Objectives
In this study we investigated the correlation between depression and frailty in older adults. Additionally, correlations among study designs (prospective vs. cross‐sectional), regions, ...depression indices, frailty indices, covariance corrections, and sexes were explored to support the analysis.
Methods
A systematic literature review and meta‐analysis were conducted. A total of 84,351 older adults, all 65 years of age or older, were analyzed. Both authors independently extracted and examined retrieved articles. Searched keywords included “depression” or “depressive”; “frailty” or “frail”; and “older people,” “elderly,” “geriatric,” or “senior.” Articles published between January 2000 and December 2016 were searched. A literature quality assessment was conducted in accordance with the guidelines of the Preferred Reporting Items for Systematic
Reviews and Meta‐Analyses
Systematic literature searches were conducted on the Embase, PubMed, MEDLINE, Cumulative Index to Nursing and Allied Health Literature, and Cochrane Library databases, and collected studies were analyzed using a random effects model.
Results
Fourteen studies on people 65 years of age or older were collected, and a correlation analysis was conducted for depression and frailty. According to the meta‐analysis, the risk for frailty due to depression was nonsignificant among the subgroups for study design (p for heterogeneity = .149), region (p = .429), depression criteria (p = .934), covariate adjustment (p = .702), and frailty criteria (p = .661). Notably, the risk for frailty due to depression was significantly higher in men than in women (pooled odds ratios for men and women: 4.76 and 2.25, respectively; Qbetween χ2 = 9.93, p = .002).
Conclusion
Older adults with depression are more prone to frailty than are those without depression. Regardless of study design, region, depression index, frailty index, and covariance corrections, no significant differences were observed in the results of studies on depression and frailty in older adults. The only factor that had a significant influence was sex; older men with depression were at a higher risk for frailty than were older women with depression.
Clinical Relevance
Depression and frailty are pertinent health concerns related to geriatric syndromes. Because older adults with depression have a high risk for frailty, nursing personnel should use a depression index as early as possible to screen for depression and further reduce the occurrence of frailty in older adults. Furthermore, based on the aforementioned differences between the sexes, special attention should be paid to older men with depression to reduce their risk for frailty.
Tumor necrosis factor (TNF)‐α activates a diverse array of signaling pathways in vascular endothelial cells (ECs), leading to the inflammatory phenotype that contributes to the vascular dysfunction ...and neutrophil emigration in patients with sepsis. To date, it is not well understood what key regulator might coordinate signaling pathways to achieve inflammatory response in TNF‐α‐stimulated ECs. This study investigated the role of dual specificity phosphatase‐6 (DUSP6) in the regulation of endothelial inflammation. Using knockout mice, we found that DUSP6 is important for TNF‐α‐induced endothelial intercellular adhesion molecule‐1 (ICAM‐1) expression in aorta and in vein. Moreover, genetic deletion of Dusp6 in pulmonary circulation significantly alleviated the susceptibility of mice to lung injury caused by neutrophil recruitment during experimental sepsis induced by TNF‐α or lipopolysaccharide (LPS). The role of DUSP6 was further investigated in primary human umbilical vein endothelial cells (HUVECs). Employing RNAi approach in which endogenous DUSP6 was ablated, we showed a critical function of DUSP6 to facilitate TNF‐α‐induced ICAM‐1 expression and endothelial leukocyte interaction. Interestingly, DUSP6‐promoted endothelial inflammation is independent of extracellular signaling‐regulated kinase (ERK) signaling. On the other hand, inducible DUSP6 leads to activation of canonical nuclear factor (NF)‐κB‐mediated transcription of ICAM‐1 gene in TNF‐α‐stimulated human ECs. These results are the first to demonstrate a positive role of DUSP6 in endothelial inflammation‐mediated pathological process and the underlying mechanism through which DUSP6 promotes NF‐κB signaling in the inflamed ECs. Our findings suggest that manipulation of DUSP6 holds great potential for the treatment of acute inflammatory diseases.
Tumour necrosis factor (TNF)‐α‐mediated signalling in vascular endothelial cells leads to inflammation, vascular dysfunction and neutrophil emigration; however, the pathways through which TNF‐α induces these phenotypes are not clear. Shu‐Fang Hsu et al. now report an important role for dual specificity phosphatase‐6 (DUSP6) in endothelial inflammation. They show that the ligand‐bound TNF‐α receptor activates DUSP6–NF‐κB signalling, leading to inducible expression of ICAM‐1 on the surface of vascular endothelium. This, in turn, promotes leukocyte recruitment and an inflammatory response. These findings provide a mechanism by which DUSP6 promotes NF‐κB signalling and suggests that targeting DUSP6 might have therapeutic benefit in acute inflammatory diseases.
