A preliminary study on the relationship between sleep, depression and cardiovascular dysfunction in a 4 sample population.

BACKGROUND: Major Depressive Disorder (MDD) has been linked in the literature to poorer prognosis in patients with cardiovascular dysfunction, although the mechanisms of this relationship remain unclear. Underlying Sleep Disordered Breathing (SDB) serves as a potential candidate to explain this effect due to its downstream effects on inflammatory activation and decreased nitric oxide (NO) bioavailability, both of which have been shown to contribute to the pathophysiology of both MDD and cardiovascular disease (CVD). METHODS: This study utilizes overnight polysomnography and an inflammation panel to examine the links between cardiovascular dysfunction and sleep difficulties in control participants and patients diagnosed with SDB only, MDD only, and both SDB and MDD. RESULTS: Results demonstrate a strong positive relationship between sleep dysfunction and the nitric oxide synthesis inhibitor Symmetric Dimethyl Arginine (SDMA) in the MDD-only cohort, suggesting a link between SDMA-mediated NO dysregulation and CVD pathogenesis in individuals with MDD. Additionally, hypopneas, a form of sleep impairment characterized by partial reduction of airflow, were found to play a significant role in the relationship between SDB and cardiovascular dysfunction in MDD-only patients. CONCLUSIONS: Results of this study demonstrate the need for widespread screening for SDB in MDD populations to detect predisposition to CVD, and also offer SDMA as a new potential target for CVD treatment in individuals with MDD.

Simultaneous and continuous multiple wavelength absorption spectroscopy on nanoliter volumes based on frequency-division multiplexing fiber-loop cavity ring-down spectroscopy.

We demonstrate a method for measuring optical loss simultaneously at multiple wavelengths with cavity ring-down spectroscopy (CRD). Phase-shift CRD spectroscopy is used to obtain the absorption of a sample from the phase lag of intensity modulated light that is entering and exiting an optical cavity. We performed dual-wavelength detection by using two different laser light sources and frequency-division multiplexing. Each wavelength is modulated at a separate frequency, and a broadband detector records the total signal. This signal is then demodulated by lock-in amplifiers at the corresponding two frequencies allowing us to obtain the phase-shift and therefore the optical loss at several wavelengths simultaneously without the use of a dispersive element. In applying this method to fiber-loop cavity ring-down spectroscopy, we achieve detection at low micromolar concentrations in a 100 nL liquid volume. Measurements at two wavelengths (405 and 810 nm) were performed simultaneously on two dyes each absorbing at mainly one of the wavelengths. The respective concentrations could be quantified independently in pure samples as well as in mixtures. No crosstalk between the two channels was observed, and a minimal detectable absorbance of 0.02 cm(-1) was achieved at 405 nm.

Heterogeneity of skin oxygen density distribution: relation to location of acupuncture points.

To investigate possible functions of acupuncture, oxygen (O(2)) levels were measured at two different acupuncture points (APs) [Hegu and Laogong] and at the corresponding non-APs (3-5 cm away from the APs) in real time using a high sensitive electrochemical O(2) microsensor. The sensor had a small planar sensing platinum disk (diameter = 25 microm) and therefore was able to monitor the O(2) levels at the localized APs. Significantly higher O(2) levels (p < 0.05) were observed at both APs (n = 5, without exceptions) in comparison with the non-APs. Sufficient sensor sensitivity to distinguish the O(2) level differences between APs and non-APs was achieved. This research provides useful information on possible functions of APs and meridians.

3-Hydroxyanthranilic acid inhibits PDK1 activation and suppresses experimental asthma by inducing T cell apoptosis.

3-Hydroxyanthranilic acid (HAA), a compound generated during tryptophan metabolism initiated by indoleamine 2,3-dioxygenase, is known to induce T cell death, but its molecular target is not known. Here we report that HAA inhibits NF-kappaB activation upon T cell antigen receptor engagement by specifically targeting PDK1. Inhibition of NF-kappaB by HAA leads to dysfunction and cell death of activated Th2 cells, which in turn suppresses experimental asthma. Inhibition of NF-kappaB and induction of apoptosis is specific to CD4 T cells because HAA does not inhibit NF-kappaB activation or induce cell death upon Toll-like receptor 4 stimulation in dendritic cells. Thus, HAA is a natural inhibitor that restrains T cell expansion and activation.