Both the generation and clearance of Aβ are regulated by cholesterol. A polymorphism of CYP46, a gene playing a major role in hydroxylation of cholesterol and thereby mediating its removal from the brain, was associated with increased Aβ load

in brain tissue. It was also associated with increased Aβ peptides and phosphorylated tau protein in cerebrospinal fluid (CSF).130 Consistent with this observation, cholesterol was higher with Inhibitors,research,lifescience,medical increasing certainty of AD neuropath ological diagnosis.131,132 However, high cholesterol was not associated with increased neuritic plaques in the neocortex or hippocampus,133 or with Ap levels in CSF.134 Since cholesterol increases atherosclerosis which in turn is associated with dysregulation of cerebral Inhibitors,research,lifescience,medical blood flow and hypoperfusion, the effects of cholesterol on dementia risk might not depend only on Ap mechanisms but also on vascular mechanisms.135 Because of some epidemiological studies suggesting an increased risk of dementia in individuals with elevated cholesterol, and because of the biological plausibility underlying this relationship, the protective effect of statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors), among the most widely prescribed cholesterollowering Inhibitors,research,lifescience,medical medications, was postulated.136 Prospective

epidemiological studies are inconsistent but not contradictor)’ in their results, with selleck kinase inhibitor several finding that statin use is associated Inhibitors,research,lifescience,medical with decreased

risk of AD and dementia137-138 and others finding no associations.140,141 A Cochrane review concluded that there is no conclusive evidence to recommend statins to reduce the risk of AD,142 but that there is a growing body of biological and epidemiological evidence suggesting that lowering cholesterol might retard the pathogenesis of AD. Table III. Risk of dementia, MCI, and cognitive decline in patients with high total cholesterol (TC). OR, relative risk, HR, hazard ratio Inflammation Blood elevations of inflammatory markers, specifically- Creactive protein (CRP) Inhibitors,research,lifescience,medical and interleukin-6 (IL-6),have however been shown to be risk factors for dementia (Table IV). Combination of high levels of several inflammatory markers in the Conselice Study of Brain Aging144 was associated with increasing hazard ratios for dementia, and specifically high CRP/IL-6 ratios (HR=1.6, 1.03-2.4). As shown in Table TV, high levels of inflammatory markers are also consistently- associated with greater rates of cognitive decline. Of interest are the results of the Health, Aging and Body Composition (ABC) study, in which subjects with the metabolic syndrome and high levels of inflammatory markers (IL-6 and CRP) had significantly higher rates of cognitive decline than subjects with the metabolic syndrome but low levels of blood markers of inflammation.

Current research has shown that elderly individuals transitioning from healthy aging to, for example, AD (sample size of 444) demonstrated a consistent and interesting trait, in that VS measures decline faster than any other cognitive abilities Johnson et al. 2009. In fact, these researchers showed that a decline in VS ability was observed on average to occur as

early as 1 year prior to any other cognitive measures demonstrating a similar trend (Johnson et al. 2009). Therefore, with the knowledge that (1) restorative approach appears to be most beneficial to helping individuals with cognitive impairments and (2) that VS ability Inhibitors,research,lifescience,medical declines early in this process, application of this pilot program was developed based on its novelty and approach in trying to address generalized cognitive learn more concerns with the stimulation of a specified brain region(s). Brain region(s) supporting VS/VM ability therefore might be the impetus Inhibitors,research,lifescience,medical for causing a cascading effect of reduced overall ability as a region of support for other brain areas affected by the progression of cognitive impairments. Rather than trying to implicitly understand the underlying brain process involved (which was well out of the Inhibitors,research,lifescience,medical scope of the program), the goal

was in trying to understand the role of this CT intervention in effectively combating the cognitive and behavioral systems related to identified cognitive impairments. Although it is Inhibitors,research,lifescience,medical still unmistakable that declines are inevitable in populations such as AD afflicted individuals, theories such as cognitive reserve (Sole-Padulles et al. 2009;

Bosch et al. 2010) and CT (Loewenstein et al. 2004) certainly suggest that individuals have options for reducing the cognitive and behavioral effects associated with illnesses such as these. In addition, as reversing or stabilizing systems of dementia-related illnesses are still genetically unattainable, it is important to identify ways to combat these impairments and find the “best practice” strategies Inhibitors,research,lifescience,medical on how to alter the progressive effects. Limitations One of the limitations of this study could be identified too as the number of available patients. However, a meta-analysis of CT tasks for individuals experiencing cognitive impairments indicates that average sample size for this type of research is approximately 16 with the range starting at 7; thus, the number of patients analyzed here is typical of this type of research (Sitzer et al. 2006), as such, although it is a drawback, it certainly is not extraordinary. Additionally, ensuring participants are able to attend each training session and maintain attendance throughout the program was another primary limitation of this research. Future research will have to consider ways to ensure full program completion for all participants.

