It has two components, Triage assessment and waiting list Every

It has two components, VX-770 cell line TRIAGE assessment and waiting list. Every staff working in ED has been given a login ID and password for logging in. After logging, in the windows shows two options: triage assessment and waiting patient work list. For triage assessment, the triage staff would click on the “TRIAGE ASSESSMENT” icon which opens up a new window asking for the

patient details like medical record number, vitals, presenting complaints etc. After entry, this information is saved in the computer and can be retrieved later for analysis. This software also helps the staff in identifying abnormal vital signs like heart rate, Inhibitors,research,lifescience,medical blood pressure and oxygen saturation according to the age of the patients by blinking vitals in red. This way, it assists the staff in triaging the patients correctly. This study had been approved by the Ethical

Review Committee (ERC) of Aga Khan University. After filling all these information, the patient triage category triage assessment number and the bed is assigned if available. Inhibitors,research,lifescience,medical In case Inhibitors,research,lifescience,medical of non-availability of bed and the patient is not life threatening or critical, then the patient is transferred to the waiting area and this information can be reviewed by the staff later on by clicking “waiting patient list”. In this way the staff completes the triage process for patients. ED staff can review bed statistics any time by using the same software. When a bed becomes available in the ED or the defined waiting time is completed, the patient is called again for reassessment or allocation of bed. At this point they are asked to go to the registration desk and were registered with their medical record number for patients who had visited Inhibitors,research,lifescience,medical the AKUH previously

Inhibitors,research,lifescience,medical as well. If that patient is visiting for the first time than a new medical record number is allocated. When patient is assigned a bed in the ED, after waiting than this time is measured as waiting time before getting a bed. When a bed is made available than the name of the patient is called for three times by triage staff at 2 minutes interval and if a patient does not reply , they are labeled as “left without being seen” and that time is noted as their waiting time. Return visits are recorded if the patient after leaving the emergency department comes back within 48 hours of visit. The return visits are Chlormezanone usually tracked down through the medical record number. Data collection All patients who were triaged in the Emergency Department of AKUH from April 1, 2010 to December 31, 2010, are included in the study. This time period was chosen to ensure consistency of results as we implemented a defined triage policy so to exclude any bias time period from Jan –March. We used an electronic ED record system to extract clinical data of all patients who were triaged in the AKUH-ED.

Methodological standards for clinical decision tools Clinical dec

Methodological standards for clinical decision tools Clinical decision tools are developed to reduce the uncertainty in medical decision-making [31-34]. Reported methodological standards for the development and validation of decision tools can be summarized as follows: [35-37] i) There must be a need for a decision tool because of the prevalence of the clinical condition and variability in current practice. Such a need must be a belief among physicians practicing in that area [38]; ii) The outcome or diagnosis to be predicted must be clearly defined. To reduce the risk of bias, outcome ascertainment should be made without knowledge of the predictor variables; iii) Inhibitors,research,lifescience,medical The clinical findings to

be used as predictors must be clearly defined, standardized, and clinically sensible and their assessment must be done without the knowledge of the outcome (Blinded predictor variable Inhibitors,research,lifescience,medical assessment);

iv) The reliability or reproducibility of the predictor variables must be clearly demonstrated; v) To increase generalizability, the subjects in the study should be selected without bias and should represent a wide spectrum of patients with and without the outcome; vi) The mathematical techniques for deriving the tools must be clearly explained; vii) Decision tools should be clinically sensible: have a clear purpose, demonstrate Inhibitors,research,lifescience,medical content validity, must be relevant, concise and easy to use in the intended clinical context; viii) The accuracy of the decision tool in classifying patients with (sensitivity) and without (specificity) the targeted outcome should be demonstrated; ix) Prospective Inhibitors,research,lifescience,medical validation on a new set of patients is an essential step in the evolution of this form of decision support. Unfortunately, many clinical decision tools are not prospectively validated to determine their accuracy, reliability, clinical sensibility, or potential impact on practice. This validation process is very important because many statistically-derived tools fail to perform well when tested Inhibitors,research,lifescience,medical in a new population.