Orexin A and B are hypothalamic peptides known to modulate arousal, feeding, and reward via OX1 and OX2 receptors. Orexins are also antinociceptive in the brain, but their mechanism(s) of action ...remain unclear. Here, we investigated the antinociceptive mechanism of orexin A in the rat ventrolateral periaqueductal gray (vlPAG), a midbrain region crucial for initiating descending pain inhibition. In vlPAG slices, orexin A (30-300 nm) depressed GABAergic evoked IPSCs. This effect was blocked by an OX1 1-(2-methylbenzoxazol-6-yl)-3-1,5naphthyridin-4-yl urea (SB 334867), but not OX2 N-acyl 6,7-dimethoxy-1,2,3,4-tetrahydroisoquinoline hydrochloride (compound 29), antagonist. Orexin A increased the paired-pulse ratio of paired IPSCs and decreased the frequency, but not amplitude, of miniature IPSCs. Orexin A-induced IPSC depression was mimicked by (R)-(+)-2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo1,2,3-de-1,4-benzoxazin-6-yl-1-napthalenylmethanone (WIN 55,212-2), a cannabinoid 1 (CB1) receptor agonist. 1-(2,4-Dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-(1-piperidyl)pyrazole-3-carboxamide (AM 251), a CB1 antagonist, reversed depressant effects by both agonists. Orexin A-induced IPSC depression was prevented by 1-6-(17β)-3-methoxyestra-1,3,5(10)-trien-17-ylaminohexyl-1H-pyrrole-2,5-dione (U73122) and tetrahydrolipstatin, inhibitors of phospholipase C (PLC) and diacylglycerol lipase (DAGL), respectively, and enhanced by cyclohexyl1,1'-biphenyl-3-ylcarbamate (URB602), which inhibits enzymatic degradation of 2-arachidonoylglycerol (2-AG). Moderate DAGLα, but not DAGLβ, immunoreactivity was observed in the vlPAG. Orexin A produced an overall excitatory effect on evoked postsynaptic potentials and hence increased vlPAG neuronal activity. Intra-vlPAG microinjection of orexin A reduced hot-plate nociceptive responses in rats in a manner blocked by SB 334867 and AM 251. Therefore, orexin A may produce antinociception by activating postsynaptic OX1 receptors, stimulating synthesis of 2-AG, an endocannabinoid, through a Gq-protein-mediated PLC-DAGLα enzymatic cascade culminating in retrograde inhibition of GABA release (disinhibition) in the vlPAG.
The orexin system consists of orexin A/hypocretin 1 and orexin B/hypocretin 2, and OX1 and OX2 receptors. Our previous electrophysiological study showed that orexin A in the rat ventrolateral ...periaqueductal gray (vlPAG) induced antinociception via an OX1 receptor-initiated and endocannabinoid-mediated disinhibition mechanism. Here, we further characterized antinociceptive effects of orexins in the mouse vlPAG and investigated whether this mechanism in the vlPAG can contribute to stress-induced analgesia (SIA) in mice. Intra-vlPAG (i.pag.) microinjection of orexin A in the mouse vlPAG increased the hot-plate latency. This effect was mimicked by i.pag. injection of WIN 55,212-2, a CB1 agonist, and antagonized by i.pag. injection of the antagonist of OX1 (SB 334867) or CB1 (AM 251), but not OX2 (TCS-OX2-29) or opioid (naloxone), receptors. Ala11, D-Leu15-orexin B (i.pag.), an OX2 selective agonist, also induced antinociception in a manner blocked by i.pag. injection of TCS-OX2-29, but not SB 334867 or AM 251. Mice receiving restraint stress for 30 min showed significantly longer hot-plate latency, more c-Fos-expressing orexin neurons in the lateral hypothalamus and higher orexin levels in the vlPAG than unrestrained mice. Restraint SIA in mice was prevented by i.pag. or intraperitoneal injection of SB 334867 or AM 251, but not TCS-OX2-29 or naloxone. These results suggest that during stress, hypothalamic orexin neurons are activated, releasing orexins into the vlPAG to induce analgesia, possibly via the OX1 receptor-initiated, endocannabinoid-mediated disinhibition mechanism previously reported. Although activating either OX1 or OX2 receptors in the vlPAG can lead to antinociception, only OX1 receptor-initiated antinociception is endocannabinoid-dependent.
•Orexins induce analgesia via endocannabinoids in the periaqueductal gray.•Restraint stress activates hypothalamic orexin neurons, leading to analgesia.•Stress-induced analgesia via OX1 and CB1 receptors in the periaqueductal gray.•Activating OX2 receptors in the periaqueductal gray also induces analgesia.