g. Larue et al. [41] report false beliefs of general practitioners and oncologists in France; negative attitudes of nurses in the use of morphine in pain management are reported from Australia [22] from the USA [23] and from Hong Kong [42]. The existence of false beliefs on pain, addiction and abuse of morphine have also been reported by Gilson et al. [21] in a study among 300 www.selleckchem.com/products/INCB18424.html American physicians. Furthermore Nwokeji et al. [43] reported that among 267 general practitioners who agreed to prescribe opioïdes to patients suffering from chronic non-cancerous pains, half feared addiction and abuse. White et al. [44] studying the attitudes of hospital physicians on opiate prescription, confirm that opiophobia is often Inhibitors,research,lifescience,medical related to fears

of dependency. Devi et al. [45]

questioning 253 Malaysian physicians reported that 83% of the respondents consider a possible addiction and the fear of exceeding sedation and respiratory depression as the main obstacles in prescribing morphine. Clinical documented experiences have Inhibitors,research,lifescience,medical proven that these fears are Inhibitors,research,lifescience,medical not justified [3,46-49]. Some physicians may also lack knowledge on morphine pharmacokinetics or may be unfamiliar with morphine prescription [50]. Ripamonti et al., [16] concluded in an Italian study of cancer patients that despite the WHO guidelines and EAPC recommendations, there was an inappropriate use of transdermal opioids by Italian physicians in situations where the use of oral morphine was not contraindicated. Our results showed a rather weak relationship between socio-demographic features and the perceptions of the use of morphine in pain management. Yet morphinofobia was highest among little-educated older men living in rural areas. The cultural and geographic influences on attitudes and beliefs regarding morphine among patients Inhibitors,research,lifescience,medical with non cancerous pains have been stressed by Monsivais et al. [51] and Cicero et al. [52]. However a literature review by Turk [53] is cautious in this regard. Ripamonti et al., [16] mentioned Inhibitors,research,lifescience,medical that patients were having a problem in taking morphine but they had no cultural problems with other

opioids. Most patients knew what morphine meant but do not know the role and the potency of other opioids. Health professionals play 17-DMAG (Alvespimycin) HCl an important role as far as morphinofobia is concerned, be it through a possible lack of knowledge regarding morphine [23,54], be it out of “more philosophical” reasons as suggested by Covington [10] and Bandieri et al., [13]. Yun et al. [55] and Edwards et al. [22] therefore suggest the necessity to develop more positive attitudes among HP regarding the use of morphine. There are limits to our study. First a generalisation to the population of Beira Interior of our observations might not be indicated because of the small sample of GP and its opportunistic nature. Second, our study focused on attitudes and perceptions on morphine of GP (potential patient) and HP and did not take in consideration the patients’ vision.

Scale bars are 10μm. … 3.4. In Vitro Transfection Using PVA/HAp/DNA Nanoparticles The expressing of the delivered DNA compositing with PVA and HAp was assayed by measuring luciferase activity (Figure 6). Low luciferase activity was shown for the HAp/DNA complex. This is caused by the strong

aggregation of HAp/DNA complexes [20]. The level of luciferase activity of PVA/DNA nanoparticles was similar Inhibitors,research,lifescience,medical to that of the HAp/DNA complex due to the slow internalization of PVA/DNA nanoparticles into cells, which could probably permit DNA degradation. In the case of the PVA/HAp/DNA nanoparticles, which can be taken up by cells quickly, high luciferase activity was shown, indicating that the encapsulation Inhibitors,research,lifescience,medical of HAp in PVA/DNA nanoparticles could enhance the transfection efficiency in vitro. However, the transection efficiency of the PVA/HAp/DNA nanoparticles was lower than in the Protein Tyrosine Kinase inhibitor high-efficient calcium phosphate transfection method, which is optimized for in vitro transfection [21]. Figure 6 In

