Observation of the Dsj(2463) and Confirmation of the Dsj*(2317)

Using 13.5 inverse-femtobarns of e+e- annihilation data in the CLEO II detector at CESR, we have observed a new narrow state decaying to Ds*+ pio, denoted the DsJ(2463). A possible interpretation holds that this is a J^P = 1+^ partner to the DsJ*(2317) state recently discovered by the BaBar Collaboration which is consistent with J^P = 0^+. We have also confirmed the existence of the DsJ*(2317) in its decay to Ds+ pio. We have measured the masses of both states, accounting for the cross-feed background that the two states represent for each other, and have searched for other decay channels for both states. No narrow resonances are seen in neutral or doubly charged Ds pi modes.Comment: Presented at MRST 2003 conference, "Joefest" Syracuse University, May 13-15, 2003; Conf. on the Intersections of Particle & Nuclear Phyiscs, New York, NY, May 19-24, 2003; Flavor Physics and CP Violation, Ecole Polytechnique, Paris, France, June 3-6, 2003; 7 pages 4 figure

Exponential chi squared distributions in infinite ergodic theory

We prove distributional limit theorems for random walk adic transformations obtaining ergodic distributional limits of exponential chi squared form.Comment: Keywords: Infinite ergodic theory, distributional convergence, random walk adic transformatio

Non-Molecular-Clock-Like Evolution following Viral Origins in Homo sapiens

Researchers routinely adopt molecular clock assumptions in conducting sequence analyses to estimate dates for viral origins in humans. We used computational methods to examine the extent to which this practice can result in inaccurate ‘retrodiction.’ Failing to account for dynamic molecular evolution can affect greatly estimating index case dates, resulting in an overestimated age for the SARS-CoV-human infection, for instance

Functional neurological disorder and multiple sclerosis: a systematic review of misdiagnosis and clinical overlap

Multiple sclerosis (MS) and functional neurological disorder (FND) are both diagnostically challenging conditions which can present with similar symptoms. We systematically reviewed the literature to identify patients with MS who were misdiagnosed with FND, patients with FND who were misdiagnosed with MS, and reports of patients with both conditions. In addition to FND, we included studies of patients with other functional and psychiatric disorders where these caused symptoms leading to investigation for or a diagnosis of MS, which in a different context would likely have been labeled as FND. Our review suggests that MS is one of the most common causes of misdiagnosis of FND and vice versa. We discuss the clinical errors that appear to result in misdiagnoses, such as over-reliance on psychiatric comorbidity when making a diagnosis of FND or over-reliance on neuroimaging for the diagnosis of MS, and practical ways to avoid them. Comorbidity between these two conditions is also likely common, has been poorly studied, and adds complexity to diagnosis and treatment in patients with both MS and FND. Misdiagnosis and comorbidity in a landscape of emerging evidence-based treatments for both MS and FND are issues not only of clinical importance to the care of these patients, but also to treatment trials, especially of MS, where FND could be a hidden confounder