A Fully-Integrated Reconfigurable Dual-Band Transceiver for Short Range Wireless Communications in 180 nm CMOS

© 2015 IEEE. Personal use of this material is permitted. Permission from IEEE must be obtained for all other users, including reprinting/ republishing this material for advertising or promotional purposes, creating new collective works for resale or redistribution to servers or lists, or reuse of any copyrighted components of this work in other works.A fully-integrated reconfigurable dual-band (760-960 MHz and 2.4-2.5 GHz) transceiver (TRX) for short range wireless communications is presented. The TRX consists of two individually-optimized RF front-ends for each band and one shared power-scalable analog baseband. The sub-GHz receiver has achieved the maximum 75 dBc 3rd-order harmonic rejection ratio (HRR3) by inserting a Q-enhanced notch filtering RF amplifier (RFA). In 2.4 GHz band, a single-ended-to-differential RFA with gain/phase imbalance compensation is proposed in the receiver. A ΣΔ fractional-N PLL frequency synthesizer with two switchable Class-C VCOs is employed to provide the LOs. Moreover, the integrated multi-mode PAs achieve the output P1dB (OP1dB) of 16.3 dBm and 14.1 dBm with both 25% PAE for sub-GHz and 2.4 GHz bands, respectively. A power-control loop is proposed to detect the input signal PAPR in real-time and flexibly reconfigure the PA's operation modes to enhance the back-off efficiency. With this proposed technique, the PAE of the sub-GHz PA is improved by x3.24 and x1.41 at 9 dB and 3 dB back-off powers, respectively, and the PAE of the 2.4 GHz PA is improved by x2.17 at 6 dB back-off power. The presented transceiver has achieved comparable or even better performance in terms of noise figure, HRR, OP1dB and power efficiency compared with the state-of-the-art.Peer reviewe

Potential role of Cyr61 induced degeneration of human Müller cells in diabetic retinopathy.

The degeneration of Müller cells has been recognized to involve in the pathogenesis of diabetic retinopathy. However, the mechanism is not yet clear. This study is to explore the potential role of Cyr61, a secreted signaling protein in extracellular matrix, in inducing human Müller cell degeneration in diabetic retinopathy (DR). Twenty patients with proliferative diabetic retinopathy (PDR) and twelve non-diabetic patients were recruited for this study. Vitreous fluid was collected during vitrectomy surgery for Cyr61 ELISA. Human Müller cell line MIO-M1 were cultured to be subconfluent, and then treated with glucose (0-20 mM) or Cyr61 (0-300 ng/ml). Cyr61 expression induced by increasing concentrations of glucose was evaluated by RT-qPCR and Western blot. Effects of Cyr61 on Müller cells viability, migration and apoptosis were observed by MTT assay, Transwell assay, and TUNEL assay. Vitreous Cyr61 levels were observed to be 8-fold higher in patients with PDR (3576.92 ± 1574.58 pg/mL), compared with non-diabetic controls (436.14 ± 130.69 pg/mL). Interestingly, the active PDR group was significantly higher than the quiescent PDR group (P<0.01). In retinal Müller cells culture, high glucose significantly and dose-dependently elevated Cyr61 expression at both mRNA and protein levels. Cyr61 at high concentrations dose-dependently inhibited the viability and migration of Müller cells. TUNEL assay further revealed that high concentration of Cyr61 significantly promoted the cell apoptosis. In conclusion, these findings demonstrated for the first time that the expression of Cyr61 was elevated by high glucose in Müller cells, and Cyr61 inhibited cell viability and migration while induced apoptosis, suggesting the potential role of Cyr61 in Müller cell degeneration. The elevated Cyr61 levels in vitreous fluid of PDR patients further support its role in diabetic retinopathy (DR)

Data from: Potential role of Cyr61 induced degeneration of human Müller cells in diabetic retinopathy

The degeneration of Müller cells has been recognized to involve in the pathogenesis of diabetic retinopathy. However, the mechanism is not yet clear. This study is to explore the potential role of Cyr61, a secreted signaling protein in extracellular matrix, in inducing human Müller cell degeneration in diabetic retinopathy (DR). Twenty patients with proliferative diabetic retinopathy (PDR) and twelve non-diabetic patients were recruited for this study. Vitreous fluid was collected during vitrectomy surgery for Cyr61 ELISA. Human Müller cell line MIO-M1 were cultured to be subconfluent, and then treated with glucose (0–20 mM) or Cyr61 (0–300 ng/ml). Cyr61 expression induced by increasing concentrations of glucose was evaluated by RT-qPCR and Western blot. Effects of Cyr61 on Müller cells viability, migration and apoptosis were observed by MTT assay, Transwell assay, and TUNEL assay. Vitreous Cyr61 levels were observed to be 8-fold higher in patients with PDR (3576.92±1574.58 pg/mL), compared with non-diabetic controls (436.14±130.69 pg/mL). Interestingly, the active PDR group was significantly higher than the quiescent PDR group (P<0.01). In retinal Müller cells culture, high glucose significantly and dose-dependently elevated Cyr61 expression at both mRNA and protein levels. Cyr61 at high concentrations dose-dependently inhibited the viability and migration of Müller cells. TUNEL assay further revealed that high concentration of Cyr61 significantly promoted the cell apoptosis. In conclusion, these findings demonstrated for the first time that the expression of Cyr61 was elevated by high glucose in Müller cells, and Cyr61 inhibited cell viability and migration while induced apoptosis, suggesting the potential role of Cyr61 in Müller cell degeneration. The elevated Cyr61 levels in vitreous fluid of PDR patients further support its role in diabetic retinopathy (DR)

