In 1909 Steinert and colleagues first clearly described the “cla

In 1909 Steinert and colleagues first clearly described the “classic”

type of myotonic dystrophy which was called Steinert’s disease (OMIM 160900). The gene defect responsible for myotonic dystrophy described by Steinert was discovered in 1992 and found to be caused by expansion of a CTG repeat in the 3′ untranslated region of DMPK, a gene encoding a protein kinase (2-4). Subsequently, in 1994, a different multisystemic disorder was described with Inhibitors,research,lifescience,medical dominantly inherited myotonia, proximal greater than distal weakness, and cataracts but lacking the gene defect responsible for Steinert’s disease (5-7). In Europe, the disease was termed proximal myotonic myopathy (PROMM, OMIM*160900) (6) or proximal myotonic dystrophy (PDM) (7) while in the United States was termed myotonic dystrophy with no CTG repeat expansion or myotonic dystrophy type 2 (DM2) (5). Later studies demonstrated that many of the families identified as having myotonic dystrophy type 2, PROMM or PDM had the same disease, a disorder caused by an unstable tetranucleotide CCTG Inhibitors,research,lifescience,medical repeat expansion in intron 1 of Zinc finger protein 9 gene (ZNF9) mapped to 3q21.3 (8, 9). Due to the existence of different types of myotonic dystrophy, the International Myotonic Dystrophy Consortium developed a new nomenclature and guidelines for DNA testing

(10). The Steinert’s disease that results from an unstable trinucleotide repeat expansion on chromosome 19, is now termed myotonic dystrophy Inhibitors,research,lifescience,medical type 1 (DM1). Patients with the clinical picture of myotonic dystrophy type 2/proximal myotonic Inhibitors,research,lifescience,medical myopathy, who have positive DNA testing for the unstable tetranucleotide repeat expansion on chromosome 3, are now classified as having myotonic dystrophy type 2 (DM2) (5, 11-12). Although DM1 and DM2 have similar symptoms, they also present a number of very dissimilar Selleck Barasertib features making them clearly separate diseases (Table 1). Table 1. Comparison of clinical manifestations between DM1 and DM2. Myotonic Dystrophy type 1 Clinical features Myotonic dystrophy type 1 is the most common inherited muscular dystrophy Inhibitors,research,lifescience,medical in adults with

an estimated prevalence of 1/8000. DM1 is characterized by the phenomenon of anticipation, by which the disease has an earlier onset and more severe course in subsequent generations. Patients with DM1 can be divided into four main categories, each presenting specific clinical features and Thiamine-diphosphate kinase management problems: congenital, childhood-onset, adult-onset, and late-onset/asymptomatic. Table 2 summarises these subtypes. Table 2. Summary of myotonic dystrophy type 1 phenotypes, clinical findings and CTG length. Congenital DM1 Congenital DM1 (CDM) shows a distinct clinical phenotype with distinct clinical features, therefore it is to be considered a severe early form of ‘classical’ DM1. CDM often presents before birth as polyhydramnios and reduced fetal movements. After delivery, the main features are severe generalized weakness, hypotonia and respiratory involvement.

A significant number of urologic patients are evaluated with imag

A significant number of urologic patients are evaluated with imaging ABT-378 ic50 studies in which iodinated contrast is administered intravenously. Contrast-induced

nephropathy is a potential sequel of such studies. It is thought that free radical generation is a causative factor of this problem.1 The administration of N-acetylcysteine, the Inhibitors,research,lifescience,medical use of the iso-osmolar contrast agent iodixanol, and hemofiltration before and after contrast administration have been used to reduce renal dysfunction after contrast loads.2–4 Free radical generation occurs more readily in an acidic environment and is attenuated by higher extracellular pH. Merten and colleagues performed a randomized controlled trial to assess whether hydration with the administration of intravenous sodium bicarbonate Inhibitors,research,lifescience,medical before, during, and after contrast administration limits the risk of renal dysfunction. Prevention of Contrast-Induced Nephropathy with Sodium Bicarbonate Merten GJ, Burgess WP, Gray LV, et al. JAMA. 2004;291:2328-2334 [PubMed].