The reason for this poor performance may be statistical (i.e., overfitting or instability of the original derived model) or due to differences in prevalence of disease or differences in the population or differences in how the decision tool is applied [39-41]; x) An implementation Etomidate phase (to demonstrate the true Doxorubicin effect on patient care) is the ultimate test for a decision tool in terms of effectiveness, uptake and cost [42]. Previous emergency department syncope studies There are nine original studies previously published to predict SAEs in ED syncope patients [7,10,11,24,43-47]. A synopsis of the available instruments and how they perform against the above-mentioned methodological standards is given in Table 1. All published studies define ‘abnormal ECG’ variable differently and none are based on evidence.

8,9 What this nonlinearity

means is that when any one med

8,9 What this nonlinearity

means is that when any one mediator is increased or decreased, there are compensatory changes in the other mediators that depend on time course and level of change of each of the mediators. Unfortunately, we cannot measure all components of this system simultaneously, and must rely on measurements of only a few of them in any one study. Yet the nonlinearity Inhibitors,research,lifescience,medical must be kept in mind in interpreting the results. Stress in the natural world The operation of allostasis in the natural world provides some insight into how animals use this response to their own benefit or for the benefit of the species. As an example of allostasis, in spring, a sudden snowstorm causes stress to birds and disrupts mating, and stress hormones are pivotal in directing the birds to suspend reproduction, to find a source of food, and to relocate to a better mating site, or at Inhibitors,research,lifescience,medical least to delay reproduction until the weather improves.10 As an example of Z-VAD-FMK cell line allostatic load, bears preparing to hibernate for the winter Inhibitors,research,lifescience,medical eat large quantities of food and put on body fat to act as an energy source during the winter.11 This accumulation of fat is used, then, to survive the winter and provide food for gestation of young; this is in contrast to the fat accumulation that occurs in bears that are captive in zoos and eating too much, partially out

of boredom, while not exercising.4 The accumulation of fat under these latter conditions can be called “allostatic overload,” referring Inhibitors,research,lifescience,medical to a condition that is associated with pathophysiology. However, allostatic overload

can also have a useful purpose for the preservation of the species, such as In migrating salmon or the marsupial mouse, which die of excessive stress after mating- the stress, and allostatic Inhibitors,research,lifescience,medical load, being caused for salmon, In part, by the migration up the rapidly flowing rivers, but also because of physiological changes that represent accelerated aging.12-14 The result is freeing up food and other resources for the next generation. In the case of the marsupial mouse, it is only the males that die after mating, due apparently to a response to mating that reduces the binding protein, corticosteroid-binding globulin (CBG), for glucocorticoids and renders them much more active throughout the body.15 Being “stressed out”, especially sleep deprivation and its during consequences The common experience of being “stressed out” has as its core the elevation of some of the key systems that lead to allostatic load- Cortisol, sympathetic activity, and proinflammatory cytokines, with a decline in parasympathetic activity. Nowhere is this better illustrated than for sleep deprivation, which is a frequent result of being “stressed out.” Sleep deprivation produces an allostatic overload that can have deleterious consequences.

5 16 −1 43 2 6 16 −0 56 4 4 16 −0 67 4 2 17 −1 06 3 4 17 −0 16 5

5 16 −1.43 2.6 16 −0.56 4.4 16 −0.67 4.2 17 −1.06 3.4 17 −0.16 5.2 17 −0.33 4.8 18 −0.68 4.1 18 0.24 6.0 18 0.00 5.5 19 −0.31 4.9 19 0.63 6.8 19 0.33 6.2 20 0.06 5.6 20 1.03 7.6 20 0.67 6.8 21 0.44 6.4 21 1.42 8.3 21 1.00 7.5 22 0.81 7.1 22 1.82 9.1 22 1.33 8.2 23 1.18 7.9 23 2.22 9.9 23 1.67 8.8 24 1.55 8.6 24 2.61 10 24 2.00 9.5 25 1.93 9.4 25 3.01 10 25 2.33 10 View it

in a separate window *Of these nonclinical norms, 579 were also included Inhibitors,research,lifescience,medical in this study and in each case were identified as having good brain health status. Conflict of Interest N. J. C. undertook analyses for this work as senior statistician employee with Brain Resource Ltd. E. G. is founder and receives income as Chairman for Brain Resource Ltd. S. D. D. receives income as VP for Productfor Brain Resource Inc, San Francisco. L. M. W., S. Inhibitors,research,lifescience,medical H. K., S. R. W., N. J. C., J. K., A. J. R., and E. G. are members of the publication committee for the international Study for Optimizing Treatment in Depression (BIBW2992 cost iSPOT-D), which is sponsored by Brain Resource and uses the BRISC as one of the hypothesized

