Percutaneous vertebroplasty — initial clinical experience in osteoporotic and myelomatous compression fractures

Background  

To review the clinical impact of vertebroplasty in osteoporotic and myelomatous compression fractures     

Identifying gaps in COVID-19 health equity data reporting in Canada using a scorecard approach

ObjectiveTo assess health equity-oriented COVID-19 reporting across Canadian provinces and territories, using a scorecard approach.MethodsA scan was performed of provincial and territorial reporting of five data elements (cumulative totals of tests, cases, hospitalizations, deaths, and population size) across three units of aggregation (province or territory level, health regions, and local areas) (15 “overall” indicators), and for four vulnerable settings (long-term care and detention facilities, schools, and homeless shelters) and eight social markers (age, sex, immigration status, race/ethnicity, healthcare worker status, occupational sector, income, and education) (180 “equity-related” indicators) as of December 31, 2020. Per indicator, one point was awarded if case-delimited data were released, 0.7 points if only summary statistics were reported, and 0 if neither was provided. Results were presented using a scorecard approach.ResultsOverall, information was more complete for cases and deaths than for tests, hospitalizations, and population size denominators needed for rate estimation. Information provided on jurisdictions and their regions, overall, tended to be more available (average score of 58%, “D”) than that for equity-related indicators (average score of 17%, “F”). Only British Columbia, Alberta, and Ontario provided case-delimited data, with Ontario and Alberta providing case information for local areas. No jurisdiction reported on outcomes according to patients’ immigration status, race/ethnicity, income, or education. Though several provinces reported on cases in long-term care facilities, only Ontario and Quebec provided detailed information for detention facilities and schools, and only Ontario reported on cases within homeless shelters and across occupational sectors.ConclusionOne year into the pandemic, socially stratified reporting for COVID-19 outcomes remains sparse in Canada. However, several “best practices” in health equity-oriented reporting were observed and set a relevant precedent for all jurisdictions to follow for this pandemic and future ones.Supplementary InformationThe online version contains supplementary material available at 10.17269/s41997-021-00496-6.     

Brain-derived neurotrophic factor genotype impacts the prenatal cocaine-induced mouse phenotype

Prenatal cocaine exposure leads to persistent alterations in the growth factor brain-derived neurotrophic factor (BDNF), particularly in the medial prefrontal cortex (mPFC) and hippocampus, brain regions important in cognitive functioning. BDNF plays an important role in the strengthening of existing synaptic connections as well as in the formation of new contacts during learning. A single nucleotide polymorphism in the BDNF gene (Val66Met), leading to a Met substitution for Val at codon 66 in the prodomain, is common in human populations, with an allele frequency of 20-30% in Caucasians. To study the interaction between prenatal cocaine exposure and BDNF, we have utilized a line of BDNF Val66Met transgenic mice on a Swiss Webster background in which BDNF(Met) is endogenously expressed. Examination of baseline levels of mature BDNF protein in the mPFC of prenatally cocaine-treated wild-type (Val66Val) and Val66Met mice revealed significantly lower levels compared to prenatally saline-treated mice. In contrast, in the hippocampus of prenatally saline- and cocaine-treated adult Val66Met mice, there were significantly lower levels of mature BDNF protein compared to Val66Val mice. In extinction of a conditioned fear, we found that prenatally cocaine-treated Val66Met mice had a deficit in recall of extinction. Examination of mature BDNF protein levels immediately after the test for extinction recall revealed lower levels in the mPFC of prenatally cocaine-treated Val66Met mice compared to saline-treated mice. However, 2 h after the extinction test, there was increased BDNF exons I, IV, and IX mRNA expression in the prelimbic cortex of the mPFC in the prenatally cocaine-treated BDNF Val66Met mice compared to prenatally saline-treated mice. Taken together, our results suggest the possibility that prenatal cocaine-induced constitutive alterations in BDNF mRNA and protein expression in the mPFC differentially poises animals for alterations in behaviorally induced gene activation, which are interactive with BDNF genotype and differentially impact those behaviors. Such findings in our prenatal cocaine mouse model suggest a gene X environment interaction of potential clinical relevance.     