At a single medical center, 119 adults with serum creatinine ranging from 1.1 to 8.0 mg/dL were randomized to receive either intravenous sodium Inhibitors,research,lifescience,medical bicarbonate or intravenous saline starting 1 hour before, during, and for 6 hours after a radiographic study in which iopamidol, a nonionic contrast agent, was administered. Contrast-induced nephropathy was defined as an increase of 25% or more in serum creatinine within 2 days Inhibitors,research,lifescience,medical of contrast administration. Contrast-induced nephropathy developed in 1.7% of those receiving sodium bicarbonate and 13.6% of those administered saline (P = .02). Urologists should consider this regimen for their patients who are at risk for contrast-induced nephropathy including those with diabetes mellitus or known renal insufficiency.

Further studies are warranted to determine whether the combination Inhibitors,research,lifescience,medical of sodium bicarbonate and N-acetylcysteine would further attenuate this risk or whether sodium bicarbonate taken orally would have the same impact.
Squamous cell carcinoma of the larynx continues to be the commonest head and neck cancer whatever in many Western countries. The larynx plays a key role for many essential functions, including breathing, voice production, airway protection, and swallowing. The goals of laryngeal cancer treatment are thus to provide best possible oncologic control, while optimizing functional outcomes. In recent decades, the treatment paradigm for advanced laryngeal cancer has shifted from one of primary surgery (total laryngectomy) as gold standard, toward non-surgical organ-preserving treatment using radiotherapy or chemoradiotherapy. However, concerns have emerged regarding functional outcomes after chemoradiotherapy, as well as possible decreased overall survival in patients with laryngeal cancer.

Synthesizing nanovectors that avoid immune clearance and thus pos

Synthesizing nanovectors that avoid immune clearance and thus possess increased circulation time is challenging since particles are typically quickly removed from the bloodstream. Approaches such as PEGylation and varying the size, shape, and composition of nanovectors may be explored to achieve this goal. Cardiovascular Targets Recent technologies have focused on discovering Inhibitors,research,lifescience,medical appropriate molecules to target for CVDs once the particle approaches the vessel wall. The vascular endothelium

that lines blood vessels and creates a natural barrier separating blood from surrounding tissue is considered an attractive target for both drug PLX-4720 in vitro delivery and imaging due to its proximity to intravenously administered therapy. Additionally, the unique markers expressed by endothelial cells during the progression of CAD offer an opportunity

for the Inhibitors,research,lifescience,medical design of molecular imaging probes and targeted nanovectors for localized treatments. Proinflammatory markers such as selectins, VCAM-1, and ICAM-1 expressed during chronic inflammation, which is prominent in most CVDs, serve as prime targets for targeted nanovectors.13 Another means of directing nanovectors to CAD is to target fibrin clots formed at the site of atherosclerosis when blood comes into contact with exposed tissue within the plaque.14 While nanovectors may be targeted to biomarkers expressed by the endothelium, Inhibitors,research,lifescience,medical the endothelial cells themselves may not be the intended target of therapeutic action. For example, cells such as monocytes, T cells, and foam cells that are recruited into atherosclerotic plaques or the underlying tissue have served as targets.15 When the final destination of imaging and drug carriers Inhibitors,research,lifescience,medical is not the vascular endothelium but rather the underlying tissue/organ, particle internalization and/or transcytosis of the nanovector must

be considered.16 17 Another possible approach for treating atherosclerosis could rely on targeting neovascularization of the vasa vasorum (network of small arteries Inhibitors,research,lifescience,medical in the vascular wall) that is strongly correlated with plaque growth and rupture.18 Particle Type Particle material and fabrication technique are important design parameters that affect the performance of nanovectors. Several types of carriers have been proposed for use in the treatment and imaging of cardiovascular diseases including soluble much carriers, viral carriers, lipid-based carriers, nano/microbubbles, polymeric, and inorganic-based nanocarriers (Figure 1). Figure 1. Schematic of (A) soluble, (B) polymer-based, and (C) lipid-based nanovectors. Soluble carriers include modified plasma proteins such as albumin, antibodies, and soluble biopolymers such as dextran and chitosan, and the design is such that the active agent is covalently linked to the carrier. For example, albumin has been conjugated to gadolinium for use as an MRI contrast agent.

