A second RA, blinded to clinical and historical data and using th

A second RA, blinded to clinical and historical data and using the hospital’s microbiology laboratory reporting selleck chemicals llc record, recorded whether or not a culture was ordered in the ED and recorded the resulting isolates’ antimicrobial susceptibilities. RAs were trained by the primary investigator (PI), who met regularly with RAs for monitoring of case selection and data management. ED visits identified by ICD-9 code that were in fact not for SSTIs (i.e. coding errors) were excluded following verification by the PI. The PI reviewed ten percent of records for data quality

and to assess interrater reliability Inhibitors,research,lifescience,medical on three key variables. The kappa statistic for performance of culture in the ED was 0.81, for performance of I&D was 0.79, and for infection type was 0.90. Outcome measures Descriptive measures included MRSA prevalence and antibiotic prescribing patterns among cultured SSTIs in the

study ED populations. Primary outcomes measured were (a) the frequency of in vitro activity of ED clinicians’ empiric antibiotic therapy against the cultured Inhibitors,research,lifescience,medical isolates among ED patients with cultured SSTIs, (b) factors associated with use of discordant antibiotic therapy or multi-drug antibiotic therapy, and (c) antibiotic resistance patterns among the most common pathogens identified. Data analysis We estimated that 25% of all SSTI patients evaluated in the ED would undergo culture and that 90% of these patients Inhibitors,research,lifescience,medical would receive antibiotics, with 50% concordance for MRSA treatment when MRSA was isolated.

Given these assumptions, between 674 and 1199 patient records Inhibitors,research,lifescience,medical would need to be abstracted to arrive at an estimate of antibiotic/culture discordance with 95% confidence intervals encompassing a range of 15 to 20 percentage points. Antibiotic usage was stratified by culture results, and age groups were compared using Pearson’s chi-square and 2-sample tests of binomial proportions. Antibiotics were categorized based Inhibitors,research,lifescience,medical on their spectrum of activity. Anti-staphylococcal antibiotics typically active against CA-MRSA include trimethoprim-sulfamethoxazole, tetracycline, doxycycline, clindamycin, rifampin, linezolid or vancomycin [1,2,13]. Antibiotics with anti-staphylococcal properties but typically ineffective against CA-MRSA were categorized as “MSSA antibiotics”: penicillins, first-generation cephalosporins, macrolides, and fluoroquinolones. “Double coverage” describes treatment with two or more antibiotics with gram-positive coverage. Three univariable logistic models Mephenoxalone were created to identify demographic or clinical variables associated with (1) in vitro coverage of any organism isolated by the empiric ED antibiotic therapy, (2) use of double antibiotic coverage, and (3) discordance between treatment and culture. In the third regression model, concordance was defined as presence of MRSA in culture when any anti-MRSA treatment was prescribed or presence of MSSA in culture when only anti-MSSA treatment was prescribed.

The fungicidal/fungistatic natures of the extracts were determine

The fungicidal/fungistatic natures of the extracts were determined as described by Thompson.9 The inhibited fungal discs from the extract treated dishes were sub-cultured in a fresh medium, and revival of their growth indicated fungistatic effect, while absence of any growth indicated fungicidal effect. Experimental Animals In this study, 72 Swiss albino mice (36 males and 36 females; 7–8 weeks old; 20–) and 50 Wistar albino

rats (25 males and 25 females; Inhibitors,research,lifescience,medical 6–8 weeks old; 120–) were used. They were bred in the animal house of the Department of Biochemistry, University of Dschang, Cameroon. The animals were housed two or three per cage in elevated wire mesh cages, and were provided with standard animal food, grower’s mash (Grand Cereals LTD, Jos-Nigeria) and water ad libitum. Acute Toxicity Study This study Inhibitors,research,lifescience,medical was carried out on Swiss albino mice (males and females) as described by Emerson and co-workers.10 A total of 72 mice, 6-8 weeks old were used. The mice of each sex were divided

into 6 subgroups of 6 animals each. Stock solution of crude extract (0.8 g/ml) was prepared using 1% aqueous solution of DMSO. Mice in subgroup 1 (control) Inhibitors,research,lifescience,medical were given (oral gavage) 1% aqueous solution of DMSO (1 ml per BW) while those of subgroups 2, 3, 4, 5 and 6 were administrated 2, 8, 16, 24

