46 Indeed, overexpression of HDAC5 in the hippocampus blocks

the behavioral effects of chronic antidepressant treatment, suggesting that increased histone acetylation on the bdnf promoter is a key mechanism to overcome the repressive effects of H3K27 methylation. Another intriguing aspect of chronic social defeat stress is that the severity of the depression-like phenotype varies within a cohort of inbred (ie, virtually genetically Inhibitors,research,lifescience,medical identical) mice. It was observed that mice susceptible to defeat stress show significantly higher firing rates of dopaminergic neurons in the ventral tegmental area (VTA) after stress exposure compared with resilient mice. These resilient mice had normal VTA firing rates because of a stress-induced upregulation of potassium channels in this brain region. Why do certain mice upregulate protective potassium channels in the VTA while others fail to do this and become “depressed?” Perhaps an epigenetic mechanism is Inhibitors,research,lifescience,medical involved Inhibitors,research,lifescience,medical in altering the promoters of certain potassium channels to ultimately determine if the gene will be induced in response to chronic stress. If so, which life experiences

trigger these chromatin remodeling events? These are important questions that may shed fundamentally new light onto an extraordinarily complex syndrome, and provide new avenues for the development of more effective antidepressants. Another important epigenetic

mechanism that may contribute to long-lasting changes in neural function and behavior is DNA methylation. Inhibitors,research,lifescience,medical Early insight into the role of DNA methylation in behavior followed from studies of maternal care that clearly demonstrate an experience-dependent rather Inhibitors,research,lifescience,medical than genetic basis for how rats treat their offspring. Rats that receive poor maternal care as pups grow up to become poor mothers to their pups. In addition to becoming poor mothers, these rats also learn more develop long-lasting heightened anxiety and stress responses. Meaney and colleagues identified a region of the glucocorticoid receptor (GR) gene, which below was hypermethylated throughout adulthood in rats who received poor maternal care. Treatment with an HDAC inhibitor not only reduced DNA methylation on the GR receptor gene but also improved anxiety and stress responses in these rats.49 More recently, these studies have been translated from rats into humans by studying the hippocampus of patients who committed suicide with or without a history of child abuse. In patients with a history of child abuse, it was observed that DNA methylation on the GR gene promoter was significantly higher, while GR mRNA expression was significantly lower than patients with no history of child abuse.

This is particularly problematic as it is imperative that these systems remain in circulation long enough such that they can accumulate within tumor tissue at levels great enough to have the intended cytotoxic effect. One obvious method for overcoming this obstacle involves the overall size reduction of the nanocarrier, which as mentioned

Inhibitors,research,lifescience,medical earlier also has the unfortunate effect of translating into less drug being delivered by the nanocarrier. Another proven method for overcoming this obstacle without compromising the amount of chemotherapeutic being delivered to tumors is the surface coating of these drug delivery vehicles with polymers, particularly polyethylene glycol (PEG). This generates “Stealth” liposomes, which is a name Inhibitors,research,lifescience,medical given to them based on their ability to evade the immune system resulting in significant increases in circulations

times in vivo [14, 19, 20]. In fact, the benefit of INK 128 cell line pegylation is quite apparent when comparing the relative half-lives of nonpegylated and pegylated liposomes which increases from just a few hours to as much as 45 hours, respectively [9]. Therefore, it is not surprising to note that the clinically approved drug Doxil is in fact pegylated (Mr 2000) in order to improve tumor site accumulation of the drug [14]. However, while surface Inhibitors,research,lifescience,medical coating liposomes with PEG achieve desirable circulation times in vivo, Inhibitors,research,lifescience,medical it also negatively influences tumor cellular uptake of these systems as the presence of the PEG moiety presents a steric barrier between the drug and cancer cells [10]. Therefore, while pegylation does not eliminate cellular uptake entirely, delivery of pegylated liposome-based chemotherapeutics is in large part based on the ability of the encapsulated drug to escape or be released from the nanocarrier

Inhibitors,research,lifescience,medical via leakage in the tumor microenvironment prior to tumor cellular uptake of the free drug. Therefore, future strategies involving the improved delivery efficiency of pegylated liposome-based drugs, particularly in the treatment of breast cancer, are aimed at various enhanced triggered release techniques to facilitate this process. One such method involves the heat-triggered release of pegylated thermosensitive liposomes. 2.1. Hyperthermia and Improved Liposome-Based Drug Delivery While liposome-based drugs of the appropriate size Resminostat retain the ability to extravasate out of circulation at tumor sites, various challenges remain involving release of the encapsulated drug from the nanocarrier. Therefore, one aspect with respect to the future design of these drugs involves the incorporation of various molecules within liposomal formulations that respond to external stimuli in a manner that disrupts liposomes to allow for the delivery of encapsulated material.

