Miracle-dz/UniFAR-FTUs huggingface dataset:
Threat to the point: improving the value of comparative extinction risk analysis for conservation action

Comparative extinction risk analysis is a common approach for assessing the relative plight of biodiversity and making conservation recommendations. However, the usefulness of such analyses for conservation practice has been questioned. One reason for underperformance may be that threats arising from global environmental changes (e.g., habitat loss, invasive species, climate change) are often overlooked, despite being widely regarded as proximal drivers of species’ endangerment. We explore this problem by (i) reviewing the use of threats in this field and (ii) quantitatively investigating the effects of threat exclusion on the interpretation and potential application of extinction risk model results. We show that threat variables are routinely (59%) identified as significant predictors of extinction risk, yet while most studies (78%) include extrinsic factors of some kind (e.g., geographic or bioclimatic information), the majority (63%) do not include threats. Despite low overall usage, studies are increasingly employing threats to explain patterns of extinction risk. However, most continue to employ methods developed for the analysis of heritable traits (e.g., body size, fecundity), which may be poorly suited to the treatment of nonheritable predictors including threats. In our global mammal and continental amphibian extinction risk case studies, omitting threats reduced model predictive performance, but more importantly (i) reduced mechanistic information relevant to management; (ii) resulted in considerable disagreement in species classifications (12% and 5% for amphibians and mammals, respectively, translating to dozens and hundreds of species); and (iii) caused even greater disagreement (20–60%) in a downstream conservation application (species ranking). We conclude that the use of threats in comparative extinction risk analysis is important and increasing but currently in the early stages of development. Priorities for future studies include improving uptake, availability, quality and quantification of threat data, and developing analytical methods that yield more robust, relevant and tangible products for conservation applications.
Selective Predictive Value of Rapid Automatized Naming in Poor Readers

This study considers the differential predictive value of rapid naming tests for various aspects of later reading, where the differential is between nondisabled and poor readers. Two large-N longitudinal samples of students who have been evaluated from third through eighth grades are studied: (a) a randomly accessed, normally distributed group including students with varying degrees of reading ability (N = 154), and (b) a group of poor readers whose single-word reading in third grade is at or below the population 10th percentile (N = 64). Outcomes in fifth and eighth grade were measured in both groups. Single-word reading in both grades was strongly predicted from third-grade rapid naming only within the poor readers, even when IQ, socioeconomc status, and third-grade single-word reading were statistically controlled. Although rapid naming had predictive value within the large, normally distributed group, its predictive power was entirely absent in the average-reading nondisabled students who were between the 10th and 90th percentiles (n = 122). The fact that rapid naming has predictive power only for poor readers but not for average readers is interpreted as suggesting that impaired readers are qualitatively different from the normal-reading population and are not simply the “tail” of a normal distribution of reading ability. It also seems that it is the automaticity of retrieval, not the knowledge of names itself (as in confrontational naming tasks), that gives the predictive power in rapid naming. These data are considered in light of the one-and two-factor theories of the underlying processes involved in reading disability or dyslexia.
Progression to AIDS: the effects of stress, depressive symptoms, and social support.

OBJECTIVE We examined the effects of stress, depressive symptoms, and social support on the progression of HIV infection. METHODS Eighty-two HIV-infected gay men without symptoms or AIDS at baseline were followed up every 6 months for up to 5.5 years. Men were recruited from rural and urban areas in North Carolina as part of the Coping in Health and Illness Project. Disease progression was defined using criteria for AIDS (CD4+ lymphocyte count of <200/microl and/or an AIDS-indicator condition). RESULTS We used Cox regression models with time-dependent covariates, adjusting for age, education, race, baseline CD4+ count, tobacco use, and number of antiretroviral medications. Faster progression to AIDS was associated with more cumulative stressful life events (p = .002), more cumulative depressive symptoms (p = .008), and less cumulative social support (p = .0002). When all three variables were analyzed together, stress and social support remained significant in the model. At 5.5 years, the probability of getting AIDS was about two to three times as high among those above the median on stress or below the median on social support compared with those below the median on stress or above the median on support, respectively. CONCLUSIONS These data are among the first to demonstrate that more stress and less social support may accelerate the course of HIV disease progression. Additional study will be necessary to elucidate the mechanisms that underlie these relationships and to determine whether interventions that address stress and social support can alter the course of HIV infection.
[Which is the role of parasites and yeasts in the genesis of chronic blepharitis?].

