Littérature scientifique sur le sujet « Academic Metabolism »

Abstract Background: Currently, there is no widely accepted clinical practice guideline for the management of severe hypercalcemia in hospitalized patients. Objective: The purpose of this project was to analyze management of hypercalcemia in hospitalized patients at an academic medical center, then establish and implement a clinical practice guideline for hypercalcemia treatment. Design: Retrospective chart review of all patients admitted for management of hypercalcemia over 37 consecutive months. Setting: Urban academic tertiary referral center Measurements: We examined which calcium- lowering medications were used, how often 2 medications were needed, average time to normocalcemia, incidence of hypocalcemia post treatment, serum phosphorus nadir and serum creatinine peak. We also assessed medication appropriateness (dose and frequency). Results: Seventy-two patients were included; 58 patients with hypercalcemia of malignancy and 14 patients with hypercalcemia of other diagnoses. In the malignancy group the most common treatment was a combination of calcitonin + bisphosphonate (43%), followed by bisphosphonate alone (29%) and calcitonin alone (24%). In the non-malignancy group, calcitonin alone was used in 50%, calcitonin + bisphosphonate in 21% and a bisphosphonate alone in 14%. Denosumab was rarely used in both groups. The median time to normocalcemia was 3.0 days irrespective of diagnostic group. Seventy two percent of the patients with malignancy and 86% of the non-malignancy group achieved normocalcemia. The incidence of hypocalcemia was 21% (12/58) in the malignancy subgroup and 29% (4/14) in the others after treatment. Serum creatinine did not change from baseline to post-treatment in either population. Median serum phosphorus dropped from 2.9 mg/dL to 1.8 mg/dL in the malignancy group and 4.2 mg/dL to 2.1 mg/dL in the non-malignancy group. Only 41% of patients that received calcitonin, were given recommended dose, route, and frequency. Conclusion: Based on the results of this study, a hypercalcemia treatment guideline was developed, highlighting appropriate medication dose and frequency. This guideline recommends zoledronic acid alone for asymptomatic malignancy patients, and in combination with calcitonin for symptomatic patients. In contrast, calcitonin alone is considered first line for non-malignant conditions.

Abstract The landscape for academic endocrinology divisions has continued to evolve rapidly;thus, finding reliable data that can be used as benchmarks has become more difficult. Resources are available for salary and relative value units, with the Association of American Medical Colleges, Medical Group Management Association, and Faculty Practice Solutions Center the most commonly used databases. However, details regarding how these data are collected and what they include are unclear. For example, does the income include bonus and/or incentive payments? How are work relative value units defined (individual rendering vs supervising advanced practitioners or fellows or residents)? How is a clinical full-time equivalent defined? In addition, other important data that would be relevant to running an academic division of endocrinology are not available from these, or any other resources, including support staff numbers and compensation or fellowship funding and training information. Therefore, an unmet need exists for reliable data that divisions can use to help shape their visions and goals. To address this demand, the Association of Endocrine Chiefs and Directors, in collaboration with the Endocrine Society, developed a detailed survey for members to address the financial, productivity, composition, and educational issues that they regularly face. Twenty academic institutions throughout the United States completed in the survey in 2018. In the present report, we have provided the results of the survey and some initial interpretations of the findings. Our hope is that the information presented will prove useful as academic endocrinology divisions continue to evolve.

