Low Threshold Multiexciton Optical Gain in Colloidal CdSe/CdTe Core/Crown Type-II Nanoplatelet Heterostructures

Colloidal cadmium chalcogenide core/crown type-II nanoplatelet heterostructures, such as CdSe/CdTe, are promising materials for lasing and light-emitting applications. Their rational design and improvement requires the understanding of the nature of single- and multiexciton states. Using pump fluence and wavelength-dependent ultrafast transient absorption spectroscopy, we have identified three spatially and energetically distinct excitons (in the order of increasing energy): interface-localized charge transfer exciton (X_CT, with electron in the CdSe core bound to the hole in the CdTe crown), and CdTe crown-localized X_CdTe and CdSe core-localized X_CdSe excitons. These exciton levels can be filled sequentially, with each accommodating two excitons (due to electron spin degeneracy) to generate one to six exciton states (with lifetimes of ≫1000, 209, 43.5, 11.8, 5.8, and 4.5 ps, respectively). The spatial separation of these excitons prolongs the lifetime of multiexciton states. Optical gain was observed in tri- (XX_CTX_CdTe) and four (XX_CTXX_CdTe) exciton states. Because of the large absorption cross section of nanoplatelets, an optical gain threshold as low as ∼43 μJ/cm² can be achieved at 550 nm excitation for a colloidal solution sample. This low gain threshold and the long triexciton (gain) lifetime suggest potential applications of these 2D type-II heterostructures as low threshold lasing materials

Image_4_Mannose inhibits Plasmodium parasite growth and cerebral malaria development via regulation of host immune responses.jpeg

D-mannose can be transported into a variety of cells via glucose transporter (GLUT), and supraphysiological levels of D-mannose impairs tumor growth and modulates immune cell function through mechanisms such as interference with glycolysis and induction of oxidative stress. Blood-stage Plasmodium mainly depends on glycolysis for energy supply and pathological immune response plays a vital role in cerebral malaria. However, it is not clear whether mannose affects malaria blood-stage infection. Here, we fed D-mannose to Plasmodium berghei-infected mice and found weight loss and reduced parasitemia without apparent side effects. Compromised parasitemia in C57BL/6 mice was accompanied by an increase in splenic macrophages compared to an untreated group. When mannose was applied to a rodent experimental cerebral malaria (ECM) model, the incidence of ECM decreased. Expression of activation marker CD69 on T cells in peripheral blood and the brain were reduced, and cerebral migration of activated T cells was prevented by decreased expression of CXCR3. These findings suggest that mannose inhibits Plasmodium infection by regulating multiple host immune responses and could serve as a potential strategy for facilitating malaria treatment.</p

Image_5_Mannose inhibits Plasmodium parasite growth and cerebral malaria development via regulation of host immune responses.jpeg

D-mannose can be transported into a variety of cells via glucose transporter (GLUT), and supraphysiological levels of D-mannose impairs tumor growth and modulates immune cell function through mechanisms such as interference with glycolysis and induction of oxidative stress. Blood-stage Plasmodium mainly depends on glycolysis for energy supply and pathological immune response plays a vital role in cerebral malaria. However, it is not clear whether mannose affects malaria blood-stage infection. Here, we fed D-mannose to Plasmodium berghei-infected mice and found weight loss and reduced parasitemia without apparent side effects. Compromised parasitemia in C57BL/6 mice was accompanied by an increase in splenic macrophages compared to an untreated group. When mannose was applied to a rodent experimental cerebral malaria (ECM) model, the incidence of ECM decreased. Expression of activation marker CD69 on T cells in peripheral blood and the brain were reduced, and cerebral migration of activated T cells was prevented by decreased expression of CXCR3. These findings suggest that mannose inhibits Plasmodium infection by regulating multiple host immune responses and could serve as a potential strategy for facilitating malaria treatment.</p

Image_6_Mannose inhibits Plasmodium parasite growth and cerebral malaria development via regulation of host immune responses.jpeg

