Peritoneal Adipocytes and Their Role in Inflammation during Peritoneal Dialysis

Adipose tissue is a major site of chronic inflammation associated with peritoneal dialysis (PD) frequently complicating peritonitis. Adiposity-associated inflammation plays a significant contributory role in the development of chronic inflammation in patients undergoing maintenance PD. However, the molecular and cellular mechanisms of this link remain uncertain. Adipose tissue synthesizes different adipokines and cytokines that orchestrate and regulate inflammation, insulin action, and glucose metabolism locally and systemically. In return, inflammation retards adipocyte differentiation and further exacerbates adipose dysfunction and inflammation. An understanding of the inflammatory roles played by adipose tissue during PD and the healing mechanism of injured mesothelium will help to devise new therapeutic approach to slow the progression of peritoneal damage during peritoneal dialysis. This article reviews the roles of peritoneal adipose tissue in chronic peritoneal inflammation under PD and in serosal repair during PD

Wave Propagation in Gravitational Systems: Completeness of Quasinormal Modes

The dynamics of relativistic stars and black holes are often studied in terms of the quasinormal modes (QNM's) of the Klein-Gordon (KG) equation with different effective potentials $V(x)$. In this paper we present a systematic study of the relation between the structure of the QNM's of the KG equation and the form of $V(x)$. In particular, we determine the requirements on $V(x)$ in order for the QNM's to form complete sets, and discuss in what sense they form complete sets. Among other implications, this study opens up the possibility of using QNM expansions to analyse the behavior of waves in relativistic systems, even for systems whose QNM's do {\it not} form a complete set. For such systems, we show that a complete set of QNM's can often be obtained by introducing an infinitesimal change in the effective potential

Eigenvector Expansion and Petermann Factor for Ohmically Damped Oscillators

Correlation functions $C(t) \sim$ in ohmically damped systems such as coupled harmonic oscillators or optical resonators can be expressed as a single sum over modes $j$ (which are not power-orthogonal), with each term multiplied by the Petermann factor (PF) $C_j$, leading to "excess noise" when $|C_j| > 1$. It is shown that $|C_j| > 1$ is common rather than exceptional, that $|C_j|$ can be large even for weak damping, and that the PF appears in other processes as well: for example, a time-independent perturbation \sim\ep leads to a frequency shift \sim \ep C_j. The coalescence of $J$ ($>1$) eigenvectors gives rise to a critical point, which exhibits "giant excess noise" ($C_j \to \infty$). At critical points, the divergent parts of $J$ contributions to $C(t)$ cancel, while time-independent perturbations lead to non-analytic shifts \sim \ep^{1/J}.Comment: REVTeX4, 14 pages, 4 figures. v2: final, 20 single-col. pages, 2 figures. Streamlined with emphasis on physics over formalism; rewrote Section V E so that it refers to time-dependent (instead of non-equilibrium) effect

Quasi-Normal Mode Expansion for Linearized Waves in Gravitational Systems

The quasinormal modes (QNM's) of gravitational systems modeled by the Klein-Gordon equation with effective potentials are studied in analogy to the QNM's of optical cavities. Conditions are given for the QNM's to form a complete set, i.e., for the Green's function to be expressible as a sum over QNM's, answering a conjecture by Price and Husain [Phys. Rev. Lett. {\bf 68}, 1973 (1992)]. In the cases where the QNM sum is divergent, procedures for regularization are given. The crucial condition for completeness is the existence of spatial discontinuities in the system, e.g., the discontinuity at the stellar surface in the model of Price and Husain.Comment: 12 pages, WUGRAV-94-

Predictors of functional deterioration in Chinese patients with Psoriatic arthritis: A longitudinal study.

10.1186/1471-2474-15-284BMC Musculoskeletal Disorders15128

Behavioral activation for dementia caregivers: scheduling pleasant events and enhancing communications

published_or_final_versio

Estimating daily and diurnal variations of illicit drug use in Hong Kong: A pilot study of using wastewater analysis in an Asian metropolitan city

