In the absence of significant mitral regurgitation and right-sided lesions, regurgitant fraction can be calculated by subtracting the RV stroke MK-8776 volume from the LV stroke volume. These internal controls help to ensure consistency of volume quantification. The reproducibility of CMR in quantifying the severity of valvular regurgitation using phase-contrast velocity mapping is superior compared to well-validated TTE volumetric methods.12 Table 4 Aortic regurgitation quantification: selected validation studies.22-24 Figure 8. In this phase-contrast sequence of a patient with aortic regurgitation, a region of interest (area) is traced at the aortic sinuses and for baseline correction at the subcutaneous fat (stationary

Inhibitors,research,lifescience,medical tissue). The highest and lowest intensity Inhibitors,research,lifescience,medical pixels at the … In aortic regurgitation, the anatomical regurgitant orifice (ARO) can be determined by obtaining

an “en-face” view of the aortic valve using sequential SSFPs cines. The smallest diastolic regurgitant orifice in mid-diastole is traced. An ARO of 0.28 cm2 has a sensitivity and specificity of 90% and 91%, respectively, in detecting severe aortic regurgitation.13 Conclusion CMR has emerged as a robust new imaging technique for assessing patients with valvular disease, and it has a number of unique advantages over other imaging modalities. Inhibitors,research,lifescience,medical CMR can help determine the mechanism of valve disease, quantify the severity of disease, and discern the consequences of the lesions including the effects on LV volume, LV systolic Inhibitors,research,lifescience,medical function, and left atrial volumes. CMR eliminates issues of image quality from inadequate imaging windows or body habitus. In most instances, information can be obtained noninvasively without the need for intravenous contrast agents or ionizing radiation. Low inter-study variability also makes it an optimal technique for serial assessment of valve disease in patients that are managed

expectantly. Funding Statement Funding/Support: Dr. Shah receives research grant funding through Siemens Medical Solutions. Footnotes Conflict of Interest Disclosure: All authors have completed and submitted the Methodist DeBakey Cardiovascular Journal whatever Inhibitors,research,lifescience,medical Conflict of Interest Statement and none were reported.
Introduction Accurate detection of cardiac thrombus affects clinical outcomes and therapeutic management as thrombus provides a substrate for thromboembolic events and a rationale for anticoagulation. Cardiac magnetic resonance (CMR) imaging enables thrombus to be detected based on intrinsic tissue characteristics related to avascular tissue composition. CMR tissue characterization for thrombus has been well validated when compared to reference standards of both pathology and clinical outcomes. Recent comparative studies have demonstrated that CMR yields superior detection of left ventricular (LV) thrombus compared to echocardiography (echo), which detects thrombus based on anatomical appearance (i.e., morphology) rather than tissue characteristics.

Al-Rashdan et al. attempt to critically evaluate this confusing maze of data and ask whether cyst fluid analysis really addresses this unmet clinical quandary of how to appropriately select patients with pancreatic cysts for surgery (4). They focus on the challenge to distinguish between mucinous subtypes by evaluating cyst fluid CEA and amylase. In the 10 year study period, they identified 134 patients with pancreatic cysts who underwent surgical resection. Of these patients,

82 underwent a preoperative EUS. Sixty-six of the 82 were mucinous cysts (14 MCN, 52 Inhibitors,research,lifescience,medical IPMN). Of these 66, 25 had preceding FNA and cyst fluid analysis performed (9 MCN, 11 SB-IPMN and 5 main duct IPMN). The median and mean CEA were not statistically different between the 9 MCN and all 16 IPMN (p=0.19), as well as, MCN and SB-IPMN (p=0.34). The median and mean Inhibitors,research,lifescience,medical amylase were not statistically different between the MCN and all IPMN (p=0.64) and MCN and SB-IPMN (p=0.92). Of note, no data was provided regarding cross-sectional

imaging or EUS findings. Their data is similar to other studies that have found limitations in the accuracy of cyst fluid CEA and amylase—as well as its selective utilization Inhibitors,research,lifescience,medical in practice. In a cohort of 33 mucinous cystadenomas and 235 IPMN patients (5), Slozek et al. showed that neither CEA nor amylase was unable to distinguish between mucinous cystadenomas and IPMN (p=0.26 and 0.23 respectively). However, for this study, how many of the pathologic diagnoses were confirmed by surgical pathology or how the definition of mucinous cystadenoma was made was not provided. Inhibitors,research,lifescience,medical Curiously, cyst fluid CA19-9 was noted to distinguish mucinous cystadenomas and IPMN (p=0.003)

