Miracle-dz/UniFAR-FTUs huggingface dataset:
Bone Preservation in Hayonim Cave (Israel): a Macroscopic and Mineralogical Study

Abstract Understanding the cause of patchy bone distributions in archaeological sites requires that one distinguish bone decomposition in place from “empty” areas where bones were never present. Marked horizontal variations in bone abundance are found in the thick Mousterian layer (E) of Hayonim Cave, a large Paleolithic site in northern Israel. Infra-red analyses of minerals in the sediments identify zones of advanced diagenesis and decomposition alongside zones whose chemistry clearly favoured the preservation of bones and wood ash. These differences adhere closely to the distribution of recognizable bones in the deposits, indicating that spatial variation in bone abundance is essentially a product of differential preservation conditions. However, the few bones present in the bone-poor units are in surprisingly good condition. The higher degree of abrasion damage and more random orientations of these bones indicate that small amounts of recent material were introduced into older layers by small burrowing animals and perhaps localized trampling. The ratio of post-Mousterian to Mousterian artifacts in layer E, and the numeric contrasts in bone abundance among stratigraphic units, indicate that time-averaging from mechanical intrusion was quantitatively unimportant (2–5%) throughout this>2·4 m thick layer. Our findings support Karkanas et al . (2000) suggestion that bone and ash mineral diagenesis in caves follow step-wise rather than gradual transformations in geological time. Good preservation environments can be distinguished from poorer ones on the basis of mineral assemblages in sediments, and deposits that once contained bone and wood ash can be identified long after the visible traces of these materials have disappeared.
Skin prick test and specific serum IgE in the diagnostic evaluation of suspected cow's milk and hen's egg allergy in children: does one replace the other?

The measurement of specific serum immunoglobulin E (sIgE) and the skin prick test (SPT) are accepted tools in the diagnostic work‐up of suspected food allergy. Often only one of the methods is used to determine sensitization; however, it is still under debate whether these two methods can be used interchangeably.
Pedicle Subtraction Osteotomy in Elderly Patients With Degenerative Sagittal Imbalance

Study Design. Retrospective, radiographical analysis. Objective. To evaluate pedicle subtraction osteotomy (PSO) as a means of correcting severe degenerative sagittal imbalance in elderly patients. Summary of Background Data. PSO in patients with degenerative sagittal imbalance is likely to cause more complications than in patients with iatrogenic flatback deformity. Methods. This study analyzed 34 patients who underwent fusion to the sacrum, with a minimum 2-year follow-up. Age of the patients were in the range from 58 to 73 with the mean at 65.5 years. PSO was performed at one segment in all cases, consisting of L3 (n = 26), L4 (n = 4), L2 (n = 3), and L1 (n = 1). The average number of levels fused was 8.15. Ten patients had structural interbody fusion at the lumbosacral junction. Results. Applying PSO at one segment, the mean correction of the lordotic angle at the osteotomy site was 33.3°, of which the loss of correction (LOC) was 4.0° at the last visit. The correction of lumbar lordosis was 33.7° and the LOC was 8.5°. The sagittal C7 plumb was 215.9 mm before surgery, corrected to 35.1 mm after surgery, and changed to 95.9 mm by the last visit. The correction of the sagittal C7 plumb was 119.9 mm and the LOC was 60.9 mm. There was substantial LOC in lumbar lordosis and sagittal C7 plumb. In 10 patients with addition of posterior lumbar interbody fusion, the LOC of lumbar lordosis was 7.4°, which was less than 9° in those without it. Conclusion. PSO for the correction of degenerative sagittal imbalance in elderly patients resulted in correction of sagittal alignment with a significant LOC of lumbar lordosis and sagittal C7 plumb. The LOC of lumbar lordosis occurred at both the osteotomy and non-osteotomy site. The addition of anterior column support is helpful to maintain correction and reduce complications. Level of Evidence: N/A
Dopaminergic regulation of striatal acetylcholine release: importance of D1 and N-methyl-D-aspartate receptors.