and 28 g/kg BW of crude extract, respectively. All the animals were fasted for 18 hours prior to the extract administration. After a single dose administration, Inhibitors,research,lifescience,medical the animals were observed for the first 3 hours for behavioral changes.11 Deaths were counted Inhibitors,research,lifescience,medical for the first 48 hours. The survived mice were closely observed for two weeks, and were monitored daily for behavioral changes, signs of toxicity and the latency of death. The KPT-330 in vivo median lethal dose (LD50) was determined by calculation.12 Sub-Acute Toxicity Study Fifty Wistar albino rats (25 males and 25 females) were used. Animals of each sex were divided into 5 subgroups of 5 animals each. They were kept under the same conditions as described above. Adenylyl cyclase Rats in subgroup 1 (control) were given daily administration of 1% DMSO (1.5 ml per BW) by oral gavage, while those of subgroups 2, 3, 4 and 5 were given 25, 50, 100 and 200 mg/kg BW of the crude extract, respectively for four weeks. All animals were provided with food and water ad libitum. They were then observed for physiological and behavioral changes. Body Weight Trend The body weight of each rat was determined during the acclimatization period, once before the commencement of vehicle or extract administration, once every day during the administration period, and once on the day of the sacrifice.

It has been suggested that a fourth mechanism exists wherein pelv

It has been suggested that a fourth mechanism exists wherein pelvic fractures in association with extraperitoneal (EP) bladder rupture are coincidental rather than causative. In one series, only 35% of bladder perforations were noted to have their injuries on the same side as the pelvic fracture.5 A proposed mechanism is that severe lower abdominal selleck chemicals trauma causes

an injury similar to that seen in a full bladder where the collapsed bladder ruptures Inhibitors,research,lifescience,medical from sheer blunt force.6 Complicated bladder lacerations involve the bladder neck and frequently there is disruption of the pelvic floor. This can result in contrast extravasation to the perineum, scrotum, penis, and anterior abdominal Inhibitors,research,lifescience,medical wall (Figure 1). Involvement of the bladder neck is often an extension of an injury. In adults, the laceration is usually a longitudinal split and can be caused by progression of the injury proximally

from a urethral tear or distally from the EP bladder. The involvement of the bladder neck or ureteric orifices converts a simple bladder perforation into one that is complex and requires surgical exploration and repair. Figure 1 Complex bladder neck injury with contrast extravasation into perineum on retrograde urethrogram. Classification Inhibitors,research,lifescience,medical Bladder trauma can be broadly classified as contusions of the bladder wall or intramural hematomas that are self-limiting and require Inhibitors,research,lifescience,medical no specific treatment (Figure 2), EP injuries that occur in 60% of all bladder traumas (Figure 3), intraperitoneal (IP) lacerations that can be seen approximately 25% of the time in patients without pelvic fracture (Figure Inhibitors,research,lifescience,medical 4), and combined IP and EP perforations that occur in 2% to 20% of all injuries.1 Bladder contusion is probably the most common type and is a relatively minor injury that

does not require specific treatment. Radiologic findings are almost L-NAME HCl always normal in these patients with gross hematuria. Two classification systems exist, one based on radiographic appearance (Table 1)7 and the other on injury severity (Table 2).8 Although these classifications may be useful for research purposes, they are of little use clinically and are rarely used in day-to-day practice. In terms of clinical relevance, classification centers on differentiating between EP and IP injury and between simple and complex injury as treatment and outcome may be different. These classifications are based on a combination of radiologic studies and/or findings at laparotomy. Figure 2 Computed tomography image revealing mural irregularity and clot at the dome of the bladder.

156 Since SSRIs and serotonin appear to modulate critical time pe

156 Since SSRIs and serotonin appear to modulate critical time period-like

plasticity in mice, it is possible that exposure to SSRIs during early stages of human development could lead to modifications in developmental plasticity in humans. This hypothesis has recently been tested using a paradigm that probes sensitive periods in human language development. Infants with gestational exposure to SSRIs exhibited a more mature pattern of language discrimination than non-exposed infants,157 suggesting that in utero SSRI exposure accelerates the Inhibitors,research,lifescience,medical closure of a critical time period in the speech perception system. Interestingly, maternal depression appeared to have the opposite effect by inducing a delay in the maturation of language discrimination.157 Conclusions Current translational research has revealed novel roles for the serotonin system in regulating the formation of cortical circuits and modulating Inhibitors,research,lifescience,medical plasticity during critical time periods of development. This has provided new insights on the impact of early-life serotonin programming in determining the risk for a wide range Inhibitors,research,lifescience,medical of behavioral phenotypes ranging from