INTRODUCTION The chronic blepharitis is a current ophthalmic disease posing a therapeutic problem. The etiologic diagnosis is essential for adapting the treatment. PURPOSE The aim of this study is to describe the role of Demodex sp, Malassezia sp and Candida sp in the pathogenesis of chronic blepharitis. PATIENTS AND METHODS It's a prospective study realized during a period of 14 months. It interested 69 patients with chronic blepharitis and 96 controls. The prevalence of Demodex sp, Malassezia sp and Candida sp on the eyelash of chronic blepharitis patients and controls was investigated. RESULTS Demodex folliculorum was found in 58% of patients with chronic blepharitis and in 15,6% of controls. The difference between the two groups was statistically significant (P<0,00001). The sex and the age intervene neither in the frequency, nor in the abundance of D. folliculorum in the two groups. Malassezia sp was identified in 10,4% of the control group and 31,88% of the group with chronic blepharitis. The difference is significant (P<0,00001). There is no correlation between frequency and abundance of Malassezia, sex and age in the two groups. CONCLUSION In our study, D. folliculorum and Malassezia sp seem to be accused in the genesis of the chronic blepharitis. Their systematic search is necessary in order to adapt the treatment.
BCG immunotherapy of bladder cancer: Inhibition of tumor recurrence and associated immune responses

Fifty‐one patients with confirmed bladder cancer have enrolled in a prospective evaluation of BCG immunotherapy. Following resection of existing tumors, patients were stratified according to tumor grade and number of previous recurrences and randomly assigned to control or BCG treatment groups. Immunotherapy consisted of six weekly administrations of Pasteur strain BCG using 120 mg intravesically and 5 mg percutaneously. Immunotherapy side effects were minimal and no patient required postponement of BCG treatments. Eleven control (46%) compared with five (22%) BCG‐treated patients had tumor recurrence (P = 0.078, χ2). Prolongation of the disease‐free interval with BCG treatment was significant at the P = 0.016 level by Wilcoxon analysis. Four control and two BCG‐treated patients had multiple recurrences. Comparing total episodes of recurrence, nineteen of 79 (24%) control and eight of 85 (7%) BCG group cystoscopic examinations revealed tumor (P = 0.006, χ2). Immunologic correlates of response to immunotherapy were not statistically significant since only five BCG‐treated patients had tumor recurrence. However, four of these five patients evidenced impaired LIF response to PPD at the time of tumor recurrence, and impairment of skin test reactivity and BCG humoral antibody response were more commonly seen in this subgroup of patients.
The Acute Treatment of Migraine in Adults: The American Headache Society Evidence Assessment of Migraine Pharmacotherapies

