Prevalence of joint-specific osteoarthritis and joint pain in British Columbia, Canada.

The objective is to determine the prevalence of self-reported physician-diagnosed osteoarthritis (OA) and musculoskeletal symptoms (pain, stiffness or discomfort) in specific joints among adults in British Columbia (BC), Canada. We carried out a cross-sectional mixed-mode survey in a random population sample of persons 18 years of age and older. Estimates were weighted to reflect the age and sex distribution of the population of BC. We obtained responses from 2,233 individuals. Overall, 18.4% (95% CI 16.8-20.1) of the adult population reported OA. Of those, more than 40% had OA in multiple sites. Prevalence ranged from 8.8% (95% CI 7.6-10.1) in the knee to 2.7% (2.1-3.5) in the foot. One-year prevalence of symptoms ranged from 49.1% (47.0-51.2) in the lower back to 23.3% (21.5-25.1) in the hip. Females reported more symptoms and OA than males in all joints. The most common site of self-reported physician-diagnosed OA in BC is the knee, but OA in the hands, hips, and feet is also common. Having OA in one joint is a strong predictor of OA in other joints.

Normal voice processing after posterior superior temporal sulcus lesion.

The right posterior superior temporal sulcus (pSTS) shows a strong response to voices, but the cognitive processes generating this response are unclear. One possibility is that this activity reflects basic voice processing. However, several fMRI and magnetoencephalography findings suggest instead that pSTS serves as an integrative hub that combines voice and face information. Here we investigate whether right pSTS contributes to basic voice processing by testing Faith, a patient whose right pSTS was resected, with eight behavioral tasks assessing voice identity perception and recognition, voice sex perception, and voice expression perception. Faith performed normally on all the tasks. Her normal performance indicates right pSTS is not necessary for intact voice recognition and suggests that pSTS activations to voices reflect higher-level processes.

Voice Recognition in Face-Blind Patients.

Right or bilateral anterior temporal damage can impair face recognition, but whether this is an associative variant of prosopagnosia or part of a multimodal disorder of person recognition is an unsettled question, with implications for cognitive and neuroanatomic models of person recognition. We assessed voice perception and short-term recognition of recently heard voices in 10 subjects with impaired face recognition acquired after cerebral lesions. All 4 subjects with apperceptive prosopagnosia due to lesions limited to fusiform cortex had intact voice discrimination and recognition. One subject with bilateral fusiform and anterior temporal lesions had a combined apperceptive prosopagnosia and apperceptive phonagnosia, the first such described case. Deficits indicating a multimodal syndrome of person recognition were found only in 2 subjects with bilateral anterior temporal lesions. All 3 subjects with right anterior temporal lesions had normal voice perception and recognition, 2 of whom performed normally on perceptual discrimination of faces. This confirms that such lesions can cause a modality-specific associative prosopagnosia.

The processing of voice identity in developmental prosopagnosia.

BACKGROUND: Developmental prosopagnosia is a disorder of face recognition that is believed to reflect impairments of visual mechanisms. However, voice recognition has rarely been evaluated in developmental prosopagnosia to clarify if it is modality-specific or part of a multi-modal person recognition syndrome. OBJECTIVE: Our goal was to examine whether voice discrimination and/or recognition are impaired in subjects with developmental prosopagnosia. DESIGN/METHODS: 73 healthy controls and 12 subjects with developmental prosopagnosia performed a match-to-sample test of voice discrimination and a test of short-term voice familiarity, as well as a questionnaire about face and voice identification in daily life. RESULTS: Eleven subjects with developmental prosopagnosia scored within the normal range for voice discrimination and voice recognition. One was impaired on discrimination and borderline for recognition, with equivalent scores for face and voice recognition, despite being unaware of voice processing problems. CONCLUSIONS: Most subjects with developmental prosopagnosia are not impaired in short-term voice familiarity, providing evidence that developmental prosopagnosia is usually a modality-specific disorder of face recognition. However, there may be heterogeneity, with a minority having additional voice processing deficits. Objective tests of voice recognition should be integrated into the diagnostic evaluation of this disorder to distinguish it from a multi-modal person recognition syndrome.

