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This is known as the _____ theory of dreams.
activation-synthesistheoryPost-Jungians tend to identify Jung’s dream theory with the concept of compensation; they tend to believe that Jung’s radically open stand constitutes his ... contemporary cognitive and neuroscientific app...
Photosynthesis, for example, is the concerted action of dozens of proteins (genes) with copy numbers in the hundreds to enable a simple chemical equation: carbon dioxide + water = sugar.
Freud’s theory about the nature of dreams can logically follow.
Of potential interest for future cannabinoid-based therapies, cannabinoid treatment does not seem to activate this pathway in normal pancreas or spleen, suggesting that these agents may activate the endoplasmic reticulum stress proapoptotic pathway selectively in tumor cells.
Pancreatic adenocarcinomas are among the most malignant forms of cancer and, therefore, it is of especial interest to set new strategies aimed at improving the prognostic of this deadly disease. The present study was undertaken to investigate the action of cannabinoids, a new family of potential antitumoral agents, in pancreatic cancer. We show that cannabinoid receptors are expressed in human pancreatic tumor cell lines and tumor biopsies at much higher levels than in normal pancreatic tissue. Studies conducted with MiaPaCa2 and Panc1 cell lines showed that cannabinoid administration (a) induced apoptosis, (b) increased ceramide levels, and (c) up-regulated mRNA levels of the stress protein p8. These effects were prevented by blockade of the CB(2) cannabinoid receptor or by pharmacologic inhibition of ceramide synthesis de novo. Knockdown experiments using selective small interfering RNAs showed the involvement of p8 via its downstream endoplasmic reticulum stress-related targets activating transcription factor 4 (ATF-4) and TRB3 in Delta(9)-tetrahydrocannabinol-induced apoptosis. Cannabinoids also reduced the growth of tumor cells in two animal models of pancreatic cancer. In addition, cannabinoid treatment inhibited the spreading of pancreatic tumor cells. Moreover, cannabinoid administration selectively increased apoptosis and TRB3 expression in pancreatic tumor cells but not in normal tissue. In conclusion, results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB(2) receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress-related genes ATF-4 and TRB3. These findings may contribute to set the basis for a new therapeutic approach for the treatment of pancreatic cancer.
The Activation-Synthesis Theory of Dreams
Cancer Cell. 2003 Jun;3(6):525-30.
Id proteins in cell growth and tumorigenesis.
Sikder HA1, Devlin MK, Dunlap S, Ryu B, Alani RM.
Since the gene encoding Id1 was cloned in 1990, Id proteins have been implicated in regulating a variety of cellular processes, including cellular growth, senescence, differentiation, apoptosis, angiogenesis, and neoplastic transformation. The development of knockout and transgenic animal models for many members of the Id gene family has been particularly useful in sorting out the biologic relevance of these genes and their expression during normal development, malignant transformation, and tumor progression. Here we review the current understanding of Id gene function, the biologic consequences of Id gene expression, and the implications for Id gene regulation of cell growth and tumorigenesis.
