Through an organometallic approach, ultrathin SnO(x)Fe(y)S(z) plates with ∼2 nm single layer-thicknesses were obtained and their graphene composites showed very promising discharge capacities of up to 736 mA h g(-1) and excellent stabilities as anode materials in lithium ion batteries.

PURPOSE: MicroRNA plays an important role in human diseases and cancer. We seek to investigate the expression status, clinical relevance, and functional role of microRNA in non-small cell lung cancer. EXPERIMENTAL DESIGN: We performed miRNA expression profiling in matched lung adenocarcinoma and uninvolved lung using 56 pairs of fresh-frozen (FF) and 47 pairs of formalin-fixed, paraffin-embedded (FFPE) samples from never smokers. The most differentially expressed miRNA genes were evaluated by Cox analysis and Log-Rank test. Among the best candidate, miR-708 was further examined for differential expression in two independent cohorts. Functional significance of miR-708 expression in lung cancer was examined by identifying its candidate mRNA target and through manipulating its expression levels in cultured cells.RESULTS: Among the 20 miRNAs most differentially expressed between tested tumor and normal samples, high expression level of miR-708 in the tumors was most strongly associated with an increased risk of death after adjustments for all clinically significant factors including age, sex, and tumor stage (FF cohort: HR, 1.90; 95% CI, 1.08-3.35; P=.025 and FFPE cohort: HR, 1.93; 95% CI, 1.02-3.63; P=.042). The transcript for TMEM88 gene has a miR-708 binding site in its 3' UTR and was significantly reduced in tumors high of miR-708. Forced miR-708 expression reduced TMEM88 transcript levels and increased the rate of cell proliferation, invasion, and migration in culture. CONCLUSIONS: MicroRNA-708 acts as an oncogene contributing to tumor growth and disease progression by directly down regulating TMEM88, a negative regulator of the Wnt signaling pathway in lung cancer.

Context:Femoral shaft cortical thickening has been mentioned in reports of atypical subtrochanteric and diaphyseal (S/D) femur fractures, but it is unclear whether thickening precedes fracture or results from a preceding stress fracture and what role bisphosphonates might play in cortical thickening.Objective:Our objective was to examine the relationship of cortical thickness to S/D fracture risk as well as establish normal reference values for femoral cortical thickness in a large population-based cohort of older women.Design:Using pelvic radiographs obtained in 1986-1988, we measured femoral shaft cortical thickness 3 cm below the lesser trochanter in women in the Study of Osteoporotic Fractures. We measured this in a random sample and in those with S/D fractures and femoral neck and intertrochanteric fractures. Low-energy S/D fractures were identified from review of radiographic reports obtained between 1986 and 2010. Radiographs to evaluate atypia were not available. Analysis used case-cohort, proportional hazards models.Outcomes:Cortical thickness as a risk factor for low-energy S/D femur fractures as well as femoral neck and intertrochanteric fractures in the Study of Osteoporotic Fractures, adjusting for age and bone mineral density in proportional hazards models.Results:After age adjustment, women with thinner medial cortices were at a higher risk of S/D femur fracture, with a relative hazard of 3.94 (95% confidence interval = 1.23-12.6) in the lowest vs. highest quartile. Similar hazard ratios were seen for femoral neck and intertrochanteric fractures. Medial or total cortical thickness was more strongly related to fracture risk than lateral cortical thickness.Conclusions:In primarily bisphosphonate-naive women, we found no evidence that thick femoral cortices placed women at higher risk for low-energy S/D femur fractures; in fact, the opposite was true. Women with thin cortices were also at a higher risk for femoral neck and intertrochanteric fractures. Whether cortical thickness among bisphosphonate users plays a role in atypical S/D fractures remains to be determined.

