Active polarization controller based on micro-ring resonators.

On-chip polarization handling is of great significance for optical interconnects to overcome polarization sensitivity. In this Letter, we propose and experimentally demonstrate a novel, to the best of our knowledge, on-chip polarization controller (PC) on a 220 nm silicon-on-insulator (SOI) platform. It is the first demonstration of a PC based on micro-ring resonators. Any input polarization states can be actively converted to the standard transverse-electric (TE) mode under the phase manipulation. Experimental results show that the insertion loss is less than 0.8 dB and the polarization dependent loss (PDL) is around 0.5 dB. The proposed device also exhibits excellent performances in wavelength tunability over the C band and 35 Gbps data transmission.

Neuroprotective effects of a novel peptide from Lignosus rhinocerotis against 6-hydroxydopamine-induced apoptosis in PC12 cells by inhibiting NF-κB activation.

According to previous studies, oxidative stress is a leading cause of dopaminergic neuron death and may contribute to the pathogenesis of Parkinson's disease (PD). In the current study, we used chromatography of gel filtration to identify a novel peptide (Lignosus rhinocerotis peptide [LRP]) from the sclerotium of Lignosus rhinocerotis (Cooke) Ryvarden. Its neuroprotective effect was evaluated using an in vitro PD model constructed by 6-hydroxydopamine (6-OHDA)-stimulated to apoptosis in PC12 cells. The molecular weight of LRP is determined as 1532 Da and the secondary structure is irregular. The simple amino acid sequence of LRP is Thr-Leu-Ala-Pro-Thr-Phe-Leu-Ser-Ser-Leu-Gly-Pro-Cys-Leu-Leu. Notably, LRP has the ability to significantly boost the viability of PC12 cells after exposure to 6-OHDA, as well as enhance the cellular activity of antioxidative enzymes like superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). LRP also lowers the level of malondialdehyde (MDA), decreases the activation performance of Caspase-3, and reduces 6-OHDA-induced apoptosis via inhibition of nuclear factor-kappa B (NF-κB) activation. These data indicate that LRP may have the potential to act as a neuroprotective agent.

Thematic trends and knowledge structure map of sentinel lymph node biopsy for breast cancer: a bibliometric analysis from 2010 to 2019.

Background: Breast cancer is the leading cancer-related deaths among women. Although great progress has been made in clinical surgical treatment, it is still urgently needed to look for a treatment model with smaller wounds, lower damage, and a better prognosis. Sentinel lymph node biopsy (SLNB) is a minimally invasive technique for breast cancer treatment, which can correctly assess the patients' condition, prognosis, and treatment response. Methods: We performed a PubMed-based bibliometric analysis to investigate publication trends of SLNB in breast cancer and determined the annual distribution of annual publication numbers, countries, authors, languages, journals, and high-frequency major Medical Subject Headings (MeSH) terms. Results: The results showed that the literature on SLNB in breast cancer has shown an upward trend, and stabilized with the most English literature in the past decade at least. The United States was the country with the most publications from 2010 to 2019. M Ahemd was the first-author who had published the most documents related to SLNB in breast cancer since 2010. The most high-frequency main MeSH words were breast neoplasms/pathology, breast neoplasms/surgery and SLNB. Conclusions: Through bicluster analysis, we divided the related articles of SLNB in breast cancer field from 2010 to 2019 into 4 clusters. Among them, indications for SLNB in breast cancer and detection of lymph node metastases and tracking methods for SLNB were considered to be current research hotspots, while assessment of axillary lymph nodes in neoadjuvant chemotherapy and application of SLNB was a potential hotspot.

AMPKα Subunit Ssp2 and Glycogen Synthase Kinases Gsk3/Gsk31 are involved in regulation of sterol regulatory element-binding protein (SREBP) activity in fission yeast.

Sterol regulatory element-binding protein (SREBP), a highly conserved family of membrane-bound transcription factors, is an essential regulator for cellular cholesterol and lipid homeostasis in mammalian cells. Sre1, the homolog of SREBP in the fission yeast Schizosaccharomyces pombe (S. pombe), regulates genes involved in the transcriptional responses to low sterol as well as low oxygen. Previous study reported that casein kinase 1 family member Hhp2 phosphorylated the Sre1 N-terminal transcriptional factor domain (Sre1N) and accelerated Sre1N degradation, and other kinases might exist for regulating the Sre1 function. To gain insight into the mechanisms underlying the Sre1 activity and to identify additional kinases involved in regulation of Sre1 function, we developed a luciferase reporter system to monitor the Sre1 activity through its binding site called SRE2 in living yeast cells. Here we showed that both ergosterol biosynthesis inhibitors and hypoxia-mimic CoCl2 caused a dose-dependent increase in the Sre1 transcription activity, concurrently, these induced transcription activities were almost abolished in Δsre1 cells. Surprisingly, either AMPKα Subunit Ssp2 deletion or Glycogen Synthase Kinases Gsk3/Gsk31 double deletion significantly suppressed ergosterol biosynthesis inhibitors- or CoCl2-induced Sre1 activity. Notably, the Δssp2Δgsk3Δgsk31 mutant showed further decreased Sre1 activity when compared with their single or double deletion. Consistently, the Δssp2Δgsk3Δgsk31 mutant showed more marked temperature sensitivity than any of their single or double deletion. Moreover, the fluorescence of GFP-Sre1N localized at the nucleus in wild-type cells, but significantly weaker nuclear fluorescence of GFP-Sre1N was observed in Δssp2, Δgsk3Δgsk31, Δssp2Δgsk3, Δssp2Δgsk31 or Δssp2Δgsk3Δgsk31 cells. On the other hand, the immunoblot showed a dramatic decrease in GST-Sre1N levels in the Δgsk3Δgsk31 or the Δssp2Δgsk3Δgsk31 cells but not in the Δssp2 cells. Altogether, our findings suggest that Gsk3/Gsk31 may regulate Sre1N degradation, while Ssp2 may regulate not only the degradation of Sre1N but also its translocation to the nucleus.