Effect of estrogen application timing on adipose tissue revascularization and immune regulation in rats after autologous fat transplantation

Purpose: To study the effect of timing of estrogen application on adipose tissue revascularization and immune regulation in rats given autologous fat transplantation.Methods: Ninety (90) healthy rats were selected for use in this study. The rats were randomly divided into a study group (n = 45) and control group (n = 45). After ovariectomy, the study group was given estrogen replacement therapy before autologous fat transplantation, while the control group was given estrogen replacement therapy after autologous fat transplantation. The rats were observed for 6 weeks after transplantation. Micro-vessel density, wet weight of transplanted fat, VEGF expression level, levels of M1 and M2 in macrophages, and macrophage infiltration rate were determined 40 days postautologous fat transplantation.Results: Forty days after autologous fat transplantation, microvessel density, wet weight of transplanted fat, expression level of VEGF and levels of M1 and M2 in macrophages were significantly higher in study group rats than in controls (p < 0.05). There was 80 % macrophage infiltration in the study group rats, while the corresponding control value (61 %) was significantly lower (p < 0.05).Conclusion: Estrogen treatment before autologous fat transplantation in rats is helpful for the revascularization of adipose tissue, enhances vascular regeneration, promotes the survival of adipose tissue after transplantation, and activates immune cells. It also promotes the production of immune factors, and improves immunoregulation in adipose tissue. Thus, this therapeutic strategy may be useful in clinical practice, but further clinical trials are required

Harrison center and products of sums of powers

This paper is mainly concerned with identities like $$(x_1^d + x_2^d + \cdots + x_r^d) (y_1^d + y_2^d + \cdots y_n^d) = z_1^d + z_2^d + \cdots + z_n^d$$ where $d>2,$ $x=(x_1, x_2, \dots, x_r)$ and $y=(y_1, y_2, \dots, y_n)$ are systems of indeterminates and each $z_k$ is a linear form in $y$ with coefficients in the rational function field \k (x) over any field \k of characteristic $0$ or greater than $d.$ These identities are higher degree analogue of the well-known composition formulas of sums of squares of Hurwitz, Radon and Pfister. We show that such composition identities of sums of powers of degree at least $3$ are trivial, i.e., if $d>2,$ then $r=1.$ Our proof is simple and elementary, in which the crux is Harrison's center theory of homogeneous polynomials.Comment: 6 page

A Pseudo DNA Cryptography Method

The DNA cryptography is a new and very promising direction in cryptography research. DNA can be used in cryptography for storing and transmitting the information, as well as for computation. Although in its primitive stage, DNA cryptography is shown to be very effective. Currently, several DNA computing algorithms are proposed for quite some cryptography, cryptanalysis and steganography problems, and they are very powerful in these areas. However, the use of the DNA as a means of cryptography has high tech lab requirements and computational limitations, as well as the labor intensive extrapolation means so far. These make the efficient use of DNA cryptography difficult in the security world now. Therefore, more theoretical analysis should be performed before its real applications. In this project, We do not intended to utilize real DNA to perform the cryptography process; rather, We will introduce a new cryptography method based on central dogma of molecular biology. Since this method simulates some critical processes in central dogma, it is a pseudo DNA cryptography method. The theoretical analysis and experiments show this method to be efficient in computation, storage and transmission; and it is very powerful against certain attacks. Thus, this method can be of many uses in cryptography, such as an enhancement insecurity and speed to the other cryptography methods. There are also extensions and variations to this method, which have enhanced security, effectiveness and applicability.Comment: A small work that quite some people asked abou

Integrating BWM and ARAS under hesitant linguistic environment for digital supply chain finance supplier section

In the era of intelligence and informatization, digital supply chain finance (DSCF) has become one of the important trends in the development of supply chain finance. With the gradual increase of DSCF suppliers and various requirements of small and medium-sized enterprises for suppliers in providing financing services, selecting the most suitable DSCF supplier is of great significance for most small and medium-sized enterprises to expand reproduction and improve competitiveness. To address such a decision-making problem, this paper proposes a new multi-expert multiple criteria decision-making model by integrating the Best Worst Method (BWM) and Additive Ratio ASsessment (ARAS) method under the hesitant fuzzy linguistic environment, in which the hesitant fuzzy linguistic BWM method is applied to determine the weights of criteria while the hesitant fuzzy linguistic ARAS method is proposed to rank the candidate suppliers. A case study is given to demonstrate the procedure of the proposed method for the selection of optimal DSCF suppliers, which shows the feasibility of the proposed method. Finally, sensitivity analysis and comparative analyses are provided to testify the applicability and superiority of the proposed method

High affinity binding of H3K14ac through collaboration of bromodomains 2, 4 and 5 is critical for the molecular and tumor suppressor functions of PBRM1.