stress-related dimensions to alterations in social domains. Genetic studies in humans have revealed that serotonin-related gene variants interact with early-life stress and modulate activation of neural circuits involved in mood and anxiety disorders as well as HPA axis responsiveness to stressors. Vulnerability or resilience to the detrimental consequences of early-life stress is likely to depend on the complex interactions between early-life adversity and serotonin-related genetic Inhibitors,research,lifescience,medical variants. In addition, data demonstrates a novel level of UMI-77 mouse transcriptional regulation Inhibitors,research,lifescience,medical suggesting that early-life stress modifies the methylation status of serotonin-related genes. Further work is needed to explore the impact of early-life stress on these novel epigenetic targets and its consequences on neural circuit activation patterns and psychiatric-relevant

dimensions. Finally, the discovery that SSRIs can reinstate juvenile-like forms of neural plasticity, GBA3 in conjunction with behavioral learning, is providing new insights on the biological mechanisms and clinical applications of antidepressants. Acknowledgments This work was supported by a Swiss National Foundation grant (PP00P3_128379) and the NCCR Synapsy grant. Selected abbreviations and acronyms SSRI selective serotonin reuptake inhibitor 5-HT serotonin SERT serotonin transporter MAOA monoamine oxidase A CR Cajal-Retzius HPA hypothalamic-pituitary axis
Depression is a widespread, devastating illness, affecting approximately 17% of the population at some point in life, resulting in enormous personal suffering and economic loss.

As a subject of clinical diagnosis, anxiety may be chronic, for i

As a subject of clinical diagnosis, anxiety may be chronic, for instance, in some types of personality disorder or in generalized anxiety disorder (GAD); in such cases, it is akin to a “trait.” In other instances, anxiety is a short-lived, noncontinuous, discrete symptom, for example, in panic disorder (PD) or in acute stress;

then it is a “state,” rather than a trait. Inhibitors,research,lifescience,medical Anxiety comprises many phenotypes and clinical descriptions. It is routinely partitioned into disorders of general anxiety, panic, phobia, and in some classifications, obsessive-compulsive disorder (OCD); and the lifetime prevalence for the group of disorders has been estimated to be as high as 25%. 1 Even this classification does not go far to encompass the Inhibitors,research,lifescience,medical complexity of anxiety, and hence the arduousness of the task of getting at its biological root. The success to date has not been overwhelming; however, some recent studies have provided more hope than was in the past thought to be realistic. OCD is sometimes classified with anxiety (eg, in the Diagnostic and Statistical Manual of

Mental Disorders [DSM]) and sometimes not (eg, in the International Statistical Classification of Diseases, 10th Revision [ICD10]). Attempts to unravel the genetics of OCD are numerous and would be best served in a treatise of their own, and so will not be included in this review. Since many genetic studies on anxiety have been performed on PD and, possibly as a direct buy Sorafenib result thereof, the Inhibitors,research,lifescience,medical most enlightening results to date have been found for PD, a proportionate Inhibitors,research,lifescience,medical amount of this review will concentrate on the findings in PD. The aim of this review is by no means to overstate

the role of genetics in anxiety, rather to highlight the evidence that exists for the role of genetics in anxiety. The term “complex trait” has been coined by geneticists Inhibitors,research,lifescience,medical to refer to any phenotype that does not exhibit classic mcndclian recessive or dominant inheritance attributable to a single gene.7 In general, complexities arise when the simple correspondence between genotype and phenotype breaks down, because either the same genotype can result in different phenotypes (due to the effects of chance, incomplete penetrance, environment, or interactions with other genes), or different genotypes Idoxuridine can result in the same phenotype (eg, phenocopies, due to environmental or random causes). In fact, most traits of medical relevance, and particularly psychiatric disorders, do not follow simple mendelian inheritance. During the last decade, geneticists have taken up the challenge of the genetic dissection of complex traits. The usual path taken to the elucidation of the genetic basis of psychiatric and other complex disorders is becoming fairly routine. Before undertaking studies aimed at genetic dissection, particularly at the molecular or DNA level, one would ideally like to infer as much as possible about the genetic basis of the trait on the basis of the pattern of disease incidence in families and populations.

