Joint and individual effectiveness of galvanic cutaneous stimulation and tactile stimulation at decreasing Simulator Adaptation Syndrome.

This research was focused on investigating the effectiveness of galvanic cutaneous stimulation and tactile stimulation jointly and individually at mitigating Simulator Adaptation Syndrome. Forty drivers (mean age = 23.1 ± 3.4 years old, twenty women) participated in a driving simulation experiment. Total scores of the Simulator Sickness Questionnaire, head movements (an index of body balance), and driving performance variables were compared across four different stimulation conditions: i) baseline (where no stimulation was presented), ii) galvanic cutaneous stimulation and iii) tactile stimulation deployed individually, and iv) both techniques deployed jointly. The results showed that both techniques presented in conjunction alleviate Simulator Adaptation Syndrome and improve driving performance more effectively than when they are presented in isolation. Importantly, reduced head movements were only revealed when galvanic cutaneous stimulation was applied. We concluded that the reduction of this syndrome is due to an improvement of body balance (elicited by galvanic cutaneous stimulation), and a distraction from the symptoms (elicited by tactile stimulation). We encourage the use of both techniques simultaneously to decrease Simulator Adaptation Syndrome.

MS-1020 is a novel small molecule that selectively inhibits JAK3 activity.

In order to identify Janus kinase/signal transducer and activator of transcription (JAK/STAT) signalling inhibitors, a cell-based high throughput screening was performed using a plant extract library that identified Nb-(alpha-hydroxynaphthoyl)serotonin called MS-1020 as a novel JAK3 inhibitor. MS-1020 potently inhibited persistently-active STAT3 in a cell type-specific manner. Further examination showed that MS-1020 selectively blocked constitutively-active JAK3 and consistently suppressed interleukin-2-induced JAK3/STAT5 signalling but not prolactin-induced JAK2/STAT5 signalling. Furthermore, MS-1020 affected cell viability only in cancer cells harbouring persistently-active JAK3/STATs, and in vitro kinase assays showed MS-1020 binds directly with JAK3, blocking its catalytic activity. Therefore, the present study suggested that this reagent selectively inhibits JAK3 and subsequently leads to a block in STAT signalling. Finally, MS-1020 decreased cell survival by inducing apoptosis via down-regulation of anti-apoptotic gene expression. These results suggest that MS-1020 may have therapeutic potential in the treatment of cancers harbouring aberrant JAK3 signalling.

Early recognition of renal toxicity of high-dose methotrexate therapy: a case report.

A 10-year-old boy with osteosarcoma and normal renal function manifested laboratory evidence of impending renal toxicity and extreme elevation of aspartate aminotrasferase and alanine aminotransferase within 2 hours after the completion of a 4-hour infusion of high-dose methotrexate (MTX) (12 g/m2), and went on to develop acute renal failure with life-threatening hyperkalemia 29 hours later. Although his renal function recovered completely with high-dose leucovorin, hemodialysis, charcoal hemoperfusion, and carboxypeptidase G2, we present this case to emphasize that signs of renal toxicity may be present as early as 2 hours after the completion of a 4-hour MTX infusion, and to suggest that monitoring for MTX toxicity should perhaps begin within a few hours after the completion of 4-hour MTX infusion.