(5). The elevated CA19-9 raises the possibility of a different biomarker to distinguish between types of mucinous cysts. Another study of 14 MCN and 52 IPMN cases confirmed by surgical pathology reported median CEA of 2844 ng/ml (range 1-14,500) in MCN and 574 ng/ml (0-38,500) in IPMN (5). While statistical analysis of this difference was not reported, the whatever overlap between Inhibitors,research,lifescience,medical CEA concentrations is readily apparent. Most recently, in a study of 126 patients, Park et al. reported overlapping median values cyst fluid CEA between MCN and IPMN (428ng/ml [5 HT Receptor inhibitor interquartile range IQR: 44-7870] and 414ng/ml [IQR 102-1223]), again without statistical analysis (7). Median values (and IQR) for cyst fluid amylase overlapped as well for MCN and IPMN (6800 IU/L [IQR 70-25,295] and 5090 IU/L [IQR 1119-38,290], respectively) (7). The data from Al-Rashdan et al. adds to the growing body of evidence that cyst fluid analysis (CEA and amylase) alone is disappointing in its ability to distinguish between the mucinous lesions, MCN and IPMN. However, the question is we would ever look at cyst fluid analysis alone to make our clinical decisions? The answer is probably not.

We found that participants using the smaller 1000 ml bag were more likely to achieve optimal tidal volumes in the simulated patient (p = 0.015). Seventy percent (n = 21) of participants produced mean tidal volumes consistent with either hypoventilation or hyperventilation of the simulated patient. Of the participants who used the 1000 ml Inhibitors,research,lifescience,medical bag, 70% (n = 21) participants were also suboptimal with their tidal volumes (Figure ​(Figure1b1b). Similarly, mean minute volumes over the two minute period revealed significant differences between the two capacity bags. We found that participants who used the smaller self-inflating bag were more likely to achieve guideline consistent

minute volumes. Ninety-three percent of participants (n = 28) using the 1600 ml bag and 70% (n

= 21) of participants using the 1000 ml bag demonstrated suboptimal minute volumes for Inhibitors,research,lifescience,medical the simulated patient (p = 0.045), see Figure ​Figure11. No statistically significant difference was found when comparing gender-specific Integrase inhibitor performance in relation to ventilation rate, tidal volume or minute volume. Discussion Ventilation of a simulated adult cardiac arrest patient by undergraduate Monash Inhibitors,research,lifescience,medical University paramedic students is better achieved by using a smaller self-inflating bag. Even when using the smaller self-inflating bag ventilation values were still predominately suboptimal. It is now well supported that the delivery of ventilation using a self-inflating bag Inhibitors,research,lifescience,medical is erratic and uncontrolled by all disciplines, not just prehospital care providers[6,10-12,1] Pitts and Kellermann proposed that hyperventilation is inevitable in real life situations and is perhaps not rescuer training that requires re-visiting, rather controlling operator emotions at the Inhibitors,research,lifescience,medical time of the incident… “When the alarm sounds, we rush to the scene uncertain of what we will find. The suddenness of these events and the high stakes involved produces an adrenaline-driven arousal response. As

a result, we do everything fast, including, perhaps, bag-valve ventilation.” [13] In an effort to exclude the emotion that is often associated with real-life GBA3 circumstances, this study explored the degree of suboptimal ventilation within the control of a simulated clinical scenario. We found that 77% (n = 23) of participants who used the 1600 ml bag and 70% (n = 21) of participants using the smaller bag were unable to reach the target ventilation rate of 8–10 VPM. Other authors have documented similar trends in ventilation rates during CPR. Aufderheide and colleagues found mean ventilation rates to be as high as 30 VPM in 7 men undergoing CPR with an advanced airway,[1] while other authors have observed rates as high as 70 VPM by some emergency care providers [14].

