Sixteen men had very high combat, exposure but no reported PTSD s

Sixteen men had very high combat, exposure but no reported PTSD symptoms either in 1946 or 40 years later. When contrasted with men who experienced PTSD symptoms after similar combat, exposure, these 16 resilient, men did not manifest less neuroticism or less severe combat; but, they did as young adults manifest, more “mature” defenses. The 16 men with high combat, exposure and mature defenses (age 20 to 47) reported only an eighth as many PTSD symptoms as the 18 men

with similarly high combat, exposure and less mature defenses (F 9.5, P=.000 two-tailed, df=33). However this Inhibitors,research,lifescience,medical example does not exclude the possibility that SGC-CBP30 supplier brains altered by PTSD, like brains Inhibitors,research,lifescience,medical altered by traumatic brain

injury (eg,Phineas Gage) or alcohol, subsequently manifest less mature mechanisms. At. present many imaging studies have illuminated the brain circuits underlying PTSD,22,23 social anxiety, and phobia.24 Only a few25-27 have begun tentatively to understand how the brain adapts (downregulates) the effects of conflict. À study by Westen et al28 helped clarify the brain pathways by which partisan voters altered unwelcome facts. The brain “reward” neurons in the striatum and nucleus accumbens appeared to be involved, providing a basis for reinforcing Inhibitors,research,lifescience,medical specific mechanism choices for downregulation. A recent study by Nili and colleagues29 illuminates a putative pathway leading to downregulation of (or dissociation from) fear. Hopefully, the next. 10 years of neuroimaging will bring increasing clarity to the field. Conclusion The concept of involuntary coping mechanisms, (the “politically correct” renaming of the now outmoded (?) Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical term, “ego mechanisms of defense”), is too valuable to be discarded by

neuroscience because of its association with Sigmund Freud and psychoanalysis. The diagnostic and prognostic validity of such “mechanisms” in longitudinal studies more than make up for their unreliability and difficulty in rating. The task of neuroscience is to continue to use neuroimaging SB-3CT to identify and to understand the neural connections of such mechanisms.
It is important to distinguish between immediate and longer-term PTSD reactions. Most diagnostic systems have distinguished between these two types of trauma response because acute stress reactions are frequent, but often transient, and they need to be distinguished from the less common persistent PTSD responses. In terms of the persistent responses, PTSD is described in the American Psychiatric Association’s DSM-IV as an anxiety disorder that comprises five major criteria.4 First, one must have been exposed to or witness an event that is threatening to safety, and one must respond to this event with fear, horror, or helplessness.

Despite these still-to-be-resolved issues, the clinical implicati

Despite these still-to-be-resolved issues, the clinical implications are already visible. Currently, the major conclusions are, (i) that most of the claimed susceptibility genes for schizophrenia also reveal genetic associations with bipolar disorder, probably even through the same at-risk haplotypes; thus, a shared genetic vulnerability to both disorders becomes an emerging scenario; (ii) although diagnoses are useful to detect susceptibility genes,

the genotype-phenotype relationship might, be more symptom- than diagnosis-based.
The high frequency of co-occurring substance use Inhibitors,research,lifescience,medical Stattic mw disorder in schizophrenia is linked to an increased risk of illness and injury.1 Apart, from impaired cognitive functioning during intoxication, substance misuse is associated with poorer outcomes in psychosis and higher rates of presentation to inpatient, and emergency Inhibitors,research,lifescience,medical services.2 Another problem relates to the high occurrence of incarceration, predominately among persons with a diagnosis from the schizophrenia spectrum, who are actively abusing substances.3 Inhibitors,research,lifescience,medical It is primarily these individuals, with comorbidity of

schizophrenia and drug addiction and who lack stable housing, who run a high risk of being incarcerated. Thus, comorbid substance abuse disorders in schizophrenic patients have been shown to be a considerable obstacle to carrying out effective treatment. The development of effective intervention programs demands a global understanding of the risk factors for developing a comorbid substance disorder, as well as the consequences of substance abuse in schizophrenia. Epidemiology Epidemiological research in this field focuses on the identification of risk factors, the temporal

