巯基化介孔硅酸钙的合成及其对Pb2+的吸附特性

以硝酸钙和硅酸钠为原料,十六烷基三甲溴化铵为模板剂,(3-巯基丙基)三甲氧基硅烷为改性剂,采用后接枝法制备巯基化介孔硅酸钙(MCS-SH),并对其结构进行了表征。考察了其对Pb2+的吸附性能,探讨了吸附热力学特征。结果表明,MCS-SH在改性后仍维持较稳定的介孔结构,为夹缝孔,比表面积和孔径范围分别为129.32 m2?g?1和5~49 nm,接入的?SH量为0.4594 mmol?g?1;MCS-SH对Pb2+的吸附符合Langmuir模型,更符合Redlich-Peterson模型;MCS-SH对Pb2+吸附是一个熵增自发进行的过程,为吸热反应,存在物理吸附和化学吸附。根据Langmuir吸附模型,在293 K下MCS-SH对Pb2+的最大吸附容量为618.09 mg?g?1,远大于文献报道的吸附剂。MCS-SH在pH 5.0~7.5的范围内对Pb2+具有优异的吸附性能。

Overcoming resistance to immunotherapy by targeting GPR84 in myeloid-derived suppressor cells

Myeloid-derived suppressor cells(MDSCs)were found to gradually accumulate in the orthotopic esophageal cancer mouse model during tumor progression.Although the roles of MDSCs in promoting tumor growth and inhibiting immune response have been extensively explored,currently,there are still no effective means for targeting MDSCs clinically.The deficiency of specific markers of MDSCs was responsible for the limited strategy to eliminating in clinic.This study identified that GPR84 was exclusively overexpressed on MDSCs.It was further found that GPR84 was prominently expressed on MDSCs in clinical samples and tumor mouse models,which drives the immunosuppression on CD8^(+)T cells by inhibiting PD-L1 degradation in lysosomes.Furthermore,G-CSF and GM-CSF were found to induce GPR84 expression through the STAT3/C/EBPβsignaling pathway.In addition,GPR84+MDSCs and PD-L1^(+)MDSCs were highly accumulated in anti-PD-1 therapy-resistant patients with esophageal cancer,and high GPR84 signature risk was verified as a negative factor for the overall survival of patients with anti-PD-1 treatment.Finally,GPR84 antagonism combined with an anti-PD-1 antibody enhanced the antitumor responses.Therefore,targeting GPR84 enhanced anti-PD-1 efficacy in esophageal cancer and other malignant tumors.This combination therapy has the potential for tumor therapy in clinics.

COVID-19:immunopathogenesis and Immunotherapeutics

The recent novel coronavirus disease(COVID-19)outbreak,caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),is seeing a rapid increase in infected patients worldwide.The host immune response to SARS-CoV-2 appears to play a critical role in disease pathogenesis and clinical manifestations.SARS-CoV-2 not only activates antiviral immune responses,but can also cause uncontrolled inflammatory responses characterized by marked pro-inflammatory cytokine release in patients with severe COVID-19,leading to lymphopenia,lymphocyte dysfunction,and granulocyte and monocyte abnormalities.These SARS-CoV-2-induced immune abnormalities may lead to infections by microorganisms,septic shock,and severe multiple organ dysfunction.Therefore,mechanisms underlying immune abnormalities in patients with COVID-19 must be elucidated to guide clinical management of the disease.Moreover,rational management of the immune responses to SARSCoV-2,which includes enhancing anti-viral immunity while inhibiting systemic inflammation,may be key to successful treatment.In this review,we discuss the immunopathology of COVID-19,its potential mechanisms,and clinical implications to aid the development of new therapeutic strategies against COVID-19.

PD-1 abrogates the prolonged persistence of CD8+CAR-T cells with 4-1BB co-stimulation

Dear Editor,The central memory differentiation critically dictates CAR-T cell persistence,which is closely associated with the therapeutic effectiveness in the clinic.It is well accepted that 4-1BB costimulation is superior over CD28 to promote the central memory differentiation and persistence of CAR-T cells.1 However,it is also noticed that CAR-T cells with either co-stimulations are comparably differentiated and persisted,2 especially under immunosuppressive conditions.Factors contributing to the discrepancy remain unknown.Mounting evidences show that programmed cell death protein 1(PD-1)directly affects memory differentiation of T cells upon PD-L1 engagement,3 in addition to limiting proliferation.It is unclear whether PD-1 is involved in the diminished difference in memory differentiation and persistence between CAR-T cells with different co-stimulations.Herein,we examined the memory differentiation of CAR-T cells when PD-1 is activated or not,and consequently the persistence and anti-tumor effects.

Four-level phase pair encoding and decoding with single interferometric phase retrieval for holographic data storage

We propose four-level phase pair encoding and decoding with single interferometric phase retrieval for holographic data storage. Inherent with phase pair encoding, phase shifting is generated by assigning a certain phase difference between two pixels of the phase pair. Multiple phase shifting operations are not required. In addition, a phase-readout reference beam can be a plane beam with an arbitrary phase in our method because phase shifting can be encoded on the phase-only spatial light modulator easily and accurately. Therefore, our method can not only increase the data transfer rate, but also improve the robustness of the holographic data storage system. Although the code rate of our method needs to be sacrificed by half, the code rate is still twice that of amplitude code when four-level phase encoding is used. We demonstrated experimentally that there is only a 1×10^-2 order of bit error rate before error correcting, which is acceptable. We believe our method will further advance the phase-modulated holographic data storage technique.