Miracle-dz/UniFAR-FTUs huggingface dataset:
A phosphatidylinositol-3 kinase binds to platelet-derived growth factor receptors through a specific receptor sequence containing phosphotyrosine

Platelet-derived growth factor (PDGF) stimulates autophosphorylation of the PDGF receptor and association of the receptor with several cytoplasmic molecules, including phosphatidylinositol-3 kinase (PI3 kinase). In this study we examined the association of PI3 kinase with immunoprecipitated autophosphorylated PDGF receptor in vitro. The PI3 kinase from cell lysates bound to the wild-type receptor but not to a mutant receptor that had a deletion of the kinase insert region. A protein of an apparent size of 85 kDa bound to the receptor, consistent with previous observations that a protein of this size is associated with PI3 kinase activity. In addition, 110- and 74-kDa proteins bound to the phosphorylated receptor. Dephosphorylated receptors lost the ability to bind PI3 kinase activity as well as the 85-kDa protein. A 20-amino-acid peptide composed of a sequence in the kinase insert region that included one of the autophosphorylation sites of the receptor (tyrosine 719) as well as a nearby tyrosine (Y708) blocked the binding of PI3 kinase to the receptor, but only when the peptide was phosphorylated on tyrosine residues. A scrambled version of the peptide did not block PI3 kinase binding to the receptor even when it was phosphorylated on tyrosine. These tyrosine-phosphorylated peptides did not block binding of phospholipase C-gamma or GTPase-activating protein to the receptor. In separate experiments (receptor blots), soluble radiolabeled receptor bound specifically to an 85-kDa protein present in sodium dodecyl sulfate-polyacrylamide gel electrophoresis-fractionated 3T3 cell lysates that were transferred to nitrocellulose paper. The binding was blocked by the same tyrosine-phosphorylated peptides that prevented binding of PI3 kinase activity to immobilized receptors. These findings show that the PDGF receptor binds directly to an 85-kDa protein and to a PI3 kinase activity through specific sequences in the kinase insert region. The association of a 110-kDa protein with the receptor also involve these sequences, suggesting that this protein may be a subunit of the PI3 kinase. Phosphotyrosine is an essential structure required for the interactions of these proteins with the PDGF receptor.
Simultaneous production of interleukin 6, interferon‐β and colony‐stimulating activity by fibroblasts after viral and bacterial infection

Different viruses were compared with the double‐stranded RNA poly(rl)· poly(rC) and interleukin (IL) 1 for their IL 6‐inducing potential in several human and animal cell types. The laboratory viruses Sendai, Mengo and Newcastle disease virus were found to dose dependently stimulate IL 6 production in diploid fibroblasts. A similar effect was obtained with the human pathogens, measles and rubella virus. Concomitantly with IL 6, two other cytokine activities, i.e., interferon‐β and colony‐stimulating activity for granulocytes and monocytes, were induced. In addition, these three activities were also produced by fibroblasts in response to Escherichia coli, whereas lipopolysaccharide was only marginally active. The specificity of the induction phenomenon was confirmed by the lack of IL 6 induction with inactivated infectious agents and by the complete neutralization of produced IL 6 by specific antibodies. This study indicates that the coordinate production of hemopoietic growth factors and interferon, originating from cells that do not classically belong to the immune system, can influence the local and systemic reactions observed during host defence against various infectious agents.
Connections of the auditory forebrain in the pigeon (columba livia)

Ascending auditory efferents in birds terminate mainly within Field L2, a cytoarchitectonically distinct region of the caudomedial telencephalon. The organization of Field L2, and that of its flanking regions, L1 and L3, was investigated with 14C‐2‐deoxyglucose (14C‐2‐DG), cytochrome oxidase, and both retrograde and anterograde tracing techniques.
Individual neuropeptides regulate gut-associated lymphoid tissue integrity, intestinal immunoglobulin A levels, and respiratory antibacterial immunity.

