Excess corticotropin releasing hormone-binding protein in the hypothalamic-pituitary-adrenal axis in transgenic mice

Corticotropin-releasing hormone (CRH) is the primary hypothalamic releasing factor that mediates the mammalian stress response. The CRH-binding protein (CRH-BP) is secreted from corticotropes, the pituitary CRH target cells, suggesting that the CRH-BP may modulate hypothalamic-pituitary-adrenal (HPA) axis activity by preventing CRH receptor stimulation. Transgenic mice were generated that constitutively express elevated levels of CRH-BP in the anterior pituitary gland. RNA and protein analyses confirmed the elevation of pituitary CRH-BP. Basal plasma concentrations of corticosterone and adrenocorticotropin hormone (ACTH) are unchanged, and a normal pattern of increased corticosterone and ACTH was observed after restraint stress. However, CRH and vasopressin (AVP) mRNA levels in the transgenic mice are increased by 82 and 35%, respectively, to compensate for the excess CRH-BP, consistent with the idea that CRH-BP levels are important for homeostasis. The transgenic mice exhibit increased activity in standard behavioral tests, and an altered circadian pattern of food intake which may be due to transgene expression in the brain. Alterations in CRH and AVP in response to elevated pituitary CRH-BP clearly demonstrate that regulation of CRH-BP is important in the function of the HPA axis.     

Reverse-engineering someone else's software: is it legal?

The author covers the legal issues of reverse-engineering someone else's software, explaining what reverse-engineering activities the courts have found to be acceptable and what legal applications are for the knowledge you gained from reverse engineering. She also defines `reverse engineering' and presents two theories regarding its use: the strict-constructionist theory, which holds that reverse-engineering copyrighted software is always illegal, and the pragmatist theory, which takes a much more liberal view of the fair-use privilege     

Erratum to: In situ observation of synthesized nanoparticles in ultra-dilute aerosols via X-ray scattering

Nano Research - The article In situ observation of synthesized nanoparticles in ultradilute aerosols via X-ray scattering, written by Sarah R. McKibbin, Sofie Yngman, Olivier Balmes, Bengt O....     

Electron beam pre-patterning for site-control of self-assembled InAs quantum dots on Inp surfaces

A site control technique for individual InAs quantum dots (QDs) formed by self-assembling has been developed, using scanning electron microscope (SEM) assisted nano-deposition and metal organic vapor phase epitaxy (MOVPE). In a first step we characterize a device with randomly distributed InAs QDs on InP, using resonant tunneling and transmission electron microscopy (TEM). Secondly, we use nano-scale deposits, created at the focal point of the electron beam on an InP based heterostructure, as “nano growth masks”. Growth of a thin InP layer produces nano-holes above the deposits. The deposits are removed by oxygen plasma etching. When InAs is supplied on this surface, QDs are self-assembled at the hole sites, while no InAs dots are observed in the flat surface region. A vertical single electron tunneling device is proposed, using the developed technique.     

Vertical Enhancement-Mode InAs Nanowire Field-Effect Transistor With 50-nm Wrap Gate

We present results on fabrication and dc characterization of vertical InAs nanowire wrap-gate field-effect transistor arrays with a gate length of 50 nm. The wrap gate is defined by evaporation of 50-nm Cr onto a 10-nm-thick HfO₂ gate dielectric, where the gate is also separated from the source contact with a 100-nm SiO_x, spacer layer. For a drain voltage of 0.5 V, we observe a normalized transconductance of 0.5 S/mm, a subthreshold slope around 90 mV/dec, and a threshold voltage just above 0 V. The highest observed normalized on current is 0.2 A/mm, with an off current of 0.2 mA/mm. These devices show a considerable improvement compared to previously reported vertical InAs devices with SiN_x, gate dielectrics.     

Nanowire single-electron memory

We demonstrate storage of electrons in semiconductor nanowires epitaxially grown from Au nanoparticles. The nanowires contain multiple tunnel junctions (MTJs) of InP barriers and InAs quantum dots designed such that the metal seed particles act as storage nodes. By positioning a second nanowire close to the seed particle it is possible to detect tunneling of individual electrons through the MTJ at 4.2 K. A strong memory effect is observed in the detector current when sweeping the writing voltage.     