Mitochondrial dysfunction is a hallmark of beta-amyloid (Aβ)-induced neurotoxicity in Alzheimer's disease (AD), and is considered an early event in AD pathology. Diammonium glycyrrhizinate (DG), the salt form of Glycyrrhizin, is known for its anti-inflammatory effects, resistance to biologic oxidation and membranous protection. In the present study, the neuroprotective effects of DG on Aβ(1-42)-induced toxicity and its potential mechanisms in primary cortical neurons were investigated. Exposure of neurons to 2 µM Aβ(1-42) resulted in significant viability loss and cell apoptosis. Accumulation of reactive oxygen species (ROS), decreased mitochondrial membrane potential, and activation of caspase-9 and caspase-3 were also observed after Aβ(1-42) exposure. All these effects induced by Aβ(1-42) were markedly reversed by DG treatment. In addition, DG could alleviate lipid peroxidation and partially restore the mitochondrial function in Aβ(1-42)-induced AD mice. DG also significantly increased the PGC-1α expression in vivo and in vitro, while knocking down PGC-1α partially blocked the protective effects, which indicated that PGC-1α contributed to the neuroprotective effects of DG. Furthermore, DG significantly decreased the escape latency and search distance and increased the target crossing times of Aβ(1-42)-induced AD mice in the Morris water maze test. Therefore, these results demonstrated that DG could attenuate Aβ(1-42)-induced neuronal injury by preventing mitochondrial dysfunction and oxidative stress and improved cognitive impairment in Aβ(1-42)-induced AD mice, indicating that DG exerted potential beneficial effects on AD.

AMP activated protein kinase (AMPK) is an energy sensing enzyme central to the regulation of metabolic homeostasis. In the heart, AMPK is activated during cardiac stress induced ATP depletion and functions to stimulate metabolic pathways that restore the AMP/ATP balance. Recently it was demonstrated that AMPK phosphorylates cardiac troponin I (cTnI) at Ser-150 in vitro. We sought to determine if the metabolic regulatory kinase AMPK phosphorylates cTnI at Ser-150 in vivo to alter cardiac contractile efficiency directly at the level of the myofilament. Rabbit cardiac myofibrils separated by two dimensional isoelectric focusing subjected to Western blot with a cTnI phosphorylation specific antibody demonstrates that cTnI is endogenously phosphorylated at Ser-150 in the heart. Treatment of myofibrils with the AMPK holoenzyme increased cTnI Ser-150 phosphorylation within the constraints of the muscle lattice. Compared to controls, cardiac fiber bundles exchanged with troponin containing cTnI pseudo-phosphorylated at Ser-150 demonstrate increased sensitivity of calcium dependent force development, blunting of both PKA dependent calcium desensitization and PKA dependent increases in length dependent activation. Thus, in addition to the defined role of AMPK as a cardiac metabolic energy gauge, these data demonstrate AMPK Ser-150 phosphorylation of cTnI directly links the regulation of cardiac metabolic demand to myofilament contractile energetics. Furthermore, the blunting effect of cTnI Ser-150 phosphorylation crosstalk can uncouple effects of myofilament PKA dependent phosphorylation from β-adrenergic signaling as a novel thin filament contractile regulatory signaling mechanism.

We investigate in this study the approach of small bowel delineation that would best correlate with acute lower GI toxicity during adjuvant intensity-modulated radiation therapy (IMRT) for endometrial cancer in this study. Thirty-two endometrial cancer patients (FIGO IB-IVA) were treated with postoperative pelvic IMRT to 48.2 6 3.1 Gy. The small bowel was delineated as separate loops, limited bowel space (BS), or an intestinal cavity (IC). The volume of the small bowel (VSB) in absolute volume or as the percentage of the total volume at various dose levels was obtained from the dose volume histograms (DVHs). Each patient's acute lower gastro-intestinal (GI) toxicity was assessed prospectively during the course of IMRT. After a median follow up of 19.6 months, the median survival, loco-regional control, progression-free-survival (PFS), and distant metastasis-free survival (DMFS) were 40.9 months, 81.2%, 62.5%, and 68.8%, respectively. Acute lower GI toxicity observed were of grade 0, 1, and 2 only: 34.4%, 31.2%, and 34.4%, respectively. The difference in %VSB with the small bowel delineated as IC at 45 Gy (%VSB(IC45)) between grade 2 and grade 0 acute lower GI toxicity reached statistical significance upon linear regression analysis ( p = 0.0347). Thus, the proportion of small bowel contoured as IC in the high dose region can potentially be an important predictor for acute lower GI toxicity during and after postoperative pelvic IMRT.

