Demetylation of the sex-determining region Y gene promoter and incidence of disorder of sex development in cloned dog males.

Canine cloning is occasionally accompanied by abnormal sexual development. Some male donor cells produce cloned pups with female external genitalia and complete male gonadal dysgenesis, which is classified as an XY disorder of sex development (XY DSD). In this study, we examine the potential of 5-aza-2'-deoxycytidine (5-aza-dC), a DNA methyltransferase inhibitor, to reduce the phenotypic abnormality XY DSD in somatic cell nuclear transfer (SCNT)- derived pups. We used a 9-year-old normal male German Shepherd dog as a cell donor. Donor cells were treated with 10 nM 5-aza-dC for 4 days before being used for SCNT. At the same stage of cell development, significantly lower levels of DNA methylation of the sex-determining region Y (SRY) promoter was observed in the treated donor cells compared to that in the untreated cells (95.2% versus 53.3% on day 4 for the control and treated groups, respectively). No significant differences were observed in the control or treatment groups concerning fusion rate, pregnancy rate (30 days or entire period), the number of pups, or the incidence of XY DSD. However, more XY DSD dogs were observed in the control group (31.25%) than in the treatment group (14.29%). Hypermethylation of the SRY promoter was observed in the XY DSD cloned pups in both the treatment (84.8%) and control groups (91.1 ± 1.4%) compared to the methylation level in the phenotypically normal male pups of the treatment (23.2 ± 20.9%) and control groups (39.1 ± 20.1%). These results suggest that 5-aza-dC treatment of donor cells can reduce the methylation level of the SRY promoter in donor cells, and thus, 5-aza-dC is advantageous for reducing the incidence of XY DSD in canine cloning.

Present and Future Trends in Consumer Health Informatics and Patient-Generated Health Data.

Objectives: Consumer Health Informatics (CHI) and the use of Patient-Generated Health Data (PGHD) are rapidly growing focus areas in healthcare. The objective of this paper is to briefly review the literature that has been published over the past few years and to provide a sense of where the field is going. Methods: We searched PubMed and the ACM Digital Library for articles published between 2014 and 2016 on the topics of CHI and PGHD. The results of the search were screened for relevance and categorized into a set of common themes. We discuss the major topics covered in these articles. Results: We retrieved 65 articles from our PubMed query and 32 articles from our ACM Digital Library query. After a review of titles, we were left with 47 articles to conduct our full article survey of the activities in CHI and PGHD. We have summarized these articles and placed them into major categories of activity. Within the domain of consumer health informatics, articles focused on mobile health and patient-generated health data comprise the majority of the articles published in recent years. Conclusions: Current evidence indicates that technological advancements and the widespread availability of affordable consumer-grade devices are fueling research into using PGHD for better care. As we observe a growing number of (pilot) developments using various mobile health technologies to collect PGHD, major gaps still exist in how to use the data by both patients and providers. Further research is needed to understand the impact of PGHD on clinical outcomes.

Reaction Gas Ratio Effect on the Growth of a Diamond Film Using Microwave Plasma-Enhanced Chemical Vapor Deposition.

In this study, diamond films were prepared using the microwave plasma-enhanced chemical vapor deposition (PECVD) system, which included a DC bias system to enhance the nucleation of the films. The films were synthesized on Si wafers with different ratios of methane (CH4) and hydrogen (H2) gases. We have studied the effects of the CH4-to-H2 ratio on the structural and optical properties of diamond films. The thickness and surface profile of the films were characterized via field emission scanning electron microscopy (FE-SEM). Raman was used to investigate the structural properties of the diamond films. The refractive indexes as functions of the CH4-to-H2 ratio were measured using an ellipsometer. The FE-SEM analysis showed that the 3 and 5 sccm CH4 created diamond films. The Raman analysis indicated that a nanocrystalline diamond film was formed at 3 sccm; a general diamond film, at 5 sccm; and films similar to the a-C:H film, at 7 sccm. The ellipsometer measurement showed that the refractive index of the synthesized diamond film was around 2.42 at 3 sccm. This value decreased as the CH4 volume increased.