The dopaminergic regulation of striatal cholinergic activity was studied using in vivo microdialysis to measure interstitial concentrations of acetylcholine (ACh) and choline in the striata of freely moving rats. The quaternary acetylcholinesterase inhibitor neostigmine (100 nM) was included in the perfusion solution to increase the recovery of ACh. d-Amphetamine (2 mg/kg, s.c.) and nomifensine (5 mg/kg, s.c.) increased the concentration of ACh in the striatal dialysate by 40 to 60%. Interstitial choline concentrations were reduced by both drugs. Administration of the selective D1 receptor antagonist SCH 23390 (0.3 mg/kg, s.c.) decreased the concentration of ACh in the striatal dialysate by 15 to 20%; in contrast, the selective D2 antagonist raclopride (1 mg/kg, s.c.) increased striatal ACh release by 50 to 60%. Raclopride also briefly increased the extracellular concentration of choline. Raclopride blocked the increase in locomotor activity produced by d-amphetamine, but did not further enhance ACh release. In contrast, SCH 23390 completely antagonized the increases in locomotion and striatal ACh release produced by d-amphetamine. These results indicate that d-amphetamine increases ACh release in the striatum via a D1 receptor mechanism. Consistent with this hypothesis, the selective D1 receptor agonist CY 208-243 (1 mg/kg, s.c.) increased striatal ACh release by approximately 60%. In contrast, local application of CY 208-243 (10 microM) and SCH 23390 (10 microM) failed to alter ACh concentrations in the striatal dialysate. Inclusion of the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 (10 microM) in the striatal perfusion solution significantly attenuated the increase in striatal ACh release produced by systemic CY 208-243. (ABSTRACT TRUNCATED AT 250 WORDS)
Neurotoxic Effects of 2,5-Hexanedione on Normal and Neurofilament-Deficient Quail

The neurotoxic effects of 2,5-hexanedione (2,5-HD) were investigated using neurofilament (NF)-deficient (Quv) Japanese quail in comparison with normal Japanese quail. Both Quv and normal Japanese quail were inoculated intraperitoneally with 350 mg/kg/day 2,5-HD for 6 consecutive wk. The results of 2,5-HD exposure differed substantially between the 2 strains of Japanese quail. The 2,5-HD-exposed normal quail showed leg paralysis about 4 wk after initiation of dosing. Some treated normal quail fell into dysstasia and died of nutritional disturbances. Histologically, 2,5-HD-treated normal quail had NF-rich axonal swellings and degeneration in the distal parts of the peripheral nerves, spinal cord, and cerebellar peduncles. In contrast, 2,5-HD-injected Quv quail showed tonic convulsion, ataxia gait, severe quivering, and excitation about 2-3 days after administration. Some treated Quv birds died immediately after systemic tonic convulsion, probably because of asphyxia. Although all treated Quv quail showed neurologic signs, there were no recognizable 2,5-HD-induced lesions in the nervous system. After about 4-6 wk of dosing, 2,5-HD induced distal axonopathy in normal quail and acute neurotoxicity in Quv quail.
Dark matter and dark energy: summary and future directions

This paper reviews the progress reported at the Discussion Meeting and advertises some possible future directions in our drive to understand dark matter and dark energy. Additionally, a first attempt is made to place in context the exciting new results from the Wilkinson Microwave Anisotropy Probe satellite, which were published shortly after this meeting. In the first part of this paper, pieces of observational evidence shown here that bear on the amounts of dark matter and dark energy are reviewed. Subsequently, particle candidates for dark matter are mentioned, and detection strategies are discussed. Finally, ideas are presented for calculating the amounts of dark matter and dark energy, and possibly relating them to laboratory data.
Registration of epidemiological studies: benefits and risks

In 1997, the Food and Drug Administration Modernization Act (FDAMA) provided for, among many other things, the establishment of a ‘‘data bank of information on clinical trials. ’’ The requirement for posting information was limited to trials of drugs for serious or life-threatening diseases. The National Library of Medicine established ClinicalTrials.gov in 2000 in response to this mandate, the primary purpose of which was to facilitate public access to investigational drugs. In 2005, the International Council of Medical Journal Editors decreed that the registration of a clinical trial would be a prerequisite for publication of the trial’s results in any of the represented journals. Although registration of clinical trials had been a cause célèbre for many years among meta-analysts concerned about publication bias, inertia prevailed until the eruption of controversies surrounding the recognition that unpublished studies of investigational drugs contained important information about drug effects that had been unavailable to health care providers and researchers. Although the motivation for trial registration stemmed from concerns about hidden information on important trial outcomes, another important feature of clinical trial registration is the ability to document the primary trial objectives. Prior to the advent of clinical trial registration, there was little to prevent investi-
Secreted tumor necrosis factor-α by human myeloid cells: a valuable parameter for evaluation of endotoxin contamination in vitro