15) The focus was set at the level of the mitral annulus and was moved to an appropriate level

when necessary. According to each coronary artery territory, the position of the transducer was adjusted to locate the region of interest in the center of the image sector, and MCE was repeated by adjusting the triggering interval. If perfusion defects were consistent with a typical ischemic territory of a coronary artery, observed in the subendocardial area, or associated Inhibitors,research,lifescience,medical with wall motion abnormalities of the same area, or if the severity of perfusion defects improved according to the lengthening triggering interval, perfusion defects were regarded as true myocardial perfusion defects and not artifacts.16) Myocardial perfusion defects present in at least one coronary territory were considered positive (Fig. 1A). MCE Selleckchem GSK1210151A results were interpreted by different reviewers blinded to the clinical data. Fig. 1 Myocardial contrast echocardiography using power Inhibitors,research,lifescience,medical harmonic Doppler imaging with a dual-frame triggering (A). Left, perfusion frame

was generated when the first packet of pulses encountered microbubbles in the myocardium and destroyed them. Right, post-destruction … Myocardial perfusion imaging with technetium-99m sestamibi As soon as possible after Inhibitors,research,lifescience,medical MCE, all patients underwent resting MPI with technetium-99m sestamibi. For SPECT imaging, 64 projections were obtained for 20 seconds, each at >180° using a dual-head rotating gamma camera. Image reconstruction was performed using standard back-projection algorithms. Short-axis slices of the left ventricles were normalized to peak heart rate. Circumferential Inhibitors,research,lifescience,medical count profiles were generated for five short-axis slices from apex to base. Scintigraphic results were analyzed by an experienced

nuclear medicine Inhibitors,research,lifescience,medical physicians who were blinded to patients’ clinical and laboratory data. Perfusion images were evaluated without gating in 35 (36%) patients and with gating in 63 (64%) patients, allowing assessment of regional function. Positive MPI was defined as a mild or definite perfusion defect on SPECT MPI performed Phosphatidylinositol diacylglycerol-lyase without gating, and a definite perfusion defect with associated abnormality in wall motion and thickening on gated MPI. Quantitative coronary angiography Coronary angiography was performed in all patients by standard techniques. Quantitative analysis of coronary angiography was done by experienced investigators using a quantitative analyzer (Ancor 2.0, Siemens, Erlangen, Germany). Significant stenosis that required urgent revascularization was defined as critical stenosis (diameter stenosis ≥90%) with the potential to affect coronary blood flow at rest and stenosis associated with ulceration or thrombus (Fig. 1B). Statistical analysis Continuous variables are presented as mean±SD.

The first universities were usually ecclesiastical institutions with close links between learning and Christian theology. The lack of access to a university medical degree did not completely restrict access for Jews to the medical profession as medical education in Europe in the Middle Ages consisted mainly of training through apprenticeship, under the guidance

of an established master. The teaching experience could be completed by the conferring of a license to practice. While the general licenses issued to Epacadostat clinical trial Jewish Inhibitors,research,lifescience,medical physicians entitled them to treat only Jewish patients, this condition was not always observed.2 Besides physicians, surgeons, and barbers, the medieval patient might also consult herbalists, pharmacists, and a wide variety of female healers.8 Though Jews were excluded from medieval universities, which became the norm for the training of physicians, Jews continued to aspire to the practice of Inhibitors,research,lifescience,medical medicine, and leaders of church and state often preferred to consult