However, functional levels remained relatively unchanged, which

However, functional levels remained relatively unchanged, which may learn more indicate that more intensive or longer duration of intervention is needed to elevate global functioning. These findings suggest that short-term treatment can delay psychosis. The authors conclude that the number needed to treat (NNT) of four (ie, four individuals would need to be treated in order to prevent conversion in one) supports continued prodromal trial research. More clarity is expected from a 12-month, randomized, controlled trial initiated in the PACE clinic in 2000, in which risperidone plus CBT will be compared Inhibitors,research,lifescience,medical with placebo plus CBT, and with placebo plus befriending. PRIME clinic randomized double-blind

study McGlashan et al44 at Yale initiated the first double-blind, placebo trial for prodromal patients in 1997. After additional sites were added, 60 subjects were enrolled in the project with 30 randomized to receive olanzapine Inhibitors,research,lifescience,medical (5 to 15 mg) and 29 to receive placebo. Medication or placebo was given for 1 year and patients were followed for Inhibitors,research,lifescience,medical an additional year. Inclusion criteria were based on the Yung UHR categories, but operationalized by the PRIME prodromal assessment tool, the Scale of Prodromal Symptoms (SOPS).48,49 Conversion to psychosis, defined by this group as any positive symptom at psychotic intensity on SQPS that was of sufficient frequency duration, or was seriously disorganizing

or dangerous, warranted removal from the trial and open-label olanzapine was initiated for 6 months. Supportive psychosocial interventions were available for all patients, but effort was made to limit the use

of concomitant psychoactive medications. Inhibitors,research,lifescience,medical Results analyzed by principal mixed-effects model after 8 weeks of treatment revealed that the olanzapine Inhibitors,research,lifescience,medical group showed significant improvement from baseline on SOPS total score, positive symptom scale, negative symptom scale, and disorganized symptom scale. The placebo group did not show any significant change on any scale at any time point. Olanzapine versus placebo group differences were found by week 8 on the SOPS total, negative, and disorganized scales, but not the positive symptom scale. Positive and Negative Symptoms Scale (PANSS) total and positive symptom scores also showed significant differences between the olanzapine and placebo groups. Weight gain was the only side effect reported significantly more others often in the olanzapine group, with over 50% of this group gaining more than 7% of their baseline body weight (versus 3% in placebo group).36 Patients receiving olanzapine showed significant within-group improvements on positive symptom scores and a trend toward greater improvement when compared to the placebo group, demonstrating the efficacy of olanzapine over placebo in the treatment of attenuated positive symptoms.

42 This is in contrast to social anxiety disorder and most other

42 This is in contrast to social anxiety disorder and most other anxiety disorders, for which the point prevalence rates in the general population are much higher than in primary care, and subjects are unlikely to present to their family doctor owing to the nature of the condition.43,44 Panic disorder Diagnosis The key feature of PD in DSM-III is the occurrence of three or more panic attacks Lonafarnib molecular weight within a 3-week period. These attacks must not have been Inhibitors,research,lifescience,medical precipitated simply by exposure to a feared situation,

must not be due to a physical disorder, and must be accompanied by at least four of the following symptoms: dyspnea, palpitations, chest pain, smothering or choking, dizziness, feelings of unreality, paresthesias, Inhibitors,research,lifescience,medical hot and cold flashes, sweating, faintness, trembling, or shaking. In DSM-III-R, the definition was revised to require four attacks in 4 weeks, or one or more attacks followed by a persistent fear of having another attack, and the list of potential symptoms was revised to include nausea or abdominal distress and to exclude depersonalization or derealization. More importantly, DSM-III-R changed the

diagnostic hierarchy Inhibitors,research,lifescience,medical such that PD could be diagnosed as a primary disorder with or without agoraphobia, and also dropped the category of agoraphobia with panic attacks. This change emphasized identifying PD as a discrete entity, and reflected the Inhibitors,research,lifescience,medical clinical experience that panic attacks tended to occur prior to the development of agoraphobia, which was increasingly viewed as a phobic avoidance response to the frightening experience of spontaneous panic attacks, near panic experiences, or limited symptom attacks.45 DSM-IV criteria require recurrent unexpected panic attacks and persistent concern about having further attacks, worry about the implications of the attacks, or a significant change in behavior due to the attacks. Epidemiological data using these criteria are not available. Symptoms (with or without agoraphobia) Unexpected, recurrent, abrupt Inhibitors,research,lifescience,medical episode