BACKGROUND Total parenteral nutrition (TPN) leads to atrophy of the gut-associated lymphoid tissue (GALT) and a significant decrease in intestinal immunoglobulin A (IgA) levels, a major constituent of mucosal immunity. Bombesin (BBS) prevents TPN-induced GALT atrophy and maintains intestinal IgA levels. BBS, a neuropeptide analogous to gastrin-releasing peptide in humans, stimulates the release of other gut neuropeptides including cholecystokinin (CCK), gastrin, and neurotensin (NT). This study investigates the ability of CCK, gastrin, or NT to individually prevent TPN-induced GALT atrophy and preserve respiratory immunity. METHODS Experiment 1: Male mice were randomly assigned to receive chow, TPN, TPN plus CCK, TPN plus gastrin, or TPN plus NT. After 5 days of feeding, Peyer's patches (PP) from the proximal and distal small bowel were harvested and analyzed for cell yields. PP cells were also analyzed for GALT cell type. Small bowel IgA levels were measured by enzyme-linked immunosorbent assay (ELISA). Experiment 2: Mice were randomly assigned to receive either liposomes containing Pseudomonas antigen or liposomes without antigen. After 10 days, mice were randomly assigned to the same five treatment groups, fed for 5 days, and then given intratracheal Pseudomonas. Mortality was assessed after 48 hours. RESULTS Experiment 1: GALT cell reductions due to IV-TPN were greater in the distal than proximal small bowel. All three neuropeptides prevented most TPN-induced GALT atrophy due mainly to the maintenance of the B-cell and T-cell populations in the PP of the distal bowel. Intestinal IgA levels were significantly higher in the animals treated with neuropeptides than animals treated with TPN only; however, these IgA levels were not maintained at levels observed in chow-fed animals. Experiment 2: Immunization resulted in significantly lower mortality in animals fed chow, TPN plus CCK, and TPN plus gastrin. TPN alone and TPN plus NT resulted in loss of immunity and mortality rate at comparable levels to unimmunized animals. CONCLUSIONS Supplementation of IV-TPN with CCK, gastrin, and NT prevents GALT atrophy, primarily in the distal bowel. Intestinal IgA levels improve but not to normal levels. CCK and gastrin reversed IV-TPN-induced effects on antibacterial pneumonia in immunized animals while NT did not.
Structural parameters optimization for the inductors used in the inductive pulse power supply

The structural parameters directly affect the energy density and the total resistance of the inductors used in the inductive pulse power supply (IPPS). In this paper, we expound the relationship between the structural parameters and electrical performances of the inductors used in IPPS, and introduce the implementation of the inductors for the experiment in Slow TRansfer of Energy Through Capacitive Hybrid (STRETCH) meat grinder circuit using Air-core Flat Spirals of Strip Coil (AFSSC). Then, we work out a program which can obtain the optimal structural parameters of the inductors with the highest energy density under the condition of providing the charging and discharging current as well as the inductance in the primary and the secondary side. The correctness of the program is verified by the measured values of the real inductors. At the end, on the condition of constant current density, we put forward a rule that along with the increase of system energy, the energy density became higher and the resistance of the inductors became lower.
A randomized trial of the effects of reducing television viewing and computer use on body mass index in young children.

OBJECTIVE To assess the effects of reducing television viewing and computer use on children's body mass index (BMI) as a risk factor for the development of overweight in young children. DESIGN Randomized controlled clinical trial. SETTING University children's hospital. PARTICIPANTS Seventy children aged 4 to 7 years whose BMI was at or above the 75th BMI percentile for age and sex. INTERVENTIONS Children were randomized to an intervention to reduce their television viewing and computer use by 50% vs a monitoring control group that did not reduce television viewing or computer use. MAIN OUTCOME MEASURES Age- and sex-standardized BMI (zBMI), television viewing, energy intake, and physical activity were monitored every 6 months during 2 years. RESULTS Children randomized to the intervention group showed greater reductions in targeted sedentary behavior (P < .001), zBMI (P < .05), and energy intake (P < .05) compared with the monitoring control group. Socioeconomic status moderated zBMI change (P = .01), with the experimental intervention working better among families of low socioeconomic status. Changes in targeted sedentary behavior mediated changes in zBMI (P < .05). The change in television viewing was related to the change in energy intake (P < .001) but not to the change in physical activity (P =.37). CONCLUSIONS Reducing television viewing and computer use may have an important role in preventing obesity and in lowering BMI in young children, and these changes may be related more to changes in energy intake than to changes in physical activity.
Magnetic resonance imaging of bone marrow in sickle cell disease: clinical, hematologic, and pathologic correlations.