Cellular differentiation programs are tightly controlled through the coordinated regulation of gene expression. Basic helix-loop-helix (bHLH) transcription factors regulate the differentiation programs of multiple cell lineages (reviewed in Norton, 2000). These proteins share a common sequence motif of a stretch of basic amino acids responsible for site-specific DNA binding adjacent to a helix-loop-helix dimerization domain. The Id family of helix-loop-helix proteins does not possess a basic DNA binding domain and functions as a dominant-negative regulator of basic HLH proteins through the formation of inactive heterodimers with intact bHLH transcription factors (Figure 1). The Id family of proteins (comprised of 4 members designated Id1–Id4) has been demonstrated to bind the ubiquitously expressed bHLH E-proteins or cell lineage-restricted bHLH transcription factors, leading to inhibition of lineage-specific gene expression and differentiation (Norton et al., 1998). Hence, the name Id refers to both inhibition of differentiation and inhibition of DNA binding. Transcriptional inhibition by Id proteins is mediated via inhibition of DNA binding of bHLH or other activator proteins at E boxes (CANNTG), N boxes (CACNAG), or Ets sites (GGAA/T) present in the promoter regions of regulated genes (reviewed in Zebedee and Hara, 2001). Since cellular differentiation programs are frequently altered during the development of neoplastic disease, it is not surprising that Id proteins would play a role in this process. Indeed, a clue to the potential role of Id genes in tumorigenesis came with the observation that, in general, high Id expression levels are found in proliferative, undifferentiated cells—a feature which is characteristic of tumor cells (Israel et al., 1999). Over the past several years, the particular mechanisms underlying the effects of Id genes on cell growth and differentiation have been investigated. Here we review data supporting the critical role of Id gene regulation in the development of normal cellular differentiation programs. We also review mechanisms of Id gene regulation of cellular growth controls and the cell cycle machinery and evaluate the contribution of dysregulated Id gene expression to the process of tumorigenesis.
In addition, we showed that CBD reduces mitochondrial membrane potential, triggers the translocation of BID to the mitochondria, the release of cytochrome c to the cytosol, and, ultimately, the activation of the intrinsic apoptotic pathway in breast cancer cells.
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Latent Content: The Hidden Meaning of Your Dreams
Further studies were done by Massi pubished in a 2006 , further elucidating the molecular pathways leading to apoptosis by CBD in her human glioma cell model. She demonstrated that Mitochondrial release of cytochrome C, Caspase activation and reactive oxygen species (ROS) induction triggered the apoptosis in the CBD treated human glioma cells. CBD treated normal glioma cells were left unharmed, again showing selectivity.
according to activation-synthesis theory dreams
Early studies in 2003 by at Hebrew University in Jerusalem showed cannabidiol (CBD) induced apoptosis via caspase activation in human leukemia cell culture (HL-60 cells). Giving the leukemia cells a short burst of radiation therapy prior to CBD enhanced the effect, attaining a 90-85% cell death rate. Normal white cells were left unharmed.
activation-synthesis hypothesis – see what you need to …
Ramer’s group at the Unviersity of Rostock in Germany has done excellent work on CBD use in lung cancer with a 2012 published in FASEB. They found early-onset upregulation (four-fold) of ICAM-1 (intercellular adhesion molecule-1) via cannabinoid receptors in CDB treated lung cancer cells. Later, 48 hrs on, they found upregulation of the tissue inhibitor of matrix metalloproteinases-1 (TIMP-1) accounting for the loss of invasiveness of the lung cancer cells. In-vivo experiments injecting lung cancer cells (A549, H358, and H460) into mice then treated with CBD showed 2-3 fold increase in ICAM-1 and TIMP-1 protein which decreased cancer cell invasiveness. Upon microscopic inspection, the number of lung metastatic lesions had been reduced in half in the CBD treated mice. In yet another study, Ramers group also a new mechanism, the downregulation of the plasminogen activator inhibitor PAI-1, a protein involved in tumor invasiveness.
Posts about activation-synthesis hypothesis written by Ryan Bowen
Shrivastava et al. studied the effect of CBD on human breast cell lines and their 2011 reported induction of cancer cell death by apoptosis and autophagy. Further studies of the molecular pathways involved, showed ER (endoplasmic reticulum stress) and production of ROS (reactive oxygen species). They found that CBD reduced mitochondrial membrane potential (opened VDAC channels) which released Cytochrome C into the cytosol, and activated programmed cell death through the intrinsic pathway. Going further, with even more elegant studies, Shrivastavs’s group blocked the apoptotic cell death pathway by adding Caspase inhibitors to the CBD treated cancer cells, after which she found compensatory increase in the autophagy pathway of cell death. This supports the “Whack-a-Mole” concept in which blocking one pathway to cell death merely leads to preferential use of an alternate pathway.
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