Miracle-dz/UniFAR-FTUs huggingface dataset:
Antibacterial Activity of Polyphenol Components in Oolong Tea Extract against Streptococcus mutans

The purpose of the present study was to determine the antibacterial activity of oolong tea extract on oral streptococci, including Streptococcus mutans and Streptococcus sobrinus, and to identify the response to its components. Antibacterial activity was found when the extract was added to S. mutans cells in chemically defined medium but not in complex broth media. Further, pretreatment with bovine serum albumin reduced the antibacterial activity. The extract showed antibacterial activity against all of the oral streptococci examined, with the highest activity against S. mutans MT8148R. This activity was found to originate from a monomeric polyphenol-rich fraction, and it was stronger than that of pure polyphenols. Moreover, some combinations of monomeric polyphenols showed the highest level of antibacterial activity. These results suggest that the antibacterial activity of oolong tea extract is caused by a synergistic effect of monomeric polyphenols, which can easily bind to proteins.
Redefining Delusion Based on Studies of Subjective Paranormal Ideation

The DSM–IV definition of delusion is argued to be unsatisfactory because it does not explain the mechanism for delusion formation and maintenance, it implies that such beliefs are necessarily dysfunctional (pathological), it underestimates the social component to some delusions, and it is inconsistent with research indicating that delusions can be modified through techniques such as contradiction, confrontation, and cognitive-behavioral therapy. However, a well-replicated mathematical model of magical/delusional thinking based on a study of paranormal beliefs and experiences is consistent with the hypothesis that attributional processes play a central role in delusion formation and maintenance. The model suggests attributional processes serve the adaptive function of reducing fear associated with ambiguous stimuli and delusional thinking is on a continuum with nonpathological forms. Based on this collective research an amendment to the definition of delusion is proposed and its clinical implications are addressed.
Freedom and happiness in mill's defence of liberty

Mill's aim in On Liberty is "to assert one very simple principle as entitled to govern absolutely the dealings of society with the individual in the way of compulsion and control". l That principle, which is often called Mill's harm principle, is this: the sole end for which mankind are warranted, individually or collectively, in interfering with the liberty of action of any of their number is self-protection . the only purpose for which power can be rightfully exercised over any member of a civilized community, against his will, is to prevent harm to others. His own good, either physical or moral, is not a sufficient warrant. He cannot rightfully be compelled to do or forbear because it will be better for him to do so, because it will make him happier, because, in the opinion of others, to do so would be wise or even right. The only part of the conduct of anyone for which he is amenable to society is that part which concerns others. In the part which merely concerns himself, his independence is, of right, absolute (pp. 95-6). What this principle is designed to preclude, of course, is "paternalism", as we now refer to it. No sane adult may be forced to do anything other than what he or she wants to do, on Mill's view, simply for paternalistic reasons. To justify the use of force, Mill says, we must show that the conduct we are attempting to control is likely to do harm to someone other than the agent. If this cannot be shown, we have no right to resort to force, whether in the form of social pressure or legal sanctions. Now Mill's defence of the harm principle is interesting not only because it is aimed at establishing such an uncompromising doctrine of individual autonomy but also because it is aimed at establishing that doctrine on strictly utilitarian grounds: his defence of the harm principle will be based solely on the principle of utility, Mill says, the principle that an action is right if it tends to promote at least as much happiness (or as little unhappiness) as any alternative action that is open to the agent and wrong if it does not (p. 97). Even if we were to imagine Mill to be arguing simply for a very strong (but defeasible) presumption against paternalistic interference with individual autonomy, which is in fact what he does in Book V of The Principles of Political Economy,2 his enterprise would nonetheless have to
Dimeric analogs of immunosuppressive decapeptide fragment of ubiquitin

