Collaborative Settings Increase Dishonesty.

The present study examines whether collaborative situations make individuals more dishonest in face-to-face settings. It also considers how this dishonesty unfolds over time. To address these questions, we employed a sequential dyadic die-rolling task in which two participants in a pair sitting face-to-face received a payoff only if both reported the same outcome when each one rolled their die. In each trial, one participant (role A) rolled a die first and reported the outcome. Then, the second participant (role B) was informed of A's reported number, rolled a die as well, and reported the outcome. If their reported outcomes were identical, both of them received a reward. We also included an individual condition in which an individual subject rolled a die twice and received a reward if he/she reported the same die-roll outcome. We found that B lied significantly more than participants in the individual condition, whereas A lied as much as participants in the individual condition. Furthermore, when collaborating, more and more participants (both A and B) became dishonest as the game progressed, whereas there was no such trend among participants in the individual condition. These findings provide evidence indicating that collaborative settings increase dishonesty and that this effect becomes more evident as the collaboration progress.

Children with Autism Spectrum Disorder's Lying is Correlated with Their Working Memory But Not Theory of Mind.

The present study examined the role of executive function in lying for children with autism spectrum disorder (ASD). The temptation resistance paradigm was used to elicit children's self-protective lies and the Hide-and-seek task was used to elicit children's self-benefiting lies. Results showed that children with ASD told fewer lies in the two deception tasks compared to children with intellectual disability (ID) and typically developing (TD) children. Furthermore, children with ASD's lying were positively correlated with their working memory, but not with their theory of mind. These findings demonstrate that the mechanisms underlying deception for children with ASD are distinct from that of TD children.

Smoking Cessation With 20 Hz Repetitive Transcranial Magnetic Stimulation (rTMS) Applied to Two Brain Regions: A Pilot Study.

Chronic smoking impairs brain functions in the prefrontal cortex and the projecting meso-cortical limbic system. The purpose of this pilot study is to examine whether modulating the frontal brain activity using high-frequency repetitive transcranial magnetic stimulation (rTMS) can improve smoking cessation and to explore the changing pattern of the brain activity after treatment. Fourteen treatment-seeking smokers were offered a program involving 10 days of rTMS treatment with a follow-up for another 25 days. A frequency of 20 Hz rTMS was sequentially applied on the left dorso-lateral prefrontal cortex (DLPFC) and the superior medial frontal cortex (SMFC). The carbon monoxide (CO) level, withdrawal, craving scales, and neuroimaging data were collected. Ten smokers completed the entire treatment program, and 90% of them did not smoke during the 25-day follow-up time. A significant smoking craving reduction and resting brain activity reduction measured by the cerebral blood flow (CBF) and brain entropy (BEN) were observed after 10 days of 20 Hz rTMS treatments compared to the baseline. Although limited by sample size, these pilot findings definitely showed a high potential of multiple-target high-frequency rTMS in smoking cessation and the utility of fMRI for objectively assessing the treatment effects.

Cetuximab enhances cisplatin-induced endoplasmic reticulum stress-associated apoptosis in laryngeal squamous cell carcinoma cells by inhibiting expression of TXNDC5.

Cisplatin and cetuximab, an anti­epidermal growth factor receptor (EGFR) monoclonal humanized antibody, have been used for treatment of laryngeal squamous cell carcinoma (LSCC). It has been demonstrated that cisplatin and inhibition of EGFR signaling may induce endoplasmic reticulum (ER) stress­associated apoptosis. However, ER protein thioredoxin domain­containing protein 5 (TXNDC5) reportedly protects cells from ER stress­associated apoptosis. The present study investigated the interaction between cisplatin, cetuximab and TXNDC5 on ER stress­associated apoptosis in LSCC cells. AMC­HN­8 human LSCC cells with or without TXNDC5 overexpression or knockdown were treated with cisplatin (5, 10, 20 and 40 µM) and/or cetuximab (10, 50, 100 and 150 µg/ml), for 12, 24, 36 and 48 h. Cisplatin and cetuximab concentration­ and time­dependently increased and decreased the expression of TXNDC5 in AMC­HN­8 cells, respectively. Knockdown of TXNDC5 markedly augmented cisplatin­induced levels of CCAAT/enhancer­binding protein homologous protein (CHOP), caspase­3 activity and apoptosis; while overexpression of TXNDC5 largely eliminated cetuximab­induced levels of CHOP, caspase­3 activity and apoptosis. Cisplatin and cetuximab demonstrated a combinatorial effect on increasing the levels of CHOP, caspase­3 activity and apoptosis, which was largely eliminated by overexpression of TXNDC5 or a reactive oxygen species (ROS) scavenger/antagonist. In addition, promoter/luciferase reporter assays revealed that cisplatin and cetuximab regulated the expression of TXNDC5 at the gene transcription/promoter level. In conclusion, the findings suggested that ER stress­associated apoptosis is a major mechanism underlying the apoptotic effect of cisplatin and cetuximab on LSCC cells; cetuximab enhanced cisplatin­induced ER stress­associated apoptosis in LSCC cells largely by inhibiting the expression of TXNDC5 and thereby increasing ROS production; cisplatin and cetuximab had stimulatory and inhibitory effects on the TXNDC5 gene promoter, respectively. The present study offered novel insights into the pharmacological effects of cisplatin and cetuximab on LSCC. It also suggested that TXNDC5 may be a potential therapeutic target for LSCC.