The study aims to provide an updated assessment of the evidence for individual pharmacological therapies for acute migraine treatment. Pharmacological therapy is frequently required for acutely treating migraine attacks. The American Academy of Neurology Guidelines published in 2000 summarized the available evidence relating to the efficacy of acute migraine medications. This review, conducted by the members of the Guidelines Section of the American Headache Society, is an updated assessment of evidence for the migraine acute medications. A standardized literature search was performed to identify articles related to acute migraine treatment that were published between 1998 and 2013. The American Academy of Neurology Guidelines Development procedures were followed. Two authors reviewed each abstract resulting from the search and determined whether the full manuscript qualified for review. Two reviewers studied each qualifying full manuscript for its level of evidence. Level A evidence requires at least 2 Class I studies, and Level B evidence requires 1 Class I or 2 Class II studies. The specific medications – triptans (almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, sumatriptan [oral, nasal spray, injectable, transcutaneous patch], zolmitriptan [oral and nasal spray]) and dihydroergotamine (nasal spray, inhaler) are effective (Level A). Ergotamine and other forms of dihydroergotamine are probably effective (Level B). Effective nonspecific medications include acetaminophen, nonsteroidal anti‐inflammatory drugs (aspirin, diclofenac, ibuprofen, and naproxen), opioids (butorphanol nasal spray), sumatriptan/naproxen, and the combination of acetaminophen/aspirin/caffeine (Level A). Ketoprofen, intravenous and intramuscular ketorolac, flurbiprofen, intravenous magnesium (in migraine with aura), and the combination of isometheptene compounds, codeine/acetaminophen and tramadol/acetaminophen are probably effective (Level B). The antiemetics prochlorperazine, droperidol, chlorpromazine, and metoclopramide are probably effective (Level B). There is inadequate evidence for butalbital and butalbital combinations, phenazone, intravenous tramadol, methadone, butorphanol or meperidine injections, intranasal lidocaine, and corticosteroids, including dexamethasone (Level C). Octreotide is probably not effective (Level B). There is inadequate evidence to refute the efficacy of ketorolac nasal spray, intravenous acetaminophen, chlorpromazine injection, and intravenous granisetron (Level C). There are many acute migraine treatments for which evidence supports efficacy. Clinicians must consider medication efficacy, potential side effects, and potential medication‐related adverse events when prescribing acute medications for migraine. Although opioids, such as butorphanol, codeine/acetaminophen, and tramadol/acetaminophen, are probably effective, they are not recommended for regular use.
Adolescents' Reported Usage of Selected Foods in Relation to Their Perceptions and Social Norms for Those Foods

This paper reports a study of factors associated with the consumption of 22 diverse foods among 2082 students aged 12-15 years in Tasmania, Australia. Students provided data by completing a printed questionnaire. Multiple linear regression was used to assess how well self-reported usual (past) frequency of consumption of a food could be estimated from their perceptions of the qualities of the food (their liking for it, its healthfulness) and their descriptive social norms for the food (its usage by parents and its usage by friends). For all foods, multiple R was significant (p < 0.0001), with values ranging from 0.28-0.64 (median for the 22 foods being 0.49). Standardized regression coefficients for liking and parental usage were highly significant (p < 0.0001) for all foods. However, consistently lower coefficients were found for friends' usage (11 with p < 0.01, but only three with p < 0.0001) and healthfulness (five with p < 0.01, but only one with p < 0.0001). The absolute and relative magnitudes of the regression coefficients varied substantially between the foods. Liking was a stronger predictor than parental usage for 11 of the foods, and parental usage out-ranked liking for the remaining 11. Regression coefficients for friends' usage and healthfulness were smaller than those for liking and parental usage for all foods studied.
Clinical significance of interleukin 33 (IL-33) in patients with eosinophilic pneumonia.

BACKGROUND Interleukin 33 (IL-33) works as a functional mediator in allergic disease by enhancing the activity of eosinophils and inducing expression of T helper 2 (Th2)-associated cytokines. However, the role of IL-33 in pulmonary eosinophilia has not been elucidated. We investigated the levels of IL-33 in eosinophilic pneumonia (EP) together with associated cytokines, and discussed the clinical significance of IL-33 in EP. METHODS Sera and bronchoalveolar lavage fluid (BALF) were obtained from 16 patients with EP, including acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP). Twelve patients with acute respiratory distress syndrome (ARDS) were also included for comparison. The concentration of IL-33 and Th2 cytokines (IL-4, IL-5, IL-13) were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS The concentration of serum IL-33 was significantly higher in patients with AEP than in CEP. In CEP, only patients with atopic factors showed mild increase of serum IL-33. The concentration of BALF IL-33 was also significantly elevated in AEP, however, it remained quite low in CEP. Among Th2 cytokines, IL-5 was significantly increased in both serum and BALF in AEP, and the level of IL-5 was positively correlated with that of IL-33. ARDS showed no increase of serum and BALF IL-33. CONCLUSIONS The remarkable increase of BALF IL-33 in AEP indicated the local production of IL-33 in lungs. IL-33 is considered to be a local key molecule for triggering pulmonary eosinophilia, together with IL-5. BALF IL-33 appears to be a useful marker for discriminating AEP from CEP and ARDS.
Molecular mechanism underlying β1 regulation in voltage- and calcium-activated potassium (BK) channels

