L-Acetylcarnitine (hydrochloride) Description: IC50: L-Acetylcarnitine, also named as ALCAR, an acetylated form of L-carnitine, fosters the uptake of acetyl coenzyme A (CoA) into mitochondria during fatty acid oxidation, raises the production of acetylcholine, and triggers the synthesis of membrane phospholipid and protein. ALCAR has been explored for use as an acetylcholine mimic as well as in targeting cardiovascular pathologies. Acetyl CoA, as the primary substrate for the Krebs cycle in mitochondria, must be re-charged with an acetyl-group in order for the Krebs cycle to maintain working when it is de-acetylated. In vitro: The proliferation of tumor antigen CA-125 expression in ovarian cancer cells was not affected by ALCAR. Higher concentration of ALCAR declined slightly but significantly in the proliferation of SKOV-3 ovarian cancer cells. In addition, ALCAR had no effect on the expression of the nerve growth factor receptors on SKOV-3 or OVCAR-3 ovarian cancer cells [1]. …show more content…
ALCAR, as a long-lasting and rapid antidepressant, functioned via the epigenetic regulation of type 2 metabotropic glutamate (mGlu2) receptors in FSL rats and in mice. Additionally, ALCAR raised the transcription of Grm2 gene encoding for the mGlu2 receptor via increasing levels of acetylated H3K27 bound to the Grm2 promoter and gaining the acetylation of NF-ĸB-p65 subunit.
In this experiment, both BALB/c and C3H mice are induced with azoxymethane (AOM) and dextran sodium sulphate (DSS). The inflammation is caused by the administration of dextran sodium sulphate to the drinking water of the mice. While azoxymethane induction plays a role in the development to colon cancer. In this project, the development of colon cancer through the inflammation pathway is being researched. The process first starts with the of inflammation foci. Over time, it develops into hyperplasia due to the increasing capacity of cell proliferation.
The IC50 values of LJI308 against RSK1, 2, and 3 were about0.004 - 0.013 mmol/L. 10 μMLJI308 could bind to nearly 100% of theRSK2. LJI308 boundtheN-terminiofRSK1, RSK3, and RSK4 to a similar extent. LJI308 inhibited S6K1 with an IC50 of 0.8 mM. In both MDA-MB-231 and H358 cell lines, 1 μM and 10 μM LJI308 exihibited an inhibitory effect on colony formation and cell growthwith a different sensitivity[1]. In HTRY-LT cell lines,treating withLJI308 (1-10 µM) after4 or 8 days decreased the cellviability by up to 90%; while little to no effect wasobserved in the non-tumorigenic HTRZ cells [2].
MCAD normally metabolizes medium-chain acyl-CoAs in the matrix of the mitochondria. In fatty acid β-oxidation, MCAD catalyzes the dehydrogenation of acyl-CoAs with four to 12 carbons in chain length (Matern & Rinaldo, 2012). In MCAD deficiency, this initial dehydrogenation step of the beta-oxidation process if significantly hindered, resulting in ineffective fatty acid degradation. A deficiency in the MCAD enzyme is caused by premature degradation due to an accumulation of improperly folded proteins and tetramer assembly. Beta-oxidation is severely impacted because the enzyme also has reduced enzymatic function due to higher Km values for medium-chain fatty acid substrates and lower affinity for its substrates (Kieweg et al., 1997).
In summary, Laurence’s article sanctioning ketamine as a cure for depression is an interesting and well-written article, however, it could give people the wrong idea about ketamine. There is a rapidly increasing interest in the discovery of drugs targeting glutamate neurotransmitter in the brain, as a hope to rapidly treat treatment-resistant patients (Duman & Ronald, 2013). While the mentioned studies in the article and this essay have given insight into ketamine’s antidepressant effects, this is still something that needs to be researched further as a lot of unresolved problems are still around with ketamine. Furthermore, the potential side effects of ketamine, including bladder and kidney damage, hepatotoxicity and psychological effects still require extreme consideration.
The underlying purpose of the experiments performed in the study, Promoter Hypermethylation of KLF4 Inactivates its Tumor Suppressor Function in Cervical Carcinogenesis, is to investigate the mechanism by which the KLF4 gene is silenced in cervical carcinomas. Cervical cancer accounts for 250,000 female deaths every year. Developing therapies for cervical cancer has been limited due to the lack of genetic and epigenetic data of the mechanism causing the cancer. The KLF4 gene is a transcriptional regulator of cell growth and differentiation. It functions as a tumor suppressor in cervical cancer, but is found to be inactivated in cervical cancer. The overexpression of KLF4 protein is known to inhibit cervical cancer cell growth and tumor formation by activating a cell cycle suppressor. Promoter CpG island hypermethylation can result in transcriptional silencing of many tumor suppressing genes. Two CpG regions, BSQ1 and BSQ3, were examined in this experiment.
