C-band superconductor/semiconductor hybrid field-effect transistor amplifier on a LaAlO3 substrate

A single-stage C-band superconductor/semiconductor hybrid field-effect transistor amplifier was designed, fabricated, and tested at 77 K. The large area (1 inch x 0.5 inches) high temperature superconducting Tl-Ba-Ca-Cu-O (TBCCO) thin film was rf magnetron sputtered onto a LaAlO3 substrate. The film had a transition temperature of about 92 K after it was patterned and etched. The amplifier showed a gain of 6 dB and a 3 dB bandwidth of 100 MHz centered at 7.9 GHz. An identical gold amplifier circuit was tested at 77 K, and these results are compared with those from the hybrid amplifier

Fabrication and Analysis of Amorphous Silicon TFT

The display technology and large area electronics got momentum with the introduction of TFT devices. TFTs can be made using different semiconducting materials or organic conducting materials as the active layer. Each one of them differ in their performance depending on the material used for the active layer. In this paper, fabrication of amorphous silicon TFT using PECVD is carried out. Simulation of the a-Si: H TFT is also carried out with the dimensions similar to that of the masks used for the fabrication. The Id-Vd plot for both the simulation and fabrication is obtained and studied

Three-Dimensional Endoscopy-Assisted Excision and Reconstruction for Metastatic Disease of the Dorsal and Lumbar Spine: Early Results

BACKGROUND: The aim of this study was to explore the role of three-dimensional (3D) endoscopy in surgical management of metastatic disease of the dorsal and lumbar spine. METHODS: This is a prospective study on 33 patients (15 men and 18 women, mean age of 61.6 ± 8.9 years) with biopsy-proven metastatic disease of the spine managed by sequential/staged posterior decompression-stabilization, followed by 3D endoscopy-assisted anterior corpectomy and stabilization with a mesh cage. All patients had significant extradural compression or spinal instability or both. Sixteen patients had neurological deficits. Visual analog scale (VAS), Frenkel grade (neurological deficits), Karnofsky performance status scale, and the 36-item short-form health survey (SF-36) were used for assessment preoperatively and at 3, 6, and 12 months from surgery. RESULTS: At a mean follow-up of 1.7 ± 0.7 years from surgery, 18 patients were alive. VAS showed significant improvement at the latest follow-up compared to preoperative levels (4.39 vs. 6.61, p = 0.001). Karnofsky status did not show any significant improvement. Frenkel grade improved in 5 patients, deteriorated in 4 patients, and remained unchanged in 24 patients. Regarding SF-36 parameters, general health showed deterioration, but role functioning—physical, role functioning—emotional, social functioning, and body pain showed statistically significant improvement. There was no change in physical health, viability, and mental health. Subjectively the surgeons felt better depth perception and smoother surgical experience with the 3D optics technology. The only complication was delayed wound healing in three patients who had a previous history of radiotherapy to the surgical site. CONCLUSIONS: 3D endoscopy is a valuable tool in the management of metastatic spinal disease requiring excision and reconstruction using the combined posterior and anterior approaches. These early results warrant confirmation with more data and longer follow-ups

Socioeconomic Inequalities in Childhood Undernutrition in India: Analyzing Trends between 1992 and 2005

India experienced a rapid economic boom between 1991 and 2007. However, this economic growth has not translated into improved nutritional status among young Indian children. Additionally, no study has assessed the trends in social disparities in childhood undernutrition in the Indian context. We examined the trends in social disparities in underweight and stunting among Indian children aged less than three years using nationally representative data.We analyzed data from the three cross-sectional rounds of National Family Health Survey of India from 1992, 1998 and 2005. The social factors of interest were: household wealth, maternal education, caste, and urban residence. Using multilevel modeling to account for the nested structure and clustering of data, we fit multivariable logistic regression models to quantify the association between the social factors and the binary outcome variables. The final models additionally included age, gender, birth order of child, religion, and age of mother. We analyzed the trend by testing for interaction of the social factor and survey year in a dataset pooled from all three surveys.While the overall prevalence rates of undernutrition among Indian children less than three decreased over the 1992-2005 period, social disparities in undernutrition over these 14 years either widened or stayed the same. The absolute rates of undernutrition decreased for everyone regardless of their social status. The disparities by household wealth were greater than the disparities by maternal education. There were no disparities in undernutrition by caste, gender or rural residence.There was a steady decrease in the rates of stunting in the 1992-2005 period, while the decline in underweight was greater between 1992 and 1998 than between 1998 and 2005. Social disparities in childhood undernutrition in India either widened or stayed the same during a time of major economic growth. While the advantages of economic growth might be reaching everyone, children from better-off households, with better educated mothers appear to have benefited to a greater extent than less privileged children. The high rates of undernutrition (even among the socially advantaged groups) and the persistent social disparities need to be addressed in an urgent and comprehensive manner

Patterning in Birthweight in India: Analysis of Maternal Recall and Health Card Data