predictors of treatment outcomes. The BRISC is also offered by Brain Resource as a for-profit screening tool, with financial interest for E. G. as employee and E. G., L. W., S. D. D., and J. G. as stockholders. Clinical Trial Registry Trial Registry:; Registration Number: NCT00693849 URL:
Amyotrophic Inhibitors,research,lifescience,medical lateral sclerosis (ALS) is heterogeneous Inhibitors,research,lifescience,medical in phenotype and genotype, and despite intense research effort, the underlying cause(s) remain obscure. Sporadic and familial forms

of ALS share common pathophysiological features, including a marked neuroinflammatory response, characterized by glial activation and innate and adaptive inflammatory components (for reviews, see Ilieva et al. 2009 and Appel et al. 2011). In murine models of ALS, activated astrocytes and microglia are observed in neuroinflammatory foci in the spinal cord prior to onset of symptoms, and such areas correlate with pronounced regional motor neuron loss (Shibata et al. 1996). Infiltration of CD8+ T-suppressor/cytotoxic and CD4+ T helper Inhibitors,research,lifescience,medical cells is also prominent (Kawamata et al. 1992). These cells alter disease progression both independently and through apparent cross-talk with microglia (Kipnis et al. 2004; Beers et al. 2008). Generally, glia secrete soluble factors that may be toxic (reactive oxygen species, proinflammatory cytokines) or protective (growth factors), however depending on local environment (Li et al. 2007). However, in models of ALS, transgenic expression of mutant hSOD1 in astrocytes and microglia results in glial phenotypes that are inherently neurotoxic compared to their wild-type counterparts (Boillee et al. 2006; Nagai et al. 2007). Thus, chronic neurodegeneration in ALS may evolve as a so-called noncell-autonomous process (Lobsiger and Cleveland 2007) that, in part, reflects a toxic glial microenvironment.

72 Recently, we investigated the role of heparanase in the place

72 Recently, we investigated the role of Talazoparib heparanase in the placenta, focusing on its effect on TF, TFPI, TFPI-2, and VEGF-A.73,74 In these two studies placenta samples of women with recurrent abortions and thrombophilia (weeks 6–10) were compared to control cases of pregnancy terminations and placentas of normal vaginal deliveries, and intrauterine growth-restricted (IUGR) babies were compared to control cases of elective cesarean sections, applying real-time RT-PCR and immunostaining. Sections obtained from miscarriages Inhibitors,research,lifescience,medical and vaginal and IUGR deliveries revealed increased (2–3-fold) levels of heparanase, VEGF-A, and TFPI-2 compared

to placentas from controls in maternal as well as in fetal placenta elements. A possible common denominator of the cases is vascular insufficiency: in vaginal deliveries lasting intermittently for a few hours; in miscarriages and IUGR babies it may represent a prolonged state. As heparanase directly activates Inhibitors,research,lifescience,medical the coagulation system,56 increased heparanase found in the placentas may contribute to placental vascular complications as summarized in Figure 2. Figure 2 Heparanase, TFPI-2, and VEGF-A are Inhibitors,research,lifescience,medical elevated in

placentas with vascular insufficiency. CONCLUSIONS Heparanase was recently revealed as an important modulator of blood coagulation. The elevation of heparanase levels in human tumors, together with the prothrombotic state of most neoplasms, suggests possible clinical relevance of the procoagulant function of heparanase. In addition its increased levels in pregnancy vascular complications accentuate heparanase significance Inhibitors,research,lifescience,medical in other proangiogenic states. In order to augment the understanding

of heparanase we lately developed an assay to evaluate heparanase Inhibitors,research,lifescience,medical procoagulant activity in the plasma,75 enabling further extensive research in the field. Targeting domains of heparanase that mediate its enzymatic activity-dependent and independent functions may prove beneficial for patients with proangiogenic and prothrombotic conditions. Abbreviations: ALL acute lymphoblastic leukemia; AML acute myeloid leukemia; ECM extracellular matrix; HS heparan sulfate; HUVEC human umbilical vein endothelial cell; IUGR intrauterine growth-restricted; LMWH low-molecular-weight heparin; MM multiple myeloma; SNPs single nucleotide polymorphism; TF tissue factor; Mephenoxalone TFPI tissue factor pathway inhibitor; VEGF vascular endothelial growth factor. Footnotes Conflict of interest: No potential conflict of interest relevant to this article was reported.
Bedside rounds have long been a time-honored component of medical education, involving performing activities of clinical care at the patient’s bedside. The patient becomes a “text,” so to speak, used to teach student doctors how to better treat other people in the future. Gonzalo et al.