Inhibitors,research,lifescience,medical relationship of the onsets of the Inhibitors,research,lifescience,medical disorders, and on specific symptoms. The proportion of schizophrenic patients with comorbidity of substance abuse varies in published studies from 10% to 70%, depending on how patients are diagnosed with schizophrenia, the types of populations studied, and the different, ways of defining drug and alcohol disorders.4 However, an increasing number of publications demonstrate a high prevalence of substance abuse in schizophrenia.2,5-7 Up to 50% of patients with schizophrenia exhibit either alcohol or illicit drug dependence, and more than 70% are nicotine-dependent.8 In particular, heavy cannabis abuse has been reported to be a stressor, eliciting relapse in patients with schizophrenia and related disorders.9 Consistent Vasopressin Receptor findings concerning demographic characteristics and gender aspects suggest, that male persons of younger age and lower educational level are associated with a greater risk for substance abuse.4 However, it seems important to mention that substance abuse difficulties among women with schizophrenia are often insufficiently identified, and that women with comorbidity of substance abuse are less likely to obtain substance abuse treatment.

Phase III studies with taxanes in GECs are limited V-325 (11) an

Phase III studies with see more taxanes in GECs are limited. V-325 (11) and CROSS (51) are pivotal studies that not only changed how we treat GECs, but also validated the role of taxanes in the management of GECs. The V-325 (11) study is a pivotal randomized study that demonstrated that docetaxel-based chemotherapy improved TTP and OS in patients with advanced GEC. The CROSS (51) study demonstrated improvements in surgical Inhibitors,research,lifescience,medical outcomes and survival in patients treated with

preoperative CRT with paclitaxel and carboplatin. Tables 2 and ​and33 summarize completed and ongoing clinical trials with taxanes-base chemotherapy, administered either alone or combined with targeted therapy. Table 3 Combination taxane-based + targeted therapy The future development of taxanes for use in GEC will require establishing optimal taxane-based chemotherapy regimens Inhibitors,research,lifescience,medical to further develop with targeted therapy, evaluating possible ways of overcoming mechanisms of resistance to taxanes,

and identifying molecular biomarkers that are predictive of response. This effort will require the collaborative efforts of many scientific disciplines. Footnotes No potential conflict of interest.
Mucinous pancreatic cysts are Inhibitors,research,lifescience,medical premalignant or malignant pancreatic neoplasms. They usually are asymptomatic and increasingly found due to widespread use of cross-sectional abdominal imaging (CT scan and MRI). Radiologic features of mucinous cysts are often not distinguishable Inhibitors,research,lifescience,medical from pseudocysts

(PCs) or other cystic neoplasms with minimal malignant potential such as serous cystadenomas (SCAs) (1). Mucinous pancreatic cysts are classified as mucinous cystic neoplasms (MCNs with or without carcinoma) and intraductal papillary mucinous neoplasms (IPMNs). Inhibitors,research,lifescience,medical The latter are further classified into whether the neoplasm involves the main pancreatic duct alone (main duct IPMN), main pancreatic duct side branches alone (branched IPMN), or both the main pancreatic and its side branches (mixed IPMN). The grade of dysplasia in mucinous pancreatic cysts is further classified as low grade dysplasia, high grade dysplasia or invasive carcinoma (2). Endoscopic Thiamine-diphosphate kinase ultrasound (EUS)-guided fine needle aspiration (EUS-FNA) cytology with cyst fluid analysis is frequently utilized to aid in classification of pancreatic cysts. However, the value of cytology is limited by the frequently low cellularity of aspirated fluid (1). The utility of several cyst fluid tumor markers studied has been variable (3). Brugge et al. concluded that a cyst fluid CEA level of 192 ng/ml has the greatest area under the curve (AUC) for differentiating mucinous from nonmucinous cysts (4). In a pooled analysis of twelve studies, amylase <250 U/L from cyst fluid was found to virtually exclude a pseudocyst.

Genetic abnormalities, as we explain below, are without doubt a m

Genetic abnormalities, as we explain below, are without doubt a major contributor to moderate and severe cognitive disability, but despite recent advances in uncovering the molecular basis of some forms of MR, our understanding of the pathogenesis of the condition is still limited. Consequently,

the chances of improving care are also limited; inadequate understanding of the origins of cognitive disability remains a major challenge for medical practice. The extent to which genes are involved The Inhibitors,research,lifescience,medical causes of cognitive disability vary with the severity of the condition: moderate-to-severe intellectual disability (defined as an intelligence quotient [IQ] score less than 50) is much more likely to be due to a single pathological cause (genetic or environmental) than mild MR (defined as an IQ score between 50 and 70), which is often thought to be multifactorial in origin. Chromosomal and genetic disorders account for 30% to 40% of moderate-to-severe MR; environmental insults explain a further 10% Inhibitors,research,lifescience,medical to 30%, and the cause is unknown in about 40% of cases.3-7