D-mannose can be transported into a variety of cells via glucose transporter (GLUT), and supraphysiological levels of D-mannose impairs tumor growth and modulates immune cell function through mechanisms such as interference with glycolysis and induction of oxidative stress. Blood-stage Plasmodium mainly depends on glycolysis for energy supply and pathological immune response plays a vital role in cerebral malaria. However, it is not clear whether mannose affects malaria blood-stage infection. Here, we fed D-mannose to Plasmodium berghei-infected mice and found weight loss and reduced parasitemia without apparent side effects. Compromised parasitemia in C57BL/6 mice was accompanied by an increase in splenic macrophages compared to an untreated group. When mannose was applied to a rodent experimental cerebral malaria (ECM) model, the incidence of ECM decreased. Expression of activation marker CD69 on T cells in peripheral blood and the brain were reduced, and cerebral migration of activated T cells was prevented by decreased expression of CXCR3. These findings suggest that mannose inhibits Plasmodium infection by regulating multiple host immune responses and could serve as a potential strategy for facilitating malaria treatment.</p

Image_3_Mannose inhibits Plasmodium parasite growth and cerebral malaria development via regulation of host immune responses.jpeg

D-mannose can be transported into a variety of cells via glucose transporter (GLUT), and supraphysiological levels of D-mannose impairs tumor growth and modulates immune cell function through mechanisms such as interference with glycolysis and induction of oxidative stress. Blood-stage Plasmodium mainly depends on glycolysis for energy supply and pathological immune response plays a vital role in cerebral malaria. However, it is not clear whether mannose affects malaria blood-stage infection. Here, we fed D-mannose to Plasmodium berghei-infected mice and found weight loss and reduced parasitemia without apparent side effects. Compromised parasitemia in C57BL/6 mice was accompanied by an increase in splenic macrophages compared to an untreated group. When mannose was applied to a rodent experimental cerebral malaria (ECM) model, the incidence of ECM decreased. Expression of activation marker CD69 on T cells in peripheral blood and the brain were reduced, and cerebral migration of activated T cells was prevented by decreased expression of CXCR3. These findings suggest that mannose inhibits Plasmodium infection by regulating multiple host immune responses and could serve as a potential strategy for facilitating malaria treatment.</p

Self-Polycondensing Hypercross-Linked Polymers from Hydroxybenzyl Alcohols for Efficient Cesium Adsorption

Demand for cesium (Cs) is increasing, and production of Cs from solid ores is energy-intensive. Isolation and extraction of Cs from salt lakes and brines could provide a more sustainable approach to help meet Cs demand, but materials with high selectivity and capacity for Cs are required due to the extremely low concentration of Cs and high concentrations of interfering ions. In this work, we developed self-polycondensing hypercross-linked polymers (HCP-HBAs) from commercial benzyl alcohols substituted by hydroxyl groups at different positions (ortho-, meta-, and para-). Through the cooperative coordination of residual hydroxymethyl groups, mesoporous HCP-HBAs displayed boosted Cs+ capacity and selectivity. Among three polymers, HCP-o-HBA possessed the highest adsorption capacity (302.1 mg g–1) and separation factor (S.F.) values for Cs+/K+ (44.7), Cs+/Rb+ (13.8), and Cs+/Mg2+ (10.1), surpassing most reported porous organic and inorganic adsorbents. Besides, HCP-o-HBA also exhibited rapid adsorption kinetics (5 min, 80% adsorption capacity) and excellent recycle performance (5 cycles, >90% removal efficiency). This study presents the promising application potential of HCP-o-HBA for highly efficient and selective cesium extraction from brines and wastewater

Image_2_Mannose inhibits Plasmodium parasite growth and cerebral malaria development via regulation of host immune responses.jpeg

