Miracle-dz/UniFAR-FTUs huggingface dataset:
Lysis of Blue-Green Algae by Myxobacter

Enrichment from local fishponds led to the isolation of a bacterium capable of lysing many species of unicellular and filamentous blue-green algae, as well as certain bacteria. The isolate is an aflagellate, motile rod which moves in a gliding, flexuous manner; the organism is capable of digesting starch and agar, but not cellulose and gelatin. Its deoxyribonucleic acid base pair composition (per cent guanine plus cytosine ∼70) shows a close resemblance to that of the fruiting myxobacteria. Algae in lawns on agar plates were lysed rapidly by the myxobacter, but only limited and slow lysis occurred in liquid media, and no lysis took place when liquid cultures were shaken. No diffusible lytic factors would be demonstrated. Continuous observation of the lytic process under a phase-contrast microscope suggested that a close contact between the polar tip of the myxobacter and the alga is necessary for lysis. The lytic action is limited to the vegetative cells of the algae, whereas heterocysts are not affected. The gas vacuoles of the algal host are the only remnant visible after completion of digestion by the myxobacter.
Histochemical Detection of Quinone Reductase Activity In Situ Using LY 83583 Reduction and Oxidation

Abstract: The application of enzymatic staining techniques, using tetrazolium dyes, to aldehyde‐treated brain sections has revealed the presence of NADPH‐diaphorase activity attributed to nitric oxide synthase. When evaluating the specificity of the putative guanylyl cyclase inhibitor LY 83583, a robust and novel staining pattern was noted in epithelial, endothelial, and astrocytic cells when LY 83583 was included in the NADPH‐diaphorase histochemical reaction. This LY 83583‐dependent staining could be blocked by the NAD(P)H:quinone oxidoreductase inhibitor dicumarol. Based on its quinone structure, we hypothesized that LY 83583 was a substrate for the enzyme NAD(P)H:quinone oxidoreductase. Transfection of human embryonic kidney 293 cells with the rat liver isoform of NAD(P)H:quinone oxidoreductase resulted in robust NADPH‐ and LY 83583‐dependent staining that was completely blocked by dicumarol and was not observed in untransfected cells. Analysis of transfected cell extracts and brain homogenates indicated that LY 83583 was a substrate for NAD(P)H:quinone oxidoreductase, with a Km similar to the well‐characterized substrate menadione. Sensitivity of the nitroblue tetrazolium reduction to superoxide dismutase indicated that the reduction of LY 83583 by NAD(P)H:quinone oxidoreductase leads to superoxide generation. The localization of NAD(P)H:quinone oxidoreductase activity to astrocytic cells suggests a role for glia in combating oxidative insults to brain and in activating quinone‐like drugs such as LY 83583.
Zebrafish larvae lose vision at night

Darkness serves as a stimulus for vertebrate photoreceptors; they are actively depolarized in the dark and hyperpolarize in the light. Here, we show that larval zebrafish essentially turn off their visual system at night when they are not active. Electroretinograms recorded from larval zebrafish show large differences between day and night; the responses are normal in amplitude throughout the day but are almost absent after several hours of darkness at night. Behavioral testing also shows that larval zebrafish become unresponsive to visual stimuli at night. This phenomenon is largely circadian driven as fish show similar dramatic changes in visual responsiveness when maintained in continuous darkness, although light exposure at night partially restores the responses. Visual responsiveness is decreased at night by at least two mechanisms: photoreceptor outer segment activity decreases and synaptic ribbons in cone pedicles disassemble.
Widespread Increase of Tree Mortality Rates in the Western United States

Persistent changes in tree mortality rates can alter forest structure, composition, and ecosystem services such as carbon sequestration. Our analyses of longitudinal data from unmanaged old forests in the western United States showed that background (noncatastrophic) mortality rates have increased rapidly in recent decades, with doubling periods ranging from 17 to 29 years among regions. Increases were also pervasive across elevations, tree sizes, dominant genera, and past fire histories. Forest density and basal area declined slightly, which suggests that increasing mortality was not caused by endogenous increases in competition. Because mortality increased in small trees, the overall increase in mortality rates cannot be attributed solely to aging of large trees. Regional warming and consequent increases in water deficits are likely contributors to the increases in tree mortality rates.
Motor units in cat soleus muscle: physiological, histochemical and morphological characteristics

1. Physiological properties of motor units in the soleus muscle were studied in anaesthetized cats using intracellular stimulation of motoneurones to ensure functional isolation of single units. The muscle fibres belonging to 6 units were identified by glycogen depletion following prolonged stimulation, permitting analysis of their histochemical profiles and anatomical organization.
Associations between work-related factors and the carpal tunnel syndrome--a systematic review.