Genetic and environmental causes explain, in roughly equal proportions, about 30% of mild intellectual disability; an etiological diagnosis is not obtained in the remaining 70% of cases.8-13 Table I summarizes data from epidemiological selleck products studies of low IQ, following the convention of separating mild disability from moderate Inhibitors,research,lifescience,medical to severe. Overall, the results reveal a distinction between the two groups. While controversy has long surrounded the extent to which genetic variation contributes to variation in intellectual function, there is now little doubt that moderate-to-severe intellectual disability is due primarily to chromosomal and genetic abnormalities. The largest Inhibitors,research,lifescience,medical individual contributors are Down’s syndrome, chromosomal rearrangements, and X-linked

mental retardation (XLMR) (Table I). Small chromosomal rearrangements, affecting the ends (telomeres) of chromosomes have emerged as a common cause in cases until recently regarded as idiopathic,14 and Inhibitors,research,lifescience,medical it is likely that a considerable proportion of cases of unknown etiology will also be found to have a genetic origin. Table I The causes of intellectual disability. IQ, intelligence quotient. The picture is less clear for IQ scores between 50 and 70. The importance of polygenic influences is inferred from the results of twin, family, and adoption studies for normal IQ measures, and rarely from Sitaxentan direct investigation of families with low IQ; studies evaluating biological and environmental risk factors in this group are singularly lacking, but there are indications that single-gene conditions and chromosomal abnormalities may be more frequent than previously assumed. Table II presents data on the genetic basis of conditions for which there is evidence that mutations give rise directly to intellectual disability.

Conclusions There is substantial evidence

that, the chron

Conclusions There is substantial evidence

that, the chronic inflammatory reaction in AD results in neuronal injury, ultimately leading to cognitive decline. Microglia activated by β-AP and cofactors such as M-CSF are likely to play a major role in generating neurotoxic agents in and around the neuritic plaque lesion. Many potential therapeutic agents that could ameliorate the inflammatory reaction in AD are available, including NOS inhibitors, agents that block the actions of proinflammatorycytokines, and antioxidants. NOS inhibitors with isoform Inhibitors,research,lifescience,medical specificity are currently under development and should soon be available for testing. Likewise, many anticytokine reagents are currently available, including older agents such as glucocorticoids, nonspecific nonsteroidal agents, and cytokine receptor Inhibitors,research,lifescience,medical antagonists, as well as newer agents such as low-molecular-weight cytokine inhibitors, convertase inhibitors, and highly specific cyclooxygenase inhibitors. However, recent, evidence using β-AP immunizations

and transgenic animals indicates that, the inflammatory response may Inhibitors,research,lifescience,medical also have a beneficial response in AD, possibly through catabolism of β-AP and other abnormal protein products.86 Therapeutic approaches to attenuating inflammation in AD may need to be precisely targeted to disrupt, deleterious aspects of the inflammatory response, while preserving beneficial effects. Selected abbreviations and acronyms AD Alzheimer’s disease β-AP Inhibitors,research,lifescience,medical beta-amyloid peptide GM-CSF gramdocyte-macrophage colony-stimulating factor IL-1 interleukin-1 M-CSF macrophage colony-stimulating factor MSR macrophage scavenger receptor NO nitric oxide NOS nitric oxide synthase ROS reactive oxygen species Notes Drs

Barbara Cordell, Philipp Kahle, Jared Tinklenberg, and Jerome Yesavage contributed to this work. Expert technical assistance was provided by Lan Yang and Nina Pascoe. Supported by grants from the National Institute of Mental Health.
Alzheimer’s disease (AD) is a significant public health problem secondary to the increased life expectancy of the general population Inhibitors,research,lifescience,medical and a better appreciation of the socioeconomic consequences of the disease. It was defined others by Alois Alzheimer in 1906 using criteria of progressive memory loss, disorientation, and pathological markers (senile plaques and neurofibrillary tangles). Initially it was assumed that AD was a rare condition, and later it was considered to be an inevitable consequence of aging. The stigma attached to aging and other factors delayed aggressive research into, and treatment of, patients with AD, but these misconceptions are fading away, and treatments, though initially modest in efficacy, are becoming available. In this paper we will review the diagnosis, etiology, genetics, epidemiology, course, and treatment of AD. Diagnosis and course The clinical manifestations of AD include disturbances in the areas of memory and language, visuospatial orientation, and higher executive function.