Polybromo-1 (PBRM1) is an important tumor suppressor in kidney cancer. It contains six tandem bromodomains (BDs), which are specialized structures that recognize acetyl-lysine residues. While BD2 has been found to bind acetylated histone H3 lysine 14 (H3K14ac), it is not known whether other BDs collaborate with BD2 to generate strong binding to H3K14ac, and the importance of H3K14ac recognition for the molecular and tumor suppressor function of PBRM1 is also unknown. We discovered that full-length PBRM1, but not its individual BDs, strongly binds H3K14ac. BDs 2, 4, and 5 were found to collaborate to facilitate strong binding to H3K14ac. Quantitative measurement of the interactions between purified BD proteins and H3K14ac or nonacetylated peptides confirmed the tight and specific association of the former. Interestingly, while the structural integrity of BD4 was found to be required for H3K14ac recognition, the conserved acetyl-lysine binding site of BD4 was not. Furthermore, simultaneous point mutations in BDs 2, 4, and 5 prevented recognition of H3K14ac, altered promoter binding and gene expression, and caused PBRM1 to relocalize to the cytoplasm. In contrast, tumor-derived point mutations in BD2 alone lowered PBRM1\u27s affinity to H3K14ac and also disrupted promoter binding and gene expression without altering cellular localization. Finally, overexpression of PBRM1 variants containing point mutations in BDs 2, 4, and 5 or BD2 alone failed to suppress tumor growth in a xenograft model. Taken together, our study demonstrates that BDs 2, 4, and 5 of PBRM1 collaborate to generate high affinity to H3K14ac and tether PBRM1 to chromatin. Mutations in BD2 alone weaken these interactions, and this is sufficient to abolish its molecular and tumor suppressor functions

PBRM1 acts as a p53 lysine-acetylation reader to suppress renal tumor growth.

p53 acetylation is indispensable for its transcriptional activity and tumor suppressive function. However, the identity of reader protein(s) for p53 acetylation remains elusive. PBRM1, the second most highly mutated tumor suppressor gene in kidney cancer, encodes PBRM1. Here, we identify PBRM1 as a reader for p53 acetylation on lysine 382 (K382Ac) through its bromodomain 4 (BD4). Notably, mutations on key residues of BD4 disrupt recognition of p53 K382Ac. The mutation in BD4 also reduces p53 binding to promoters of target genes such as CDKN1A (p21). Consequently, the PBRM1 BD4 mutant fails to fully support p53 transcriptional activity and is defective as a tumor suppressor. We also find that expressions of PBRM1 and p21 correlate with each other in human kidney cancer samples. Our findings uncover a tumor suppressive mechanism of PBRM1 in kidney cancer and provide a mechanistic insight into the crosstalk between p53 and SWI/SNF complexes

Multiple tumor suppressors regulate a HIF-dependent negative feedback loop via ISGF3 in human clear cell renal cancer.

Whereas VHL inactivation is a primary event in clear cell renal cell carcinoma (ccRCC), the precise mechanism(s) of how this interacts with the secondary mutations in tumor suppressor genes, including PBRM1, KDM5C/JARID1C, SETD2, and/or BAP1, remains unclear. Gene expression analyses reveal that VHL, PBRM1, or KDM5C share a common regulation of interferon response expression signature. Loss of HIF2α, PBRM1, or KDM5C in VHL-/-cells reduces the expression of interferon stimulated gene factor 3 (ISGF3), a transcription factor that regulates the interferon signature. Moreover, loss of SETD2 or BAP1 also reduces the ISGF3 level. Finally, ISGF3 is strongly tumor-suppressive in a xenograft model as its loss significantly enhances tumor growth. Conversely, reactivation of ISGF3 retards tumor growth by PBRM1-deficient ccRCC cells. Thus after VHL inactivation, HIF induces ISGF3, which is reversed by the loss of secondary tumor suppressors, suggesting that this is a key negative feedback loop in ccRCC. © 2018, Liao et al

Cdc42-Interacting Protein-4 Promotes TGF-Β1-Induced Epithelial-Mesenchymal Transition and Extracellular Matrix Deposition in Renal Proximal Tubular Epithelial Cells

Cdc42-interacting protein-4 (CIP4) is an F-BAR (Fer/CIP4 and Bin, amphiphysin, Rvs) family member that regulates membrane deformation and endocytosis, playing a key role in extracellular matrix (ECM) deposition and invasion of cancer cells. These processes are analogous to those observed during the initial epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. The role of CIP4 in renal tubular EMT and renal tubulointerstitial fibrosis was investigated over the course of the current study, demonstrating that the expression of CIP4 increased in the tubular epithelia of 5/6-nephrectomized rats and TGF-β1 treated HK-2 cells. Endogenous CIP4 evidenced punctate localization throughout the cytosol, with elevated levels observed in the perinuclear region of HK-2 cells. Subsequent to TGF-β1 treatment, CIP4 expression increased, forming clusters at the cell periphery that gradually redistributed into the cytoplasm. Simultaneously, EMT induction in cells was confirmed by the prevalence of morphological changes, loss of E-cadherin, increase in α-SMA expression, and secretion of fibronectin. Overexpression of CIP4 promoted characteristics similar to those commonly observed in EMT, and small interfering RNA (siRNA) molecules capable of CIP4 knockdown were used to demonstrate reversed EMT. Cumulatively, results of the current study suggest that CIP4 promotes TGF-β1-induced EMT in tubular epithelial cells. Through this mechanism, CIP4 is capable of inducing ECM deposition and exacerbating progressive fibrosis in chronic renal failure