Symmetric inclusion-exclusion

One form of the inclusion-exclusion principle asserts that if A and B are functions of finite sets then A(S) is the sum of B(T) over all subsets T of S if and only if B(S) is the sum of (-1)^|S-T| A(T) over all subsets T of S. If we replace B(S) with (-1)^|S| B(S), we get a symmetric form of inclusion-exclusion: A(S) is the sum of (-1)^|T| B(T) over all subsets T of S if and only if B(S) is the sum of (-1)^|T| A(T) over all subsets T of S. We study instances of symmetric inclusion-exclusion in which the functions A and B have combinatorial or probabilistic interpretations. In particular, we study cases related to the Polya-Eggenberger urn model in which A(S) and B(S) depend only on the cardinality of S.Comment: 10 page

Differential disease restriction of Moloney and Friend murine leukemia viruses by the mouse Rmcf gene is governed by the viral long terminal repeat.

Neonatal CxD2 (Rmcfr) and Balb/c (Rmcfs) mice inoculated with Moloney murine leukemia virus (M-MuLV) exhibited approximately equivalent time course and pathology for disease. CxD2 mice showed only slightly reduced presence of Moloney mink cell focus-forming virus (M-MCF) provirus as seen by Southern blot analysis compared to Balb/c mice. This lack of restriction for disease and spread of MCF was in sharp contrast to that seen for CxD2 mice inoculated with Friend murine leukemia virus (F-MuLV), where incidence of disease and propagation of MCFs were severely restricted, as previously reported. Inoculation of CxD2 mice with FM-MuLV, a recombinant F-MuLV virus containing M-MuLV LTR sequences (U3 and R), resulted in T cell disease of time course equal to that seen in Balb/c mice; there also was little restriction for propagation of MCFs. This indicated that presence of the M-MuLV long terminal repeat (LTR) was sufficient for propagation of MCFs in CxD2 mice. Differing restriction for F-MuLV vs. M-MuLV in CxD2 mice was explained on the basis of different "MCF propagator cells" for the two viruses. It was suggested that cells propagating F-MCF (e.g., erythroid progenitors) are blocked by endogenous MCF-like gp70env protein, whereas cells propagating M-MCF (e.g., lymphoid) do not express this protein on their surface. F-MuLV disease in CxD2 mice was greatly accelerated when neonates were inoculated with a F-MuLV/F-MCF pseudotypic mixture. However, F-MCF provirus was not detectable or only barely detectable in F-MuLV/F-MCF-induced tumors, suggesting that F-MCF acted indirectly in induction of these tumors

Effect of screening abdominal ultrasound examination on the decision to pursue advanced diagnostic tests and treatment in dogs with neurologic disease.

BackgroundAbdominal ultrasound examinations (AUS) are commonly performed before advanced neurodiagnostics to screen for diseases that might affect diagnostic plans and prognosis.ObjectivesDescribe the type and frequency of abnormalities found by AUS in dogs presenting with a neurological condition, identify risk factors associated with abnormalities, and evaluate treatment decisions based on findings.AnimalsSeven hundred and fifty-nine hospitalized dogs.MethodsRetrospective study. Medical records of dogs presented from 2007 to 2009 for neurologic disease were searched for signalment, neuroanatomic localization, and AUS findings. Whether dogs had advanced neurodiagnostics and treatment was analyzed.ResultsFifty-eight percent of dogs had abnormal findings on AUS. Probability of abnormalities increased with age (P < 0.001). Nondachshund breeds had higher probability of abnormal AUS than dachshunds (odds ratio [OR] = 1.87). Eleven percent of dogs did not have advanced neurodiagnostics and in 1.3%, this was because of abnormal AUS. Dogs with ultrasonographic abnormalities were less likely than dogs without to have advanced neurodiagnostics (OR = 0.3 [95% confidence interval [CI]: 0.17, 0.52]), however, the probability of performing advanced diagnostics was high regardless of normal (OR = 0.95 [95% CI: 0.92, 0.97]) or abnormal (OR = 0.85 [95% CI: 0.81, 0.88]) AUS. Treatment was more often pursued in small dogs and less often in dogs with brain disease.Conclusions and clinical importanceFindings from screening AUS had a small negative effect on the likelihood of pursuing advanced neurodiagnostics. Although it should be included in the extracranial diagnostic workup in dogs with significant history or physical examination abnormalities, AUS is considered a low-yield diagnostic test in young dogs and dachshunds

Healthcare Data Analytics on the Cloud

Meaningful analysis of voluminous health information has always been a challenge in most healthcare organizations. Accurate and timely information required by the management to lead a healthcare organization through the challenges found in the industry can be obtained using business intelligence (BI) or business analytics tools. However, these require large capital investments to implement and support the large volumes of data that needs to be analyzed to identify trends. They also require enormous processing power which places pressure on the business resources in addition to the dynamic changes in the digital technology. This paper evaluates the various nuances of business analytics of healthcare hosted on the cloud computing environment. The paper explores BI being offered as Software as a Service (SaaS) solution towards offering meaningful use of information for improving functions in healthcare enterprise. It also attempts to identify the challenges that healthcare enterprises face when making use of a BI SaaS solution

Characterization of an Inherited Neurologic Syndrome in Toyger Cats with Forebrain Commissural Malformations, Ventriculomegaly and Interhemispheric Cysts.

BackgroundIn children, frequent congenital malformations with concomitant agenesis of the corpus callosum are diagnosed by neuroimaging in association with other cerebral malformations, including interhemispheric cysts and ventriculomegaly. Similar studies providing full characterization of brain defects by in vivo magnetic resonance imaging (MRI), and correlations with the pertinent anatomic pathologic examinations are absent in veterinary medicine.Hypothesis/objectivesCongenital brain defects underlie the neurologic signs observed in Toyger cats selectively bred for a short ear phenotype.AnimalsUsing proper pedigree analysis and genetic evaluations, 20 related Oriental-derived crossbred Toyger cats were evaluated. Seven clinically healthy (carrier) cats and 13 clinically affected cats that had neurologic signs, short ear phenotype and concomitant complex brain anomalies were studied.MethodsComplete physical and neurologic examinations and MRI were performed in all clinically healthy and affected cats. Postmortem and histopathologic examinations were performed in 8 affected cats and 5 healthy cats.ResultsNeurologic and MRI investigations confirmed 13 clinically affected cats with structural brain abnormalities. Ventriculomegaly with frequent concomitant supratentorial interhemispheric, communicating ventricular type-1b cysts and multiple midline and callosal malformations were detected in all cats displaying neurologic signs. Genetic analysis confirmed autosomal recessive mode of inheritance with no chromosomal abnormalities.Conclusions and clinical importanceNeuroanatomic dissections and histopathology were helpful for evaluation of abnormalities in midline brain structures, and for the full characterization of cysts. However, MRI was more sensitive for detection of small cysts. In this feline model, MRI diagnosis had extremely good correlation with pathologic abnormalities noted in the subset of animals that were examined by both modalities