Although poorly understood, normal cells and cancerous cells of the same type exhibit different patterns of nutrient consumption, processing and utility of metabolic substrates. Differences in substrate uptake, preference, and alternately emphasized metabolic pathways offer opportunities for selective targeting of cancer versus stroma. This may be accomplished by using a sequential approach of nutrient deprivation and pharmaceutical perturbation of metabolic pathways to inhibit cellular proliferation. The purpose of this study was to investigate the effects of restricting glucose and glutamine concentrations, in vitro, to levels that resemble a potential human fasting state. The mammalian target of rapamycin (mTOR), a mediator of nutrient sensation, was then inhibited with rapamycin in the nutrient-restricted conditions. Because active Akt/mTOR is implicated in cancer cell pro-survival, the hypothesis is that pharmaceutical inhibition of active Akt/mTOR signaling in combination with the stress of restricted nutrient supply will be more effective than nutrient deprivation alone at disrupting metabolic processes to impair cancer cell proliferation and/or pro-survival mechanisms. Untreated and treated conditions were tested to determine if an additive or synergistic effect would result from a sequential insult of nutrient deprivation followed by inhibited mTORC1 signaling. The cell line used for this study was cultivated from a murine pancreatic intraepithelial neoplasia (PANIN) derived from a transgenic mouse with pancreatic tissue-specific expression of constitutively active Akt. The transgene of Akt, isoform 1, contains a myristoyl tag that facilitates co-localization of Akt to the plasma membrane, thereby promoting the activation of this signaling protein.; This aberrantly activated Akt represents a prosurvival condition observed in most cancers, and impacts metabolic balance with increased downstream signaling to metabolic sensors and regulators, including mTORC1. Several methods were used to evaluate changes in metabolic and physiological response to nutrient deprivation and mTORC1 inhibition. These included tetrazolium reduction/absorbance readings to qualitatively evaluate differences in cell proliferation, and Western immunoblots for observing changes in protein expression and phosphorylation. ATP luminescence assays were applied to quantify intracellular ATP content, and citrate synthase spectrophotometry used to quantify specific activity/indicate changes in the TCA/OXPHOS production of ATP. Results from the above methods suggest that, individually, nutrient deprivation and rapamycin treatment share some similar effects on metabolically-related protein phosphorylation and in reducing cellular proliferation. Collectively, nutrient deprivation plus rapamycin treatment, however, resulted in unanticipated metabolic alterations under conditions used for this study, the complexities of which would need to be delineated in future studies.
B.S.
Bachelors
Burnett School of Biomedical Sciences
Molecular Biology and Microbiology

The weightless environment results in atrophy of the anti-gravity muscles. Hindlimb suspension is a model for weightlessness induced atrophy. This study evaluated the effects of hindlimb suspension, microgravity and exercise training followed by suspension on skeletal muscle. Soleus mass, myofibrillar and sarcoplasmic protein content were measured in one to four day hindlimb suspended animals. Protein synthesis was measured by intramuscular injection of ³H phenylalanine with correction for the difference between tRNA and intracellular specific activities. Myofibrillar protein loss was minimal after two days of unweighting but significant after three days. Although sarcoplasmic protein content showed no change, synthesis of both protein pools declined in parallel. Myofibrillar degradation increased during the first three days of unweighting, partially accounting for protein loss. The decline in degradation during day four explained the slower rate of protein loss at this time. Sarcoplasmic protein degradation increased slightly during the first two days of unweighting then declined sharply, thus explaining the sparing of sarcoplasmic proteins. Animals exposed to weightlessness showed soleus atrophy similar to suspended animals. The plantaris and gastrocnemius had reduced growth while the extensor digitorum longus and tibialis anterior grew normally in flight and suspended animals. Insulin stimulated glucose uptake was enhanced in soleus, but not extensor digitorum longus of flight and suspended animals. In situ insulin and IGF-1 stimulated 2-deoxyglucose uptake was greater after six days of suspension. Voluntary wheel training increased soleus mass, protein content and in vivo protein synthesis which plateaued by three weeks. Suspended or trained-suspended animals showed reductions in soleus mass, protein content and synthesis compared to trained animals. However, trained-suspended animals showed higher values for protein content and synthesis compared to suspended animals. In conclusion, these studies show that unweighting atrophy is characterized by decreased synthesis and increased degradation of myofibrillar proteins, and a sparing of sarcoplasmic proteins due to slower degradation. Tail-cast hindlimb suspension may be used as a ground based model to mimic the effects of weightlessness on muscle proteins. Wheel training causes muscle hypertrophy; and although training prior to suspension provides some protection against protein loss, it does not prevent atrophy.