vitro transfection using HAp/DNA, PVA/DNA and PVA/HAp/DNA complexes. Each value represents the mean ± SD (n = 3). *P < .05. 3.5. In Vivo Transfection Using Hydrodynamic Injection In vivo transfection was performed by using a hydrodynamic Inhibitors,research,lifescience,medical method (Figure 7). This method is known as an effective plasmid DNA transfection method without gene carrier to liver [35]. Figure 7(a) shows the results of in vivo hydrodynamic injection using various nanoparticles. The luciferase activity of the PVA/DNA complex (PVA: 0.001w/v%) was lower than that of DNA injection, whereas high luciferase activity was achieved Inhibitors,research,lifescience,medical for PVA/HAp/DNA

nanoparticles at the PVA concentration of 0.001w/v% (HAp: 0.0001w/v%). At PVA concentration of 0.01w/v% (HAp: 0.001w/v%), Inhibitors,research,lifescience,medical the luciferase activity of PVA/HAp/DNA nanoparticles decreased compared to that of 0.001w/v%. This is thought to be caused by the insignificant uptake of the large particles of PVA/HAp/DNA nanoparticles (about 780nm, Figure 2, Table 1) by hepatocytes [36]. When the luciferase activity in lung was also investigated, the low activity was detected in lung compared to that in liver, irrespective of type of nanoparticles. Figure 7 Transgene expression below (luciferase activity) of plasmid DNA, PVA/DNA, and PVA/HAp/DNA complexes injected by in vivo hydrodynamic method. (b) Time course of transgene expression of plasmid DNA and PVA/HAp/DNA complexes injected by in vivo hydrodynamic method. … The time-course of transgene activity was also investigated (Figure 7(b)). For plasmid DNA, the highest value for luciferase activity was detected after 12 hours, and the level of gene expression significantly decreased over time. On the other hand, in the case of PVA/HAp/DNA nanoparticles, the highest value for luciferase activity was achieved for 24 hours. This result indicates that the PVA/HAp/DNA nanoparticles could prolong the gene expression.

Statistical guidelines forjudging validity of selleck chemicals llc linkage reports in complex disorders have been suggested.36,40 These guidelines suggest thresholds for an initial report of “significant” linkage (LOD score ≈3.6 or nominal P≈0.00002) and for confirmation (LOD score =1.2 or P≈0.01). These guidelines should limit false positives

to less than 5%. It should be remembered that these guidelines refer to analysis of a single phenotypic definition (eg, BP I and BP II disorders). If multiple (overlapping) phenotypes are analyzed, some statistical adjustments for multiple hypothesis testing may be necessary. An associated critical issue is the Inhibitors,research,lifescience,medical power of a confirmation study to detect the Inhibitors,research,lifescience,medical effect size initially described. Effect sizes are often expressed as the increased relative risk41 due to a specific genetic locus.42 This increased relative risk refers to the ratio of the risk to a BP proband’s relative (eg, sibling) to develop the disorder divided by the risk for the general population.

For BP disorder, family studies suggest that the relative risk for siblings is increased by a factor of ≈8 to 9 (see Gershon et al,20 for Inhibitors,research,lifescience,medical example). Because BP disorder is almost certainly an oligogenic syndrome, in which at least several loci contribute to Inhibitors,research,lifescience,medical the increased relative risk, locus-specific relative risk

(the increased risk due to a single locus) is expected to be much less than 9. For complex traits, such as hypertension, diabetes, and BP disorder, loci that increase risk by factors greater than 2 are unusual. One such locus is near the ITLA locus for insulin-dependent diabetes mellitus (relative risk ≈3),43 another is the apolipoprotein E locus in late-onset Alzheimer’s disease.44 If three loci of equal effect size are used in an interactive Inhibitors,research,lifescience,medical multiplicative model to explain the increased relative risk in BP disorder (each locus increases relative risk by ≈2), then these three hypothetical interactive loci explain most of the relative risk (2 × 2 × 2 = 8). Thus, loci that increase risk for BP disorder Sclareol will have minor to moderate effects. Substantial sample sizes are required to detect such loci of minor effect. As Hauser and Boehnke45 have shown, ≈400 affected sibling pairs are needed to have >95% power to detect initially (LOD >3) loci which increase risk by a factor of 2, while 200 pairs are needed to have >95% power to provide confirmation (P≤0.01) of a previously detected locus. Review of bipolar molecular linkage studies Molecular methods have been used in BP linkage studies to localize susceptibility genes. A linkage study of Old Order Amish pedigrees described evidence (LOD score >4.