Jewish doctors.9 At the same time, Jewish community leaders worried about the risks that accompanied the exposure of their sons to university learning in the Christian world. Rabbis, like Joseph Solomon Delmedigo (Figure 1), frequently expressed their concern or even expressed their complete opposition to such studies. Rabbi Jacob David Provenzal wrote, in 1490, to Rabbi David Messer Leon his total Inhibitors,research,lifescience,medical opposition to all secular learning, including even that of medicine.10 Rabbi Joseph Solomon Delmedigo (1591–1655), a native of Crete and a former Inhibitors,research,lifescience,medical student in Padua, had a knowledge of logic, natural philosophy, metaphysics, and divinity and devoted himself to medicine, writing Refu’ot Te’alah (Healing Medicine), and to mathematics and astronomy. Nevertheless, in

his Sefer Elim, he warned parents against sending their sons to Padua before “the light of the Torah has shined upon them Inhibitors,research,lifescience,medical … in order that they not turn away from it.” Tuviya Cohen, a physician whose writings illustrate the exposure to the sciences he encountered at university, counseled that “No one (Jew) in all the lands of Italy, Oxymatrine Poland, Germany and France should consider studying medicine without first filling his belly with the written and oral Torah and other subjects.”11 There were bold attempts to provide Jewish facilities for medical studies in Sicily in 1466 and in Mantua in 1564, but these proved unsuccessful.12,13 Cecil Roth considered that there was some “inconclusive evidence” that the college in Mantua did operate for a few years.10 Studying in Padua did give Jewish students access to the local Jewish communities, both in Padua and in Venice, where there were opportunities for Jewish students to familiarize themselves with the language and subjects required for the medical course, and which were not available to them in their own communities, in an encompassing Jewish environment.

Il faut tenir compte toutefois de l’extrême rareté des cas d’hépatopathies décrits lors des grossesses, des incidences psychologiques et financières des substitutions hormonales en ces circonstances. Enfin, dans un tiers des cas, la thérapeutique antithyroïdienne peut être interrompue vers la fin du 2e trimestre ou au début du 3e trimestre, lorsque l’hyperfonctionnement est bien contrôlé par

une petite dose d’antithyroïdien et qu’a été constatée une normalisation du titre des anticorps antirécepteurs de la TSH (la grossesse est une période de tolérance immunitaire). Au cours de l’allaitement, le PTU a été privilégié du fait de Autophagy inhibitor in vivo son moindre passage dans le lait. Mais l’efficacité et la bonne tolérance de doses modérées de thiamazole (15 à 30 mg par jour) ont aussi été établies. La surveillance de l’hémogramme est recommandée dans le dictionnaire Vidal durant les six premières semaines du traitement antithyroïdien. Sa non-réalisation pourrait être source de difficultés médicolégales. Elle par sa détermination est de plus immédiatement impérative en cas de fièvre ou d’angine. Bien que le risque hépatique soit imparfaitement prévisible sous ATS, on suggère

aussi la surveillance des fonctions hépatiques (transaminases, phosphatases alcalines) avant l’initiation du traitement et lors de la réévaluation hormonale après trois ou quatre semaines. L’arrêt au moins temporaire du traitement est recommandé en cas de valeurs des transaminases ou des phosphatases alcalines BIBW2992 excédant 2 à 3 fois la limite supérieure des normes et restant

accrues après une semaine. La surveillance des fonctions hépatiques est particulièrement recommandée chez la femme enceinte, mensuellement, parallèlement à celle de l’équilibre hormonal, et l’arrêt des ATS est impératif en cas d’ictère. Même si la recommandation n’est pas formelle chez les patients soumis au long cours à un antithyroïdien de synthèse, le contrôle annuel du titre des ANCA est aussi suggéré, Oxalosuccinic acid et lors de toute manifestation suggestive de vascularite (fièvre, arthralgies, signes cutanés, pulmonaires, rénaux, syndrome inflammatoire…). les auteurs déclarent un conflit d’intérêt avec les laboratoires Merckx-Lipha et HAC Pharma. “
“Obésité, syndrome métabolique (SMet) et diabète de type II (DT2), qui sont susceptibles de constituer les étapes évolutives d’un même processus inhibitors pathologique, partagent en outre de nombreux points communs. L’obésité androïde, qui prédispose au DT2, est un des éléments constitutifs du SMet, au même titre que l’intolérance au glucose. Image en miroir, le DT2 est quasi-constamment associé à une surcharge pondérale et à son cortège d’éléments constitutifs du SMet. Considérés individuellement, obésité, SMet et DT2 sont associés à un risque cardiovasculaire significativement accru. Une insulino-résistance, d’intensité plus ou moins marquée, est observée dans chacune de ces trois situations.