Pyrrolizidine alkaloids are proposed to be metabolized in the liver to reactive pyrrole species, or dehydroalkaloids. These reactive pyrroles are hypothesized to be responsible for pyrrolizidine alkaloid toxicity. This dissertation research has established that dehydroalkaloids are, in fact, metabolites of pyrrolizidine alkaloids. It was first determined that dehydromonocrotaline is produced during hepatic microsomal metabolism of monocrotaline and that it has the ability to bind in vitro with a synthetic thiol-containing resin, Thiopropyl Sepharose 6B. Similarly, synthetic dehydromonocrotaline binds to this resin. Dehydromonocrotaline was identified as a pyrrolizidine alkaloid metabolite based upon its resin cleavage products. When resin-bound pyrrole, synthetic or microsomally generated, was cleaved in a buffered, ethanolic silver nitrate solution, O⁷-ethyl dehydroretronecine was the major product, supporting the suggestion that the pyrrole generated by hepatic microsomes is dehydromonocrotaline. This system was then used to determine the formation of dehydroalkaloids from other pyrrolizidine alkaloids. These other alkaloids--trichodesmine, retrorsine, senecionine and heliotrine--cause toxicity to the liver as well as to extrahepatic organs. Their metabolism in this system reveals that alkaloids which produce extrahepatic toxicity have an increased percentage of reactive metabolites formed by phenobarbital-induced hepatic microsomes. Therefore, this system in vitro can be a good predictor of alkaloids which may produce extrahepatic toxicity in vivo. Trichodesmine is a pyrrolizidine alkaloid that is unique in its neurotoxicity. It is structurally similar to monocrotaline, yet it varies widely in its toxicity. It was determined that trichodesmine is more toxic in the rat than monocrotaline as indexed by LD₅₀ values. The distribution of pyrrolic metabolites reveals that trichodesmine treatment results in brain pyrrole levels 4 times higher than monocrotaline, retrorsine, or control. Histopathologic investigation of trichodesmine-treated animals reveals severe neuronal death in the cerebral cortex. These results suggest that neurotoxicity observed with trichodesmine is a result of pyrrole metabolites reaching the brain, thus providing further evidence for the involvement of pyrrole metabolites in pyrrolizidine alkaloid-induced extrahepatic toxicity.

1,2,3-Trichloropropane (TCP) causes rat hepatic DNA damage in the form of DNA single strand breaks. This damage was dose and time dependent. In vivo ¹⁴C-TCP equivalents covalently bound to hepatic protein, RNA and DNA. Glutathione depletion with L-buthionine-(R,S)-sulfoximine increased binding to protein by 342% while it decreased binding to DNA by 56%. The in vivo binding data suggest a dual role for glutathione in the bioactivation of TCP. In vitro rat hepatic microsomes activated TCP to species which covalently bound to microsomal protein. Rat liver microsomes also bioactivated TCP to the direct acting mutagen 1,3-dichloroacetone. 1,3-Dichloroacetone was identified as the major microsomal protein binding species through conjugation with N-acetylcysteine to form 1,3-(2-propanone)-bis-S-(N-acetylcysteine) which accounted for 87% of all TCP microsomal metabolism. These findings support a role for 1,3-dichloroacetone as a mutagenic metabolite of TCP. Carbon-13 nuclear magnetic resonance was used to identify directly the urinary metabolite of ¹³C₃-TCP (99 atom % enrichment). Urine was investigated directly using proton-decoupled ¹³C and two-dimensional homonuclear correlated nuclear magnetic resonance spectroscopy. Spectral shifts have been assigned to N-acetyl-S-(2-hydroxy-3-chloropropyl)cysteine, 1,3-(2-propanol)-bis-S-(N-acetylcysteine), N-acetyl-S-(2-hydroxy-2-carboxyethyl)cysteine, 2,3-dichloropropionic acid, 2-chloroethanol, ethylene glycol and oxalic acid by comparison to spectra of authentic standards. No unchanged TCP was detected. From the results obtained it is concluded that metabolism of TCP by cytochromes P450 and by glutathione conjugation can result in the formation of reactive metabolites of TCP which may be responsible for TCP genotoxicity.

Thesis (Ph. D.)--University of California, San Diego, 2010.
Title from first page of PDF file (viewed June 3, 2010). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (leaves 141-143).