Properties of Dye-Sensitized Solar Cells Using Carbon Nanowall Counter Electrodes.

This research investigates plasma-treated and metal-coated carbon nanowalls (CNWs) for use as counter electrodes of dye-sensitized solar cells (DSSCs). The CNWs were synthesized on a fluorine-tin-oxide (FTO) glass substrate using the microwave plasma-enhanced chemical vapor deposition (PECVD) system with methane (CH4) gas. The post-plasma treatment was performed on the CNWs with hydrogen (H2) plasma using PECVD, and the CNWs were sputter-coated with metal films using the RF magnetron sputtering system with a four-inch tungsten (W) target. Then the post-plasma-treated and metal-coated CNWs were used as counter electrodes for the fabrication of the DSSCs. Field-emission scanning electron microscopy (FE-SEM) was performed to obtain cross-sectional and planar images of the grown CNWs. The energy conversion efficiencies of the DSSCs manufactured using the post-plasma-treated and metal-layer-coated CNWs as the counter electrodes were measured.

Association between prolonged breastfeeding and bone mineral density and osteoporosis in postmenopausal women: KNHANES 2010-2011.

UNLABELLED: This study showed that a negative correlation between duration of breastfeeding and bone mineral density (BMD) in the lumbar spine and prolonged breastfeeding is an independent risk for osteoporosis in postmenopausal women. The present study suggests that postmenopausal women with a history of prolonged breastfeeding require more careful screening for osteoporosis. INTRODUCTION: Several studies suggest that breastfeeding and childbirth lead to maternal calcium loss and a decline in BMD. While the association between breastfeeding and BMD immediately after weaning is well-established, the effects of breastfeeding on postmenopausal women have been controversial. The aim of this study was to examine the effects of breastfeeding on bone mineral density (BMD) and the prevalence of osteoporosis in postmenopausal women. METHODS: The present study was a cross-sectional survey based on the Korea National Health and Nutrition Examination Survey (KNHANES) 2010 and 2011 data. The association between breastfeeding and BMD and osteoporosis was examined in 1222 postmenopausal women. RESULTS: The duration of breastfeeding and BMD in the lumbar spine showed a negative correlation. The association between duration of breastfeeding and BMD remained significant after adjustment for reproductive factors and other confounding factors (P = 0.008). However, the number of deliveries and age at the time of delivery did not correlate with BMD at any site after adjustment. Moreover, the prevalence of osteoporosis in postmenopausal women with a history of prolonged breastfeeding was significantly higher than that in women with a short history of breastfeeding (≥37 months, OR = 3.292; 95 % CI 1.485-7.299). The prevalence of lumbar spine fracture showed a significant increasing trend with the increase in the duration of breastfeeding. CONCLUSION: Prolonged breastfeeding was significantly associated with low BMD in the lumbar spine and higher prevalence of osteoporosis. However, the number of deliveries or age at the time of childbirth did not influence BMD.

Implementation of secondary stroke prevention protocol for ischaemic stroke patients in primary care.

