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The electronic structure of a Ga-rich wide-gap CuIn0.1Ga0.9Se2thin-film solar cell absorber and its interface with a solution-grown CdS buffer layer were directly investigated by using a combination of X-ray and ultraviolet photoelectron spectroscopy with inverse photoemission spectroscopy. After a state-of-the-art RbF postdeposition treatment, we observe a small amount of Rb at the absorber surface, but no indication of a Rb-(In,Ga)-Se layer. The surface band gap of the absorber is determined to 1.79 ± 0.14 eV, which is approximately 0.2 eV larger than its optical bulk band gap. The special character of the Cu-poor and Rb-containing absorber surface highlights the need for a direct and all-experimental determination of the conduction band. For the CdS/CuIn0.1Ga0.9Se2interface, we find a significant cliff in the conduction band (−0.53 ± 0.15 eV), which we identify as a limiting factor for the performance of such Ga-rich wide-gap devices.

The mechanism by which chlorpropamide (CP) treatment promotes antidiuresis is unknown. CP competitively inhibited antidiuretic hormone (ADH) binding and adenylyl cyclase (AC) stimulation (inhibition constants KiandK′iof 2.8 mM and 250 μM, respectively) in the LLC-PK1cell line. CP (333 μM) increased the apparent Kaof ADH for AC activation (0.31 vs. 0.08 nM) without affecting a maximal response, suggesting competitive antagonism. Because CP lowers “basal” AC activity and the AC activation-ADH receptor occupancy relationship (A-O plots), it is an ADH inverse agonist. Twenty-four-hour CP exposure (100 μM) upregulated the ADH receptors without affecting affinity. This lowered Kaand increased basal AC activity and maximal response (1.86 vs. 1.35 and 14.9 vs. 10.6 fmol cAMP ⋅ min−1⋅ 103cells−1, n= 6, P< 0.05). NaCl, which potentiates ADH stimulation, also increased basal AC activity. This, together with the CP-ADH inverse agonism and increased basal AC activity at higher receptor density, unmasks constitutive receptor signaling. The CP-ADH inverse agonism explains receptor upregulation and predicts the need for residual ADH with functional isoreceptors for CP-mediated antidiuresis. This could be why CP ameliorates partial central diabetes insipidus but not nephrogenic diabetes insipidus.

Background:Urodilatin is a 32-amino-acid (AA) peptide formed in the kidney. Methods:High-performance gel permeation chromatography and high-pressure liquid chromatography evaluation of plasma followed by sensitive urodilatin and atrial natriuretic peptide (ANP) assays revealed that urodilatin does circulate distinctly from ANP. Results:Urodilatin circulates at very low levels (i.e 9–12 pg/ml). Infusion of ANP increased the circulating concentration of urodilatin 135-fold (p < 0.001), suggesting that some of the effects of ANP may be mediated by urodilatin while long-acting natriuretic peptide, vessel dilator, and kaliuretic peptide did not affect urodilatin in healthy humans (n = 30). Only ANP decreased the renal clearance of urodilatin (60–75%, p < 0.01). Urodilatin was metabolized into peptides smaller than 5 AAs as well as excreted intact into urine. Conclusion:Urodilatin circulates and is increased by ANP in humans.

The article discusses the tips for attaching the rein to the horse.

Focuses on the measures done by the National Education Association in the U.S. to reform flaws in the No Child Left Behind Act educational law. Protests to boost the annual salary of paraeducators; Development of workshops to prepare paraeducators in North Carolina for the state's para assessment examination ; Development of an assessment scheme for paraeducators in New Jersey.