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are the most up-to-date type of questions that you will experience on the AP Chemistry Exam. . Periodic relationships including, for example, atomic radii, ionization energies, Balancing of equations including those for redox reactions. 3. Chemistry homework help yahoo answer help with my thesis statement and other sites — far too many for one person to review, let alone to keep up to date. Includes numerous examples of application of kinetic molecular theory and a of how to balance redox reactions; also covers cell potentials and Faraday's laws. Example:Mg2CO3 heat> magnesium carbonate is break the following key: a) combination b) decomposition PERIOD____ DATE ______.

The most important glomerular lesions are capillary basement membrane thickening. Excessive glomerulosclerosis can produce adequate levels of ischemia to the kidneys that can develop into end-stage renal diseaserequiring dialysis or renal transplantation [ 3 ]. Increased DM prevalence rates, predominantly in developing countries, follow the trend of lifestyle changes and certain diets.

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One particular area in research is zinc Zn. The sufficient availability of this transition metal has shown to be essential for biological processes [ 4 ] including optimal nucleic acid and protein metabolism as well as cell growth, division, and function [ 5 ].

Interestingly, some studies have shown DM patients had increased levels of Zn excretion in urine compared to non-DM controls [ 6 ] and that DM patients are usually Zn deficient. This has encouraged further research into the possible positive effects of Zn supplementation on DM patients. Several studies have shown its beneficial effects on renal pathological changes in T1D and T2D subjects by reducing oxidative stress, glomerular damage, lymphocytic infiltration, and urinary albumin excretion.

As DM incident rates increase rapidly worldwide, and the UK health service is predicted to spend Therefore, this particular study includes analysis of published findings and have found promising results that show Zn reducing, and in some cases completely preventing renal damage. The intention of this paper is to highlight the significance of Zn and encourage further research in this area, and its potential use as a treatment against renal pathological symptoms in DM patients.

Diagnosis of DM Blood glucose level tests are the common methods of diagnosis for DM, which include fasting glucose concentration test, poststandard carbohydrate load, and oral glucose tolerance test OGTT. Patients with abnormally high levels of glucose in any of these tests are considered to have impaired glucose tolerance and recognised as prediabetics or diabetics. Another diagnostic test is to measure levels of glycated haemoglobin HbA1cwhich identifies the average plasma glucose concentration over a long period of time, for a period of two to three months.

High levels of HbA1c are usually seen in DM patients and individuals with renal failure. HbA1c is formed when haemoglobin binds to plasma glucose. Due to high numbers of glucose molecules binding to haemoglobin in DM patients, high levels of HbA1c is typically expected. Together with the fasting plasma glucose test, the HbA1c test is mainly used to diagnose T2D.

Most patients depend on exogenous insulin for survival. Without insulin they develop severe metabolic complications such as ketoacidosis and coma. T2D is a complex multifactorial disease where both genetic [ 7 - 9 ] and environmental factors [ 10 - 12 ] play a role.

Other types of DM fall into monogenic and secondary causes. Although the major types of DM arise by different pathogenic mechanisms, the long-term complications in kidneys, eyes, nerves, and blood vessels are the same and are the principal causes of morbidity and death. DM includes a group of metabolic disorders caused by the disruption of glucose reabsorption in kidney tubules. High concentration of glucose in urine leads to saturation of transport proteins in the epithelium, restricting glucose molecules from leaving the kidney tubules.

Urine containing high glucose solute glycosuria causes osmotic diuresis, increasing the volume of urine excreted out of the body polyuria. Normal glucose homeostasis is regulated by three interrelated processes including the production of glucose in the liver, glucose uptake and utilization by peripheral tissues, and actions of insulin and other regulatory hormones such as glucagon.

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Insufficient levels of insulin in the body, which occurs in DM, can cause accumulation of glucose in cells and lead to cell damage, including in renal cells. As glomerulosclerosis progresses in DM patients with nephrotic syndrome, symptoms such as proteinuria, hypoalbuminemia, and oedema become evident.

Excessive glomerulosclerosis can produce adequate levels of ischemia to the kidneys that can be seen as granular lesions on its surface [ 15 ].

Zinc in the Human Body Zn is a trace element found in microorganisms, plants, and animals. Although trace quantities are contained within organisms, the presence of this transition metal has shown to be essential for biological processes [ 4 ].

Approximately enzymes and more proteins contain Zn components, which emphasizes its essential role for human health.


Optimal nucleic acid and protein metabolism, as well as cell growth, division, and function require sufficient availability of Zn [ 5 ]. In the human body, most Zn is found in the muscle and bone and smaller concentrations are found in some organs including the liver, gastrointestinal tract, and kidney.

Oral ingestion of Zn leads to its absorption through the small intestine and then its release into blood serum where it can be absorbed into different areas of the body and ultimately excreted by binding to proteins such as albumin and transferrin [ 16 ]. Cellular Zn involves efficient homeostatic control that avoids accumulation of excess Zn [ 17 ] and redistributes Zn to avoid its deficiency in specific organs e.

