Comorbid anxiety with depression predicts poor outcomes with a higher percentage of treatment resistance than either disorder occurring alone. Overlap of anxiety and depression complicates diagnosis and renders treatment challenging. A vital step in treatment of such comorbidity is careful and comprehensive diagnostic assessment. We attempt to explain various psychosocial and pharmacological approaches for treatment of comorbid anxiety and depression. For the psychosocial component, we focus only on generalized anxiety disorder based on the following theoretical models: (1) "the avoidance model"; (2) "the intolerance of uncertainty model"; (3) "the meta-cognitive model"; (4) "the emotion dysregulation model"; and (5) "the acceptance based model". For depression, the following theoretical models are explicated: (1) "the cognitive model"; (2) "the behavioral activation model"; and (3) "the interpersonal model". Integration of these approaches is suggested. The treatment of comorbid anxiety and depression necessitates specific psychopharmacological adjustments as compared to treating either condition alone. Serotonin reuptake inhibitors are considered first-line treatment in uncomplicated depression comorbid with a spectrum of anxiety disorders. Short-acting benzodiazepines (BZDs) are an important "bridging strategy" to address an acute anxiety component. In patients with comorbid substance abuse, avoidance of BZDs is recommended and we advise using an atypical antipsychotic in lieu of BZDs. For mixed anxiety and depression comorbid with bipolar disorder, we recommend augmentation of an antidepressant with either lamotrigine or an atypical agent. Combination and augmentation therapies in the treatment of comorbid conditions vis-à-vis monotherapy may be necessary for positive outcomes. Combination therapy with tricyclic antidepressants, gabapentin and selective serotonin/norepinephrine reuptake inhibitors (e.g., duloxetine) are specifically useful for comorbid chronic pain syndromes. Aripiprazole, quetiapine, risperidone and other novel atypical agents may be effective as augmentations. For treatment-resistant patients, we recommend a "stacking approach" not dissimilar from treatment of hypertension In conclusion, we delineate a comprehensive approach comprising integration of various psychosocial approaches and incremental pharmacological interventions entailing bridging strategies, augmentation therapies and ultimately stacking approaches towards effectively treating comorbid anxiety and depression.

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A 1.8 GHz power amplifier for a polar transmitter application is implemented with 0.18 µm RF CMOS technology, and a differential line inductor is proposed for the differential circuit. The differential line inductor is used as a low power matching network in the stage-convertible power amplifier in order to increase the efficiency of a low output power region. The power amplifier achieved a power-added efficiency of 41% at a maximum output power of 31.5 dBm. The low power efficiency improvement for the power amplifier is 81% at an output power of 20 dBm.

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A fully integrated CMOS RF power amplifier for a 1.8 GHz band EDGE polar transmitter is presented. It is implemented with 0.18-µm CMOS process. The output power is 33.4 ~ 33.5 dBm and the power added efficiency is 39 ~ 41 percent when the frequency varies from 1.71 to 1.91 GHz. The dynamic range is increased by 12 dB with the use of the proposed switchable transformer, which meets the EDGE dynamic range requirement of 37 dB when the supply voltage changes from 0.8 to 3.3 V.Index Terms -CMOS integrated circuits, MOSFET power amplifiers, MMIC power amplifiers, UHF power amplifiers.