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Superfine wool fiber has a soft and luxurious texture, excellent moisture absorption and is warmer and more comfortable than ordinary wool. Liquid ammonia, which has exceptional permeability, exerts a certain modification effect on the surface scales of wool in the finishing and processing of wool fabric, thereby enhancing its wear performance. However, limited research has been conducted on the impact of liquid ammonia on valuable wool fibers such as superfine wool and cashmere. In this article, superfine wool tops were treated with continuous liquid ammonia finishing equipment and the effects of liquid ammonia on the microstructure and surface morphology of superfine wool fiber were investigated. In addition, the changes in length, fineness, anti-felting, and dyeing properties of superfine wool fiber after liquid ammonia treatment were examined. The results demonstrated that the interstitial integrity of intercellular substance of superfine wool was compromised following treatment with liquid ammonia, which had a greater tendency to infiltrate cortical cells and induce alterations in wool structure and performance. Furthermore, the surface scales of superfine wool were damaged after treatment with liquid ammonia, leading to improved anti-felting and dyeing properties. [ABSTRACT FROM AUTHOR]

Aplastic anaemia (AA) is an autoimmune disease characterized by haematopoietic failure in the bone marrow. Abnormal activation and hyperfunction of T lymphocytes are believed to cause bone marrow damage, which plays a major role in AA pathogenesis. Dendritic cells (DCs) play a vital role in the immune system by processing antigens for presentation to T cells and regulating their differentiation and function. DC dysfunction may cause abnormal T‐cell activation. Recent studies have associated the occurrence and development of AA with DC function. In this review, we have discussed the role of DCs in AA pathogenesis and their potential as putative therapeutic targets for AA. [ABSTRACT FROM AUTHOR]

Liquid ammonia as a non-aqueous medium has many physical properties close to water, such as small molecular weight and strong permeability. It has been widely used for the ecological processing of cellulosic fibers to improve their luster, softness and dyeing properties. However, there are few reports on the dyeing of wool treated with liquid ammonia, especially at a lower temperature. Herein, a continuous liquid ammonia finishing machine was used to batch process wool followed by dyeing in a commonly-used wool dyeing machine. The results showed that many scale flakes and some cuticle cracking were seen on the fiber surface, and the disulfide bonds of cystine were broken down after liquid ammonia treatment, which promoted the diffusion of dyestuff into the fiber. Moreover, the uptakes and K/S value of wool dyed with Lanaset and Lanasol CE dyes were higher than the untreated wool, and the dyeing temperature could decrease to 85 °C, while the degree of fiber strength reduction merely decreased by 3–5%. Furthermore, for the reactive dyes, the dyeing temperature can reduce to 70 °C with the chemical auxiliaries Miralan LTD, while the degree of strength reduction decrease by 8–10%. Liquid ammonia treatment can be used for dyeing at a lower temperature than boiling temperature (100 °C), reduce energy consumption and reduce the degree of fiber strength reduction of wool. The method shows considerable to great value and is significant in providing a feasible approach for the industrial application of low-temperature dyeing technology. [ABSTRACT FROM AUTHOR]

Embryonic metanephros is the mammalian renal anlagen, which is considered as a potential source for the regeneration of functional whole kidneys. Some studies reported that metanephros implanted into unilateral nephrectomized animals can develop into kidney tissue. However, kidneys are nephrotoxic in renal failure patients, and whether metanephros can grow in nephrotoxic has not been reported. This study aims to investigate the growth of metanephros in acute nephrotoxic environment and analyze the therapeutic effect of metanephros microenvironment on acute kidney injury (AKI). AKI was induced in 200 g Wistar rats by giving intramuscular injections of 50% glycerol (10 mL/kg) in their hind limbs. 45 rats were divided randomly into three groups (control, glycerin, and metanephros). Metanephros group was transplanted two metanephroi (embryonic day 15) into the renal capsule of AKI rats. Glycerin group was AKI rats without transplantation. Control group was untreated. Mature glomeruli and tubules were detected in the grafts in metanephros group, which means that metanephroi can grow into tissues with mature kidney structure under acute nephrotoxic. Then, we assessed the renal function of host rats and found that there were fewer tubular necrosis in metanephros group than glycerin group, and the serum creatinine and urea nitrogen were significantly lower in metanephros group than glycerin group. These results suggested that embryonic metanephroi can grow into tissues with mature kidney structure under acute nephrotoxic, and the graft microenvironment was effective in inhibiting the progression of AKI, which provides a new approach for the treatment of acute renal injury. [ABSTRACT FROM AUTHOR]

