Previous work on assigning tasks to robots has proposed extensive categorizations of allocation of tasks with and without constraints. The main contribution of this paper is a specific categorization of problems that have temporal and ordering constraints. We propose a novel taxonomy that emphasizes the differences between temporal and ordering constraints, and organizes the current literature according to the nature of those constraints. We summarize widely used models and methods from the task allocation literature and related areas, such as vehicle routing and scheduling problems, showing similarities and differences.

Ingestion of omega-3 fatty acids is known to exert favorable health effects on a number of biological processes such as improved immune profile, enhanced cognition, and optimized neuromuscular function. Recently, data have emerged demonstrating a positive influence of omega-3 fatty acid intake on skeletal muscle. For instance, there are reports of clinically-relevant gains in muscle size and strength in healthy older persons with omega-3 fatty acid intake as well as evidence that omega-3 fatty acid ingestion alleviates the loss of muscle mass and prevents decrements in mitochondrial respiration during periods of muscle-disuse. Cancer cachexia that is characterized by a rapid involuntary loss of lean mass may also be attenuated by omega-3 fatty acid provision. The primary means by which omega-3 fatty acids positively impact skeletal muscle mass is via incorporation of eicosapentaenoic acid (EPA; 20:5n−3) and docosahexaenoic acid (DHA; 22:6n−3) into membrane phospholipids of the sarcolemma and intracellular organelles. Enrichment of EPA and DHA in these membrane phospholipids is linked to enhanced rates of muscle protein synthesis, decreased expression of factors that regulate muscle protein breakdown, and improved mitochondrial respiration kinetics. However, exactly how incorporation of EPA and DHA into phospholipid membranes alters these processes remains unknown. In this review, we discuss the interaction between omega-3 fatty acid ingestion and skeletal muscle protein turnover in response to nutrient provision in younger and older adults. Additionally, we examine the role of omega-3 fatty acid supplementation in protecting muscle loss during muscle-disuse and in cancer cachexia, and critically evaluate the molecular mechanisms that underpin the phenotypic changes observed in skeletal muscle with omega-3 fatty acid intake.

Summary Co-option of host components by solid tumors facilitates cancer progression and can occur in both local tumor microenvironments and remote locations. At present, the signals involved in long-distance communication remain insufficiently understood. Here, we identify PF4 (platelet factor 4, CXCL4) as an endocrine factor whose over-expression in tumors correlates with decreased overall patient survival. Furthermore, engineered PF4 over-production in a Kras-driven lung adenocarcinoma genetic mouse model expanded megakaryopoiesis in bone marrow, augmented platelet accumulation in lungs and accelerated de novo adenocarcinogenesis. Additionally, anti-platelet treatment controlled mouse lung cancer progression, further suggesting that platelets can modulate the tumor microenvironment to accelerate tumor outgrowth. These findings support PF4 as a cancer-enhancing endocrine signal that controls discrete aspects of bone marrow hematopoiesis and tumor microenvironment and should be considered as a molecular target in anticancer therapy.

Previous studies have shown that n-3 polyunsaturated fatty acids n-3 (n-3 PUFA) have several anticancer effects, especially attributed to their ability to modulate a variety of genomic and immune responses. In this context, this randomized, prospective, controlled clinical trial was conducted in order to check whether supplementation of 2 g/day of fish oil for 9 weeks alters the production of inflammatory markers, the plasma fatty acid profile and the nutritional status in patients with colorectal cancer (CRC). Eleven adults with CRC in chemotherapy were randomized into two groups: (a) supplemented (SG) daily with 2 g/day of encapsulated fish oil [providing 600 mg/day of eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA)] for 9 weeks (n = 6), and (b) control (CG) (n = 5). All outcomes were evaluated on the day before the first chemotherapy session and 9 weeks later. Plasma TNF-α, IL-1β, IL-10 and IL-17A, the pro/anti-inflammatory balance (ratio TNF-α/IL-10 and IL-1β/IL10) and serum albumin, showed no significant changes between times and study groups (p > 0.05). C-reactive protein (CRP) and the CRP/albumin ratio showed opposite behavior in groups, significantly reducing their values in SG (p < 0.05). Plasma proportions of EPA and DHA increased 1.8 and 1.4 times, respectively, while the ARA reduced approximately 0.6 times with the supplementation (9 weeks vs baseline, p < 0.05). Patients from SG gained 1.2 kg (median) while the CG lost -0.5 kg (median) during the 9 weeks of chemotherapy (p = 0.72). These results demonstrate that 2 g/day of fish oil for 9 weeks of chemotherapy improves CRP values, CRP/albumin status, plasma fatty acid profile and potentially prevents weight loss during treatment.

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Here, we investigated the effect of jump exercise on tumor growth, cancer cachexia, lymphocyte proliferation and macrophage function in Walker 256 tumor-bearing rats. Male Wistar rats (60 days) were divided into sedentary (C) and exercised (E) groups. Jump training consisted of six sets of 10 jumps in water with overload of 50% of body mass with 1 min of resting, four times per week for 8 weeks. After 6 weeks of training, half of each group was inoculated with 2 x 10(7) cells of Walker 256 tumor. Sedentary tumor-bearing and exercised tumor-bearing are referred to as T and TE, respectively. Tumor weight in the T group was 25 g. These animals display loss of weight, hypertriacylglycerolemia, hyperlacticidemia, depletion of glycogen stores and increase in PIF expression. Jump exercise (TE) induced a significant lower tumor weight, preserves liver glycogen stores, partly prevented the hypertriacylglycerolemia, hyperlacticidemia and, prevented the fall in body weight and reduced PIF expression. Lymphocyte was increased by tumor burden (T) and was higher by including exercise (TE). The same was observed regarding phagocytosis and lysosomal volume. Anaerobic exercise decreases tumor growth, cancer cachexia and increases innate and adaptative immune function.

Obesity is a metabolic, multifactorial disease that is underpinned by factors such as genetics, epigenetics, as well as high-energy food intake and sedentarism. Obesity is often associated with, and exacerbated by, other metabolic disorders such as type 2 diabetes mellitus (T2DM). A hallmark of T2DM is failure of insulin secretion from pancreatic β-cell to regulate blood glucose disposal into peripheral tissues, such as skeletal muscle, termed insulin resistance, as well as deregulation of pancreatic α-cell function. It has been proposed that insulin resistance is, in part, a consequence of impaired signal transduction of insulin caused by several molecules released from adipose tissue that include (adipo)cytokines and fatty acids. However, not all fatty acids exert a negative impact on insulin sensitivity. In fact, it has been suggested that palmitoleic acid (16:1n-7) has hormone-like properties and improves some metabolic parameters that are impaired in obesity and T2DM. Moreover, in vitro approaches reveal that cis-16:1n-7 can influence pancreatic β-cell survival, insulin secretion, and skeletal muscle insulin response and adipocyte metabolism. In vivo experiments using animal models show that the ingestion of cis-16:1n-7 or sources of it (e.g., macadamia oil) can partially prevent the metabolic alterations caused by high-fat/carbohydrate diets. In general, studies in humans found positive associations between higher trans-16:1n-7 proportion in plasma phospholipids and improved insulin sensitivity or decreased the onset of T2DM. However, plasma cis-16:1n-7 data are still controversial. In this brief review, we discuss the main studies on 16:1n-7 effects on obesity and T2DM and their potential for clinical application.