A longitudinal, prospective, controlled evaluation of magnetic resonance images (MRI) of long bones in sickle cell patients was undertaken simultaneously with assessment of clinical status and hematologic parameters, including dense erythrocytes. MRI of bone marrow in sickle cell patients during steady states appeared patchy and were markedly different from those in matched controls (P approximately 0). Patients with severe patchiness were older than those with mild or moderate patchiness (P less than .03). Sixty-nine MRI were performed during 28 painful episodes occurring in 14 subjects with sickle cell disease (SCD). Increased signals on intermediate and T2-weighted images were detected in 35.7% of painful episodes. These abnormalities were distinct and not observed to occur spontaneously during the steady-state examinations (P approximately 0). Bone marrow infarcts were confirmed by biopsy in two instances and autopsy in one instance. Dense red cells decreased by 40.81% of baseline during pain crises (P = .00005), more remarkably in those who had pain in the lower extremities (P = .0145). Patients with change in MRI during pain crises had a greater percentage change in the dense cells than those without the change in MRI (69.7% v 31.3%, P = .0120).
Tumour‐cell apoptosis after cisplat in treatment is not telomere dependent

Cisplatin is a major chemotherapeutic agent, especially for the treatment of neuroblastoma. Telomeres with their sequence (TTAGGG)n are probable targets for cisplatin intrastrand cross‐linking, but the role of telomeres in mediating cisplatin cytotoxicity is not clear. After exposure to cisplatin as single dose or continuous treatment, we found no loss of telomeres in either SHSY5Y neuroblastoma cells (telomere length, ∼4 kbp), HeLa 229 cells (telomere length, 20 kbp) or in the acute lymphoblastic T cell line 1301 (telomere length, ∼80 kbp). There was no induction of telomeric single strand breaks, telomeric overhangs were not degraded and telomerase activity was down‐regulated only after massive onset of apoptosis. In contrast, cisplatin induced a delayed formation of DNA strand breaks and induced DNA damage foci containing γ‐H2A.X at nontelomeric sites. Interstitial DNA damage appears to be more important than telomere loss or telomeric damage as inducer of the signal pathway towards apoptosis and/or growth arrest in cisplatin‐treated tumour cells. © 2005 Wiley‐Liss, Inc.
Ap53genetic polymorphism as a modulator of hepatocellular carcinoma risk in relation to chronic liver disease, familial tendency, and cigarette smoking in hepatitis B carriers

This study evaluated whether the codon 72 p53 polymorphism was related to hepatocellular carcinoma (HCC). Genotypes of p53were determined in 80 incident cases of HCC and 328 controls nested in a cohort study of 4,841 male chronic hepatitis B carriers. No overall increase in HCC risk with thePro variant allele of thep53 polymorphism was apparent. However, there were synergistic effects on HCC development for the Pro allele with chronic liver disease and family history of HCC in first‐degree relatives. Compared with subjects without the Pro allele and chronic liver disease, the increase in HCC risk associated with chronic liver disease among those without the Pro allele was only threefold. Subjects with both chronic liver disease and the Pro allele were at an increased risk of 7.60 (95% CI = 2.28‐25.31). When subjects without family history of HCC and the Pro allele were considered as the reference group, there was no apparent increased risk of HCC for those without thePro allele who had family history of HCC. Among those with both factors, there was a significantly increased risk of 3.29 (95% CI = 1.10‐9.85). Both cigarette smoking and glutathioneS‐transferase M1 genotype modified the risk of HCC associated with the p53polymorphism. Significantly increased risk associated with the p53genotype was observed only among smokers who were glutathione S‐transferase–null (Pro/Pro vs. Arg/Arg: odds ratio = 6.46; 95% CI = 1.55‐26.94). The p53polymorphism also interacted with the cytochrome P4501A1and carotenoid levels in smoking‐related hepatocarcinogenesis.
Hexaaquanickel(II) bis[2-carboxylato-2-(isothiouronium-S-ylmethyl)propane-1,3-diyl phosphate] hexahydrate.

