Estimating infant upper extremities motion with an RGB-D camera and markerless deep neural network tracking: A validation study.

Quantitative biomarkers of infant motion may be predictive of the development of movement disorders. This study presents and validates a low cost, markerless motion tracking method for the estimation of upper body kinematics of infants from which proper biomarkers may be extracted. The method requires a single RGB-D camera, a 2D motion tracking software publicly available (DeepLabCut) and an algorithm generating 3D point coordinates from the 2D tracked points, dealing with missing data, originating from various sources, for estimating joint kinematics. The proposed method is validated using known point kinematics obtained from a doll, with size and shape of an infant, lying on a turntable rotating at 33⅓ rpm. Two camera image plane orientations are tested: parallel to the turntable motion plane and forming a 45° angle with respect to the motion plane. The latter enhances the occurrence of body parts occlusions during motion as expected in live infant motion recordings. The length of upper body segments, elbow and shoulder joint angles and the linear point velocity determined with the proposed method are evaluated against reference values obtained from the known motion of the turntable. The relevant Mean Absolute Errors (MAE) found indicate the margin of error to expect when processing live infant motion. The proposed method may be improved if enhanced hardware and tracking software are employed, therefore reducing the above-mentioned margin of error. Clinical Relevance - The validation of the proposed method carried out in this study allows clinicians to select proper quantitative biomarkers obtained from infants upper body motion that may be useful for predicting movement disorders.

Origin of the Resistive Anisotropy in the Electronic Nematic Phase of BaFe(2)As(2) Revealed by Optical Spectroscopy.

We perform, as a function of uniaxial stress, an optical-reflectivity investigation of the representative "parent" ferropnictide BaFe(2)As(2) in a broad spectral range, across the tetragonal-to-orthorhombic phase transition and the onset of the long-range antiferromagnetic (AFM) order. The infrared response reveals that the dc transport anisotropy in the orthorhombic AFM state is determined by the interplay between the Drude spectral weight and the scattering rate, but that the dominant effect is clearly associated with the metallic spectral weight. In the paramagnetic tetragonal phase, though, the dc resistivity anisotropy of strained samples is almost exclusively due to stress-induced changes in the Drude weight rather than in the scattering rate, definitively establishing the anisotropy of the Fermi surface parameters as the primary effect driving the dc transport properties in the electronic nematic state.

Susceptibility anisotropy in an iron arsenide superconductor revealed by x-ray diffraction in pulsed magnetic fields.

In addition to unconventional high-T(c) superconductivity, the iron arsenides exhibit strong magnetoelastic coupling and a notable electronic anisotropy within the a-b plane. We relate these properties by studying underdoped Ba(Fe(1-x)Co(x))2As2 by x-ray diffraction in pulsed magnetic fields up to 27.5 T. We exploit magnetic detwinning effects to demonstrate anisotropy in the in-plane susceptibility, which develops at the structural phase transition despite the absence of magnetic order. The degree of detwinning increases smoothly with decreasing temperature, and a single-domain condition is realized over a range of field and temperature. At low temperatures we observe an activated behavior, with a large hysteretic remnant effect. Detwinning was not observed within the superconducting phase for accessible magnetic fields.

Massive Dirac fermion on the surface of a magnetically doped topological insulator.

In addition to a bulk energy gap, topological insulators accommodate a conducting, linearly dispersed Dirac surface state. This state is predicted to become massive if time reversal symmetry is broken, and to become insulating if the Fermi energy is positioned inside both the surface and bulk gaps. We introduced magnetic dopants into the three-dimensional topological insulator dibismuth triselenide (Bi2Se3) to break the time reversal symmetry and further position the Fermi energy inside the gaps by simultaneous magnetic and charge doping. The resulting insulating massive Dirac fermion state, which we observed by angle-resolved photoemission, paves the way for studying a range of topological phenomena relevant to both condensed matter and particle physics.

Photodissociation of dibromoethanes at 248 nm: an ignored channel of Br2 elimination.