Our previous studies revealed that ubiquitin and its decapeptide fragment with the LEDGRTLSDY sequence, located on the exposed molecule loop, strongly suppressed the immune response. This suggested that the loop may serve as a functional epitope of ubiquitin molecule and that a possible mechanism of biological action of the synthesized peptides is associated with interfering in interactions of ubiquitin with other molecules. Ubiquitin is known to exist in oligomeric forms, which can interact with various oligomeric receptors. We designed and synthesized new dimeric analogs of the ubiquitin fragment, to probe whether dimeric peptides may have higher affinity towards the ubiquitin receptors responsible for immunosuppression, which are believed to form oligomeric structures. Three dimerization strategies, N‐terminus to N‐terminus, C‐terminus to C‐terminus, and N‐terminus to C‐terminus (head‐to‐tail) via PEG derivatives were used to synthesize the dimeric peptides on solid support. In the course of our research, we developed a new and straightforward procedure of dimerization where α‐amino groups of the C‐terminal lysine residues of two peptide fragments were linked by PEG spacer directly on solid support.
The B‐cell‐activating factor signalling pathway is associated with Helicobacter pylori independence in gastric mucosa‐associated lymphoid tissue lymphoma without t(11;18)(q21;q21)

We previously reported that activation of the B‐cell‐activating factor (BAFF) pathway upregulates nuclear factor‐κB (NF‐κB) and induces BCL3 and BCL10 nuclear translocation in Helicobacter pylori (HP)‐independent gastric diffuse large B‐cell lymphoma (DLBCL) tumours with evidence of mucosa‐associated lymphoid tissue (MALT). However, the significance of BAFF expression in HP independence of gastric low‐grade MALT lymphomas without t(11;18)(q21;q21) remains unexplored. Sixty‐four patients who underwent successful HP eradication for localized HP‐positive gastric MALT lymphomas without t(11;18)(q21;q21) were studied. BAFF expression was significantly higher in the HP‐independent group than in the HP‐dependent group [22/26 (84.6%) versus 8/38 (21.1%); p < 0.001]. Similarly, BAFF receptor (BAFF‐R) expression (p = 0.004) and nuclear BCL3 (p = 0.004), BCL10 (p < 0.001), NF‐κB (p65) (p = 0.001) and NF‐κB (p52) (p = 0.005) expression were closely correlated with the HP independence of these tumours. Moreover, BAFF overexpression was significantly associated with BAFF‐R expression and nuclear BCL3, BCL10, NF‐κB (p65) and NF‐κB (p52) expression. These findings were further validated in an independent cohort, including 40 HP‐dependent cases and 18 HP‐independent cases of gastric MALT lymphoma without t(11;18)(q21;q21). The biological significance of BAFF signalling in t(11;18)(q21;q21)‐negative lymphoma cells was further studied in two types of lymphoma B cell: OCI‐Ly3 [non‐germinal centre B‐cell origin DLBCL without t(11;18)(q21;q21) cell line] and MA‐1 [t(14;18)(q32;q21)/IGH‐MALT1‐positive DLBCL cell line]. In both cell lines, we found that BAFF activated the canonical NF‐κB and AKT pathways, and induced the formation of BCL10–BCL3 complexes, which translocated to the nucleus. BCL10 and BCL3 nuclear translocation and NF‐κB (p65) transactivation were inhibited by either LY294002 or by silencing BCL3 or BCL10 with small interfering RNA. BAFF also activated non‐canonical NF‐κB pathways (p52) through tumour necrosis factor receptor‐associated factor 3 degradation, NF‐κB‐inducing kinase accumulation, inhibitor of κB kinase (IKK) α/β phosphorylation and NF‐κB p100 processing in both cell lines. Our data indicate that the autocrine BAFF signal transduction pathway contributes to HP independence in gastric MALT lymphomas without the t(11;18)(q21;q21) translocation. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Efferent projections of the suprachiasmatic nucleus: I. Studies using anterograde transport of Phaseolus vulgaris leucoagglutinin in the rat