OBJECTIVES The aim of this study was to make a quantitative assessment of the exposure-response relationships between work-related physical and psychosocial factors and the occurrence of carpal tunnel syndrome (CTS) in occupational populations. METHODS A systematic review of the literature was conducted on the associations of type of work, physical load factors, and psychosocial aspects at work to the occurrence of CTS. The associations between work factors and CTS were expressed in quantitative measures, namely, odds ratios (OR) or relative risks. RESULTS Jobs with the highest risk of CTS included work in the meat- and fish-processing industry, forestry work with chain saws, and electronic assembly work (OR 76.5, 21.3, and 11.4, respectively). The occurrence of CTS was associated with high levels of hand-arm vibration, prolonged work with a flexed or extended wrist, high requirements for hand force, high repetitiveness, and their combination. No association was found between any psychosocial risk factor and CTS. Contradictory findings were reported for associations between computer work and CTS. CONCLUSIONS This review provides consistent indications that CTS is associated with an average hand force requirement of >4 kg, repetitiveness at work (cycle time 50% of cycle time performing the same movements), and a daily 8-hour energy-equivalent frequency-weighted acceleration of 3.9 m/s2.
Simvastatin, 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitor, suppresses osteoclastogenesis induced by receptor activator of nuclear factor‐κB ligand through modulation of NF‐κB pathway

Simvastatin, an inhibitor of 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase, is a cholesterol‐lowering drug that may play a role in bone metabolism through a mechanism that is not fully understood. Recently, receptor activator of NF‐κB ligand (RANKL), a member of the TNF superfamily, has emerged as a major mediator of bone loss via activation of osteoclastogenesis. The latter is also associated with certain cancers such as multiple myeloma and breast cancer. Whether simvastatin can modulate RANKL‐induced or cancer induced osteoclastogenesis was investigated. The effect of simvastatin on RANKL signaling and consequent osteoclastogenesis was investigated. RANKL induced NF‐κB activation, whereas pretreatment with simvastatin completely suppressed such activation and correlated with suppression of RANKL‐induced activation of IκBα kinase, IκBα phosphorylation and IκBα degradation. Similarly, RANKL induced the differentiation of monocytic cells to osteoclasts, whereas simvastatin suppressed it. The inhibition was maximal when cells were exposed to both simvastatin and RANKL simultaneously and minimal when simvastatin was added 1 day after RANKL treatment. Simvastatin also inhibited the osteoclastogenesis induced by human breast cancer and by multiple myeloma cells. Together, our results indicate that simvastatin inhibits the RANKL‐induced NF‐κB activation pathway that leads to suppression of osteoclastogenesis induced by RANKL and by tumor cells, thereby suggesting its therapeutic potential in osteoporosis and in cancer‐related bone loss. © 2008 Wiley‐Liss, Inc.
Complement factor H 402H variant and reticular macular disease.

OBJECTIVE To determine the association of high-risk alleles in the complement factor H (CFH; Y402H, rs1061170) and age-related maculopathy susceptibility (ARMS2; A69S, rs10490924) genes with reticular macular disease (RMD), a major clinical subphenotype of age-related macular degeneration (AMD). METHODS Using retinal images from the Columbia Macular Genetics Study, we identified 67 subject individuals with RMD. A comparison group of 64 subjects with AMD without RMD was matched by ethnicity, age, sex, and AMD clinical stage. RESULTS In the RMD group, 53 of 67 subjects (79.1%) were female, the mean age was 83 years, and 47 of 67 (70.1%) had late AMD, with closely matched values in the non-RMD group. The frequencies of the CFH 402H allele were 39.6% in the RMD group (53 of 134 individuals) and 58.6% in the non-RMD group (75 of 128 individuals) (χ(2) = 8.8; P = . 003; odds ratio, 0.46 [95% confidence interval, 0.28-0.76]). The corresponding frequencies of the risk allele for ARMS2 were 44.0% (40 of 128 individuals) and 31.3% (40 of 128 individuals), respectively (χ(2) = 4.0; P = . 045; odds ratio, 1.73 [95% confidence interval, 1.04-2.90]). Homozygosity for 402H was particularly associated with the absence of RMD, occurring in 8 of 67 subjects (11.9%) with RMD vs 24 of 64 subjects (37.5%) without RMD (P < .001). Retinal macular disease also was associated with hypertension among male patients. CONCLUSIONS The AMD-associated CFH 402H risk variant is significantly associated with the absence of RMD but enhanced risk for RMD is conferred by the ARMS2 69S AMD risk allele. These results are consistent with the hypothesis that 402H may confer a survival benefit against certain infections, some of which may cause RMD. CLINICAL RELEVANCE Reticular macular disease may be genetically distinct from the rest of AMD.
The Day-of-the-Week Effect’ Asymmetry in Return and Volatility in China: An Empirical Study