miR-23a promotes cisplatin chemoresistance and protects against cisplatin-induced apoptosis in tongue squamous cell carcinoma cells through Twist.

Tongue squamous cell carcinoma (TSCC) is one of the most common head and neck cancers. Cisplatin is effective as a single agent or in combination with other drugs for the treatment of TSCC. Treatment with cisplatin-based chemotherapy has been found to improve the prognosis of patients with TSCC. However, one of the most important clinical issues of cisplatin-based TSCC chemotherapy is the intrinsic/acquired chemoresistance to cisplatin. Increased expression of miR-23a reportedly promotes cisplatin chemoresistance in TSCC cells. High expression of Twist is also associated with cancer chemoresistance and poor prognosis of TSCC patients. In the present study, we explored the interaction between miR-23a and Twist in TSCC cells, and assessed its impact on TSCC chemoresistance to cisplatin. miR-23a and/or Twist were overexpressed or knocked down in SCC-4 and Tca8113 human TSCC cells. The expression levels of miR-23a and Twist were determined. The half maximal inhibitory concentration (IC50) of cisplatin and cell apoptosis rate under cisplatin treatment were used as measures of cisplatin chemoresistance. Overexpression of miR-23a in both SCC-4 and Tca8113 cells markedly increased Twist expression, c-Jun N-terminal kinase (JNK) activity and the half maximal inhibitory concentration (IC50) of cisplain, and decreased cisplatin-induced apoptosis, all of which was abolished by knockdown of Twist or selective JNK inhibitor SP600125. On the other hand, knockdown of miR-23a significantly decreased Twist expression, JNK activity and IC50 of cisplain, and increased cisplatin-induced apoptosis, all of which was completely reversed by overexpression of Twist. In conclusion, the present study for the first time demonstrates that miR-23a promotes cisplatin chemoresistance and protects cisplatin-induced apoptosis in TSCC cells through inducing Twist expression by a JNK-dependent mechanism. It adds new insights into the molecular mechanisms underlying TSCC chemoresistance.

Effects of aminoguanidine and vitamin C on collagen type IV in diabetic nephropathy rats.

The aim of this article is to investigate the effects of Aminoguanidine and vitamin C (VitC) on type IV collagen in diabetic nephropathy rats. Diabetic nephropathy rats were induced by intraperitoneal injection of STZ. Rats were randomly divided into five groups: normal control group (n = 10), diabetes group (n = 10), aminoguanidine group (n = 10), VitC group (n = 10), aminoguanidine and VitC group (n = 10). After 16 weeks, the general conditions, blood gloucose, glycosylated hemoglobin, blood urea nitrogen, serum creatinine, serum type IV collagen, urinary albumin excretion rate, and creatinine clearance rate were detected, type IV collagen protein was determined by immunohistochemical analysis as well as the expression of collagen type IVα1 mRNA were determined by in situ hybridization analysis in the kidneys of each group. The results were (1) diabetes mellitus and renal lesions occurred in the diabetes group, aminoguanidine group, VitC group, VitC and aminoguanidine group; (2) aminoguanidine and VitC improved the general conditions of diabetic nephropathy rats, decreased blood urea nitrogen, serum creatinine, and urinary albumin excretion rate as well as increased creatinine clearance rate. The expressions of collagen type IV were significantly down-regulated in treatment groups in contrast to the diabetes group. Aminoguanidine and VitC protect renal lesions in diabetic nephropathy, respectively, by inhibiting expression of type IV collagen, while aminoguanidine and VitC have a synergistic effect on them.