Cellular Zn homeostasis is mediated by two protein families; the Zn-importer Zip, Zrt, Irtlike proteins family containing 14 proteins that transport Zn into the cytosol, and the Zn transporter ZnT family, comprising 10 proteins transporting Zn out of the cytosol [ 19 ]. Regulation of homeostasis is crucial to maintain cellular viability and prevent deregulation, which can lead to damage of the cell and ultimately cell death.

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Cellular Zn homeostasis is mediated by three main mechanisms Figure 1. One is the transportation of Zn into the cytosol through the plasma membrane by importers from the Zip-family, and it is exported out of the cytosol by proteins from the ZnT-family. Another is due to Zn-binding proteins such as metallothionein MT that maintain Zn homeostasis.

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To enable Zn re-distribution, it needs to be mobilized from its tight binding sites by coordinating Zn to sulphur donors. This allows direct Zn transfer and redox reactions to occur to the redox-inert Zn ion. The final main mechanism is transportermediated sequestration of Zn into intracellular organelles, including endoplasmic reticulum, Golgi, and lysosomes. Cellular Zn homeostasis and its impact on cytotoxicity and during Zn deficiency. A Cellular Zn homeostasis. Zn is transported into the cytosol by Zip-family and exported out by ZnT-family.

MT maintain Zn homeostasis. It coordinates Zn to sulphur donors, allowing Zn transfer and redox reactions to occur. Elevated levels of free Zn ions can bind to Zn finger structures of the metal-regulatory transcription factor MTF -1, inducing the expression of Tred.

Oxidation of thiols by reactive oxygen ROS or nitrogen RNS species triggers the formation of the oxidized protein thionin Toxwhich generates Zn signals and reduces oxidant signals, thereby reducing oxidative stress [ 20 ] Figure 1. MTs have been widely recognised in their involvement with Zn homeostasis. Overall, MT has a variety of functions including the regulation of apoptosis and more relevantly, the maintenance of Zn homeostasis.

Due to the unique structural characteristics of MT, it can bind up to seven Zn ions. A study on the effects of MT on tubular epithelial cells in the kidney showed the up-regulation of MT stimulated the hypoxia-inducible factor and hypoxia-responsive elements HIFHRE pathway, which stabilizes protein expression in cells and reduces renal injury caused by hypoxia [ 21 ].

Decreased levels of Zn in the body can cause damaging effects towards growth, neuronal development, and immunity. There are several causes of Zn deficiency including insufficient dietary intake e. Zinc and Diabetes InZn was discovered as a component of insulin crystals therefore suggested the importance of Zn to maintain normal biological processes in the body.

The deregulation of Zn homeostasis can lead to Zn deficiency or excess Zn in the body, which can affect the formation of insulin crystals that may lead to insufficient levels of insulin and result in DM. Possible components that may be involved in Zn deregulation include defects in MT as this protein is predominantly involved in Zn homeostasis. Alternatively it could be caused by defects in the Zn transporter protein ZnT-8, which delivers Zn ion from the cytoplasm into insulin granules [ 25 - 27 ].

As well as being a significant component of insulin, Zn also relates to DM in the sense that studies on animal DM models and human have shown increase levels of Zn excretion in urine compared to non-DM controls [6]. This indicates that DM patients are usually Zn deficient. The definite cause for this is yet unknown, however a number of studies have indicated a positive correlation between increased zincuria with polyuriasince osmotic diuresis is one of the symptoms of DM [ 28 - 30 ].

Therefore high levels of Zn are excreted in urine, resulting in Zn deficiency in the body. Also hyperzincuria has been linked with blood glucose concentration, glycosuria and proteinuria [ 293132 ]. Improvements in control diabetic glycaemic level after zinc supplementation The relationship between Zn deficiency and DM has been the subject of many studies, some using animal models [ 33 - 35 ] and some human subjects [ 3637 ].

Diabetic subjects are commonly tested for blood glucose levels due to inadequate levels of insulin produced by the pancreas. A study on T1D rats by STZ administration showed lower blood glucose levels and hour urinary protein levels after 3 months of Zn supplication in DM subjects Blood glucose level This suggested that Zn might be involved in preventing hyperglycaemia and proteinuriawhich are common symptoms of DM-induced renal damage.

A study on T2D patients suffering from microalbuminuria showed that HbA1c was significantly reduced from 8. Another paper studied the effects of Zn supplementation on T2D patients and the level of glycaemic control.

Group 1, which included 50 patients, were given Zn, and 51 patients in Group 2 were given a placebo. Results showed a positive correlation between serum Zn levels and Zn intake. Improvements in diabetic glomerular function after zinc supplementation The effects of a mixture of vitamins and minerals, including Zn have also shown improvements in glomerular function in T2D patients. Factors that significantly reduced are urinary albumin excretion UAE levels, fasting serum glucose and malondialdehyde concentrations.

Malondialdehyde is a common marker for oxidative stress [ 43 ]. Several studies have investigated the effects of Zn supplementation on microalbuminuria in DM patients [ 4144 - 46 ].

