No abstract

Malnutrition has been considered to be associated with the prognosis of cancer. the Geriatric nutritional Risk index (GnRi), based on serum albumin levels, present body weight, and ideal body weight, is a simple screening tool to predict the risk of nutrition-related morbidity and mortality in elderly patients. We aimed to evaluate whether preoperative GnRi was associated with postoperative complications and prognosis in elderly patients with colorectal cancer (cRc). We retrospectively enrolled 313 CRC patients aged ≥65 years after curative surgery and classified them into an all-risk GnRi (≤98) group and a no-risk GNRI (>98) group. Kaplan-Meier analysis showed overall survival was significantly worse in the all-risk GNRI group than in the no-risk GNRI group (P = 0.009). Multivariable analyses showed low GnRi (≤98) was an independent risk factor for postoperative complications (P = 0.048) and overall survival (P = 0.001) in the patients. Among the complications, the incidence of surgical site infection, in particular, was significantly higher in the all-risk GNRI group (P = 0.008). In conclusion, low preoperative GnRi (≤98) was associated with increased postoperative complications and poor prognosis. Preoperative GNRI can be used as an identifier for potential high-risk group of morbidity and mortality in elderly cRc patients. Colorectal cancer (CRC) is the third most commonly diagnosed cancer and the second leading cause of cancer-related mortality worldwide 1,2. According to the World Health Organization GLOBOCAN database, there were an estimated 1,849,518 new CRC cases and 880,792 CRC-related deaths in 2018 3. As life expectancy increases and the population ages, the number of elderly patients undergoing surgery also increases 4,5. For instance, in the United States, 60.7% of all the incident CRC patients in 2018 were 65 years or older, and then 81% of the elderly patients and even 64% of the patients aged ≥85 years underwent surgery from 2011 to 2015 3,6. Elderly patients often have some comorbidities, such as cardiovascular disease and respiratory dysfunction 7,8 , and often become malnourished 9,10. In elderly patients, disease-related malnutrition is associated with increased morbidity and mortality 9-12 and prolonged length of stay in hospital due to decrease in their life activity, performance status, and immune function 11-14. The Geriatric Nutritional Risk Index (GNRI) is an elderly-specific index that has been proposed to assess the nutrition-related risk of morbidity and mortality for elderly patients in hospital 15,16. This index was first reported by Bouillanne et al. They divided patients into four groups-a major-risk group (GNRI: <82), a moderate-risk group (GNRI: 82-<92), a low-risk group (GNRI: 92-98), and a no-risk group (GNRI: >98)-and suggested that the risk of infectious complications or mortality was significantly higher in the major-, moderate-, and low-risk groups than in the no-risk group 17. The GNRI is also used for prognosis of chronic diseases 18-20 , and in recent

Although the venous tributaries of the right colon are variable, preoperative 3D-CT is informative and helpful for surgeons performing laparoscopic CME for right colon cancer.

Radiation-induced intestinal fibrosis (RIF) is a serious complication after abdominal radiotherapy for pelvic tumor or peritoneal metastasis. Herein, we show that RIF is mediated by eosinophil interactions with α-smooth muscle actin-positive (α-SMA) stromal cells. Abdominal irradiation caused RIF especially in the submucosa (SM) of the small intestine, which was associated with the excessive accumulation of eosinophils in both human and mouse. Eosinophil-deficient mice showed markedly ameliorated RIF, suggesting the importance of eosinophils. After abdominal irradiation, chronic crypt cell death caused elevation of extracellular adenosine triphosphate, which in turn activated expression of C-C motif chemokine 11 (CCL11) by pericryptal α-SMA cells in the SM to attract eosinophils in mice. Inhibition of C-C chemokine receptor 3 (CCR3) by genetic deficiency or neutralizing antibody (Ab) treatment suppressed eosinophil accumulation in the SM after irradiation in mice, suggesting a critical role of the CCL11/CCR3 axis in the eosinophil recruitment. Activated α-SMA cells also expressed granulocyte-macrophage colony-stimulating factor (GM-CSF) to activate eosinophils. Transforming growth factor-β1 from GM-CSF-stimulated eosinophils promoted collagen expression by α-SMA cells. In translational studies, treatment with a newly developed interleukin-5 receptor α-targeting Ab, analogous to the human agent benralizumab, depleted intestinal eosinophils and suppressed RIF in mice. Collectively, we identified eosinophils as a crucial factor in the pathogenesis of RIF and showed potential therapeutic strategies for RIF by targeting eosinophils.

In patients with UC, CD103 DCs show the impaired ability to generate Treg cells, but exhibit a colitogenic function inducing Th1/Th2/Th17 responses. These findings show how human CD103 DCs could contribute to the pathogenesis of UC.

Electrochemical deposition of Bi-Te alloy films from acidic solutions containing Bi(NO3)3 and TeO2 has been investigated. The thickness, compound, and composition of the Bi-Te alloy films have been examined using stylus-type surface profiling techniques, x-ray diffraction peak measurement, and inductively coupled plasma/Auger electron spectroscopy measurements. At potentials where limiting current was observed, the compositions of films were controlled by the mole ratio [Bi3 § in the solutions and the relationship between the composition of electrodeposited films and the composition of electrolyte solutions was derived.

Innate lymphoid cells (ILCs) are responsible for mucosal tissue homeostasis and are involved in the progression and suppression of several types of cancer. However, the effects of ILCs on colorectal cancer (CRC) are poorly understood. We characterized human ILCs in normal colon and CRC tissue, investigating their role in the tumor immune microenvironment. Normal mucosa and tumor tissues were obtained from CRC patients and the cells were isolated by enzymatic digestion. NKp44 + ILC3s with high expression of tertiary lymphoid structure (TLS) formation-related genes, including LTA, LTB, and TNF, accumulated in the normal colonic mucosa and T1/T2 tumors. However, the number of NKp44 + ILC3s was significantly reduced in T3/T4 tumors compared to normal colonic mucosa and T1/T2 tumors. NKp44 + ILC3s present in T3/T4 tumors had decreased expression of TLS formation-related genes, whereas stromal cells had decreased expression of CXCL13, CCL19, and CCL21. The decreasing number of NKp44 + ILC3s during tumor progression correlated with the TLS density in tumors. Thus, our results indicate that NKp44 + ILC3s infiltrate CRC tissue but the number of cells decreases in T3/T4 tumors, with associated decreases in TLS induction.Research.

Inappropriate activation of T helper (Th) cells, such as Th1 and Th17 cells, is implicated in the pathogenesis of chronic inflammatory disorders including ulcerative colitis (UC). CXCR1 macrophages contribute to intestinal homeostasis through various mechanisms in mice. However, whether mononuclear phagocytes with regulatory functions are present in the human colon is not clearly defined. We investigated whether innate myeloid cells that suppress activation of effector T cells exist in the human intestinal mucosa. Among intestinal lamina propria cells, Lin HLA-DR CD14 CD163 cells were subdivided into CD160 and CD160 cells. Both subsets produced high levels of IL-10. CD163 CD160 cells suppressed effector T cell proliferation, whereas CD163 CD160 cells induced Th17 differentiation. Patients with UC exhibited increased numbers of CD163 CD160 cells, while showing profoundly decreased numbers of CD163 CD160 cells. In this context, CD163 CD160 cells had higher CD80/CD86 expression and lower IL10RB expression, and these cells did not suppress effector T cell proliferation. The CD163 CD160 subset in normal intestinal mucosa inhibits inappropriate Th1/Th17 responses through suppression of their proliferation, and its number and suppressive activity are impaired in patients with UC. These findings indicate how human innate immune cells might prevent UC development.