Human promyelocytic leukemic cells (HL-60) possess well regulated expression of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, acylCoA:cholesterol acyltransferase (ACAT), and receptor-mediated low density lipoprotein (LDL) catabolism, but lack receptor-mediated acetyl-LDL processing. Differentiation of HL-60 cells with tetramyristic phorbol acetate (TPA) is accompanied by the loss of receptor-mediated LDL degradation and no expression of a functionally active scavenger receptor. 1,25-Dihydroxyvitamin D₃ (D₃)-induced HL-60 macrophages possess specific and saturable receptor-mediated binding for LDL, with an apparent K(d) of 29 μg/ml and a B(max) of 219 ng/mg. Receptor-mediated LDL degradation is specific for apoB and apoE containing lipoproteins; it is calcium dependent, and is inhibited by pronase and chloroquine. Differentiation of HL-60 cells with D₃ for 2 days induces a 45-fold increase in acetyl-LDL degradation rate compared to undifferentiated cells. Receptor-mediated degradation of acetyl-LDL is specific for acetyl-LDL, calcium independent, inhibited by chloroquine, pronase and fucoidin treatment, and is not regulated by cellular cholesterol. Acetyl-LDL binding studies demonstrated a K(d) of 36 μg/ml and a B(max) 313 ng/mg. Delivery of cholesterol via receptor-mediated catabolism of LDL or acetyl-LDL results in significant suppression of sterol synthesis and HMG-CoA reductase activity, and significant induction of ACAT activity relative to macrophages incubated with LPDS (P < 0.001). However, receptor-mediated degradation of acetyl-LDL, but not LDL, significantly increases cholesteryl ester content (P < 0.001). D₃-induced HL-60 macrophages incubated with or without LDL for 48 hr exhibited large empty vacuoles with little or no lipid stainable material. In contrast, macrophages incubated with acetyl-LDL exhibited a dramatic increase in lipid stainable material which imparted the macrophages with a foamy appearance. In conclusion, HL-60 cells treated with D₃ for 48 hr undergo activation differentiation assuming the structural and functional characteristics of human monocyte-derived macrophages. Thus, D₃-induced HL-60 macrophages are a suitable in vitro system to study lipoproteins and cholesterol regulation as related to macrophage involvement in atherosclerosis.

Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed August 6, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 147-190).

There are an increasing number of ecological distribution conflicts around the world ultimately caused from the increase in the metabolism of the economy in terms of flows of energy and materials. There are resource extraction conflicts, transport conflicts, and also waste disposal conflicts. Therefore, there are many local complaints. Since the 1980s and 1990s there has been a globalizing environmental justice movement that in its strategy meetings and practices has developed a set of concepts and slogans to describe and intervene in such conflicts. They include “environmental racism,” “popular epidemiology,” “the environmentalism of the poor and the indigenous,” “biopiracy,” “tree plantations are not forests,” “the ecological debt,” “climate justice,” “food sovereignty,” “water justice,” and so on . . . These notions have been born from socio-environmental activism but sometimes they have been taken up also by academic political ecologists and used in their analyses.