Myeloid cells respond to external stimuli such as gram negative bacterial lipopolysaccharides (LPS) or endotoxin by producing a large array of intermediates and proteins, including the pro-inflammatory cytokines such as, tumor necrosis factor-α (TNF-α), free radicals, nitric oxide, and other intermediates. The aim of this research was to investigate the response of human myeloid cells to endotoxin, and correlate secreted TNF-α concentration with endotoxin exposure. For this purpose, human myeloid cell lines such as, U937, HL-60 (undifferentiated and differentiated) and the human peripheral blood Mononuclear (hpMN) and Polymorphonuclear (hpPMN) cells were treated by bacterial endotoxin in a dose and time dependent manner. Then the cells were isolated from supernatants. The nitro-blue tetrazolium (NBT) reduction potential of isolated cells was quantitatively assessed. The secreted TNF-α was assessed by the ELISA and TNF-α dependent L929 cells cytotoxicity methods. The hpPMN, hpMN, and differentiated U937 cells showed a higher ability to reduce NBT in response to endotoxin. The amount of produced TNF-α by hpPMN and hpMN cells were higher than that of other cells (Up to 300 pg/ml at 15 min and 6000 pg/ml at 24 hrs in response to 10 ng/ml of endotoxin, r = 0.974). The results of this study indicated that, human myeloid cells specially the hpPMN and hpMN cells provide a useful in vitro system for evaluating the endotoxin contamination in culture medium. In response to endotoxin, these cells synthesize and secrete TNF-α in a dose and time dependent manner.
Using Behavior Rating Scales forADHD Across Ethnic Groups

In this study we examined the normative and construct equivalence of the teacher IOWA Conners Rating Scale (IOWA) in a sample of 3,998 elementary school children (2,124 African American and 1,874 European American) ages 5 to 11 years in an urban school district. Risk odds ratios (% > 2 SD) were calculated by gender and ethnicity. An exploratory Principal Axis factor analysis was performed to determine the appropriateness of the 2-factor model. Structural equation modeling was used to estimate the degree of fit for the 2-factor model. Both African American boys and girls received significantly higher scores than their European American counterpoints.There was a 2.48 to 3.51 greater likelihood forAfrican American boys and a 3.60 to 5.27 greater likelihood of African American girls to be rated > 2 SD above the mean for inattention/overactivity, aggression, or IOWA Conners Rating Scale scores. A rater ethnicity by student ethnicity (European American vs. African American) interaction was also found. Confirmatory factor analysis indicated that the same 2-factor model was appropriate for the African American and European American groups. The results suggest that although there is construct equivalence across the African American and European American groups, there is still a question as to normative equivalence.
The p38/Reactivating Kinase Mitogen-activated Protein Kinase Cascade Mediates the Activation of the Transcription Factor Insulin Upstream Factor 1 and Insulin Gene Transcription by High Glucose in Pancreatic β-Cells*