D-mannose can be transported into a variety of cells via glucose transporter (GLUT), and supraphysiological levels of D-mannose impairs tumor growth and modulates immune cell function through mechanisms such as interference with glycolysis and induction of oxidative stress. Blood-stage Plasmodium mainly depends on glycolysis for energy supply and pathological immune response plays a vital role in cerebral malaria. However, it is not clear whether mannose affects malaria blood-stage infection. Here, we fed D-mannose to Plasmodium berghei-infected mice and found weight loss and reduced parasitemia without apparent side effects. Compromised parasitemia in C57BL/6 mice was accompanied by an increase in splenic macrophages compared to an untreated group. When mannose was applied to a rodent experimental cerebral malaria (ECM) model, the incidence of ECM decreased. Expression of activation marker CD69 on T cells in peripheral blood and the brain were reduced, and cerebral migration of activated T cells was prevented by decreased expression of CXCR3. These findings suggest that mannose inhibits Plasmodium infection by regulating multiple host immune responses and could serve as a potential strategy for facilitating malaria treatment.</p

Image_1_Mannose inhibits Plasmodium parasite growth and cerebral malaria development via regulation of host immune responses.jpeg

D-mannose can be transported into a variety of cells via glucose transporter (GLUT), and supraphysiological levels of D-mannose impairs tumor growth and modulates immune cell function through mechanisms such as interference with glycolysis and induction of oxidative stress. Blood-stage Plasmodium mainly depends on glycolysis for energy supply and pathological immune response plays a vital role in cerebral malaria. However, it is not clear whether mannose affects malaria blood-stage infection. Here, we fed D-mannose to Plasmodium berghei-infected mice and found weight loss and reduced parasitemia without apparent side effects. Compromised parasitemia in C57BL/6 mice was accompanied by an increase in splenic macrophages compared to an untreated group. When mannose was applied to a rodent experimental cerebral malaria (ECM) model, the incidence of ECM decreased. Expression of activation marker CD69 on T cells in peripheral blood and the brain were reduced, and cerebral migration of activated T cells was prevented by decreased expression of CXCR3. These findings suggest that mannose inhibits Plasmodium infection by regulating multiple host immune responses and could serve as a potential strategy for facilitating malaria treatment.</p

Characteristics of eligible studies.

<p>Characteristics of eligible studies.</p

The prognostic and clinicopathologic characteristics of CD147 and esophagus cancer: A meta-analysis

<div><p>Objective</p><p>The prognostic significance of CD147 expression in esophageal cancer patients remains controversial. Using a meta-analysis, we investigated the prognostic and clinicopathologic characteristics of CD147 in esophageal cancer.</p><p>Methods</p><p>A comprehensive literature search of the PubMed (1966–2016), EMBASE (1980–2016), Cochrane Library (1996–2016), Web of Science (1945–2016), China National Knowledge Infrastructure (1982–2016), and Wanfang databases (1988–2016) was performed to identify studies of all esophageal cancer subtypes. Correlations between CD147 expression and survival outcomes and clinicopathological features were analyzed using meta-analysis methods.</p><p>Results</p><p>Seventeen studies were included. High CD147 expression reduced the 3-year survival rate (OR = 3.26, 95% CI = (1.53, 6.93), p = 0.02) and 5-year survival rate(OR = 4.35, 95% CI = (2.13, 8.90), p < 0.0001). High CD147 expression reduced overall survival in esophageal cancer (HR = 1.60, 95% CI = (1.19, 2.15), p = 0.02). Additionally, higher CD147 expression was detected in esophageal cancer tissues than noncancerous tissues (OR = 9.45, 95% CI = (5.39, 16.59), p < 0.00001), normal tissues (OR = 12.73, 95% CI = (3.49, 46.46), p = 0.0001), para-carcinoma tissues (OR = 12.80, 95% CI = (6.57, 24.92), p < 0.00001), and hyperplastic tissues (OR = 3.27, 95% CI = (1.47, 7.29), p = 0.004). CD147 expression was associated with TNM stage (OR = 3.66, 95% CI = (2.20, 6.09), p < 0.00001), tumor depth (OR = 7.97, 95% CI = (4.13, 15.38), p < 0.00001), and lymph node status (OR = 5.14, 95% CI = (2.03,13.01), p = 0.0005), but not with tumor differentiation, age, or sex.</p><p>Conclusion</p><p>Our meta-analysis suggests that CD147 is an efficient prognostic factor in esophageal cancer. High CD147 expression in patients with esophageal cancer was associated with worse survival outcomes and common clinicopathological indicators of poor prognosis.</p></div