For the in vitro skin permeation experiments, the effects of FFP, PE, and DE concentration and the screened PE content on skin permeation were investigated to optimize the DE MTDS formulation. The results of F1 to 4 were shown in

Figure 1, and the control group was F9 described in Table 1. In order to confirm the permeation enhancement of the ethanol evaporation, we added the pure drug group, which meant that the equal amount of drug to other groups was uniformly put on the skin. The transdermal permeation profiles of formulations containing different FFPs did not show significant difference. The formulation including FFP reduced the permeation of DE Inhibitors,research,lifescience,medical significantly compared with the control group, indicating that the FFP would inhibit the transdermal delivery of DE. The significant difference between the control

and pure drug group, indicating the evaporation of ethanol, would www.selleckchem.com/Sir2-like-Family.html enhance the permeation Inhibitors,research,lifescience,medical effect. Figure 1 Percutaneous permeation profiles of DE MTDS containing different film forming polymers (mean ± SD; n = 3). The results of F5 to 8 were shown in Figure 2. The control and pure drug group was the same as the one in Figure 1. As seen from the figure, the transdermal flux of them was LA > IPM > AZO > PG. LA and IPM showed comparable transdermal Inhibitors,research,lifescience,medical flux without significant difference at this concentration level. Though PG had the greatest solubility for DE, its transdermal flux was the lowest. This might attribute to the fact proven by Trottet that PG would permeate through the skin and might carry the drug with it, as shown by correlations Inhibitors,research,lifescience,medical in vitro between the permeation of both PG and the drug [28]. As the PG permeated through the skin, the “drug reservoir” in the skin would not be formed. Besides, the investigation of influence Inhibitors,research,lifescience,medical of penetration enhancer on drug permeation from volatile formulations by Hadgraft reconfirmed the

conclusion stated by Trottet. In addition, Hadgraft presented that, after administration, IPM remained in the skin to form a “patchless drug reservoir” instead of permeating through the skin like PG did [29]. The AZO group showed a relatively low tansdermal flux compared with the IPM and LA group; to some extent, it indicated that the solubility of DE in PE was a critical fact determining the transdermal flux [30, 31]. The transdermal flux of the control group is much higher compared with the group containing pure drug. This might attribute to the fact that the evaporation to of ethanol could increase the thermodynamic energy of drug. Besides, ethanol also can be used as permeation enhancer in some cases [32]. Figure 2 Percutaneous permeation profiles of dexketoprofen MTDS containing different penetration enhancers (mean ± SD; n = 3). As the results shown in Figure 1, we can see that the transdermal flux of the formulations incorporating different FFPs did not show significant difference.

2011; Phillips, 2011]. The other benzodiazepines most commonly used worldwide for rapid tranquillization are clonazepam and midazolam. TGX-221 Midazolam has a faster onset than lorazepam but requires

more frequent re-administration and has an increased risk of respiratory depression [Bak et al. 2011]. Many units have been using intramuscular clonazepam as an alternative benzodiazepine although the intramuscular route of administration is unlicensed in the Inhibitors,research,lifescience,medical UK (Marion Wetherill, Personal communication, Medical Information Department, Roche Products Ltd, 2010). Clonazepam has been reported to be used in doses up to 6 mg for rapid tranquillization in adults since the early 1990s with few side effects to produce similar tranquillization to haloperidol in a similar timeframe [Chouinard

Inhibitors,research,lifescience,medical et al. 1993]. However, there are no reports about its use in adolescent patients. Compared with lorazepam, clonazepam is associated with pharmacokinetic differences that have the potential to cause concern. Clonazepam has a slower time to peak concentration Inhibitors,research,lifescience,medical of 3 hours [Crevoisier et al. 2003] compared with a time of 1.5 hours for lorazepam [Wyeth Pharmaceuticals, 2005]. In terms of dose equivalence, 1 mg lorazepam is reported to be equivalent to 0.25–0.5 mg clonazepam [Curtin and Schulz, 2004]; however, the Maudsley guidelines [Taylor et al. 2009] state that 1 mg lorazepam is equivalent to 1–2 mg clonazepam. Information obtained from the manufacturer in 2005 gave a dose equivalence of 1–2 mg lorazepam being equivalent to 4 mg clonazepam. These differences illustrate the uncertainty of actual dose equivalence. The elimination half-life of clonazepam

is relatively long with estimates varying between 20 and 80 hours [Greenblatt et al. 1987; Berlin and Dahlstrom, 2010]. Another Inhibitors,research,lifescience,medical source reports clonazepam’s half-life to be 39 hours with that of lorazepam being 11 hours [Davies et al. 2010]. This gives the potential for dose accumulation when doses are repeated in succession. In addition, it is reported that there are secondary peaks observed following intravenous or intramuscular clonazepam, thought to be due to enterohepatic Inhibitors,research,lifescience,medical recycling, because the glucuronide of clonazepam may be deconugated by intestinal flora and reabsorbed from the intestine in the form of the parent drug [Davies Calpain et al. 2010]. In terms of brain uptake and benzodiazepine receptor occupancy, clonazepam has been found to be similar to lorazepam [Greenblatt et al. 1987]. Respiratory depression is a well-recognized but rare side effect of benzodiazepine’s, although this is increased if the benzodiazepine is taken with alcohol or is given to someone who has underlying pulmonary problems [McNaught et al. 1989]. In an adolescent forensic secure hospital it is not uncommon to require the use of intramuscular rapid tranquillization medication in the management of severe aggression and agitation for patients as young as 13 years [Hill et al. 2012].