Insulin upstream factor 1 (IUF1), a transcription factor present in pancreatic β-cells, binds to the sequence C(C/T)TAATG present at several sites within the human insulin promoter. Here we isolated and sequenced cDNA encoding human IUF1 and exploited it to identify the signal transduction pathway by which glucose triggers its activation. In human islets, or in the mouse β-cell line MIN6, high glucose induced the binding of IUF1 to DNA, an effect mimicked by serine/threonine phosphatase inhibitors, indicating that DNA binding was induced by a phosphorylation mechanism. The glucose-stimulated binding of IUF1 to DNA and IUF1-dependent gene transcription were both prevented by SB 203580, a specific inhibitor of stress-activated protein kinase 2 (SAPK2, also termed p38 mitogen-activated protein kinase, reactivating kinase, CSBP, and Mxi2) but not by several other protein kinase inhibitors. Consistent with this finding, high glucose activated mitogen-activated protein kinase-activated protein kinase 2 (MAPKAP kinase-2) (a downstream target of SAPK2) in MIN6 cells, an effect that was also blocked by SB 203580. Cellular stresses that trigger the activation of SAPK2 and MAPKAP kinase-2 (arsenite, heat shock) also stimulated IUF1 binding to DNA and IUF1-dependent gene transcription, and these effects were also prevented by SB 203580. IUF1 expressed in Escherichia coli was unable to bind to DNA, but binding was induced by incubation with MgATP, SAPK2, and a MIN6 cell extract, which resulted in the conversion of IUF1 to a slower migrating form. SAPK2 could not be replaced by p42 MAP kinase, MAPKAP kinase-2, or MAPKAP kinase-3. The glucose-stimulated activation of IUF1 DNA binding and MAPKAP kinase-2 (but not the arsenite-induced activation of these proteins) was prevented by wortmannin and LY 294002 at concentrations similar to those that inhibit phosphatidylinositide 3-kinase. Our results indicate that high glucose (a cellular stress) activates SAPK2 by a novel mechanism in which a wortmannin/LY 294002-sensitive component plays an essential role. SAPK2 then activates IUF1 indirectly by activating a novel IUF1-activating enzyme.
Down-regulation of dendritic spine and glutamic acid decarboxylase 67 expressions in the reelin haploinsufficient heterozygous reeler mouse

Heterozygous reeler mice (HRM) haploinsufficient for reelin express ≈50% of the brain reelin content of wild-type mice, but are phenotypically different from both wild-type mice and homozygous reeler mice. They exhibit, (i) a down-regulation of glutamic acid decarboxylase 67 (GAD67)-positive neurons in some but not every cortical layer of frontoparietal cortex (FPC), (ii) an increase of neuronal packing density and a decrease of cortical thickness because of neuropil hypoplasia, (iii) a decrease of dendritic spine expression density on basal and apical dendritic branches of motor FPC layer III pyramidal neurons, and (iv) a similar decrease in dendritic spines expressed on the basal dendrite branches of CA1 pyramidal neurons of the hippocampus. To establish whether the defect of GAD67 down-regulation observed in HRM is responsible for neuropil hypoplasia and decreased dendritic spine density, we studied heterozygous GAD67 knockout mice (HG67M). These mice exhibited a down-regulation of GAD67 mRNA expression in FPC (about 50%), but they expressed normal amounts of reelin and had no neuropil hypoplasia or down-regulation of dendritic spine expression. These findings, coupled with electron-microscopic observations that reelin colocalizes with integrin receptors on dendritic spines, suggest that reelin may be a factor in the dynamic expression of cortical dendritic spines perhaps by promoting integrin receptor clustering. These findings are interesting because the brain neurochemical and neuroanatomical phenotypic traits exhibited by the HRM are in several ways similar to those found in postmortem brains of psychotic patients.
In search of evidence: family practitioners' use of the Internet for clinical information.

PURPOSE The aim of the study was to determine the extent of use of the Internet for clinical information among family practitioners in New Zealand, their skills in accessing and evaluating this information, and the ways they dealt with patient use of information from the Internet. METHOD A random sample of members of the Royal New Zealand College of General Practitioners was surveyed to determine their use of the Internet as an information source and their access to MEDLINE. They were asked how they evaluated and applied the retrieved information and what they knew about their patients' use of the Internet. Structured interviews with twelve participants focused in more depth on issues such as the physicians' skills in using MEDLINE and in evaluating retrieved material, their searches for evidence-based information, their understanding of critical appraisal, their patients' use of the Internet, and the ways they handle this use. RESULTS More than 80% (294/363) of members in the sample completed and returned the questionnaire. Of these, 48.6% reported that they used the Internet to look for clinical information. Gender and age were more significant in determining use than practice type or location. Information was primarily sought on rare diseases, updates on common diseases, diagnosis, and information for patients. MEDLINE was the most frequently accessed source. Search skills were basic, and abstracts were commonly used if the full text of an item was not readily available. Most reported that up to 10% of patients bring information from the Internet to consultations. Both Internet users and non-Internet users encouraged patients to search the Web. Internet users were more likely to recommend specific sites. CONCLUSIONS Practitioners urgently need training in searching and evaluating information on the Internet and in identifying and applying evidence-based information. Portals to provide access to high-quality, evidence-based clinical and patient information are needed along with access to the full text of relevant items.
Effect of slope and footwear on running economy and kinematics