The efferent projections of the suprachiasmatic nucleus (SCh) in the rat hypothalamus have been reexamined with the anterograde tracer Phaseolus vulgaris leucoagglutinin (PHA‐L), which displays labeled axons with the clarity of a Golgi impregnation. Fibers from the SCh can be divided into six pathways for descriptive purposes. By far the densest terminal field arising from cells in the SCh ends in a roughly comma‐shaped zone between the SCh and paravontricular nucleus on the one hand and the periventricular nucleus and anterior hypothalamic area on the other. A few axons continue dorsally from this “subparaventricular zone” to pass through parvicellular parts of the paraventricular nucleus and the overlying midline thalamic nuclei to end in midrostrocaudal parts of the paraventricular nucleus of the thalamus, and a larger number continue caudally to end in the dorsomedial nucleus, dorsal parts of the cell‐sparse zone surrounding the ventromedial nucleus, and the posterior hypothalamic area. The other five pathways all consist of relatively small numbers of fibers and give rise to relatively sparse terminal fields. The second pathway consists of rostrally directed fibers that end in ventral parts of the medial preoptic area and anteroventral periventricular nucleus. The third consists of anterodorsally oriented fibers that pass through the medial preoptic nucleus and adjacent regions to end ventrally in the intermediate lateral septal nucleus. The fourth consists of fibers just caudal to the third group that end in the preoptic continuation of the bed nucleus of the stria terminalis, as well as in the parataenial nucleus and rostral part of the paraventricular nucleus of the thalamus. The fifth consists of laterally directed fibers that course over the optic tract to end in the ventral lateral geniculate nucleus. And the sixth consists of fibers that course posteriorally through the anterior hypothalamic and retrochiasmatic areas to end in the cell‐sparse zone between the arcuate nucleus and ventral parts of the ventromedial nucleus, as well as in adjacent parts of the lateral hypothalamic area.
Epidemiology of Hodgkin's disease.

Hodgkin's disease displays an intriguing variation in incidence with age. For adult disease, there is striking bimodality in incidence with peaks in young adulthood and in older adulthood. On epidemiologic grounds, there appear to be three different diseases: childhood (0-14 years), young adult (15-34 years), and older adult Hodgkin's disease (55+ years). There are marked geographic variations in Hodgkin's disease incidence, but the variations are different for the three age groups. There are also interesting associations between Hodgkin's disease and markers of social class. For the young adult disease, the higher the socioeconomic status of a person, the greater the Hodgkin's disease risk. Additionally, Hodgkin's disease patients appear to have had fewer of the childhood infectious diseases or to have had these diseases at older ages than controls. These factors suggest an analogy between young adult Hodgkin's disease and Epstein-Barr virus, poliomyelitis, and tuberculosis infections. Thus, the descriptive epidemiology of Hodgkin's disease suggests an infectious disease process underlying its etiology in young adulthood and perhaps in childhood. There is a curious relationship between Hodgkin's disease and Epstein-Barr virus infection. Persons with Epstein-Barr virus infection have an increased risk of developing Hodgkin's disease, and the Epstein-Barr virus infection precedes the development of Hodgkin's disease. The virus has never been isolated from or identified in Hodgkin's disease tissue. The mechanisms underlying this association are unknown and may provide important clues to the etiology of Hodgkin's disease and other lymphomas. It is likely that there is no direct person-to-person spread of Hodgkin's disease. This is suggested by several negative studies of linkages between cases, time-space clustering, and aggregation of exposures at schools. Studies have shown that neither physicians nor nurses, groups with greater likelihood of encountering Hodgkin's disease patients than the general public, have an increased risk. There appears to be familial aggregation of Hodgkin's disease. Siblings of young adult cases are at increased risk, whereas siblings of older adult cases have no increase in risk. Among sibling pairs with Hodgkin's disease, there is a marked excess of like-sex pairs. Like-sex siblings have almost twice the risk of discordant-sex siblings, suggesting an interaction between environmental and genetic factors. Thus, it would be of interest to known the risk to spouses of cases who share environments but who do not share genes. (ABSTRACT TRUNCATED AT 400 WORDS)
Role of genes and environments for explaining Alzheimer disease.