57-59 Prevention of tau pathology has begun to emerge as a viable

57-59 Prevention of tau pathology has begun to emerge as a viable approach to prevention of neurodegeneration, although efforts in this area lag significantly behind the

anti-amyloid research. There are currently two major approaches in this area: i) prevention of tau aggregation; and ii) inhibition of tau phosphorylation. Prevention of tau aggregation The major function of tau in neurons is thought to be the stabilization of microtubles, and tau can be demonstrated Inhibitors,research,lifescience,medical to both increase the rate of assembly of tubulin into microtubules and stabilize existing microtubules.60 This activity appears to be controlled by phosphorylation of tau, in that phosphorylation of

tau renders it less efficient in promoting assembly, and is believed to dissociate tau from assembled microtubules. Tau is ordinarily a soluble protein, but forms insoluble, filamentous aggregates in the Inhibitors,research,lifescience,medical course of neurofibrillary tangle formation. Early-methods for purification of tangles took advantage of this insolubility, and employed harsh detergent and acid extraction techniques to dissolve away contaminating proteins.61,62 Both toxic gain of function and loss of function models have been PRT062607 manufacturer proposed for tau’s role Inhibitors,research,lifescience,medical in neuronal degeneration. The formation of tau aggregates may be toxic to neurons,63 or

conversely, conversion of tau into insoluble polymers Inhibitors,research,lifescience,medical may reduce the effectiveness of tau in stabilizing microtubules. It is still too early in this research to decide which model is more plausible. The mechanisms responsible for the conversion of a normally soluble monomeric protein into the insoluble filamentous aggregates have been the subject of intense study and the target for some drug development. Although tau in neurofibrillary tangles is hyperphosphorylated (see Inhibitors,research,lifescience,medical below),64 there is still much debate about the role of phosphorylation in aggregation of tau. Indeed, many of the studies of tau aggregation have shown the formation of filamentous aggregates from nonphosphorylated tau,65,66 and have the used such systems to screen for potential inhibitors of tau aggregation. These studies usually include polyanions such as heparin, RNA,65 or arachidonic acid67 to stimulate tau aggregation. Using such a system, unpublished results apparently revealed that methylene blue could inhibit tau aggregation, and this compound, under the name Rember, has been reported to be effective in preventing decline in clinical test scores in patients with Alzheimer’s disease.

162 Such a mechanism may contribute to trap glutamine in

162 Such a mechanism may contribute to trap glutamine in astrocytes and promote swelling. In contrast with its acute form, chronic hepatic encephalopathy, which is associated with more modest increases in brain ammonia, does not result in overt cerebral edema,163 suggesting the existence of compensatory mechanisms taking place in astrocytes in order to

prevent excessive swelling. This is thought to be accomplished by the release of osmolytes such as taurine and myo-inositol by astrocytes in response to glutamine accumulation. However, it appears that when osmolyte pools Inhibitors,research,lifescience,medical are depleted as a result of excessive hyperammonemia, for example during acute liver failure, this protective mechanism is exhausted and astrocytes swell as a result. This, together with an impaired capacity of astrocytes to fulfill their role in ammonia detoxification, seriously compromises brain function in acute liver

failure. Conclusion Astrocytes Inhibitors,research,lifescience,medical are known to be the most important neural cell type for the maintenance of brain click here homeostasis. It is safe to assume that, as technology advances in the years to come, we will continue to uncover the multiple facets of astroglia. It has already become quite clear however that it is unrealistic to approach brain Inhibitors,research,lifescience,medical function and dysfunction from a uniquely neuronal standpoint. Because of their involvement in such a wide range of homeostatic functions, any brain insult is likely to have an impact on astrocytes. Their capacity to adapt to these changes Inhibitors,research,lifescience,medical weighs heavily in the fine balance between neuroprotection and neurotoxicity as illustrated by the three neuropathological conditions discussed above. In this context, understanding astrocytic function is key to providing a better grasp of brain function in general and how it may go awry. This may lead to the identification Inhibitors,research,lifescience,medical of