Significance β-Subunits (β1–β4) play a critical role in defining the properties of the voltage- and calcium-activated potassium (BK) channel, which in turn determines the physiological role that this channel can perform in different tissues. In particular, the β1-subunit causes an increase in the apparent BK Ca2+ sensitivity due to a stabilization of the voltage sensor in the active configuration. We investigated the molecular details of such voltage-sensor stabilization by mutagenesis and gating current measurements. Mixing regions of β1 and β3 made it possible to identify the N terminus, in particular the third and fourth lysine residues, as the structural element necessary to recover the full effect of β1 on the voltage sensor. Being activated by depolarizing voltages and increases in cytoplasmic Ca2+, voltage- and calcium-activated potassium (BK) channels and their modulatory β-subunits are able to dampen or stop excitatory stimuli in a wide range of cellular types, including both neuronal and nonneuronal tissues. Minimal alterations in BK channel function may contribute to the pathophysiology of several diseases, including hypertension, asthma, cancer, epilepsy, and diabetes. Several gating processes, allosterically coupled to each other, control BK channel activity and are potential targets for regulation by auxiliary β-subunits that are expressed together with the α (BK)-subunit in almost every tissue type where they are found. By measuring gating currents in BK channels coexpressed with chimeras between β1 and β3 or β2 auxiliary subunits, we were able to identify that the cytoplasmic regions of β1 are responsible for the modulation of the voltage sensors. In addition, we narrowed down the structural determinants to the N terminus of β1, which contains two lysine residues (i.e., K3 and K4), which upon substitution virtually abolished the effects of β1 on charge movement. The mechanism by which K3 and K4 stabilize the voltage sensor is not electrostatic but specific, and the α (BK)-residues involved remain to be identified. This is the first report, to our knowledge, where the regulatory effects of the β1-subunit have been clearly assigned to a particular segment, with two pivotal amino acids being responsible for this modulation.
Protein kinase Cα‐responsive polymeric carrier: its application for gene delivery into human cancers

For cancer‐targeting gene delivery, we applied a protein kinase C (PKC)α‐responsive polymeric carrier to human cancers (U‐87 MG [human glioblastoma‐astrocytoma, epithelial‐like cell line] and A549 [human lung adenocarcinoma epithelial cell line]). Two polymers, one a PKCα‐responsive polymer (PPC[S]) containing the phosphorylation site serine, and the other a negative control polymer (PPC[A]), in which the serine was substituted with alanine, were synthesized. No cytotoxicity of the polymer was identified. When the complexes were transfected into cancer cells or tissues in which PKCα was hyper‐activated, the luciferase expression from the PPC(S)/plasmid (pDNA) complex was higher than that from the PPC(A)/pDNA complex. These results show that the phosphorylation of complex by PKCα in cancer cells leads to high gene expression and that our system can be used as a human cancer cell–targeting gene delivery system. (Cancer Sci 2009)
Mitochondrial DNAs and plasmids as taxonomic characteristics in Trichoderma viride

Mitochondrial DNA (mtDNA) was purified from 12 isolates of the Trichoderma viride aggregate and found to be, on the average, 32.7 kb in size. Plasmids were present in the mtDNA preparations from 8 of 12 strains of T. viride examined. Plasmids in four of the strains produced ladderlike banding patterns on gels, and these plasmids were studied in detail. The ladderlike patterns were produced by single molecules that were supercoiled to various degrees. Plasmids from two of the strains do not have homology with the mtDNA but do have a limited amount of homology with each other. No phenotype could be associated with the presence of a plasmid. Restriction endonuclease digestion of the mtDNAs produced patterns in which the presence or absence of certain fragments correlated with the classification of the strains into T. viride group I or II. Phenetic cluster analysis and parsimony analysis of the fragment patterns produced groups that corresponded to T. viride groups I and II. The fragment patterns were very diverse, with nearly all strains having a unique pattern. However, two strains of T. viride group I from widely different geographical locations did have identical restriction patterns for all the enzymes used in this study. This result indicates that it may not be possible to use mtDNA restriction patterns alone to identify Trichoderma strains.
Morphine‐induced in vivo release of spinal cholecystokinin is mediated by δ‐opioid receptors – effect of peripheral axotomy