In the title complex, [Ni(H(2)O)(6)](C(6)H(10)N(2)O(6)PS)(2) x 6 H(2)O, the asymmetric unit consists of one-half of an Ni atom (which lies on an inversion centre) with three coordinated water molecules, one complete 2-carboxylato-2-(isothiouronium-S-ylmethyl)propane-1,3-diyl phosphate anion and three noncoordinated water molecules. The hexaaquanickel(II) cations have distorted octahedral coordination and are connected via water chains to form two-dimensional supramolecular networks parallel to the ab plane. The phosphate ester anion is linked via N-H.O and O-H.O hydrogen bonds, thus creating various ring, dimer and chain hydrogen-bonding patterns, and building up a second two-dimensional supramolecular network parallel to the ab plane. The crystal structure is further stabilized by an intra- and interlayer hydrogen-bond network. This work illustrates that a carboxylate with a caged phosphate ester can open its ring in the presence of dichloridotetrakis(thiourea)nickel, and the resulting polyfunctional anion can be used for constructing a complex hydrogen-bonding scheme.
Presidential address: Experimenting with the scientific past†

Abstract When it comes to knowledge about the scientific pasts that might have been – the so-called ‘counterfactual’ history of science – historians can either debate its possibility or get on with the job. Taking the latter course means re-engaging with some of the most general questions about science. It can also lead to fresh insights into why particular episodes unfolded as they did and not otherwise. Drawing on recent research into the controversy over Mendelism in the early twentieth century, this address reports and reflects on a novel teaching experiment conducted in order to find out what biology and its students might be like now had the controversy gone differently. The results suggest a number of new options: for the collection of evidence about the counterfactual scientific past, for the development of collaborations between historians of science and science educators, for the cultivation of more productive relationships between scientists and their forebears, and for heightened self-awareness about the curiously counterfactual business of being historical.
Life events and severe anorexia nervosa in adolescence

The purpose of the study was to study the influence of life events on adolescent patients suffering from anorexia nervosa. Twenty one hospitalized adolescent inpatients with severe anorexia nervosa were compared with 79 adolescent nonanorectic psychiatric inpatients and 40 healthy adolescents for stressful life events throughout their lives. The nonanorectic patients suffered from schizophrenia, affective disorders, anxiety disorders, borderline personality disorder or conduct disorder. The assessment of the contribution of life events to the development of anorexia and the control mental disorders was based on semistructured interviewing of the patients, their parents and the patients' therapists. The instrument used was that developed by Pfeffer. The anorectic patients showed significantly higher negative life event scores than healthy controls in all the areas of life events examined. In addition, they showed significantly more negative life events concerning parents than patients in the other psychiatric diagnostic categories. These findings have relevance for the growing literature on the association between eating disorders and certain forms of child abuse.
Kinetics of HbA1c, Glycated Albumin, and Fructosamine and Analysis of Their Weight Functions Against Preceding Plasma Glucose Level

OBJECTIVE To examine the kinetics of HbA1c, glycated albumin (GA), and fructosamine (FA) levels in response to plasma glucose change and their relationship with the preceding plasma glucose level. RESEARCH DESIGN AND METHODS The time courses of HbA1c, GA, and FA after acute glycemic normalization were observed in nine patients with newly diagnosed non-insulin-dependent diabetes mellitus and compared with theoretical ones. Their weight functions against preceding plasma glucose level were analyzed assuming a stepwise plasma glucose change and compared with the theoretical prediction. RESULTS The fasting plasma glucose level was acutely normalized after admission with a half-time of 6.3 ± 2.4 days (mean ± SD). The HbA1c level decreased linearly during the initial 2 months with a half-time of 34.6 ± 10.1 days, followed by a gradual decrease thereafter. GA and FA levels decreased very rapidly during the initial 2–3 weeks with half-times of 17.1 ± 2.8 and 12.2 ± 4.8 days, respectively, followed by a gradual decrease thereafter. The time courses of HbA1c, GA, and FA agreed well with theoretically estimated decay curves. Experimental values of weight functions against the preceding plasma glucose level agreed well with the theoretical prediction. The weight functions for glycated proteins had maximum values on the days just before the measurement of glycated proteins and gradually decreased with an increasing time interval. The lengths of the periods over which the weight functions for HbA1c, GA, and FA extend back were estimated to be roughly 100, 40, and 30 days, respectively. CONCLUSIONS The levels of HbA1c, GA, and FA do not reflect the simple mean but reflect the weighted mean of the preceding plasma glucose level over a considerably longer period than was previously speculated.
Molecular cloning of silkworm paralytic peptide and its developmental regulation.

