Authors:Rui He, Xuxia Wang, Ke Fang, Nianqing Liu, Zhiyong Zhang, Yuying Huang, Wei He, and Hao Lei
In this work, elemental distributions in the rat olfactory bulbs (OB) were measured by synchrotron radiation X-ray fluorescence
(SRXRF) 9 hours after unilateral intranaris application of MnCl2 solution. The effects of deposition of exogenous Mn in the OB on the distributions of other elements, particularly calcium,
were also investigated. The results show that the application of MnCl2 solution in the nasal cavity resulted in inhomogeneous deposition of Mn in the OB, with the highest Mn content found in the
ipsilateral glomerular layer (GL). Locations in the ipsilateral hemisphere of the OB with higher Mn content were found to
be associated with significantly higher calcium and zinc contents, suggesting the presence of excess exogenous Mn may affect
the homeostasis of other trace elements such as calcium and zinc.
Authors:Lung-Chang Tsai, Jyun-Wei Chen, Hung-Yi Hou, Shang-Hao Liu, and Chi-Min Shu
The decomposition of organic peroxides by their relatively weak oxygen linkage and hydroperoxide radical in the presence of reaction solution is one of the thermal hazards for triggering a runaway reaction. Runaway incidents may occur in oxidation reactors, vacuum condensation reactors, tank lorries, or storage tanks. In NFPA 432 organic peroxides in NFPA 432 are classified as flammable. The exothermic behaviors of solid organic peroxides, dicumene peroxide, benzoyl peroxide, and lauroyl peroxide, were determined by differential scanning calorimetry (DSC), and vent sizing package 2 (VSP2). Relevant data detected by DSC provided thermal stability information, such as exothermic onset temperature (T0), maximum heat-releasing peak (Tmax), and heat of decomposition (ΔHd). VSP2 was used to perform the bench scale situation for pushing the expected or unexpected reaction to undergo runaway reaction. Onset temperature, maximum pressure, self-heating rate ((dT dt−1)max), and pressure-release rate ((dP dt−1)max) were therefore obtained and explained. These results are essentially crucial in process design for an inherently safer approach.
Authors:Joël Billieux, Daniel L. King, Susumu Higuchi, Sophia Achab, Henrietta Bowden-Jones, Wei Hao, Jiang Long, Hae Kook Lee, Marc N. Potenza, John B. Saunders, and Vladimir Poznyak
This commentary responds to Aarseth et al.’s (in press) criticisms that the ICD-11 Gaming Disorder proposal would result in “moral panics around the harm of video gaming” and “the treatment of abundant false-positive cases.” The ICD-11 Gaming Disorder avoids potential “overpathologizing” with its explicit reference to functional impairment caused by gaming and therefore improves upon a number of flawed previous approaches to identifying cases with suspected gaming-related harms. We contend that moral panics are more likely to occur and be exacerbated by misinformation and lack of understanding, rather than proceed from having a clear diagnostic system.
Authors:Chao-Chuan Chi, Chiang-Ting Chou, Chun-Chi Kuo, Yao-Dung Hsieh, Wei-Zhe Liang, Li-Ling Tseng, Hsing-Hao Su, Sau-Tung Chu, Chin-Man Ho, and Chung-Ren Jan
The effect of 2,4,6-trimethyl-N-(meta-3-trifluoromethyl-phenyl)-benzenesulfonamide (m-3M3FBS), a presumed phospholipase C activator, on cytosolic free Ca2+ concentrations ([Ca2+]i) in OC2 human oral cancer cells is unclear. This study explored whether m-3M3FBS changed basal [Ca2+]i levels in suspended OC2 cells by using fura-2 as a Ca2+-sensitive fluorescent dye. M-3M3FBS at concentrations between 10–60 μM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced partly by removing extracellular Ca2+. M-3M3FBS-induced Ca2+ influx was inhibited by the store-operated Ca2+ channel blockers nifedipine, econazole and SK&F96365, and by the phospholipase A2 inhibitor aristolochic acid. In Ca2+-free medium, 30 μM m-3M3FBS pretreatment inhibited the [Ca2+]i rise induced by the endoplasmic reticulum Ca2+ pump inhibitors thapsigargin and 2,5-di-tert-butylhydroquinone (BHQ). Conversely, pretreatment with thapsigargin, BHQ or cyclopiazonic acid partly reduced m-3M3FBS-induced [Ca2+]i rise. Inhibition of inositol 1,4,5-trisphosphate formation with U73122 did not alter m-3M3FBS-induced [Ca2+]i rise. At concentrations between 5 and 100 μM m-3M3FBS killed cells in a concentration-dependent manner. The cytotoxic effect of m-3M3FBS was not reversed by prechelating cytosolic Ca2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA). Propidium iodide staining data suggest that m-3M3FBS (20 or 50 μM) induced apoptosis in a Ca2+-independent manner. Collectively, in OC2 cells, m-3M3FBS induced [Ca2+]i rise by causing inositol 1,4,5-trisphosphate-independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx via phospholipase A2-sensitive store-operated Ca2+ channels. M-3M3FBS also induced Ca2+-independent cell death and apoptosis.
