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Various Hormonal Supplementations Activate Sugarcane Regeneration In-Vitro  [cached]
Ghulam Zahra Jahangir,Idrees Ahmad Nasir,Riaz Ahmad Sial,Muhammad Aslam Javid
Journal of Agricultural Science , 2010, DOI: 10.5539/jas.v2n4p231
Abstract: Influence of different hormonal concentrations in plant growth medium on the onset of callus and somatic embryoid induction chased by plantlet regeneration and multiplication of regenerated shoots was the main goal of these studies. Results concluded that MS medium supplemented with auxin alone (3 to 4mg/l 2, 4-D) induces callus formation (3mg/l 2, 4-D alone produced embryogenic calli) and auxin-cytokinin combination like 2, 4-D and IAA (both in 1mg/l and 2mg/l concentration) with BAP (1mg/l) found very effective for somatic embryoid induction. Plantlet regeneration from embryogenic calli, as somatic embryogenesis, found good in auxin-cytokinin combination of 2, 4-D and IAA with BAP but in different concentrations i.e. 2, 4-D and IAA 2mg/l with 2 and 3mg/l BAP.
Plasticizers May Activate Human Hepatic Peroxisome Proliferator-Activated Receptor Less Than That of a Mouse but May Activate Constitutive Androstane Receptor in Liver  [PDF]
Yuki Ito,Toshiki Nakamura,Yukie Yanagiba,Doni Hikmat Ramdhan,Nozomi Yamagishi,Hisao Naito,Michihiro Kamijima,Frank J. Gonzalez,Tamie Nakajima
PPAR Research , 2012, DOI: 10.1155/2012/201284
Abstract: Dibutylphthalate (DBP), di(2-ethylhexyl)phthalate (DEHP), and di(2-ethylhexyl)adipate (DEHA) are used as plasticizers. Their metabolites activate peroxisome proliferator-activated receptor (PPAR) α, which may be related to their toxicities. However, species differences in the receptor functions between rodents and human make it difficult to precisely extrapolate their toxicity from animal studies to human. In this paper, we compared the species differences in the activation of mouse and human hepatic PPARα by these plasticizers using wild-type (mPPARα) and humanized PPARα (hPPARα) mice. At 12 weeks old, each genotyped male mouse was classified into three groups, and fed daily for 2 weeks per os with corn oil (vehicle control), 2.5 or 5.0?mmol/kg DBP (696, 1392?mg/kg), DEHP (977, 1953?mg/kg), and DEHA (926, 1853?mg/kg), respectively. Generally, hepatic PPARα of mPPARα mice was more strongly activated than that of hPPARα mice when several target genes involving β-oxidation of fatty acids were evaluated. Interestingly, all plasticizers also activated hepatic constitutive androstane receptor (CAR) more in hPPARα mice than in mPPARα mice. Taken together, these plasticizers activated mouse and human hepatic PPARα as well as CAR. The activation of PPARα was stronger in mPPARα mice than in hPPARα mice, while the opposite was true of CAR. 1. Introduction Dibutylphthalate (DBP), di(2-ethylhexyl)phthalate (DEHP), and di(2-ethylhexyl)adipate (DEHA) are used as representative industrial plasticizers, though the use of the first two considerably decreased recently. These chemicals are involved in peroxisome proliferations, similar to endogenous fatty acids, exogenous fibrates, and thiazolidinediones [1–4]. Once most plasticizers are taken into the body, they are metabolized by lipase in several organs such as liver and small intestine, and their metabolites, especially mono-carboxylic acids, activate peroxisome proliferator-activated receptor alpha (PPARα), and influence the receptor-related lipid metabolism, anti-inflammation, glucose metabolism, and ketogenesis [5]. Peroxisome proliferators (PPs) cause hepatocarcinogenesis in rodents, and PPARα is involved in the mode of action [6]. However, the lower expression of PPARα in human liver [7] and ligand affinity for the agonists [2, 3] has been discussed within the context of how the risk of these chemicals is extrapolated to human from the animal data [8]. Indeed, the International Agency for Research on Cancer downgraded the DEHP carcinogenicity potential from 2B to 3, which produced some conflicting views over the
Cancer cachexia
Marcus E Martignoni, Philipp Kunze, Helmut Friess
Molecular Cancer , 2003, DOI: 10.1186/1476-4598-2-36
Abstract: Cancer cachexia occurs most frequently in malignancy and is associated with more than 20% of cancer deaths [1]. Patients with upper gastrointestinal cancer are especially likely to suffer from substantial weight loss, and patients with pancreatic cancer have the highest frequency of developing a cachectic syndrome. Thus the research groups and physicians dealing with pancreatic cancer are very interested in finding an effective treatment for cachectic patients. But there is still little known about this clinical issue, and our knowledge grows slowly. Much more research and many more clinical trials are needed to increase our understanding of the syndrome and to develop therapeutic strategies for one of the major symptoms of cancer.The word "cachexia" comes from the Greek words "kakos" and "hexis", meaning "bad conditions" [2]. Cachexia is a complex metabolic status with