Depression has often been associated with increased negative affect reactivity to stress (Stress-Sensitivity) and reduced capacity to experience pleasure or positive affect (Reward Experience). To ...date, no studies have prospectively examined changes in Stress-Sensitivity and Reward Experience following antidepressant treatment. The sample included 83 depressed patients and 22 healthy controls. A randomized controlled trial was carried out with patients receiving either imipramine or placebo for 6 weeks. At baseline and 6 weeks, patients and controls participated in an Experience Sampling procedure, prospectively measuring ecologically valid daily life appraisals of activities and mood states. The course of depression was assessed with the Hamilton Depression Rating Scale (HDRS). Multilevel linear regression analyses showed that patients had higher negative and lower positive appraisals of activities than controls. In addition, patients showed increased Stress-Sensitivity (negative affect reactivity to negatively appraised activities). Treatment with imipramine decreased Stress-Sensitivity and increased Reward Experience (positive affect reactivity to positively appraised activities). Changes in Stress-Sensitivity and Reward Experience were in part reducible to changes in the process of activity appraisal itself. However, increase in Reward Experience, but not decrease in Stress-Sensitivity, discriminated between patients who responded and those who did not, independent of changes in the process of activity appraisal itself. Response to treatment in depression may be conditional on restoration of hedonic capacity, the cerebral substrate of which requires further study in relation to antidepressant response. A search for (synergistic) antidepressant therapies specifically targeting ability to experience reward may be warranted.
For the first time, a full platform using FDSOI technology is presented. This work demonstrates 32% and 84% speed boost at 1.0V and 0.6V respectively, without adding process complexity compared to ...standard bulk technology. We show how memory access time can be significantly reduced thanks to high Iread, by keeping competitive leakage values. Yield of ~14Mb SRAM cells is demonstrated, allowing to measure for the first time Vmin of SRAM arrays.
Epitaxy of Si or SiGe on Si substrates needs perfectly cleaned substrates. When bulk substrates can be cleaned at high temperature, FD-SOI substrates must be cleaned at low temperature that means by ...wet or plasma cleans (or any combination). The defectivity, chemical contamination and morphology of surfaces cleaned by different methods described in Table I have been checked by different experimental methods.
Display omitted
•Conventional cleaning processes of Si and SiGe surfaces require high temperature treatments incompatible with ultra-thin film technology.•We propose a low temperature surface cleaning process, based on a combination of wet-clean and plasma-clean processes that avoids the film dewetting and enables subsequent epitaxial growth.•The so-proposed new recipe is perfectly suited for FD-SOI technology nodes.
Ultra thin Silicon films of Silicon-on-Insulator technology are metastable and thus cannot be submitted to high temperature treatments that may roughen or disrupt the film during the set of technological steps required for device fabrication. This paper concerns the development of an efficient low temperature cleaning process of Si and SiGe surfaces that enables a subsequent good-quality epitaxy of raised source and drain. For this purpose wet-clean, plasma-clean and several combinations of both are used. We thus propose two effective surface cleaning processes with low thermal budget optimized for FD-SOI technology.
Andersen-Tawil syndrome (ATS) and Noonan syndrome (NS) are both autosomal dominantly inherited disorders that share anomalies in the same body systems, i.e. cardiovascular system, skeleton, growth, ...and face morphology. Here we report a patient meeting clinical diagnostic criteria for NS in whom no variant in one of the genes known to cause NS was found and a pathogenic variant in KCNJ2 (c.653G > C, p.(Arg218Pro)) was demonstrated. Because of manifestations typical for NS and previously not described in ATS (broad neck, low hairline and pectus excavatum), this may indicate there is a phenotypical overlap between ATS and NS, although we cannot exclude that the patient has an additional, hitherto undetected variant in another gene that explains the NS features. Further studies into a functional relation between KCNJ2 and the RAS/MAPK pathway are needed to determine this further.
Background
Mutations in the myosin heavy chain 7 (
MYH7
) gene commonly cause cardiomyopathy but are less frequently associated with congenital heart defects.
Methods
In this study, we describe ...a mutation in the
MYH7
gene, c. 5754C > G; p. (Asn1918Lys), present in 15 probands and 65 family members.
Results
Of the 80 carriers (age range 0–88 years), 46 (57.5%) had cardiomyopathy (mainly dilated cardiomyopathy (DCM)) and seven (8.8%) had a congenital heart defect. Childhood onset of cardiomyopathy was present in almost 10% of carriers. However, in only a slight majority (53.7%) was the left ventricular ejection fraction reduced and almost no arrhythmias or conduction disorders were noted. Moreover, only one carrier required heart transplantation and nine (11.3%) an implantable cardioverter defibrillator. In addition, the standardised mortality ratio for
MYH7
carriers was not significantly increased. Whole exome sequencing in several cases with paediatric onset of DCM and one with isolated congenital heart defects did not reveal additional known disease-causing variants. Haplotype analysis suggests that the
MYH7
variant is a founder mutation, and is therefore the first Dutch founder mutation identified in the
MYH7
gene. The mutation appears to have originated in the western region of the province of South Holland between 500 and 900 years ago.
