Optical properties of heavily doped GaAs nanowires and electroluminescent nanowire structures.

We present GaAs electroluminescent nanowire structures fabricated by metal organic vapor phase epitaxy. Electroluminescent structures were realized in both axial pn-junctions in single GaAs nanowires and free-standing nanowire arrays with a pn-junction formed between nanowires and substrate, respectively. The electroluminescence emission peak from single nanowire pn-junctions at 10 K was registered at an energy of around 1.32 eV and shifted to 1.4 eV with an increasing current. The line is attributed to the recombination in the compensated region present in the nanowire due to the memory effect of the vapor-liquid-solid growth mechanism. Arrayed nanowire electroluminescent structures with a pn-junction formed between nanowires and substrate demonstrated at 5 K a strong electroluminescence peak at 1.488 eV and two shoulder peaks at 1.455 and 1.519 eV. The main emission line was attributed to the recombination in the p-doped GaAs. The other two lines correspond to the tunneling-assisted photon emission and band-edge recombination in the abrupt junction, respectively. Electroluminescence spectra are compared with the micro-photoluminescence spectra taken along the single p-, n- and single nanowire pn-junctions to find the origin of the electroluminescence peaks, the distribution of doping species and the sharpness of the junctions.

Genetics of susceptibility for radiation-induced leukemia. Mapping of genes involved to chromosomes 1, 2, and 4, and implications for a viral etiology in the disease.

Susceptibility to radiation-induced leukemia in (A/J x B10)F2 mice is encoded for by genes in chromosomes 1, 2, and 4. The loci involved in chromosomes 1 and 4 are close to or similar to xenotropic virus inducibility locus on chromosome 1 and a locus-affecting expression of xenotropic MuLV envelope-related cell surface antigens. Radiation-induced leukemia-1 (Ril-1) on chromosome 2 plays an overriding influence in susceptibility to the disease. This locus might encode ecotropic viral-associated genetic information or might contain cellular sequences with oncogenic potential. These findings are of interest in view of the importance of recombinant viruses to leukemogenesis. Furthermore, it is intriguing that Ril-1 is located in a chromosomal site rich in thymus differentiation-specific loci. An explanation for tissue-specific activation of endogenous viruses is that activation of the virus in question is dependent on differentiation-specific steps.

Microplasma-based flowing atmospheric-pressure afterglow (FAPA) source for ambient desorption-ionization mass spectrometry.

A new direct-current microplasma-based flowing atmospheric pressure afterglow (FAPA) source was developed for use in ambient desorption-ionization mass spectrometry. The annular-shaped microplasma is formed in helium between two concentric stainless-steel capillaries that are separated by an alumina tube. Current-voltage characterization of the source shows that this version of the FAPA operates in the normal glow-discharge regime. A glass surface placed in the path of the helium afterglow reaches temperatures of up to approximately 400 °C; the temperature varies with distance from the source and helium flow rate through the source. Solid, liquid, and vapor samples were examined by means of a time-of-flight mass spectrometer. Results suggest that ionization occurs mainly through protonation, with only a small amount of fragmentation and adduct formation. The mass range of the source was shown to extend up to at least m/z 2722 for singly charged species. Limits of detection for several small organic molecules were in the sub-picomole range. Examination of competitive ionization revealed that signal suppression occurs only at high (mM) concentrations of competing substances.

Use of Interrupted Helium Flow in the Analysis of Vapor Samples with Flowing Atmospheric-Pressure Afterglow-Mass Spectrometry.

The flowing atmospheric-pressure afterglow (FAPA) source was used for the mass-spectrometric analysis of vapor samples introduced between the source and mass spectrometer inlet. Through interrupted operation of the plasma-supporting helium flow, helium consumption is greatly reduced and dynamic gas behavior occurs that was characterized by schlieren imaging. Moreover, mass spectra acquired immediately after the onset of helium flow exhibit a signal spike before declining and ultimately reaching a steady level. This initial signal appears to be due to greater interaction of sample vapor with the afterglow of the source when helium flow resumes. In part, the initial spike in signal can be attributed to a pooling of analyte vapor in the absence of helium flow from the source. Time-resolved schlieren imaging of the helium flow during on and off cycles provided insight into gas-flow patterns between the FAPA source and the MS inlet that were correlated with mass-spectral data. Graphical Abstract ᅟ.

Bilateral profound sudden sensorineural hearing loss presenting a diagnostic conundrum in a child with sickle cell anaemia.

