Nodeless superconductivity in a quasi-two-dimensional superconductor AuTe2Se(4/3)

We performed ultra-low temperature thermal conductivity measurements on the single crystal of a new gold-based quasi-two-dimensional superconductor Au Te2Se（4/3）, which has a superconducting transition temperature Tc = 2.70 K. A negligible residual linear term κ0/T in zero magnetic field is observed, which suggests fully gapped superconducting state.Furthermore, the field dependence of κ0/T is similar to that of the multi-band s-wave superconductor Ba Fe1.9 Ni0.1 As2 at low field. These results reveal multiple nodeless superconducting gaps in this interesting quasi-two-dimensional superconductor with Berezinsky–Kosterlitz–Thouless topological transition.

T cell infiltration is associated with kidney injury in patients with anti-glomerular basement membrane disease

Cell-mediated autoimmunity, particularly that involving autoreactive T cells, participates in mediating anti-glomerular basement membrane(GBM) disease. However, direct kidney injury mediated by renal infiltrated T cells has not been clearly elucidated in humans. The T cell profile(CD3, CD4, CD8, IL-17, and foxp3) and macrophage(CD68) were examined by immunohistochemistry on renal biopsy tissues from 13 patients with anti-GBM disease. The correlation between cell infiltration and clinical data was also analyzed. We found that the distribution of T cell infiltration was predominant in the peri-glomerular and interstitial areas. CD3^+ T cell infiltratrion around the glomeruli with cellular crescent formations was significantly higher than that around the glomeruli with mild mesangial proliferation. CD8^+ T cells significantly accumulated around the glomeruli with cellular crescents without Ig G deposits compared to those with Ig G deposits. The prevalence of infiltrating CD8^+ T cells was correlated with the percentage of ruptured Bowman's capsules. In conclusion, cellular immunity may play a crucial role in the inflammatory kidney injury in anti-GBM patients. The periglomerular infiltration of T cells, especially CD8^+ T cells, may participate in the pathogenic mechanism of glomerular damage.

Shenqi Xingnao Granules ameliorates cognitive impairments and Alzheimer’s disease-like pathologies in APP/PS1 mouse model

Objective:Alzheimer’s disease(AD)is along with cognitive decline due to amyloid-β(Aβ)plaques,tau hyperphospho rylation,and neuron loss.Shenqi Xingnao Granules(SQXN),a traditional Chinese medicine,significantly ameliorated the cognitive function and daily living abilities of patients with AD.However,till date,no study has investigated the mechanism of action of SQXN on AD.The present study aimed to verify the effects of SQXN treatment on cognitive impairments and AD-like pathologies in APP/PS1 mice.Methods:Four-month-old APP/PS1 transgenic(Tg)mice were randomly divided into a model group and SQXN-treated(3.5,7,14 g/kg per day)groups.Learning-memory abilities were determined by Morris water maze and object recognition test.All mice were sacrificed and the brain samples were collected after 75 d.The soluble Aβcontents were detected by Elisa kit;The levels of expression of NeuN,APP,phosphorylated tau and related protein were measured by Western blotting;The inflammation factors were detected by the proinflammatory panel kit.Results:Four-month-old APP/PS1 mice were administered SQXN by oral gavage for 2.5 months.Using the Morris water maze tests and Novel object recognition,we found that SQXN restored behavioral deficits in the experimental group of Tg mice when compared with the controls.SQXN also inhibited neuronal loss(NeuN marker).SQXN treatment decreased soluble Aβ42 through inhibiting the expression of sAPPβand BACE-1 without regulating full-length amyloid precursor protein(FL APP).Insulin degrading enzyme(IDE),the Aβdegrading enzyme,were increased by SQXN.In addition,SQXN reduced hyperphosphorylated tau protein levels and prevented excessive activation of p-GSK-3βin the brain of APP/PS1 mice.Compared with APP/PS1 transgenic negative mice,IFN-γ,IL-1β,IL-2,IL-4,IL-5,IL-6,IL-12 p70,KC/GRO and TNF-αwere not obviously changed in the brain of 6.5-month-old APP/PS1 transgenic(Tg)mice.However,SQXN could inhibited the expression of IL-2.Conclusion:These results demonstrate that SQXN ameliorates the cognitive impairments in APP/PS1 mice.The possible mechanisms involve its inhibition of neuronal loss,soluble Aβdeposition,tau hyperphosphorylation and inflammation.