Social media disorder (SMD) is an increasing problem, especially in adolescents. The lack of a consensual classification for SMD hinders the further development of the research field. The six components of Griffiths’ biopsychosocial model of addiction have been the most widely used criteria to assess and diagnosis SMD. The Bergen social media addiction scale (BSMAS) based on Griffiths’ six criteria is a widely used instrument to assess the symptoms and prevalence of SMD in populations. This study aims to: (1) determine the optimal cut-off point for the BSMAS to identify SMD among Chinese adolescents, and (2) evaluate the contribution of specific criteria to the diagnosis of SMD.
Structured diagnostic interviews in a clinical sample (n = 252) were performed to determine the optimal clinical cut-off point for the BSMAS. The BSMAS was further used to investigate SMD in a community sample of 21,375 adolescents.
The BSMAS score of 24 was determined as the best cut-off score based on the gold standards of clinical diagnosis. The estimated 12-month prevalence of SMD among Chinese adolescents was 3.5%. According to conditional inference trees analysis, the criteria “mood modification”, “conflict”, “withdrawal”, and “relapse” showed the higher predictive power for SMD diagnosis.
Results suggest that a BSMAS score of 24 is the optimal clinical cut-off score for future research that measure SMD and its impact on health among adolescents. Furthermore, criteria of “mood modification”, “conflict”, “withdrawal”, and “relapse” are the most relevant to the diagnosis of SMA in Chinese adolescents.
Authors:John B. Saunders, Wei Hao, Jiang Long, Daniel L. King, Karl Mann, Mira Fauth-Bühler, Hans-Jürgen Rumpf, Henrietta Bowden-Jones, Afarin Rahimi-Movaghar, Thomas Chung, Elda Chan, Norharlina Bahar, Sophia Achab, Hae Kook Lee, Marc Potenza, Nancy Petry, Daniel Spritzer, Atul Ambekar, Jeffrey Derevensky, Mark D. Griffiths, Halley M. Pontes, Daria Kuss, Susumu Higuchi, Satoko Mihara, Sawitri Assangangkornchai, Manoj Sharma, Ahmad El Kashef, Patrick Ip, Michael Farrell, Emanuele Scafato, Natacha Carragher, and Vladimir Poznyak
Online gaming has greatly increased in popularity in recent years, and with this has come a multiplicity of problems due to excessive involvement in gaming. Gaming disorder, both online and offline, has been defined for the first time in the draft of 11th revision of the International Classification of Diseases (ICD-11). National surveys have shown prevalence rates of gaming disorder/addiction of 10%–15% among young people in several Asian countries and of 1%–10% in their counterparts in some Western countries. Several diseases related to excessive gaming are now recognized, and clinics are being established to respond to individual, family, and community concerns, but many cases remain hidden. Gaming disorder shares many features with addictions due to psychoactive substances and with gambling disorder, and functional neuroimaging shows that similar areas of the brain are activated. Governments and health agencies worldwide are seeking for the effects of online gaming to be addressed, and for preventive approaches to be developed. Central to this effort is a need to delineate the nature of the problem, which is the purpose of the definitions in the draft of ICD-11.
Authors:Hans-Jürgen Rumpf, Sophia Achab, Joël Billieux, Henrietta Bowden-Jones, Natacha Carragher, Zsolt Demetrovics, Susumu Higuchi, Daniel L. King, Karl Mann, Marc Potenza, John B. Saunders, Max Abbott, Atul Ambekar, Osman Tolga Aricak, Sawitri Assanangkornchai, Norharlina Bahar, Guilherme Borges, Matthias Brand, Elda Mei-Lo Chan, Thomas Chung, Jeff Derevensky, Ahmad El Kashef, Michael Farrell, Naomi A. Fineberg, Claudia Gandin, Douglas A. Gentile, Mark D. Griffiths, Anna E. Goudriaan, Marie Grall-Bronnec, Wei Hao, David C. Hodgins, Patrick Ip, Orsolya Király, Hae Kook Lee, Daria Kuss, Jeroen S. Lemmens, Jiang Long, Olatz Lopez-Fernandez, Satoko Mihara, Nancy M. Petry, Halley M. Pontes, Afarin Rahimi-Movaghar, Florian Rehbein, Jürgen Rehm, Emanuele Scafato, Manoi Sharma, Daniel Spritzer, Dan J. Stein, Philip Tam, Aviv Weinstein, Hans-Ulrich Wittchen, Klaus Wölfling, Daniele Zullino, and Vladimir Poznyak
The proposed introduction of gaming disorder (GD) in the 11th revision of the International Classification of Diseases (ICD-11) developed by the World Health Organization (WHO) has led to a lively debate over the past year. Besides the broad support for the decision in the academic press, a recent publication by van Rooij et al. (2018) repeated the criticism raised against the inclusion of GD in ICD-11 by Aarseth et al. (2017). We argue that this group of researchers fails to recognize the clinical and public health considerations, which support the WHO perspective. It is important to recognize a range of biases that may influence this debate; in particular, the gaming industry may wish to diminish its responsibility by claiming that GD is not a public health problem, a position which maybe supported by arguments from scholars based in media psychology, computer games research, communication science, and related disciplines. However, just as with any other disease or disorder in the ICD-11, the decision whether or not to include GD is based on clinical evidence and public health needs. Therefore, we reiterate our conclusion that including GD reflects the essence of the ICD and will facilitate treatment and prevention for those who need it.