The measurement of illicit drug metabolites in raw wastewater is increasingly being adopted as an approach to objectively monitor population-level drug use, and is an effective complement to traditional epidemiological methods. As such, it has been widely applied in western countries. In this study, we utilised this approach to assess drug use patterns over nine days during April 2011 in Hong Kong. Raw wastewater samples were collected from the largest wastewater treatment plant serving a community of approximately 3.5 million people and analysed for excreted drug residues including cocaine, ketamine, methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA) and key metabolites using liquid chromatography coupled with tandem mass spectrometry. The overall drug use pattern determined by wastewater analysis was consistent with that have seen amongst people coming into contact with services in relation to substance use; among our target drugs, ketamine (estimated consumption: 1400-1600. mg/day/1000 people) was the predominant drug followed by methamphetamine (180-200. mg/day/1000 people), cocaine (160-180. mg/day/1000 people) and MDMA (not detected). The levels of these drugs were relatively steady throughout the monitoring period. Analysing samples at higher temporal resolution provided data on diurnal variations of drug residue loads. Elevated ratios of cocaine to benzoylecgonine were identified unexpectedly in three samples during the evening and night, providing evidence for potential dumping events of cocaine. This study provides the first application of wastewater analysis to quantitatively evaluate daily drug use in an Asian metropolitan community. Our data reinforces the benefit of wastewater monitoring to health and law enforcement authorities for strategic planning and evaluation of drug intervention strategies

Treatment of human astrocytoma U87 cells with silicon dioxide nanoparticles lowers their survival and alters their expression of mitochondrial and cell signaling proteins

Recent evidence suggests silicon dioxide micro- and nanoparticles induce cytotoxic effects on lung cells. Thus, there is an increasing concern regarding their potential health hazard. Nevertheless, the putative toxicity of nanoparticles in mammalian cells has not yet been systematically investigated. We previously noted that several metallic oxide nanoparticles exert differential cytotoxic effects on human neural and nonneural cells. Therefore, we hypothesized that silicon dioxide nanoparticles induce cytotoxicity in U87 cells by lowering their survival by decreasing cell survival signaling and disturbing mitochondrial function. To investigate this hypothesis, we determined the activities of the key mitochondrial enzymes, citrate synthase and malate dehydrogenase, in astrocytoma U87 cells treated with silicon dioxide nanoparticles. In addition, we studied the expression of the mitochondrial DNA-encoded proteins, cytochrome C oxidase II and nicotinamide adenine dinucleotide (NADPH) dehydrogenase subunit 6, and cell signaling pathway protein extracellular signal-regulated kinase (ERK) and phosphorylated ERK in treated U87 cells. The activated form of ERK controls cell growth, differentiation, and proliferation. In parallel, we determined survival of U87 cells after treating them with various concentrations of silicon dioxide nanoparticles. Our results indicated that treatment with silicon dioxide nanoparticles induced decreases in U87 cell survival in a dose-related manner. The activities of citrate synthase and malate dehydrogenase in treated U87 cells were increased, possibly due to an energetic compensation in surviving cells. However, the expression of mitochondrial DNA-encoded cytochrome C oxidase subunit II and NADH dehydrogenase subunit 6 and the cell signaling protein ERK and phosphorylated ERK were altered in the treated U87 cells, suggesting that silicon dioxide nanoparticles induced disruption of mitochondrial DNA-encoded protein expression, leading to decreased mitochondrial energy production and decreased cell survival/proliferation signaling. Thus, our results strongly suggest that the cytotoxicity of silicon dioxide nanoparticles in human neural cells implicates altered mitochondrial function and cell survival/proliferation signaling

Early Microglial Activation Following Closed-Head Concussive Injury Is Dominated by Pro-Inflammatory M-1 Type

Microglial activation is a pathological hallmark of traumatic brain injury (TBI). Following brain injury, activated microglia/macrophages adopt different phenotypes, generally categorized as M-1, or classically activated, and M-2, or alternatively activated. While the M-1, or pro-inflammatory phenotype is detrimental to recovery, M-2, or the anti-inflammatory phenotype, aids in brain repair. Recent findings also suggest the existence of mixed phenotype following brain injury, where activated microglia simultaneously express both M-1 and M-2 markers. The present study sought to determine microglial activation states at early time points (6–72 h) following single or repeated concussive injury in rats. Closed-head concussive injury was modeled in rats using projectile concussive impact injury, with either single or repeated impacts (4 impacts, 1 h apart). Brain samples were examined using immunohistochemical staining, inflammatory gene profiling and real-time polymerase chain reaction analyses to detect concussive injury induced changes in microglial activation and phenotype in cortex and hippocampal regions. Our findings demonstrate robust microglial activation following concussive brain injury. Moreover, we show that multiple concussions induced a unique rod-shaped microglial morphology that was also observed in other diffuse brain injury models. Histological studies revealed a predominance of MHC-II positive M-1 phenotype in the post-concussive microglial milieu following multiple impacts. Although there was simultaneous expression of M-1 and M-2 markers, gene expression results indicate a clear dominance in M-1 pro-inflammatory markers following both single and repeated concussions. While the increase in M-1 markers quickly resolved after a single concussion, they persisted following repeated concussions, indicating a pro-inflammatory environment induced by multiple concussions that may delay recovery and contribute to long-lasting consequences of concussion