National data on birthweight from birth certificates or medical records are not available in India. The third Indian National Family Health Survey included data on birthweight of children obtained from health cards and maternal recall. This study aims to describe the population that these data represent and compares the birthweight obtained from health cards with maternal recall data in terms of its socioeconomic patterning and as a risk factor for childhood growth failure.The analytic sample consisted of children aged 0 to 59 months with birthweight data obtained from health cards (n = 3227) and maternal recall (n = 16,787). The difference between the card sample and the maternal recall sample in the distribution across household wealth, parental education, caste, religion, gender, and urban residence was compared using multilevel models. We also assessed the ability of birthweight to predict growth failure in infancy and childhood in the two groups. The survey contains birthweight data from a majority of household wealth categories (>5% in every category for recall), both genders, all age groups, all caste groups, all religion groups, and urban and rural dwellers. However, children from the lowest quintile of household wealth were under-represented (4.73% in card and 8.62% in recall samples). Comparison of data across health cards and maternal recall revealed similar social patterning of low birthweight and ability of birthweight to predict growth failure later in life. Children were less likely to be born with low birthweight if they had mothers with over 12 years of education compared to 1-5 years of education with relative risk (RR) of 0.79 (95% confidence interval [CI]: 0.52, 1.2) in the card sample and 0.70 (95% CI: 0.59, 0.84) in the recall sample. A 100 gram difference in a child's birthweight was associated with a decreased likelihood of underweight in both the card (RR: 0.95; 95% CI: 0.94, 0.96) and recall (RR: 0.96; 95% CI: 0.96, 0.97) samples.Our results suggest that in the absence of other sources, the data on birthweight in the third Indian National Family Health Survey is valuable for epidemiologic research

Alteration of Proteins and Pigments Influence the Function of Photosystem I under Iron Deficiency from Chlamydomonas reinhardtii

BACKGROUND: Iron is an essential micronutrient for all organisms because it is a component of enzyme cofactors that catalyze redox reactions in fundamental metabolic processes. Even though iron is abundant on earth, it is often present in the insoluble ferric [Fe (III)] state, leaving many surface environments Fe-limited. The haploid green alga Chlamydomonas reinhardtii is used as a model organism for studying eukaryotic photosynthesis. This study explores structural and functional changes in PSI-LHCI supercomplexes under Fe deficiency as the eukaryotic photosynthetic apparatus adapts to Fe deficiency. RESULTS: 77K emission spectra and sucrose density gradient data show that PSI and LHCI subunits are affected under iron deficiency conditions. The visible circular dichroism (CD) spectra associated with strongly-coupled chlorophyll dimers increases in intensity. The change in CD signals of pigments originates from the modification of interactions between pigment molecules. Evidence from sucrose gradients and non-denaturing (green) gels indicates that PSI-LHCI levels were reduced after cells were grown for 72 h in Fe-deficient medium. Ultrafast fluorescence spectroscopy suggests that red-shifted pigments in the PSI-LHCI antenna were lost during Fe stress. Further, denaturing gel electrophoresis and immunoblot analysis reveals that levels of the PSI subunits PsaC and PsaD decreased, while PsaE was completely absent after Fe stress. The light harvesting complexes were also susceptible to iron deficiency, with Lhca1 and Lhca9 showing the most dramatic decreases. These changes in the number and composition of PSI-LHCI supercomplexes may be caused by reactive oxygen species, which increase under Fe deficiency conditions. CONCLUSIONS: Fe deficiency induces rapid reduction of the levels of photosynthetic pigments due to a decrease in chlorophyll synthesis. Chlorophyll is important not only as a light-harvesting pigment, but also has a structural role, particularly in the pigment-rich LHCI subunits. The reduced level of chlorophyll molecules inhibits the formation of large PSI-LHCI supercomplexes, further decreasing the photosynthetic efficiency

Substrate Binding Mode and Its Implication on Drug Design for Botulinum Neurotoxin A

The seven antigenically distinct serotypes of Clostridium botulinum neurotoxins, the causative agents of botulism, block the neurotransmitter release by specifically cleaving one of the three SNARE proteins and induce flaccid paralysis. The Centers for Disease Control and Prevention (CDC) has declared them as Category A biowarfare agents. The most potent among them, botulinum neurotoxin type A (BoNT/A), cleaves its substrate synaptosome-associated protein of 25 kDa (SNAP-25). An efficient drug for botulism can be developed only with the knowledge of interactions between the substrate and enzyme at the active site. Here, we report the crystal structures of the catalytic domain of BoNT/A with its uncleavable SNAP-25 peptide 197QRATKM202 and its variant 197RRATKM202 to 1.5 Å and 1.6 Å, respectively. This is the first time the structure of an uncleavable substrate bound to an active botulinum neurotoxin is reported and it has helped in unequivocally defining S1 to S5′ sites. These substrate peptides make interactions with the enzyme predominantly by the residues from 160, 200, 250 and 370 loops. Most notably, the amino nitrogen and carbonyl oxygen of P1 residue (Gln197) chelate the zinc ion and replace the nucleophilic water. The P1′-Arg198, occupies the S1′ site formed by Arg363, Thr220, Asp370, Thr215, Ile161, Phe163 and Phe194. The S2′ subsite is formed by Arg363, Asn368 and Asp370, while S3′ subsite is formed by Tyr251, Leu256, Val258, Tyr366, Phe369 and Asn388. P4′-Lys201 makes hydrogen bond with Gln162. P5′-Met202 binds in the hydrophobic pocket formed by the residues from the 250 and 200 loop. Knowledge of interactions between the enzyme and substrate peptide from these complex structures should form the basis for design of potent inhibitors for this neurotoxin