OBJECTIVE: To present the first published case of a child with bilateral profound sudden sensorineural hearing loss found in association with sickle cell anaemia, and to demonstrate the importance of early recognition, investigation and empirical treatment of sudden sensorineural hearing loss. METHOD: Case report and review of world literature. CASE REPORT: The authors present the case of a seven-year-old child with known sickle cell anaemia, who presented with bilateral profound sensorineural hearing loss developing over a period of five days. There was a history of ophthalmological disease in the preceding weeks, and inflammatory markers were raised. The differential diagnosis included a vaso-occlusive or inflammatory aetiology such as Cogan's syndrome, and treatment for both was instigated. Hearing thresholds did not recover, and the patient underwent cochlear implantation 12 weeks later. CONCLUSION: Sudden sensorineural hearing loss has a variable aetiology and is rare in children. Immediate treatment for all possible aetiologies is essential, along with targeted investigations and early referral for cochlear implantation if no recovery is demonstrated.

A new lymphocyte cell surface antigen, Ly-22.2, controlled by a locus on chromosome 4 and a second unlinked locus.

A serum raised by immunizing (B10.A(4R) X B10.HTT)F1 mice against A.AL lymphocytes detects a new antigenic determinant designated Ly-22.2. Ly-22.2 expression is under the control of two independently segregating genes, one of which maps to chromosome 4 adjacent to a locus affecting XenCSA expression. Ly-22.2 is present in varying amounts in all lymphoid organs, but appears to be expressed primarily on T lymphocytes. Ly-22.2 is not detectable in brain, kidney, lung, liver, or erythrocytes. Strain distribution studies show Ly-22.2 is present in all strains examined except B10-derived congenic strains. It is of interest that C57BL/6 and C57BL/10 mice differ in the expression of this antigen.

Induction of leukemia by both fractionated x-irradiation and radiation leukemia virus involves loci in the chromosome 2 segment H-30-A.

A common link between the induction of leukemia by (i) fractionated doses of x-irradiation and (ii) radiation leukemia virus in mice may be established by the observation that the segment of chromosome 2 between the loci for the minor histocompatibility antigen H-30 and color coat agouti (H-30-A) includes distinct loci involved in susceptibility to leukemogenesis induced by factors i and ii.

Evidence for a major cluster of lymphocyte differentiation antigens on murine chromosome 2.

The region of chromosome 2 between H-13 and H-3 has been shown to contain loci coding for a variety of other alloantigens, including Ly-4 and the locus coding for beta 2-microglobulin. Herein we show that Ly-6 and Ly-11 are coded for by genes in a segment of chromosome 2 adjacent to the H-3-H-13 region and that this segment of chromosome also contains the tightly linked loci coding for antigens Ala-1, DAG, H9/25, H-30, Ly-8, and ThB. In addition, at least one locus (and probably more) affecting susceptibility to leukemia induction is found within this gene cluster.

Definition of a new T lymphocyte cell surface antigen, Ly 11.2.

The present communication defines a new cell surface antigen, Ly 11.2, which appears from its strain and tissue distribution to be distinct from all other previously defined normal or virally coded antigens or traits of the mouse. Lymphocytes of the T cell lineage, but not B cells or nonlymphoid cells, bear this marker. Although the locus coding for this antigen appears to be closely linked to the minor histocompatibility locus H-30 and to the locus coding for Ly 6.2, a chromosome assignment has not yet been made for my of these loci.

Functional properties of Ly 11.2 lymphocytes: a role for these cells in leukemia?

Functional studies of lymphocyte subpopulations reveal that Ly 11.2, a newly defined T cell surface antigen, is present on prothymocytes and natural killer cells, but not on suppressor T cells for antigen-specific IgE antibody responses, Ly 1+, 2-, 3- helper T cells nor on tumor-specific cytotoxic effector cells. Changes in the expression of Ly 11.2 regularly accompany leukemogenesis and are quite distinct from changes of other cell surface antigens thus far observed. After intrathymic inoculation of radiation leukemia virus (RadLV), many more Ly 11.2-positive cells are found expressing viral antigens than cells expressing other cell surface phenotypes. In addition, after RadLV inoculation, significantly more Ly 11.2-positive cells can be found in the thymus of susceptible mice than in the thymus of resistant mice. The greater availability of permissive (Ly 11.2-positive) cells in susceptible vs resistant hosts at the time when infectious virus is present may account for the shorter latency period and high leukemia incidence of susceptible vs resistant mice.

Association of endogenous viral loci with genes encoding murine histocompatibility and lymphocyte differentiation antigens.

Several polymorphic DNA restriction endonuclease fragments hybridizing with xenotropic and ecotropic envelope virus probes map adjacent to minor histocompatibility and lymphocyte (H/Ly) antigen-encoding loci. Viral DNA restriction fragments are associated with Ly-17 on chromosome 1, H-30, H-3, and H-13 on chromosome 2, Ly-21 on chromosome 7, H-28 on chromosome 3, and H-38 (chromosomal location as yet undetermined). In each case no recombinant can be found between the H/Ly locus in question and the virus-related restriction fragment, suggesting that linkage is very tight. Although some viral loci map to locations where no H/Ly has yet been mapped, the frequency and tightness of linkage in the seven instances described, coupled with the large number of as yet unmapped H/Ly loci, suggests that the associations found are significant.