Fourier sum of squares certificates

The non-negativity of a function on a finite abelian group can be certified by its Fourier sum of squares (FSOS). In this paper, we propose a method of certifying the non-negativity of an integer-valued function by an FSOS certificate, which is defined to be an FSOS with a small error. We prove the existence of exponentially sparse polynomial and rational FSOS certificates and we provide two methods to validate them. As a consequence of the aforementioned existence theorems, we propose a semidefinite programming (SDP)-based algorithm to efficiently compute a sparse FSOS certificate. For applications, we consider certificate problems for maximum satisfiability (MAX-SAT) and maximum k-colorable subgraph (MkCS) and demonstrate our theoretical results and algorithm by numerical experiments

Effect of triptolide on proliferation and apoptosis of angiotensin II-induced cardiac fibroblasts in vitro: a preliminary study

Background: The effect of triptolide (TPL) on cardiac fibroblasts (CFbs) and cardiac fibrosis remain unknown till now. This study was conducted to explore the effects of TPL on proliferation and apoptosis of angiotensin II (Ang II)-induced CFbs.Materials and Methods: Ang II was used to promote proliferation of CFbs. Two dosages of TPL (10ng/ml and 100ng/ml) were chosen. MTT assay was used to detect cell survival rate in vitro. Flow cytometer was performed to analyze apoptosis of CFbs. Hydroxyproline concentration was detected with hydroxyproline assay kit. Quantitative real-time PCR was used to detect the expression of TGF-β1 and Smad3 mRNA.Results: Ang II promoted CFbs proliferation significantly. Compared to Ang II group, TPL markedly reduced the viability of CFbs and its Hydroxyproline concentration (P<0.05). Besides, TPL can significantly promote apoptosis of CFbs (P<0.05). Furthermore, TPL reduced the expressions of TGF-β1 and Smad3 mRNA in Ang II-induced CFbs (P<0.05).Conclusion: TPL can inhibit the proliferation of CFbs in rats by down-regulating TGF-β1/Smad3 signaling pathway. TPL might be a promising therapeutic drug for myocardial fibrosis.Keywords: Cardiac fibroblast; triptolide; proliferation; apoptosis; angiotensi

Different effects of morning and nocturnal hypertension on target organ damage in chronic kidney disease

Both morning hypertension (MH) and nocturnal hypertension (NH) are associated with severe target organ damage in patients with chronic kidney disease (CKD). However, the isolated or combined effects of MH and NH on target organ damage are less well‐defined. A cross‐sectional study was conducted among 2386 non‐dialysis CKD patients with ambulatory blood pressure monitoring. The authors categorized patients into four groups based on the presence or absence of MH and NH. Multivariate logistic analyses were used to evaluate the correlation between hypertension subtypes and target organ damage, including left ventricular hypertrophy (LVH), abnormal carotid intima‐media thickness (CIMT), low estimated glomerular filtration rate (eGFR), and albuminuria. The percentages of isolated MH, isolated NH, and combined MH and NH were 2.3%, 24.0%, and 49.3%, respectively. Compared to patients without MH and NH, isolated MH was only related to low eGFR (2.26 [95% confidence interval: 1.00–5.09]) and albuminuria (2.17 [95% CI: 1.03–4.54]). Meanwhile, combined MH and NH group compared to the group without MH and NH had a higher risk of LVH (2.87 [95% CI: 2.01–4.09]), abnormal CIMT (2.01 [95% CI: 1.47–2.75]), low eGFR (3.18 [95% CI: 2.23–4.54]), and albuminuria (1.79 [95% CI: 1.33–2.40]), even in patients without daytime hypertension. The risk of cardiovascular and renal damage was also observed in the isolated NH group. In conclusion, morning hypertension is associated with kidney dysfunction and has combined effects with nocturnal hypertension on cardiovascular damage in chronic kidney disease patients

Prognostic value of inflammation-based scores in patients receiving radical resection for colorectal cancer

Abstract Background The modified Glasgow Prognostic Score (mGPS) and the neutrophil-to-lymphocyte ratio (NLR) are conventional inflammation-based scores for colorectal cancer (CRC). The systemic inflammation score (SIS) has been shown to be more informative than the mGPS in CRC. The albumin-NLR, composed of albumin and the NLR, can also be a candidate for a valuable inflammation score. However, about the utility of the mGPS, SIS, and albumin-NLR for CRC patients who have received radical resections remains unclear. Methods This study enrolled 877 CRC patients, who underwent radical surgical resection between January 1, 2007 and December 31, 2014. The prognostic values of the mGPS, SIS, and albumin-NLR were compared by the Kaplan-Meier survival analysis, multivariate Cox regression modelling, and the time-dependent receiver operating characteristic curve analysis (ROC). Results In the Kaplan-Meier analysis, all three inflammation scores were significantly associated with overall survival (OS) in the group including all the patients (mGPS, p = 0.016; SIS, p < 0.001; albumin-NLR, p = 0.007) and in the left-sided colon tumour subgroup (mGPS, p = 0.029; SIS p = 0.0013; albumin-NLR, p = 0.001). In the right-sided colon tumour subgroup, only the albumin-NLR was associated with OS (p = 0.048). The albumin-NLR was the only independent prognostic factor of the three scores for OS in the multivariate survival analysis. Conclusions The albumin-NLR outperformed both the SIS and mGPS in predicting OS in CRC patients undergoing radical resection

Overexpression of Circulating Soluble Nogo-B Improves Diabetic Kidney Disease by Protecting the Vasculature

Damage to the vasculature is the primary mechanism driving chronic diabetic microvascular complications such as diabetic nephropathy, which manifests as albuminuria. Therefore, treatments that protect the diabetic vasculature have significant therapeutic potential. Soluble neurite outgrowth inhibitor-B (sNogo-B) is a circulating N-terminus isoform of full-length Nogo-B, which plays a key role in vascular remodeling following injury. However, there is currently no information on the role of sNogo-B in the context of diabetic nephropathy. We demonstrate that overexpression of sNogo-B in the circulation ameliorates diabetic kidney disease by reducing albuminuria, hyperfiltration, and abnormal angiogenesis and protecting glomerular capillary structure. Systemic sNogo-B overexpression in diabetic mice also associates with dampening vascular endothelial growth factor-A signaling and reducing endothelial nitric oxide synthase, AKT, and GSK3β phosphorylation. Furthermore, sNogo-B prevented the impairment of tube formation, which occurred when human endothelial cells were exposed to sera from patients with diabetic kidney disease. Collectively, these studies provide the first evidence that sNogo-B protects the vasculature in diabetes and may represent a novel therapeutic target for diabetic vascular complications