The synthesis of cisplatin is very well established and is one of the most classic examples of synthesis in inorganic chemistry (figure 1). Dhara reported in 1970 “A rapid method for the synthesis of cis-[PtCl2(NH3)2].”8 The starting material, K2[PtCl4], is treated with excess of KI to be converted into K2[PtI4]. The product is subsequently treated with NH3 to obtain yellow colored cis-[PtI2(NH3)2] that is collected and dried. cis-[PtI2(NH3)2] is then dissolved in AgNO3 to precipitate out AgI that is removed. The solution containing cis-[Pt(OH2)2(NH3)2]2+ is lastly treated with KCl to produce the final, yellow-colored product, cisplatin.
The synthesis scheme of cisplatin is deeply related to the trans effect. Chernyaev introduced the trans effect in platinum chemistry9. The theory is based on empirical observation that the rate of substitution of a ligand in a square planar complex is dependent on the group opposite (or trans) to it8. The trans effect can be explained by two factors: sigma-bonding effect and pi-bonding effect.
The sigma-bonding effect is the weakening of the bonding between platinum and X, or the leaving group, by the sigma bonding between platinum and the sigma-bonding ligand (T in figure 2) trans to X. The Pt-X bond is affected by Pt-T bond because both bondings make use of platinum Px and dx2-y2 orbitals. If the bonding between Pt-T becomes stronger, less of platinum dx2-y2 orbital is available for Pt-X bond, making the bond weaker as a result. Thus a strong sigma-bonding ligand “labilizes” the metal-ligand bond trans to it, which is sigma-bonding effect.
The pi-bonding effect is another factor that contributes to trans effect. When pi-bonding ligand (T in figure 2) that is trans to X result in strong pi-b...
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... c, which leads to APAF1 activation, followed by CASP9 activation that can also activate CASP3 and CASP711.
Studies have shown that the transduction of cisplatin-DNA adduct recognition signal occurs through pathways other than p53, including the following: AKT pathway, c-ABL, MAPK/JNK/ERK, and MKP1/CL10011. These other pathways are not covered in this paper due to page limits.
Reference
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14. Ohndorf, Nature, 1999, 399, 708-712.
15. Jayaraman, Genes & Development, 1998, 12, 462-472.
16. Vousden, Nature Reviews, 2002, 2, 594-604.
The immunologic events that are happening at the local level during Carlton's acute inflammatory response would be:
The positive charge on the phosphorus atom is a strong EWG (electron-withdrawing group), which will trigger the adjacent carbon as a weak acid. 5 Very strong bases are required for deprotonation such as an alkyl lithium, however in this experiment 50% sodium hydroxide was used as reiterated. Lastly, the reaction between ylide and aldehyde/ketone produces alkene. (Eq. 1) As shown in equation 2, the reaction between the phosphonium salt and the sodium hydroxide produces the ylide/carbanion that is stabilized due to the positive charge on phosphorus and the conjugation that occurs in the benzene ring as shown by the structure B in equation 2.
Some possible errors raised during the synthesis and spectrometric analysis of TPCP include the insufficient mixing of the hexane and TPCP, in which will result in the low absorbance of the compound. Additionally, the low yield is contributed from the loss of product during filtration.
...s to interfere with bonding to the receptors. The final possibility uses CNP, which downregulates the activation in MAP kinase pathways in the chondrocytes (4).
In this lab 4-tert-butylcyclohexanone is reduced by sodium borohydride (NaBH4) to produce the cis and trans isomers of 4-tert-butylcyclohexanol. Since the starting material is a ketone, NaBH4 is strong enough to perform a reduction and lithium aluminum hydride is not needed. NaBH4 can attack the carbonyl group at an equatorial (cis) or axial (trans) position, making this reaction stereoselective. After the ketone is reduced by the metal-hydride, hydrochloric acid adds a proton to the negatively charged oxygen to make a hydroxyl group. The trans isomer is more abundant than the cis based on the results found in the experiment and the fact that the trans isomer is more stable; due to having the largest functional groups in equatorial positions.
