The Economic Impact of Loss of Performance Due to Absenteeism and Presenteeism Caused by Depressive Symptoms and Comorbid Health Conditions among Japanese Workers

We aimed to determine the economic impact of absenteeism and presenteeism from five conditions potentially comorbid with depressive symptoms—back or neck disorders, depression, anxiety, or emotional disorders, chronic headaches, stomach or bowel disorders, and insomnia—among Japanese workers aged 18–59 yr. Participants from 19 workplaces anonymously completed Stanford Presenteeism Scale questionnaires. Participants identified one primary health condition and determined the resultant performance loss (0–100%) over the previous 4-wk period. We estimated the wage loss by gender, using 10-yr age bands. A total of 6,777 participants undertook the study. Of these, we extracted the data for those in the 18–59 yr age band who chose targeted primary health conditions (males, 2,535; females 2,465). The primary health condition identified was back or neck disorders. We found that wage loss due to presenteeism and absenteeism per 100 workers across all 10-yr age bands was high for back or neck disorders. Wage loss per person was relatively high among those identifying depression, anxiety, or emotional disorders. These findings offer insight into developing strategies for workplace interventions on increasing work performance.     

Beneficial biological effects and the underlying mechanisms of molecular hydrogen - comprehensive review of 321 original articles -

Molecular hydrogen (H2) is clinically administered; however, in some hospitals, H2 is given to patients without consideration of its safe use. In the present study, we prepared convenient and safe devices for the drinking of super-saturated H2 water, for intravenous drip infusion of H2-rich saline, and for the inhalation of H2 gas. In order to provide useful information for researchers using these devices, the changes in H2 concentration were studied. Our experimental results should contribute to the advance of non-clinical and clinical research in H2 medicine.     

Effects of high-intensity and blood flow-restricted low-intensity resistance training on carotid arterial compliance: role of blood pressure during training sessions

We examined the effects of high-intensity resistance training (HIT) and low-intensity blood flow-restricted (LI-BFR) resistance training on carotid arterial compliance. Nineteen young men were randomly divided into HIT (n = 9) or LI-BFR (n = 10) groups. The HIT and LI-BFR groups performed 75 and 30 %, respectively, of one-repetition maximum (1-RM) bench press exercise, 3 days per week for 6 weeks. During the training sessions, the LI-BFR group wore elastic cuffs around the most proximal region of both arms. Muscle cross-sectional area (CSA), 1-RM strength, and carotid arterial compliance were measured before and 3 days after the final training session. Acute changes in systolic arterial pressure (SAP), plasma endothelin-1 (ET-1), nitrite/nitrate (NOx), and noradrenalin concentrations were also measured during and after a bout of training session. The training led to significant increases (P < 0.01) in bench press 1-RM and arm and chest muscle CSA in the two training groups. Carotid arterial compliance decreased significantly (P < 0.05) in the HIT group, but not in the LI-BFR group. There was a significant correlation (r = ?0.533, P < 0.05) between the change in carotid arterial compliance and the acute change in SAP during training sessions; however, ET-1 and NOx did not correlate with carotid arterial compliance. Our results suggest that muscle CSA and strength increased following 6 weeks of both HIT and LI-BFR training. However, carotid arterial compliance decreased in only the HIT group, and the changes were correlated with SAP elevations during exercise sessions.     

Prediction of healing progress of pressure ulcers by distribution analysis of protein markers on necrotic tissue: A retrospective cohort study

