The Hospital Elder Life Program is effective in reducing incidence of delirium and rate of falls, with a trend toward decreasing length of stay and preventing institutionalization. With ongoing efforts in continuous program improvement, implementation, adaptations, and sustainability, HELP has emerged as a reference standard model for improving the quality and effectiveness of hospital care for older persons worldwide.

Malignant ascites-derived exosomes have been demonstrated to participate in tumor metastasis. In peritoneal metastasis, normal mesothelial cells (MCs) can be converted into carcinoma-associated fibroblasts (CAFs) by mesothelial-mesenchymal transition (MMT). Herein, we evaluated the effect of malignant ascites-derived exosomes on peritoneal MCs in vitro and in vivo experiments to determine whether exosomes could educate MCs and contribute to peritoneal metastasis.Under the treatment of ascites-derived exosomes, peritoneal MCs showed increased ability to proliferate and migrate. Expression of CAFs specific proteins markers in MCs, including fibroblast activation protein (FAP), alpha-smooth muscle actin (α-SMA), and fibronectin, were increased after treatment of exosomes. In clinical samples test, TGF-β1 was found to be overexpressed in both malignant ascites and malignant ascites-derived exosomes, and the high volume of TGF-β1 may be responsible for peritoneum fibrosis. In addition, exosomes can increase xenograft tumor growth by suppressing the inhibitive ability on tumor cells by MCs. Besides, CAFs specific proteins markers including FAP, α-SMA, and vimentin were increased in clinical peritoneal biopsies. The immunohistochemical staining for mice tumor biopsies also revealed increased expression of fibronectin and FAP, along with decreased expression of E-cadherin and VCAM-1 after exosomes treatment.Thus, malignant ascites-derived exosomes may be of importance in the development of peritoneal metastasis by facilitating MCs to proliferate and convert into CAFs by TGF-β1 induced MMT.

The transhiatal approach for cancers of the esophagogastric junction, especially types III, should be recommended, and its long-term outcome benefits should be further evaluated.

BackgroundCachexia has a devastating impact on survival and quality of life for many cancer patients and contributes to nearly one‐third of all cancer deaths; also, it is associated with poor responses to chemotherapy and survival. A better understanding of the underlying mechanisms of cancer‐associated cachexia (CAC), coupled with effective therapeutic approaches, will improve management of progressive functional impairment in cancer patients. Salidroside, a phenylpropanoid glycoside in Rhodiola rosea L, has been reported to possess potential anti‐fatigue, anti‐ageing, and anti‐Alzheimer's disease properties. It is widely consumed as a nutritional supplement, but its effects on CAC and the possible mechanism remain a mystery.MethodsIn the murine models of cachexia induced by CT‐26 and Lewis lung carcinoma (LLC) tumour, respectively, main features of CAC were determined after treatment of salidroside or chemotherapy. In vitro experiments were performed using murine C2C12 myotubes, which were treated by tumour necrosis factor‐α. Levels of several critical muscle‐related signal proteins such as mammalian target of rapamycin (mTOR), p‐mTOR, and myosin heavy chain (MyHC) were examined using western blot both in vitro and in vivo.ResultsIn the present study, we showed the exciting effect of salidroside on the treatment of CAC. In CT‐26 and LLC models, respectively, salidroside treatment could effectively preserve the tumour‐free body weight, decrease loss of adipose and gastrocnemius muscles, alleviate tumour burden, and prolong their survival time. Additionally, in combined chemotherapy, salidroside could synergistically enhance the anti‐tumour activity of cisplatin, especially decreased or eliminated chemotherapy‐induced cachexia. Further analysis demonstrated that salidroside could significantly increase expression of mTOR, p‐mTOR, and MyHC in gastrocnemius muscle. Also, results in vitro showed that salidroside could not only obviously increase mTOR, p‐mTOR, and MyHC expression in C2C12 myotubes but also effectively rescue their down‐regulation induced by tumour necrosis factor‐α.ConclusionsIn the current study, the exciting effect of salidroside on CAC suggested that salidroside supplementation might be a promising approach for a multi‐targeted therapy for the treatment of CAC.

These results indicate that ANXA2 is a biomarker with diagnostic and prognostic potential for patients with CRC.