Prevalence and Clinical Correlates of Insomnia in Depressive Disorders: The CRESCEND Study

Objective

To investigate the prevalence, clinical manifestations, and clinical correlates of insomnia in a large cohort of Korean patients with depressive disorders.

Methods

We recruited 944 patients with depressive disorders from the Clinical Research Center for Depression of South Korea (CRESCEND) study. Psychometric scales were used to assess depression (HAMD), anxiety (HAMA), psychotic symptoms (BPRS), global severity (CGI-S), and functioning (SOFAS). Insomnia levels were determined by adding the scores for all items on the HAMD insomnia subscale. The clinical characteristics of the patients with ''low insomnia'' (summed score ≤3 on the HAMD subscale) and ''high insomnia'' (score ≥4) were compared using statistical analyses. A logistic regression model was constructed to identify factors associated with ''high insomnia'' status.

Results

Symptoms of insomnia were present in 93% of patients, while simultaneous early, middle, and late insomnia affected 64.1%. The high insomnia patients were characterized by significantly greater age, higher symptom levels (including core, gastrointestinal somatic and anxiety symptoms, and suicidal ideation), higher global severity and incidence of physical disorders, and greater insight. Explanatory factors of ''high insomnia'' status were older age, higher gastrointestinal somatic and anxiety symptom levels, higher global severity, and greater insight.

Conclusion

In clinical psychiatry, insomnia has been significantly underdiagnosed and undertreated. It affects most patients with depressive disorders, and is indicative of the global severity of depression. Active efforts to diagnose and treat insomnia in patients with depressive disorders should be strongly encouraged. Further research is needed to improve the diagnosis and treatment of insomnia in depressive patients.     

Association of CXCL1 promoter polymorphism with ischaemic stroke in Korean population

This is a pilot study analysing association of chemokine gene polymorphisms (CXCL1, rs3117604; CXCL2, rs3806792; CCL2, rs2857656 and rs3760396; CCL5, rs2107538) in Korean patients with ischemic stroke (IS) (n = 120) and age‐matched controls (n = 267). The CXCL1 gene and particularly T allele of rs3117604 was associated with IS.     

Bone mineral density: Methods of measurement and its influence on primary stability of miniscrews

Objective:To verify whether bone mineral density (BMD) of cortical bone, trabecular bone, and total bone influence the primary stability of orthodontic miniscrews and to verify whether there is a correlation between the measurement of BMD by cone-beam computed tomography (CBCT) and central dual-energy x-ray absorptiometry (DEXA).Materials and Methods:Twenty bovine bone sections were extracted from the pubic and iliac bones from regions with cortical thicknesses of approximately 1 mm. The BMD of the total bone block was evaluated using two methods: CBCT and DEXA. The BMD of cortical, trabecular, and total bone in the region of interest (ROI) were also evaluated by CBCT. After scanning the bone blocks, 20 self-drilling miniscrews (INP®) 1.4 mm in diameter and 6 mm long were inserted into them. The peak implant insertion torque (IT) was registered. After this, the pull-out test (PS) was performed and the maximum force registered. The Pearson correlation test was applied to verify the correlations between variables.Results:The BMD of the total bone block verified by CBCT and DEXA showed a positive and strong correlation (r  =  0.866, P  =  .000). The BMD of the ROI for cortical bone influenced the IT (r  =  0.518, P  =  .40) and the PS of miniscrews (r  =  0.713, P  =  .001, Table 2). However, the total bone BMD (verified by CBCT and DEXA) and trabecular bone BMD presented weak and not statistically significant correlations with primary stability.Conclusions:There was a positive correlation between total bone block BMD measured by DEXA and CBCT. The cortical BMD influenced the IT and PS.     

Xanthohumol ameliorates 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin–induced cellular toxicity in cultured MC3T3‐E1 osteoblastic cells

2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) is an environmental contaminant. Xanthohumol is a prenylated flavonoid found in hops (Humulus lupulus) and beer. The aim of the current study was to explore the role of xanthohumol in modulating the toxicity of TCDD in MC3T3‐E1 osteoblastic cells. In cells treated with TCDD alone, intracellular Ca²⁺ concentrations, mitochondrial membrane potential disruption, reactive oxygen species production, cardiolipin peroxidation, nitric oxide release and cytochrome P450 1A1 expression were significantly increased. TCDD treatment increased the mRNA levels of extracellular signal‐regulated kinase 1 and nuclear factor kappa B, and significantly decreased the level of protein kinase B (AKT) in MC3T3‐E1 osteoblastic cells. However, the presence of xanthohumol alleviated the pathological effects of TCDD. In addition, xanthohumol treatment significantly increased the expression of genes associated with osteoblast differentiation (alkaline phosphatase, osteocalcin, osteoprotegerin and osterix). We conclude that xanthohumol has a beneficial influence and may antagonize TCDD toxicity in osteoblastic cells.     