Predicting the short‐term healing progress of pressure ulcers is important for providing timely and appropriate intervention. Although there are some prediction methods available, these are unsuitable for ulcers with abundant necrotic tissue. We aimed to elucidate the relationship between necrotic tissue alteration and protein distributions on ulcers to establish a new prediction method. Thirty‐eight pressure ulcers were retrospectively analyzed. Protein distributions on necrotic tissue were evaluated by the wound blotting at three levels: marker protein positivity, signal patterns (speckled, heterogeneous, or homogeneous), and the occupation of heterogeneous pattern. Peroxidase, alkaline phosphatase, tumor necrosis factor α, and matrix metalloproteinase‐2 were used as marker proteins. One‐week necrotic tissue alteration was classified as liquefaction or nonliquefaction, and associations with protein distributions were analyzed. The peroxidase positivity was significantly higher in the liquefaction than in the nonliquefaction (p = 0.031). In peroxidase‐positive samples, the proportion of nonliquefaction samples was significantly higher in the heterogeneous pattern (p = 0.029). In the heterogeneous‐patterned samples, the proportion of samples with an occupation values greater than the median value tended to be higher in the nonliquefaction (p = 0.087). There was no significant relationship between liquefaction and other markers. Peroxidase positivity predicts 1‐week liquefaction of necrotic tissue, while a heterogeneous pattern indicates nonliquefaction.     

Discovery and structure–activity relationship of plastoquinone analogs as anticancer agents against chronic myelogenous leukemia cells

Two series of amino‐1,4‐benzoquinones ( AQ1–18 ) based on the structural analogs of plastoquinones were synthesized and the structure–activity relationship against chronic myelogenous leukemia activity was examined. All of the synthesized compounds were tested for their cytotoxic effects on different leukemic cell lines. Of interest, AQ15 exhibited a better selectivity than the reference drug imatinib on cancer cells. Owing to this, AQ15 was selected for a further apoptosis/necrosis evaluation where AQ15 ‐treated K562 cells demonstrated similar apoptotic effects like imatinib‐treated cells at their IC₅₀ values. The inhibitory effects of AQ15 and the other three compounds with various activities against eight tyrosine kinases, including ABL1, were investigated. AQ15 showed weak activity against ABL1, and a correlation was observed between the anti‐K562 and anti‐ABL1 activities. The binding mode of AQ15 into the ATP binding pocket of ABL1 kinase was predicted in silico, showing the formation of some key interactions. In addition, AQ15 was shown to suppress the downstream signaling of BCR‐ABL in K562 cells. Finally, AQ15 obviously cleaved DNA in the presence of an iron(II) complex system, indicating that this can be the major mechanism of its antiproliferative action, whereas the mild inhibition of ABL kinase is just in‐part mechanism of its overall outstanding cellular activity.     

SUMO and Alzheimer’s Disease

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline and is the most common cause of dementia in the elderly. Histopathologically, AD features insoluble aggregates of two proteins in the brain, amyloid-β (Aβ) and the microtubule-associated protein tau, both of which have been linked to the small ubiquitin-like modifier (SUMO). A large body of research has elucidated many of the molecular and cellular pathways that underlie AD, including those involving the abnormal Aβ and tau aggregates. However, a full understanding of the etiology and pathogenesis of the disease has remained elusive. Consequently, there are currently no effective therapeutic options that can modify the disease progression and slow or stop the decline of cognitive functioning. As part of the effort to address this lacking, there needs a better understanding of the signaling pathways that become impaired under AD pathology, including the regulatory mechanisms that normally control those networks. One such mechanism involves SUMOylation, which is a post-translational modification (PTM) that is involved in regulating many aspects of cell biology and has also been found to have several critical neuron-specific roles. Early studies have indicated that the SUMO system is likely altered with AD-type pathology, which may impact Aβ levels and tau aggregation. Although still a relatively unexplored topic, SUMOylation will likely emerge as a significant factor in AD pathogenesis in ways which may be somewhat analogous to other regulatory PTMs such as phosphorylation. Thus, in addition to the upstream effects on tau and Aβ processing, there may also be downstream effects mediated by Aβ aggregates or other AD-related factors on SUMO-regulated signaling pathways. Multiple proteins that have functions relevant to AD pathology have been identified as SUMO substrates, including those involved in synaptic physiology, mitochondrial dynamics, and inflammatory signaling. Ongoing studies will determine how these SUMO-regulated functions in neurons and glial cells may be impacted by Aβ and AD pathology. Here, we present a review of the current literature on the involvement of SUMO in AD, as well as an overview of the SUMOylated proteins and pathways that are potentially dysregulated with AD pathogenesis.