OBJECTIVE: To investigate the effectiveness of a secondary stroke prevention protocol in the general out-patient clinic. DESIGN: Cohort study with pre- and post-intervention comparisons. SETTING: Two general out-patient clinics in Hong Kong. PATIENTS: Ischaemic stroke patients who had long-term follow-up in two clinics were recruited. The patients of one clinic received the intervention (intervention group) and the patients of the second clinic did not receive the intervention (control group). The recruitment period lasted for 6 months from 1 September 2008 to 28 February 2009. The pre-intervention phase data collection started within this 6-month period. The protocol implementation started at the intervention clinic on 1 April 2009. The post-intervention phase data collection started 9 months after the protocol implementation, and ran for 6 months from 1 January 2010 to 30 June 2010. MAIN OUTCOME MEASURES: Clinical data before and after the intervention, including blood pressure, glycated haemoglobin level, low-density lipoprotein level and prescription pattern, were compared between the two groups to see whether there was enhancement of secondary stroke management. RESULTS: A total of 328 patients were recruited into the intervention group and 249 into the control group; data of 256 and 210 patients from these groups were analysed, respectively. After intervention, there were significant reductions in mean (± standard deviation) systolic blood pressure (135.2 ± 17.5 mm Hg to 127.7 ± 12.2 mm Hg), glycated haemoglobin level (7.2 ± 1.0% to 6.5 ± 0.8%), and low-density lipoprotein level (3.4 ± 0.8 mmol/L to 2.8 ± 1.3 mmol/L) in the intervention group (all P<0.01). There were no significant reductions in mean systolic blood pressure, glycated haemoglobin level, or low-density lipoprotein level in the control group. There was a significant increase in statin use (P<0.01) in both clinics. CONCLUSION: Through implementation of a clinic protocol, the standard of care of secondary stroke prevention for ischaemic stroke patients could be improved in a general out-patient clinic.

Fibroblast growth factor 21 analogue LY2405319 lowers blood glucose in streptozotocin-induced insulin-deficient diabetic mice by restoring brown adipose tissue function.

AIM: To investigate the effects of LY2405319, an analogue of fibroblast growth factor 21 (FGF21), on glucose homeostasis in streptozotocin (STZ)-induced insulin-deficient mice (STZ mice). METHODS: Nine-week-old male C57BL/6J mice were administered a single intraperitoneal injection of STZ (150 mg/kg). One week later, after confirmation of hyperglycaemia, saline or LY2405319 (5 mg/kg) was injected subcutaneously daily for 4 weeks. Changes in glucose homeostasis, energy metabolism and brown adipose tissue (BAT) function were assessed. RESULTS: The STZ mice had elevated blood glucose and reduced plasma FGF21 levels, impaired glucose uptake in the BAT, and BAT mitochondria with absent or swollen cristae and fewer lipid vacuoles. LY2405319 significantly reduced blood glucose levels and this was associated with increased BAT glucose uptake and changes in gene expression and morphology, indicating improved mitochondrial lipid metabolism in the BAT. Importantly, the ability of LY2405319 to lower blood glucose in STZ mice was compromised after removing interscapular BAT. CONCLUSIONS: Our results show that LY2405319 reduces blood glucose levels in insulin-deficient diabetes by improving BAT metabolism. Additional studies investigating the therapeutic potential of FGF21 for the treatment of type 1 diabetes are warranted.

Relationship between prosthodontic status and nutritional intake in the elderly in Korea: National Health and Nutrition Examination Survey (NHANES IV).

OBJECTIVES: Many health issues have been reported to be associated with poor nutritional status. We sought to examine the association between nutritional intake and oral health status in elderly people. METHODS: The association between perceived disability in mastication and prosthodontic status was analysed using multiple logistic regression. Multiple linear regression was used to analyse the association between prosthodontic status and nutritional intake. RESULTS: The elderly subjects with partial or full dentures reported chewing difficulties 1.62-fold more frequently (95% CI: 1.06-2.49) than those with natural teeth or a fixed prosthesis after adjusting for gender, TMD (temporomandibular disorder), household income and education level. Additionally, daily nutritional intakes of energy, protein, fat, ash, calcium, phosphorus and thiamine were decreased significantly in elderly with partial or full dentures compared with those with no prosthesis or with a fixed prosthesis (P < 0.05). CONCLUSIONS: Our findings underline oral health status and perceived disability in mastication are associated with dietary imbalances in the elderly. We suggest that the evaluation of patients' nutritional status should be considered as a part of an overall plan for dental hygiene care.

cAMP response element binding protein H mediates fenofibrate-induced suppression of hepatic lipogenesis.