of intense fear or discomfort (ie, panic attacks) that peak within 10 min and may involve multiple systems. Feelings of unreality, detachment from self, and intense fear of losing control, choking, going crazy, having a heart attack, or dying during a panic attack. Suplatast tosilate Recurrent and unexpected panic attacks and, for at least 1 month after an episode, concerns about the consequences of a prior attack or having another attack (ie, PD). Symptoms of agoraphobia may be present: fear of getting into situations or going to places where a panic attack may occur and there is no escape or availability of help. Prevalence Table VI 7,8,11,14,25,46-52 shows prevalence rates for PD from a cross-national collaborative study in 10 countries, using DIS and DSM-III criteria.

This has been shown in three studies of pyramidal neurons in the

This has been shown in three studies of pyramidal neurons in the hippocampus,39-41 and has also been reported in dorsolateral prefrontal cortex42 and cerebellar Purkinje cells.”43 Some studies found that the neurons are also more closely packed. Outside the cerebral cortex, extensive cytoarchitectural data are limited to the thalamus, for which there are reports of a loss of neurons from the Inhibitors,research,lifescience,medical dorsomedial and anterior nuclei, though the matter remains controversial. Synapses and dendrites Synapses and dendrites represent a potential site for pathologies that

are undetectable using standard approaches. Because they are hard to visualize directly, proteins localized to these parts of the neuron are used as this website Markers for them.44 Markers of presynaptic terminals are generally reduced in the hippocampus in schizophrenia.44,45 Inhibitors,research,lifescience,medical Hie magnitude of the loss varies according to the individual synaptic proteins (and hippocampal subfields) studied, implying that the

synaptic pathology is not uniform. There is some evidence for preferential involvement of excitatory connections.46 Presynaptic markers may also be reduced in prefrontal cortex, but in this region it is a subset of inhibitory neurons and terminals which appears most Inhibitors,research,lifescience,medical affected.47 Complementing these changes, alterations in dendrites have been shown in the neocortex and in the subiculum, with a decreased density of dendritic spines seen in three studies.18 Although unproven, the usual and simplest interpretation is that these changes together reflect fewer (or otherwise aberrant) synaptic contacts being formed and received.44,45,49 There is an encouraging convergence between these synaptic findings and the cytoarchitectural alterations. In particular, Inhibitors,research,lifescience,medical the decreases in presynaptic and dendritic markers are in keeping with the smaller neuronal cell bodies, since the size of the latter is proportional to the dendritic and axonal spread of the neuron.50 It is also consistent with an Inhibitors,research,lifescience,medical increased neuronal density, in that dendrites and synapses comprise most of the neuropil and, if this is reduced,

neurons will pack more closely.51 Moreover, it also corresponds with the results of proton magnetic resonance studies, which have shown reductions in the neuronal marker N-acctylaspartate (NAA), as one would predict, if the neurons are on average smaller and have less extensive projections.52 Where and what is the pathology? Most also of the positive findings reported in schizophrenia are in the hippocampal formation, dorsolateral prefrontal cortex, and cingulate gyrus.6,7 However, this may be merely a sign that these areas have been the most intensively studied. Few studies have included a comparison region (eg, striate cortex), and those which have do not provide a clear picture as to the uniformity versus selectivity of cerebral involvement, in schizophrenia.

This provides the basis of TME technique, as sharp dissection alo

This provides the basis of TME technique, as sharp dissection along the mesorectal fascia yields the entire mesorectum, which is the lymph node-bearing mesentery of the rectum. Secondarily, it removes any small regional metastases. Removing lymph nodes with the surgical click here specimen removes cancer cells, but more importantly provides information about staging, prognosis, and guides treatment decisions. For example, the United States