Whether similar changes can also be found in other stimulant abuse populations, such as cocaine, MDMA, nicotine, or caffeine abusers is still unknown. Section 4: Decision making and executive control in stimulant dependence Task paradigms and behavioral findings of decision making and executive control Decision making, memory, working memory, attention, cognitive flexibility, conflict monitoring, and planning are often conceptualized as Inhibitors,research,lifescience,medical separate selleck inhibitor elements of executive functioning, generally linked to intact (dorsal) PFC function (Smith and

Jonides 1999; Funahashi 2001). In drug dependence, executive dysfunction may result in maladaptive decision making, preventing sound judgments regarding health benefits related to drug use, or cognitive inflexibility resulting in dependent individuals being unable to steer away from drug-related thoughts. Here we discuss task paradigms and behavioral findings regarding Inhibitors,research,lifescience,medical decision making, memory, and cognitive flexibility. Decision making Decision making

can be Inhibitors,research,lifescience,medical assessed using the Iowa Gambling task (IGT) (Bechara et al. 1994) or a two-choice prediction task. The IGT stimulates the participant to gain money by turning cards of their choice from four virtual card decks: two containing large gains but even greater losses, and two decks with small rewards but even smaller losses. Thus, perseveration of risky choices will Inhibitors,research,lifescience,medical make the participant lose money. Using the IGT, methamphetamine and amphetamine abusers favored the risky high reward option (resulting in losses) compared with HCs (Rogers et al. 1999; Bechara et al. 2001). Moreover, decision-making speed and accuracy Inhibitors,research,lifescience,medical were impaired in amphetamine abusers and associated with duration of abuse,

suggesting that repeated stimulant use may contribute to impaired decision making (Rogers et al. 1999). On the other hand, even small differences in decision-making strategies predicted future ecstasy use in ecstasy naive individuals (Schilt et al. 2009), implying a causal role for decision-making impairments in the development of stimulant abuse. Finally, STK38 in methadone-maintained abstinent heroin abusers, smokers showed impaired decision making during a gambling task as compared with nonsmokers (Rotheram-Fuller et al. 2004). The two-choice prediction task presents only two options: a risky option (high gains, but more losses) and a low-risk option (low gains, but few losses). The IGT and the two-choice prediction task are closely related to the PRLT discussed in Section 1, as they also involve positive and negative feedback. The IGT and the two-choice prediction task also address cognitive flexibility, which can also be measured using the Wisconsin Card Sorting Task (WCST) or the PRLT.

Newer biomarkers could evaluate treatment response in older adults in whom anxiety is most likely to have long-term adverse health or cognitive

consequences. These may include HPA axis functioning through cortisol sampling, or genome-wide expression analysis, a powerful high-throughput technology that provides a systems approach for examining complex clinical disease in terms of dynamic changes in gene expression.221 Genome-wide expression analysis assays the current activity level of all transcripts known in humans. Thus, for example, a researcher can determine whether stress results in higher or lower levels of RNA transcripts in peripheral immunological cells.222 Such data, combined with bioinformatic Inhibitors,research,lifescience,medical techniques, allow researchers to infer the functioning of all of the intracellular pathways at a given point in time (ie, at baseline and then after a treatment), as well as their interactions.223,224 Inhibitors,research,lifescience,medical Additionally, as we previously noted, chronic stress hyperactivity (as seen in anxiety disorders) may cause accelerated aging; thus, telomere length measurement, during the

course of a treatment study, might provide a precise and quantitative estimate of benefits of treatment for health and cognition of older adults. Finally, novel Trichostatin A research buy neuroimaging markers might include neurogenesis, functional connectivity, and peripheral Inhibitors,research,lifescience,medical and central inflammation. In all, recent advances in technology in studies of anxiety could increase our precision for measurement, a need most pressing in geriatrics. What we do know: Inhibitors,research,lifescience,medical eight rules for managing anxiety disorders from a lifespan perspective

In this last section, we provide a blueprint for managing older (and equally so, younger) adults with anxiety disorders, based on empirical findings and our own clinical experience. 1. Assessment should Inhibitors,research,lifescience,medical measure severity and provide objective criteria for assessing response, and should assess comorbidity, prior treatment, cognitive status, and need for a medical workup Assessment of anxiety is often overlooked by mental health providers. A helpful introduction to the topic is to ask about stress; eg, “older adults often deal with stress; many how do you feel in times of stress?“ Patients who describe symptoms suggestive of anxiety or worry can then be further queried. Use nondirective questioning to determine the severity of anxiety symptoms, by: (i) level of distress (asking how much the anxiety symptoms bother the patient, what strategies they are trying in order to control or avoid it, and what somatic symptoms they are having); (ii) how much of their time it takes; and (iii) avoidance. Avoidance is a key component of all anxiety disorders yet often is not recognized. For example, older adults may rationalize changes in behavior patterns to perceived poor health or environmental limitations. Inquire about behavioral changes including activities given up or, conversely, intrusive overinvolvement with family members.