AIMS/HYPOTHESIS: Fenofibrate is a drug used to treat hyperlipidaemia that works by inhibiting hepatic triacylglycerol synthesis. Sterol regulatory element binding protein-1c (SREBP-1c) is a major regulator of the expression of genes involved in hepatic triacylglycerol synthesis. In addition, endoplasmic reticulum (ER)-bound transcription factor families are involved in the control of various metabolic pathways. Here, we show a novel function for an ER-bound transcription factor, cAMP response element binding protein H (CREBH), in fenofibrate-mediated inhibition of hepatic lipogenesis. METHODS: The effects of fenofibrate and adenovirus-mediated Crebh (also known as Creb313) overexpression (Ad-Crebh) on hepatic SREBP-1c production and lipogenesis in vitro and in vivo were investigated. We also examined whether downregulation of endogenous hepatic Crebh by small interfering (si)RNA restores the fenofibrate effect on hepatic lipogenesis and SREBP-1c production. Finally, we examined the mechanism by which CREBH inhibits hepatic SREBP-1c production. RESULTS: Fasting and fenofibrate treatment induced CREBH production and decreased SREBP-1c levels. Indeed, Ad-Crebh inhibited insulin- and liver X receptor agonist TO901317-induced Srebp-1c (also known as Srebf1) mRNA expression in cultured hepatocytes. Moreover, increased production of CREBH in the liver of mice following tail-vein injection of Ad-Crebh inhibited high-fat diet-induced hepatic steatosis through inhibition of Srebp-1c expression. The inhibition of endogenous Crebh expression by siRNA restored fenofibrate-induced suppression of Srebp-1c expression and hepatic lipid accumulation both in vitro and in vivo. CONCLUSIONS/INTERPRETATION: These results show that fenofibrate decreases hepatic lipid synthesis through induction of CREBH. This study suggests CREBH as a novel negative regulator of SREBP-1c production and hepatic lipogenesis.

A novel PRKAR1A mutation in Korean Carney complex family.

Carney complex (CNC) is an autosomal dominant hereditary or sporadic multiple neoplastic syndrome that shows variable clinical symptoms. Generally, CNC appears as skin pigmentation, cardiac or cutaneous myxomas, and multiple endocrine tumours. We performed an extensive evaluation of 9 individuals within 1 family in whom CNC was suspected. Among them, 5 had CNC with various clinical manifestations. We also performed mutational analysis of suspected genes in these patients. Although all patients were members of the same family, variable CNC-related manifestations were observed in each patient. An analysis showed a novel deletion mutation (c.537delA) in exon 6 of the PRKAR1A gene in the patients. Based on our results, the patients were determined to have CNC type I. This is the first such mutational report in Korea.

Autotransplantation of an ectopic impacted premolar with sinus lift and allogenic bone graft.

AIM: This article presents a case report of autogenous tooth transplantation to a site which had insufficient bone volume using a sinus lift and allogenic bone graft. SUMMARY: An ectopic, fully impacted premolar tooth was autotransplanted from its ectopic impaction site into its original site, where there was insufficient recipient vertical bone volume because of sinus expansion. The deciduous tooth was extracted from the recipient site, and the sinus membrane detached and elevated via the alveolar socket. Allogenic bone grafting was performed, and the impacted premolar was transplanted into the prepared site. To improve adaptation, the recipient site was prepared using a rapid prototype tooth model, a replica tooth which allowed complete socket preparation in advanced of the actual removal of the donor tooth. The donor tooth was fixed with sutures and maintained for 17 days to allow physiologic movement. Root canal treatment was initiated 24 days after autotransplantation, and an intra-canal medicament was used for 4 months. Canal filling was completed 5 months after autotransplantation. There was no root resorption of the transplanted tooth, and the grafted bone was well preserved and had no signs of infection. KEY LEARNING POINTS: When the recipient bone volume is insufficient, autotransplantation can be preceded by bony augmentation. The preparation of the recipient tooth socket using a tooth replica from CBCT reduces the extra-oral time of the actual tooth and promotes better periodontal ligament healing. Careful evaluation of the pulp status of the donor tooth is important in advance of timely endodontic treatment.

Pitx3-deficient aphakia mice display unique behavioral responses to psychostimulant and antipsychotic drugs.