One study found that 13 5% of 539 of a visiting nurse agency’s ho

One study found that 13.5% of 539 of a visiting nurse agency’s homecare clients, aged

65 or older, were diagnosed with major depressive disorder (MDD), a rate twice as high as was found in those receiving ambulatory care; it also found that 71% of those who were depressed were experiencing their first episode of depression (Bruce et al. 2002). Other studies found 10–12% rates of clinically significant depressive symptoms—a score of 10 or higher on the Patient Health Questionnaire-9 Inhibitors,research,lifescience,medical (PHQ-9)—among homebound older adults (Ell et al. 2005; Sirey et al. 2008). When younger age groups (50–64) of homebound adults were included, 17.5% had clinically significant depressive symptoms (PHQ-9 ≥ 10), and 8.8% had probable MDD (Choi et al. 2010). Older adults with greater medical burden and functional impairment are more vulnerable to depression, and depression can lead to further exacerbation of physical, functional, and mental health problems (Charlson and Peterson 2002; Taylor et al. Inhibitors,research,lifescience,medical 2004; Alexopoulos 2005; Covinsky et al. 2010; Pinquart and Duberstein 2010; Celano and Huffman 2011). Higher rates of depression in homebound older adults than in their ambulatory age peers are likely to stem from stresses

Inhibitors,research,lifescience,medical associated with their chronic illnesses and disability. Among low-income homebound older adults, financial worries and social isolation created by their homebound state as well as by the stresses that arise from managing chronic illnesses were found

to increase their vulnerability to depression (Choi and McDougall 2007). For a large proportion Inhibitors,research,lifescience,medical of low-income, depressed, homebound older adults, their depression may also be a continuation of poor mental health that they have experienced for many years, associated with long-term economic adversities, poor physical health, and family/relationship Inhibitors,research,lifescience,medical conflicts (Rush et al. 2005; Qiu et al. 2010). Despite their suffering from depression, low-income, depressed, homebound older adults face significant barriers to accessing treatment in selleckchem general and psychotherapy in particular, due to their homebound state and lack of financial resources (Choi and McDougall 2007; Qiu et al. 2010). The most common depression treatment for them tends to be antidepressant medication Phosphoprotein phosphatase prescribed by their primary care or family physician (PCP) (Crystal et al. 2003; Weissman et al. 2011). Previous studies also found that PCPs did not routinely refer older patients to a psychiatrist or psychotherapist, that they were skeptical about the effectiveness of psychotherapy, that they took responsibility for diagnosing and treating depression in their older patients mostly with selective serotonin reuptake inhibitors (SSRIs) as first-line agents, and that they reported their confidence in prescribing antidepressants as high or very high (Gallo et al. 1999; Fischer et al. 2003; Wang et al. 2006).

Evaluation of intention was based on all information available in

Evaluation of intention was based on all Vorinostat molecular weight information available in each case, including patients’ own reported intentions, when known. Special attention was given to letters confirming suicidal intent, supposed intake of lethal doses of the toxic agent(s), or other active procedures to ensure a lethal outcome. Information from other sources such as ambulance personnel and companions was also taken into consideration. In the forensic cases, the evaluation of intention was according to the assessment of the forensic pathologist. In fatal poisonings not

subjected to medico-legal autopsy, the attending physician classified the intention. Substance use disorders were classified according to the ICD-10 criteria Inhibitors,research,lifescience,medical [14], i.e. drug dependence as for ethanol, prescription drugs, or illegal drugs. One category was chosen Inhibitors,research,lifescience,medical in each case, but among those who were dependent on illegal drugs, six patients fulfilled the criteria for other substance use disorders as well: four as ethanol dependent, and two as dependent on prescription drugs. Statistics The standardized Inhibitors,research,lifescience,medical registration forms were optically scanned and processed using TeleForm Desktop version

9.1 (TeleForm, Verity Inc., Sunnyvale, California). Statistics were analysed using SPSS, version 16.0 (SPSS, Chicago, Illinois), except 95% confidence intervals for case fatality rates, where NCSS version 2007 (NCSS, Kaysville, Utah) was used. An independent samples t test was used to compare Inhibitors,research,lifescience,medical continuous data, and χ2 tests were used to compare categorical data. Ethics The study was carried out according to the Helsinki declaration. Permission was obtained from the National Data Inspectorate and the Regional Ethics Committee. The links between patients’ names and social security numbers and the study case numbers were

stored by Statistics Norway. Results During one year, 103 subjects aged 16 years or older died of acute poisoning in Oslo, giving an annual mortality rate of 24 per 100 000 for Oslo. Eleven subjects (11%) were treated Inhibitors,research,lifescience,medical in hospital because of acute poisoning but died in spite of treatment (Figure ​(Figure1),1), of whom three were medico-legally examined. In one of these cases, the death was not registered as caused by acute poisoning at the time of death. Eight people (8%) treated on scene by ambulance services were declared dead on scene, whereas 84 (82%) were declared dead on scene by physicians outside to hospital or ambulance services. Figure 1 Deaths by acute poisoning in Oslo during one year. Sixty-nine (67%) of all deaths were males (Table ​(Table1).1). The mean age was 44 years (range 19-86 years); 42 years among males and 49 years among females (p = 0.025). Ninety-three (90%) were originally from Norway. In eight cases, the deceased had previously been treated by ambulance services because of acute poisoning in the same year.

