14 research outputs found

    The asymptotic variance rate of the output process of finite capacity birth-death queues

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    We analyze the output process of finite capacity birth-death Markovian queues. We develop a formula for the asymptotic variance rate of the form λ *+σvi where λ * is the rate of outputs and v i are functions of the birth and death rates. We show that if the birth rates are non-increasing and the death rates are non-decreasing (as is common in many queueing systems) then the values of v i are strictly negative and thus the limiting index of dispersion of counts of the output process is less than unity. In the M/M/1/K case, our formula evaluates to a closed form expression that shows the following phenomenon: When the system is balanced, i.e. the arrival and service rates are equal, σvi\λ* is minimal. The situation is similar for the M/M/c/K queue, the Erlang loss system and some PH/PH/1/K queues: In all these systems there is a pronounced decrease in the asymptotic variance rate when the system parameters are balanced

    Novel FOXF1 Mutations in Sporadic and Familial Cases of Alveolar Capillary Dysplasia with Misaligned Pulmonary Veins Imply a Role for its DNA Binding Domain.

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    Alveolar capillary dysplasia with misalignment of pulmonary veins (ACD/MPV) is a rare and lethal developmental disorder of the lung defined by a constellation of characteristic histopathological features. Nonpulmonary anomalies involving organs of gastrointestinal, cardiovascular, and genitourinary systems have been identified in approximately 80% of patients with ACD/MPV. We have collected DNA and pathological samples from more than 90 infants with ACD/MPV and their family members. Since the publication of our initial report of four point mutations and 10 deletions, we have identified an additional 38 novel nonsynonymous mutations of FOXF1 (nine nonsense, seven frameshift, one inframe deletion, 20 missense, and one no stop). This report represents an up to date list of all known FOXF1 mutations to the best of our knowledge. Majority of the cases are sporadic. We report four familial cases of which three show maternal inheritance, consistent with paternal imprinting of the gene. Twenty five mutations (60%) are located within the putative DNA-binding domain, indicating its plausible role in FOXF1 function. Five mutations map to the second exon. We identified two additional genic and eight genomic deletions upstream to FOXF1. These results corroborate and extend our previous observations and further establish involvement of FOXF1 in ACD/MPV and lung organogenesis
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