We demonstrate the conditional detection of time-bin qubits after storage in and retrieval from a photon-echo-based waveguide quantum memory. Each qubit is encoded into one member of a photon pair produced via spontaneous parametric down-conversion, and the conditioning is achieved by the detection of the other member of the pair. By performing projection measurements with the stored and retrieved photons onto different bases, we obtain an average storage fidelity of 0.885±0.020, which exceeds the relevant classical bounds and shows the suitability of our integrated light-matter interface for future applications of quantum information processing.

BACKGROUND The diagnosis of tuberculosis remains difficult. This study aimed to assess performance of interferon-gamma release assay (IGRA) in diagnosis of active tuberculosis (ATB) with pulmonary and extrapulmonary involvements, and to determine the diagnostic role of IGRA (T-SPOT.TB) and tuberculin skin test (TST) in BCG-vaccinated population. METHODS AND FINDINGS Two hundred twenty-six ATB suspects were recruited and examined with T-SPOT.TB. Among them, fifty-two and seventy-six subjects were simultaneously tested by TST with 5TU or 1TU of purified protein derivative (PPD). The sensitivity of T-SPOT.TB was 94.7%(71/75), comparable in pulmonary and extrapulmonary disease groups (95.6% vs. 93.3%, P>0.05), while the specificity was 84.10%(90/107) but differed in two groups (69.2% vs. 88.9%, P = 0.02). Compared to T-SPOT.TB, TST with 5TU-PPD showed less sensitivity (92.3% vs. 56.4%) and specificity (84.6% vs. 61.5%)(both P<0.01); the sensitivity of TST with 1TU-PPD was 27.8%, and despite its specificity identical to T-SPOT.TB (both 82.8%) positive predictive value (PPV) was only 33.3%. By combining T-SPOT.TB with TST (1TU), the specificity rose to 95%, but the PPV stayed unchanged. CONCLUSIONS IGRA could function as a powerful immunodiagnostic test to explore pulmonary and extrapulmonary TB, while TST failed to play a reliable or auxiliary role in identifying TB disease and infection in the BCG-vaccinated population.

The aim of this study was to investigate whether some biomarkers could predict cognitive impairment after stroke. One hundred fifty-two first-ever stroke patients were recruited within 6-72 h after the onset of symptoms. Blood was drawn within 1 h after admission for determining biomarkers. Cognitive function was assayed 2 weeks after stroke. The patients were divided into four groups: stroke, vascular cognitive impairment with no dementia (VCIND), vascular dementia (VaD), and mixed dementia (MD). Forty healthy subjects were used as controls. The results indicated that lower soluble receptor levels for advanced glycation end products (sRAGE) and higher β-secretase enzyme (BACE1) and neprilysin (NEP) levels were found in the VCIND, VaD, and MD groups. In addition, the percentages of ε3/ε4 genotypes and ε4 alleles in the VCIND, VaD, and MD groups were higher than in the stroke group. Correlation analysis determined that sRAGE, BACE1, and NEP were significantly related to the results of neuropsychological assessments. Logistic regression analysis, however, suggested that only sRAGE and BACE1 changed ahead of cognitive impairment after stroke. In conclusion, only BACE1 and sRAGE, not NEP or APOE genotypes, may be biomarkers diagnosing post-stroke cognitive impairment.

The pedicled paraumbilical flap is a reliable tissue transfer for hand and forearm reconstruction. However, its size, pedicle length and/or thickness limit its application in resurfacing of extensive defects of the upper limb. To conquer those limitations, this flap was pre-expanded for 10-24 weeks prior to transfer in 25 patients and used as a pedicle flap to cover upper extremity defects. Extensive defects of upper limb were reconstructed by the pre-expanded paraumbilical flaps. The flaps ranged in size from 10cm×8cm to 30cm×14cm. The donor sites were closed directly in all cases. All flaps survived, but two had partial flap necrosis due to venous congestion or infection. With pre-transfer expansion, a large, well-perfused abdominal pedicle flap can be raised and transferred based on the paraumbilical perforators. This pre-expanded flap might be useful in the patients who have the extensive upper limb defects and sufficient time to allow tissue expansion.