The reality is that physicians are

often unaware of the indicated disorders for many medicines. In one large US study of primary care physicians and psychiatrists, less than 50% could identify the FDA approved diagnoses for selected medicines [Chen et al. 2009]. Similar rates are seen in the UK. General practitioners (GPs) are unaware of the extent of off- label prescribing [Ekins Daukes et al. 2005], although many are aware of the explicit problems with dosing in children [Ekins Daukes et al. 2005]. Perhaps Inhibitors,research,lifescience,medical most importantly clinicians often have only a limited understanding of the issues around off-label prescribing, the frequency of side effects and lack of efficacy data. There can also be problems concerning informed consent [Ekins Daukes et al. Inhibitors,research,lifescience,medical 2005], as while prescribers of psychotropics may be aware that the prescription is off-label, it is clear that it is only rarely known by the patient [Haw and Stubbs,

2005]. Overall there are few established systems to support and manage off-licence medicine prescribing [Ansani et al. 2006]. Psychiatrists continue to express unease about the extent of prescribing off-licence in the mental health field and the legal, as well as clinical risk that they expose themselves to [Lowe-Ponsford and Baldwin, 2000]. Furthermore, while it is not considered a Inhibitors,research,lifescience,medical breach of care to prescribe off-licence, if and when that decision is supported by clinical evidence and a broad body of clinical opinion, it is possible to face sanction if a off-label treatment is withheld [Henry, 1999]. In reality, only a small minority are ever involved Inhibitors,research,lifescience,medical in such a grievance [Lowe-Ponsford and Baldwin, 2000]. Safeguards can be implemented to ensure drug accessibility is controlled, and that prescribing remains the prerogative of appropriately

trained clinical practitioners. Medicines prescriber information sheets list patient safety data, while black-box warnings continue to update clinicians when extra vigilance is needed [Stafford, 2008]. In the UK at least there appears to be a confusing range of opinion on what can Inhibitors,research,lifescience,medical be prescribed and for whom, from national medicines information services, expert opinion such as the Maudsley Prescribing Guidelines [Taylor et al. 2012], the MHRA and NICE, to guidance from individual hospitals, NHS trusts and insurance companies [Bücheler et al. 2002]. A framework to protect unlicensed groups Blinded randomised controlled trials remain the highest quality individual study design. They ALOX15 provide the most reliable and objective data to support effectiveness, efficacy and safety of innovative treatments, and need to be conducted before regulators award full licensed approval for a medicine. However, change in the current regulatory process is required, to generate greater Neratinib chemical structure incentive to conduct new drug research for mental disorders and, to guarantee long-term added efficacy and safety [Segman and Weizman, 2008].

Gene variants (ie, alleles or polymorphisms) that code for the enzymes responsible for drug metabolism

can Autophagy Compound Library affect pharmacokinetics, and therefore the amount of drug available in the bodyto elicit a response. In addition, gene variants can affect pharmacodynamics, the therapeutic effect of a drug in the target organ (Figure 1 , “PK and PD”). Representative examples in breast cancer research include the overexpression of the ITER2 gene, a positive predictor of response Inhibitors,research,lifescience,medical to the drug trastuzumab (Herceptin), and the predictive value of active cytochrome P450 (CYP) 2D6 alleles in tamoxifen discontinuation.3 Figure 1. The influence of pharmacokinetic, pharmacodynamic and environmental Inhibitors,research,lifescience,medical factors on pharmacotherapy response and side effects (source: www.silvermedia.ca). In psychiatry, we lack basic laboratory investigations to diagnose mental illness, let alone genetic advances to guide treatment. A primary goal of current research is to characterize the etiologies and biological susceptibilities of heterogeneous, complex conditions, such as depression and psychosis. We are at the threshold of being able to predict treatment response, primarilythrough genetics and neuroimaging. Personalized medicine in psychiatry is a broad topic. As such, we will confine our review Inhibitors,research,lifescience,medical to the most promising markers of treatment response and adverse effects emerging from the areas of pharmacogenetics