Enhanced functional integration of human photoreceptor precursors into human and rodent retina in an ex vivo retinal explant model system.

Retinal disease is the major cause of irreversible blindness in developed countries. Transplantation of photoreceptor precursor cells (PPCs) derived from human embryonic stem cells (hESCs) is a promising and widely applicable approach for the treatment of these blinding conditions. Previously, it has been shown that after transplantation into the degenerating retina, the percentage of PPCs that undergo functional integration is low. The factors that inhibit PPC engraftment remain largely unknown, in part, because so many adverse factors could be at play during in vivo experiments. To advance our knowledge in overcoming potential adverse effects and optimize PPC transplantation, we have developed a novel ex vivo system. Harvested neural retina was placed directly on top of cultured retinal pigment epithelial (RPE) cells from a number of different sources. To mimic PPC transplantation into the subretinal space, hESC-derived PPCs were inserted between the retinal explant and underlying RPE. Explants cocultured with hESC-derived RPE maintained normal gross morphology and viability for up to 2 weeks, whereas the explants cultured on ARPE19 and RPE-J failed by 7 days. Furthermore, the proportion of PPCs expressing ribbon synapse-specific proteins BASSOON and RIBEYE was significantly higher when cocultured with hESC-derived RPE (20% and 10%, respectively), than when cocultured with ARPE19 (only 6% and 2%, respectively). In the presence of the synaptogenic factor thrombospondin-1 (TSP-1), the proportion of BASSOON-positive and RIBEYE-positive PPCs cocultured with hESC-derived RPE increased to ∼30% and 15%, respectively. These data demonstrate the utility of an ex vivo model system to define factors, such as TSP-1, which could influence integration efficiency in future in vivo experiments in models of retinal degeneration.

Moderate or deep local hypothermia does not prevent the onset of ischemia-induced dendritic damage.

We studied the acute (up to 2 hours after reperfusion) effects of localized cortical hypothermia on ischemia-induced dendritic structural damage. Moderate (31°C) and deep (22°C) hypothermia delays, but does not block the onset of dendritic blebbing or spine loss during global ischemia in mouse in vivo. Hypothermic treatment promoted more consistent recovery of dendritic structure and spines during reperfusion. These results suggest that those using therapeutic hypothermia will need to consider that it does not spare neurons from structural changes that are the result of ischemia, but hypothermia may interact with mechanisms that control the onset of damage and recovery during reperfusion.

Reversible cyclosporin A-sensitive mitochondrial depolarization occurs within minutes of stroke onset in mouse somatosensory cortex in vivo: a two-photon imaging study.

Neuronal structure and function are rapidly damaged during global ischemia but can in part recover during reperfusion. Despite apparent recovery in the hours/days following an ischemic episode, delayed cell death can be initiated, making it important to understand how initial ischemic events affect potential mediators of apoptosis. Mitochondrial dysfunction and the opening of the mitochondrial permeability transition pore (mPTP) are proposed to link ischemic ionic imbalance to mitochondrially mediated cell death pathways. Using two-photon microscopy, we monitored mitochondrial transmembrane potential (Deltapsi(m)) in vivo within the somatosensory cortex during ischemia and reperfusion in a mouse global ischemia model. Our results indicated a synchronous loss of Deltapsi(m) within 1-3 min of ischemic onset that was linked to within seconds of plasma membrane potential (Deltapsi(p)) depolarization. Deltapsi(m) recovered rapidly upon reperfusion, and no delayed depolarization was observed over 2 h. Cyclosporin A treatment largely blocked Deltapsi(m) collapse during ischemia, suggesting a role for the mPTP. Blocking Deltapsi(m) depolarization did not affect structural damage to dendrites, indicating that the opening of the mPTP and damage to dendrites are separable pathways that are activated during Deltapsi(p) depolarization. Our findings using in vivo imaging suggest that mitochondrial dysfunction and specifically the activation of the mPTP are early reversible events during brain ischemia that could trigger delayed cell death.