More than 80% of ammonia (NH₃) in the steel manufacturing process wastewater is contributed from the coking wastewater, which is usually treated by biological processes. However, the NH₃ in the ...coking wastewater is typically too high for biological treatment due to its inhibitory concentration. Therefore, a two-stage process including a hollow fiber membrane contactor (HFMC) and a modified membrane distillation (MD) system was developed and applied to reduce and recover NH₃ from coking wastewater. The objectives of this paper are to evaluate different membrane materials, receiving solutions, and operation parameters for the system, remove NH₃ from the coking wastewater to less than 300 mg N/L, which is amenable to the biological process, and recover ammonia solution for reuse. As a result, the polytetrafluoroethylene (PTFE) HFMC using sulfuric acid as a receiving solution can achieve a maximum NH₃-N transmembrane flux of 1.67 g N/m²·h at pH of 11.5 and reduce NH₃ in the coking wastewater to less than 300 mg N/L. The NH₃ in the converted ammonium sulfate ((NH₄)₂SO₄) was then recovered by the modified MD using ice water as the receiving solution to produce ≥3% of ammonia solution for reuse.
Purpose
To compare corneal haze between active ulcer and healed scarring using a Scheimpflug densitometry.
Materials and methods
A prospective longitudinal study enrolled 30 patients (30 eyes) with ...ulcerative keratitis (UK). Each subject’s corneal optical density (COD) was measured with a Scheimpflug corneal densitometry, Pentacam® AXL (Oculus GmbH, Wetzlar, Germany), at the active ulcerative and complete scarring stage. The COD data were analyzed through distinct methods (inbuilt, sorted annular partitions, and ulcer-matching densitometric maps). We compared different CODs to select the better index for clinically monitoring the transition from corneal ulceration to healed scar.
Results
The CODs of the periphery (
P
= 0.0024) and outside of the active ulcer (
P
= 0.0002) significantly decreased after scarring. Partitioning the cornea into different depths and annular zones, the anterior layer, center layer, and the 2−6 mm annular zone had a more remarkable COD decrease after scar formation. The 3rd-sorted COD in the anterior layer revealed the highest area under the receiver-operating characteristic curves (0.709), in which 90% of subjects had COD reduction during the ulcer-to-scar transition.
Conclusions
Aside from subjective judgment based on clinical signs, the Scheimpflug tomography–based densitometry could provide objective and efficient monitoring of the corneal opacity evolution in UK patients. Because the 3rd-sorted annular COD is a better index than the inbuilt or mapping CODs in differentiating active ulcers from healed scars, this COD could be a clinically promising parameter to monitor the progression of UK patients.
Aim: To investigate the effect of whole-body vibration on older people with sarcopenia, and their physical capability, activities of daily living, and sleep quality. Methods: This study is ...quasi-experimental and adopts single-group pretest–posttest design. The study included participants aged older than 65 years who lived in nursing homes and care centers in Taipei, Taiwan. The whole-body vibration training was performed for 3 months, and during each training session, a participant received ten cycles of 60-sec vibration with 30-sec breaks between the cycles. The physical capability, activities of daily living, and sleep quality of the participants were examined to understand the pretest and posttest results of whole-body vibration training. Concerning the statistical methods adopted, nonparametric method-based tests were employed. Results: In addition to sleep quality (z = 7.367, p > 0.05), significant differences were observed between before and after whole-body vibration training intervention for one-foot balance (z = −2.447, p < 0.05), shoulder and arm flexibility (z = −3.159, p < 0.05), walking speed (z = −2.692, p < 0.05), right-hand grip (z = −3.388, p < 0.05), left-hand grip (z = −3.264, p < 0.05), five sit–stand repetitions (z = −2.936, p < 0.05), skeletal muscle mass index (z = −3.621, p < 0.05), and activities of daily living (z = 1.163, p < 0.05). Conclusions: According to this study, with the 12-week whole-body vibration training in older people with sarcopenia, their physical capability and activities of daily living have improved, though sleeping quality is not statistically significant.
In Singapore General Hospital (SGH), patients with chronic obstructive pulmonary disease (COPD) are referred for advance care planning (ACP) at the specialist outpatient clinics with about 50 cases ...referred a year and a completion rate of 10%. One of the commonly cited reasons by patients is that they are feeling well currently and do not need to talk about ACP at that moment. The Emergency Department (ED) saw about 240 COPD patients of P2 or P3 acuity yearly and might be a strategic place for ACP advocacy to take place for COPD patients who are triaged as P2 or P3 acuity. While the memory of the recent exacerbation remains fresh, it could be an opportune moment to start an ACP conversation with such patients in the ED. A quality improvement project (QIP) led by both ED nurses and doctors was executed to increase the number of ACP referrals for COPD patients from the ED. A total of 16 COPD ACP referrals were made, up from the previous baseline of zero. Of note, two of the 16 referrals (12.5%) completed the ACP process. Four more (25%) are still in midst of ACP completion at time of project conclusion.
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