Surveillance, Epidemiology and End Results (SEER) cancer registry Inhibitors,research,lifescience,medical database shows that for each T stage, 5-year overall and disease-free survival decreases with increasing LN involvement. The presence of lymph node metastases determines the patients most likely to benefit from adjuvant therapy (2). The American Joint Committee on Cancer (AJCC) and the International Union Against Cancer (IUAC) Inhibitors,research,lifescience,medical recommends removing at least 12 lymph nodes to properly assess the adequacy of surgical resection and provide adequate information for staging. Having a minimal lymph node cut off value is problematic as the number of lymph nodes is highly individual, varying with age, location, and tumor characteristics such as growth Inhibitors,research,lifescience,medical factors and microsatellite instability. Even with standardized surgical technique and pathologic evaluation (including the use

of fat clearing to optimize lymph node harvest), the total number of lymph nodes harvested after neoadjuvant chemoradiation is highly variable and frequently less than 12, and with the possibility of fewer positive lymph nodes, downstaging can occur (3,4). To address this issue, we previously proposed calculating lymph node Inhibitors,research,lifescience,medical ratios as a method that incorporates the negative impact on survival of finding as few as one positive lymph node and the uncertainty Inhibitors,research,lifescience,medical regarding the optimal number of total lymph nodes to harvest (5). This lymph node ratio is valuable as an independent prognostic factor for overall survival, not only in rectal cancer,

but also in gastric, breast, bladder, pancreatic cancer, and colon cancer (6). Rolziracetam Interestingly, increasing the number of lymph nodes retrieved is associated with increased survival among patients with colorectal cancer (7,8). The article by Denham and colleagues in the current issue of the Journal of Gastrointestinal Oncology provides a wide-ranging review of multiple studies and biologic principles to determine the underlying basis of this observation. Given the lack of consensus in the literature, the authors conclude that the explanation for the association of increased survival with increased lymph node retrieval is multifactorial and lies in tumor-host biology (9). Clinically, deciding how many lymph nodes to retrieve is less relevant, as a surgeon performing a “cancer operation” should, by virtue of optimal surgical technique, maximize the mesenteric lymph nodes harvested.

Among inpatients treated with amitriptylinc, approximately one th

Among inpatients treated with amitriptylinc, approximately one third had been found to be complete responders, partial responders, and nonresponders, respectively.7 Weissman et al8 reported a follow-up study to

4 years in a sample of female depressives who had responded to initial treatment with amitriptyline and had been included in a controlled trial of Inhibitors,research,lifescience,medical continuation antidepressant and psychotherapy. Many showed moderate or fluctuating symptoms, corresponding approximately to residual chronicity, but. included some subjects who relapsed and then remitted. Occurrence of residual symptoms had been noted in general practice patients with depression and anxiety, 9 and in 38% of elderly dépressives at 1 year, and 20% at 2 to 4 years.10 More recently, one or more residual symptoms have been found in 82% of elderly depression remitters below 8 on the Hamilton Depression scale.11 At. these levels the subjects would be below the usual threshold for partial remission, however. More recent, Inhibitors,research,lifescience,medical studies of residual symptoms have been reviewed by Fava et al.12 They have been reported both after drug treatment and psychotherapy. Fava et al, 13 in a study of their own, reported a strong relationship between prodromal and residual Inhibitors,research,lifescience,medical symptoms. The most common symptoms were irritability and anxiety. The influential

Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study, 14 which has reported higher nonremission rates for depression than hitherto thought, Inhibitors,research,lifescience,medical to occur, did not use a criterion for partial remission. Residual symptoms and relapse Following remission, the patients in our original study4 were followed for another 15 months. As in other followup studies, there was a high rate of subsequent relapse, with 40% of subjects relapsing over the next. 15 months. All the relapses occurred in the first 10 months, giving some support to the concept, of relapse as an early phenomenon that is distinguished from Inhibitors,research,lifescience,medical recurrence later in time. An

important, finding emerged when we separated out the subjects with residual symptoms at remission. Among these, 76% relapsed in the next 10 months, compared with 25% of subjects without residual symptoms.3 Residual symptoms were a key indicator of subsequent relapse. A number of other studies have drawn attention to high relapse rates in residual dépressives.10,15-18 One study19 found that patients Calpain with residual symptoms of depression obtained greater benefit from maintenance antidepressant therapy than those who had completely recovered. Prien and Kupfer20 found that relapse was less common after full remission of at. least. 16 weeks, a finding on which they based a TSA HDAC purchase recommendation that continuation treatment should comprise at least 4 months of complete remission. After 9 months, 49% of a Dutch sample were found to be in full remission and 45% in partial remission.