A promising method
has been demonstrated to fabricate quantum dot
(QD)-converted full-color micro-light emitting diodes (LEDs) by inkjet
printing (IJP) instead of the mass transfer of three red-green-blue
(RGB) color chips. By introducing an additional medium, that is, NaCl
into a formulated ink, QD deposition is manipulated by the NaCl-QD
adhesive force and the capillary flow inside the liquid drop via varying
the substrate hydrophobicity, which enabled spontaneous self-encapsulation
of QDs in a single NaCl crystal. An RGB QD@NaCl array with a small
pixel size and uniform size distribution (diameter = 3.74 ± 0.5
μm) is obtained in the IJP process, which demonstrated a full-color
micro-LED display with a color gamut of approximately 110% of the
National Television System Committee (NTSC) standard.
It has been postulated that folic acid (folate) deficiency (FD) may be a risk factor for the pathogenesis of a variety of oxidative stress-triggered chronic degenerative diseases including diabetes, however, the direct evidence to lend support to this hypothesis is scanty. For this reason, we set out to study if FD can trigger the apoptotic events in an insulin-producing pancreatic RINm5F islet β cells. When these cells were cultivated under FD condition, a time-dependent growth impediment was observed and the demise of these cells was demonstrated to be apoptotic in nature proceeding through a mitochondria-dependent pathway. In addition to evoke oxidative stress, FD condition could also trigger nitrosative stress through a NF-κB-dependent iNOS-mediated overproduction of nitric oxide (NO). The latter compound could then trigger depletion of endoplasmic reticulum (ER) calcium (Ca2+) store leading to cytosolic Ca2+ overload and caused ER stress as evidence by the activation of CHOP expression. Furthermore, FD-induced apoptosis of RINm5F cells was found to be correlated with a time-dependent depletion of intracellular gluthathione (GSH) and a severe down-regulation of Bcl-2 expression. Along the same vein, we also demonstrated that FD could severely impede RINm5F cells to synthesize insulin and their abilities to secret insulin in response to glucose stimulation were appreciably hampered. Even more importantly, we found that folate replenishment could not restore the ability of RINm5F cells to resynthesize insulin. Taken together, our data provide strong evidence to support the hypothesis that FD is a legitimate risk factor for the pathogenesis of diabetes.
Background: Solid cancers with bone marrow metastases are rare but lethal. This study aimed to identify clinical factors predictive of survival in adult patients with solid cancers and bone marrow metastases. Methods: A total of 83 patients were enrolled consecutively between January 1, 2000 and December 31, 2012. Bone marrow metastases were confirmed by biopsies. Patient clinical features and laboratory data were analyzed for associations. Results: The median age of the patients was 54 years (range, 23-88 years), and 58% were male. The 3 most common primary tumor locations were the stomach (32 patients, 39%), prostate (16 patients, 19%), and lungs (12 patients, 15%). The median overall survival was 49 days (range, 3-1423 days). Patients with Eastern Cooperative Oncology Group performance status 1, cancers of prostate origin, platelet counts over 50,000/ml, and undergoing antitumor therapies had a significantly better prognosis in the multivariate analysis. The median survival times were 173 and 33 days for patients with 2-3 more favorable parameters (n=24) and those with 0-1 (n=69), respectively (hazard ratio 0.30; 95% CI 0.17-0.52, p<0.001). Conclusions: Solid cancers with bone marrow metastases are dismal and incurable diseases. Understanding prognostic factors to these diseases helps medical personnel to provide appropriate treatments and better inform patients about outcomes. Antitumor therapies may improve outcomes in selected patient cohorts.
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