Impact of Depression on Work Productivity and Its Improvement after Outpatient Treatment with Antidepressants

AbstractObjectiveDepressive disorders influence socioeconomic burden at both the individual and organizational levels. This study estimates the lost productive time (LPT) and its resulting cost among workers with major depressive disorder (MDD) compared with a comparison group. It also estimates the change in productivity after 8 weeks of outpatient psychiatric treatment with antidepressants.MethodsWorking patients diagnosed with MDD without other major physical or mental disorders were recruited (n = 102), along with age- and sex-matched healthy controls from the Seoul Metropolitan area (n = 91). The World Health Organization's Health and Work Performance Questionnaire and the Hamilton Rating Scale for Depression were utilized to measure productivity and severity of depression, respectively, at baseline and at 8 weeks of treatment.ResultsThe LPT from absenteeism and presenteeism (reduced performance while present at work) was significantly higher among the MDD group. Workers with MDD averaged costs due to LPT at 33.4% of their average annual salary, whereas the comparison group averaged costs of 2.5% of annual salary. After 8 weeks of treatment, absenteeism and clinical symptoms of depression were significantly reduced and associated with significant improvement in self-rated job performance (31.8%) or cost savings of $7508 per employee per year.ConclusionsWe confirmed that significant productivity loss arises from MDD and that this loss can be reduced with psychiatric intervention after a time period as short as 8 weeks. Mental health professionals should work with employers to devise a cost-effective system to provide workers with accessible quality care

A Synonymous Genetic Alteration of LMX1B in a Family with Nail-Patella Syndrome

The gene responsible for nail-patella syndrome, LMX1B, has recently been identified on chromosome 9q. Here we present a patient with nail-patella syndrome and an autosomal dominant pattern of inheritance. A 17-year-old girl visited our clinic for the evaluation and treatment of proteinuria. She had dystrophic nails, palpable iliac horns, and hypoplastic patellae. Electron microscopy of a renal biopsy showed irregular thickening of the glomerular basement membrane. A family history over three generations revealed five affected family members. Genetic analysis found a change of TCG to TCC, resulting in a synonymous alteration at codon 219 in exon 4 of the LMX1B gene in two affected family members. The same alteration was not detected in an unaffected family member. This is the first report of familial nail-patella syndrome associated with an LMX1B in Korea mutation, However, we can not completely rule out the possibility that the G-to-C change may be a single nucleotide polymorphism as this genetic mutation cause no alteration in amino acid sequence of LMX1B

Two Cases of Adrenal Abscesses Following Histoacryl® (N-butyl-2-cyanocrylate) Injection

We report two cases of adrenal abscesses that occurred following a Histoacryl® (N-butyl-2-cyanocrylate) injection for variceal bleeding. Patients had been diagnosed with alcoholic liver cirrhosis and gastric varices bleeding and received a Histoacryl® injection for the variceal bleeding. Patients had fever and abdominal tenderness and were diagnosed with an adrenal abscess at 2 months following the Histoacryl® injection. One patient received open drainage and the other underwent percutaneous drainage. When a patient has previously been injected with Histoacryl® for the treatment of variceal bleeding and presents with fever, an evaluation for an unusual complication such as adrenal abscess is recommended

Pyruvate Dehydrogenase Kinase Is a Metabolic Checkpoint for Polarization of Macrophages to the M1 Phenotype

Metabolic reprogramming during macrophage polarization supports the effector functions of these cells in health and disease. Here, we demonstrate that pyruvate dehydrogenase kinase (PDK), which inhibits the pyruvate dehydrogenase-mediated conversion of cytosolic pyruvate to mitochondrial acetyl-CoA, functions as a metabolic checkpoint in M1 macrophages. Polarization was not prevented by PDK2 or PDK4 deletion but was fully prevented by the combined deletion of PDK2 and PDK4; this lack of polarization was correlated with improved mitochondrial respiration and rewiring of metabolic breaks that are characterized by increased glycolytic intermediates and reduced metabolites in the TCA cycle. Genetic deletion or pharmacological inhibition of PDK2/4 prevents polarization of macrophages to the M1 phenotype in response to inflammatory stimuli (lipopolysaccharide plus IFN-γ). Transplantation of PDK2/4-deficient bone marrow into irradiated wild-type mice to produce mice with PDK2/4-deficient myeloid cells prevented M1 polarization, reduced obesity-associated insulin resistance, and ameliorated adipose tissue inflammation. A novel, pharmacological PDK inhibitor, KPLH1130, improved high-fat diet-induced insulin resistance; this was correlated with a reduction in the levels of pro-inflammatory markers and improved mitochondrial function. These studies identify PDK2/4 as a metabolic checkpoint for M1 phenotype polarization of macrophages, which could potentially be exploited as a novel therapeutic target for obesity-associated metabolic disorders and other inflammatory conditions