Bones are multifunctional passive organs of movement that supports soft tissue and directly attached muscles. They also protect internal organs and are a reserve of calcium, phosphorus and magnesium. Each bone is covered with periosteum, and the adjacent bone surfaces are covered by articular cartilage. Histologically, the bone is an organ composed of many different tissues. The main component is bone tissue (cortical and spongy) composed of a set of bone cells and intercellular substance (mineral and organic), it also contains fat, hematopoietic (bone marrow) and cartilaginous tissue. Bones are a tissue that even in adult life retains the ability to change shape and structure depending on changes in their mechanical and hormonal environment, as well as self-renewal and repair capabilities. This process is called bone turnover. The basic processes of bone turnover are: • bone modeling (incessantly changes in bone shape during individual growth) following resorption and tissue formation at various locations (e.g. bone marrow formation) to increase mass and skeletal morphology. This process occurs in the bones of growing individuals and stops after reaching puberty • bone remodeling (processes involve in maintaining bone tissue by resorbing and replacing old bone tissue with new tissue in the same place, e.g. repairing micro fractures). It is a process involving the removal and internal remodeling of existing bone and is responsible for maintaining tissue mass and architecture of mature bones. Bone turnover is regulated by two types of transformation: • osteoclastogenesis, i.e. formation of cells responsible for bone resorption • osteoblastogenesis, i.e. formation of cells responsible for bone formation (bone matrix synthesis and mineralization) Bone maturity can be defined as the completion of basic structural development and mineralization leading to maximum mass and optimal mechanical strength. The highest rate of increase in pig bone mass is observed in the first twelve weeks after birth. This period of growth is considered crucial for optimizing the growth of the skeleton of pigs, because the degree of bone mineralization in later life stages (adulthood) depends largely on the amount of bone minerals accumulated in the early stages of their growth. The development of the technique allows to determine the condition of the skeletal system (or individual bones) in living animals by methods used in human medicine, or after their slaughter. For in vivo determination of bone properties, Abstract 10 double energy X-ray absorptiometry or computed tomography scanning techniques are used. Both methods allow the quantification of mineral content and bone mineral density. The most important property from a practical point of view is the bone’s bending strength, which is directly determined by the maximum bending force. The most important factors affecting bone strength are: • age (growth period), • gender and the associated hormonal balance, • genotype and modification of genes responsible for bone growth • chemical composition of the body (protein and fat content, and the proportion between these components), • physical activity and related bone load, • nutritional factors: – protein intake influencing synthesis of organic matrix of bone, – content of minerals in the feed (CA, P, Zn, Ca/P, Mg, Mn, Na, Cl, K, Cu ratio) influencing synthesis of the inorganic matrix of bone, – mineral/protein ratio in the diet (Ca/protein, P/protein, Zn/protein) – feed energy concentration, – energy source (content of saturated fatty acids - SFA, content of polyun saturated fatty acids - PUFA, in particular ALA, EPA, DPA, DHA), – feed additives, in particular: enzymes (e.g. phytase releasing of minerals bounded in phytin complexes), probiotics and prebiotics (e.g. inulin improving the function of the digestive tract by increasing absorption of nutrients), – vitamin content that regulate metabolism and biochemical changes occurring in bone tissue (e.g. vitamin D3, B6, C and K). This study was based on the results of research experiments from available literature, and studies on growing pigs carried out at the Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences. The tests were performed in total on 300 pigs of Duroc, Pietrain, Puławska breeds, line 990 and hybrids (Great White × Duroc, Great White × Landrace), PIC pigs, slaughtered at different body weight during the growth period from 15 to 130 kg. Bones for biomechanical tests were collected after slaughter from each pig. Their length, mass and volume were determined. Based on these measurements, the specific weight (density, g/cm3) was calculated. Then each bone was cut in the middle of the shaft and the outer and inner diameters were measured both horizontally and vertically. Based on these measurements, the following indicators were calculated: • cortical thickness, • cortical surface, • cortical index. Abstract 11 Bone strength was tested by a three-point bending test. The obtained data enabled the determination of: • bending force (the magnitude of the maximum force at which disintegration and disruption of bone structure occurs), • strength (the amount of maximum force needed to break/crack of bone), • stiffness (quotient of the force acting on the bone and the amount of displacement occurring under the influence of this force). Investigation of changes in physical and biomechanical features of bones during growth was performed on pigs of the synthetic 990 line growing from 15 to 130 kg body weight. The animals were slaughtered successively at a body weight of 15, 30, 40, 50, 70, 90, 110 and 130 kg. After slaughter, the following bones were separated from the right half-carcass: humerus, 3rd and 4th metatarsal bone, femur, tibia and fibula as well as 3rd and 4th metatarsal bone. The features of bones were determined using methods described in the methodology. Describing bone growth with the Gompertz equation, it was found that the earliest slowdown of bone growth curve was observed for metacarpal and metatarsal bones. This means that these bones matured the most quickly. The established data also indicate that the rib is the slowest maturing bone. The femur, humerus, tibia and fibula were between the values of these features for the metatarsal, metacarpal and rib bones. The rate of increase in bone mass and length differed significantly between