Acupuncture for dry eye: a randomised controlled trial protocol

<p>Abstract</p> <p>Background</p> <p>Dry eye is usually managed by conventional medical interventions such as artificial tears, anti-inflammatory drugs and surgical treatment. However, since dry eye is one of the most frequent ophthalmologic disorders, safer and more effective methods for its treatment are necessary, especially for vulnerable patients. Acupuncture has been widely used to treat patients with dry eye. Our aim is to evaluate the effectiveness and safety of acupuncture for this condition.</p> <p>Methods/Design</p> <p>A randomised, patient-assessor blinded, sham (non-acupuncture point, shallow acupuncture) controlled study was established. Participants allocated to verum acupuncture and sham acupuncture groups will be treated three times weekly for three weeks for a total of nine sessions per participant. Seventeen points (GV23; bilateral BL2, GB4, TE23, Ex1 (Taiyang), ST1 and GB20; and left SP3, LU9, LU10 and HT8 for men, right for women) have been selected for the verum acupuncture; for the sham acupuncture, points have been selected that do not coincide with a classical acupuncture point and that are located close to the verum points, except in the case of the rim of the eye. Ocular surface disease index, tear film breakup time, the Schirmer I test, medication quantification scale and general assessment of improvement will be used as outcome variables for evaluating the effectiveness of acupuncture. Safety will also be assessed at every visit. Primary and secondary outcomes will be assessed four weeks after screening. All statistical analyses will be performed using analysis of covariance.</p> <p>Discussion</p> <p>The results of this trial will be used as a basis for clarifying the efficacy of acupuncture for dry eye.</p> <p>Trial registration</p> <p>ClinicalTrials.gov NCT00969280.</p

Sleep-Dependent Changes in the Coupling Between Heart Period and Arterial Pressure in Newborn Lambs

This study assessed whether sleep-dependent changes in the relationship between heart period (HP) and mean arterial pressure (MAP) occur in newborn life. Electrodes for electrocorticographic, electromyographic, and electrooculographic monitoring and an arterial catheter for blood pressure recordings were implanted in 11 newborn lambs. HP and MAP beat-to-beat values were computed from 120-s blood pressure recordings during quiet wakefulness, active sleep, and quiet sleep. For each recording, the time shift at which the maximum of the HP versus MAP cross-correlation function was attained was identified. For each lamb and wake-sleep state, an average correlation coefficient was then computed corresponding to the median value of such time shifts. The maximum of the cross-correlation function was attained with HP lagging behind MAP. The corresponding mean correlation coefficient was significantly higher in quiet sleep (0.51 ± 0.05) than either in quiet wakefulness (0.31 ± 0.05) or in active sleep (0.29 ± 0.03). Sleep-related differences in the correlation between HP and MAP were maintained after HP and MAP data were low-pass filtered at 0.3 Hz to remove their fast ventilatory oscillations. In conclusion, data indicate that the relationship between spontaneous fluctuations in HP and those in MAP is sleep-state dependent in newborn lambs. A positive HP versus MAP correlation with HP lagging behind MAP is consistent with baroreflex control of HP. Heart rhythm thus may be more tightly controlled by the baroreceptor reflex and less dependent on central autonomic commands in quiet sleep than either in quiet wakefulness or in active sleep

Mitochondrial optic neuropathies – Disease mechanisms and therapeutic strategies

Leber hereditary optic neuropathy (LHON) and autosomal-dominant optic atrophy (DOA) are the two most common inherited optic neuropathies in the general population. Both disorders share striking pathological similarities, marked by the selective loss of retinal ganglion cells (RGCs) and the early involvement of the papillomacular bundle. Three mitochondrial DNA (mtDNA) point mutations; m.3460G>A, m.11778G>A, and m.14484T>C account for over 90% of LHON cases, and in DOA, the majority of affected families harbour mutations in the OPA1 gene, which codes for a mitochondrial inner membrane protein. Optic nerve degeneration in LHON and DOA is therefore due to disturbed mitochondrial function and a predominantly complex I respiratory chain defect has been identified using both in vitro and in vivo biochemical assays. However, the trigger for RGC loss is much more complex than a simple bioenergetic crisis and other important disease mechanisms have emerged relating to mitochondrial network dynamics, mtDNA maintenance, axonal transport, and the involvement of the cytoskeleton in maintaining a differential mitochondrial gradient at sites such as the lamina cribosa. The downstream consequences of these mitochondrial disturbances are likely to be influenced by the local cellular milieu. The vulnerability of RGCs in LHON and DOA could derive not only from tissue-specific, genetically-determined biological factors, but also from an increased susceptibility to exogenous influences such as light exposure, smoking, and pharmacological agents with putative mitochondrial toxic effects. Our concept of inherited mitochondrial optic neuropathies has evolved over the past decade, with the observation that patients with LHON and DOA can manifest a much broader phenotypic spectrum than pure optic nerve involvement. Interestingly, these phenotypes are sometimes clinically indistinguishable from other neurodegenerative disorders such as Charcot-Marie-Tooth disease, hereditary spastic paraplegia, and multiple sclerosis, where mitochondrial dysfunction is also thought to be an important pathophysiological player. A number of vertebrate and invertebrate disease models has recently been established to circumvent the lack of human tissues, and these have already provided considerable insight by allowing direct RGC experimentation. The ultimate goal is to translate these research advances into clinical practice and new treatment strategies are currently being investigated to improve the visual prognosis for patients with mitochondrial optic neuropathies