better suited therapeutic targets, as they should take into account the multiple interactions and interdependencies between neural cell types. Acknowledgments Acknowledgements: The authors wish to thank Drs Igor Allaman and Nicolas Aznavour for their help with the manuscript. Work in Parvulin PJM’s laboratory is supported by the Swiss National Science Foundation (grant no. 3100AO-108336/1 to PJM). MB was supported by the Fonds de la Recherche en Santé du Québec (FRSQ). Selected abbreviations and acronyms Aβ amyloid-beta AD Alzheimer’s disease GSH glutathione MCT monocarboxylate transporter ROS reactive oxygen species
Amphetamines and ring substituted methylenedioxyamphetamines are the most commonly used illicit drugs after cannabis. Amphetamines are psychostimulants, and methylenedioxyamphetamines are entactogens – psychoactive drugs with emotional and social effects.

The patient told us, “I do not get tired from biting, and I can e

The patient told us, “I do not get tired from biting, and I can eat more kinds of food than before.” Discussion This is the first report on the increase of the occlusal force of DMD patients. The jaw ROM exercise gave the DMD patients a feeling of satisfaction with their appetite. This means that the applicability of jaw ROM exercise was confirmed subjectively and objectively. Occlusal force increases up to approximately 20 years of age in healthy persons. In the natural history of DMD, occlusal force does not increase in patients in their teens or older (2). On the basis of this

finding, we did Inhibitors,research,lifescience,medical not compare the training effect between the groups of patients with and without the jaw ROM exercise, but we compared the effect in terms of the time course. The occlusal force of DMD patients is markedly lower than that in healthy persons of the same age (5). Muscles Ponatinib manufacturer contributing to the occlusion of the mouth are the masseter, temporal muscle, and medial pterygoid Inhibitors,research,lifescience,medical muscle. The masseter acts mainly to generate occlusal force. The factors causing the degradation of occlusal force are muscle atrophy,

Inhibitors,research,lifescience,medical muscle and soft tissue consolidation (7, 10), and malocclusion (11, 12). Among these factors, we consider that the effect of the jaw ROM exercise is mainly on the amelioration of the consolidation of the masseter and soft tissue. In this study, we applied a hot pack on Inhibitors,research,lifescience,medical the cheek of the masseter muscle region and massaged the masseter

before the jaw ROM exercise. These actions were useful to reduce the consolidation of the masseter and soft tissue. The hot pack enhances hypodermal blood flow by warming the body surface and increases the intramuscular temperature in a deep part of hypodermal tissue (13). It is confirmed that the temperature of the muscle depends on hypodermal Inhibitors,research,lifescience,medical thickness (14). In the case of DMD, the hypodermal tissue is thin, and the temperature of the masseter increases sufficiently to increase the blood flow in the masseter and soft tissue. Then, the extensibility of the masseter and soft tissue increases (15, 16), and the muscle softens (17, 18). The masseteric massage performed immediately after a hot pack application also increased the extensibility of the masseter and soft tissue around the muscle (15, 16). The increase in the extensibility of the masseter augmented muscle force: as a result, the greatest occlusal force mafosfamide increases. The self-training served to maintain the effect. In animal experiments, it was observed that there is a muscle force augmentation effect when we let an animal exercise after a hot pack application (13, 19). It is considered that the heat shock protein increased muscle protection from heat load other than blood flow improvement, which contributes to muscle force augmentation (20, 21). In DMD, a similar muscle protection may have been provided by a hot pack.

These patients were similar to the PARTNER high-risk group in age

These patients were similar to the PARTNER high-risk group in age, sex, pre-op ejection fraction, and severity of Roscovitine manufacturer aortic stenosis. The perioperative mortality was 2.7% (3 of 92), and the perioperative stroke rate was 4.3% (4 of 92). The 1-year survival rate was 85% (Kaplan-Meier).

There were no periprosthetic leaks. These outcomes indicate that in selected elderly patients treated in an experienced center, surgical results superior to those receiving AVR in the PARTNER trial high-risk cohort can be achieved with fewer late complications such as ongoing strokes and progressive aortic insufficiency. Current Intrinsic Limitations of TAVI A comparison of the capabilities of TAVI vs. AVR is shown in Table 2. In our unselected Inhibitors,research,lifescience,medical total series of 1,514 AVR

