The combination of 10th percentile ADC, average ADC, and T2-weighted skewness with CAD is promising in the differentiation of prostate cancer from normal tissue. ADC image features and K(trans) moderately correlate with GS.

T follicular helper (TFH) cells are critical for B cell activation in germinal centers and are often observed in human inflamed tissue. However, it is difficult to know if they contribute in situ to inflammation. Expressed markers define TFH subsets associated with distinct functions in vitro. However, such markers may not reflect in situ function. The delivery of T cell help to B cells requires direct cognate recognition. We hypothesized that by visualizing and quantifying such interactions we could directly assess TFH cell competency in situ. Therefore, we developed computational tools to quantify spatial relationships between different cell subtypes in tissue (Cell Distance Mapping, CDM). Analysis of inflamed human tissues indicated that measurement of internuclear distances between TFH and B cells could be used to discriminate between cognate and non-cognate interactions. Furthermore, only cognate-competent TFH cell populations expressed high levels of Bcl-6 and IL-21. These data suggest that CDM can be used to identify adaptive immune cell networks driving in situ inflammation. Such knowledge should help identify diseases, and disease subsets, that may benefit from therapeutics targeting of specific T cell:antigen presenting cell interactions.

The aim of this study was to determine the efficacy of immunonutrition vs standard nutrition in cancer patients treated with surgery. Cochrane Central Register of Controlled Trials, EMBASE, MEDLINE, EBSCOhost, and Web of Science were searched. Sixty‐one randomized controlled trials were included. Immunonutrition was associated with a significantly reduced risk of postoperative infectious complications (risk ratio [RR] 0.71 [95% CI, 0.64–0.79]), including a reduced risk of wound infection (RR 0.72 [95% CI, 0.60–0.87]), respiratory tract infection (RR 0.70 [95% CI, 0.59–0.84]), and urinary tract infection (RR 0.69 [95% CI, 0.51–0.94]) as well as a decreased risk of anastomotic leakage (RR 0.70 [95% CI, 0.53–0.91]) and a reduced hospital stay (MD −2.12 days [95% CI −2.72 to −1.52]). No differences were found between the 2 groups with regard to sepsis or all‐cause mortality. Subgroup analyses revealed that receiving arginine + nucleotides + ω‐3 fatty acids and receiving enteral immunonutrition reduced the rates of wound infection and respiratory tract infection. The application of immunonutrition at 25–30 kcal/kg/d for 5–7 days reduced the rate of respiratory tract infection. Perioperative immunonutrition reduced the rate of wound infection. For malnourished patients, immunonutrition shortened the hospitalization time. Therefore, immunonutrition reduces postoperative infection complications and shortens hospital stays but does not reduce all‐cause mortality. Patients who are malnourished before surgery who receive arginine + nucleotides + ω‐3 fatty acids (25–30 kcal/kg/d) via the gastrointestinal tract during the perioperative period (5–7 days) may show better clinical efficacy.

Heme oxygenase-1 (HO-1) has been implicated in cardiac dysfunction, oxidative stress, inflammation, apoptosis and autophagy associated with heart failure, and atherosclerosis, in addition to its recognized role in metabolic syndrome and diabetes. Numerous studies have presented contradictory findings about the role of HO-1 in diabetic cardiomyopathy (DCM). In this study, we explored the role of HO-1 in myocardial dysfunction, myofibril structure, oxidative stress, inflammation, apoptosis and autophagy using a streptozotocin (STZ)-induced diabetes model in mice systemically overexpressing HO-1 (Tg-HO-1) or mutant HO-1 (Tg-mutHO-1). The diabetic mouse model was induced by multiple peritoneal injections of STZ. Two months after injection, left ventricular (LV) function was measured by echocardiography. In addition, molecular biomarkers related to oxidative stress, inflammation, apoptosis and autophagy were evaluated using classical molecular biological/biochemical techniques. Mice with DCM exhibited severe LV dysfunction, myofibril structure disarray, aberrant cardiac oxidative stress, inflammation, apoptosis, autophagy and increased levels of HO-1. In addition, we determined that systemic overexpression of HO-1 ameliorated left ventricular dysfunction, myofibril structure disarray, oxidative stress, inflammation, apoptosis and autophagy in DCM mice. Furthermore, serine/threonine-specific protein kinase (Akt) and AMP-activated protein kinase (AMPK) phosphorylation is normally inhibited in DCM, but overexpression of the HO-1 gene restored the phosphorylation of these kinases to normal levels. In contrast, the functions of HO-1 in DCM were significantly reversed by overexpression of mutant HO-1. This study underlines the unique roles of HO-1, including the inhibition of oxidative stress, inflammation and apoptosis and the enhancement of autophagy, in the pathogenesis of DCM.

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