A Systematic Review of the Extent and Measurement of Healthcare Provider Racism

BACKGROUND

Although considered a key driver of racial disparities in healthcare, relatively little is known about the extent of interpersonal racism perpetrated by healthcare providers, nor is there a good understanding of how best to measure such racism.

OBJECTIVES

This paper reviews worldwide evidence (from 1995 onwards) for racism among healthcare providers; as well as comparing existing measurement approaches to emerging best practice, it focuses on the assessment of interpersonal racism, rather than internalized or systemic/institutional racism.

METHODS

The following databases and electronic journal collections were searched for articles published between 1995 and 2012: Medline, CINAHL, PsycInfo, Sociological Abstracts. Included studies were published empirical studies of any design measuring and/or reporting on healthcare provider racism in the English language. Data on study design and objectives; method of measurement, constructs measured, type of tool; study population and healthcare setting; country and language of study; and study outcomes were extracted from each study.

RESULTS

The 37 studies included in this review were almost solely conducted in the U.S. and with physicians. Statistically significant evidence of racist beliefs, emotions or practices among healthcare providers in relation to minority groups was evident in 26 of these studies. Although a number of measurement approaches were utilized, a limited range of constructs was assessed.

CONCLUSION

Despite burgeoning interest in racism as a contributor to racial disparities in healthcare, we still know little about the extent of healthcare provider racism or how best to measure it. Studies using more sophisticated approaches to assess healthcare provider racism are required to inform interventions aimed at reducing racial disparities in health.     

Differential expression of VGLUT1 or VGLUT2 in the trigeminothalamic or trigeminocerebellar projection neurons in the rat

The vesicular glutamate transporters, VGLUT1 and VGLUT2, reportedly display complementary distribution in the rat brain. However, co-expression of them in single neurons has been reported in some brain areas. We previously found co-expression of VGLUT1 and VGLUT2 mRNAs in a number of single neurons in the principal sensory trigeminal nucleus (Vp) of the adult rat; the majority of these neurons sent their axons to the thalamic regions around the posteromedial ventral nucleus (VPM) and the posterior nuclei (Po). It is well known that trigeminothalamic (T-T) projection fibers arise not only from the Vp but also from the spinal trigeminal nucleus (Vsp), and that trigeminocerebellar (T-C) projection fibers take their origins from both of the Vp and Vsp. Thus, in the present study, we examined the expression of VGLUT1 and VGLUT2 in Vp and Vsp neurons that sent their axons to the VPM/Po regions or the cortical regions of the cerebellum. For this purpose, we combined fluorescence in situ hybridization (FISH) histochemistry with retrograde tract-tracing; immunofluorescence histochemistry was also combined with anterograde tract-tracing. The results indicate that glutamatergic Vsp neurons sending their axons to the cerebellar cortical regions mainly express VGLUT1, whereas glutamatergic Vsp neurons sending their axons to the thalamic regions express VGLUT2. The present data, in combination with those of our previous study, indicate that glutamatergic Vp neurons projecting to the cerebellar cortical regions express mainly VGLUT1, whereas the majority of glutamatergic Vp neurons projecting to the thalamus co-express VGLUT1 and VGLUT2.     

Exercise responses in children and adults with a Fontan circulation at simulated altitude

Background: Traveling to high altitude has become more popular. High‐altitude exposure causes hypobaric hypoxia. Exposure to acute high altitude, during air travel or mountain stays, seems to be safe for most patients with congenital heart disorders (CHD). Still, current guidelines for CHD patients express concerns regarding safety of altitude exposure for patients with a Fontan circulation. Therefore, investigating hemodynamic and pulmonary responses of acute high‐altitude exposure (±2500 m) at rest and during maximal exercise in patients with Fontan circulation can provide clarity in this dispute and may contribute to improvement of clinical counseling.
Methods: Twenty‐one Fontan patients with 21 age‐matched healthy controls, aged 8‐40 years, were enrolled in an observational study. Participants performed two car‐ diopulmonary exercise tests on a cycle ergometer with breath‐by‐breath respiratory gas analyses combined with noninvasive impedance cardiac output measurements: one at sea level (±6 m) and one at simulated high altitude (±2500 m), respectively.
Results: The effect of altitude exposure was different in rest for saturation (−2.3% vs −4.1%) between Fontan patients and healthy controls (P < .05). At peak exercise the effects of high altitude exposure was different on VO₂ (−5.1% vs 9.6%) and AvO₂‐diff (−0.3% vs −12.8%) between Fontan patients and healthy controls.
Conclusion: Although, acute high‐altitude exposure has a detrimental effect on exer‐ cise capacity, the impact on pulmonary and hemodynamic responses of high‐altitude exposure is comparable between Fontan patients and healthy controls.     