Lower energy cost of running (Cr) has been reported when wearing minimal (MS) vs traditional shoes (TS) on level terrain, but the effect of slope on this difference is unknown. The aim of this study was to compare Cr, physiological, and kinematic variables from running in MS and TS on different slope conditions. Fourteen men (23.4 ± 4.4 years; 177.5 ± 5.2 cm; 69.5 ± 5.3 kg) ran 14 5‐min trials in a randomized sequence at 10 km/h on a treadmill. Subjects ran once wearing MS and once wearing TS on seven slopes, from −8% to +8%. We found that Cr increased with slope gradient (P < 0.01) and was on average 1.3% lower in MS than TS (P < 0.01). However, slope did not influence the Cr difference between MS and TS. In MS, contact times were lower (P < 0.01), flight times (P = 0.01) and step frequencies (P = 0.02) were greater at most slope gradients, and plantar‐foot angles – and often ankle plantar‐flexion (P = 0.01) – were greater (P < 0.01). The 1.3% difference between footwear identified here most likely stemmed from the difference in shoe mass considering that the Cr difference was independent of slope gradient and that the between‐footwear kinematic alterations with slope provided limited explanations.
School functioning of children at risk for behavioral pathology.

URCAFS provides an opportunity to study the development of the child before the onset of psychological disorder. With this in mind, measures need to be developed to assess the child not only for descriptive purposes but also to look for signs which could be precursors or predictors of later disability. The present study will report (a) the development of a battery of assessment materials suitable for use in risk studies, and (b) a description of present functioning of a group of children at risk to behavioral disorder vis-a-vis comparisons with a low-risk peer group. In previous studies, Rolf (1972) found no differences between high-risk children and low-risk controls on teacher ratings; but on peer ratings, offspring of hospitalized parents were more frequently selected for externalizing negative roles than were controls. Weintraub, Neale, and Liebert (1975) and Neale and Weintraub (1975) found that a combined sample of offspring of schizophrenic and neurotically depressed parents scored more negatively than controls on a variety of teacher-rated behavioral dimensions, but only sons of neurotically depressed patients scored more negatively than controls. No differences between the offspring of these two diagnostic groups occurred under direct comparison, however. Because URCAFS children, by definition, are only at risk for a psychiatric disorder, they may not display clear signs of psychopathology during childhood. Garmezy (1974a, 1974b, 1974c), following White (1959), has suggested that competence and the mastery of basic life tasks be used as the primary concept underlying the assessment of children at risk. A cluster of competence variables can then be used to describe a child's current functioning and also to act as a differential predictor of later outcome. Competence has been defined in various ways, but we have defined
Mechanism of action and pharmacology of unfractionated heparin.

An updated statement by the American Heart Association (AHA) on the pharmacology and clinical use of heparin and low-molecular-weight heparin (LMWH) is published online at http://www.atvb. org and also appears in the June 19, 2001 issue of Circulation . The following is a summary of the AHA statement. We have not cited references; these can be accessed from the full text. Heparin is a sulfated polysaccharide with a molecular weight range of 3000 to 30 000 Da (mean, 15 000 Da). It produces its major anticoagulant effect by inactivating thrombin and activated factor X (factor Xa) through an antithrombin (AT)-dependent mechanism. Heparin binds to AT through a high-affinity pentasaccharide, which is present on about a third of heparin molecules. For inhibition of thrombin, heparin must bind to both the coagulation enzyme and AT, whereas binding to the enzyme is not required for inhibition of factor Xa. Molecules of heparin with fewer than 18 saccharides lack the chain length to bridge between thrombin and AT and therefore are unable to inhibit thrombin. In contrast, very small heparin fragments containing the pentasaccharide sequence inhibit factor Xa via AT. By inactivating thrombin, heparin not only prevents fibrin formation but also inhibits thrombin-induced activation of platelets and of factors V and VIII. The main limitation of heparin results from its propensity to bind to positively charged proteins and surfaces. Pharmacokinetic limitations are caused by AT-independent binding of heparin to plasma proteins, proteins released from platelets, and endothelial cells, resulting in a variable anticoagulant response and the phenomenon of heparin resistance. AT-independent binding to macrophages and endothelial cells also results in dose-dependent clearance. Other limitations include (1) …