Türkçeden garp dillerine tercümeler

Taha Toros Arşivi, Dosya Adı: Namık Kemalİstanbul Kalkınma Ajansı (TR10/14/YEN/0033) İstanbul Development Agency (TR10/14/YEN/0033

Effect of Behavioral Precaution on Braking Operation of Elderly Drivers under Cognitive Workloads

The number of accidents by elderly drivers caused by the erroneous tread of a brake pedal or accelerator pedal has increased. A recent study reported that the number of accidents could be reduced by preparing for braking mistakes due to driving behavior by using a simulator. However, related studies have pointed out that driving behavior in simulators does not always reflect driving behavior in the real world. This paper focuses on the posture of the left foot as a behavioral precaution and provides insights into braking mistakes by comparing behavioral precautions taken on simulators and on public roads. In the experimental results, cognitive and action errors increased with age, but elderly drivers are less likely to have an accident when they are exposed to the risk of collision in situations with a mental workload by making space for the right foot to step on the brake pedal. Elderly drivers with coping skills had their left foot perpendicular to the ground and their body was unstable. This result was different from the driving behavior in the simulator, but it was not possible to identify that this difference was the cause of the collision accidents. Coping skills were predicted with 70% accuracy from the left foot posture of an elderly driver near the intersection. We expanded the system’s range of use and enhanced its usefulness by predicting coping skills derived from natural driving behavior in the real world. The contributions of this study are as follows. We clarify the effect of behavioral precautions on the braking operation of elderly drivers when under a cognitive workload. We provide new insights into the use of behavioral precautions in older drivers’ braking operations in the real world. We predicted coping skills from natural driving behavior near intersections in the real world

Impact of intrapartum oxytocin administration on neonatal sucking behavior and breastfeeding

Abstract This study aimed to examine the effect of intrapartum oxytocin administration on neonatal sucking behavior and breastfeeding. A total of 64 pairs (29 in the group treated with intrapartum oxytocin and 35 in the control group) of normal infants within 24–48 h of birth and their mothers were recruited. Sucking ability was evaluated by measuring Non-Nutritive Sucking (NNS) for 5 min. Data on the rate of exclusive breastfeeding at 1 month postpartum were collected. In the adjusted multiple regression models, intrapartum oxytocin exposure was significantly associated with fewer total NNS bursts (95% confidence interval (CI), −7.02 to −0.22), longer pause times (95% CI, 1.33 to 10.21), and greater pause-time variability (95% CI, 3.63 to 63.92). Effects estimated using structural equation modeling revealed that intrapartum oxytocin exposure had a significant negative and direct effect on the practice of exclusive breastfeeding 1 month postpartum (β = −0.238, p = 0.047). However, no NNS-mediated indirect effects were observed. This report demonstrates that infants born to mothers who receive intrapartum oxytocin may have impaired sucking ability for at least the first 48 h after birth, and breastfeeding support should be provided

Persistence of Viremia and Production of Neutralizing Antibodies Differentially Regulated by Polymorphic APOBEC3 and BAFF-R Loci in Friend Virus-Infected Mice▿

Several host genes control retroviral replication and pathogenesis through the regulation of immune responses to viral antigens. The Rfv3 gene influences the persistence of viremia and production of virus-neutralizing antibodies in mice infected with Friend mouse retrovirus complex (FV). This locus has been mapped within a narrow segment of mouse chromosome 15 harboring the APOBEC3 and BAFF-R loci, both of which show functional polymorphisms among different strains of mice. The exon 5-lacking product of the APOBEC3 allele expressed in FV-resistant C57BL/6 (B6) mice directly restricts viral replication, and mice lacking the B6-derived APOBEC3 exhibit exaggerated pathology and reduced production of neutralizing antibodies. However, the mechanisms by which the polymorphisms at the APOBEC3 locus affect the production of neutralizing antibodies remain unclear. Here we show that the APOBEC3 genotypes do not directly affect the B-cell repertoire, and mice lacking B6-derived APOBEC3 still produce FV-neutralizing antibodies in the presence of primed T helper cells. Instead, higher viral loads at a very early stage of FV infection caused by either a lack of the B6-derived APOBEC3 or a lack of the wild-type BAFF-R resulted in slower production of neutralizing antibodies. Indeed, B cells were hyperactivated soon after infection in the APOBEC3- or BAFF-R-deficient mice. In contrast to mice deficient in the B6-derived APOBEC3, which cleared viremia by 4 weeks after FV infection, mice lacking the functional BAFF-R allele exhibited sustained viremia, indicating that the polymorphisms at the BAFF-R locus may better explain the Rfv3-defining phenotype of persistent viremia

Electron-Deficient Pt₂M₂Pt₂ Hexanuclear Metal Strings (M = Pt, Pd) Supported by Triphosphine Ligands

