Dual-mode frequency multiplier in graphene-base hot electron transistor.

Since quantum computers have been gradually introduced in countries around the world, the development of the many related quantum components that can operate independently of temperature has become more important for enabling mature products with low power dissipation and high efficiency. As an alternative to studying cryo-CMOSs (complementary metal-oxide-semiconductors) to achieve this goal, quantum tunneling devices based on 2D materials can be examined instead. In this work, a vertical graphene-based quantum tunneling transistor has been used as a frequency modulator. The transistor can operate via different quantum tunneling mechanisms and generates, by applying the appropriate bias, voltage-resistance curves characteristic of variable nonlinear resistance for both base and emitter voltages. We experimentally demonstrate frequency modulation from input signals over the range of 100 kHz to 10 MHz, enabling a tunable frequency doubler or tripler in just a single transistor. This frequency multiplication with a tunneling mechanism makes the graphene-based tunneling device a promising option for frequency electronics in the emerging field of quantum technologies.

Effects of Arsenic Trioxide on K562 Cell Proliferation and Its Mechanisms / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To investigate the effects of arsenic trioxide (AsO) on K562 cell proliferation by regulating cell cycle protein D1 and cyclin-dependent kinase inhibitor p27kip1.</p><p><b>METHODS</b>MTT was used to detect the effect of AsOon K562 cell proliferation, so as to screen out the appropriate drug concentration. Furthermore, the K562 cell apoptosis was observed by microscopy. The expression of CyclinD1 and p27kip1 in K562 cells treated with AsOwas analyzed by reverse transcription-polymerase chain reaction(RT-PCR), immunohistochemistry and Western blot.</p><p><b>RESULTS</b>AsOcould inhibit the proliferation of K562 cells in a dose- and time- dependent manner (r= 0.967). And the apoptosis cell number in AsOgroup was significantly higher than that in the control group(P<0.05). AsOcould markedly inhibit the expression of CyclinD1 in K562 cells(P<0.05), but the expression of P27kip1 was not significantly changed after AsOtreatment.</p><p><b>CONCLUSIONS</b>AsOcan induce K562 cell apoptosis and inhibit K562 cell proliferation by regulating the expression of CyclinD1.</p>

Micro gel column technique is fit for detecting mixed fields post ABO incompatible hematopoietic stem cell transplantation.

How to choose suitable serologic method for assessment of the actual stages of ABO chimera is more important to establish transfusion strategy for patients post-ABO incompatible hematopoietic stem cell transplantation. We reported ABO phenotypes of a patient post-ABO minor incompatible hematopoietic stem cell transplantation from 1+ weak agglutination by tube method was obviously reaffirmed to mixed fields with 4+ positive reaction by micro gel column card. Hence, blood bank technologists must continually work together with hematologist to establish appropriate transfusion strategy, and micro gel column technique can be more appropriate for detecting mixed fields during the whole period of transplantation.

[Effects of tumor metastasis suppressor gene nm23-H1 on invasion and proliferation of cervical cancer cell lines].

BACKGROUND AND OBJECTIVE: Previous studies have shown that nm23-H1 is a tumor metastasis suppressor gene. Nucleotide diphosphate kinase 1 (NDPK1) encoded by nm23-H1 is involved in cancer cellular differentiation, proliferation, apoptosis and metastasis. This study was to investigate the effects of nm23-H1 on proliferation and invasion of cervical cancer cells. METHODS: The eukaryotic expression vector pcDNA3.1-nm23-H1 was transfected into cervical cancer cells. Cell invasion potential was determined by the Transwell assay. Cell proliferation was measured by MTT assay and changes in cell cycle distribution were analyzed by flow cytometry (FCM). RESULTS: Compared with parent cells (Caski and SiHa) and vector control cells (Caski-3.1 and SiHa-3.1), the proliferation and invasion of pcDNA3.1-nm23-H1 transfected cells (SiHa-N and Caski-N) were apparently decreased (P<0.05); the proportions of G2/M and S cells were obviously decreased while that of G0/G1 cells was increased (P<0.05). However, transfection of nm23-H1 gene had no influence on proliferation, cell cycle and invasion of HeLa cells (P>0.05). CONCLUSION: nm23-H1 gene could inhibit proliferation and invasion of cervical cancer cells in a cell-dependent manner.