However, some patients present atypical CDS features, with myopathy and cardiomyopathy but without ichthyosis and mutation in ABHD5. This phenotype was called NLSDM and further facilitated the discovery of new causative gene, patatin-like phospholipase domain containing 2 (PNPLA2), encoding ATGL (37). So far, the AMD3100 ic50 mutations in ABHD5 Inhibitors,research,lifescience,medical have been reported to cause protein truncations but not absence, suggesting that the mutant protein is not completely deficient but functionally impaired (33). In NLSDM, almost all mutations in PNPLA2 are located on C-terminal region, preserving the proposed

active site of the enzyme. These truncated enzyme Inhibitors,research,lifescience,medical variants have later been shown impaired in their ability to bind to cellular lipid droplets in vitro (38). NLSD is characterized by systemic TG deposition in multiple tissues, including skin, muscle, liver, central nervous

system, and blood leukocytes. Clinically, it is often present with ichthyosis, mild myopathy, hepatomegaly and, variably, ophthalmologic symptoms, neurosensory hearing loss, mental retardation and short stature (39-41). In NLSDI, the ichthyosis represents nonbullous congenital ichthyosiform erythroderma and the weakness is usually mild and predominant proximal. However, in NLSDM, no ichthyosis is observed and the slowly progressive muscle involvement Inhibitors,research,lifescience,medical could be in both proximal and distal limbs, with a predominant distal weakness in some patients. Importantly, the cardiomyopathy is exclusively seen in almost half of the patients with NLSDM (41), but not NLSDI while neurosensory defects and mental retardation are commonly seen in NLSDI but not NLSDM. Inhibitors,research,lifescience,medical CK level is usually mildly to moderately elevated. The detection Inhibitors,research,lifescience,medical of lipid accumulation in leukocytes, muscle fibers and fibroblasts is critical for the diagnosis of NLSD as the clinical manifestations of NLSD are inconstant and the biochemical investigations

for lipid dysmetabolism usually do not show any abnormality. The intracytoplasmic lipid storage in leukocytes is visible on peripheral blood smear, which is called Jordan’s anomaly. In skeletal muscles, increased lipid droplets could be observed even in presymptomatic period. Noteworthily, rimmed vacuoles in the muscles were reported in some NLSDM patients (Fig. 2D) (42, 43), suggesting a different pathomechanism from other LSMs, either which might be associated with membrane phospholipid abnormalities caused by decreased DG availability. So far, there is still no effective treatment in NLSD. The functions of ATGL and CGI-58 are still largely unknown. However, the production of the mice lacking ATGL has provided an opportunity to prompt the understanding of NSLDM (44), though unfortunately, the phenotype of CGI-58-deficient mice has not been reported yet.

A recent study has demonstrated that the expression of ACE and other target genes is enhanced by ACE-associated kinases and, therefore, ACE might have an influence on signal transduction mechanisms in the CNS and the periphery.34 Future aspects: from pharmacogenetics to pharmacogenomics Although the above findings in the field of pharmacogenetics Inhibitors,research,lifescience,medical are important, none of the positive

results can fully account for the heterogeneity in response to AD treatment. Moreover, due to the complexity of drug response, single mutations in one gene are unlikely to cause the continuous variability in response. The pharmacogenomic approach uses recent advances in experimental genomics and proteomics (the investigation of all the proteins in a cell or organism), together with the available sequence information of the Human Genome Project. These developments will not only enable genome-wide screens of several millions of SNPs without the use of specific hypotheses and a candidate gene strategy but also functional investigations of gene and/or Inhibitors,research,lifescience,medical protein expression over the whole genome or proteome.35 Although most of the data available so far derived from animal studies, the finding of Landgrebe et al,36 who Blebbistatin manufacturer performed Inhibitors,research,lifescience,medical a gene expression analysis in mice

treated with paroxetine and mirtazapine, is remarkable. The authors found that both drugs led to a downregulation of four common genes, thus suggesting that ADs with different pharmacological principles of action can share the same molecular targets even through the primary pathways on which they act are different. This finding underlines the Inhibitors,research,lifescience,medical recent hypothesis that the initial mechanisms of action trigger subsequent events in the signal transduction cascade and, finally, protein expression. Although all the above results have to be replicated and validated in further experiments and also analyzed in vivo, there is no doubt that large-scale gene and/or protein expression analysis will be performed in Inhibitors,research,lifescience,medical the near future in many laboratories by using all these rapidly growing technologies of functional genomics.