the examined bones, but in all cases it was lower (coefficient b <1) than the growth rate of the whole body of the animal. The fastest growth rate was estimated for the rib mass (coefficient b = 0.93). Among the long bones, the humerus (coefficient b = 0.81) was characterized by the fastest rate of weight gain, however femur the smallest (coefficient b = 0.71). The lowest rate of bone mass increase was observed in the foot bones, with the metacarpal bones having a slightly higher value of coefficient b than the metatarsal bones (0.67 vs 0.62). The third bone had a lower growth rate than the fourth bone, regardless of whether they were metatarsal or metacarpal. The value of the bending force increased as the animals grew. Regardless of the growth point tested, the highest values were observed for the humerus, tibia and femur, smaller for the metatarsal and metacarpal bone, and the lowest for the fibula and rib. The rate of change in the value of this indicator increased at a similar rate as the body weight changes of the animals in the case of the fibula and the fourth metacarpal bone (b value = 0.98), and more slowly in the case of the metatarsal bone, the third metacarpal bone, and the tibia bone (values of the b ratio 0.81–0.85), and the slowest femur, humerus and rib (value of b = 0.60–0.66). Bone stiffness increased as animals grew. Regardless of the growth point tested, the highest values were observed for the humerus, tibia and femur, smaller for the metatarsal and metacarpal bone, and the lowest for the fibula and rib. Abstract 12 The rate of change in the value of this indicator changed at a faster rate than the increase in weight of pigs in the case of metacarpal and metatarsal bones (coefficient b = 1.01–1.22), slightly slower in the case of fibula (coefficient b = 0.92), definitely slower in the case of the tibia (b = 0.73), ribs (b = 0.66), femur (b = 0.59) and humerus (b = 0.50). Bone strength increased as animals grew. Regardless of the growth point tested, bone strength was as follows femur > tibia > humerus > 4 metacarpal> 3 metacarpal> 3 metatarsal > 4 metatarsal > rib> fibula. The rate of increase in strength of all examined bones was greater than the rate of weight gain of pigs (value of the coefficient b = 2.04–3.26). As the animals grew, the bone density increased. However, the growth rate of this indicator for the majority of bones was slower than the rate of weight gain (the value of the coefficient b ranged from 0.37 – humerus to 0.84 – fibula). The exception was the rib, whose density increased at a similar pace increasing the body weight of animals (value of the coefficient b = 0.97). The study on the influence of the breed and the feeding intensity on bone characteristics (physical and biomechanical) was performed on pigs of the breeds Duroc, Pietrain, and synthetic 990 during a growth period of 15 to 70 kg body weight. Animals were fed ad libitum or dosed system. After slaughter at a body weight of 70 kg, three bones were taken from the right half-carcass: femur, three metatarsal, and three metacarpal and subjected to the determinations described in the methodology. The weight of bones of animals fed aa libitum was significantly lower than in pigs fed restrictively All bones of Duroc breed were significantly heavier and longer than Pietrain and 990 pig bones. The average values of bending force for the examined bones took the following order: III metatarsal bone (63.5 kg) <III metacarpal bone (77.9 kg) <femur (271.5 kg). The feeding system and breed of pigs had no significant effect on the value of this indicator. The average values of the bones strength took the following order: III metatarsal bone (92.6 kg) <III metacarpal (107.2 kg) <femur (353.1 kg). Feeding intensity and breed of animals had no significant effect on the value of this feature of the bones tested. The average bone density took the following order: femur (1.23 g/cm3) <III metatarsal bone (1.26 g/cm3) <III metacarpal bone (1.34 g / cm3). The density of bones of animals fed aa libitum was higher (P<0.01) than in animals fed with a dosing system. The density of examined bones within the breeds took the following order: Pietrain race> line 990> Duroc race. The differences between the “extreme” breeds were: 7.2% (III metatarsal bone), 8.3% (III metacarpal bone), 8.4% (femur). Abstract 13 The average bone stiffness took the following order: III metatarsal bone (35.1 kg/mm) <III metacarpus (41.5 kg/mm) <femur (60.5 kg/mm). This indicator did not differ between the groups of pigs fed at different intensity, except for the metacarpal bone, which was more stiffer in pigs fed aa libitum (P<0.05). The femur of animals fed ad libitum showed a tendency (P<0.09) to be more stiffer and a force of 4.5 kg required for its displacement by 1 mm. Breed differences in stiffness were found for the femur (P <0.05) and III metacarpal bone (P <0.05). For femur, the highest value of this indicator was found in Pietrain pigs (64.5 kg/mm), lower in pigs of 990 line (61.6 kg/mm) and the lowest in Duroc pigs (55.3 kg/mm). In turn, the 3rd metacarpal bone of Duroc and Pietrain pigs had similar stiffness (39.0 and 40.0 kg/mm respectively) and was smaller than that of line 990 pigs (45.4 kg/mm). The thickness of the cortical bone layer took the following order: III metatarsal bone (2.25 mm) <III metacarpal bone (2.41 mm) <femur (5.12 mm). The feeding system did not affect this indicator. Breed differences (P <0.05) for this trait were found only for the femur bone: Duroc (5.42 mm)> line 990 (5.13 mm)> Pietrain (4.81 mm). The cross sectional area of the examined bones was arranged in the following order: III metatarsal bone (84 mm2) <III metacarpal bone (90 mm2) <femur (286 mm2). The feeding system had no effect on the value of this bone trait, with the exception of the femur, which in animals fed the dosing system was 4.7% higher (P<0.05) than in pigs fed ad libitum. Breed differences (P<0.01) in the coross sectional area were found only in femur and III metatarsal bone. The value of this indicator was the highest in Duroc pigs, lower in 990 animals and the lowest in Pietrain pigs. The cortical index of individual bones was in the following order: III metatarsal bone (31.86) <III metacarpal bone (33.86) <femur (44.75). However, its value did not significantly depend on the intensity of feeding or the breed of pigs.