This paper aims to investigate the day-of-the-week effects’ asymmetry based on the CSI300 Index, the Shanghai Composite Index and the Shenzhen Component Index. The Kruskal–Wallis test established that the day-of-the-week effects exist in Chinese stock markets. In addition, the Brown–Forsythe test was applied to investigating the constancy of variances across the days of the week, which demonstrated that only the Shanghai Composite Index satisfies the null hypothesis of constancy variances. Furthermore, the first-generation threshold models were used to assess the day-of-the-week effects’ asymmetry. Comparative analysis of ARMA-GARCH, ARMA-GJR-ARCH and ARMA-APARCH using the Engle and Ng test implied that ARMA-GJR-GARCH and ARMA-APARCH could explain Chinese stock markets better; the Nyblom test showed the parameters’ constancy in these models. Finally, and most importantly, with the aid of the sensible proxy variable of the volatility, the Diebold–Mariano test was used to compare the forecasting performance of competing models; the results indicated that for the CSI300 and Shanghai Composite Indices, ARMA-GJR-GARCH displays better performance than ARMA-APARCH. However, for the Shenzhen Component Index, no significant difference was observed between the two models.
Limb Reduction Defects after Prenatal Inhibition of Nitric Oxide Synthase in Rats

ABSTRACT: To determine the influence of nitric oxide (NO) on vascular tone during fetal development, timed pregnant rats received the NO synthase inhibitor NG-nitro-L-arginine methyl ester for consecutive 4, 7, or 14 d before parturition (postorganogenesis). Offspring demonstrated limb reduction defects (incidence, 53%) involving either or both hindlimbs, whereas forelimbs were uniformly spared. Defects were dose-dependent but independent of the duration of administration occurring with equal frequency in 4-, 7-, and 14-d treatment groups. Histologic analysis revealed features characteristic of vascular disruption with hemorrhagic necrosis and loss of structure. The defects were prevented by concurrent maternal administration of L-arginine or the NO donors S-nitroso-N-acetyl-penicillamine and sodium nitroprusside. Defects were not seen after prenatal treatment with aminoguanidine. To study basal and agonist-mediated NO release, newborn femoral and brachial arteries were cannulated with a glass micropipette under constant pressure, and changes in intraluminal diameter (micrometers) were measured in response to acetylcholine and the NO synthase inhibitor Nω-nitro-L-arginine. Newborn femoral and brachial vessels demonstrated a dramatic (59%) decrease in resting diameter compared with adult vessels (16%). These findings suggest that basal NO release is upregulated during fetal development concurrent with the processes that increase maternal NO release. The data also suggest that up-regulation of NO release occurs throughout the fetal systemic circulation and is not restricted to hindlimbs. This is the first study to demonstrate inhibition of NO release in the pathogenesis of limb reduction defects.
Characterization of CHEK2 mutations in prostate cancer