Currently some biomarkers are regarded as state markers such as g

Currently some biomarkers are regarded as state markers such as genetics and related findings, in addition, several markers are putative trait markers. Both state and trait markers carry distinct information which provides the possibility of characterizing treatment Panobinostat molecular weight outcome better than mere

subjective measures. Definition The term “biomarker” is not always appropriately used, given the great diversity of methods and investigational procedures to identify the origin or “state” of psychiatric disorders. Moreover, for drug development it also appears necessary to identify “trait” alterations; this is of importance for identification of parameters monitoring Inhibitors,research,lifescience,medical the intrinsic course of illness on one hand and predicting the efficacy of treatment procedures on this intrinsic course on the other hand. From this point

of view for biomarkers individual dynamic responsiveness to interventions is also interesting. Absolute measures are helpful in identifying, Inhibitors,research,lifescience,medical eg, alterations in comparison of patients vs controls. However, of further interest is the way the individual response has to be classified: within the physiological bandwidth of homeostasis or at the borders of individual Inhibitors,research,lifescience,medical regulatory capacity. According to Frank and Hargreaves,1 biomarkers are characteristics which are objectively measured and evaluated as an indicator of the intrinsic causes

of illnesses, the clinical course, and its modification by treatment. In this Inhibitors,research,lifescience,medical context the authors point to the differentiation of clinical end points of treatment and surrogate end points: the former is for psychiatric approaches reflected by behavior and subjective feelings. For the latter the surrogate end point substitutes a clinical end point, to predict clinically wanted or unwanted effects. In addition, different types of biomarkers can in general be classified as shown in Table I 3: Table I Types of biomarkers. Inhibitors,research,lifescience,medical Another aspect comprises the terms sensitivity and specificity. Sensitivity and specificity are statistical Dipeptidyl peptidase measures of the performance of binary classification tests. Sensitivity measures the proportion of measures or markers which correctly identify a condition, specificity measures the proportion of negative measures, which resembles the concept of Type I and Type II errors.4 In the spectrum of biomarkers there is considerable variability with regard to sensitivity and specificity. Up to now, and especially in the past decade, a multitude of procedures have been developed, which may be listed as follows (adapted from ref 5, but not an exhaustive list of approaches – Table II): Table II Targets of biomarkers.

The incorporation of functional neuroimaging into genetic studies

The incorporation of functional neuroimaging into genetic studies is challenging. Since the expected effects of any single polymorphism are small, it is essential to pay close attention to experimental design in neuroimaging genomics. As highlighted above, it is important to use well-characterized neurobehavioral probes, and to evaluate and control confounding variables such as age, gender, basal abilities, performance, and clinical status. In addition, neuroimaging genomic studies require large samples

that can optimally be obtained by multisite studies. Such efforts introduce the additional variability related to scanner characteristics Inhibitors,research,lifescience,medical and image acquisition. Nonetheless, the field is making rapid progress and is poised to make new discoveries that will illuminate neural pathways to specific features of schizophrenia in ways that will lead to novel interventions. Conclusions

Considerable advances with fMRI have been made in efforts to elucidate the neurobiology of schizophrenia, and fMRI Inhibitors,research,lifescience,medical has become a dominant method to examine brain systems. It provides noninvasive measures with high anatomic resolution, acceptable temporal resolution, and increasingly reliable quantitation. Abnormalities in schizophrenia have been documented at multiple levels of neurobehavioral processing and across several Inhibitors,research,lifescience,medical neural systems. These abnormalities are manifested in failure of some regions to activate to a task, while other regions overactivate and there are alterations in the connectivity among regions. A clearer picture