AbstractAquaponics’ potential to transform urban food production has been documented in a rapid increase of academic research and public interest in the field. To translate this publicity into real-world impact, the creation of commercial farms and their relationship to the urban environment have to be further examined. This research has to bridge the gap between existing literature on growing system performance and urban metabolic flows by considering the built form of aquaponic farms. To assess the potential for urban integration of aquaponics, existing case studies are classified by the typology of their building enclosure, with the two main categories being greenhouses and indoor environments. This classification allows for some assumptions about the farms’ performance in their context, but a more in-depth life cycle assessment (LCA) is necessary to evaluate different configurations. The LCA approach is presented as a way to inventory design criteria and respective strategies which can influence the environmental impact of aquaponic systems in the context of urban built environments.

Yoga is an ancient mind-body practice originated in India more than 2.000 years ago and is described systematically early on. The research on the psychophysiological benefits of yoga in children has been found to improve concentration, attention, memory, resilience, mood, self-control, academic performance, psychomotor and cardiac functions, as well as metabolic parameters. Consequently, yoga seems to help children with attention problems such as ADHD, and with special needs or during physical rehabilitation. Therefore, yoga might represent an important life skill tool for all children to deal with health issues, cognitive challenges and emotinal self-regulation. In this chapter, the supporting evidence of yoga for children will be discussed, as well as the effectiveness of frequency, duration and the issue of age appropriateness. Among many reasons, but specially due to their brain maturity, children's yoga is not a version of yoga for adults, it is a unique practice where children should allow to have fun while they experience the well known health benefits of yoga.

Few biologists today have likely heard of cell biologist Alex Novikoff (1913–1987) (Figure 3.1). But the fruits of his science are well known. He helped discover the cell organelle called the lysosome. In 1955 he visualized what Christian de Duve had characterized only by chemical means. He documented the first known enzyme of the Golgi body, another cell organelle. He developed ways to stain lysosomes and peroxisomes (also cell organelles) that were critical to identifying them and studying them with the electron microscope. Novikoff also was targeted by the anti-Communist movement in the mid-twentieth century. In 1953 he was dismissed from the University of Vermont for declining to answer questions before a congressional committee. In 1974 he was elected to the National Academy of Sciences. His FBI file then contained 822 pages. Novikoff ’s fascinating case raises important issues about how science and political ideology relate. In 1982 the American Society for Cell Biology honored Novikoff with its prestigious E. B. Wilson Award for his foundational contributions to the emerging field. Yet much earlier, in the late 1930s, he was indeed a member of the Communist Party. For him, it expressed a quest for social justice and an appreciation of Karl Marx’s scientific posture toward society. While he researched experimental embryology as a PhD student at Columbia University, he also helped write and distribute the Communist newsletter at Brooklyn College, where he taught. When the college tried to disrupt the teachers’ union, Novikoff was secretly listed as a suspected Communist. When World War II began, Novikoff wanted to serve the nation. He applied for a medical commission in the military. He was twice denied, however, owing to doubts about his loyalty. He later consulted for the army on two biological films—until it found his vague Communist record. (One wonders: Did someone imagine that he could link enzymes and carbohydrate metabolism to the violent overthrow of the US government?) Later, Novikoff lost his faculty position—not for any political activity but for invoking the Fifth Amendment in anti-Communist hearings, and despite recommendations from fellow faculty describing his “tireless” research efforts.

The day Erin Brockovich was driving in Reno and got hit by another driver, brought her in close contact not only with the bumper of the other car, but eventually also with the US legal system, and this would change her life completely. The day Steven Soderbergh asked Julia Roberts to play the part of Erin Brockovich in the film with the same name didn’t really change her life, one presumes, but it would show the world’s moviegoers and critics that the star and Academy Award winning actress of 1990 was really back on the right track. What is the link between these events? The answer is the element chromium. It was chromium that made law-firm clerk Brockovich start a David-against-Goliath struggle with the California energy conglomerate Pacific Gas and Electric Company, that made director Soderbergh make the blockbuster movie that gave Roberts an Oscar for best female actress in 2000 and revitalized her career. I will try not to spoil the picture for those who have not seen it, because it is well worth watching, but the fact that the good guys win in the end is probably not a surprise anyway. However, the role of chromium in this play is not at all evident. And are the good guys really the good guys? There is usually a proper amount of, and a proper place for, everything, and this includes the elements of the periodic table. The main component in steel, a material which has a role to play in this story, is iron, and while we sometimes have too low a level of this element in our bodies, too much of it will kill us. The same goes for chromium: we can’t live without it. Or so it was thought until very recently. It was supposed to help us to break down and metabolize sugars, and thus ‘chromium deficiency’ could possibly be related to diabetes. Now, while low levels seems to do no harm, there are still possibilities of a therapeutic window—that is, concentrations where it may do some good—but it does not any longer seem to be considered an essential element, although official consensus on this has not yet been proclaimed.