Summary Genetic studies in schizophrenia are on the cusp of an e

Summary Genetic studies in schizophrenia are on the cusp of an exciting new era

of utilizing specific laboratory-based endophenotypes to parse the complex genetic architecture of the “groups of schizophrenia.” The template described above for P50 suppression studies has already yielded a sequence of findings leading to the identification of a specific abnormality that accounts for P50 suppression deficits in schizophrenia Inhibitors,research,lifescience,medical patients and their clinically unaffected relatives. In addition to this, there are many studies examining heritability of other strong candidate endophenotypes, as listed in Table I Other study strategies are now being utilized in endophenotypic research in schizophrenia. Investigations

are underway in a number of settings to identify genes that convey a risk for schizophrenia. For example, whole genome Inhibitors,research,lifescience,medical linkage studies have revealed loci that might be of functional importance. In addition, the endophenotypic strategy, however, allows us to understand the underlying neurobiology and neural substrates of these genetic abnormalities. Inhibitors,research,lifescience,medical Many conundrums and obstacles must be overcome in this endeavor. For example, the improvement of endophenotypic abnormalities via the use of second-generation96 antipsychotic medications may (or may not) impede our ability to carefully conduct family heritability studies, which will allow us to ultimately identify genetic abnormalities characteristic of schizophrenia. With the use of statistical Inhibitors,research,lifescience,medical genetics methods, unmedicated patients, animal model identification of quantitative trait loci, and specific genetic abnormalities, the exciting possibility

exists for matching endophenotypes with their underlying genetic abnormalities and then constructing “composite endophenotypes” consisting of neurobiologically Inhibitors,research,lifescience,medical coherent selleck compound combinations of more than one of the identified biomarkers. It is very important to identify the convergence and divergence of these endophenotype–gene abnormality linkages in schizophrenia patients in order to see whether a single genetic abnormality is likely to induce the multiple observed deficits of schizophrenia patients. Ultimately, the specification either of how different gene–environment interactions contribute to neuronal pathology associated with psychosis may enable us to further clarify the nosology of schizophrenia. Quantitative endophenotype-based strategies play an important role that will help elucidate the genetic basis of schizophrenia and point the way toward molecularly derived strategies for the treatment of important subgroups of patients with this complex disorder.

This result suggests for the first time that sleep need is under

This result suggests for the first time that sleep need is under strong genetic control, and genes can

be identified underlying sleep homeostasis. Conclusions The functions of sleep remain elusive. Understanding the regulation of sleep at the molecular level represents a powerful step to gaining access to the enigma of sleep. Although evidence has accumulated to indicate a major role for genetic factors in normal and pathological sleep, the underlying molecular mechanisms have not been elucidated, except in a few rare sleep disorders. Like most other complex traits, sleep is controlled by many genetic and environmental factors. Inhibitors,research,lifescience,medical New strategies are becoming available for genetic dissection of complex phenotypes. Inhibitors,research,lifescience,medical The hope of finding single genes that determine the presence or absence of any vigilance states in an all-or-nothing manner is highly unrealistic. However, as reviewed here, sleep-related endophenotypes, such as the sleep EEG features, can be controlled by single or major genes. A noteworthy discovery is that such genes indicate unpredicted pathways (eg, β-oxidation and vitamin A signaling) that are not only implicated in sleep but link sleep to other complex Inhibitors,research,lifescience,medical behaviors. Selected abbreviations and acronyms EEG

electroencephalogram LTP long-term potentiation NREM non-rapid eye movement QTL quantitative trait loci REM rapid eye movement SCN suprachiasmatic nucleus TPF theta peak frequency Notes This work was supported by the State of Vaud and the Swiss National Inhibitors,research,lifescience,medical Science Foundation.
Biologlcal clocks are devices that can measure time In the absence of environmental timing cues, such as changes In light Intensity, temperature, or humidity.1 The discovery of circadian clocks dates back to 1729, when the French astronomer Jean Jacques Ortous de Malran observed that mimosa plants continued to open and close their Inhibitors,research,lifescience,medical leaves in a daily manner when kept in the absence of sunlight.2 Selleck AZD6244 Obviously, other environmental