Br(2) molecular elimination is probed in the photodissociation of 1,1- and 1,2-C(2)H(4)Br(2) isomeric forms at 248 nm by using cavity ring-down absorption spectroscopy. Their photodissociation processes differ markedly from each other. The quantum yield of the Br(2) fragment in 1,2-dibromoethane is 0.36+/-0.18, in contrast to a value of 0.05+/-0.03 in 1,1-dibromoethane. The vibrational population ratios of Br(2)(v=1)/Br(2)(v=0) are 0.8+/-0.1 and 0.5+/-0.2 for 1,2- and 1,1-dibromoethanes, respectively. The Br(2) yield densities are found to increase by a factor of 35% and 190% for 1,2- and 1,1-dibromoethanes within the same temperature increment. In the ab initio potential energy calculations, the transition state (TS) along the adiabatic ground state surface may correlate to the Br(2) products. The TS energy for 1,2-dibromoethane is well below the excitation energy at 483 kJ/mol, whereas that for 1,1-dibromoethane is slightly above. Such a small TS energy barrier impedes the photodissociation of the ground state 1,1-dibromoethane such that the production yield of Br(2) may become relatively low, but rise rapidly with the temperature. The TS structure shows a larger bond distance of Br-Br in 1,2-dibromoethane than that in 1,1-dibromoethane. That explains why the former isomer may result in hotter vibrational population of the Br(2) fragments.

Formation of interstellar 2,4-pentadiynylidyne, HCCCCC(X 2Pi), via the neutral-neutral reaction of ground state carbon atom, C(3P), with diacetylene, HCCCCH(X 1Sigma(g)+).

The interstellar reaction of ground-state carbon atom with the simplest polyyne, diacetylene (HCCCCH), is investigated theoretically to explore probable routes to form hydrogen-deficient carbon clusters at ultralow temperature in cold molecular clouds. The isomerization and dissociation channels for each of the three collision complexes are characterized by utilizing the unrestricted B3LYP/6-311G(d,p) level of theory and the CCSD(T)/cc-pVTZ calculations. With facilitation of RRKM and variational RRKM rate constants at collision energies of 0-10 kcalmol, the most probable paths, thus reaction mechanism, are determined. Subsequently, the corresponding rate equations are solved that the evolutions of concentrations of collision complexes, intermediates, and products versus time are obtained. As a result, the final products and yields are identified. This study predicts that three collision complexes, c1, c2, and c3, would produce a single final product, 2,4-pentadiynylidyne, HCCCCC(X (2)Pi), C(5)H (p1)+H, via the most stable intermediate, carbon chain HC(5)H (i4). Our investigation indicates the title reaction is efficient to form astronomically observed 2,4-pentadiynylidyne in cold molecular clouds, where a typical translational temperature is 10 K, via a single bimolecular gas phase reaction.

Genotoxicity of low dose N-nitroso propoxur to human gastric cells.

Propoxur is among the most popular insect control agents in subtropical countries such as Taiwan. As a member of the N-methylcarbamate insecticide group, propoxur is notorious for its potential for conversion into highly genotoxic N-nitroso derivatives. Due to the fact that the stomach has been identified as the major target for N-nitroso N-methylcarbamates, this investigation used a human gastric cell line, SC-M1, in order to obtain results pertinent to the authentic adverse effects of this compound on human health. This report reveals that at dose levels inhibiting < or = 10% cell growth, a 2-h pulsed treatment of N-nitroso propoxur induced significant amounts of DNA damage. Most of the damaged DNA was repaired within 24 h after treatment removal, such that an outcome with a significant induction of chromosomal aberrations was not observed. Gene mutations and anchorage independence, on the other hand, were significantly induced by this same treatment. In conclusion, exposure to low doses of N-nitroso propoxur is not cytotoxic nor clastogenic, nevertheless, has the potential to increase genetic instability and, possibly as a result, to enhance the malignant potential of treated cells. We suggest that although the damaged DNA was repaired during the transient G2/M arrest period, it was probably not done in an appropriate way which would preserve the original genetic stability.

Human gastric cells resistant to (-)-epigallocatechin gallate show cross-resistance to several environmental pollutants.

After a long-term culture in (-)-epigallocatechin gallate (EGCG, 20 microM), a major constituent of green tea, human gastric AGS cells developed 2.2-fold resistance to EGCG. The resistant AGS (AGS-R) cells were cross-resistant to several N-methylcarbamate insecticides, which are among the major control agents for pest insects in Taiwan. The AGS-R cells also showed protective effects against both the cytotoxicity and DNA damage induced by one of the mutagenic derivatives of N-methylcarbamate insecticide, N-nitroso methomyl, which is known to target the mammalian gastric tract. Therefore, acquisition of resistance by AGS cells through chronic exposure to EGCG implies that the tea-drinking habit of the Taiwanese is probably beneficial for the health of the gastric tract. In addition, AGS-R cells were cross-resistant to sodium arsenite and hydrogen peroxide, indicating that tolerance to oxidative stress might play a role in the development of resistance described in this investigation.