RAB-5 and RAB-10 cooperate to regulate neuropeptide release in Caenorhabditis elegans

Neurons secrete neuropeptides from dense core vesicles (DCVs) to modulate neuronal activity. Little is known about how neurons manage to differentially regulate the release of synaptic vesicles (SVs) and DCVs. To analyze this, we screened all Caenorhabditis elegans Rab GTPases and Tre2/Bub2/Cdc16 (TBC) domain containing GTPase-activating proteins (GAPs) for defects in DCV release from C. elegans motoneurons. rab-5 and rab-10 mutants show severe defects in DCV secretion, whereas SV exocytosis is unaffected. We identified TBC-2 and TBC-4 as putative GAPs for RAB-5 and RAB-10, respectively. Multiple Rabs and RabGAPs are typically organized in cascades that confer directionality to membrane-trafficking processes. We show here that the formation of release-competent DCVs requires a reciprocal exclusion cascade coupling RAB-5 and RAB-10, in which each of the two Rabs recruits the other’s GAP molecule. This contributes to a separation of RAB-5 and RAB-10 domains at the Golgi–endosomal interface, which is lost when either of the two GAPs is inactivated. Taken together, our data suggest that RAB-5 and RAB-10 cooperate to locally exclude each other at an essential stage during DCV sorting.     

Using willingness to pay to assess the benefits of assisted reproductive techniques

Current economic evaluations of Assisted Reproductive Techniques (ARTs) are criticized for assuming that the only factor important to users is whether they leave the service with a child. Such an approach ignores, first, outcomes beyond some narrow medical definition of success, second, the majority of users who leave the service childless and, third, the actual process of treatment. The aim of this study was to establish the importance of factors beyond some medical definition of success in the provision of ARTs, using the economic instrument of willingness to pay (WTP). The results suggest that there is some value in going through the service, even if the couple leaves it childless. It is concluded that the WTP technique is potentially useful in evaluating ARTs but further studies need to be undertaken to assess its reliability and validity.     

A Homozygous PDE6D Mutation in Joubert Syndrome Impairs Targeting of Farnesylated INPP5E Protein to the Primary Cilium

Joubert syndrome (JS) is characterized by a distinctive cerebellar structural defect, namely the « molar tooth sign ». JS is genetically heterogeneous, involving 20 genes identified to date, which are all required for cilia biogenesis and/or function. In a consanguineous family with JS associated with optic nerve coloboma, kidney hypoplasia, and polydactyly, combined exome sequencing and mapping identified a homozygous splice‐site mutation in PDE6D, encoding a prenyl‐binding protein. We found that pde6d depletion in zebrafish leads to renal and retinal developmental anomalies and wild‐type but not mutant PDE6D is able to rescue this phenotype. Proteomic analysis identified INPP5E, whose mutations also lead to JS or mental retardation, obesity, congenital retinal dystrophy, and micropenis syndromes, as novel prenyl‐dependent cargo of PDE6D. Mutant PDE6D shows reduced binding to INPP5E, which fails to localize to primary cilia in patient fibroblasts and tissues. Furthermore, mutant PDE6D is unable to bind to GTP‐bound ARL3, which acts as a cargo‐release factor for PDE6D‐bound INPP5E. Altogether, these results indicate that PDE6D is required for INPP5E ciliary targeting and suggest a broader role for PDE6D in targeting other prenylated proteins to the cilia. This study identifies PDE6D as a novel JS disease gene and provides the first evidence of prenyl‐binding‐dependent trafficking in ciliopathies.