progressive weight loss and depletion of host reserves of adipose tissue and skeletal muscle. Cachexia should be suspected if involuntary weight loss of greater than five percent of premorbid weight occurs within a six-month period [3]. Cachexia represents the clinical consequence of a chronic, systemic inflammatory response, with high hepatic synthesis of acute-phase proteins resulting in depletion of essential amino acids [4]. In contrast, in starvation only fat metabolism is increased while the organism tries to conserve lean body mass [5].In addition to metabolic changes, cachexia is often associated with anorexia. In cancer patients there can be mechanical interference such as obstructions, as well as treatment-related toxicity. In patients receiving chemotherapy or radiation, subsequent nausea, vomiting and diarrhea can contribute to weight loss. But the lack of nutrients alone cannot explain the metabolic changes seen in cachexia. In clinical trials, nutritional supplementation and dietary counseling failed to increase body weight [6]. Several appetite-stimulating drugs have been tested in an
Fast Growth May Impair Regeneration Capacity in the Branching Coral Acropora muricata  [PDF]
Vianney Denis, Mireille M. M. Guillaume, Madeleine Goutx, Stéphane de Palmas, Julien Debreuil, Andrew C. Baker, Roxane K. Boonstra, J. Henrich Bruggemann
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072618
Abstract: Regeneration of artificially induced lesions was monitored in nubbins of the branching coral Acropora muricata at two reef-flat sites representing contrasting environments at Réunion Island (21°07′S, 55°32′E). Growth of these injured nubbins was examined in parallel, and compared to controls. Biochemical compositions of the holobiont and the zooxanthellae density were determined at the onset of the experiment, and the photosynthetic efficiency (Fv/Fm) of zooxanthellae was monitored during the experiment. Acropora muricata rapidly regenerated small lesions, but regeneration rates significantly differed between sites. At the sheltered site characterized by high temperatures, temperature variations, and irradiance levels, regeneration took 192 days on average. At the exposed site, characterized by steadier temperatures and lower irradiation, nubbins demonstrated fast lesion repair (81 days), slower growth, lower zooxanthellae density, chlorophyll a concentration and lipid content than at the former site. A trade-off between growth and regeneration rates was evident here. High growth rates seem to impair regeneration capacity. We show that environmental conditions conducive to high zooxanthellae densities in corals are related to fast skeletal growth but also to reduced lesion regeneration rates. We hypothesize that a lowered regenerative capacity may be related to limited availability of energetic and cellular resources, consequences of coral holobionts operating at high levels of photosynthesis and associated growth.
Heterogeneous response of adipose tissue to cancer cachexia
Bertevello, P.S.;Seelaender, M.C.L.;
Brazilian Journal of Medical and Biological Research , 2001, DOI: 10.1590/S0100-879X2001000900009
Abstract: cancer cachexia causes disruption of lipid metabolism. since it has been well established that the various adipose tissue depots demonstrate different responses to stimuli, we assessed the effect of cachexia on some biochemical and morphological parameters of adipocytes obtained from the mesenteric (mes), retroperitoneal (rpat), and epididymal (eat) adipose tissues of rats bearing walker 256 carcinosarcoma, compared with controls. relative weight and total fat content of tissues did not differ between tumor-bearing rats and controls, but fatty acid composition was modified by cachexia. adipocyte dimensions were increased in mes and rpat from tumor-bearing rats, but not in eat, in relation to control. ultrastructural alterations were observed in the adipocytes of tumor-bearing rat rpat (membrane projections) and eat (nuclear bodies).
Heterogeneous response of adipose tissue to cancer cachexia  [cached]
Bertevello P.S.,Seelaender M.C.L.
Brazilian Journal of Medical and Biological Research , 2001,
Abstract: Cancer cachexia causes disruption of lipid metabolism. Since it has been well established that the various adipose tissue depots demonstrate different responses to stimuli, we assessed the effect of cachexia on some biochemical and morphological parameters of adipocytes obtained from the mesenteric (MES), retroperitoneal (RPAT), and epididymal (EAT) adipose tissues of rats bearing Walker 256 carcinosarcoma, compared with controls. Relative weight and total fat content of tissues did not differ between tumor-bearing rats and controls, but fatty acid composition was modified by cachexia. Adipocyte dimensions were increased in MES and RPAT from tumor-bearing rats, but not in EAT, in relation to control. Ultrastructural alterations were observed in the adipocytes of tumor-bearing rat RPAT (membrane projections) and EAT (nuclear bodies).