Human p16gamma, a novel transcriptional variant of p16(INK4A), coexpresses with p16(INK4A) in cancer cells and inhibits cell-cycle progression.

The INK4A locus encodes two tumor suppressor genes, p16(INK4A) and p14(ARF), transcribed using alternative exons 1alpha or 1beta spliced onto the same exons 2 and 3. Both p16(INK4A) and p14(ARF) are capable of inhibiting the cell-cycle progression, albeit in different manner; p16(INK4A) is phosphorylation of retinoblastoma (pRB) dependent while p14(ARF) is p53-dependent. In this study, we report the discovery of a novel variant of p16(INK4A), termed p16gamma, in a primary T-cell acute lymphoblastic leukemia (T-ALL) patient sample and a neuroblastoma cell line, which was expressed at both the transcriptional and translational levels. Cloning and sequencing of the p16gamma cDNA revealed that p16gamma was identical to p16(INK4A), except that it contained an in-frame insertion of 197 bp between exons 2 and 3. p16gamma expression was detected in the majority of p16(INK4A)-expressing primary T-ALL and B-ALL patient samples and other p16(INK4A)-expressing tumor samples, but was only barely detectable in some normal mononuclear cells and other non-tumor samples. Structural analysis by nuclear magnetic resonance and circular dichroism confirmed that p16gamma, like p16(INK4A), is also an ankyrin-repeat protein. Functional analysis of p16gamma revealed that p16gamma protein interacted with cyclin D-dependent kinase4 and inhibited its kinase activity. Using a luciferase reporter assay, the transfection of p16gamma repressed the E2F response, the downstream target of pRB, with an efficacy equivalent to that of p16(INK4A). Moreover p16gamma, like p16(INK4A), induced cell-cycle arrest at G(0)/G(1), and inhibited cell growth in colony formation assay.

Epstein-barr virus nuclear antigen 2 retards cell growth, induces p21(WAF1) expression, and modulates p53 activity post-translationally.

The Epstein-Barr virus (EBV) nuclear antigen 2 (EBNA2) has been shown to be required for promotion of cell-cycle progression in EBV-immortalized B-lymphocytes. However, other studies have indicated that EBNA2 alone, in the absence of other EBV genes, may retard cell growth. To resolve this discrepancy, we investigated the effect of EBNA2 on the growth of various cells, including EBV target nasopharyngeal carcinoma cells, NPC-TW01 and NPC-TW04. We found that EBNA2 could retard cell growth, in stable Vero, HEp-2, and U2OS cell clones expressing EBNA2, and in Vero, 293, NPC-TW01, and NPC-TW04 cells transiently transfected with EBNA2. While investigating the mechanism underlying the growth-retarding function of EBNA2, we found that EBNA2 induced p21(WAF1) expression in these cells. This induction of p21(WAF1) expression was mediated through p53. EBNA2 was found to stimulate p53 to bind to the p53-response element within the p21(WAF1) promoter, possibly by promoting p53 phosphorylation. This enhancement of p53 sequence-specific DNA-binding activity may be the mechanism through which EBNA2 activates the expression of p53-regulated genes, including p21(WAF1) and mdm-2. Together, these studies reveal a possible intrinsic function of EBNA2 in cell-growth regulation and elucidate a novel mechanism by which EBNA2 modulates transcription.

Use of the transurethral prostatectomy clinical path to monitor health outcomes.

