Design and Analysis of a Gain-Enhanced,Fully Differential Telescopic Operational Transconductance Amplifier

This paper describes the design and analysis of a fully differential,gain-enhanced CMOS telescopic operational transconductance amplifier （OTA） used in a pipeline analog-to-digital converter （ADC）. Specifications of the OTA are derived from the requirements of ADC. Simulation shows that for a lpF load capacitance, this OTA achieves a high DC gain （approximately 145dB） and a wide unity-gain bandwidth （above 750MHz） at a phase margin 58°. In a configuration where the closed loop-gain is 4,the design spends about 18ns for settling with 0.05% accuracy. Simulations of this design are performed in SMIC CMOS 0.18μm technology.

Proliferation in rat gastric mucosal cells induced by chronic ethanol feeding through the ROS/BMK1 pathway

Objective: To investigate the correlation between the gastric mucosal cell proliferation and low-concentration alcohol intake in a chronic drinking rat model, and to investigate the possible role of ROS/BMK1 pathway in this process. Methods: SD rats were randomly divided into 4 groups: control group, administered with tap water; ethanol group, with 6% ethanol in the drinking water; quercetin group, with quercetin (100 mg/kg) by intragastric gavage twice a day; ethanol+quercetin group, administered with quercetin combined with 6% ethanol. The cell proliferation in rat gastric mucosa was analyzed by flow cytometery and proliferating cell nuclear antigen (PCNA) immunohistochemical staining. Activation of ERKs and BMK1 was evaluated by the expression and phosphorylation of these kinases using Western Blot analysis. Results: Compared to the controls, the cell proliferation in gastric mucosa of rats exposed to the ethanol for 7 d was enhanced, and the activation of BMK1 was also increased in this period. Otherwise quercetin, as a free radical scavenger, attenuated increased cell proliferation and activation of BMK1 in rat stomach treated with ethanol. However, no changes of ERKs expression and phosphorylation occurred in the rats in all groups. Conclusion: These results suggested that the ROS and BMK1 activation may be a central mechanism, which underlies cell proliferation in rat gastric mucosa stimulus with the chronic low-concentration ethanol.

Adenovirus-mediated gene transfer of TIMP-4 reduces neointimal hyperplasia in balloon-injured rat carotid artery

Objective:To determine the effects of a recombinant replication-deficient adenovirus encoding human tissue inhibitor of metalloproteinase-4(Ad.TIMP-4) on vascular smooth muscle cell(VSMC) function in vitro and neointimal development in the injured rat carotid artery.Methods:Western blotting,gelatin zymography and reverse zymography were used to characterize the expression and functional activity of the TIMP-4 secreted by Ad.TIMP-4-infected VSMCs.The migration and proliferation of VSMCs in vitro were separately detected by using Millicell-PCF invasion chambers and [3H]-thymidine incorporation assay.Immunohistochemistry and morphometric analysis were used to determine the local expression of TIMP-4 and its effect on neointima development in a rat carotid artery balloon injury model.Results:VSMCs infected with Ad.TIMP-4 expressed functionally active human TIMP-4 which increased with the duration of infection.TIMP-4 expression inhibited VSMC migration,but not significantly affect VSMC proliferation.In a balloon-injured rat carotid artery model,a significant 62% reduction in neointimal area was found in Ad.TIMP-4-infected vessels at 14 days after injury.Ad.TIMP-4 infection had no effect on medial area.Conclusion:Our results indicated TIMP-4 over expression can significantly inhibit the migration of cultured VSMCs and prevent neointimal formation after vascular injury.Our findings provide additional evidence that TIMP-4 could play an important role in vascular pathophysiology,and may be an important therapeutic target for future drug development.