The expected results will provide new insights in the pathophysiology of psychiatric disorders. Such detailed knowledge will have profound effects on the diagnosis, prevention, and treatment of these diseases. Conclusion Although many investigations have shown Thymidine kinase that genetic variations in target proteins influence their interaction with ADs, the results are still not conclusive and far from the original concept of tailoring the drug regimen to an individual’s predisposition and predicting a patient’s response to therapeutic agents. We have to be aware that the phenotype of drug response is highly complex, representing a classical example of the outcome of gene-gene or gene-environment interactions.

Typical phenotypes of glycogenosis type II include the severe classic infantile form, characterized by severe muscle weakness and hypertrophic cardiomyopathy, almost invariably fatal by 12 months, a “non-classic” form presenting between 1 and 2 years of age and the lateonset form, presenting at any time after the age of 1 year, including juvenile and adult-onset subtypes, which are considered as part of a continuous

clinical spectrum (1). In particular the adult-onset form presents with slowly progressive proximal lower limb and/or paraspinal muscle weakness, often followed by Inhibitors,research,lifescience,medical restrictive respiratory failure, which could be life-threatening, as it is in infants and children (2). However the clinical Inhibitors,research,lifescience,medical spectrum of adultonset form is wide, ranging from asymptomatic patients with increased CK to muscle cramps and pain syndrome or rigid-spine syndrome (2, 3). Furthermore clinical severity and disease progression is greatly variable. We report on a family with 3 siblings with an unusual adult-onset Pompe disease clinically characterized by weakness of bulbar, axial and limb-girdle muscles in association with Inhibitors,research,lifescience,medical atypical histopathological changes. Case report Clinical features Patients were siblings

born from non-consanguineous parents. Patient 1 is a 47 year-old male, who came to our attention because of difficulty in moving tongue and lips and swallowing, occurring since the age of 43. Inhibitors,research,lifescience,medical Furthermore he noticed mild limb muscle wasting and weakness during the disease course. Neurological examination at the age of

45 years showed tongue selleckchem hypotrophy and weakness without fasciculations (Fig. 1), moderate orbicularis oculi and oris weakness, waddling gait with knee hyperextension and marked spine lordosis, mild neck flexor, moderate proximal upper and lower limb muscle weakness and mild thoracic scoliosis. Electromyography showed neurogenic changes Inhibitors,research,lifescience,medical in all examined limb muscles, myopathic at genioglossum and neuromyogenic at orbicularis oculi and oris. Sensory and motor nerve conduction studies were normal. Figure 1. Tongue hypotrophy in patient 2 (A) and tongue weakness against moderate resistance by the examiner in patient 1 (B). Photographs are printed with permission of the patients. Patient unless 2 is a 56-year-old woman, having CK mildly increased (range 564-634 U/L; normal value 24-195) since the age of 38, when it was assessed for the first time, and not further investigated. At the age of 48 she noticed lower limb weakness and at the age of 53 respiratory problems and mild dysphagia. On examination at first admission in our institute at the age of 54 years she displayed marked head flexors and thigh extensor muscle weakness with waddling gate, tongue hypotrophy and weakness (Fig. 1).

We were surprised to find that the sinusoids were diffusely filled with macrophages (obstructed) all of which stained heavily for CD163 and not so heavily for CD68. The CD163 (M2c) plays an immuno-regulation role (34). The soluble form of CD163 can be measured in the serum to assess the degree of macrophage activation since CD163 is an activated macrophage marker (35). To assess the sinusoidal macrophages morphologically, we performed electron microscopy (Figure 2B, C). The morphology was that of two types of macrophages. The first type was Inhibitors,research,lifescience,medical smaller and filled with phagocytic bodies (secondary

lysosomes). The second type was much larger and less common and contained lysosomes and rough ER Inhibitors,research,lifescience,medical (Figure 2). Figure 2 CD-163 positive macrophages fill all the sinusoids in a liver biopsy from an AH patient ×612 (A); EM of the same liver as A showing 2 types of macrophages in the sinusoids, phagocytic on the left (B arrow) and (C) secretory on the right ×1973 … The marked increase in the activity of CD163 positive macrophages involves a cascade of intracellular signals which lead to the secretion of IL6 and CSF1. CD163 positive macrophages are positive for the CD14 and CD16 subunits. CD-163 expression is down regulated by proinflammatory mediators

