In this paper, we present differential cross sections and complete sets of polarization transfer coefficients, D i j , obtained in the 13 C(p ជ ,n ជ) 13 N reaction studied at zero degree and at 197 MeV incident proton energy. The complete set of polarization observables is used to obtain the Fermi and Gamow-Teller ͑GT͒ cross section contributions in the ground state transition, which are then used to deduce GT transition strengths. The sum of the GT strength up to 20 MeV of excitation is compared with shell model calculations. In the region between 20 to 46 MeV of excitation, the differential cross section has been separated in spin and nonspin components.

New elastic and inelastic neutron scattering data for 6 Li taken at 24.0 MeV have been analyzed in conjunction with existing proton scattering data for these targets at 24.4 MeV. The new data allow us to infer that p"=p~i n Li and Li in contrast with the results p"=(N/Z)p~deduced from earlier proton and electron work.

Plant polyphenols, such as hydrolysable tannins, are present in the human diet and known to exhibit anti-diabetic and anti-obesity activity. We previously reported that the representative hydrolysable tannin compound α-penta-galloyl-glucose (α-PGG) is a small molecule insulin mimetic that, like insulin, binds to insulin receptor (IR) and activates the IR-Akt-GLUT4 signaling pathway to trigger glucose transport and reduce blood glucose levels in db/db and ob/ob diabetic mice. However, its effects on adipogenesis and lipid metabolism were not known. In this study, high fat diet (HFD)-induced diabetic and obese mice were treated with α-PGG to determine its effects on blood glucose and triglycerides. 3T3-L1 preadipocytes were used as a cell model for identifying the anti-adipogenic activity of α-PGG at molecular and cellular levels as a first step in elucidating the mechanism of action of the compound. In vivo, oral administration of α-PGG significantly reduced levels of blood glucose, triglyceride, and insulin in HFD-induced diabetic/obese mice (P<0.05). In vitro, α-PGG inhibited the differentiation of 3T3-L1 preadipocytes into mature adipocytes. α-PGG suppressed the expression of positive adipogenic factors PPARγ C/EBPα and mTOR and augmented the negative adipogenic factor Pref-1. Furthermore, α-PGG induced upregulation of p21 and G1 phase cell cycle arrest. In contrast, adipogenic signaling pathways mediated by insulin, the cAMP response element binding protein (CREB) and glucocorticoid receptor (GR), were not inhibited. RNAi knockdown of p21 led to a 4-fold increase in triglyceride level in 3T3-L1 preadipocytes treated with MDI and α-PGG compared to regular preadipocytes. These results indicate, for the first time, that α-PGG is blood triglyceride- and glucose-lowering in HFD-induced obese and diabetic mice. It selectively inhibited some but not all major adipogenic pathways as well as the mTOR-p21-mediated cell cycle regulatory pathway. It is very likely that these apparently diverse but coordinated activities together inhibited adipogenesis. These results expand our knowledge on how PGG works in adipocytes and further confirm that α-PGG functions as an orally-deliverable natural insulin mimetic with adipogenetic modulatory functions.

We present zero-degree differential cross sections and transverse spin-transfer coefficients D NN (0°) for the 17,18 O(p ជ ,n ជ ) 17,18 F reactions at E p ϭ118 MeV. For the transition to the 17 F(g.s.) to which several multipoles contribute, the measured D NN (0°)ϭϪ0.13Ϯ0.05 is used to separate the Fermi and Gamow-Teller contributions at 0°. The empirical Gamow-Teller strengths and the Fermi strengths are employed to estimate the solar neutrino absorption cross section in 17 O and 18 O.