First, the role

of Sir2 as a key regulator of yeast lifespan was challenged.24 Second, at that time, no ortholog for PNC1 in other organisms was found. Therefore, the answer as to whether this model is unique only for yeast SCH 900776 mw remains elusive. The first uncertainty about the role Sir2 plays in modulating replicative longevity in yeast via regulation of the rate of ERC formation arose from the observation that the lifespan extension by overexpressing Sir2 was strain-dependent.24 In addition, it was noticed that in the BY4742 yeast strain, mutation of fob1, which blocks the formation of ERCs, Inhibitors,research,lifescience,medical or Sir2 overexpression, together with DR has a cumulative effect on yeast lifespan.24 Put simply, DR extended the lifespan of fob1 or sir2 double mutation. Thus, at least in this yeast strain the effect of DR cannot be Sir2 or ERC-dependent, as an additional increase of lifespan was seen with each treatment. In response to these claims other groups have shown that in the absence of Sir2 another yeast sirtuin, Inhibitors,research,lifescience,medical Hst2, takes over and regulates the positive effect of DR on Inhibitors,research,lifescience,medical yeast lifespan via ERC formation.25 However, this was not the end of the debate. Soon after, two researchers published that in the BY4742 yeast strain, double mutation of sir2 and fob1 along with a mutation in one of the hst isoforms hst1/hst2/hst4 has no significant effect on the yeast lifespan.26

Treatment with DR extended the lifespan of these combinations. Notably, Inhibitors,research,lifescience,medical the role of Hst3 in this study was complex. Mutations in hst3 only, or triple mutation sir2hst3fob1,

have a small but significant effect on yeast lifespan. However, once combined with hst4 mutation, yeast lifespan was significantly reduced. Moreover, DR was not able to extend the lifespan of yeast carrying mutations in fob1 and all yeast sirtuins. Interestingly, the authors did not report whether DR can extend the lifespan Inhibitors,research,lifescience,medical in hst3hst4 double mutations. Thus, the role of hst3 in DR response remains elusive. Taken together, despite extensive research, the question whether Sir2 or other sirtuins regulate yeast lifespan Rolziracetam during DR via controlling ERCs formation is still under debate. Recent studies have reported that Sir2 regulates yeast replicative lifespan by additional rDNA-independent mechanisms. During cytokinesis, the majority of proteins damaged due to oxidative stress are maintained in the mother cell. Nystrom and his associates showed that Sir2 is required for this asymmetric inheritance, and absence of Sir2 results in an inheritance of oxidatively damaged proteins and reduced capacity to respond to oxidative stress in daughter cells.27 Others have shown that an age-associated decrease in Sir2 protein levels is accompanied by an increase in histone H4 K16 acetylation and regions.

Finally the potential research participant or his or her legal guardian must evaluate the institutionally approved acceptable relationship of potential risks,

burdens, and inconvenience to the expected benefits of the research study with regard to his or her personal idiosyncrasies, interests, and values, and in case of his Inhibitors,research,lifescience,medical or her GSK J4 cost individual acceptability of the relationship he or she may consent to participate. Informed consent All medical interventions in human beings must be authorized personally by the concerned individual. This is particularly important for a research intervention because it is aimed not only for the benefit of the individual but also or even only at the benefit of

others. This is much less regulated in naturalistic studies, although they offer no or at best minor Inhibitors,research,lifescience,medical individual benefit but potentially considerable risks, eg, with unexpected incidental findings. Therefore, the basic precondition for research with human beings is their voluntary and valid informed consent. However, the voluntariness may be jeopardized by conditions such as imprisonment, poverty, or personal dependency, and the validity may be impaired by insufficient information, its inadequate understanding, or incapability of making decisions. Populations with such risk factors are called vulnerable populations. Mentallyill persons are a vulnerable population. Inhibitors,research,lifescience,medical Their specific vulnerability is given by the risk that their competence to consent may be impaired or does not exist at all. In such conditions they are at risk to be used without authorization for other than their own benefit. Inhibitors,research,lifescience,medical This may also happen in naturalistic studies, eg, in those that include children, but in general participants of such studies are healthy adults with competence to consent. Nevertheless, the researcher and the design of the study should be aware of the possible incapacity of potential participants in order to deal Inhibitors,research,lifescience,medical with it. The underlying concept of informed consent is that the consenting research participant makes the objective of the research intervention

Ms or her own. However, practice is more or less distant from this concept, particularly with incompetent patients, eg, with minors or mentally ill people. Assessment of capacity to consent Details and open questions of the informed consent process are eg, embedding ADAMTS5 it into the development of the physician-patient-relationship and improving the patient’s capacity to understand and to consent, particularly the assessment of the capacity.39 Recently a broad range of instruments for a standardized assessment of the capacity to consent has been developed, but up to now its application is limited by a restricted practicability or unproven validity or specific indications for only some dimensions of the capacity to consent.