Zarate C. A., Du J., Quiroz J., Gray N. A., Denicoff K., Singh J. B., et al. (2003). Regulation of cellular plasticity cascades in the pathophysiology and treatment of mood disorders: role of the glutamatergic system. Ann N Y Acad Sci 1003, 273−291.
My family has a history of bad teeth with weak enamel. We could brush, floss, and use mouthwash five times a day and still get cavities. When my son's teeth came in, they had very weak enamel, and he had to have a lot of dental repair done when he was only two. This was when I started searching the internet for something that could help his teeth; and I discovered Xylitol. Xylitol is a white substance that tastes like sugar. It is found in various items in nature including hardwood, raspberries, berries, and lettuce-it is truly a natural sweetener. It is often derived from birch. Testing confirms that Xylitol reduces tooth decay in people who are prone to dental cavities, and even in those who are not. Children who chewed the recommended amount
According to the University of Edinburgh, “Brain study confirms gene mutation link to psychiatric disorders.” A highly anticipated genetic engineering called genome editing has had controversies. Genome editing is inserting, deleting, or replacing the genome of an organism. This means bad DNA strands such as cancer could be cut out of humans’ genes, but genome editing could have major drawbacks. Brain scans have shown that genetic mutation has effects on the structure, function and chemistry of the brain, which ultimately can lead to major psychiatric disorders such as bipolar disorder, depression, and schizophrenia. Researchers led by the University of Edinburgh found mutation had lower levels of a chemical called glutamate in major areas in the brain. Low levels of glutamate have been strong links with schizophrenia and severe symptoms of mental ill health. They hope to continue studying people with mutation will one day reveal new insights to biological
Over the years, the fight against ovarian cancer has proven to be even more difficult due to the cancer being asymptomatic at its early stages. For this reason, there are constantly late diagnoses made on women who unfortunately develop this cancer (Stack).... ... middle of paper ... ...
Yu, Wounger W.Y, Shih-Jen Tsai, Chen-Jee Hong, Tai-Jui Chen, Ming-Chao Chen, and Chih-Wei Yang. 2005. “Association Study of a Monoamine Oxidase A Gene Promoter Polymorphism with Major Depressive Disorder and Antidepressant Response.” Neuropsychoparmacology 30:1719-1723.
With heart-related problems on the rise with each passing year, more people than ever before are looking for preventative supplements and solutions for these issues. Heart disease is one of the most prevalent, yet preventable, health problems despite the continuation of countless prescription medications. This has led people to seek out alternatives and natural supplements that can protect, repair and restore their heart health. Arginine, also known as L-arginine, is one such remedy that has enjoyed an increase in popularity.
Other forms of human cancer that involve oncogenes are neuroblastoma and breast cancer. In neuroblastoma patients there is a large presence of abnormality of the N-myc proto-oncogene associated with a conversion to an oncogene. In neuroplastic cells there is an abnormal increase in the N-myc gene resulting from gene amplification, which is the repeating of DNA sequences multiple times. In addition, breast cancer also is caused through gene amplification resulting in the development of oncogenes. Gene amplification of the c-erb B-2 proto-oncogene results in increased production of the c-erb B-2 protein.7 Oncogenes in these two cases bypass the G phases and proceed straight to either the S phase or mitosis, initiating abnormal cell proliferation unimpeded by cell growth regulation.
... The limited research that has been performed using these cells has yielded contradictory results: some results say that the alpha5beta1 integrins destroy cancer cells, other results have shown that cell division and other necessary cell functions have been encouraged by the integrin. But the research has predominantly shown that the results of the expression of alpha5beta1 integrins yield beneficial results in terms of cancer tumor reduction. More research needs to be done, but the knowledge obtained from this experiment that alpha5beta1 integrin prevents premature cell death is an excellent step forward in the fight against cancer. There are untold possibilities for the medical applications of not only alpha5beta1 integrins, but all of the many integrins and cell adhesion molecules that play important roles in cell function.
Uterine cancer is an important women health problem developing rapidly, killing over 200,000 women each year. No one has discovered the actual cause, but there is a leading factor that has great suspicions to what is causing this cancer to grow rapidly.
1. The labels have fallen off of three bottles thought to contain hydrochloric acid, or sodium chloride solution, or sodium hydroxide solution. Describe a simple experiment which would allow you to determine which bottle contains which solution.