5-bisphosphate's interaction with the enzyme is independent of the flattened face. It is concluded that the flattened face of type II beta phosphatidylinositol phosphate kinase binds to membranes through nonspecific interactions, and that this interaction is essential for efficient catalysis.     

Prospective identification, isolation by flow cytometry, and in vivo self-renewal of multipotent mammalian neural crest stem cells

Multipotent and self-renewing neural stem cells have been isolated in culture, but equivalent cells have not yet been prospectively identified in neural tissue. Using cell surface markers and flow cytometry, we have isolated neural crest stem cells (NCSCs) from mammalian fetal peripheral nerve. These cells are phenotypically and functionally indistinguishable from NCSCs previously isolated by culturing embryonic neural tube explants. Moreover, in vivo BrdU labeling indicates that these stem cells self-renew in vivo. NCSCs freshly isolated from nerve tissue can be directly transplanted in vivo, where they generate both neurons and glia. These data indicate that neural stem cells persist in peripheral nerve into late gestation by undergoing self-renewal. Such persistence may explain the origins of some PNS tumors in humans.     

Pulsed-light inactivation of food-related microorganisms

The effects of high-intensity pulsed-light emissions of high or low UV content on the survival of predetermined populations of Listeria monocytogenes, Escherichia coli, Salmonella enteritidis, Pseudomonas aeruginosa, Bacillus cereus, and Staphylococcus aureus were investigated. Bacterial cultures were seeded separately on the surface of tryptone soya-yeast extract agar and were reduced by up to 2 or 6 log10 orders with 200 light pulses (pulse duration, approximately 100 ns) of low or high UV content, respectively (P < 0.001).     

Contact analysis of a posterior cervical spine plate using a three-dimensional canine finite element model

The development of a three-dimensional finite element model of a posteriorly plated canine cervical spine (C3-C6) including contact nonlinearities is described. The model was created from axial CT scans and the material properties were derived from the literature. The model demonstrated sufficient accuracy from the results of a mesh convergence test. Significant steps were taken toward establishing model validation by comparison of plate surface strains with a posteriorly plated canine cervical spine under three-point bending. This model was developed to better characterize the contact pressures at the various interfaces under average physiologic canine loading. The analysis showed that the screw-plate interfaces had the highest values of all the mechanical parameters evaluated.     

EDTA chelation therapy does not selectively increase chromium losses

Chelation therapy and supplemental Cr have both been shown to lead to improved blood glucose, lipids, and insulin activity. Chelation therapy leads to the removal of toxic as well as essential metals. To determine if chelation therapy leads to increased urinary Cr losses and altered Cr homeostasis, 2 groups of subjects (1 group that had undergone only 1 or no chelation therapy and 1 group in which all subjects had undergone at least 19 chelation sessions) were evaluated for differences in possible Cr homeostasis based on urinary Cr losses. There were no significant differences in urinary Cr losses between the two groups of subjects and there were no significant increases in urinary Cr losses resulting from chelation therapy. Increases in urinary Cr losses were strongly influenced by supplementation but not chelation therapy.     

Naked DNA vaccination of Atlantic salmon Salmo salar against IHNV

A naked plasmid DNA encoding the glycoprotein (pCMV4-G) of a 1976 isolate of infectious hematopoietic necrosis virus (IHNV) obtained from steelhead Oncorhynchus mykiss was used to vaccinate Atlantic salmon Salmo salar against IHNV. Eight weeks post-vaccination the fish were challenged with a strain of IHNV originally isolated from farmed Atlantic salmon undergoing an epizootic. Fish injected with the glycoprotein-encoding plasmid were significantly (p < 0.05) protected against IHNV by both immersion and cohabitation challenge. Survivors of the first challenges were pooled and re-challenged by immersion 12 wk after the initial challenge. Significant (p < 0.05) protection was observed in all of the previously challenged groups including those receiving the complete vaccine. Fish injected with the glycoprotein-encoding plasmid produced low levels of virus-neutralizing antibodies prior to the first challenge. Neutralizing antibodies increased in all groups after exposure to the IHNV. Passive transfer of pooled sera from pCMV4-G vaccinates and IHN survivors provided relative survivals of 40 to 100% compared to fish injected with sera collected from fish immunized with control vaccines or left unhandled. In this study, DNA vaccination effectively protected Atlantic salmon smolts against challenges with IHNV.