Orthogonality catastrophe and quantum speed limit for spin chain at finite temperature.

We present an interesting relationship between the orthogonality catastrophe (OC) and the quantum speed limit (QSL) for a spin chain with uniform nearest neighbour couplings perturbed by an impurity spin. We thoroughly study the catastrophic QSL that specifies a bound on the evolution time between the initial and final states and in this respect, link it to the emerging OC effect. It is found that the speed of state evolution subtle but fundamental, and the bound characterized by QSL shows the same behaviours as the OC effect in the thermodynamic limit. It allows us to reveal some universal properties, in particular finite temperature effects. Significantly, the threshold of temperature and system size is clearly demonstrated for the QSL under finite temperature.

Predictors of primary patency after percutaneous balloon angioplasty for stenosis of Brescia-Cimino hemodialysis arteriovenous fistula.

OBJECTIVE: Percutaneous transluminal balloon angioplasty (PTA) is recommended as the first choice to treat stenosis of Brescia-Cimino arteriovenous fistulas (B-C AVFs). The ability to predict which B-C AVFs are at risk for recurrent stenosis post-PTA would allow closer monitoring of patients, and possibly result in surgical intervention rather than repeat PTA. The purpose of this study was to identify predictive factors of primary patency after PTA in B-C AVFs. METHODS: Patients diagnosed with B-C AVF primary stenosis and treated by PTA between November 2013 and March 2018 were included in the study. Patient and stenotic lesion characteristics and PTA procedure factors were included in the analysis. The Kaplan-Meier method was used to analyze the primary patency rate. Cox proportional hazard regression analysis was used to identify factors predictive of decreased primary patency. RESULTS: 74 patients (35 males, 39 females) with a mean age of 61.68 ± 11.44 years (range, 36-84 years) were included in the study. The mean B-C AVF age was 16.34 ± 12.93 months (range, 2-84 months), and the median primary patency time was 7.79 ± 0.48 months. Cox proportional hazard regression analysis revealed stenosis location at the inflow artery [hazard ratio (HR)=3.83, 95% confidence interval (CI): 1.46-10.09] or anastomosis (HR = 1.90, 95% CI: 1.09-3.32), dilation >2 times during PTA (HR = 2.30, 95% CI: 1.22-4.34), and residual stenosis >30% (HR = 2.42, 95% CI: 1.26-4.63) were significantly associated with decreased patency. CONCLUSION: In conclusion, the primary patency rate of PTA for B-C AVF dysfunction is reduced by dilation >2 times, residual stenosis >30%, and stenosis located at the inflow artery or anastomosis. These results may help in tailoring surveillance programs, multiple PTA, or a proximal re-anastomosis surgery in patients with AVF dysfunction. ADVANCES IN KNOWLEDGE: A number of studies have been conducted to examine the predictors of primary patency after PTA, however, no definitive conclusions have been reached. Our study revealed that stenosis location at the inflow artery or anastomosis, dilation >2 times during PTA, and residual stenosis >30% were the predictors of primary patency after PTA, which may help in tailoring surveillance programs, multiple PTA, or a proximal re-anastomosis surgery in patients with arteriovenous fistulas dysfunction.

MiR-140-3p is Involved in In-Stent Restenosis by Targeting C-Myb and BCL-2 in Peripheral Artery Disease.

AIM: In-Stent Restenosis (ISR) is the major reason for recurrent ischemia and amputation after endovascular treatment of Peripheral Artery Disease (PAD). Our previous study demonstrated that miR-140-3p is significantly down-regulated in PAD arteries. However, expression and function of miR-140-3p in ISR of human PAD are currently unclear.The aim of this study is to determine the miR-140-3p expression and its regulative role in ISR of PAD. METHODS: The RNA level was determined by quantitative real-time polymerase chain Reaction (qRT-PCR) and in situ hybridization. Primary cultured ASMCs were isolated from human femoral arterial of the healthy donors or ISR patients. Cell proliferation was determined by Edu incorporation and CCK-8 assay. Apoptosis was determined by Annexin-Ⅴ/PI Double-Staining assay and TUNEL assay. A rat carotid artery balloon angioplasty model was used to investigate the effect of miR-140-3p on restenosis. RESULTS: MiR-140-3p was significantly down-regulated in PAD and ISR arteries than normal arteries. Primary cultured ISR ASMCs exhibited elevated proliferation and down-regulated miR-140-3p than normal ASMCs. Transfection of miR-140-3p mimic attenuated PDGF-BB-induced proliferation in cultured ASMCs and induced apoptosis. Luciferase reporter assay indicated that miR-140-3p transfection significantly down-regulated C-Myb and BCL-2 in ISR ASMCs by targeting to their 3'-UTRs. MiR-140-3p transfection induced anti-proliferation and apoptosis in ASMCs, which were ameliorated by over-expression of C-Myb or BCL-2. Moreover, the animal study showed that miR-140-3p can reduce restenosis following angioplasty via targeting C-Myb and BCL-2. CONCLUSIONS: The result suggests that miR-140-3p regulates ASMC function via targeting C-Myb and BCL-2 in the process of ISR in PAD. The novel findings may offer a hopeful therapeutic target for human PAD.

3-(4-Chloro-phen-yl)-2-(diisopropyl-amino)-1-benzofuro[3,2-d]pyrimidin-4(3H)-one.

In the mol-ecule of the title compound, C(22)H(22)ClN(3)O(2), the three fused rings of the benzofuro[3,2-d]pyrimidine system are almost coplanar. This ring system is oriented with respect to the substituted benzene ring at a dihedral angle of 79.05 (3)°. Intra-molecular C-H⋯N hydrogen bonding results in the formation of a six-membered ring. In the crystal structure, π-π stacking inter-actions involving the furan, pyrimidinone and benzene rings are present [centroid-to-centroid distances in the range 3.258 (1)-3.870 (1) Å].

Ethyl 2-[1-(4-chloro-phen-yl)-2,5-dioxo-1,2,3,5-tetra-hydro-imidazo[1',2':1,2]pyrimidino[5,4-b][1]benzofuran-3-yl]acetate.

The asymmetric unit of the title compound, C(22)H(16)ClN(3)O(5), consists of two crystallographically independent mol-ecules. The fused rings of the imidazo[1,2-a]benzo[4,5]furo[3,2-d]pyrimidine system are nearly coplanar and the chlorophenyl rings are twisted with respect to the two pyrimidinone ring systems by 71.00 (2) and 62.59 (2)°. The C atoms of the ethyl side chain are disordered and were refined using a split model. In the crystal structure, the mol-ecules are connected via weak intra- and inter-molecular C-H⋯O inter-actions are present. The ethyl group in one molecule is disordered over two positions, with site occupancy factors 0.55 and 0.45; in the other molecule only the methyl group is disordered over two positions, with site occupancy factors 0.6 and 0.4.