Measurements of stratospheric carbon dioxide (CO2) and nitrous oxide (N2O) concentrations were analyzed to investigate stratospheric transport rates. Temporal variations in tropospheric CO2 were observed to propagate into the stratosphere, showing that tropospheric air enters the lower tropical stratosphere continuously, ascends, and is transported rapidly (in less than 1 month) to both hemispheres. The mean age A of stratospheric air determined from CO2 data is approximately 5 years in the mid-stratosphere. The mean age is mathematically equivalent to a conserved tracer analogous to exhaust from stratospheric aircraft. Comparison of values for A from models and observations indicates that current model simulations likely underestimate pollutant concentrations from proposed stratospheric aircraft by 25 to 100 percent.

Abstract. The influence of the quasi-biennial oscillation (QBO) on the transport of long-lived tracers out of the tropics and the mechanism responsible for the QBO in subtropical ozone and its dependence on the seasonal cycle are examined with a two-dimensional model. The modeled QBO induces a meridional circulation which modulates transport of long-lived tracers out of the tropics. The induced circulation also produces a QBO in ozone in the subtropics by advection of ozone out of the tropics and down from higher altitudes. In agreement with observations, the subtropical anomalies in ozone are greatest in the winter season. This seasonal synchronization of the subtropical anomalies occurs because the induced circulation is stronger always in the winter hemisphere as a result of nonlinear momentum advection in the tropics and subtropics. Meridional transport in the model is enhanced by the QBO through an "upper" and a "lower" transport regime, in agreement with the analysis by Hitchman et al. [ 1994]. When there are descending westerly winds in the tropics in the model, transport out of the tropics is enhanced in the lower stratosphere. When there are descending easterlies, transport out of the tropics is enhanced in the middle stratosphere. This modulation of transport out of the tropics significantly influences the stratospheric distribution of long-lived tracers. Depending on the phase of the QBO, mixing ratio surfaces of long-lived tracers (such as N20 ) in the extratropics can be displaced poleward by more than 10 ø.

Abstract. A coupled two-dimensional model of the dynamics, chemistry, and radiation of the stratosphere is described. The effects of Rossby wave mixing are parameterized by externally specified coefficients Kyy, which are used consistently

The study of pathological laughter and crying (PLC) allows insights into the neural basis of laughter and crying, two hallmarks of human nature. PLC is defined by brief, intense and frequent episodes of uncontrollable laughter or crying provoked by trivial stimuli. It occurs secondary to CNS disorders such as stroke, tumours or neurodegenerative diseases. Based on case studies reporting various lesions locations, PLC has been conceptualized as dysfunction in a cortico-limbic-subcortico-thalamo-ponto-cerebellar network. To test whether the heterogeneous lesion locations are indeed linked in a common network, we applied ‘lesion network-symptom-mapping’ (LNSM) to 70 focal lesions identified in a systematic literature search for case reports of PLC. In LNSM normative connectome data (resting state functional MRI, n = 100) is used to identify the brain regions which are likely affected by diaschisis based on the lesion locations. With LNSM we were able to identify a common network specific for PLC when compared with a control cohort (n = 270). This bilateral network is characterized by positive connectivity to the cingulate and temporomesial cortices, striatum, hypothalamus, mesencephalon and pons and negative connectivity to the primary motor and sensory cortices. In the most influential pathophysiological model of PLC, a center for the control and coordination of facial expressions, respiration and vocalization in the periaqueductal grey is assumed which is controlled via two pathways: an emotional system that exerts excitatory control of the periaqueductal grey descending from the temporal and frontal lobes, basal ganglia and hypothalamus and a volitional system descending from the lateral premotor cortices which can suppress laughter or crying. To test whether the positive and negative PLC subnetworks identified in our analyses can indeed be related to an emotional system and a volitional system, we identified lesions causing emotional (n = 15) or volitional facial paresis (n = 46) in a second literature search. Patients with emotional facial paresis show preserved volitional movements but cannot trigger emotional movements in the affected hemiface, while the reverse is true for volitional facial paresis. Importantly, these lesions map differentially onto the PLC subnetworks: the ‘positive PLC subnetwork’ is part of the emotional system and the ‘negative PLC subnetwork’ overlaps with the volitional system for the control of facial movements. Based on this network analysis we propose a two-hit model of PLC: a combination of direct lesion and indirect diaschisis effects cause PLC through the loss of inhibitory cortical control of a dysfunctional emotional system.