INFLUENCE OF 24-HOUR SLEEP DEPRIVATION ON CARDIOVASCULAR AND NEURAL CONTROL AT REST AND DURING ACUTE STRESS IN HUMANS

Recent epidemiological studies report a consistent association between short sleep and incidence of hypertension, as well as short sleep and cardiovascular disease-related mortality. While the association between short sleep and hypertension appears to be stronger in women than men, the mechanisms underlying the relations between sleep deprivation, stress, risks of cardiovascular diseases, and sex remain unclear. We conducted two studies to investigate the underlying neural mechanisms of these relations. In study 1, we examined sympathetic neural and blood pressure responses to experimentally-induced sleep deprivation in men and women. We further investigated the influence of sleep deprivation on cardiovascular reactivity to acute stress. In study 2, we examined the neural and cardiovascular function throughout the ovarian cycle in sleep deprived women. Twenty-eight young healthy subjects (14men and 14 women) were tested twice in study 1, once after normal sleep (NS) and once after 24-h total sleep deprivation (TSD). We measured the blood pressure, heart rate (HR), muscle sympathetic nerve activity (MSNA) and forearm blood flow (FBF) during 10min baseline, 5min of mental stress (MS) and 2 min cold pressor test (CPT). We demonstrated that TSD increased resting arterial blood pressure to a similar extent in both men and women, but MSNA decreased only in men following TSD. This MSNA response was associated with altered baroreflex function in women and divergent testosterone responses to TSD between men and women. Regarding TSD and cardiovascular reactivity, TSD elicited augmented HR reactivity and delayed recovery during both MS and CPT in men and women, and responses between sexes were not statistically different. Fourteen young healthy women participated in study 2. Subjects were tested twice, once during their early follicular (EF) phase after TSD, once during their mid-luteal (ML) phase after TSD. Blood pressure, HR, MSNA, and FBF were recorded during 10min baseline, 5 min MS, and 2 min CPT. We observed an augmented resting supine blood pressure during EF compared to ML in sleep deprived women. In contrast, resting MSNA, as well as cardiovascular responses to stressors, were similar between EF and ML after TSD. In conclusion, we observed sex differences in MSNA responses to TSD that demonstrate reductions of MSNA in men, but not women. TSD elicited augmented HR reactivity and delayed HR recovery to acute stressors similarly in men and women. We also reported an augmented supine blood pressure during EF compared to ML in sleep deprived women. These novel findings provide new and valuable mechanistic insight regarding the complex and poorly understood relations among sleep deprivation, sex, stress, and risk of cardiovascular disease.

Sleep Deprivation and Pain Intensity

Little or poor quality sleep is often reported in patients suffering from acute or chronic pain. Conversely, sleep loss has been known to elevate pain perception; thus a potential bi-direction relationship exists between sleep deprivation and pain. The effect of sleep deprivation on the thermal pain intensity has yet to be determined, furthermore, sex differences in pain have not been examined following sleep deprivation. There is also a higher prevalence of insomnia in women, and reports indicate that sleep quality is diminished and pain sensitivity may be greater during high hormone phases of the menstrual cycle. In Study 1 we examined the effects of 24-hour total sleep deprivation (TSD) on pain intensity during a 2-minute cold pressor test (CPT). We hypothesized that TSD would augment thermal pain intensity during CPT and women would demonstrate an elevated response compare to men. In Study 2 we investigated the effects of menstrual phase on pain intensity during CPT following TSD. We hypothesized that pain intensity would be augmented during the mid-luteal (ML) phase of the menstrual cycle. In Study 1, pain intensity was recorded during CPT in 14 men and 13 women after normal sleep (NS) and TSD. Pain intensity responses during CPT were elevated in both conditions; however, pain intensity was augmented (~ 1.2 a.u.) following TSD. When analyzed for sex differences, pain intensity was not different between men and women in either condition. In Study 2, pain intensity was recorded during CPT in 10 female subjects during the early follicular (EF) and ML phases of the menstrual cycle after TSD. Estradiol and progesterone levels were elevated during the ML phase, however, pain intensity was not different between the two phases. We conclude that TSD significantly augments pain intensity during CPT, but this response is not sex dependent. We further demonstrate that the collective effect of TSD and elevated gonadal hormone concentrations do not result in a differential pain response during the EF and ML phases of the menstrual cycle. Collectively, sleep loss augments pain intensity ratings in men and women and may contribute to sleep loss in painful conditions.

Systemic analysis of microarray data sets towards identifying genes regulating root development

Nitrogen and water are essential for plant growth and development. In this study, we designed experiments to produce gene expression data of poplar roots under nitrogen starvation and water deprivation conditions. We found low concentration of nitrogen led first to increased root elongation followed by lateral root proliferation and eventually increased root biomass. To identify genes regulating root growth and development under nitrogen starvation and water deprivation, we designed a series of data analysis procedures, through which, we have successfully identified biologically important genes. Differentially Expressed Genes (DEGs) analysis identified the genes that are differentially expressed under nitrogen starvation or drought. Protein domain enrichment analysis identified enriched themes (in same domains) that are highly interactive during the treatment. Gene Ontology (GO) enrichment analysis allowed us to identify biological process changed during nitrogen starvation. Based on the above analyses, we examined the local Gene Regulatory Network (GRN) and identified a number of transcription factors. After testing, one of them is a high hierarchically ranked transcription factor that affects root growth under nitrogen starvation. It is very tedious and time-consuming to analyze gene expression data. To avoid doing analysis manually, we attempt to automate a computational pipeline that now can be used for identification of DEGs and protein domain analysis in a single run. It is implemented in scripts of Perl and R.