oscillations such as daily temperature fluctuations could have driven the cyclic leaf openings in de Mairan’s experiment, thereby challenging his conclusion about the existence of a mimosa clock. However, in 1832 the Swiss physician and botanist Augustin Pyrame de Candolle heptaminol demonstrated that in constant light mimosa plants opened and closed their leaves with a cycle of 22 hours rather than 24 hours.3 This observation provided irrefutable evidence that the leaf movement rhythm was not merely driven by cyclic environmental cues depending on the earth’s rotation, but by a self-sustained biological clock. Incidentally, “circadian” is derived from the Latin words “circa diem” and indicates that circadian clocks can measure days only approximately. Hence, the phase of circadian oscillators must be corrected daily to stay in resonance with geophysical time. The photoperiod (ie, daily variations in light intensity) is the primary Zeitgeber for the synchronization of circadian clocks.

3% to 28 4% [18F]FDG PET contributed more to the improvement in

3% to 28.4%. [18F]FDG PET contributed more to the improvement in the accuracy than CSF or MRI, showing the usefulness of molecular learn more imaging in the early diagnosis of AD.169 Current drugs for AD include acetylcholinerase inhibitors such as donepezil and rivastigmine; memantine, a drug that blocks NMDA receptors,170 and drugs that combat the neurotoxic effect of Aβ plaques including the

L-type calcium channel antagonist nimopidine, and antioxidants such as vitamin E.171 Candidate drugs Inhibitors,research,lifescience,medical for AD include beta and gamma secretase inhibitors, and immunogenic synthetic Aβ42 or monoclonal antibodies (eg, bapineuzumab) against Aβ42.172 Molecular imaging is not only useful for the early detection

Inhibitors,research,lifescience,medical of AD and MCI, but also for predicting treatment response to anti-amyloid and other drugs, and may serve as a surrogate outcome measure.172,173 For example, some PET studies reported reduction of brain Aβ plaques measured by [11C]PIB after the treatment with Inhibitors,research,lifescience,medical anti-amyloid agents, though the disease modifying effects need further confirmation.174-176 The imaging of inflammatory mediators such as microglia may help assess the effectiveness of drugs that are targeted toward reducing inflammation in the brain, such as NSAIDs. Moreover, since abnormalities in cholinergic, noradrenergic, serotonergic,

and dopaminergic Inhibitors,research,lifescience,medical systems are all thought to contribute to AD pathophysiology, imaging of these neurotransmitter systems will help develop further drug targets and evaluate their efficacy.173 Conclusions How molecular imaging has uniquely changed thinking about these illnesses Molecular imaging enables molecular processes to be related to the clinical presentation, and subsequent course of CNS disorders. Inhibitors,research,lifescience,medical For example, in the case of schizophrenia it has provided data on the regional nature of the dopamine alterations in the brain at the onset, and even predating the illness. Furthermore, molecular imaging has narrowed down the nature of the dopaminergic alterations at onset of the disorder- identifying that the major alterations are presynaptic and not at the receptor or transporter level- and tuclazepam related this to subsequent clinical outcomes. This has enabled the dopamine hypothesis of schizophrenia to be revised in ways that would not have been possible with other techniques. Molecular imaging also clarified how antipsychotics work — demonstrating that D2/3, but not D1 or 5-HT2A, receptor occupancy is linked to subsequent treatment response and side effects. This finding has contributed to a change in clinical practice away from the use of high dose antipsychotics towards lower doses.

In this recent study, dynorphin, at four different doses, was inf

In this recent study, dynorphin, at four different doses, was infused into the caudate-putamen, and dopamine levels were quantitatively measured, using high-performance liquid chromatography, in the

extracellular fluid obtained during in vivo microdialysis in that brain region.23 Also, the effect of a relatively high dose of Selleckchem Bcl 2 inhibitor dynorphin A on increases in dopamine levels caused by 15 mg/kg of cocaine was measured using in vivo microdialysis. In related studies, the effect of this dose of dynorphin A on cocaine-induced conditioned place preference Inhibitors,research,lifescience,medical was studied.23 We found that dynorphin significantly decreased basal dopamine levels in a dose-dependent manner and by more than 60% at the highest dose. Further, this effect Inhibitors,research,lifescience,medical was blocked by preinjection with a selective kappa-opioid receptor antagonist, nor-binaltorphimine (nor-BNI).23 Further, it was found that the highest dose of dynorphin studied (4.4 nanomolar) resulted in a complete block of the cocaineinduced increases in dopamine levels, and also attenuated locomotor activity induced by 15 mg/kg of cocaine, and blocked the formation of cocaine-induced conditioned place preference.23