严重事故下吸湿性气溶胶的自然去除研究

反应堆发生严重事故时,堆芯释放出的吸湿性气溶胶会在潮湿的安全壳内增大,从而影响其自然去除过程。本文理论推导了吸湿性气溶胶的增大模型并通过多种方法对其进行了验证。模型计算结果表明,气溶胶的增大过程由于受到溶解度的限制而存在临界湿度值,在该临界值以下时气溶胶不发生吸湿,但这未被其他严重事故分析程序所考虑。同时,基于某三代先进压水堆的特定严重事故工况,本文分析了干颗粒半径及湿度对气溶胶的平衡半径和自然去除系数的影响。结果表明:气溶胶的自然去除系数随干颗粒半径的增大将先减小后增加,并在1μm时达到最小值;相同湿度下,干颗粒半径对气溶胶半径的最大增大比例的影响不大;湿度的增加对不同干颗粒半径气溶胶去除系数的影响不同。

Fangjihuangqi Tang improved lower urinary tract dysfunction in benign prostatic hyperplasia rats model

OBJECTIVE: To investigated the effect and mechanism of Fangjihuangqi Tang (FHT) on lower urinary tract dysfunction induced by benign prostatic hyperplasia (BPH) in rats. METHODS: Male rats were randomly divided into seven groups: normal, model, finasteride (0.5 mg/ kg), terazosin (0.5 mg/kg), and FHT (10, 5, 2.5 g/kg). Rats were administered testosterone (0.5 mg sc) for 6 weeks after orchiectomy, excluding the normal group. All rats were intragastrically administered assigned drugs for 4 weeks from the third week. Urodynamics were assessed in rats under anesthesia. Serum dihydrotestosterone (DHT) and prostatic acid phosphatase (PAP) were measured. The prostate index (PI), bladder index (BI), and pathological detection were evaluated. RESULTS: In the model group, the PI, BI, serum DHT, serum PAP, threshold pressure (TP), micturition pressure (MP), and residual urine volume (RV)were significantly higher. Moreover, inter-micturition duration (IMD) was significantly lower and the prostatic and bladder showed obvious pathological changes. The IMD was significantly higher, while BI, TP, MP, and RV were significantly lower and bladder pathological changes were alleviated in the FHT (10, 5 g/kg), finasteride, and terazosin groups. The PI, DHT, and PAP were significantly lower in the finasteride group, but they did not change significantly in the FHT (10, 5, 2.5 g/kg) and terazosin groups. CONCLUSION: FHT could relieve symptoms of lower urinary tract dysfunction in BPH rats but with no apparent effect on reducing the volume of the enlarged prostate itself.

Modulation of expression of P16 and Her2 in rat breast tissues of mammary hyperplasia model by external use of Rupifang Extract

tract in external use on expression of proto-onco- genes her2 and tumor suppression genes p16 in rat breast tissues of mammary hyperplasia model. To explore the mechanisms of Rupifang Extract in external use for preventing and treating mammary hyperplasia. METHODS Thirty virginal female Wistar rats were randomized into 5 groups, 6 in each, A： blank con- trol group; B： model group; C： the low dose group of Rupifang; D： the middle dose group of Rupifang; and E： The high dose group of Rupifang. The mam- mary hyperplasia rat models were produced by in- jecting estradiol benzoate and progesterone and ir- ritating by tail nipping. Drug intervention was also launched during the model formation. After 30 days, the expression of her2 and p16 in breast tis- sues of rats in each group were detected by the SP immunohistochemical method. RESULTS： Compared with Blank control group, the expression of her2 in breast tissues in Model group was higher, and the expression of p16 was lower （P〈O.05 or P〈O.01）. After intervention with Rupi- fang Extract, compared with Model group, the ex- pression of her2 in breast tissues in Rupifang groups was lower, and the expression of p16 higher （P〈O.05 or P〈O.01）. CONCLUSION： The mechanisms of Rupifang Ex- tract in external application for preventing and treating mammary hyperplasia may be reducing the expression of proto-oncogenes her2 and in- creasing the expression of tumor suppression genes p16.