Mapping the relationship between subgenual cingulate cortex functional connectivity and depressive symptoms across adolescence

Changes in the functional connectivity of the subgenual anterior cingulate cortex (SGC) have been linked with depressive symptoms. The aim of this study was to map this relationship across mid to late adolescence. Employing a longitudinal functional magnetic resonance imaging (fMRI) design, associations between patterns of resting-state SGC functional connectivity and symptoms of depression were examined at two time points in an initial sample of 72 adolescents. Using a region-of-interest approach, these associations were evaluated cross-sectionally and longitudinally. Cross-sectionally, weaker SGC functional connectivity with the posterior cingulate cortex (PCC), angular gyrus and dorsal prefrontal cortex at baseline, and weaker SGC connectivity with the dorsomedial prefrontal cortex (DMPFC) and ventromedial prefrontal cortex at follow-up, were associated with higher depressive symptoms. Longitudinally, a decrease in SGC functional connectivity with DMPFC, PCC, angular gyrus and middle temporal gyrus was associated with higher depressive symptoms at follow-up. The observation of weaker SGC connectivity predicting increased symptoms contrasts with the majority of resting-state fMRI studies in clinically depressed populations. Taken together with these past studies, our findings suggest depression-related changes in SGC functional connectivity may differ across developmental and illness stages.     

Identifying subtypes of mild cognitive impairment in Parkinson’s disease using cluster analysis

Journal of Neurology - The concept of Mild Cognitive Impairment (MCI) in Parkinson’s disease (PD) has shown the potential for identifying at-risk dementia patients. Identifying subtypes of...     

Association between serotonin transporter genotype,brain structure and adolescent-onset major depressive disorder: a longitudinal prospective study

The extent to which brain structural abnormalities might serve as neurobiological endophenotypes that mediate the link between the variation in the promoter of the serotonin transporter gene (5-HTTLPR) and depression is currently unknown. We therefore investigated whether variation in hippocampus, amygdala, orbitofrontal cortex (OFC) and anterior cingulate cortex volumes at age 12 years mediated a putative association between 5-HTTLPR genotype and first onset of major depressive disorder (MDD) between age 13–19 years, in a longitudinal study of 174 adolescents (48% males). Increasing copies of S-alleles were found to predict smaller left hippocampal volume, which in turn was associated with increased risk of experiencing a first onset of MDD. Increasing copies of S-alleles also predicted both smaller left and right medial OFC volumes, although neither left nor right medial OFC volumes were prospectively associated with a first episode of MDD during adolescence. The findings therefore suggest that structural abnormalities in the left hippocampus may be present prior to the onset of depression during adolescence and may be partly responsible for an indirect association between 5-HTTLPR genotype and depressive illness. 5-HTTLPR genotype may also impact upon other regions of the brain, such as the OFC, but structural differences in these regions in early adolescence may not necessarily alter the risk for onset of depression during later adolescence.     

Perceptions of disadvantage, ethnicity and psychosis

BACKGROUND: People from Black ethnic groups (African-Caribbean and Black African) are more prone to develop psychosis in Western countries. This excess might be explained by perceptions of disadvantage. AIMS: To investigate whether the higher incidence of psychosis in Black people is mediated by perceptions of disadvantage. METHOD: A population-based incidence and case-control study of first-episode psychosis (Aetiology and Ethnicity in Schizophrenia and Other Psychoses (AESOP)). A total of 482 participants answered questions about perceived disadvantage. RESULTS: Black ethnic groups had a higher incidence of psychosis (OR= 4.7, 95% CI 3.1-7.2). After controlling for religious affiliation, social class and unemployment, the association of ethnicity with psychosis was attenuated (OR=3.0, 95% CI 1.6-5.4) by perceptions of disadvantage. Participants in the Black non-psychosis group often attributed their disadvantage to racism, whereas Black people in the psychosis group attributed it to their own situation. CONCLUSIONS: Perceived disadvantage is partly associated with the excess of psychosis among Black people living in the UK. This may have implications for primary prevention.