The dorsal (A9) and ventral striatum (A10) of the midbrain mediate many of the effects of psychoactive drugs that alter emotion, cognition, and motor activity within the contexts of therapy or abuse. Although transgenic and knockout technologies have enabled development of genetic models to dissect contributions of specific dopamine (DA) receptor subtypes to psychoactive drug effects, few models exist that can distinguish contributions of A9 versus A10 circuits. Pitx3 is a transcription factor enriched in DA neurons. Aphakia (ak) mice deficient in Pitx3 show selective loss of nigrostriatal DA, while other DA pathways are relatively spared, and therefore could be a useful tool for investigating the role of this subclass of DA projections. We investigated the effects of stimulants amphetamine, apomorphine, and MK-801 and the antipsychotic drug haloperidol on behavior in ak mice. Whereas wild-type mice showed the characteristic locomotor hyperactivity in response to amphetamine (5 mg/kg) and apomorphine (4 mg/kg), these drugs caused a paradoxical suppression of locomotor hyperactivity in ak mice. MK-801 (0.2 mg/kg) induced hyperactivity was maintained in both wt and ak mice. Additionally, mutant but not wild-type mice were insensitive to the cataleptic effects of haloperidol (1 mg/kg). These studies indicate that the nigrostriatal DA circuit plays a critical role in maintaining normal responsiveness to psychotropic drugs that either stimulate or block DA neurotransmission. We propose that ak mice may represent a valuable genetic model not only to study Parkinson's disease, but also to dissect the pathophysiologic and pharmacotherapuetic mechanisms of other DA-mediated disorders such as attention-deficit hyperactivity disorder, drug abuse and schizophrenia.

Effects of maintaining a remifentanil infusion on the recovery profiles during emergence from anaesthesia and tracheal extubation.

BACKGROUND: Emergence from anaesthesia and tracheal extubation can be associated with hyperdynamic circulatory responses. We examined the effects of maintaining a remifentanil infusion on recovery profiles such as coughing and cardiovascular responses after general anaesthesia. METHODS: Forty patients undergoing endoscopic sinus surgery under general anaesthesia using total i.v. anaesthesia (propofol and remifentanil) were randomly allocated to a control group (n=20) or remifentanil group (n=20) during emergence from anaesthesia. At the end of surgery, propofol was ceased and the infusion of remifentanil was stopped in the control group and maintained in the remifentanil group at a target organ concentration of 1.5 ng ml(-1) until extubation. Heart rate (HR), mean arterial pressure (MAP), and recovery profiles were measured and evaluated. RESULTS: There was no significant difference in sex ratio, age, weight, height, time to eye opening, time to extubation, nausea, visual analogue scale, and time to discharge. Increases in HR and MAP occurred during emergence in the control group compared with baseline values. Increases in HR were attenuated in the remifentanil group and MAP decreased during recovery compared with baseline values. HR and MAP values were significantly higher in the control group [103 (23) beats min(-1), 129 (17) mm Hg] compared with the remifentanil group [79 (17) beats min(-1), 112 (15) mm Hg] during emergence and tracheal extubation. Moderate or severe coughing was observed only in the control group (8/20 vs 0/20, P<0.001). CONCLUSIONS: Maintaining a remifentanil infusion reduced haemodynamic changes and coughing associated with tracheal extubation almost without significantly delaying recovery from anaesthesia.

Effects of bupivacaine and ropivacaine on field potential in rat hippocampal slices.