The shortage of transplantable organs impedes the development of tissue-engineered alternatives. Producing tissues similar to immature kidneys from pluripotent stem cells is possible in vitro, but the size of the organoids is limited. Furthermore, in vivo implantation is necessary for organoid development and functional maturation. In the present study, the induction procedure was optimized and kidney organoids derived from induced pluripotent stem cells in vitro were produced. The kidney organoids were examined by immunofluorescence and quantitative PCR. Then, a unilateral nephrectomy model was established that was beneficial to the compensatory proliferation of the other kidney. Finally, these organoids were implanted below the kidney capsules of immunodeficient mouse hosts that had been nephrectomized unilaterally. This implantation resulted in the enlargement of the organoids and the production of vascular cells. Although signs of organoid maturation were lacking in short-term culture in vivo, the present study provided a method for studying kidney organoid development in vivo. [ABSTRACT FROM AUTHOR]

Retigeric acid B (RAB), a natural compound isolated from lichen, has been demonstrated to inhibit cell growth and promote apoptosis in prostate cancer (PCa) cells. The present study evaluated the function of RAB combined with clinical chemotherapeutic drugs in PCa cell lines by MTT assay, reverse transcription quantitative polymerase chain reaction and western blot analysis, and identified that RAB at low doses produced significant synergistic cytotoxicity in combination with cisplatin (CDDP); however, no marked synergism between RAB and the other chemotherapeutics was observed. Additional studies revealed that RAB exerted an inhibitory effect on DNA damage repair pathways, including the nucleotide excision repair and mismatch repair pathways, which are involved in the sensitivity to CDDP‑based chemotherapy, as suggested by the significantly downregulated expression of certain associated repair proteins. Notably, Excision repair cross‑complementing 1, a critical gene in the nucleotide excision repair pathway, exhibited the most significant decrease. When combined with CDDP, RAB‑mediated impairment of DNA repair resulted in prolonged DNA damage, as demonstrated by the long‑lasting appearance of phosphorylation of histone H2AX at Ser139, which potentially enhanced the chemosensitivity to CDDP. Concurrently, the proapoptotic protein death receptor 5 (DR5) was activated by RAB, which also enhanced the chemotherapeutic response of CDDP. Knockdown of DR5 partially blocked RAB‑CDDP synergism, suggesting the crucial involvement of DR5 in this event. The results of the present study identified that RAB functioned synergistically with CDDP to increase the efficacy of CDDP by inhibiting DNA damage repair and activating DR5, suggesting the mechanistic basis for the antitumor effect of RAB in combination with current chemotherapeutics. [ABSTRACT FROM AUTHOR]

Abstract: To establish a recellularization kidney model by using adipose tissue‐derived stem cells (ADSCs) as seeding cells and to investigate the growth and differentiation of ADSCs in decellularized kidney scaffolds. ADSCs were isolated using a modified method and then identified using flow cytometry analysis. Osteogenesis and adipogenesis differentiation were performed. Rat kidneys were decellularized using 0.5% sodium dodecyl sulfate. Immunofluorescence, immunohistochemistry, and scanning electron microscope were conducted to examine the scaffold microstructure. The decellularized kidney scaffold was seeded with ADSCs antegrade through the artery or retrograde through the ureter and cultured for 5–10 days. Hematoxylin and eosin staining, immunofluorescence, and immunohistochemistry were applied to assess growth and differentiation of seeding cells within the scaffold. ADSCs populated within the glomerular, vascular, and tubular area of kidney scaffolds. Cells differentiated toward endothelial or tubular cells. Stromal cell‐derived factor 1 promoted cell attachment in the scaffold. These findings suggest that ADSCs can be used as an additional new source of seeding cells within decellularized kidney scaffold. This combination may offer an alternative to donor kidney transplant. In this way, autologous ADSCs can be utilized as seeding cells in cell‐scaffold kidney regeneration for further clinical transplantation. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 805–814, 2018. [ABSTRACT FROM AUTHOR]