Electron-deficient Pt₂M₂Pt₂ hexanuclear clusters, [Pt₄M₂(μ-dpmp)₄(XylNC)₂]­(PF₆)₄ (M = Pt (<b>7</b>), Pd (<b>8</b>); dpmp = bis­((diphenylphosphino)­methyl)­phenylphosphine), were synthesized by oxidation of hydride-bridged hexanuclear clusters [Pt₄M₂(μ-H)­(μ-dpmp)₄(XylNC)₂]­(PF₆)₃ (M = Pt (<b>2</b>), Pd (<b>3</b>)) and were revealed to involve a linearly ordered Pt₂M₂Pt₂ array joined by delocalized bonding interactions with 84 cluster valence electrons, which are discussed on the basis of DFT calculations. The central M–M distances of <b>7</b> and <b>8</b> are significantly reduced upon the apparent loss of a hydride unit from the M–H–M central part of <b>2</b> and <b>3</b>, indicating that the bonding electrons in the adjacent M–Pt bonds migrate into the central M–M bond to result in a dynamic structural change during two-electron oxidation of the hexanuclear metal strings. A similar Pt₆ complex terminated by two iodide anions, [Pt₆I₂(μ-dpmp)₄]­(PF₆)₂ (<b>9</b>), was synthesized from [Pt₆(μ-H)­I₂(μ-dpmp)₄]­(PF₆) (<b>5</b>) by treatment with [Cp₂Fe]­[PF₆]. Complexes <b>7</b> and <b>8</b> were readily reacted with the neutral two-electron donors XylNC, CO, and phosphines to afford the trinuclear complexes [Pt₂M­(μ-dpmp)₂(XylNC)­L]­(PF₆)₂ (M = Pt, L = XylNC (<b>1a</b>), CO (<b>10</b>), PPh₃ (<b>11</b>); M = Pd, L = XylNC (<b>1b</b>)) through cleavage of the electron-deficient central M–M bond. When complex <b>7</b> was reacted with the diphosphines (<b>PP</b>) <i>trans</i>-Ph₂PCHCHPPh₂ (dppen) and Ph₂P­(CH₂)₂PPh₂ (dppe), the diphosphine was inserted into the central M–M bond to afford [(XylNC)­Pt₃(μ-dpmp)₂(<b>PP</b>)­Pt₃(μ-dpmp)₂(XylNC)]­(PF₆)₄ (<b>12</b>), which was transformed by treatment with another 1 equiv of diphosphine into the asymmetric trinuclear complexes [Pt₃(μ-dpmp)₂(XylNC)­(<b>PP</b>)]­(PF₆)₂ (<b>13</b>). A further ligand exchange reaction of <b>13a</b> (<b>PP</b> = <i>trans</i>-dppen) provided the diphosphine-terminated symmetrical Pt₃ complex [Pt₃(μ-dpmp)₂(L)₂]­(PF₆)₂ (L = <i>trans</i>-dppen (<b>14a</b>)). Complexes <b>7</b> and <b>8</b> were also reacted with [AuCl­(PPh₃)] to yield the Pt₂MAu heterotetranuclear complexes [Pt₂MAuCl­(μ-dpmp)₂(PPh₃)­(XylNC)]­(PF₆)₂ (M = Pt (<b>15</b>), Pd (<b>16</b>)), in which the Pt₂M trinuclear fragment is inserted into the Au–Cl bond in a 1,1-fashion on the central M atoms of the Pt₂M₂Pt₂ string

Characteristics of Patients in the Validation Set.

<p>Characteristics of Patients in the Validation Set.</p

Prediction of Kidney Histopathology.

<p>Subjects with a molecular score > Threshold I or > Threshold II were considered to be ≥ 3 or ≥ 4, respectively.</p><p>*Histopathology grades were consistent with the predicted value using Threshold I.</p><p>^†Histopathology grades were consistent with the predicted value using Threshold II.</p><p>Prediction of Kidney Histopathology.</p

The Transcriptional Profile Related to Chronic Kidney Disease (CKD).

<p>(<b>A</b>) Distribution of differences in gene expression between control kidney RNA (Control) and RNA extracted from 48 CKD biopsies. Microarray analysis was performed and genes down-regulated (z-score < -2.0, green) or up-regulated (z-score > 2.0, blue) in CKD are indicated. (<b>B</b>) Biological functions of the genes showing differential expression in CKD samples were classified according to their Gene Ontology and P values were calculated with MetaCore software. (<b>C</b>) Relationship between P values from Kruskal-Wallis test on tubulointerstitial fibrosis and tubular cell damage. Each symbol represents one gene. Gray or black circles indicate genes with any P values < 0.05; open circles represent genes with both P values > 0.05. HAVCR1, hepatitis A virus cellular receptor 1; LCN2, lipocalin 2; SOX9, SRY-box 9; WFDC2, WAP four-disulfide core domain 2; NKX6-2, NK6 homeobox 2.</p

Analysis of the Molecular Score Performance.

<p>(<b>A</b>) Relative signal intensity heatmaps for hepatitis A virus cellular receptor 1 (HAVCR1), lipocalin 2 (LCN2), SRY-box 9 (SOX9), WAP four-disulfide core domain 2 (WFDC2), and NK6 homeobox 2 (NKX6-2) in relation to renal histopathology. (<b>B</b>) The distribution of molecular score based on histological grades. (<b>C</b>) The area under the receiver operating characteristics curve (AUC) for the molecular score of each biopsy, plotted against the grade of tubulointerstitial fibrosis and tubular cell damage.</p