BACKGROUND: In spite of more than 20 yr of research, the mechanism whereby local anaesthetics act on the brain to mediate anaesthesia still remains unclear. Furthermore, the effect of local anaesthetics on neuronal excitability and synaptic transmission in the hippocampus has not been reported. Thus, the purpose of the present study was to find out the differences between the local anaesthetics, bupivacaine and ropivacaine, in their actions on synaptic transmission of brain in the context of hippocampal field potential. METHODS: Brains were removed from 3- to 4-week-old rats and transverse slices (300 microm thick) were prepared using a microslicer. A slice was then placed on the centre on a multielectrode dish probe. To record evoked field potentials at 64 sites, a pair of single planar microelectrodes delivering bipolar constant current pulses (45-90 microA, 0.1 ms) was applied. Electrophysiological recordings were measured using the 64-channel multielectrode dish. RESULTS: The amplitude of field potential in the rat CA1 region was inhibited by both bupivacaine and ropivacaine. The inhibitory effects of bupivacaine and ropivacaine on field potential amplitudes in CA1 were similar. For bupivacaine 10 microg ml(-1), inhibited field potentials were incompletely recovered; in contrast, for 10 ropivacaine microg ml(-1), inhibited field potentials were completely recovered after washing out with incubation solution. CONCLUSIONS: Inhibitory effects of bupivacaine and ropivacaine on hippocampal field potential amplitude and recovery rate after washout after bupivacaine or ropivacaine treatment represent the underlying mechanisms of the systemic toxicity of local anaesthetics.

Human alpha 1-antitrypsin therapy induces fatal anaphylaxis in non-obese diabetic mice.

Previous studies have shown that human alpha-1 antitrypsin (hAAT) gene delivery prevents type 1 diabetes (T1D) in non-obese diabetic (NOD) mice. Furthermore, hAAT protein administration prolongs acceptance of islet allografts. Therefore, we evaluated the use of purified hAAT protein therapy to prevent T1D in NOD mice. Female NOD, non-obese resistant (NOR), Balb/c and C57BL/6 mice were injected intraperitoneally with vehicle alone or vehicle containing hAAT, human albumin or mouse albumin (or mg/injection/mouse; 2x/week). Preparations of clinical-grade hAAT included API(R), Aralast, Prolastin and Zemaira. Surprisingly, hAAT administration was associated with a high rate of fatal anaphylaxis. In studies seeking T1D prevention at 4 weeks of age, 100% mice died after six injections of hAAT. When administrated at 8-10 weeks of age, most (80-100%) NOD mice died following the fourth injection of hAAT, while 0% of Balb/c and C57BL/6 mice and 10% of NOR mice died. Interestingly, repeated injections of human albumin, but not mouse albumin, also induced sudden death in NOD mice. Antibodies to hAAT were induced 2-3 weeks after hAAT administration and death was prevented by treatment with anti-platelet-activating factor along with anti-histamine. In studies of disease reversal in NOD mice, using the four pharmaceutical grade formulations of hAAT, anaphylactic deaths were observed with all hAAT preparations. The propensity for fatal anaphylaxis following antigenic administration appears to be NOD- but not hAAT-specific. The susceptibility of NOD mice to hypersensitivity provides a significant limitation for testing of hAAT. Development of strategies to avoid this unwanted response is required to use this promising therapeutic agent for T1D.

25-hydroxycholesterol induces mitochondria-dependent apoptosis via activation of glycogen synthase kinase-3beta in PC12 cells.

25-hydroxycholesterol (25-OH-chol) induces apoptosis in many cell types. The present study investigated the possible involvement of mitochondria-dependent apoptotic signalling molecules in the death of PC12 cells treated with 25-OH-chol. 25-OH-chol increased the production of reactive oxygen species and opened mitochondrial permeability transition pore, resulting in release of cytochrome c and subsequent activation of caspase-9 and -3. 25-OH-chol induced the activation of c-Jun N-terminal kinase (JNK) and glycogen synthase kinase-3beta (GSK-3beta). The JNK inhibitor SP600125 attenuated the activation of caspase-9 and -3 and reduced 25-OH-chol-induced cell death. GSK inhibitors SB415286 and SB216763 significantly down-regulated JNK activity and attenuated the cytotoxicity of 25-hydroxycholesterol. However, SP600125 did not alter the activity of GSK-3beta. The results indicate that 25-OH-chol induces cell death via activation of GSK-3beta and subsequent up-regulation of JNK. Pharmacological intervention of GSK-3beta-JNK-caspase signalling pathway may be useful for the reduction of cytotoxicity of oxysterols.