Context: Bisbibenzyl compounds have gained our interests for their potential antitumor activity in malignant cell-types. Objective: The objective of this study is to investigate the effect of bisbibenzyl compounds riccardin C (RC), marchantin M (MM), and riccardin D (RD) on androgen receptor (AR) in prostate cancer (PCa) cells. Materials and methods: After exposure to 10 μM of the compounds for 24 h, cell cycle and cell survival analyses were performed using FACS and MTT assay to confirm the effect of these bisbibenzyls on PCa LNCaP cells. Changes in the AR expression and function, as the result of exposure to the compounds, were investigated using real-time PCR, ELISA, transient transfection, western blotting (WB), immunoprecipitation, and immunofluorescence staining (IF). Chemical-induced autophagy was examined by WB, IF, and RNAi. Results: RC, MM, and RD reduced the viability of LNCaP cells accompanied with arrested cell cycle in the G0/G1 phase and induction of apoptosis. Further investigation revealed that these compounds significantly inhibited AR expression at mRNA and protein levels, leading to the suppression of AR transcriptional activity. Moreover, inhibition of proteasome activity by bisbibenzyls, which in turn caused the induction of autophagy, as noted by induction of LC3B expression, conversion, and accumulation of punctate dots in treated cells. Co-localization of AR/LC3B and AR/Ub suggested that autophagy contributed to the degradation of polyubiquitinated-AR when proteasome activity was suppressed by the bisbibenzyls. Discussion and conclusion: Suppression of proteasome activity and induction of autophagy were involved in bisbibenzyl-mediated modulation of AR activities and apoptosis, suggesting their potential in treating PCa. [ABSTRACT FROM PUBLISHER]

Purpose: Our previous studies had shown that Riccardin D (RD) exhibited cytotoxic effects by induction of apoptosis and inhibition of angiogenesis and topoisomerase II. Here, we reported that apoptosis is not the sole mechanism by which RD inhibits tumor cell growth because low concentrations of RD caused cellular senescence in prostate cancer (PCa) cells. Methods: Low concentrations of RD were used to treat PCa cells in vitro and in vivo, and senescence-associated β-galactosidase activity, DNA damage response markers, and/or colony-forming ability, cell cycle were analyzed, respectively. We then used siRNA knockdown to identify key factor in RD-triggered cellular senescence. Results: RD treatment caused growth arrest at G0/G1 phase with features of cellular senescence phenotype such as enlarged and flattened morphology, increased senescence-associated-beta-galactosidase staining cells, and decreased cell proliferation in PCa cells. Induction of cellular senescence by RD occurred through activation of DNA damage response including increases in the phosphor-H2AX, inactivation of Chk1/2, and suppression of repair-related Ku70/86 and phosphor-BRCA1 in PCa cells in vitro and in vivo. Analysis of expression levels of p53, p21, p16, p27, pRb and E2F1 and genetic knockdown of p21 demonstrated an important role of p21 in RD-triggered cellular senescence. Conclusions: Involvement of the DNA damage response and p21 defines a novel mechanism of RD action and indicates that RD could be further developed as a promising anticancer agent for cancer therapy. [ABSTRACT FROM AUTHOR]

It has been suggested that ezrin activation plays a key role in the regulation of cancer metastasis. In this study, we immunohistochemically investigated the expression patterns of total ezrin and its two phosphorylated forms, pEzrin − Thr567 and pEzrin − Tyr353, in 66 samples of invasive pancreatic carcinomas and 11 samples of normal pancreas tissues. Positive expressions of ezrin and pEzrin − Thr567 were detected in most PDAC tissues, significantly higher than that of pEzrin − Tyr353. Furthermore, overexpression of pEzrin − Tyr353 in pancreatic cancers was associated with positive lymph node metastasis, less differentiation, pAkt overexpression, and shorter survival times. pEzrin − Tyr353 may be a potent prognosis predictor for pancreatic cancer. [ABSTRACT FROM AUTHOR]

We identified a group of hypoxia-regulated proteins upregulated in microdissected pancreatic cancer nests compared with normal pancreatic ducts. Immunohistochemical study further validated that pancreatic cancers had significantly higher expression levels of glucose-regulated protein 78, macrophage migration inhibitory factor and annexin A5 than normal pancreas tissues, these protein biomarkers also demonstrated high receiver operating characteristic curves in discriminating pancreatic cancers from normal pancreas. In conclusion, our study indicated a link between pancreatic cancer and hypoxia-regulated proteins. Glucose-regulated protein 78, macrophage migration inhibitory factor and annexin A5 might be promising targets for pancreatic cancer diagnosis and therapy. [ABSTRACT FROM AUTHOR]