Increased Cell Fusion in Cerebral Cortex May Contribute to Poststroke Regeneration  [PDF]
Alexander Paltsyn,Svetlana Komissarova,Ivan Dubrovin,Aslan Kubatiev
Stroke Research and Treatment , 2013, DOI: 10.1155/2013/869327
Abstract: In this study, we used a model of a hemorrhagic stroke in a motor zone of the cortex in rats at the age of 3 months The report shows that cortical neurons can fuse with oligodendrocytes. In formed binuclear cells, the nucleus of an oligodendrocyte undergoes neuron specific reprogramming. It can be confirmed by changes in chromatin structure and in size of the second nucleus, by expression of specific neuronal markers and increasing total transcription rate. The nucleus of an oligodendrocyte likely transforms into a second neuronal nucleus. The number of binuclear neurons was validated with quantitative analysis. Fusion of neurons with oligodendrocytes might be a regenerative process in general and specifically following a stroke. The appearance of additional neuronal nuclei increases the functional outcome of the population of neurons. Participation of a certain number of binuclear cells in neuronal function might compensate for a functional deficit that arises from the death of a subset of neurons. After a stroke, the number of binuclear neurons increased in cortex around the lesion zone. In this case, the rate of recovery of stroke-damaged locomotor behavior also increased, which indicates the regenerative role of fusion. 1. Introduction Protection, rehabilitation, and stroke outcome are determined by the extent of the preserved neuronal tissue. Thus, the maintenance and regeneration of stroke-injured neurons is a prominent topic on which there are many publications, all of which represent neuronal regeneration exclusively as a result of neurogenesis. This tendency can be justified only in one case, when a stroke occurs in the dentate gyrus (fascia dentata hippocampus) or in the olfactory bulb. These two zones are reasonably considered neurogenic because they are sites of the replacement of granular neurons. Granular neurons are formed in two other neurogenic zones: the subgranular layer of the dentate gyrus [1–5] and the subventricular layer of the cerebral ventricles [6–8]. Neuroblasts migrate from these zones to the granular layer of the dentate gyrus [9–11] and to the olfactory bulbs [8, 12], where they differentiate into granular neurons. Reports of neurogenesis in other brain regions, as in the review of Gould [13], contradict other experiments [14–17]. Therefore, scientific consensus purports that, in other brain regions, neurogenesis does not occur. According to one hypothesis, neurogenesis does not normally occur in the cortex but appears after stroke [18, 19]. However, some publications do not confirm this point of view [20]. These issues
Pathophysiology of cancer cachexia
Younes, Riad N.;Noguchi, Yoshikazu;
Revista do Hospital das Clínicas , 2000, DOI: 10.1590/S0041-87812000000500005
Abstract: cancer cachexia is a frequent complication observed in patients with malignant tumors. although several decades have passed since the first focus on the metabolic dysfunction's associated with cancer, few effective therapeutic interventions have been successfully introduced into the medical armamentarium. the present study thoroughly reviews the basic pathophysiology of cancer cachexia and the treatment options already investigated in that field. experimental and clinical studies were evaluated individually in order to clarify the intricate alterations observed in tumor-bearing patients. the difficulties in introducing sound and effective nutritional support or metabolic manipulation to reverse cancer cachexia are outlined in this review.
Pathophysiology of cancer cachexia  [cached]
Younes Riad N.,Noguchi Yoshikazu
Revista do Hospital das Clínicas , 2000,
Abstract: Cancer cachexia is a frequent complication observed in patients with malignant tumors. Although several decades have passed since the first focus on the metabolic dysfunction's associated with cancer, few effective therapeutic interventions have been successfully introduced into the medical armamentarium. The present study thoroughly reviews the basic pathophysiology of cancer cachexia and the treatment options already investigated in that field. Experimental and clinical studies were evaluated individually in order to clarify the intricate alterations observed in tumor-bearing patients. The difficulties in introducing sound and effective nutritional support or metabolic manipulation to reverse cancer cachexia are outlined in this review.
Treatment of cachexia in oncology  [cached]
Tazi E,Errihani H
Indian Journal of Palliative Care , 2010,
Abstract: Background: Cachexia is a complex metabolic syndrome associated with many chronic or end-stage diseases, especially cancer, and is characterized by loss of muscle with or without loss of fat mass. The management of cachexia is a complex challenge that should address the different causes underlying this clinical event with an integrated or multimodal treatment approach targeting the different factors involved in its pathophysiology. Aims and Objectives : The purpose of this article was to review the current medical treatment of cancer-related cachexia, in particular focusing on combination therapy and ongoing research. Results : Among the treatments proposed in the literature for cancer-related cachexia, some proved to be ineffective, namely, cyproheptadine, hydrazine, metoclopramide, and pentoxifylline. Among effective treatments, progestagens are currently considered the best available treatment option for cancer-related cachexia, and they are the only drugs approved in Europe. Drugs with a strong rationale that have failed or have not shown univocal results in clinical trials so far include eicosapentaenoic acid, cannabinoids, bortezomib, and anti-TNF-alpha MoAb. Several emerging drugs have shown promising results but are still under clinical investigation (thalidomide, selective cox-2 inhibitors, ghrelin mimetics, insulin, oxandrolone, and olanzapine). Conclusions : To date, despite several years of coordinated efforts in basic and clinical research, practice guidelines for the prevention and treatment of cancer-related muscle wasting are lacking, mainly because of the multifactorial pathogenesis of the syndrome. From all the data presented, one can speculate that one single therapy may not be completely successful in the treatment of cachexia. From this point of view, treatments involving different combinations are more likely to be successful.
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