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Journal of Behavioral Addictions
Authors:
Lu Li
,
Dan-Dan Xu
,
Jing-Xin Chai
,
Di Wang
,
Lin Li
,
Ling Zhang
,
Li Lu
,
Chee H. Ng
,
Gabor S. Ungvari
,
Song-Li Mei
, and
Yu-Tao Xiang

Background and aims

Internet addiction disorder (IAD) is common in university students. A number of studies have examined the prevalence of IAD in Chinese university students, but the results have been inconsistent. This is a meta-analysis of the prevalence of IAD and its associated factors in Chinese university students.

Methods

Both English (PubMed, PsycINFO, and Embase) and Chinese (Wan Fang Database and Chinese National Knowledge Infrastructure) databases were systematically and independently searched from their inception until January 16, 2017.

Results

Altogether 70 studies covering 122,454 university students were included in the meta-analysis. Using the random-effects model, the pooled overall prevalence of IAD was 11.3% (95% CI: 10.1%–12.5%). When using the 8-item Young Diagnostic Questionnaire, the 10-item modified Young Diagnostic Questionnaire, the 20-item Internet Addiction Test, and the 26-item Chen Internet Addiction Scale, the pooled prevalence of IAD was 8.4% (95% CI: 6.7%–10.4%), 9.3% (95% CI: 7.6%–11.4%), 11.2% (95% CI: 8.8%–14.3%), and 14.0% (95% CI: 10.6%–18.4%), respectively. Subgroup analyses revealed that the pooled prevalence of IAD was significantly associated with the measurement instrument (Q = 9.41, p = .024). Male gender, higher grade, and urban abode were also significantly associated with IAD. The prevalence of IAD was also higher in eastern and central of China than in its northern and western regions (10.7% vs. 8.1%, Q = 4.90, p = .027).

Conclusions

IAD is common among Chinese university students. Appropriate strategies for the prevention and treatment of IAD in this population need greater attention.

Open access
Acta Physiologica Hungarica
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.

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