Top 100 influential manuscripts in obstructive sleep apnea: a bibliometric analysis.

OBJECTIVE: This study aimed to explore the characteristics of the top 100 influential manuscripts on obstructive sleep apnea (OSA). METHODS: All manuscripts in English were searched from the Thomson Reuters Web of Science database by using OSA-related terms and ranked based on citation frequency. The top 100 influential manuscripts were selected and further analyzed by author, subject, journal, year of publication, country of origin, and institution. RESULTS: A total of 42,878 manuscripts were searched from the Web of Science. The top 100 influential manuscripts were published from 2005 to 2017, with a total citation frequency of 38,463 and a median citation frequency of 303 (range: from 210 to 2, 707). The American Journal of Respiratory and Critical Care Medicine published the largest number of manuscripts from the top 100 (n = 18; 5340 citations), followed by Sleep (n = 11; 3516 citations) and Chest (n = 7; 1784 citations). The most cited manuscript (Marin, J.M et al., Lancet 2005; 2707 citations) mainly analyzed long-term cardiovascular outcomes in men with OSA with/without continuous positive airway pressure. The most prevalent subject was associated diseases (n = 41), followed by treatments (n = 40). Most of the manuscripts were original articles (n = 63) based on observational clinical studies and published from American institutions (n = 60). CONCLUSIONS: Our study identified the top 100 influential manuscripts on OSA and provides insights into the characteristics of the most highly cited manuscripts to improve our understanding and management of OSA.

Nigrostriatal Dopamine Acting on Globus Pallidus Regulates Sleep.

Lesions of the globus pallidus externa (GPe) produce a profound sleep loss (∼45%) in rats, suggesting that GPe neurons promote sleep. As GPe neuronal activity is enhanced by dopamine (DA) from the substantia nigra pars compacta (SNc), we hypothesized that SNc DA via the GPe promotes sleep. To test this hypothesis, we selectively destroyed the DA afferents to the caudoputamen (CPu) using 6-hydroxydopamine and examined changes in sleep-wake profiles in rats. Rats with 80-90% loss of SNc neurons displayed a significant 33.7% increase in wakefulness (or sleep reduction). This increase significantly correlated with the extent of SNc DA neuron loss. Furthermore, these animals exhibited sleep-wake fragmentation and reduced diurnal variability of sleep. We then optogenetic-stimulated SNc DA terminals in the CPu and found that 20-Hz stimulation from 9 to 10 PM increased total sleep by 69% with high electroencephalograph (EEG) delta power. We finally directly optogenetic-stimulated GPe neurons and found that 20-Hz stimulation of the GPe from 9 to 10 PM increased total sleep by 66% and significantly increased EEG delta power. These findings elucidate a novel circuit for DA control of sleep and the mechanisms of abnormal sleep in BG disorders such as Parkinson's disease and Huntington's disease.

Protective effects of early hypoxic post-conditioning in cultured cortical neurons.

PRIMARY OBJECTIVE: Recent evidence suggests that delayed hypoxic post-conditioning is neuroprotective. The aim of the present study was to test whether early post-conditioning applied immediately after hypoxia could protect cultured neurons from hypoxia/reoxygenation (H/R)-induced injuries. METHODS: Primary cortical neuronal culture depleted of microglia was exposed to H/R. Post-conditioning started immediately after hypoxia and consisted of three cycles of 15-minutes of reoxygenation and 15-minutes of hypoxia. Cell viability assay was performed using Cell Counting Kit-8 (CCK-8). Apoptosis was evaluated by Hoechst 33258 staining, FITC-Annexin V/PI double staining and Western blot assay (testing the cleaved caspase-3 expression). Reactive oxygen species (ROS), intracellular Ca(2+) and mitochondrial membrane potential (MMP) were examined using confocal laser-scanning microscopy. MAIN RESULTS: H/R significantly reduced cell viability and increased neuronal apoptosis and necrosis. Furthermore, the expression of cleaved caspase-3, ROS production and intracellular Ca(2+) were increased. MMP was attenuated. Injuries induced by H/R were substantially attenuated by early hypoxic post-conditioning. Changes in cleaved caspase-3 expression, ROS production, intracellular Ca(2+) level and MMP in response to H/R were significantly decreased by the post-conditioning. CONCLUSIONS: The findings demonstrated that early hypoxic post-conditioning could protect neurons against H/R-induced injuries independent of microglial cells, possibly by inhibiting ROS over-production and intracellular Ca(2+) accumulation and maintaining MMP.