Purely excitonic lasing in ZnO microcrystals: Temperature-induced transition between exciton-exciton and exciton-electron scattering

Since the seminal observation of room-temperature laser emission from ZnO thin films and nanowires, numerous attempts have been carried out for detailed understanding of the lasing mechanism in ZnO. In spite of the extensive efforts performed over the last decades, the origin of optical gain at room temperature is still a matter of considerable discussion. In this work, we show that a ZnO film consisting of well-packed micrometer-sized ZnO crystals exhibits purely excitonic lasing at room temperature without showing any symptoms of electron-hole plasma emission, even under optical excitation more than 25 times above the excitonic lasing threshold. The lasing mechanism is shifted from the exciton-exciton scattering to the exciton-electron scattering with increasing temperature from 3 to 150 K. The exciton-electron scattering process continues to exist with further increasing temperature from 150 to 300 K. Thus, we present distinct experimental evidence that the room-temperature excitonic lasing is achieved not by exciton-exciton scattering, as has been generally believed, but by exciton-electron scattering. We also argue that the long carrier diffusion length and the low optical loss nature of the micrometer-sized ZnO crystals, as compared to those of ZnO nanostructures, plays a key role in showing room-temperature excitonic lasing

Stress responsive miR-23a attenuates skeletal muscle atrophy by targeting MAFbx /atrogin-1

Muscle atrophy occurs in many pathological states and results primarily from accelerated protein degradation by the ubiquitin-proteasome pathway. We used dexamethasone to induce muscle wasting and investigated the role of a microRNA (miRNA) in the control of muscle-specific E3 ubiquitin ligase MAFbx/atrogin-1. Here we show that miR-23a suppresses MAFbx/atrogin-1 translation by binding to 3'UTR of the mRNA. Furthermore, ectopic expression of miR-23a is sufficient to protect myocytes from atrophy in vitro and in vivo in response to dexamethasone treatment, and heat stress-induced miR-23a protects muscle from dexamethasone-induced muscle atrophy. Our surprising discovery of the physiological role of miR-23a in preventing the atrophy program should lay the basis not only for further understanding of the mechanisms of muscle wasting in diverse diseases, but also for developing novel therapies for these debilitating conditions

Evaluation of calibration factor of OSLD toward eye lens exposure dose measurement of medical staff during IVR

The eye lens is a sensitive organ of which an x‐ray exposure dose should be managed during interventional radiology (IVR). In the actual situations, the eye lens is exposed to scattered x‐rays; they have different from the standard x‐ray energies which are used for general dose calibration of the dosimeter. To perform precise dose measurement, the energy dependence of the dosimeter should be properly accounted for when calibrating the dosimeter. The vendor supplies a calibration factor using 80‐kV diagnostic x‐rays under a free‐air condition. However, whether it is possible to use this calibration factor to evaluate the air kerma during the evaluation of the eye lens dose is unclear. In this paper, we aim to precisely determine calibration factors, and also examine the possible application of using a vendor‐supplied calibration factor. First, the x‐ray spectrum at the eye lens position during fluoroscopy was measured with a CdTe x‐ray spectrometer. We mimicked transfemoral cardiac catheterization using a human‐type phantom. Second, we evaluated the doses and calibration factors at three dosimetric points: front and back of protective goggles, and the front of the head (eye lens position). We used the measured x‐ray spectrum to determine the incident photon distribution in the eye lens regions, and x‐ray spectra corresponding to the dosimetric points around the eye lens were estimated using Monte Carlo simulation. Although the calibration factors varied with dosimetric positions, we found that the factors obtained were similar to the vendor‐supplied calibration factor. Furthermore, based on the experiment, we propose a practical way to calibrate an OSL dosimeter in an actual clinical situation. A person evaluating doses can use a vendor‐supplied calibration factor without any corrections for energy dependences, only when they add a systematic uncertainty of 5%. This evidence will strongly support actual exposure dose measurement during a clinical study

Expression and localization of connective tissue growth factor (CTGF/Hcs24/CCN2) in osteoarthritic cartilage

AbstractObjectiveThe investigation of the expression and localization of connective tissue growth factor/hypertrophic chondrocyte-specific gene product 24/CCN family member 2 (CTGF/Hcs24/CCN2) in normal and osteoarthritic (OA) cartilage, and quantification of CTGF/Hcs24-positive cells.MethodsCartilage samples of patients (n=20) with late stage OA were obtained at total joint replacement surgery. Morphologically normal cartilage was harvested for comparison purposes from the femoral heads of 6 other patients with femoral neck fracture. Paraffin-embedded sections were stained by Safranin O. The severity of the OA lesions was divided into four stages (normal, early, moderate, and severe). The localization of protein and mRNA for CTGF/Hcs24 was investigated by immunohistochemistry and in situ hybridization, respectively. The population of CTGF/Hcs24-positive chondrocytes in OA cartilage and chondro-osteophyte was quantified by counting the number of the cells under light microscopy.ResultsSignals for CTGF/Hcs24 were detected in a small percentage of chondrocytes throughout the layers of normal cartilage. In early stage OA cartilage, the CTGF/Hcs24-positive chondrocytes were localized mainly in the superficial layer. In moderate to severe OA cartilage, intense staining for CTGF/Hcs24 was observed in proliferating chondrocytes forming cell clusters next to the cartilage surface. In chondro-osteophyte, strong signals were found in the chondrocytes of the proliferative and hypertrophic zones.ConclusionCTGF/Hcs24 expression was detected in both normal and OA chondrocytes of human samples. The results of the current study suggested that expression of CTGF/Hcs24 was concomitant with development of OA lesions and chondrocyte differentiation in chondro-osteophyte

