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Yatham LN, Kennedy SH, Parikh SV, Schaffer A, Beaulieu S, Alda M, O’Donovan C, MacQueen G, McIntyre RS, Sharma V, Ravindran A, Young LT, Milev R, Bond DJ, Frey BN, Goldstein BI, Lafer B, Birmaher B, Ha K, Nolen WA, Berk M.
Canadian Network for Mood and Anxiety Treatments (CANMAT) and International Society for Bipolar Disorders (ISBD) collaborative update of CANMAT guidelines for the management of patients with bipolar disorder: update 2013.
Bipolar Disord 2012: 00: 000–000. © 2012 John Wiley & Sons A/S.Published by Blackwell Publishing Ltd. The Canadian Network for Mood and Anxiety Treatments published guidelines for the management of bipolar disorder in 2005, with updates in 2007 and 2009. This third update, in conjunction with the International Society for Bipolar Disorders, reviews new evidence and is designed to be used in conjunction with the previous publications.The recommendations for the management of acute mania remain largely unchanged. Lithium, valproate, and several atypical antipsychotic agents continue to be first‐line treatments for acute mania. Monotherapy with asenapine, paliperidone extended release (ER), and divalproex ER, as well as adjunctive asenapine, have been added as first‐line options.For the management of bipolar depression, lithium, lamotrigine, and quetiapine monotherapy, as well as olanzapine plus selective serotonin reuptake inhibitor (SSRI), and lithium or divalproex plus SSRI/bupropion remain first‐line options. Lurasidone monotherapy and the combination of lurasidone or lamotrigine plus lithium or divalproex have been added as a second‐line options. Ziprasidone alone or as adjunctive therapy, and adjunctive levetiracetam have been added as not‐recommended options for the treatment of bipolar depression. Lithium, lamotrigine, valproate, olanzapine, quetiapine, aripiprazole, risperidone long‐acting injection, and adjunctive ziprasidone continue to be first‐line options for maintenance treatment of bipolar disorder. Asenapine alone or as adjunctive therapy have been added as third‐line options.  相似文献   
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The objective of this study was to evaluate the critical time period between the onset of sensorineural hearing loss and cochlear implantation with respect to normal voice production in children with post-meningitic hearing loss. Acoustic measures of voice production were obtained from ten paediatric cochlear implant recipients with post-meningitic hearing loss. Acoustic measures were obtained utilising the Multi-Dimensional Voice Program and Computerized Speech Laboratory (Kay Elemetrics Corp.). Measures were based on sustained phonation of the vowel /a/. Acoustic parameters included fundamental frequency, short- and long-term frequency perturbation, and short- and long-term amplitude perturbation. Measures of fundamental frequency and short-term frequency and amplitude perturbation were comparable to values of children with normal hearing. Long-term control of frequency was within normal limits for subjects with a period of auditory deprivation of less than four months. Measures of long-term amplitude perturbation were normal for all patients except those with cochlear ossification. Early restoration of auditory feedback with cochlear implantation, the absence of cochlear ossification, residual aided hearing following meningitis, and auditory-verbal therapy were identified as factors in preserving the long-term control of frequency and amplitude in the setting of post-meningitic hearing loss.  相似文献   
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PURPOSE OF STUDY: To investigate whether the addition of triiodothyronine (T3) helps relieve depressive symptoms in non-hypothyroid major depressive disorder patients who failed to respond to an adequate course of standard SSRI antidepressant treatments. METHODS: Patients who fulfilled the DSM-IV criteria for non-psychotic major depression, able to give informed consent, and failed to show satisfactory antidepressant response after a minimum of six weeks adequate treatment were recruited. To enter the study their Hamilton Depression (17-item HAMD) score had to be 18 or more, thyroid-stimulating hormone (TSH) value within the normal range, and a normal thyrotropin releasing hormone-stimulation test (TRH-ST). All patients continued taking the same SSRI which they had been taking before they entered the study. At the completion of TRH-SH they were all started on 25 microg of T3 and the dose was increased to 50 microg within a week when tolerated; they continued the combination of T3 and the SSRI for a minimum of three weeks. RESULTS: Twelve patients, comprising eight females and four males, entered the study. One female patient withdrew during the first week of side effects, eleven patients completed the trial. The patients ranged from 26 to 77 years of age, with the mean age for males and females being 52.3 and 45.1 years, respectively. Five patients were taking sertraline (mean dose = 130 mg/day) and 4 were taking citalopram (mean dose = 50 mg/day), two were on fluvoxamine (150 mg/day) and one patient was on 40 mg of paroxetine. The women took a mean daily dose of 40.6 microg of T3 for a mean duration of 3.75 weeks, while the men were on a mean daily dose of 43.8 mug of T3 for 3.5 weeks. T3 augmentation was associated with a statistically significant drop (p < .003) in the mean HAMD at end of the three weeks compared to baseline scores. Five patients (42%) showed >or=50% improvement on HAMD scores, with three achieving full remission (HAMD scores相似文献   
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The pathophysiology of platelet dysfunction in the Wiskott-Aldrich immune deficiency syndrome (WAS) remains unclear. Using flow cytometry, we have characterized the functional properties of platelets from 10 children with WAS. Patients with WAS had thrombocytopenia, small platelets, increased platelet-associated IgG and reduced platelet-dense granule content. Levels of reticulated 'young' platelets were normal in the WAS patients. Although the mean numbers of platelet glycoprotein (GP) Ib, GPIIbIIIa and GPIV molecules per platelet appeared lower in WAS patients than in healthy controls, analysis of similar-sized platelets revealed the mean number of GPIb molecules per platelet to be comparable in patients and normal controls. Surface GPIIbIIIa and GPIV expression was, however, significantly lower on the WAS platelets than on normal platelets. Compared with normal platelets, WAS platelets showed a reduced ability to modulate GPIIbIIIa expression following thrombin stimulation. In addition, thrombin- and ADP-induced expression of CD62P and CD63 was defective in WAS platelets. Phallacidin staining of the WAS platelets revealed less F-actin content than in normal platelets. Together, these data suggest that the reduced platelet number and function in WAS reflects, at least in part, a defect in bone marrow production as well as an intrinsic platelet abnormality.  相似文献   
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