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Research was conducted to study the functions of NifS in the maturation of glutamine phosphoribosylpyrophosphate amidotransferase from Bacillus subtilis. The glutamine was synthesized as an inactive proenzyme while the enzyme activity in cell extracts was determined by measuring the formation of the product glutamate. Results showed that a NifS-like protein is involved in Fe-S cluster synthesis in the enzyme. They also indicated that the coexpression of nifS may increase heterologous metallocluster synthesis in other proteins during overexpression.

An analysis of the purification of the Azotobacter vinelandii nifV-encoded homocitrate synthase was conducted. The nifV gene was expressed at high levels in Escherichia coli and was later on purified. Results of the study revealed that nifV is capable of catalyzing the condensation of acetyl-CoA and other keto acids. Furthermore, E. coli cells produces homocitrate into a growth medium.

It is known that [[Beta].sub.2] integrins are crucial for leukocyte cell-cell and cell-matrix interactions, and accumulating evidence now suggests that integrins serve not only as a structural link but also as a signal-transducing unit that controls adhesion-induced changes in cell functions. In the present study, we plated human neutrophils on surface-bound anti-[[Beta].sub.2] (CD18) antibodies and found that the small GTP-binding protein [p21.sup.ras] is activated by [[Beta].sub.2] integrins. Pretreatment of the cells with genistein, a tyrosine kinase inhibitor, led to a complete block of [p21.sup.ras] activation, an effect that was not achieved with either U73122, which abolishes the [[Beta].sub.2] integrin-induced [Ca.sup.2+] signal, or wortmannin, which totally inhibits the phosphatidylinositol 3-kinase activity. Western blot analysis revealed that antibody-induced engagement of [[Beta].sub.2] integrins causes tyrosine phosphorylation of several proteins in the cells. One of these tyrosine-phosphorylated proteins had an apparent molecular mass of 95 kDa and was identified as the protooncogene product Vav, a [p21.sup.ras] guanine nucleotide exchange factor that is specifically expressed in cells of hematopoietic lineage. A role for Vav in the activation of [p21.sup.ras] is supported by the observations that antibody-induced engagement of [[Beta].sub.2] integrins causes an association of Vav with [p21.sup.ras] and that the effect of genistein on [p21.sup.ras] activation coincided with its ability to inhibit both the tyrosine phosphorylation of Vav and the Vav-[p21.sup.ras] association. Taken together, these results indicate that antibody-induced engagement of [[Beta].sub.2] integrins on neutrophils triggers tyrosine phosphorylation of Vav and, possibly through its association, a downstream activation of [p21.sup.ras].

L-cysteine is desulfurized to sulfur and L-alanine by the nifS gene product (NIFS), which is a pyridoxal phosphate binding enzyme. NIFS is necessary for metallocluster's biosynthesis in nitrogenase that contains MoFe and Fe proteins as it provides inorganic sulfur necessary iron-sulfur core development. A substrate cysteine-pyridoxal phosphate ketimine adduct is formed during desulfurization, causing the production protein-bound persulfide, which is the sulfur donor for the core formation.

Investigations of nitrogen fixation pathways help define and characterize the structure, distribution and biosynthesis of nitrogenase-associated metalloclusters which are essential for the electron transfer pathway and substrate reduction. Nitrogenase is a metalloenzyme comprising two constituent proteins, MOFe and Fe. It effects the catalytic reaction involving the reduction of nitrogen to NH3.

In the present work, a structure-dependent ratiometric fluorescence (RF) sensor constructed with boric acid–modified carbon quantum dots (B-CQDs) and Tb-MOF(MOF-76) was developed for sensing 2,6-pyridinedicarboxylic acid (DPA). Based on the distinct fluorescent responses of B-CQDs and MOF-76 to DPA, MOF-76/B-CQDs can be developed as a RF sensor for DPA detection. In this RF sensor, the reticulated cross-linked structure of MOF-76/B-CQDs can be destroyed by DPA due to a strong coordination effect between DPA and the Tb of MOF-76, resulting in the quenching of the fluorescence of B-CQD and the restoration of the fluorescence of MOF-76 after the addition of DPA. Benefiting from the confinement effect of the special structure change, the presented sensor showed high sensitivity toward DPA with a detection limit of 3.05 μM and excellent selectivity over the monochromatic fluorescence sensor. [ABSTRACT FROM AUTHOR]

This study aimed at understanding the diabetic prevalence, awareness, treatment and control rates and their influencing factors among people aged ≥ 40 years in Shenyang, China. A face-to-face cross-sectional epidemiological survey was conducted on the respondents using the national unified questionnaire. A total of 3922 respondents were enrolled, including 609 cases of diabetes. The diabetic prevalence rate was 15.5%, and was higher in rural areas than that in urban areas (17.7% vs. 14.2%, p = 0.004), while no difference was observed between men and women (14.8% vs. 16.1%, p = 0.242). Advanced age, hypertension and dyslipidemia were the diabetes influencing factors. Among the 609 respondents with diabetes, the diabetic awareness and treatment rates, and the control rate of fasting plasma glucose were 82.3%, 36.6% and 17.1%, respectively. In different age groups, the diabetic awareness rate was higher in men than that in women, and the treatment rate was higher in women than that in men. The diabetic patients, who consumed fruit for ≥ 5 days a week, accounted for 16.3%, and their diabetic treatment (28.1%) and control rates (44.1%) were lower. Shenyang people aged ≥ 40 years have higher diabetic prevalence and awareness rates, and lower diabetic treatment and control rates. Finally, it is necessary to enhance awareness and education about diabetes, to improve its treatment and control rates. [ABSTRACT FROM AUTHOR]

Many positive-sense RNA viruses, especially those infecting plants, are known to experience stringent, stochastic population bottlenecks inside the cells they invade, but exactly how and why these populations become bottlenecked are unclear. A model proposed ten years ago advocates that such bottlenecks are evolutionarily favored because they cause the isolation of individual viral variants in separate cells. Such isolation in turn allows the viral variants to manifest the phenotypic differences they encode. Recently published observations lend mechanistic support to this model and prompt us to refine the model with novel molecular details. The refined model, designated Bottleneck, Isolate, Amplify, Select (BIAS), postulates that these viruses impose population bottlenecks on themselves by encoding bottleneck-enforcing proteins (BNEPs) that function in a concentration-dependent manner. In cells simultaneously invaded by numerous virions of the same virus, BNEPs reach the bottleneck-ready concentration sufficiently early to arrest nearly all internalized viral genomes. As a result, very few (as few as one) viral genomes stochastically escape to initiate reproduction. Repetition of this process in successively infected cells isolates viral genomes with different mutations in separate cells. This isolation prevents mutant viruses encoding defective viral proteins from hitchhiking on sister genome-encoded products, leading to the swift purging of such mutants. Importantly, genome isolation also ensures viral genomes harboring beneficial mutations accrue the cognate benefit exclusively to themselves, leading to the fixation of such beneficial mutations. Further interrogation of the BIAS hypothesis promises to deepen our understanding of virus evolution and inspire new solutions to virus disease mitigation. [ABSTRACT FROM AUTHOR]