CONTEXT Twin studies using selected samples have shown high heritability for Alzheimer disease (AD). OBJECTIVE To evaluate genetic and environmental influences on AD in a fully ascertained population of older twins, including like- and unlike-sex pairs. DESIGN Five-group quantitative genetic model: male monozygotic twins, female monozygotic twins, male dizygotic twins, female dizygotic twins, and unlike-sex twins. SETTING AND PARTICIPANTS All twins in the Swedish Twin Registry aged 65 years and older. The study included 11,884 twin pairs, among whom were 392 pairs in which 1 or both members had AD. MAIN OUTCOME MEASURES All individuals were screened for cognitive dysfunction. Suspected cases of dementia and their co-twins received complete clinical diagnostic evaluations for AD. Estimates of heritability, shared environmental influences, and nonshared environmental influences, adjusting for age, were derived from the twin data. RESULTS Heritability for AD was estimated to be 58% in the full model and 79% in the best-fitting model, with the balance of variation explained by nonshared environmental influences. There were no significant differences between men and women in prevalence or heritability after controlling for age. Within pairs concordant for AD, intrapair difference in age at onset was significantly greater in dizygotic than in monozygotic pairs, suggesting genetic influences on timing of the disease. CONCLUSIONS In the largest twin study to date, we confirmed that heritability for AD is high and that the same genetic factors are influential for both men and women. However, nongenetic risk factors also play an important role and might be the focus for interventions to reduce disease risk or delay disease onset.
Pharmacogenetic pathway analysis for determination of sunitinib-induced toxicity.

5006 Background: To identify genetic markers in the pharmacokinetic and pharmacodynamic pathways of sunitinib that predispose for development of toxicities; thrombocytopenia, leukopenia, mucosal inflammation, hand-foot syndrome and 'any toxicity according to Common Terminology Criteria > grade 2. ' METHODS A multicenter pharmacogenetic association study was performed in 219 patients treated with single agent sunitinib. A total of 31 single nucleotide polymorphisms in 12 candidate genes, together with several non-genetic variants, were analyzed for a possible association with toxicity. In addition, genetic haplotypes were developed and related to toxicity. RESULTS The risk for leukopenia was increased when the G-allele in CYP1A1 2455A/G (OR = 6.24; p = 0.029) or the T-allele in FLT3 738T/C (OR = 2.8; p = 0.008) were present or CAG in the NR1I3 (5719C/T, 7738A/C, 7837T/G) haplotype (OR = 1.74; p = 0.041) was absent. 'Any toxicity > grade 2' prevalence was increased when the T-allele of VEGFR-2 1191C/T (OR = 2.39; p = 0.046) or a copy of TT in the ABCG2 (-15622C/T, 1143C/T) haplotype (OR = 2.63; p = 0.016) were present. The risk for mucosal inflammation was increased in the presence of the G-allele in CYP1A1 2455A/G (OR = 4.03; p = 0.021) and the prevalence of hand-foot syndrome was increased when a copy of TTT in the ABCB1 (3435C/T, 1236C/T, 2677G/T) haplotype (OR = 2.56; p = 0.035) was present. CONCLUSIONS This exploratory study suggests that polymorphisms in specific genes encoding for metabolizing enzymes, efflux transporters and drug targets are associated with sunitinib related toxicities. A better understanding of genetic and non-genetic determinants of sunitinib toxicity should help to optimize drug treatment in individual patients. [Table: see text].
Bare hands interaction with the projected images combined with a real object

In this paper, we propose a bare hands recognition system which can be used in the projection environment and also can be used in both fixed and mobile systems. Particularly, for its robust and fast operation under the projected images, we designed structured infrared lights using diffraction gratings and a laser module. Performance measurements of the system and user tests were conducted.
[High-frequency echocardiography for assessment of regional wall motion abnormality and cardiac function in mice with myocardial infarction].

OBJECTIVE To evaluate the value of high-frequency echocardiography in assessing cardiac structure and function in a mouse model of myocardial infarction. METHODS Twenty-five C57BL/6 mice were randomly divided into sham-operated group (n=10) and myocardial infarction model group (n=15) established by ligation of the left anterior descending artery. The cardiac structure, regional wall motion and cardiac function of mice were examined with pulsed wave Doppler (PWD), tissue Doppler imaging (TDI), EKV and M-mode echocardiography 3 days before and at 1 week after the operation. The histological changes and myocardial structure of the heart were observed at 1 week after the operation. RESULTS High-frequency echocardiography and HE staining detected obvious myocardial infarction in the mice in the model group. Compared with the sham-operated mice, the mice with myocardial infarction showed significant left ventricular expansion, obvious thinning of the ventricular wall, and significantly decreased ventricular systolic function and diastolic function with regional wall motion abnormality and ventricular remodeling. CONCLUSION s 2D-type echocardiography combined with M-mode, PWD, TDI and EKVTM for allows accurate and sensitive detection of the loci and severity of myocardial infarction to provide important evidence for clinical diagnosis and treatment of myocardial infarction.
Apolipoprotein B and apolipoprotein A‐I: risk indicators of coronary heart disease and targets for lipid‐modifying therapy