The checkpoint kinase 2 (CHEK2, also known as CHK2) is a tumor suppressor that participates in the DNA damage‐signaling pathway. It is phosphorylated and activated following DNA damage, resulting in cell cycle arrest and apoptosis. Previously, we reported germline CHEK2 mutations in patients with prostate cancer. In this study, we have identified two novel somatic CHEK2 mutations, c.349A>G (p.R117G) and c.967A>C (p.E321K), in prostate tumor specimens and investigated the functions of these mutants in vivo. We have shown that most of the germline CHEK2 mutations and one somatic mutation (p.R117G) within FHA domain have modestly reduced CHEK2 kinase activity in comparison with wild‐type CHEK2 while the other somatic mutation (p.E321K) within the kinase domain of CHEK2 totally abolished CHEK2 kinase activity. Given that several clinical CHEK2 mutations reside in the Forkhead‐associated (FHA) domain, we further generated a series of missense mutations within this domain and demonstrated the requirement of an intact FHA domain for the full activation of CHEK2. Taken together, these results provide evidence that both germline and somatic CHEK2 mutations identified in prostate cancer may contribute to the development of prostate cancer through the reduction of CHEK2 activation in response to DNA damage and/or oncogenic stress. Hum Mutat 27(8), 742–747, 2006. Published 2006 Wiley‐Liss, Inc.
Dust exposure and the risk of cancer in cement industry workers in Korea.

BACKGROUND Cement is used widely in the construction industry, though it contains hazardous chemicals such as hexavalent chromium. Several epidemiological studies have examined the association between cement dust exposure and cancer, but these associations have proved inconclusive. In the present study, we examined the association between dust exposure and cancer in cement industry workers in Korea. METHODS Our cohort consisted of 1,324 men who worked at two Portland cement manufacturing factories between 1997 and 2005. We calculated cumulative dust exposures, then categorized workers into high and low dust exposure groups. Cancer cases were identified between 1997 and 2005 by linking with the national cancer registry. Standardized incidence ratios (SIRs) were calculated for all workers and the high and low dust exposure groups, respectively. RESULTS The SIR for overall cancers in all workers was increased (1.35, 95% CI: 1.01-1.78). The SIR for stomach cancer in the high dust exposure group was increased (2.18, 95% CI: 1.19-3.65), but there was no increased stomach cancer risk in the low dust exposure group. The SIR for rectal cancer in all workers was increased (3.05, 95% CI: 1.32-6.02). Rectal cancer risk was similar in the high and low exposure groups. CONCLUSIONS Our findings suggest a potential association between exposure in the cement industry and an increased risk of stomach and rectal cancers. However, due to the small number of cases, this association should be further investigated in a study with a longer follow-up period and adjustment for confounders.
Sex differences in subclinical and DSM-IV pathological gambling: results from the National Epidemiologic Survey on Alcohol and Related Conditions

Background. To examine sex differences in DSM-IV subclinical and pathological gambling in nationally representative data of the US population. Method. Data come from a large (n=43093) representative sample of the adult US population. Results. The lifetime prevalence rate of DSM-IV pathological gambling was 0·64% (95% CI 0·50–0·78) for men and 0·23% (95% CI 0·17–0·29) for women, whereas the lifetime prevalence of subclinical pathological gambling was 6·79% (95% CI 6·32–7·26) for men and 3·26% (95% CI 2·93–3·59) for women. For subclinical pathological gambling, men were significantly (p<0·01) more likely than women to have smoked more than two packs of cigarettes a day, to be classified as heavy drinkers and to have lifetime diagnoses of alcohol and drug use disorders. Women with subclinical and pathological gambling were significantly more likely than men to have lifetime mood and anxiety disorders. With respect to pathological gambling, women had later ages of onset of the disorder, and were significantly more likely than men to report gambling to relieve depressed mood and to prefer casino gambling. Rates of treatment-seeking for DSM-IV pathological gambling were low for both men and women. Conclusions. There are important sex differences in the prevalence, symptom pattern, sociodemographic and clinical correlates and course of DSM-IV subclinical and pathological gambling. Results underscore the need to investigate sex differences in the social determinants, neurobiology and treatment response of DSM-IV subclinical and pathological gambling.
The Quarterly Projection Model of the SARB

The macroeconomic modelling and forecasting process at the South African Reserve Bank makes use of a suite of models. This paper provides an update of the Quarterly Projection Model (QPM) – a so-called gap model – which has played an integral role in the suite since 2007. Details of the structure and functioning of the QPM model, with particular focus on the four most important gaps – the output gap, real exchange rate gap, real interest rate gap, and inflation gap (or inflation from target) – are provided. The model is then used to decompose these four gaps in order to tell a coherent story of South Africa's macroeconomic dynamics since the inception of inflation targeting. From the perspective of the policy maker, the QPM provides a tool that quantifies the consequences of its actions on the economy, while adequately highlighting the trade-offs that are faced in the process.
Tyrosine Residues Direct the Ubiquitination and Degradation of the NY-1 Hantavirus G1 Cytoplasmic Tail