of these abnormalities and their relation to genetic vulnerability, clinical manifestation, and the potential modulation with treatment will require the combined application of cross-modal measures. In this context fMRI will play a critical role by offering procedures Inhibitors,research,lifescience,medical for establishing whether a specific neural system is adequately recruited for its role in the information processing cascade and whether it GS-1101 ic50 communicates adequately Inhibitors,research,lifescience,medical with other systems on which it depends, or that may depend on its output. Acknowledgments Supported by NIH grants MH64045 and MH60722.
Research interest in investigating brain abnormalities in schizophrenia thus waned until 1976, when the first computed tomography (CT) study showed enlarged lateral ventricles in schizophrenia.10 Following this study, a PD184352 (CI-1040) large number of CT and magnetic resonance imaging (MRI) studies followed, with the first MRI study of schizophrenia conducted in 1984 by Smith and coworkers.11 The first quantitative MRI study of schizophrenia was subsequently conducted by Andreasen and coworkers in 1986,12 and the first quantitative MRI study that included contiguous slices of the entire brain and correlations with specific clinical symptoms was conducted by Shenton and coworkers in 1992.13 An example of a CT scan is depicted in Figure 1 , which shows a clear differentiation between bone, brain, and cerebrospinal fluid (CSF).

S P and P K analyzed the data and wrote the article Conflict

S. P. and P. K. analyzed the data and wrote the article. Conflict of BLZ945 chemical structure interest The authors have no conflict of interest to declare. Supporting Information Additional Supporting Information may be found in the online version of this article: Figure S1. Data plotted per animal. Each point at each gap distance is from one animal. The number of attempts for control Inhibitors,research,lifescience,medical (A) and P0 (B) animals. The duration of an attempt in control (C) and P0 (D) animals. Error bars show mean ± SEM. Not all animals crossed

at all gap distances (Control: n = 12; P0: n = 15). Click here to view.(26K, pdf) Click here to view.(142K, png) Click here to view.(596 bytes, txt)
Researchers investigating associative learning in invertebrates have made significant breakthroughs in understanding

Inhibitors,research,lifescience,medical the conditioning process in animals like Aplysia and honey bees (Couvillon and Bitterman 1980; Kandel and Schwartz 1982; Burmeitser et al. 1995). Studying invertebrate learning systems provides the opportunity to ask complex questions in relatively Inhibitors,research,lifescience,medical simple systems, as compared with vertebrates. An area of particular interest is the role of conditioning in learning through changes in behavior. Behavior is modulated by experience, through the acquisition of new information (learning) about the environment. Thus, instinctive behaviors can be modified based on the information provided in the environment. Several invertebrate studies show that these organisms modify Inhibitors,research,lifescience,medical their behavior, especially avoidance behavior. This is seen in mollusks with habituation of the rapid gill withdrawal reflex (Castellucci and Kandel 1974), food aversion with electric shock (Mpitsos and Davis 1973; Mpitsos and Collins 1975), and CO2 poisoning (Gelperin 1975). One

technique to demonstrate learning is using studies of operant learning, specifically the animal’s ability to Inhibitors,research,lifescience,medical complete a task. A key study showed that Carcinus maenas (a crab) are able to perform a lever-press motor task (Abramson and Feinman 1990). Precise manipulation of appendages is a powerful behavior in learning abilities because it tests the degree to which manipulative and motor behaviors are part of paradigm motor command. This is especially interesting given our developing knowledge click here of neural circuitry and neuronal control in decapods such as crayfish and lobster (Krasne 1969; Davis 1970; Larimer et al. 1971). Learning and memory formation are important in the natural environment and this is especially true for social animals, because many social hierarchies depend on recognition. As seen with many crustaceans, agonistic outcomes between conspecifics create a history of social experience that can influence future behavior (Goessmann et al. 2000; Daws et al. 2002; Bergman et al. 2003). Studies in mollusks have shown that they use sign or goal tracking (Kemenes and Benjamin 1989; Purdy et al. 1999).

It is not yet possible to prove that the deficits or excesses of

It is not yet possible to prove that the deficits or excesses of activity are primary or secondary, but the analyses of anhedonic nonclinical subjects, nonanhedonic depressed patients, and depressed patients with various levels of anhedonia seems to favor this

way of thinking. This oversimplified way of assessing the role of two major structures in anhedonia Inhibitors,research,lifescience,medical as a pivotal symptom of depression also has to be confronted with the complexity of the concept of anhedonia. Indeed, in order to get a pleasurable, hedonic feeling, a large number of steps have to be efficient, such as arousal (being able to globally detect potentially rewarded stimuli), appraisal (having the capacity Inhibitors,research,lifescience,medical to detect which specific stimuli are hedonically relevant), and expression of this JNK-IN-8 ic50 emotion (being detected). The role of dopamine and the ventral striatum in anhedonia, as a symptom of depression,