Although LDL cholesterol (LDL‐C) is associated with an increased risk of coronary heart disease, other lipoproteins and their constituents, apolipoproteins, may play an important role in atherosclerosis. Elevated levels of apolipoprotein (apo) B, a constituent of atherogenic lipoproteins, and reduced levels of apo A‐I, a component of anti‐atherogenic HDL, are associated with increased cardiac events. Apo B, apo A‐I and the apo B/apo A‐I ratio have been reported as better predictors of cardiovascular events than LDL‐C and they even retain their predictive power in patients receiving lipid‐modifying therapy. Measurement of these apolipoproteins could improve cardiovascular risk prediction.
Follow-up Recommendation Detection on Radiology Reports with Incidental Pulmonary Nodules

The management of follow-up recommendations is fundamental for the appropriate care of patients with incidental pulmonary findings. The lack of communication of these important findings can result in important actionable information being lost in healthcare provider electronic documents. This study aims to analyze follow-up recommendations in radiology reports containing pulmonary incidental findings by using Natural Language Processing and Regular Expressions. Our evaluation highlights the different follow-up recommendation rates for oncology and non-oncology patient cohorts. The results reveal the need for a context-sensitive approach to tracking different patient cohorts in an enterprise-wide assessment.
A Communication-Efficient Distributed Algorithm for Kernel Principal Component Analysis

Principal Component Analysis (PCA) is a fundamental technology in machine learning. Nowadays many high-dimension large datasets are acquired in a distributed manner, which precludes the use of centralized PCA due to the high communication cost and privacy risk. Thus, many distributed PCA algorithms are proposed, most of which, however, focus on linear cases. To efficiently extract non-linear features, this brief proposes a communication-efficient distributed kernel PCA algorithm, where linear and RBF kernels are applied. The key is to estimate the global empirical kernel matrix from the eigenvectors of local kernel matrices. The approximate error of the estimators is theoretically analyzed for both linear and RBF kernels. The result suggests that when eigenvalues decay fast, which is common for RBF kernels, the proposed algorithm gives high quality results with low communication cost. Results of simulation experiments verify our theory analysis and experiments on GSE2187 dataset show the effectiveness of the proposed algorithm.
Substance P-induced respiratory excitation is blunted by delta-receptor specific opioids in the rat medulla oblongata.

The effects of substance P (SP) and the naturally occurring met-enkephalin and the synthetic mu-specific opioid agonist, DAGO (Tyr-D-Ala-Gly-N-Methy-Phe-Gly-ol) and the delta-specific opioid agonist DADL (Tyr-D-Ala-Gly-Phe-D-Leu) on basal ventilation were investigated in halothane-anaesthetized rats. Local injections of SP (0.75-1.5 nmol) in the ventrolateral medulla oblongata (VLM), e.g. nucleus paragigantocellularis, and nucleus reticularis lateralis increased ventilation because of an elevation of tidal volume. Met-enkephalin induced a short-lasting ventilatory depression mainly because of a depression of tidal volume. Activation of delta- and mu-opioid receptors in the VLM by local application of DADL and DAGO, respectively, induced ventilatory depression, which was later in onset and more long-lasting. Local administration of met-enkephalin into the VLM also produced a long-lasting inhibition of the SP-induced ventilatory excitation. A similar blockade of the SP-induced excitatory ventilatory response could be elicited by DADL but not by DAGO. This antagonistic effect was attenuated by local application of the delta-opioid receptor antagonist ICI 154. 129. We conclude that the naturally occurring met-enkephalin as well as synthetic mu- and delta-specific enkephalin analogues (DAGO and DADL, respectively) in VLM depress basal ventilation by an effect on inspiratory drive. There is a functional antagonism between activation of delta-opioid receptors and SP receptors into the VLM in respect to respiratory regulation.