Difference in direct charge-parity violation between charged and neutral B meson decays.

Equal amounts of matter and antimatter are predicted to have been produced in the Big Bang, but our observable Universe is clearly matter-dominated. One of the prerequisites for understanding this elimination of antimatter is the nonconservation of charge-parity (CP) symmetry. So far, two types of CP violation have been observed in the neutral K meson (K(0)) and B meson (B(0)) systems: CP violation involving the mixing between K(0) and its antiparticle (and likewise for B(0) and ), and direct CP violation in the decay of each meson. The observed effects for both types of CP violation are substantially larger for the B(0) meson system. However, they are still consistent with the standard model of particle physics, which has a unique source of CP violation that is known to be too small to account for the matter-dominated Universe. Here we report that the direct CP violation in charged B(+/-)-->K(+/-)pi(0) decay is different from that in the neutral B(0) counterpart. The direct CP-violating decay rate asymmetry, (that is, the difference between the number of observed B(-)-->K(-)pi(0) event versus B(+)-->K(+) pi(0) events, normalized to the sum of these events) is measured to be about +7%, with an uncertainty that is reduced by a factor of 1.7 from a previous measurement. However, the asymmetry for versus B(0)-->K(+)pi(-) is at the -10% level. Although it is susceptible to strong interaction effects that need further clarification, this large deviation in direct CP violation between charged and neutral B meson decays could be an indication of new sources of CP violation-which would help to explain the dominance of matter in the Universe.

Measurements of branching fractions for B --> K pi and B --> pi pi decays.

We report measurements of branching fractions for B --> K pi and B --> pi pi decays based on a data sample of 449 x 10(6) BB[over] pairs collected at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy e(+)e(-) collider. We also measure the ratios of partial widths for B-->Kpi decays, namely R(c) identical with 2Gamma(B(+) --> K(+) pi(0))/Gamma(B(+) --> K(0) pi(+)) = 1.08+/-0.06+/-0.08 and R(n) identical with Gamma(B(0) --> K(+) pi(-))/2 Gamma(B(0) --> K(0) pi(0)) = 1.08+/-0.08+/-0.08, where the first and the second errors are statistical and systematic, respectively. These ratios are sensitive to enhanced electroweak penguin contributions from new physics; the new measurements are, however, consistent with standard model expectations.

Measurement of Einstein-Podolsky-Rosen-type flavor entanglement in Upsilon(4S) --> B0 B0 decays.

The neutral B meson pair produced at the Upsilon(4S) should exhibit a nonlocal correlation of the type discussed by Einstein, Podolsky, and Rosen. We measure this correlation using the time-dependent flavor asymmetry of semileptonic B(0) decays, which we compare with predictions from quantum mechanics and two local realistic models. The data are consistent with quantum mechanics, and inconsistent with the other models. Assuming that some B pairs disentangle to produce B(0) and B(0) with definite flavor, we find a decoherent fraction of 0.029 +/ -0.057, consistent with no decoherence.

Measurement of D0-D0 mixing parameters in D0 --> Ks pi+ pi- decays.

We report a measurement of D0-D(0) mixing parameters in D(0) --> K(s)(0) pi(+) pi(-) decays using a time-dependent Dalitz-plot analysis. We first assume CP conservation and subsequently allow for CP violation. The results are based on 540 fb(-1) of data accumulated with the Belle detector at the KEKB e(+)e(-) collider. Assuming negligible CP violation, we measure the mixing parameters x = (0.80 +/- 0.29(-0.07-0.14)(+0.09+0.10))% and y = (0.33+/-0.24(-0.12-0.08)(+0.08+0.06))%, where the errors are statistical, experimental systematic, and systematic due to the Dalitz decay model, respectively. Allowing for CP violation, we obtain the CP-violating parameters |q / p| = 0.86(-0.29-0.03)(+0.30+0.06) +/- 0.08 and arg(q/p) = (-14(-18-3-4)(+16+5+2)) degrees .