PURPOSE: We evaluated the effect on cost and medical care quality of use of the transurethral prostatectomy clinical path. MATERIALS AND METHODS: Results in 100 patients treated when the transurethral prostatectomy clinical path was used were compared to those of 100 treated by the same physicians before implementation of this path. RESULTS: After implementation of the transurethral prostatectomy clinical path the length of hospital stay was significantly decreased from 5.9 to 5.0 days (p < 0.01) and Foley catheterization time was significantly decreased from 3.13 to 2.84 days (p < 0.01). Antibiotics were routinely used from the day before surgery to the day of hospital discharge as required by patient conditions. Therefore, a shorter hospital stay will significantly decrease the use of antibiotics. After implementation of the clinical path the average admission charges were decreased significantly by 17% (p < 0.01). Although some results from use of this path will not significantly affect costs, they will reflect some quality improvement. The effect of clinical path implementation on length of hospital stay between patients treated by junior and senior attending physicians was not significant. However, there was a statistically significant difference (p < 0.01) between results obtained by junior and senior attending physicians regarding average admission charges. CONCLUSIONS: Implementation of the transurethral prostatectomy clinical path can improve health care outcome by decreasing length of stay and admission charges, and improving quality of medical care, particularly for patients treated by junior attending physicians.

Complex marital histories and economic well-being: the continuing legacy of divorce and widowhood as the HRS cohort approaches retirement.

We use data from the first wave of the Health and Retirement Survey (HRS) to examine the marital histories of this cohort of women and men on the verge of retirement. The legacy of past increases in divorce rates is evident in the complex marital histories of HRS households and the relationship between those histories and current economic status. Couples in a first marriage now make up only one-quarter of black households and fewer than half of all white and Hispanic households. In over one-third of all married-couple households, at least one spouse had a previous marriage that ended in divorce or widowhood. These couples have significantly lower incomes and assets than couples in first marriages. Contrary to the popular notion that private and public insurance better provide for the security of widows than divorced persons, currently widowed households and couples in which the prior marriage of one spouse had ended in widowhood are no better off than are their divorced peers. This holds true for both black and white households. From a single cross-section, one cannot tell what caused these differences in income and wealth across marital status groups although it is clear that women and blacks spend a higher percentage of their lifetime outside of marriage than do men and whites. We also speculate from estimates of widowhood expectations for a subset of married respondents that underestimating the chances of widowhood--because both men and women overestimate their chances of joint survival--may be a factor in the relatively low economic status of widows. Because couples in life-long marriages have been the traditional standard upon which marital property reform and the survivorship rules of private and public programs are based, their diminishing importance among all households raises concern about the protection provided by these institutions against the long-term economic consequences of past and future marital dissolution.

Gender, family configuration, and the effect of family background on educational attainment.

A comprehensive model of family influences on educational resemblance of siblings expands the traditional sibling pair model to a full sibship model in order to investigate how gender, gender composition of sibships, and a measure of ordinal position moderate the effect of social origins on educational attainments of siblings. One common family factor is sufficient to explain the variation of educational attainment among brothers and sisters. Although effects of social origins variables on brothers are larger than on sisters, the relative effects of measured social origins are virtually the same among sisters and brothers. The disparity between educational attainments of brothers and sisters persists across sex composition and family size. Ordinal position does not alter the effects of social origins on educational attainment nor does it directly affect educational attainment. Father's and mother's education are equally important for all siblings regardless of birth order, gender composition, and family size.

Preeclampsia in multiple pregnancy.

BACKGROUND: Preeclampsia is one of the most common pregnancy-induced complications, and results in a large number of maternal deaths. How pregnancy incites or aggravates hypertension remains unresolved; despite decades of intensive research directed to hypertensive disorders, they remain among the most important unresolved problems in obstetrics. The incidence of preeclampsia is increased in multiple pregnancies, and several preeclampsia-related fetal risks may be particularly hazardous to the babies of multiple gestations. METHODS: The records of 561 women with multiple pregnancies delivered consecutively at Mackay Memorial Hospital were reviewed retrospectively. Thirteen mild cases and 39 severe cases of preeclampsia in multiple pregnancies were compared with 52 control cases of multiple pregnancies without preeclampsia, but matched for maternal age and parity. The categories for comparison included parity, gestational age, time of onset of preeclampsia, route of delivery, mean birth weight, growth discordancy, maternal complications, neonatal morbidity and mortality. RESULTS: The incidence of preeclampsia in our consecutive series of 561 multiple pregnancies was 9.3% compared with 1.8% in singleton pregnancies (p < 0.0001). In primiparas with multiple pregnancies, the incidence of preeclampsia was 12.2% compared with 6.2% (p < 0.05) in multiparas. Breech presentation was the most common indication for Cesarean section in all groups. The preeclamptic group had a significantly higher rate of Cesarean section compared with the control group (p < 0.006), with prolonged labor and fetal distress were the two main reasons for this difference. Severe preeclamptic patients had babies with significantly lower mean birth weights (p < 0.05), higher incidence of intrauterine growth retardation (p < 0.025) and neonatal respiratory distress syndrome (p < 0.0008) compared with those of the control group. All seven cases with maternal complications were in the severe preeclamptic group. CONCLUSIONS: An unfavorable perinatal outcome was found to be associated with severe, but not with mild, preeclampsia in multiple pregnancies.

