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Dexmedetomidine hydrochloride (DEX) is a α2-adrenergic receptor agonist that causes vasoconstriction by acting on α2B-adrenergic receptors in peripheral blood vessels. The authors aimed to determine the influence of DEX on tissue distribution, anesthetic action, and hemodynamic effects of lidocaine in rats. The investigators injected indigo carmine-containing (14)C-labeled lidocaine hydrochloride (2 %) without and with 3.1, 12.5, or 50 μg/mL DEX or 10 μg/mL epinephrine into the right palatal mucosa mesial to the maxillary first molar of specific pathogen-free male Wistar rats. Autoradiography and liquid scintillation counting were performed to evaluate (14)C-labeled lidocaine concentrations in the palatal mucosa, maxillary bone, maxillary nerve, and peripheral blood. Somatosensory-evoked potentials were measured to analyze anesthetic action, and blood pressure and pulse rate were measured to compare hemodynamic effects. DEX extended the tissue distribution of lidocaine in a concentration-dependent manner. Lidocaine with 12.5 μg/mL DEX had similar blood peak arrival time and peak-to-peak amplitude as lidocaine with 10 μg/mL epinephrine, but it reduced pulse rate. The results of this study suggest that 12.5 μg/mL DEX improves tissue distribution, anesthetic action, and hemodynamic effects of lidocaine in rats. Therefore, 12.5 μg/mL DEX may be a suitable alternative to epinephrine in lidocaine formulations, especially for patients with ischemic heart disease and hypertension.

This report demonstrates a late presenter and long-term survivor (38 months old) of alveolar capillary dysplasia with misalignment of the pulmonary veins (ACD/MPV) and with a heterozygous frameshift mutation in FOXF1. The mild phenotype may be due to his residual normal lung tissue as demonstrated in the chest computed tomography (CT) and histopathological findings.We report the longest survivor of ACD/MPV. The mild phenotype is most likely due to the patient's residual normal lung tissue.

In infinite ergodic theory, two distributional limit theorems are well-known. One is characterized by the Mittag-Leffler distribution for time averages of \(L^1(m)\) functions, i.e., integrable functions with respect to an infinite invariant measure. The other is characterized by the generalized arc-sine distribution for time averages of non-\(L^1(m)\) functions. Here, we provide another distributional behavior of time averages of non-\(L^1(m)\) functions in one-dimensional intermittent maps where each has an indifferent fixed point and an infinite invariant measure. Observation functions considered here are non-\(L^1(m)\) functions which vanish at the indifferent fixed point. We call this class of observation functions weak non-\(L^1(m)\) function. Our main result represents a first step toward a third distributional limit theorem, i.e., a distributional limit theorem for this class of observables, in infinite ergodic theory. To prove our proposition, we propose a stochastic process induced by a renewal process to mimic a Birkoff sum of a weak non-\(L^1(m)\) function in the one-dimensional intermittent maps.

BACKGROUND: Genetic variations associated with interstitial lung diseases (ILD) have not been extensively studied in Japanese infants. METHODS: Forty-three infants with unexplained lung dysfunction were studied. All 43, 22, and 17 infants underwent analyses of surfactant protein (SP)-C gene (SFTPC) and ATP-binding cassette A3 gene (ABCA3), SP-B gene (SFTPB), and SP-B western blotting, respectively. Two and four underwent assessment of granulocyte macrophage colony-stimulating factor-stimulating phosphorylation of signal transducer and activator of transcription-5 (pSTAT-5) and analyses of FOXF1 gene (FOXF1), respectively. RESULTS: ILD were diagnosed clinically in nine infants: four, three, and two had interstitial pneumonitis, hereditary pulmonary alveolar proteinosis (hPAP), and alveolar capillary dysplasia with misalignment of pulmonary veins (ACD/MPV), respectively. Genetic variations considered responsible were detected in six (67%) of the nine infants with ILD: three with hPAP (SFTPC p.Leu45Arg and p.Gln145fs, and ABCA3 p.Arg1583Trp/p.Val1495CysfsX21), two with interstitial pneumonitis (SFTPC p.Lys63Glu and p.Ser72Asn/p.Gly100Ala), and one with ACD/MPV (FOXF1 p.Leu300ArgfsX79). None showed SFTPB mutations or defects in pSTAT-5. The 17 bron-choalveolar lavage or tracheal aspirates contained enough SP-B protein. CONCLUSION: The SP-C abnormality was most prevalent, and SP-B deficiency was rare in Japanese infants with hereditary-ILD.