Direct imaging of the atomic structure inside a nanowire by scanning tunnelling microscopy

Semiconductor nanowires are expected to be important components in future nano-electronics and photonics. Already a wide range of applications has been realized, such as high-performance field-effect transistors, bio/chemical sensors, diode logics and single-nanowire lasers. As nanowires have small cross-sections and large surface-to-bulk ratios, their properties can be significantly influenced by individual atomic-scale structural features, and they can have properties or even atomic arrangements with no bulk counterparts. Hence, experimental methods capable of directly addressing the atomic-scale structure of nanowires are highly desirable. One such method is scanning tunnelling microscopy (STM), which, by direct imaging of the atomic and electronic structure of surfaces has revolutionized the perception of nanoscale objects and low-dimensional systems. Here we demonstrate how combining STM with an embedding scheme allows us to image the interior of semiconductor nanowires with atomic resolution. Defect structures such as planar twin segments and single-atom impurities are imaged inside a GaAs nanowire. Further, we image an intriguing GaAs nanowire that is separated into two distinct nanocrystallites along the growth direction of the wire.     

Involvement of p21racA, phosphoinositide 3-kinase, and vacuolar ATPase in phagocytosis of bacteria and erythrocytes by Entamoeba histolytica: suggestive evidence for coincidental evolution of amebic invasiveness

Trophozoites of Entamoeba histolytica, the protozoan parasite that causes amebic dysentery, phagocytose bacteria in the colonic lumen and erythrocytes (RBC) in host tissues. Because tissue invasion is an evolutionary dead end, it is likely that amebic pathogenicity is coincidentally selected, i.e., the same methods used to kill bacteria in the colonic lumen are used by parasites to damage host cells and cause disease. In support of this idea, the amebic lectin and pore-forming peptide are involved in binding and killing, respectively, bacteria and host epithelial cells. Here amebic phagocytosis of bacteria, RBC, and mucin-coated beads was disrupted by overexpression of E. histolytica p21(racA-V12), a ras-family protein involved in selection of sites of actin polymerization, which had been mutated to eliminate its GTPase activity. p21(racA-V12) transformants were also defective in capping and cytokinesis, while pinocytosis of fluorescent dextrans was not affected. Wortmannin, a fungal inhibitor of phosphoinositide 3-kinase, markedly inhibited phagocytosis of bacteria, RBC, and mucin-coated beads by wild-type amebae. In contrast to p21(racA-V12) overexpression, wortmannin abolished amebic pinocytosis of dextrans but had no inhibitory effects on capping. Inhibition of amebic vacuolar acidification by bafilomycin also decreased bacterial and RBC uptake. These results, which demonstrate similarities between mechanisms of phagocytosis of bacteria and RBC by amebae and macrophages, support the idea of coincidental selection of amebic genes encoding proteins that mediate destruction of host cells.     

Ultrastructural, physiological, and molecular defects in the inner ear of a gene-knockout mouse model for autosomal Alport syndrome

It is well documented that damage to the chick cochlea caused by acoustic overstimulation or ototoxic drugs is reversible. Second-order auditory neurons in nucleus magnocellularis (NM) are sensitive to changes in input from the cochlea. However, few experiments studying changes in NM during cochlear hair cell loss and regeneration have been reported. Chicks were given a single systemic dose of gentamicin, which results in maximal hair cell loss in the base of the cochlea after 5 days. Many new hair cells are present by 9 days. These new hair cells are mature but not completely recovered in organization by 70 days. We counted neurons in Nissl-stained sections of the brainstem within specific tonotopic regions of NM, comparing absolute cell number between gentamicin- and saline-treated animals at both short and long survival times. Our data suggest that neuronal number in rostral NM parallels hair cell number in the base of the cochlea. That is, after a single dose of gentamicin, we see a loss of both cochlear hair cells and NM neurons early, followed by a recovery of both cochlear hair cells and NM neurons later. These results suggest that neurons, like cochlear hair cells, can recover following gentamicin-induced damage.