Determination of free progesterone in an ultrafiltrate of saliva collected in situ.

We have investigated the utility of an ultrafiltrate of saliva for measuring progesterone as an indicator of luteal function during the menstrual cycle of women. A filtrate of saliva is collected in the mouth by means of an osmotic pump that accumulates medium containing only molecules less than 12,000 Da. We analyzed the nonextracted ultrafiltrate by a solid-phase immunoassay for progesterone and monitored the mid-luteal surge of lutropin in urine with a liquid-phase radioimmunoassay. Progesterone concentrations in the ultrafiltrate are significantly lower during the follicular phase and increase after the release of lutropin. The concentration of progesterone in the ultrafiltrate correlates closely with total progesterone in matched blood samples (r = 0.84, cycle 1; and r = 0.89, cycle 2). Likewise, we found a good correlation between the results in whole saliva and in the ultrafiltrate (r = 0.95). The described method of obtaining a pre-processed specimen noninvasively simplifies the self-collection of samples by patients (including collection at home); excludes potential interference from microorganisms, desquamated cells, and salivary components; and simplifies the processing of the biological fluid in the laboratory.

Interferon-mediated inhibition of prostaglandin synthesis in human mononuclear leukocytes.

In this study, the question of whether human leukocyte-derived and fibroblast-derived interferon had an effect on prostaglandin metabolism in human peripheral blood mononuclear cells has been considered. Both leukocyte- and fibroblast-derived interferon were potent inhibitors of mononuclear cell prostaglandin synthesis at low physiological concentrations. Inhibition required a minimum incubation of 1 hr. Interferon had no effect on release of arachidonic acid; synthesis of hydroxy fatty acids was slightly increased.

Modulation of T-lymphocyte differentiation antigens: potential relevance for multiple sclerosis.

Effects of the anti-T-cell monoclonal antibodies OKT3, OKT5, and OKT8 on T-cell surface properties and cell functions were evaluated. Incubation of mononuclear cells isolated from peripheral blood for 48 hr with each monoclonal antibody in the absence of complement resulted in modulation of their respective surface antigens; i.e., the number of cells detected by immunofluorescence as positive for the T3, T5, and T8 surface antigens was reduced. T3, T5, and T8 antigens modulated independently. A radiolabeled second antibody technique confirmed modulation by OKT3 and OKT8 and indicated that T-cell differentiation antigens can regenerate in culture. Incubation of mononuclear cells with OKT3 increased the number of sheep erythrocyte-binding lymphocytes (E+-rosetting cells) and markedly increased the number of avidly E+-rosetting cells. Incubation with OKT8 reduced the number of E+- and of avidly E+-rosetting cells. OKT3 induced both mitogenic reactivity and suppressor cell activity; cells modulated by OKT8 exhibited reduced mitogenic reactivity and reduced suppressor cell function. The decreases in total T cells, in avid T cells, in suppressor cell number, and in suppressor cell function that follow modulation by OKT8 mimic changes observed in multiple sclerosis patients.

Influence of azathioprine (imuran) on in vitro immune function in multiple sclerosis.

In vitro immune function was assessed in patients with multiple sclerosis (MS) who were receiving Imuran therapy, in untreated MS patients, and in controls. In untreated stable MS patients, concanavalin A (Con A)-driven mitogenic reactivity (T effector function) and Con A-induced suppressor activity were modestly reduced compared to controls; pokeweed mitogen-induced immunoglobulin G (IgG) secretion was increased. Untreated patients with active MS demonstrated high levels of IgG secretion and marked decreases in suppressor activity. In Imuran-treated patients, Con A mitogenic responses and suppressor activity were comparable to those observed in untreated stable patients, and IgG secretion was reduced. The results in the treated patients likely reflect a direct effect of Imuran on B cell function rather than an indirect effect mediated via suppressor cells.