These are partly based on functional genetic polymorphisms of the responsible genes. Pharmacokinetics, ie, the distribution

and metabolism of drugs, is dependent, on genetic variants of the metabolizing enzymes and transport proteins. Some of these are: The P450 cytochromes, which are members of the phase I metabolizing enzymes responsible for oxidation of functional groups. The phase II metabolizing enzyme N-acetyltransferase (NAT), which is responsible Inhibitors,research,lifescience,medical for the conjugation of substances with hydrophilic molecules for facilitated renal excretion. The multidrug resistance protein (MDR1), which controls the active transport, through the membranes of cells. These determine the plasma AG-014699 ic50 levels and also the spectrum of metabolites, and are thus responsible for the effects and side effects of drugs. In addition, psychotropic drugs interact, at this level and influence each Inhibitors,research,lifescience,medical other. Table I. Reasons for nonresponse

to treatment Cytochrome P450 enzymes Various cytochromes are responsible for the metabolism of psychotropic drugs,5 most, notably cytochromes CYP2C19, CYP3 A4, CYP1A2, and CYP2D6. Halopcridol, for example, is metabolized by CYP2D6, CYP3A4, and CYP1A2. Notably, the enzyme CYP2D6 exists in more than 20 different genetic Inhibitors,research,lifescience,medical variants, so-called polymorphisms, which show different enzymatic activities. Next, there are slow metabolizers, extensive metabolizers, and ultrarapid metabolizers. Several allelic variants of the CYP2D6 gene can lead to a nonfunctional enzyme or reduced CYP2D6 activity. The most common mutations in Caucasians associated with a slow metabolizer phenotype are the CYP2D6*3*4*5*6 alleles, or combinations of these, Inhibitors,research,lifescience,medical leading to a nonfunctional enzyme or reduced activity when they occur as heterozygous combinations with the wild-type allele. The ultrarapid metabolizer CYP2D6 phenotype is associated with a gene duplication. Up to 13 CYP2D6 copies Inhibitors,research,lifescience,medical could be the result of this mutation.6 The extensive metabolizer phenotype

could therefore be a result, of a homozygeous CYP2D6 wild-type genotype or a combination of alleles coding for reduced or abundant activity (CYP2D6*3*4*5*6*10*17) and alleles MTMR9 coding for increased activity. In a study with haloperidol, which is degraded to reduced halopcridol, a pipcridine metobolite, and a presumably neurotoxic substance haloperidol pyridinium (HPP+) (Figure 3), we noted that patients with the allele CYP2D6*4, which exists in around 10% of the Caucasian population and determines a slow metabolizer, show higher plasma levels of haloperidol and reduced haloperidol. At the same time, these patients showed a poorer response to treatment and more side effects. CYP3A4 is responsible for the increased occurrence of the possibly neurotoxic metabolite HPP+,7,8 showing similarities to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinium (MPTP), which provoked symptoms similar to Parkinson’s disease in heroin addicts.

For example, female rats who lick their newborn offspring more often during the first week of life Induce In them a lesser responsivity to stressors, lasting into adulthood. These behavioral changes

are accompanied by a higher number of glucocorticoid receptors in the hippocampus due to an epigenetlc modification of a transcription factor of this receptor.16 Feelings and words The above facts could induce resignation (“we are the puppets of our genes and environment; we are molded by our experiences”), were there not the option of reworking our representation through speech. How we talk about our past, and the stories we tell ourselves about our present and our future, reflect our feelings and emotions.17 The same Inhibitors,research,lifescience,medical facts can induce different Inhibitors,research,lifescience,medical feelings because each person has a different history, and does not attribute the same emotion to the same verbal representation. The fact that

