Perturbative QCD analysis of B→ϕK∗B \to \phi K^* decays

We study the first observed charmless $B\to VV$ modes, the $B\to\phi K^*$ decays, in perturbative QCD formalism. The obtained branching ratios $B(B\to\phi K^*)\sim 15 \times 10^{-6}$ are larger than $\sim 9\times 10^{-6}$ from QCD factorization. The comparison of the predicted magnitudes and phases of the different helicity amplitudes, and branching ratios with experimental data can test the power counting rules, the evaluation of annihilation contributions, and the mechanism of dynamical penguin enhancement in perturbative QCD, respectively.Comment: 14 pages, 2 tables, brief disscussion on hard sacle added, version to appear in PR

Nonfactorizable contributions to B→D(∗)MB \to D^{(*)} M decays

While the factorization assumption works well for many two-body nonleptonic $B$ meson decay modes, the recent measurement of $\bar B\to D^{(*)0}M^0$ with $M=\pi$, $\rho$ and $\omega$ shows large deviation from this assumption. We analyze the $B\to D^{(*)}M$ decays in the perturbative QCD approach based on $k_T$ factorization theorem, in which both factorizable and nonfactorizable contributions can be calculated in the same framework. Our predictions for the Bauer-Stech-Wirbel parameters, $|a_2/a_1|= 0.43\pm 0.04$ and $Arg(a_2/a_1)\sim -42^\circ$ and $|a_2/a_1|= 0.47\pm 0.05$ and $Arg(a_2/a_1)\sim -41^\circ$, are consistent with the observed $B\to D\pi$ and $B\to D^*\pi$ branching ratios, respectively. It is found that the large magnitude $|a_2|$ and the large relative phase between $a_2$ and $a_1$ come from color-suppressed nonfactorizable amplitudes. Our predictions for the ${\bar B}^0\to D^{(*)0}\rho^0$, $D^{(*)0}\omega$ branching ratios can be confronted with future experimental data.Comment: 25 pages with Latex, axodraw.sty, 6 figures and 5 tables, Version published in PRD, Added new section 5 and reference

Relationship of serum bilirubin concentration to kidney function and 24-hour urine protein in Korean adults

<p>Abstract</p> <p>Background</p> <p>The relationships among serum bilirubin concentration, kidney function and proteinuria have yet to be fully elucidated, nor have these relationships been investigated in Korean adults.</p> <p>Method</p> <p>We retrospectively reviewed the medical records of Korean adults who were evaluated at Kosin University Gospel Hospital (Busan, Republic of Korea) during a five-year period from January 2005 to December 2009. We evaluated the relationships among serum bilirubin concentration, estimated glomerular filtration rate (eGFR) and 24-hour urinary protein excretion in a sample of 1363 Korean adults aged 18 years or older.</p> <p>Results</p> <p>The values of eGFR <60 mL/min/1.73 m²and 24-hour urine albumin ≥150 mg/day were observed in 26.1% (n = 356) and 40.5% (n = 553) of subjects, respectively. Fasting glucose levels ≥126 mg/dL were observed in 44.9% (n = 612) of the total sample. After adjustment for potential confounding factors including demographic characteristics, comorbidities and other laboratory measures, total serum bilirubin was positively associated with eGFR and negatively associated with proteinuria both in the whole cohort and in a subgroup of diabetic individuals.</p> <p>Conclusions</p> <p>To our knowledge, this is the first hospital-based study specifically aimed at examining the relationships among serum total bilirubin concentration, 24-hour urine protein and kidney function in Korean adults. We demonstrated that serum total bilirubin concentration was negatively correlated with 24-hour urine protein and positively correlated with eGFR in Korean non-diabetic and diabetic adults.</p

Differences in Clinical Features According to Boryoung and Karp Genotypes of Orientia tsutsugamushi

Scrub typhus is an infectious disease caused by Orientia tsutsugamushi. The differences in virulence of O. tsutsugamushi prototypes in humans are still unknown. We investigated whether there are any differences in the clinical features of the Boryoung and Karp genotypes.Patients infected with O. tsutsugamushi, as Boryoung and Karp clusters, who had visited 6 different hospitals in southwestern Korea were prospectively compared for clinical features, complications, laboratory parameters, and treatment responses. Infected patients in the Boryoung cluster had significantly more generalized weakness, eschars, skin rashes, conjunctival injection, high albumin levels, and greater ESR and fibrinogen levels compared to the Karp cluster. The treatment response to current antibiotics was significantly slower in the Karp cluster as compared to the Boryoung cluster.The frequency of occurrence of eschars and rashes may depend on the genotype of O. tsutsugamushi

Ndel1 Promotes Axon Regeneration via Intermediate Filaments

Failure of axons to regenerate following acute or chronic neuronal injury is attributed to both the inhibitory glial environment and deficient intrinsic ability to re-grow. However, the underlying mechanisms of the latter remain unclear. In this study, we have investigated the role of the mammalian homologue of aspergillus nidulans NudE, Ndel1, emergently viewed as an integrator of the cytoskeleton, in axon regeneration. Ndel1 was synthesized de novo and upregulated in crushed and transected sciatic nerve axons, and, upon injury, was strongly associated with neuronal form of the intermediate filament (IF) Vimentin while dissociating from the mature neuronal IF (Neurofilament) light chain NF-L. Consistent with a role for Ndel1 in the conditioning lesion-induced neurite outgrowth of Dorsal Root Ganglion (DRG) neurons, the long lasting in vivo formation of the neuronal Ndel1/Vimentin complex was associated with robust axon regeneration. Furthermore, local silencing of Ndel1 in transected axons by siRNA severely reduced the extent of regeneration in vivo. Thus, Ndel1 promotes axonal regeneration; activating this endogenous repair mechanism may enhance neuroregeneration during acute and chronic axonal degeneration

Suppression of NLRX1 in chronic obstructive pulmonary disease

Cigarette smoke (CS) and viruses promote the inflammation and remodeling associated with chronic obstructive pulmonary disease (COPD). The MAVS/RIG-I–like helicase (MAVS/RLH) pathway and inflammasome-dependent innate immune pathways are important mediators of these responses. At baseline, the MAVS/RLH pathway is suppressed, and this inhibition must be reversed to engender tissue effects; however, the mechanisms that mediate activation and repression of the pathway have not been defined. In addition, the regulation and contribution of MAVS/RLH signaling in CS-induced inflammation and remodeling responses and in the development of human COPD remain unaddressed. Here, we demonstrate that expression of NLRX1, which inhibits the MAVS/RLH pathway and regulates other innate immune responses, was markedly decreased in 3 independent cohorts of COPD patients. NLRX1 suppression correlated directly with disease severity and inversely with pulmonary function, quality of life, and prognosis. In murine models, CS inhibited NLRX1, and CS-induced inflammation, alveolar destruction, protease induction, structural cell apoptosis, and inflammasome activation were augmented in NLRX1-deficient animals. Conversely, MAVS deficiency abrogated this CS-induced inflammation and remodeling. Restoration of NLRX1 in CS-exposed animals ameliorated alveolar destruction. These data support a model in which CS-dependent NLRX1 inhibition facilitates MAVS/RHL activation and subsequent inflammation, remodeling, protease, cell death, and inflammasome responses