Specifically “TP53, p16INK4A, and SMAD4. The p53 nuclear protein activates transcription of a cyclin kinase inhibitor p21WAF1/CIP1. Following genomic stress, inappropriate growth factor stimulation or expression of oncogenic ras increased expression of p53, and thus p21WAF1/CIP1 resulted in inactivation of specific CDK/cyclin complexes” (MedScape). If this transformed cell can escape internal and external fail-safe mechanisms, receive nutrients, and activate its proliferative program, it can form a mass of cancerous cells. Tumor growth can cause the loss of pancreatic functions. Another characteristic of pancreatic cancer is metastasis happens early in tumor growth, which is most likely responsible for pancreatic cancer’s aggressive
Chemotherapy is the treatment of a tumor with chemical agents to reduce mass or eradicate a tumor completely. There are certain mechanisms by which chemotherapy inhibits cancer. The first mechanism is cell death by cytotoxicity. Some chemical agents in certain amounts are toxic to cells. The cells die due to the toxic...
... had a higher induction effect on HBD1 than their counterpart at the same concentration (Figure 3). While on LL-37, 5-phenyl valeric acid (C5), 6-phenyl hexanoic acid (C6) and 7-phenyl heptanic acid (C7) had a higher response than their fatty acids, the peak expression observed at 5-phenyl valeric acid (C5) (Figure 3).
Thought to be an oncogene, a gene that has potential in transforming normal cells into tumor cells, p53 was regarded as the most prominent tumor suppressor gene [1]. P53 is a gene which signals apoptosis (programmed cell death) if a cell cannot be repaired due to an extensive amount of damage. As stated in the textbook, p53 regulation occurs by an E3 ubiquitin-protein ligase known as MDM2 [1]. "Controlling the controller" is a statement that describes the molecular interaction where the presence of MDM2 targets the p53 for proteosome via degradation. With three main checkpoints in cell cycle, the literature states p53 functioning from G1 into S phase in a chaotic cell [2]. The normal state of cells is to keep p53 levels low in order to prevent uncontrolled apoptosis and random cell cycle arrest from occurring. In a further note, although p53 promotes apoptosis and cell cycle arrest, cancer may result from p53 unable to recognize the problematic site. In turn, a mutation in p53 may result engaging in new activities. These activities include cellular transformation, tumor metastasis,...
...-1 (PAI-1) from the endothelial cells and monocytes, activating the extrinsic coagulation pathway. This also leads to activation of factor X and fibrin production.
Frey, Regina F., and Maureen J. Donlin. "Chemistry 257." Olfaction Tutorial. Washington University, 1998. Web. 4 Dec. 2013.
The American Cancer Society publishes current advances made in cancer research on their website. Many of the exciting discoveries about how best to treat the disease focus on the genetic aspects associated with certain types of cancer. In addition, treatments aimed at genetic solutions to cancer may be more effective and may cause fewer adverse side effects than traditional cancer treatments (American Can...
Figure 1: The hexacyanoferrate iron (III) ion: contains 6 ligands which are bound to the central metal therefore has a coordination number of 6 (n=6¬). (Hussain,2007) [13]
... magnetic orbitals on the metal and the valence orbitals of the ligands. In the present case where the nickel centres are bridged by long N-C-N hmt and N-C-N-C-N dca ligands it is reasonable to assume that only minor exchange interactions can be mediate by these bridges and, as observed here, this type of magnetic pathways generally promotes antiferromagnetic interactions [38,45-48]. Nevertheless spin canting is often observed and usually associated with single-ion magnetic anisotropy or antisymmetric exchange interaction. From structural considerations the existence of two crystallographically independent Ni(II) ions with non-collinear anisotropy axes might be at the origin of the suspected canting phenomena. To clearly ascertain for the existence of a spin canting magnetic order, as the data suggests, neutron diffractions measurements are foreseen.
Plontke, R. (2003, March 13). Chemnitz UT. TU Chemnitz: - Technische Universität Chemnitz. Retrieved April 1, 2014, from http://www.tu-chemnitz.de/en/