The silkworm paralytic peptide (PP) is a member of the ENF peptide family that exerts multiple biological activities involved in defense reaction and growth regulation. We isolated its cDNA and examined mRNA expression profiles. cDNA encoded 131 amino acids from which the 23-residue PP sequence was found at the C-terminal portion. Immunoblot analysis and paralytic activity assay indicated that inactive pro-protein in larval hemolymph was processed into active peptide immediately after bleeding. In the last larval instar, 0.6-kb PP mRNA was expressed in various tissues, of which the fat body was predominant. Its expression in the fat body decreased during the feeding period and then increased during metamorphic process. Juvenile hormone and 20-hydroxyecdysone upregulated its expression. At the embryonic stage, 1.5-kb mRNA, in addition to 0.6-kb mRNA, was expressed from 1 day after oviposition to hatching. PP was thus expressed stage-specifically under hormonal control.
Seven‐site versus three‐site method of body composition using BodyMetrix ultrasound compared to dual‐energy X‐ray absorptiometry

Obesity is a steadily growing epidemic affecting all segments of the population including college‐aged students. The weight gain that is evidenced amid the transitional stage of college years increases the risks associated with cardiovascular and metabolic diseases. The BodyMetrix® BX‐2000 (ULTRA) using a seven‐site method has been evaluated against dual‐energy X‐ray absorptiometry (DXA) for estimation of body composition, which has yielded conflicting results. To date, no studies have compared the three‐site method Jackson and Pollock three‐site method to DXA.
mGluR5 antagonism increases autophagy and prevents disease progression in the zQ175 mouse model of Huntington’s disease

Inhibiting the glutamate receptor mGluR5 may prevent the progression of neuronal loss and motor impairment in patients with Huntington’s disease. A treatment for Huntington’s disease? There are currently no therapies that stop or reverse Huntington’s disease (HD), a progressive neurodegenerative disease caused by an expansion in the huntingtin protein that promotes its toxic accumulation in the central nervous system. Impaired autophagy, the process of breaking down and removing cellular debris and dysfunctional proteins, is implicated in HD. Blocking the kinase mTOR therapeutically can activate autophagy, but these drugs have serious side effects and poor penetrance into the brain. Abd-Elrahman et al. found that inhibiting the neuronal cell-surface glutamate receptor mGluR5 with the drug CTEP stimulated autophagy of huntingtin aggregates and improved motor and cognitive performance in HD model mice, without any apparent side effects. Given that CTEP analog is already in clinical trials for other neuronal-associated disorders, these findings suggest that the trials ought to be expanded to include HD patients. Huntington’s disease (HD) is a neurodegenerative disease caused by an expansion in the huntingtin protein (also called Htt) that induces neuronal cell death with age. We found that the treatment of 12-month-old symptomatic heterozygous and homozygous zQ175 huntingtin knockin mice for 12 weeks with CTEP, a negative allosteric modulator of metabotropic glutamate receptor 5 (mGluR5), reduced the size and number of huntingtin aggregates, attenuated caspase-3 activity, and reduced both neuronal apoptosis and neuronal loss in brain tissue. Both motor and cognitive impairments were improved in CTEP-treated zQ175 mice. The reduction in huntingtin protein aggregate burden by CTEP correlated with the activation of an autophagy pathway mediated by the kinase GSK3β, the transcription factor ZBTB16, and the autophagy factor ATG14. Inhibition of mGluR5 with CTEP also reduced the inhibitory phosphorylation of the autophagosome biogenesis–related kinase ULK1, increased the phosphorylation of the autophagy factor ATG13, and increased the abundance of the autophagy-related protein Beclin1 in homozygous zQ175 mice. The findings suggest that mGluR5 antagonism may activate autophagy through convergent mechanisms to promote the clearance of mutant huntingtin aggregates and might be therapeutic in HD patients.