Objective. Renal involvement in systemic lupus erythematosus (SLE) is associated with poor prognosis. Currently available renal biomarkers are relatively insensitive and nonspecific for diagnosing SLE nephritis. Previous research suggests that neutrophil gelatinaseassociated lipocalin (NGAL) is a high-quality renal biomarker of acute kidney injury, while its usefulness in SLE is unclear. We undertook this study to determine the relationship between urinary NGAL excretion and SLE disease activity or damage, with a focus on nephritis.Methods. A cohort of 35 patients diagnosed as having SLE prior to age 16 years (childhood-onset SLE) was assessed for disease activity (using the Systemic Lupus Erythematosus Disease Activity Index 2000 update) and damage (using the Systemic Lupus International Collaborating Clinics/American College of Rheumatology SLE Damage Index) in a double-blind, crosssectional study. Information on current markers of renal function and disease was obtained and compared with NGAL levels (ng/mg of urinary creatinine) measured by enzyme-linked immunosorbent assay. Eight children with juvenile idiopathic arthritis (JIA) served as controls.Results. NGAL levels did not differ with the age, weight, height, sex, or race of the patients. Patients with childhood-onset SLE had significantly higher NGAL levels than did those with JIA (P < 0.0001). NGAL levels were strongly to moderately correlated with renal disease activity and renal damage (Spearman's r > 0.47, P < 0.0001 for both comparisons), but not with extrarenal disease activity or extrarenal damage. NGAL levels of >0.6 ng/mg urinary creatinine were 90% sensitive and 100% specific for identifying childhood-onset SLE patients with biopsy-proven nephritis.Conclusion. Urinary NGAL is a promising potential biomarker of childhood-onset SLE nephritis. The results of the current study require validation in a larger cohort to more accurately delineate urinary NGAL excretion in relation to the diverse SLE phenotypes.Among the main determinants of poor prognosis of systemic lupus erythematosus (SLE) (1) is renal involvement, which is more frequently encountered in children than in adults with SLE. Currently available renal biomarkers (e.g., measures of the degree of SLE renal disease activity and severity) are too insensitive to allow for the early identification of patients with active SLE nephritis, prohibiting timely therapy to avoid permanent renal damage (2). Randomized clinical trials in SLE are hindered by the lack of high-quality biomarkers with which to verify the effects of therapies within a short period of time (3).

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Graphene‐based composites have received attention as part of the drive towards next‐generation electronic and energy‐storage technologies. However, current graphene synthesis methods are limited by complex, time‐consuming, toxic, costly, and/or often low‐yield procedures. The synthesis of a novel stretchable graphene‐polyurethane‐poly(3,4‐ethylenedioxythiophene):polystyrene sulfonate ink aimed at printing wearable electronics is reported. The procedure is based on low‐cost high‐yield production of high‐performance graphene ink produced by laser induction of polyimide film followed by harvesting the graphene. Screen printing is used to fabricate flexible and intrinsically stretchable micro‐supercapacitors (S‐MSCs) printed on different substrates. The resulting graphene‐based printed S‐MSCs display a remarkably high capacitive performance and attractive mechanical resiliency. High specific areal capacitance, above 23 mF cm−2, is achieved, which is the highest areal capacitance reported for highly stretchable, printed graphene supercapacitors. A repeated (200 cycles) stretchability beyond 100% is obtained while maintaining more than 85% of the S‐MSCs' original capacitance. This unique and highly scalable graphene ink synthesis method holds considerable promise for application in low‐cost graphene‐based chemical formulation, especially in the field of printed and wearable electronics toward multifunctional, energy‐storage systems capable of withstanding severe mechanical deformation while maintaining their optimal electrochemical performance.

Although it is accepted that the environment within the granuloma profoundly affects Mycobacterium tuberculosis (Mtb) and infection outcome, our ability to understand Mtb gene expression in these niches has been limited. We determined intragranulomatous gene expression in human-like lung lesions derived from nonhuman primates with both active tuberculosis (ATB) and latent TB infection (LTBI). We employed a non-laser-based approach to microdissect individual lung lesions and interrogate the global transcriptome of Mtb within granulomas. Mtb genes expressed in classical granulomas with central, caseous necrosis, as well as within the caseum itself, were identified and compared with other Mtb lesions in animals with ATB (n = 7) or LTBI (n = 7). Results were validated using both an oligonucleotide approach and RT-PCR on macaque samples and by using human TB samples. We detected approximately 2,900 and 1,850 statistically significant genes in ATB and LTBI lesions, respectively (linear models for microarray analysis, Bonferroni corrected, P < 0.05). Of these genes, the expression of approximately 1,300 (ATB) and 900 (LTBI) was positively induced. We identified the induction of key regulons and compared our results to genes previously determined to be required for Mtb growth. Our results indicate pathways that Mtb uses to ensure its survival in a highly stressful environment in vivo. A large number of genes is commonly expressed in granulomas with ATB and LTBI. In addition, the enhanced expression of the dormancy survival regulon was a key feature of lesions in animals with LTBI, stressing its importance in the persistence of Mtb during the chronic phase of infection.

Yeast Saccharomyces cerevisiae genes TIFI and TIF2 (translation initiation factor) encode a protein tentatively called translation initiation factor (Tif) due to the similarity of its amino acid sequence and its molecular weight to mammalian eukaryotic initiation factor 4A. To clarify whether Tif is involved in translation, we produced an affinitypurified anti-Tif antibody by using Tif isolated from a Tifoverproducing yeast strain as immunogen and an Escherichia coli strain expressing Tif from an expression vector to provide the extract for affinity purification of the antibody. By using chromatographic procedures and the affinity-purified anti-Tif antibody as probe to identify Tif-containing fractions, we purified Tif from wild-type yeast cells. When yeast cells containing the only TIF) gene on a plasmid under the control of the galactose-inducible CYCI-GALIO promoter were grown in medium containing glucose as the carbon source, the production of Tif was shut off and growth was arrested. Lysates made from these cells were inactive in in vitro translation.Addition of Tif to these lysates restored in vitro protein synthesis. These results show that Tif is a translation factor, the yeast homologue of mammalian translation initiation factor 4A.According to current models of translation initation in eukaryotes, initiation factors recognize and bind to the 5' terminal cap structure of mRNA and melt RNA secondary structure. Ribosomes then bind to or near the 5' end of the mRNA and reach the initiator AUG codon by scanning the mRNA in the 5' to 3' direction (for reviews, see refs.