Association between Cognitive Impairment,Vascular Disease and All-Cause Mortality

Objective

The purpose of this study was to investigate the association between elder’s cognitive impairment and mortality. Additionally, interaction between cognitive impairment and cardio- and cerebrovascular diseases was considered.

Methods

Data from the Korean Longitudinal Study of Aging (KLoSA) from 2006 to 2014 was assessed using 10,026 participants at baseline with no missing information. Chi-square test, log-rank test, and Cox proportional hazards models were used to investigate the association between cognitive impairment and mortality.

Results

Cognitive impairment was significantly associated with mortality. With normal cognitive functioning group as reference: HR=2.329 (p<.0001) for severe cognitive impairment, HR=1.238 (p.009) for mild cognitive impairment. The association remained significant even after considering for cardio- and cerebrovascular diseases.

Conclusion

This study provided additional support to previous findings in regards to the relationship between cognitive impairment and mortality. Worse cognitive functioning increased the risk of mortality and the presence of cardio- and cerebrovascular diseases exacerbated this relationship.

     

Effectiveness and acceptability of a multidisciplinary approach in improving the care of patients with advanced chronic kidney disease: a pilot study

International Urology and Nephrology - This study aimed at determining the feasibility of conducting a large-scale pragmatic effectiveness study on the implementation of multidisciplinary care...     

alpha-MSH acetylation in the pituitary gland of the sea bream (Sparus aurata L.) in response to different backgrounds, confinement and air exposure

MSH is a pituitary hormone derived by post-translational processing from POMC and involved in stress and background adaptation. N-terminal acetylation of MSH to monoacetyl alpha-MSH or diacetyl alpha-MSH increases the bioactivity of the peptide. The aim of this study was to characterize alpha-MSH acetylation in the sea bream (Sparus aurata L.) pituitary gland in response to the stressors air exposure and confinement, as well as in fish adapted for 15 days to a white, gray or black background. Pituitary homogenates were purified by reversed-phase HPLC (RP-HPLC). The alpha-MSH content of fractions was measured by RIA. Immunoreactive RP-HPLC fractions were further analyzed by electrospray mass spectrometry and the peptide sequence determined as SYSMEHFRWGKPV-NH2. In the pituitary gland of sea bream, des-, mono- and diacetyl alpha-MSH were identified. Then plasma alpha-MSH levels were measured in sea bream adapted to different backgrounds. Surprisingly, we found the highest plasma alpha-MSH levels in white-adapted as compared with black-adapted sea bream with intermediate values for gray-adapted fish. This observation is in contrast with results that have been obtained in eel, trout or terrestrial vertebrates. Next, des-, mono- and diacetyl alpha-MSH forms were measured in homogenates of the pituitary gland and in plasma of sea bream exposed to air, to confinement, or to different backgrounds. Monoacetyl alpha-MSH was the predominant form in all control and experimental groups. The lowest content of monoacetyl alpha-MSH relative to des- and diacetyl alpha-MSH was found in white-adapted fish. Levels of des- and diacetyl alpha-MSH forms were similar under all conditions. We observed that monoacetyl alpha-MSH is the most abundant isoform in the pituitary gland after background adaptation, confinement and air exposure, in sea bream. These data indicate that the physiologically most potent isoform of alpha-MSH may vary from species to species.     

Transforming growth factor-beta trans-modulates the expression of colony stimulating factor receptors on murine hematopoietic progenitor cell lines

Transforming growth factor beta (TGF-beta) is a potent and selective growth inhibitor of early hematopoietic progenitors and leukemic cells. The cellular mechanism(s) underlying this antiproliferative effect is, however, currently unknown. In the present study, we demonstrate that TGF-beta inhibits the expression of granulocyte-macrophage colony stimulating factor (GM-CSF), interleukin 3 (IL-3), and granulocyte-CSF (G-CSF) receptors on murine factor-dependent and independent hematopoietic progenitor cell lines without a significant change in receptor affinity. A maximum reduction in GM-CSF receptor numbers of 65% to 77% was observed by 96-hour incubation with TGF-beta. The TGF- beta induced trans-down-modulation of GM-CSF receptors was prolonged, noncytotoxic but reversible, and not due to endogenous production of GM- CSF. The TGF-beta induced reduction in CSF receptor numbers preceded TGF-beta's growth inhibitory action. In addition, the ED50 (1 to 10 pmol/L) for TGF-beta's CSF receptor modulatory and antiproliferative effect was similar. The effect of TGF-beta on cell surface CSF receptor expression was specific, because the expression of other cell surface proteins (Ly 5 and Ly 17) was not affected by TGF-beta treatment, and because other growth inhibitors (tumor necrosis factor and interferon) did not affect CSF receptor expression. These data suggest that the downregulation of the growth of hematopoietic progenitor cells by TGF- beta involves reducing the cell surface expression on growth factor receptors.