Conclusion
Clinically, the p. (Asn1918Lys) mutation is associated with congenital heart defects and/or cardiomyopathy at young age but with a relatively benign course.
The Fully-Depleted Silicon-on-Insulator (FD-SOI) technology for advanced CMOS devices is based on SOI substrates formed by an ultra-thin Si or SiGe film on a thick insulator. A reduction of parasitic ...resistances of such CMOS components is obtained with the Raised Source and Drain (RSD) technology. In this work we show that modifying the Siconi™ plasma-based etching process widely used in microelectronic and/or combining it to wet-etching methods allows to improve the principal steps of fabrication of RSD FD-SOI CMOS devices.
More precisely, using sampling areas on 300mm wafers that simulate the principal stages of FD-SOI building, (i) we show that a modified SiCoNi process may be used to increase the etching selectivity necessary to dissolve the oxide layer while maintaining a low-k spacer of high quality, (ii) we propose a combination of optimized SiCoNi-dry and wet etching that reduces the post-etching roughness and the contamination level of the channel surface before the subsequent epitaxy.
Description of different SiGe samples (300mm SOI wafer) under study: 1) initial silicon bulk used as a reference material, 2) SiGe layer grown by epitaxy (channel layer), 3) nitride silicon deposition (low-k dielectric layer), 4) silicon nitride etching, 5) surfaces cleaned by various processes, 6) SiGe:B layer grown by epitaxy (Raised-Source-Drain epitaxy). Display omitted
•FD-SOI technology requires the use of very thin channel and thus the use of raised sources and drains.•The quality of the epitaxially grown RSD depends on the surface quality of the channel and thus depends on many technological steps preliminar to the RSD subsequent growth.•The present report describes how etching and cleaning methods may be improved to reach high quality FD-SOI based CMOS devices.
In this small series, local intrasinus catheter-directed heparin infusion with or without balloon thrombectomy was safe in the treatment of dural venous sinus thrombosis (DVST). Although systemic ...anticoagulation (SAC) is the treatment of choice, there is a lack of consensus regarding the best treatment should SAC fail or be contraindicated. We present our institutional experience with 16 patients in whom failure of, or contraindication to, SAC occurred and who subsequently underwent intrasinus catheter-directed heparin infusion with or without balloon thrombectomy.
A retrospective review of 16 patients ranging in age from 14 days to 77 years who had intrasinus catheter-directed heparin infusion was undertaken with 9 male and 7 female patients identified. Of these 16 patients, 4 (25%) had a contraindication to SAC and SAC failed in 12 (75%). Technically successful intrasinus infusion catheter placement was achieved in all 16 patients (100%). Mean duration of infusion was 3.3 days (range, 1-6 days). Adjunctive balloon thrombectomy was performed in 9 (56.3%) of 16 patients. No procedure-related mortality occurred.
Partial and complete sinus recanalization occurred in 10 (62.5%) of 16 patients and 1 (6.3%) of 16 patients, respectively. There were 3 deaths (18.8%) attributed to disease progression. At most recent clinical follow-up (mean, 9.3 months), 11 (84.6%) of 13 surviving patients were independent, with a modified Rankin Scale (mRS) score of 1 or less.
Local intrasinus catheter-directed heparin infusion with or without adjunctive balloon thrombectomy seems to be a safe and effective treatment of DVST in patients in whom SAC failed or in whom there was a contraindication to SAC. In addition, the risk for symptomatic intracranial hemorrhage may be significantly lower than intrasinus infusion of thrombolytics.
More than 11 genetic causes of severe combined immunodeficiency (SCID) have been identified, affecting development and/or function of T lymphocytes, and sometimes B lymphocytes and natural killer ...(NK) cells. Deletion of 22q11.2 is associated with immunodeficiency, although less than 1% of cases are associated with T-B + NK + SCID phenotype. Severe immunodeficiency with CHARGE syndrome has been noted only rarely Omenn syndrome is a rare autosomal recessive form of SCID with erythroderma, hepatosplenomegaly, lymphadenopathy and alopecia. Hypomorphic recombination activating genes 1 and 2 mutations were first described in patients with Omenn syndrome. More recently, defects in Artemis, RMRP, IL7Rα and common gamma chain genes have been described. We describe four patients with mutations in CHD7, who had clinical features of CHARGE syndrome and who had T-B + NK + SCID (two patients) or clinical features consistent with Omenn syndrome (two patients). Immunodeficiency in patients with DiGeorge syndrome is well recognized - CHARGE syndrome should now be added to the causes of T-B + NK + SCID, and mutations in the CHD7 gene may be associated with Omenn-like syndrome.
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