ABSTRACT The hantavirus G1 protein contains a long C-terminal cytoplasmic tail of 142 residues. Hantavirus pulmonary syndrome-associated hantaviruses contain conserved tyrosine residues near the C terminus of G1 which form an immunoreceptor tyrosine activation motif (ITAM) and interact with Src and Syk family kinases. During studies of the G1 ITAM we observed that fusion proteins containing the G1 cytoplasmic tail were poorly expressed. Expression of G1 cytoplasmic tail constructs were dramatically enhanced by treating cells with the proteasome inhibitor ALLN, suggesting that the protein is ubiquitinated and degraded via the 26S proteasome. By using a 6-His-tagged ubiquitin, we demonstrated that the G1 cytoplasmic tail is polyubiquitinated and degraded in the absence of proteasome inhibitors. Expression of only the ITAM-containing domain also directed protein ubiquitination and degradation in the absence of upstream residues. Deleting the C-terminal 51 residues of G1, including the ITAM, stabilized G1 and blocked polyubiquitination and degradation of the protein. Site-directed mutagenesis of both ITAM tyrosines (Y619 and Y632) to phenylalanine also blocked polyubiquitination of G1 proteins and dramatically enhanced G1 protein stability. In contrast, the presence of Y627, which is not part of the ITAM motif, had no effect on G1 stability. Mutagenesis of just Y619 enhanced G1 stability, inhibited G1 ubiquitination, and increased the half-life of G1 by threefold. Mutating only Y632 had less of an effect on G1 protein stability, although Y619 and Y632 synergistically contributed to G1 instability. These findings suggest that Y619, which is conserved in all hantaviruses, is the primary signal for directing G1 ubiquitination and degradation. Collectively these findings indicate that specific conserved tyrosines within the G1 cytoplasmic tail direct the polyubiquitination and degradation of expressed G1 proteins and provide a potential means for down-regulating hantavirus G1 surface glycoproteins and cellular proteins that interact with G1.
In Vivo Th1 and Th2 Cytokine Modulation Effects of Rhodiola rosea Standardised Solution and its Major Constituent, Salidroside

Although Rhodiola rosea (L.) is used widely and disseminated in Oriental medicine, its in vivo effects on cytokine modulation remain unclear. Among the biologically active components of Rhodiola rosea, salidroside was suggested to be the most active compound. The objectives of this study were to assess the toxicity and cytokine modulation effects of Rhodiola rosea standardised solution (RRSS) and salidroside. Quantitative high pressure liquid chromatography (HPLC) analysis determined the content of salidroside in RRSS to be 4.39% (w/v). Groups of Balb/c mice were fed daily with different doses of RRSS or salidroside, with CAPE or distilled water used as positive and negative controls, respectively. The acute and subacute toxicity tests did not reveal weight differences, pathological changes, or abnormalities in liver or kidney function indices among the treated groups. Ovalbumin‐primed mouse cytokine assays demonstrated that both T helper (Th1) (IL‐2 and IFN‐γ) and Th2 (IL‐4 and IL‐10) cytokines were significantly increased by feeding with RRSS in a dose‐ and time‐dependent manner (p < 0.05). Moreover, the cytokine modulation effects of salidroside were less prominent than that of RRSS treatment and not dose‐dependent. These findings suggest that increased secretion of both Th1‐ and Th2‐pattern cytokines can be achieved with RRSS and salidroside treatment. Copyright © 2011 John Wiley & Sons, Ltd.
Query processing techniques in probabilistic databases

Probabilistic databases have many diverse applications due to inherent uncertainty in those applications. In this paper, we review how uncertainty is managed in probabilistic databases. Two techniques of query evaluation on probabilistic databases exist, namely extensional and intensional. Extensional query evaluation directly operates on tuple probability and thus it is quiet efficient. But, for some queries it gives wrong results. We have to find safe query plan if one exists for a given query. Intensional query evaluation derives probability inference using lineage expression. Intensional semantics can become impractical for complex queries as data complexity depends on the query and the instance. We discuss various queries including joins, top-k, skyline, aggregates on probabilistic databases. In addition, we provide outline of most popular probabilistic databases: MayBMS and Trio. As commercial probabilistic database management system is still lacking, we hope this review will motivate database researchers to develop concrete probabilistic database management system.