Robust H∞ Control For Uncertain Nonlinear Active Magnetic Bearing Systems Via Takagi-Sugeno Fuzzy Models

In this paper, a systematic procedure to design the robust H ∞, fuzzy controller for a nonlinear active magnetic bearing (AMB) system affected by time-varying parametric uncertainties is presented. First, the continuous-time Takagi-Sugeno (T-S) fuzzy model is employed to represent the nonlinear AMB system. Next, based on the obtained fuzzy model, sufficient conditions are derived in terms of linear matrix inequalities (LMIs) for robust stability and H∞, performance of the control system. The main feature of this paper is that some drawbacks existing in the previous approaches such as truncation errors and nonconvex bilinear matrix inequality (BMI) problem are eliminated by utilizing the homogeneous fuzzy model which includes no bias terms in the local state space models rather than the affine one which includes bias terms. Hence, the design method presented here will prove to be more tractable and accessible than the previous ones. Finally, numerical simulations demonstrate the effectiveness of the proposed approach. © ICROS, KIEE and Springer 2010

A Comparative Study of Fault Diagnosis for Train Door System: Traditional versus Deep Learning Approaches

A fault diagnosis of a train door system is carried out using the motor current signal that operates the door. A test rig is prepared, in which various fault modes are examined by applying extreme conditions, as well as the natural and artificial wears of critical components. Two approaches are undertaken toward the fault classification for comparative purposes: one is the traditional feature-based method that requires several steps for the processing features such as signal segmentation, the extraction of time-domain features, selection by Fisher’s discrimination, and K-nearest neighbor. The other is the deep learning approach by employing the convolutional neural network (CNN) to skip the hand-crafted features extraction process. In the traditional approach, good accuracy is found only after the current signal is segmented into the three velocity regimes, which enhances the discrimination capability. In the CNN, superior accuracy is obtained even by the original raw signal, which is more convenient in terms of implementation. However, in view of practical applications, the traditional approach is more useful in that the features processing can be easily applied to assess the health state of each fault and monitor the progression over time in the real operation, which is not enabled by the deep learning approach

CRISPR-Cas9 Mediated Telomere Removal Leads to Mitochondrial Stress and Protein Aggregation

Aging is considered the major risk factor for neurodegenerative diseases including Parkinson’s disease (PD). Telomere shortening is associated with cellular senescence. In this regard, pharmacological or genetic inhibition of telomerase activity has been used to model cellular aging. Here, we employed CRISPR-Cas9 technology to instantly remove the telomere to induce aging in a neuroblastoma cell line. Expression of both Cas9 and guide RNA targeting telomere repeats ablated the telomere, leading to retardation of cell proliferation. Instant deletion of telomere in SH-SY5Y cells impaired mitochondrial function with diminished mitochondrial respiration and cell viability. Supporting the pathological relevance of cell aging by CRISPR-Cas9 mediated telomere removal, alterations were observed in the levels of PD-associated proteins including PTEN-induced putative kinase 1, peroxisome proliferator-activated receptor γ coactivator 1-α, nuclear respiratory factor 1, parkin, and aminoacyl tRNA synthetase complex interacting multifunctional protein 2. Significantly, α-synuclein expression in the background of telomere removal led to the enhancement of protein aggregation, suggesting positive feed-forward interaction between aging and PD pathogenesis. Collectively, our results demonstrate that CRISPR-Cas9 can be used to efficiently model cellular aging and PD