Children’s involuntary exposure to tobacco smoke is a common and substantial health problem that has been receiving increasing attention from the pediatric, public health and research communities. According to the 2006 Surgeon General’s Report, there is no safe level of tobacco smoke exposure, yet at least 30% of children in the United States live in households with at least one adult smoker, and nearly 60% have evidence of recent exposure (Machlin, Hill, and Liang 2006). Tobacco smoke exposure has been causally linked to numerous adverse health outcomes and is currently a leading preventable cause of both low birth weight and sudden infant death syndrome, and a major contributor to lower respiratory infections, otitis media, and increased asthma severity (American Academy of Pediatrics, Committee on Environmental Health 1997; Cook and Strachan 1999; DiFranza et al. 2004). Recently, associations between tobacco smoke exposure and other childhood health problems, such as increased rates of dental caries (Aligne et al. 2003; Iida et al. 2007), food insecurity (Cutler et al. in press), and the metabolic syndrome (Weitzman et al. 2005) have been identified. As discussed in this chapter, a growing human and animal literature, which expands upon a more than 25-year-old body of work, also indicates that involuntary exposure to tobacco smoke during the pre- and/or postnatal periods is associated with adverse cognitive and behavioral outcomes in children. Tobacco smoke exposure has been associated with decrements in IQ, problems with learning and memory, difficulty with auditory processing, neonatal hyperactivity, attention-deficit hyperactivity disorder (ADHD), internalizing and externalizing behavioral problems, and conduct disorder. Animal models have provided evidence that tobacco is toxic to the developing brain, and there are plausible biologic pathways that appear to mediate these effects. Exciting new studies have begun to identify specific genes that play a role in the relationship between tobacco smoke exposure and adverse cognitive and behavioral outcomes in children. The term “secondhand smoke” (SHS), also referred to as “environmental tobacco smoke” (ETS), refers to the smoke that is exhaled from a smoker’s lungs, as well as the smoke from the smoldering end of a cigarette.

Background: The teaching of the subject “Biochemical Basis of Human Nutrition” of the Degree in Biochemistry is based on the premise that students apply the knowledge acquired in previous courses concerning biochemistry and metabolism. However, for many topics covered in this subject, not rigorously application of this knowledge has been detected, existing influences derived from non-expert information available in the media. To a large extent, this problem lies in the fact that nutrition is a topic widely covered in the media, although often in a generalized, incomplete and not very rigorous way. Methodologies: In this project we proposed students to apply a critical view on nutrition-related information available in the media, with special emphasis on the hottest topics, such as transgenic foods and Mediterranean diet. For this purpose, we designed two strategies: (1) a mini-workshop activity in connection with the subject “Food Biotechnology” focused on the use of transgenic foods; (2) involving students in the creation and management of a web page aimed at dealing with topics related to nutrition, worked from two approaches (informative and scientific). For the development of these activities, students were assigned to different working groups and information about the knowledge of the students in the topics was collected in pre- and post-activity tests. In this way, we involved students in real activities of expert search and screening of information, in order to communicate it in different environments. Results: The project was developed during two academic years, involving students from two successive promotions (30 students in the first year and 39 in the second year). The activities proposed within the project were voluntary, and the percentage of adherence to them was 100% in both cases, indicating the high degree of acceptance among the students. We created a website (www.lawebnatural.com) in the context of this project. In the activities aimed at researching and writing articles on specific topics within the web page environment, questionnaires were carried out prior to the development of the activities to evaluate the degree of knowledge that the students had about the topics to be worked on in the activities. The implementation of post-activities questionnaires showed an improvement percentage of 85% in the knowledge of the topics. The elaboration of graphic material on transgenic foods for the mini-workshop activity, was another profitable activity contributing to a better understanding of the topics. Conclusions and implications: The use of these dynamics concerning the active participation of students in creative tasks based on information search improves the quality of learning. The choice of current topics in nutrition awakens the students' critical spirit, as they confront their pre-established ideas about these topics with the new knowledge acquired. Findings: This communication is derived from the Educative Innovation Project PIE19-068, funded by University of Malaga. Websites were supported by funds from My Scientific.