and neuroimaging in depression Inhibitors,research,lifescience,medical and schizophrenia. Genetics of antipsychotic drug metabolism, response, and side effects in schizophrenia Antipsychotic drugs remain the cornerstone of treatment in schizophrenia. However, more than 20% of patients do not initially respond to treatment with drug therapy.4 In addition to lack of response, many patients discontinue their medication due to side effects, which can have serious and devastating consequences.5 In the following sections we discuss the genetics of antipsychotic drug metabolism, response, and side effects in schizophrenia. Genetics of antipsychotic Inhibitors,research,lifescience,medical drag metabolism The vast majority of antipsychotic drugs are metabolized by

the liver enzymes CYP2D6 and CYP2C19, which play critical roles in determining plasma drug levels. Gene variants that confer altered enzymatic activity influence plasma drug levels, and therefore can predict effective drug doses and potential side effects. The CYP2D6 gene codes for an enzyme that is responsible for metabolizing the Thymidine kinase majority of antipsychotic medications.6 This enzyme shows genetic variability in activity and is highly polymorphic, with over 70 single nucleotide polymorphisms (SNPs) and copy number variations (CNVs).7 These variations can influence antipsychotic drug activity and a patient’s ability to metabolize them. Individuals can be classified, based on their gene polymorphisms, as poor (PM), intermediate (IM), extensive/normal (EM), or ultrarapid drug metabolizers (UM).

These results suggest that SBE7-β-CyD increased the bioavailability and persistence of the blood-glucose lowering effect of insulin glargine after subcutaneous administration of an insulin glargine solution to rats. Table 3 In vivo pharmacodynamics parameters of insulin glargine with or without SBE7-β-CyD (200mM). (1) Time to nadir blood glucose concentration. (2)

Nadir blood glucose concentration. (3) The cumulative percentage of change in serum glucose Inhibitors,research,lifescience,medical … 4. Conclusions In the present study, we revealed that Sul-β-CyD and SBE7-β-CyD increased solubility of insulin glargine. Furthermore, SBE7-β-CyD suppressed the formation of oligomer and enhanced the dissolution rate of insulin glargine from its precipitate, compared to that of Sul-β-CyD. In addition, we Inhibitors,research,lifescience,medical demonstrated that SBE7-β-CyD increased the bioavailability and persistence of the blood-glucose lowering effect of insulin glargine after subcutaneous administration of an insulin glargine solution to rats, probably due to the inhibitory effects of SBE7-β-CyD on the enzymatic degradation at the injection site, resulting from

the interaction with insulin glargine molecules. These www.selleckchem.com/products/lee011.html findings indicate that SBE7-β-CyD can be a useful excipient for a peakless profile of insulin Inhibitors,research,lifescience,medical glargine. Acknowledgments The work described in this paper presents additional results from a Joint Research Project by Kumamoto University and its collaboration partner CyDex

Pharmaceuticals, Inc. and the authors wish to acknowledge this collaboration as well as funding support from CyDex Pharmaceuticals, Inc. The authors oblige Inhibitors,research,lifescience,medical to Sanofi-Aventis for the supply of insulin glargine.
Doxorubicin (Adriamycin) is a commonly used anti-cancer drug. It is most often used against breast and esophageal carcinomas, Inhibitors,research,lifescience,medical osteosarcoma and soft-tissue sarcomas, and Hodgkin’s and non-Hodgkin’s lymphomas [1]. The effectiveness of doxorubicin (DOX) in treating various types of cancers is greatly limited by the serious side effects caused by the drug. The initial side effects caused as a result of DOX administration include less serious symptoms, such as nausea, vomiting, myelosuppression, and arrhythmia, which are usually reversible [1]. However, DOX-associated cardiomyopathy Phosphoprotein phosphatase and congestive heart failure have raised grave concern among health practitioners [2]. A widely researched approach of increasing the efficacy, while lowering the deleterious side effects caused by anti-cancer agents such as doxorubicin, is of developing nanoparticle-based drug delivery systems [3–5]. Various kinds of nanoparticles have been studied for the delivery of DOX, which include poly(butylcyanoacrylate) [6], poly(isohexylcyanoacrylate) [7], poly(lactic-co-glycolic acid [8], chitosan [9], gelatine [10], and liposomes [11]). In addition, Dreis et al.