like LPS, IFNg and TNFα. IL-6 and IL-10 strongly up regulate CD-163 (36). Thus, up Inhibitors,research,lifescience,medical regulation of CD-163 as noted in the livers of AH implies that the positive staining macrophages are functionally anti-inflammatory (36). The link

between the activated macrophage in the sinusoids in the liver of patients with AH and the development of HCC is through chronic activation of TLR4 in response to a “leaky gut” increase in LPS into the portal vascular system (4). The link to Inhibitors,research,lifescience,medical HCC pathogenesis was first developed using a model of alcohol-fed NSSA Tg mice with a diet supplement of LPS. The combination, over time led to synergistic liver damage and Inhibitors,research,lifescience,medical liver tumor formation due to alcohol-induced endotoxemia (37). In this mouse model, Nanog, a stem cell/progenitor cell marker, was up regulated by TLR4 activation. CD133/Nanog positive cells were found in the mouse liver tumors that formed (38). These observations Phosphatidylinositol diacylglycerol-lyase supported the concept that the synergism between alcohol abuse and HCV leads to liver BAY 73-4506 datasheet tumorigenesis through TLR signaling up regulation of the Nanog expressing stem cells, causing them to transform into cancer stem cells in HCC formation (TISCs). Nanog is up regulated by TLR4 activation. CD133/Nanog positive cells are consequently found in the HCCs of affected Tg mice (39) (Figures 3, ​,4,4, ​,5).5). CD133, a marker for cancer stem cells, is regulated epigenetically by TGFβ (40). In fact there is compelling evidence that TGFβ signals the expansion of progenitor liver stem cells, which lead to HCC formation and stimulate the progression of the HCCs (41-43).

143 In particular, the DSPS appears to be associated with present or past depression in more than 75% of patients.144 It could be hypothesized that the failure in their social life causes social withdrawal and consequently a loss of the social cues necessary to synchronize their circadian rhythm. This might lead to an even more delayed Inhibitors,research,lifescience,medical phase shift and an enforcement of the psychological characteristics of DSPS patients, such as introversion and depressive

feelings. This situation becomes a vicious circle. The advanced sleep phase syndrome is a much less prevalent entity, characterized by habitual and involuntary sleep and wake times that are at least several hours earlier than societal means. Patients complaint of earlymorning awakening, and a diagnosis of depression may be made selleck erroneously. The maladjustment of these patients to social Inhibitors,research,lifescience,medical life occurs less frequently than in DSPS, probably because societal constraints on sleep time are less

rigid than on wake time. Conclusion Even though most psychiatric patients have a complaint about sleep, a primary sleep disorder may also result in neuropsychiatrie complications. Assessment of psychiatric status in patients with organic sleep disorders is necessary to optimize Inhibitors,research,lifescience,medical treatment strategies. An adequate assessment of psychiatric manifestations should be part of their sleep evaluation. Psychiatrists need to be alert to the possibility that patients who present with cognitive and/or affective disorders may have an organic sleep Inhibitors,research,lifescience,medical disorder such as OSAS, narcolepsy, or RLS/PLMD. In particular, an organic sleep disorder should be considered in the differential diagnosis of atypical or resistant psychiatric disorders. Selected abbreviations and acronyms CPAP continuous positive airway pressure DSPS delayed sleep phase syndrome MMPI Minnesota Multiphasic Personality Inventory OSAS Inhibitors,research,lifescience,medical obstructive

sleep apnea/hypopnea syndrome PLMD periodic leg movement disorder PLMS periodic leg movements during sleep REM rapid eye movement RLS restless legs syndrome SF-36 Short Form 36 Health Survey
Since the discovery by Kupfer and Foster1 of a link between depression and a shorter Interval between sleep onset from and the first episode of rapid eye movement sleep (REMS) than In controls, the relationship between psychiatric disorders and sleep has been the focus of intense research. Twenty years later, the results of a large meta-analysis2 could be summarized as follows. The sleep of depressive patients is usually accompanied by several anomalies when compared with controls: (1) increased sleep onset latency; (ii) increased percentage of REMS; (iii) increased REMS density; (iv) decreased sleep maintenance; (v) decreased percentage of slow-wave sleep (SWS); and (vi) shortened REMS latency (RL).