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Results from studies show a significant decrease in UAE in subjects given Zn, whereas subjects not given Zn exhibited consistent high UAE levels [ 41 ]. This study has shown the renal-protective effects of Zn by significantly reducing UAE after Zn supplementation, which suggests reduced permeability of renal glomerulus to albumin in patients supplied with Zn.

This also demonstrates the effectiveness of Zn as these improvements were seen within only 3 months, therefore shows the potential of Zn to possibly prevent renal damage at a relatively fast rate. However, the limitations of this study include only measuring fasting plasma glucose and not postprandial plasma glucose concentration.

Hence these levels may change after Zn supplementation and alter the results. Also high homocysteine concentrations in plasma are associated with glomerular filtration impairment [ 45 ]. Hence a decrease in this amino acid after Zn supplementation shows promising results.

In addition to research on damaged renal tubules, other substances involved in renal damage have been studied. For example, renal tissues from Zn-deficient DM rats that were given Zn supplementation showed a reduction in levels of connective tissue growth factor CTGF.

A number of studies have shown a positive correlation between the level of renal CTGF mRNA expression and glomerulosclerosis in diabetic mice [ 47485051 ]. Inhibition of diabetic oxidative stress after zinc supplementation A study on the antioxidant effects of Zn on T2D showed initial increases in oxidative stress, which was measured according to the presence of plasma thiobarbituric acid reactive substances TBARSin T2D patients compared to healthy patients 3.

After six months of Zn supplementation, T2D patients showed a significant reduction in plasma TBARS, in contrast to the placebo group where no significant changes were seen [ 52 ]. Another similar study also showed the potential antioxidant effects of Zn, although when combined with chromium.

However a study on T2D male patients showed Zn supplementation does not decrease oxidative stress in patients with normal Zn levels [ 54 ]. Recent advance in cancer research has strongly suggests that cancer stem cells contribute to the formation and maintenance of the heterogeneous cellular society in the tumor tissue.

After all, this heterogeneity is the major cause of the acquired resistance to anti-tumor therapies. Accumulating evidence suggests that tumor cells educate stroma cells as they enhance the malignant potential of tumor cells [ 1 ].

Given that cancer cells frequently have mutations in the cell-cycle regulatory proteins, tumor cells are mistaken as homogeneous. However, there exists a cellular heterogeneity in tumor tissues [ 2 ], which is why therapeutic response to the molecular targeting drugs is different depending on the genetic or epigenetic background of each tumor cell. An emerging concept of the cancer stem cells CSCs simply explains how the hierarchy of tumor cells is formed.

CSCs have the selfrenewal ability and multi-lineage differentiation potential [ 45 ], both of which are necessary to architect the secondary heterogeneous tumor lesion from a single cell Figure 1. This diversity is responsible for the formation of minimal residual disease MRD [ 2 ], which leads to the latent relapse and the distant metastasis.

Bilateral perspectives into the entity of cancer stem cells CSCs.

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CSCs are defined to show the self-renewal and multi-lineage differentiation potential, which contribute to the formation of the heterogeneous cellular population in the tumor tissue. It still remains elusive, however, these two cell populations are exactly the same entity each other. We would like to focus on the biological characteristics of CSCs, which contributed to the therapeutic resistance.

Stemness is composed of the various phenotypes of CSCs; resistance to redox stress via the synthesis of glutathione GSH and G0 cell cycle arrest under hypo-nutrient or growth factor conditions Figure 1. Epithelial-mesenchymal transition EMT has widely been recognized as a crucial step in the invasion and metastasis as well as normal tissue development and wound healing [ 9 ]. EMT has long been believed to increase the number of CSCs at the invasive front and metastatic foci [ 1011 ].

CD44 is an adhesion molecule to extracellular matrix such as osteopontin and hyaluronic acids [ 12 ]. CD44 has a numerous isoforms because of alternative splicing machinery mainly regulated by RNA binding protein epithelial splicing regulatory protein 1 ESRP1 and epigenetic modulation of the HistoneH3lysine9trimethylation H3K9me3 [ 13 - 15 ].

While CD44 variant isoform CD44v is predominantly expressed in epithelial cancer cells, the CD44 standard isoform CD44s is mainly expressed in mesenchymal cancer cells. Redox stress-induced Wnt activation and EMT.

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That is why the knockdown of Prrx1 induces MET and promotes the lung metastasis of breast cancer cells [ 18 ]. Furthermore, it has been demonstrated that tumor cells maintain epithelial phenotype with the high expression of CD44v at the invasive front [ 10 ].

This seems paradoxical to the current concept, but some researcher insist on the presence of CAFs with CSCs at the invasive front [ 19 ]. Indeed, CD44v is strongly expressed at the invasive front and negatively correlated with the expression of oncogenic protein c-Myc. Redox stress-induced Wnt signal activation is responsible for the inversed relationship between CD44v and c-Myc [ 10 ]. The irreversible quiescence of CSCs is finely regulated by the modulation of several kinds of stress derived from tumor microenvironment.