133 research outputs found
Proton spectra from Non-Mesonic Weak Decay of p-shell Lambda-Hypernuclei and evidence for the two-nucleon induced process
New spectra from the FINUDA experiment of the Non Mesonic Weak Decay (NMWD)
proton kinetic energy for 9(Lambda)Be, 11(Lambda)B, 12(Lambda)C, 13(Lambda)C,
15 (Lambda)N and 16(Lambda)O are presented and discussed along with the
published data on 5(Lambda)He and 7(Lambda)Li. Exploiting the large mass number
range and the low energy threshold (15 MeV) for the proton detection of FINUDA,
an evaluation of both Final State Interactions (FSI) and the two nucleon
induced NMWD contributions to the decay process has been done. Based on this
evaluation, a linear dependence of FSI on the hypernuclear mass number A is
found and for the two nucleon stimulated decay rate the experimental value of
Gamma2/Gammap=0.43+-0.25 is determined for the first time. A value for the two
nucleon stimulated decay rate to the total decay rate
Gamma2/GammaNMWD=0.24+-0.10 is also extracted.Comment: 11 pages and 2 figure
Rare spontaneous monochorionic dizygotic twins: a case report and a systematic review
Background: Monochorionic dizygotic twins are a rare condition, mostly related to assisted reproductive technology. This type of twinning is burdened by the same risk of pregnancy complications found in monochorionic monozygotic pregnancies. Case presentation: We report a case of spontaneous monochorionic dizygotic twins sharing situs inversus abdominalis and isolated levocardia, with only one twin affected by biliary atresia with splenic malformation syndrome. We also conducted a literature review of the 14 available documented monochorionic dizygotic twin gestations spontaneously conceived. Conclusions: It is still unclear how this unusual type of twinning can occur in spontaneous conception. The evidence so far suggest the importance to timely diagnose the chorionicity, in order to adequately manage the typical complications associated with monochorionicity
Precise Measurements of Branching Fractions for Meson Decays to Two Pseudoscalar Mesons
We measure the branching fractions for seven two-body decays to
pseudo-scalar mesons, by analyzing data collected at
GeV with the BESIII detector at the BEPCII collider. The branching fractions
are determined to be ,
,
,
,
,
,
,
where the first uncertainties are statistical, the second are systematic, and
the third are from external input branching fraction of the normalization mode
. Precision of our measurements is significantly improved
compared with that of the current world average values
Measurements of Weak Decay Asymmetries of , , , and
Using production from a 567 pb
data sample collected by BESIII at 4.6 GeV, a full angular analysis is carried
out simultaneously on the four decay modes of , , , and . For the first time, the
transverse polarization is studied in unpolarized
collisions, where a non-zero effect is observed with a statistical significance
of 2.1. The decay asymmetry parameters of the weak
hadronic decays into , , and
are measured to be ,
,
, and
, respectively. In comparison with
previous results, the measurements for the and
modes are consistent but with improved precision, while the parameters for the
and modes are measured for the first time
3,5-Diiodo-L-thyronine modulates the expression of genes of lipid metabolism in a rat model of fatty liver.
Recent reports demonstrated that 3,5-diiodo-l-thyronine (T(2)) was able to prevent lipid accumulation in the liver of rats fed a high-fat diet (HFD). In this study, we investigated how the rat liver responds to HFD and T(2) treatment by assessing the transcription profiles of some genes involved in the pathways of lipid metabolism: oxidation, storage and secretion. The mRNA levels of the peroxisome proliferator-activated receptors (PPARα, PPARγ and PPARδ), and of their target enzymes acyl-CoA oxidase and stearoyl-CoA desaturase were evaluated by real-time RT-PCR. Moreover, the expression of the adipose triglyceride lipase involved in lipid mobilisation, of the main PAT proteins acting in lipid droplet (LD) turnover, and of apoprotein B (apo B), the major protein component of very low-density lipoproteins (VLDLs) were analysed. Overall, our data demonstrated that T(2) administration to HFD rats counteracts most of the hepatic transcriptional changes that occurred in response to the excess exogenous fat. In particular, our results suggest that T(2) may prevent the pathways leading to lipid storage in LDs, promote the processes of lipid mobilisation from LDs and secretion as VLDL, in addition to the stimulation of pathways of lipid oxidation. In conclusion, our findings might give an insight into the mechanisms underlying the anti-steatotic ability of T(2) and help to define the potential therapeutic role of T(2) for preventing or treating liver steatosis
Observation of the Singly Cabibbo-Suppressed Decay and Evidence for
Based on 2.93 fb collision data taken at center-of-mass
energy of 3.773 GeV by the BESIII detector, we report searches for the singly
Cabibbo-suppressed decays and .
A double tag technique is used to measure the absolute branching fractions
and
, with
statistical significances of and , respectively. We also
present measurements of the absolute branching fractions for the related decay modes. We find
and
, which are
consistent with the current world averages. The first and second uncertainties
are statistical and systematic, respectively
Fluorescent RT in situ PCR detection of MRP1 mRNA in human HCV infected liver.
Chronic hepatitis C is now a major cause of chronic liver disease, cirrhosis and hepatocellular carcinoma. Approximately 20% of cases of acute viral hepatitis are due to hepatitis C. Cirrhosis develops in more than 25% of patients with chronic infection and each year hepatocellular carcinoma occurs in 1-3% of patients with cirrhosis due to HCV (Hoofnagle 1999). Patients with hepatocellular carcinoma are characterized by nonresponsiveness to chemotherapeutic agents. A cause of refractivity to treatment has been ascribed to the overexpression of the Pgp (MDR) protein (Kim et al. 1999), and the additional involvement of multidrug resistance-associated proteins (MRPs) has been also hypothesized (Minemura et al. 1999)
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