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Yoga practice has been associated with various indices of positive embodiment in correlational and intervention studies. Yet, systematic, theoretically-grounded models detailing specific mechanisms by which yoga supports positive embodiment are lacking. In this article, we present a conceptual model that describes mechanisms (i.e., mediators and moderators) that can be used to guide research to help answer how, for whom, and under what conditions yoga practice may promote positive embodiment. Based on existing theoretical frameworks and empirical findings, this model suggests that (a) yoga practice may cultivate embodying experiences during yoga (e.g., state mindfulness), (b) these embodying experiences may build stable embodying experiences that generalize beyond the yoga context (e.g., trait mindfulness), and (c) these stable embodying experiences may then promote embodying practices (e.g., mindful self-care). This mediational chain is likely moderated by the yoga context (e.g., instructional focus, presence of mirrors, diversity of bodies represented) and yoga practitioners' social identities (e.g., body size, physical limitations), social and personal histories (e.g., experiences with weight stigma and trauma), and personality traits and motives (e.g., body comparison, appearance-focused motives to practice yoga). Using the structure of this conceptual model, we offer researchers ideas for testable models and study designs that can support them. [ABSTRACT FROM AUTHOR]

The article focuses on intuitive approach on dysfunctional eating and exercise behaviors leading to obesity, eating disorders and dysfunctional exercise patterns. Topics discussed include the intricate link between body image, food and exercise, intuitive eating based on psychological cues of hunger and fullness rather than intense and triggering emotions, and intuitive exercise that refers to listening to the body for cues when to start and stop exercise.

Lantana (Lantana camara Linn) is a noxious weed that grows in many tropical and subtropical parts of the world. Ingestion of lantana foliage by grazing animals causes cholestasis and hepatotoxicity. Both ruminants and nonruminant animals such as guinea pigs, rabbits, and female rats are susceptible to the hepatotoxic action of lantana toxins. The hepatotoxins are pentacyclic triterpenoids called lantadenes. Molecular structure of lantadenes has been determined. Green unripe fruits of the plant are toxic to humans. Lantana spp. exert allelopathic action on the neighboring vegetation. The allelochemicals have been identified as phenolics, with umbelliferone, methylcoumarin, and salicylic acid being the most phytotoxic. In addition to phenolics, a recent report indicates lantadene A and B as more potent allelochemicals. Management of lantana toxicosis in animals is achieved by drenching with activated charcoal and supportive therapy. Recent reports on the bilirubin clearance effect of Chinese herbal tea Yin Zhi Huang (decoction of the plant Yin Chin, Artemisia capillaries, and three other herbs) or its active ingredient 6,7-dimethylesculetin, in jaundice are very exciting and warrant investigations on its, possible, ameliorative effects in lantana intoxicated animals. Research is being conducted on new drug discovery based on natural products in different parts of the lantana plant. [ABSTRACT FROM AUTHOR]

This paper reviews a wide range of recent studies that have linked AD-associated biochemical and physiological changes with oxidative stress and damage. Some of these changes include disruptions in metal ion homeostasis, mitochondrial damage, reduced glucose metabolism, decreased intracellular pH and inflammation. Although the changes mentioned above are associated with oxidative stress, in most cases, a cause and effect relationship is not clearcut, as many changes are interlinked. Increases in the levels of Aβ peptides, the main protein components of the cerebral amyloid deposits of AD, have been demonstrated to occur in inherited early-onset forms of AD, and as a result of certain environmental and genetic risk factors. Aβ peptides have been shown to exhibit superoxide dismutase activity, producing hydrogen peroxide which may be responsible for the neurotoxicity exhibited by this peptide in vitro. This review also discusses the biochemical aspects of oxidative stress, antioxidant defence mechanisms, and possible antioxidant therapeutic measures which may be effective in counteracting increased levels of oxidative stress. In conclusion, this review provides support for the theory that damage caused by free radicals and oxidative stress is a primary cause of the neurodegeneration seen in AD with Aβ postulated as an initiator of this process. [ABSTRACT FROM AUTHOR]

Background: Obstetric cholestasis, attributed to maternal hypersensitivity to estrogens, is a pregnancy-specific disorder characterized by pruritus and biochemical cholestasis in the second or third trimester of pregnancy. The pathophysiology of the disorder is incompletely understood, but the familial nature of the disease has long been recognized. Carriership of long-chain 3-hydroxyacyl-coenzyme A dehydrogenase (LCHAD) deficiency has been reported to be associated with an increased risk of obstetric cholestasis and the gene is located in the p23 region of chromosome 2. Methods: On the basis of this information, we conducted population-based linkage disequilibrium (LD) screening to find potential cholestasis-associated loci on chromosome 2. The study was carried out in 47 unrelated control women and in 45 cholestatic women, eight of whom had a positive family history. Results: During initial screening with chromosome 2-specific microsatellite markers, the tetranucleotide marker D2S1394 was found to be in LD in the 2p13 region. Screening this region with additional microsatellite markers revealed that the adjacent marker D2S1374 was also significantly associated with obstetric cholestasis, whereas no association was found with the markers located in the vicinity of the hydroxyacyl-CoA dehyrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase, alpha subunit (HADHA) gene. Conclusions: Collectively, these data suggest that there may be a novel obstetric cholestasis-associated gene located in the vicinity of the 2p13 LD region. [ABSTRACT FROM AUTHOR]

Cross-bred, anesthetized female swine were given intravascularly a lethal (72 µg/kg; n = 6) or toxic-sublethal (25 µg/kg; n = 6) dose of microcystin-LR (MCLR), from Microcystis aeruginosa, or the vehicle (n = 4). At the high dose, from 12 to 18 min after administration, central venous pressure and hepatic perfusion were significantly lower, and shortly thereafter, portal venous pressure was significantly higher and aortic mean pressure was significantly lower than controls. By 45 min postdosing, serum bile acids, lactate, potassium, and total bilirubin, as well as blood pO[sub 2], were significantly higher, while hematocrit, platelet count, and blood bicarbonate, pCO[sub 2], and base excess were significantly lower than controls. By 90 min, serum arginase, urea nitrogen, inorganic phosphorus, and creatinine were significantly higher, while glucose and blood pH were significantly. [ABSTRACT FROM AUTHOR]