Morphine and other opioid agonists induce spinal in vivo release of cholecystokinin (CCK), a neuropeptide with anti‐opioid properties. However, so far the opioid receptor subtype responsible for this effect has not been determined. In the present in vivo microdialysis study, the morphine‐induced release of cholecystokinin‐like immunoreactivity (CCK‐LI) in the dorsal horn was completely blocked by the δ‐opioid antagonist naltrindole (10 µm in the perfusion fluid). Neither the µ‐opioid receptor antagonist d‐Phe‐Cys‐Tyr‐d‐Trp‐Orn‐Thr‐Pen‐Thr amide (CTOP; 10 µm in the perfusion fluid), nor the κ‐opioid receptor antagonist nor‐binaltorphimine (nor‐BNI); 10 µm in the perfusion fluid) had any significant effect in this respect. In addition, systemic administration of the δ‐opioid receptor agonist BW373U86 (1 mg/kg, s.c.) and spinal administration of the δ2‐opioid receptor agonist, Tyr‐d‐Ala‐Phe‐Glu‐Val‐Val‐Gly amide ([d‐Ala2] deltorphin II) (1 µm in the perfusion fluid) induced a significant increase of the CCK‐LI level. The effect of BW373U86 on spinal CCK‐LI release was completely blocked by spinal administration of naltrindole. The µ‐opioid receptor agonist [D‐ala2‐N‐Me‐Phe4‐Gly5‐ol]‐enkephalin (DAMGO) (1 µm in the perfusion fluid or 1 mg/kg, s.c.) failed to alter the CCK‐LI level. Peripheral nerve lesions have previously been shown to down‐regulate µ‐ and δ‐opioid receptors in the dorsal horn, to increase the gene‐expression of CCK and CCK‐receptor mRNA in dorsal root ganglion neurons and to alter the potassium‐induced spinal CCK‐LI release. After complete sciatic nerve transection, administration of the two selective δ‐opioid receptor agonists induced a significant release of CCK‐LI, which was comparable to controls. In contrast, neither systemic nor spinal administration of morphine and DAMGO altered the spinal CCK‐LI release in axotomized animals. The present data indicate that the δ‐opioid receptor mediates morphine‐induced CCK‐LI release in the spinal cord.
Role of calcium in nitric oxide‐induced cytotoxicity: EGTA protects mouse oligodendrocytes

Active nitrogen species are overproduced in inflammatory brain lesions in multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE). NO has been shown to mediate the death of oligodendrocytes (OLs), a primary target of damage in MS. To develop strategies to protect OLs, we examined the mechanisms of cytotoxicity of two NO donors, S‐nitroso‐N‐acetyl‐penicillamine (SNAP) and sodium nitroprusside (SNP) on mature mouse OLs. Nitrosonium ion (NO+) rather than NO · mediates damage with both SNAP and SNP, as shown by significant protection with hemoglobin (HbO2), but not with the NO · scavenger PTIO. SNAP and SNP differ in time course and mechanisms of killing OLs. With SNAP, OL death is delayed for at least 6 hr, but with SNP, OL death is continuous over 18 hr with no delay. Relative to NO release, SNP is more toxic than SNAP, due to synergism of NO with cyanide released by SNP. SNAP elicits a Ca2+ influx in over half of the OLs within min. Further, OL death due to NO release from SNAP is Ca2+‐dependent, because the Ca2+ chelator EGTA protects OLs from killing by SNAP, and also from killing by the NONOates NOC‐9 and NOC‐18, which spontaneously release NO ·. SNP does not elicit a Ca2+ influx, and EGTA is not protective. In comparison to the N20.1 OL cell line (Boullerne et al., [1999] J. Neurochem. 72:1050–1060), mature OLs are (1) more sensitive to SNAP, (2) much more resistant to SNP, (3) sensitive to cyanide, but not iron, and (4) exhibit a Ca2+ influx and EGTA protection in response to NO generated by SNAP. J. Neurosci. Res. 63:124–135, 2001. © 2001 Wiley‐Liss, Inc.