Associations of Diet Quality and Heavy Metals with Obesity in Adults: A Cross-Sectional Study from National Health and Nutrition Examination Survey (NHANES)

A poor diet cannot fully explain the prevalence of obesity. Other environmental factors (e.g., heavy metals) have been reported to be associated with obesity. However, limited evidence is available for the combined effect of these factors on obesity. Therefore, we conducted a cross-sectional study and used the data from the National Health and Examination Survey (2007–2018) to explore the associations between diet quality and heavy metals and obesity. Diet quality was evaluated by the Healthy Eating Index-2015 (HEI-2015) score. Heavy metals included serum cadmium (Cd), lead (Pb), and mercury (Hg). We included 15,959 adults, with 5799 of obesity (body mass index ≥ 30 kg/m2). After adjustment for covariates, every interquartile range increase in HEI-2015 scores, Pb, Cd and Hg was associated with a 35% (odds ratios [OR] = 0.65, 95% confidence interval [CI]: 0.60, 0.70), 11% (OR = 0.89, 95% CI: 0.82, 0.98), 9% (OR = 0.91, 95% CI: 0.87, 0.96), 5% (OR = 0.85, 95% CI: 0.82, 0.89) reduction in risk of peripheral obesity, respectively. In addition, the association between the HEI-2015 scores and peripheral obesity was attenuated by higher levels of heavy metals (All p interaction < 0.05). Results remained similar for abdominal obesity. Our study reveals the distinct effects of a high-quality diet and heavy metals on obesity prevalence, and the beneficial effect of a high-quality diet could be weakened by higher levels of heavy metals

Recapitulating X-Linked Juvenile Retinoschisis in Mouse Model by Knock-In Patient-Specific Novel Mutation

X-linked juvenile retinoschisis (XLRS) is a retinal disease caused by mutations in the gene encoding retinoschisin (RS1), which leads to a significant proportion of visual impairment and blindness. To develop personalized genome editing based gene therapy, knock-in animal disease models that have the exact mutation identified in the patients is extremely crucial, and that the way which genome editing in knock-in animals could be easily transferred to the patients. Here we recruited a family diagnosed with XLRS and identified the causative mutation (RS1, p.Y65X), then a knock-in mouse model harboring this disease-causative mutation was generated via TALEN (transcription activator-like effector nucleases). We found that the b-wave amplitude of the ERG of the RS1-KI mice was significantly decreased. Moreover, we observed that the structure of retina in RS1-KI mice has become disordered, including the disarray of inner nuclear layer and outer nuclear layer, chaos of outer plexiform layer, decreased inner segments of photoreceptor and the loss of outer segments. The novel knock-in mice (RS1-KI) harboring patient-specific mutation will be valuable for development of treatment via genome editing mediated gene correction

Long-Term Exposure to PM_2.5 and Mortality: A Cohort Study in China

We investigated the association of long-term exposure to atmospheric PM2.5 with non-accidental and cause-specific mortality in Yinzhou, China. From July 2015 to January 2018, a total of 29,564 individuals aged ≥ 40 years in Yinzhou were recruited for a prospective cohort study. We used the Cox proportional-hazards model to analyze the relationship of the 2-year average concentration of PM2.5 prior to the baseline with non-accidental and cause-specific mortality. The median PM2.5 concentration was 36.51 μg/m3 (range: 25.57–45.40 μg/m3). In model 4, the hazard ratios per 10 μg/m3 increment in PM2.5 were 1.25 (95%CI: 1.04–1.50) for non-accidental mortality and 1.38 (95%CI:1.02–1.86) for cardiovascular disease mortality. We observed no associations between PM2.5 and deaths from respiratory disease or cancer. In the subgroup analysis, interactions were observed between PM2.5 and age, as well as preventive measures on hazy days. The observed association between long-term exposure to atmospheric PM2.5 at a relatively moderate concentration and the risk of non-accidental and cardiovascular disease mortality among middle-aged and elderly Chinese adults could provide evidence for government decision-makers to revise environmental policies towards a more stringent standard

experimental data

data for the: (1) Vitreous levels of Cyr61 in PDR and non-diabetic patients were determined by ELISA;(2) Cyr61 expression in Müller cells was observed at mRNA and protein level. (3) Effect of Cyr61 on the viability, migration and apoptosis of Müller cells was observe