Foster Caregiver Experience of Pediatric Hospital-to-Home Transitions: A Qualitative Analysis.

Objective: Children entering foster care after discharge from the hospital are at risk for adverse events associated with the hospital-to-home transition. Education of foster caregivers regarding transitional care needs is key. However, little is known about the unique needs of foster caregivers as they transition from hospital to home with a new foster child or how hospital-based health care teams can better support foster caregivers.

Improving Hospital-to-Home Transitions for Children Entering Foster Care.

Background And Objectives: Hospital-to-home transitions present safety risks for patients. Children discharged with new foster caregivers may be especially vulnerable to poor discharge outcomes. With this study, our objective is to identify differences in discharge quality and outcomes for children discharged from the hospital with new foster caregivers compared with children discharged to their preadmission caregivers.

The Economic Burden of Schizophrenia in the United States in 2013.

Objective: The objective of this study was to estimate the US societal economic burden of schizophrenia and update the 2002 reported costs of $62.7 billion given the disease management and health care structural changes of the last decade.

Methods: A prevalence-based approach was used to assess direct health care costs, direct non-health care costs, and indirect costs associated with schizophrenia (ICD-9 codes 295.

Single-dose intracerebroventricular administration of galactocerebrosidase improves survival in a mouse model of globoid cell leukodystrophy.

Globoid cell leukodystrophy (GLD), also known as Krabbe disease, is a devastating, degenerative neurological disorder. It is inherited as an autosomal recessive trait caused by loss-of-function mutations in the galactocerebrosidase (GALC) gene. Previously, we have shown that peripheral injection of recombinant GALC, administered every other day, results in a substantial improvement in early clinical phenotype in the twitcher mouse model of GLD.

Alzheimer disease with amygdala Lewy bodies: a distinct form of alpha-synucleinopathy.

Lewy bodies (LBs) are alpha-synuclein-immunoreactive neuronal inclusions with a predilection for specific cortical and subcortical regions, including the amygdala. In this study, the presence of LBs was assessed in 347 cases of Alzheimer disease (AD). In 87 cases, LB pathology was diagnostic of brainstem (n=3), transitional (n=32), or diffuse (n=52) Lewy body disease (LBD).

Argyrophilic grain disease in demented subjects presenting initially with amnestic mild cognitive impairment.

A previous autopsy study of patients with amnestic-type mild cognitive impairment (MCI) suggested an overrepresentation of argyrophilic grain disease (AGD). We studied 34 patients who had diagnoses of amnestic MCI during progression to dementia and who came to autopsy. Neuropathologic evaluation included routine histochemical and immunohistochemical methods, including a 4-repeat tau-specific marker (ET3).

Suppression of galactosylceramidase (GALC) expression in the twitcher mouse model of globoid cell leukodystrophy (GLD) is caused by nonsense-mediated mRNA decay (NMD).

The twitcher mouse is a pathologically and enzymatically authentic model of globoid cell leukodystrophy (GLD, Krabbe disease) that has been widely used for the evaluation of potential therapeutic approaches. This naturally occurring mouse model contains a premature stop codon (W339X) in the galactosylceramidase (GALC) gene that abolishes enzymatic activity. Using either immunocytochemical approaches or Western blot methodology, we have been unable to detect the truncated form of GALC expected to be produced in these animals.

Hereditary diffuse leukoencephalopathy with spheroids: clinical, pathologic and genetic studies of a new kindred.

Hereditary diffuse leukoencephalopathy with spheroids (HDLS) is a rare autosomal dominant disorder characterized by cerebral white matter degeneration with axonal spheroids leading to progressive cognitive and motor dysfunction. We report clinical and pathological features, as well as molecular genetic analysis, of a family with HDLS. A pedigree consisting of 27 persons in 5 generations contained 6 affected individuals.

Abeta42 is essential for parenchymal and vascular amyloid deposition in mice.

Considerable circumstantial evidence suggests that Abeta42 is the initiating molecule in Alzheimer's disease (AD) pathogenesis. However, the absolute requirement for Abeta42 for amyloid deposition has never been demonstrated in vivo. We have addressed this by developing transgenic models that express Abeta1-40 or Abeta1-42 in the absence of human amyloid beta protein precursor (APP) overexpression.

Enzyme replacement therapy results in substantial improvements in early clinical phenotype in a mouse model of globoid cell leukodystrophy.

Globoid cell leukodystrophy (GLD) or Krabbe disease is a devastating, degenerative neurological disorder caused by mutations in the galactosylceramidase (GALC) gene that severely affect enzyme activity. Currently, treatment options for this disorder are very limited. Enzyme replacement therapy (ERT) has been shown to be effective in lysosomal storage disorders with predominantly peripheral manifestations such as type I Gaucher's and Fabry's disease.

Alpha-synuclein immunoreactivity in neuronal nuclear inclusions and neurites in multiple system atrophy.

We examined neuronal and oligodendroglial nuclear inclusions and neurites in the pontine base of multiple system atrophy brains using an antibody to alpha-synuclein. Immunohistochemistry showed alpha-synuclein positive inclusions in the nuclei of some neurons and oligodendroglia. Immunoelectron microscopy showed that the labeled inclusions were composed of bundles of tightly packed straight filaments with a diameter of 10-20 nm.