patients, only 44% had undergone an isolated AVR. The remainder have received concurrent CAB, ascending aortic aneurysm repair, or mitral or tricuspid valve surgery. While Inhibitors,research,lifescience,medical most patients had pure aortic stenosis, about one-third had some degree of aortic insufficiency, which is a contraindication to TAVI. AVR allows treatment of any size of aortic “annulus” because prosthetic valves are available up to a diameter of 33 mm. Table 2 Differences in indications Inhibitors,research,lifescience,medical for TAVI vs. AVR. Ascending aortic aneurysm surgery may be required in conjunction with AVR most commonly because of atherosclerotic degeneration, Marfan’s syndrome, or aneurysmal disease from bicuspid aortic valve Inhibitors,research,lifescience,medical disease. The latter may be present in a significant proportion of these patients. Bicuspid aortic valve disease is currently considered to be a contraindication for TAVI because the single-slit opening may not conform to the circular shape of the deployed prosthesis. The aortic root and ascending aorta also tend to be larger in these patients. Patient-Prosthesis Mismatch (PPM) The TAVI prostheses are designed to have maximal geometrical orifice area. This is achieved Inhibitors,research,lifescience,medical through direct attachment of the tissue leaflets to the stent and the absence of an external sewing ring. The Medtronic CoreValve has the leaflets attached above the “annular”

fixation zone to further enhance the post-implantation effective orifice area (EOA). Despite these technical advantages, the EOA achieved by TAVI is intrinsically limited by the presence of the retained calcified aortic leaflets (which are not removed) and by the extent to which the calcified ascending aortic root and annulus can be safely dilated. In addition, the range of sizes currently available is limited. Ewe et al.11 reported on data Bumetanide from a multicenter study in which 165 patients were evaluated for PPM. Studies were performed at baseline, before hospital discharge, and 6 months after TAVI. They found that 30 patients (18.2%) had an indexed EOA of <0.85 cm2/m2. A substantially higher proportion of these patients with PPM did not show clinical improvement compared with those without PPM (36.7% vs. 1.5%, P <0.001). The major adverse cardiovascular- and valve-related events did not differ.

The results of this study therefore show that IM olanzapine had a

The results of this study therefore show that IM Flavopiridol purchase olanzapine had a small effect on blood pressure. Treatment with olanzapine may result in fatal outcomes due to diabetic ketoacidosis, diabetic coma, etc. because of a marked increase in the glucose level. Consistent with the results of previous research, the results of this study found that IM olanzapine did not result in an increase in the glucose level to the extent seen with IM haloperidol, and suggested that IM olanzapine may have little effect on the glucose level. Most adverse events were rated mild

or moderate. Furthermore, in this study, no serious adverse events such as paralytic ileus, diabetic ketoacidosis, neuroleptic Inhibitors,research,lifescience,medical malignant syndrome or tardive dyskinesia occurred. Limitations This study had a relatively Inhibitors,research,lifescience,medical small sample size and was a short-term study (2 hours). Furthermore it was an open-label and not a double-blind study, so the possibility that bias was introduced to the results cannot be ruled out. There are consequently limits to the conclusions that can be drawn from this study. Since the doses of IM olanzapine and IM haloperidol used in this study were not equivalent, we cannot rule out the possibility that this affected the

study results. Inhibitors,research,lifescience,medical Furthermore, because only those patients who could give informed consent in this study were included, there is a limit to the results of this study. The greatest problem with this study is that the patients received IM olanzapine or IM haloperidol while

being treated concomitantly with antipsychotic Inhibitors,research,lifescience,medical medications, and it is therefore impossible to completely rule out the possibility that the antipsychotic drugs that the patients were receiving affected the results of this study. A double-blind, randomized, controlled study in subjects who are not taking concomitant medication potentially affecting efficacy and safety may be necessary in the future to clarify the differences in efficacy and safety between IM olanzapine, IM haloperidol and other first-generation injectable formulations. Inhibitors,research,lifescience,medical Conclusion This study was a comparative investigation of the clinical efficacy and safety Idoxuridine of IM olanzapine and IM haloperidol in agitated elderly patients. The results of this study suggest the possibility that agitated elderly patients may result in superior efficacy and safety after IM olanzapine without serious adverse events in comparison with IM haloperidol. Footnotes Funding: This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Conflict of interest statement: H.S. received honoraria from Janssen, Otsuka and Dainippon Sumitomo. K.G. received a honoraria from Janssen. Y.T. received honoraria from Otsuka. Contributor Information Hidenobu Suzuki, Department of Psychiatry, Suzuki Clinic, 3-34-16 Hamadayama, Suginami, Tokyo, 168-0065, Japan.