Measurement of the νμ charged current quasielastic cross section on carbon with the T2K on-axis neutrino beam

We report a measurement of the νµ charged current quasi-elastic cross-sections on carbon in the T2K on-axis neutrino beam. The measured charged current quasi-elastic cross-sections on carbon at mean neutrino energies of 1.94 GeV and 0.93 GeV are (11.95 ± 0.19(stat.) +1.82−1.47(syst.)) ×10^−39 cm^2/neutron, and (10.64 ± 0.37(stat.)+2.03−1.65(syst.)) × 10^−39 cm^2/neutron, respectively. These results agree well with the predictions of neutrino interaction models. In addition, we investigated the effects of the nuclear model and the multi-nucleon interaction.

Triple-junction solar cell performance under Fresnel-based concentrators taking into account chromatic aberration and off-axis operation

Concentration photovoltaic (CPV) systems might produce quite uneven irradiance distributions (both on their level and on their spectral distribution) on the solar cell. This effect can be even more evident when the CPV system is slightly off-axis, since they are often designed to assure good uniformity only at normal incidence. The non-uniformities both in absolute irradiance and spectral content produced by the CPV systems, can originate electrical losses in multi-junction solar cells (MJSC). This works is focused on the integration of ray-tracing methods for simulating the irradiance and spectrum maps produced by different optic systems throughout the solar cell surface, with a 3D fully distributed circuit model which simulates the electrical behavior of a state-of-the-art triple-junction solar cell under the different light distributions obtained with ray-tracing. In this study four different CPV system (SILO, XTP, RTP, and FK) comprising Fresnel lenses concentrating sunlight onto the same solar cell are modeled when working on-axis and 0.6 degrees off-axis. In this study the impact of non-uniformities on a CPV system behavior is revealed. The FK outperforms other Fresnel-based CPV systems in both on-axis and off-axis conditions.

Field experiment of 800× off-axis XR-Köhler concentrator module on a carousel tracker

This paper presents the design and preliminary experimental results of a concentrator-type photovoltaic module based on a free-form off-axis 800×XR-Köhler concentrator. The off-axis XR-Köhler concentrator is one of the advanced concentrators that perform high concentration with a large acceptance angle and excellent irradiance uniformity on a solar cell. As a result of on-sun characterization of the unglazed single-cell unit test rig, the temperature-corrected DC module efficiency was 32.2% at 25 °C without an anti-reflective (AR) coating on the secondary optics, and the acceptance angle was more than ±1.0°. In addition, the non-corrected DC efficiency of an individual cell in a glazed 8-cell unit module mounted on a carousel tracking system was measured. The individual efficiency deviated in the range of 24.3-27.4%, owing to the mirror shape and alignment errors. The resultant series-connected efficiency was approximately 25% at direct normal irradiation (DNI) of 770 W/m2.

RB-mediated suppression of spontaneous multiple neuroendocrine neoplasia and lung metastases in Rb+/− mice

Alterations in pathways mediated by retinoblastoma susceptibility gene (RB) product are among the most common in human cancer. Mice with a single copy of the Rb gene are shown to develop a syndrome of multiple neuroendocrine neoplasia. The earliest Rb-deficient atypical cells were identified in the intermediate and anterior lobes of the pituitary, the thyroid and parathyroid glands, and the adrenal medulla within the first 3 months of postnatal development. These cells form gross tumors with various degrees of malignancy by postnatal day 350. By age of 380 days, 84% of Rb+/− mice exhibited lung metastases from C-cell thyroid carcinomas. Expression of a human RB transgene in the Rb+/− mice suppressed carcinogenesis in all tissues studied. Of particular clinical relevance, the frequency of lung metastases also was reduced to 12% in Rb+/− mice by repeated i.v. administration of lipid-entrapped, polycation-condensed RB complementary DNA. Thus, in spite of long latency periods during which secondary alterations can accumulate, the initial loss of Rb function remains essential for tumor progression in multiple types of neuroendocrine cells. Restoration of RB function in humans may prove an effective general approach to the treatment of RB-deficient disseminated tumors.

Galanin regulates prolactin release and lactotroph proliferation

The neuropeptide galanin is predominantly expressed by the lactotrophs (the prolactin secreting cell type) in the rodent anterior pituitary and in the median eminence and paraventricular nucleus of the hypothalamus. Prolactin and galanin colocalize in the same secretory granule, the expression of both proteins is extremely sensitive to the estrogen status of the animal. The administration of estradiol-17β induces pituitary hyperplasia followed by adenoma formation and causes a 3,000-fold increase in the galanin mRNA content of the lactotroph. To further study the role of galanin in prolactin release and lactotroph growth we now report the generation of mice carrying a loss-of-function mutation of the endogenous galanin gene. There is no evidence of embryonic lethality and the mutant mice grow normally. The specific endocrine abnormalities identified to date, relate to the expression of prolactin. Pituitary prolactin message levels and protein content of adult female mutant mice are reduced by 30–40% compared with wild-type controls. Mutant females fail to lactate and pups die of starvation/dehydration unless fostered onto wild-type mothers. Prolactin secretion in mutant females is markedly reduced at 7 days postpartum compared with wild-type controls with an associated failure in mammary gland maturation. There is an almost complete abrogation of the proliferative response of the lactotroph to high doses of estrogen, with a failure to up-regulate prolactin release, STAT5 expression or to increase pituitary cell number. These data further support the hypothesis that galanin acts as a paracrine regulator of prolactin expression and as a growth factor to the lactotroph.

Steroid disorders in children: Congenital adrenal hyperplasia and apparent mineralocorticoid excess

Our research team and laboratories have concentrated on two inherited endocrine disorders, congenital adrenal hyperplasia (CAH) and apparent mineralocorticoid excess, in thier investigations of the pathophysiology of adrenal steroid hormone disorders in children. CAH refers to a family of inherited disorders in which defects occur in one of the enzymatic steps required to synthesize cortisol from cholesterol in the adrenal gland. Because of the impaired cortisol secretion, adrenocorticotropic hormone levels rise due to impairment of a negative feedback system, which results in hyperplasia of the adrenal cortex. The majority of cases is due to 21-hydroxylase deficiency (21-OHD). Owing to the blocked enzymatic step, cortisol precursors accumulate in excess and are converted to potent androgens, which are secreted and cause in utero virilization of the affected female fetus genitalia in the classical form of CAH. A mild form of the 21-OHD, termed nonclassical 21-OHD, is the most common autosomal recessive disorder in humans, and occurs in 1/27 Ashkenazic Jews. Mutations in the CYP21 gene have been identified that cause both classical and nonclassical CAH. Apparent mineralocorticoid excess is a potentially fatal genetic disorder causing severe juvenile hypertension, pre- and postnatal growth failure, and low to undetectable levels of potassium, renin, and aldosterone. It is caused by autosomal recessive mutations in the HSD11B2 gene, which result in a deficiency of 11β-hydroxysteroid dehydrogenase type 2. In 1998, we reported a mild form of this disease, which may represent an important cause of low-renin hypertension.