These findings suggest that a dynorphin agonist might be helpful in managing cocaine and other stimulant dependency by preventing cocaine or other stimulant-induced Inhibitors,research,lifescience,medical dopamine surges. However, on the other hand, any significant lowering of basal dopaminergic tone could lead to dysphoria, and thus more craving for a drug of abuse such as cocaine. Therefore, it has made our laboratory suggest that a potentially effective kappa-opioid receptor-directed compound for management of cocaine addiction would probably be a kappa partial agonist, that is, with modest agonist activity, but also Inhibitors,research,lifescience,medical antagonist activity, which should render stable basal dopaminergic tones, yet significantly attenuate cocaineor other stimulant-induced dopamine surges, as well as “liking of” cocaine. In related studies, Zhang et al studied a related potent

synthetic kappa-agonist, R-84760, on cocaine-induced Inhibitors,research,lifescience,medical increases in striatal dopamine levels in cocaine-induced Dipeptidyl peptidase conditioned place preference in C57BL/6J mice.24 R-84760 is a novel nonpeptidic potent synthetic selective kappa-opioid receptor agonist that has been studied to a limited extent in humans for other indications. It was found that, similarly to dynorphin itself, this compound would effect a dose-dependent reduction in dopaminergic tone, as measured during in vivo microdialysis in the striatum.24 Also, it was shown that, like dynorphin, a low dose (0.1 mg/kg) of R-84760 would block cocaineinduced increases in the dopamine levels. Also, it was found that similarly low doses of R-84760 would completely prevent the development of cocaine-induced conditioned place preference and would attenuate locomotor activity in the conditioning chamber.

Pezawas et al102 studied longitudinally recurrent brief depressio

Pezawas et al102 studied longitudinally recurrent brief depression in an adolescent community sample. Recurrent brief depression was defined according to DSM-IV-TR research criteria. The frequency of all depressive disorders was 21%; the frequency of recurrent brief depression was 1% without history of major depressive disorder and 1% with history of major depressive disorder. Compared with major depressive disorder, recurrent brief depression did

not occur more in females than in males (a typical feature of nonbipolar depression), and frequency of comorbid axis Inhibitors,research,lifescience,medical I disorders was different. The frequency of suicide attempts, compared with major depressive disorder, was 8% vs 12%. Recurrent brief depression was not associated Inhibitors,research,lifescience,medical with bipolar disorders. However, use of fully structured PD 332991 interviews by lay interviewers underreports bipolar II disorder.4, 24, 25

Angst and Hochstrasser100 found Inhibitors,research,lifescience,medical that recurrent brief depression (defined as in DSM-IV-TR) had a lifetime community prevalence of 10% to 16%, it could shift to major depressive disorder and vice versa, had a 35% diagnostic stability, usually lasted 1 to 3 days, had different axis I comorbidity compared with major depressive disorder (more anxiety disorders), high frequency of suicide attempts (14% Inhibitors,research,lifescience,medical vs 21% in major depressive disorder), and high treatment seeking. Angst et al also found that recurrent brief depression was similar to major depressive disorder

on most validators such as age at onset, family history, and impairment of functioning. Carta et al103 found a community lifetime prevalence of recurrent brief depression of 8%. A literature review by Merikangas et al104 on recurrent brief Inhibitors,research,lifescience,medical depression Oxygenase found that validation criteria did not discriminate between recurrent brief depression and major depressive disorder, that it did not appear to be a milder subtype of depressive disorders, and that it was unrelated to the premenstrual syndrome. The current status of recurrent brief depression is unclear. Seasonal affective disorder According to DSM-IV-TR, seasonal affective disorder is not a distinct disorder, but a specifier of the major depressive episode of bipolar disorders and depressive disorders. It is unclear if it is more common in bipolar disorders, but it seems to be more common in bipolar II disorder than in bipolar I disorder.