Relationship between the cAMP levels in leukocytes and the cytokine balance in patients surviving gram negative bacterial pneumonia

Lipopolysaccharide-stimulated leukocytes secrete proinflammatory cytokines including tumor necrosis factor-α and interleukin-12. Over-activation of host defense systems may result in severe tissue damage and requires regulation. Granulocyte colony-stimulating factor and interleukin-10 are candidate cytokines for inducing tolerance to lipopolysaccharide re-stimulation. We compared cytokines secreted by lipopolysaccharide-stimulated blood cells from patients who had survived gram negative bacterial pneumonia (Pseudomonas aeruginosa, Escherichia coli or Proteus mirabilis, n = 26) and age-matched healthy volunteers (n = 18). Interleukin-12p70 and tumor necrosis factor-α expression was significantly lower in patients (p = 0.0039 and p<0.001) compared to healthy controls, while granulocyte colony-stimulating factor production was markedly higher in patients (p<0.001). Levels of interleukin-10 were comparable. Granulocyte colony-stimulating factor expression was inversely correlated with interleukin-12p70 (R = −0.71, p<0.001) and tumor necrosis factor-α (R = −0.64, p<0.001) expression; interleukin-10 showed no significant correlation. In unstimulated leukocytes from patients, cAMP levels were significantly raised (p = 0.020) and were correlated inversely with interleukin-12p70 levels (R = −0.81, p<0.001) and directly with granulocyte colony-stimulating factor (R = 0.72, p = 0.0020), matrix metalloproteinase-9 (R = 0.67, p = 0.0067) and interleukin-10 (R = 0.54, p = 0.039) levels. Our results demonstrate that granulocyte colony-stimulating factor production by lipopolysaccharide-stimulated leukocytes is a useful indicator of tolerance induction in surviving pneumonia patients and that measuring cAMP in freshly isolated leukocytes may also be clinically significant

MicroRNA-125b regulates the expression of aggrecanase-1 (ADAMTS-4) in human osteoarthritic chondrocytes

INTRODUCTION: Increased expression of aggrecanase-1 (ADAMTS-4) has emerged as an important factor in osteoarthritis (OA) and other joint diseases. This study aimed to determine whether the expression of ADAMTS-4 in human chondrocytes is regulated by miRNA. METHODS: MiRNA targets were identified using bioinformatics. Chondrocytes were isolated from knee cartilage and treated with interleukin-1 beta (IL-1β). Gene expression was quantified using TaqMan assays and protein production was determined by immunoblotting. Luciferase reporter assay was used to verify interaction between miRNA and target messenger RNA (mRNA). RESULTS: In silico analysis predicted putative target sequence of miR-125b on ADAMTS-4. MiR-125b was expressed in both normal and OA chondrocytes, with significantly lower expression in OA chondrocytes than in normal chondrocytes. Furthermore, IL-1β-induced upregulation of ADAMTS-4 was suppressed by overexpression of miR-125b in human OA chondrocytes. In the luciferase reporter assay, mutation of the putative miR-125b binding site in the ADAMTS-4 3'UTR abrogated the suppressive effect of miR125. CONCLUSIONS: Our results indicate that miR-125b plays an important role in regulating the expression of ADAMTS-4 in human chondrocytes and this identifies miR-125b as a novel therapeutic target in OA

Involvement of resistin-like molecule β in the development of methionine-choline deficient diet-induced non-alcoholic steatohepatitis in mice

Resistin-like molecule β (RELMβ) reportedly has multiple functions including local immune responses in the gut. In this study, we investigated the possible contribution of RELMβ to non-alcoholic steatohepatitis (NASH) development. First, RELMβ knock-out (KO) mice were shown to be resistant to methionine-choline deficient (MCD) diet-induced NASH development. Since it was newly revealed that Kupffer cells in the liver express RELMβ and that RELMβ expression levels in the colon and the numbers of RELMβ-positive Kupffer cells were both increased in this model, we carried out further experiments using radiation chimeras between wild-type and RELMβ-KO mice to distinguish between the contributions of RELMβ in these two organs. These experiments revealed the requirement of RELMβ in both organs for full manifestation of NASH, while deletion of each one alone attenuated the development of NASH with reduced serum lipopolysaccharide (LPS) levels. The higher proportion of lactic acid bacteria in the gut microbiota of RELMβ-KO than in that of wild-type mice may be one of the mechanisms underlying the lower serum LPS level the former. These data suggest the contribution of increases in RELMβ in the gut and Kupffer cells to NASH development, raising the possibility of RELMβ being a novel therapeutic target for NASH