the emotional response to the same story differs between listeners Invites the speaker to make the effort of empathy, by which he or she looks at himself or herself from the outside. This cognitive leap can act upon and transform Inhibitors,research,lifescience,medical the Initial emotion. This use of speech―this rhetoric―expresses the emotions of the Inner world, organizes the behavioral consequences of these emotions, and thus explains the possibility of mental transmission. Between molecular biology on the one hand and emotion-structuring speech on the other, mood stands at a confluence of determinants, and is subject to modification by each. Selected abbreviations and acronyms COMT catechol-O-methyltransferase CSPT cortico-striato-pallido-thalamic (circuitry) ERP event-related potential PPI prepulse inhibition SNP single nucleotide polymorphism
The Inhibitors,research,lifescience,medical observation that a large majority of psychiatric patients smoke cigarettes leads to the question about the possible relationship between smoking, dependence, and neurological diseases.1,2 Several studies have reported Inhibitors,research,lifescience,medical an association between smoking and depression.3,4 This question takes on a new dimension when we consider that

nicotine, the natural alkaloid contained in tobacco INK 128 clinical trial leaves, is a powerful and addictive compound acting on the central nervous system (CNS). A pivotal point in this line of thinking is what we know about the mechanisms by which nicotine acts on the CNS and what we can gain from a better understanding oxyclozanide of the intimate processes that drive to tobacco consumption.5,6 In this article, we will examine the basic functioning of the key players in nicotine addiction, ie, the neuronal nicotinic acetylcholine (ACh) receptors, and their possible role in depression. The ACh receptors First called Vagustoff by Loewi, due to its discovery in the heart muscle in 1921, the neurotransmitter ACh exerts many different actions. ACh is synthesized in the terminal bouton and stored in clear vesicles, and is released by nerve activity in the synaptic cleft.

Moreover, a single dose of 1mg ZOL is able to induce a significant reduction of circulating

VEGF in patients with bone metastases suggesting an in vivo biological activity of low ZOL concentrations in humans [93]. 6. Nanotechnology and BPs: Macrophage Targeting PCI 32765 macrophages are the major differentiating cell of the mononuclear phagocyte system (MPS). They derive from monocytes that migrate from Inhibitors,research,lifescience,medical the peripheral blood to extravascular tissue where they differentiate into macrophages [94]. Macrophages play a critical role in host defense because they migrated to an infected focus following attraction by a variety of substances, such as components from bacteria, complement components, immune complexes, and collagen fragments. Once at the infected focus, macrophages may phagocytose and kill infectious agents by a variety of mechanisms [95]. Moreover, following uptake of protein antigens, macrophages generated immunogenic fragments activating Inhibitors,research,lifescience,medical and regulating the immune response [96]. Finally, macrophages infiltrate

tumors, Inhibitors,research,lifescience,medical where they represent an important mechanism of host defense against tumor cells, either inhibiting tumor cell division or killing the cells following secretion of soluble mediators or by other means [97, 98]. However, most tumors can be infiltrated by a different macrophage phenotype, which provides an immunosuppressive microenvironment for tumor growth. Furthermore, these tumor-associated macrophages (TAM) secrete many cytokines, chemokines, and proteases, which promote tumor angiogenesis, growth, metastasis, and immunosuppression [99]. Thus, due to their pivotal role in a number of physiological and pathological processes including tumors, Inhibitors,research,lifescience,medical macrophages represent an attractive target for therapy. While in the case

of small soluble drug, only a small fraction can reach the macrophages, these latter can be the preferential accumulation site for intravenously injected colloidal carriers. Indeed, once into the bloodstream plasma proteins adsorb on particle surface and this process, also named opsonization, facilitates particle recognition and Inhibitors,research,lifescience,medical clearance from the blood by circulating phagocytes as well as tissue macrophages that are in direct contact with the blood [100]. Thus, the localization all of intravenously injected nanocarriers in cells of the mononuclear phagocytes system (MPS) offers a potential and powerful method to target therapeutic agents to these cells. Nowadays, various lipid and polymeric carriers such as liposomes and nanoparticle are under investigation to deliver drugs to macrophages. However, nanocarrier characteristics, in terms of size, shape, and particle surface, affect the pharmacokinetics of the nanocarrier and need to be carefully evaluated when designing nanocarriers for macrophage targeting. For more details, the readers are directed to more specific reviews on this theme, for example, an excellent review by Moghimi [100].