is nevertheless a largely replicated finding; this does not mean that they explain the trait, but more likely, that they are definitely Inhibitors,research,lifescience,medical involved…among others.
Despite their obvious clinical relevance, the terms “sad” or “sadness” are not defined in some major psychiatric dictionaries, such as the Campbell Psychiatric Dictionary1 and the Lexicon of Psychiatry, Neurology and the Neurosciences2 or the French Academy of Medicine’s Dictionary.3

This is even more surprising, given that sadness (“tristis” in classical Latin) was commonly given a psychological meaning in the ancient Latin world. In Latin-based languages, Inhibitors,research,lifescience,medical the meaning was linked to melancholia and sorrow later, during the 14th century. The term was used to nickname Inhibitors,research,lifescience,medical Don Quixote the “knight of the sad face,” in the 17th century.4 From a medical historical, perspective, sadness was described in patients for a long time before the term depression was introduced. For example, Hippocrates defined melancholia as a state of persistent fear and sadness. In the middle of the 19th century, when the concept of depressive disorder appeared, sadness was closely linked to motor retardation, and sometimes delusions, both included in the depressive syndrome. By the end of the 19th century, Kraepelin had described several types Ketanserin of depression, corresponding to various states of motor and psychic retardation. Beginning with Kraepelin, successive classifications have been developed, so as to better identify depressive disorders, mainly in dimensional ways. Beyond the symptomatic clusters that nowadays define depression, the importance of the core symptoms of depression, and in particular of sadness, could be crucial from a clinical point of view.

In clear contrast, a desmin-related myopathy-associated CRYAB mut

In clear contrast, a desmin-related myopathy-associated CRYAB mutation Arg120Gly decreased binding not only to the N2-B region but also to the I26/27 region which is expressed in both cardiac and skeletal muscle, and led to the accumulation of mutant αB-crystallin aggregations (28). These differences in the functional changes might also contribute to the difference in the distribution of affected muscles. Conclusions Many intensive studies have been performed to elucidate the molecular mechanisms of ICM, over the last two decades, and pathophysiological analyses have shed light on the pathogenesis of ICM. However, the entire molecular

basis underlying the development Inhibitors,research,lifescience,medical of ICM is not yet fully solved. In fact, the genetic defects or mutations in the disease genes could be identified only in about half or in an even smaller proportion of HCM and DCM patients, respectively. In addition, linkage studies have suggested many different disease loci Inhibitors,research,lifescience,medical which are distinct from the known disease gene loci in different multiplex families with ICM (5). These observations indicate that there are still many other disease genes to be identified.

Further genetic, molecular and functional analyses are crucial for a complete understanding of ICM and for developing new therapeutic strategies Inhibitors,research,lifescience,medical to prevent cardiac dysfunction in ICM. Acknowledgements This work was supported in part by Grant-in-aids from Ministry of Education, Culture, Inhibitors,research,lifescience,medical Sports, Science and Technology, Japan, research

grants from Ministry of Health, Labour and Welfare, Japan, Program for Promotion of Fundamental Studies in Health Sciences of National Institute of Biomedical Innovation (NIBIO), and “Association Française contre les Myopathies” (AFM, Grant No. 11737).
selleck chemical cachexia is a condition associated with Inhibitors,research,lifescience,medical a variety of serious life-threatening diseases, including cancer, sepsis, AIDS, and congestive heart failure. The weight loss in cancer cachexia involves both adipose and muscle tissue. The muscle wasting is not simply due to malnutrition and nutritional supplements have been shown to be ineffective in restoring skeletal muscle protein content in patients with cancer cachexia (1) and the molecular events underlying cancer cachexia have been the subject of increasing scientific interest (2, 3). There whatever has been an increasing interest in the role played by inflammatory cytokines in cancer cachexia such as tumor necrosis factor (TNF-α), interleukin(IL)-1, IL-6, and interferon-γ. In a myogenic cell culture and an experimental rodent cancer model, Acharya et al. (4) reported that none of these cytokines induced dramatic cachexia-like effects by themselves, but in combination they promoted severe muscle wasting by selectively targeting myosin, the dominating sarcomeric protein in skeletal muscle, i.e., the molecular motor protein.