Public Reporting and Transparency

Provides a short history of efforts to report information on health system performance; identifies policy issues to consider when advancing such efforts; and offers lessons from the experience of public reporting efforts to date

The Insulin Resistance Intervention after Stroke trial: a perspective on future practice and research

The prevention of recurrent events after ischaemic stroke and transient ischaemic attack is well established and based on lifestyle changes, antithrombotics, statins, antihypertensives and carotid surgery. The international IRIS trial assessed whether pioglitazone, a glucose-lowering insulin-sensitizing drug, would reduce recurrent vascular events in patients with ischaemic stroke or transient ischaemic attack. After 4.8 years, pioglitazone therapy was associated with reduced vascular events and new diabetes, and an increase in weight, oedema and bone fractures. Pioglitazone may add to the strategies for preventing further events in patients with stroke or transient ischaemic attack

Understanding the Relationship Between Type 2 Diabetes and Bladder Cancer

Individuals with type 2 diabetes (T2DM) have an increased risk of bladder cancer, relative to non-diabetic individuals. We aimed to investigate factors that may influence this association. Some reports suggest an association between the glucose-lowering drug pioglitazone and bladder cancer. Our first objective was to quantify the potential risk of bladder cancer with pioglitazone use, using meta-analytic techniques. Other studies observed a time-varying risk of cancer in T2DM. Our second objective was to assess temporal trends in the risk of bladder cancer in newly diagnosed T2DM vs. non-diabetic individuals. In our systematic review, we saw that pioglitazone use was associated with an increased risk of bladder cancer, but this was not seen with other drugs in the same class. In our administrative cohort study, bladder cancer risk was significantly elevated only in the first year following T2DM diagnosis, and only in the lowest category of physician visits before T2DM diagnosis

Assessment of emergency medicine residents: a systematic review

Background: Competency-based medical education is becoming the new standard for residency programs, including Emergency Medicine (EM). To inform programmatic restructuring, guide resources and identify gaps in publication, we reviewed the published literature on types and frequency of resident assessment.Methods: We searched MEDLINE, EMBASE, PsycInfo and ERIC from Jan 2005 - June 2014. MeSH terms included “assessment,” “residency,” and “emergency medicine.” We included studies on EM residents reporting either of two primary outcomes: 1) assessment type and 2) assessment frequency per resident. Two reviewers screened abstracts, reviewed full text studies, and abstracted data. Reporting of assessment-related costs was a secondary outcome.Results: The search returned 879 articles; 137 articles were full-text reviewed; 73 met inclusion criteria. Half of the studies (54.8%) were pilot projects and one-quarter (26.0%) described fully implemented assessment tools/programs. Assessment tools (n=111) comprised 12 categories, most commonly: simulation-based assessments (28.8%), written exams (28.8%), and direct observation (26.0%). Median assessment frequency (n=39 studies) was twice per month/rotation (range: daily to once in residency). No studies thoroughly reported costs.Conclusion: EM resident assessment commonly uses simulation or direct observation, done once-per-rotation. Implemented assessment systems and assessment-associated costs are poorly reported. Moving forward, routine publication will facilitate transitioning to competency-based medical education

Loss of PV Interneurons in the BLA May Contribute to Altered Network and Behavioral States in Chronically Epileptic Mice.

Psychiatric disorders, including anxiety and depression, are highly comorbid in people with epilepsy. However, the mechanisms mediating the shared pathophysiology are currently unknown. There is considerable evidence implicating the basolateral amygdala (BLA) in the network communication of anxiety and fear, a process demonstrated to involve parvalbumin-positive (PV) interneurons. The loss of PV interneurons has been well described in the hippocampus of chronically epileptic mice and in postmortem human tissue of patients with temporal lobe epilepsy (TLE). We hypothesize that a loss of PV interneurons in the BLA may contribute to comorbid mood disorders in epilepsy. To test this hypothesis, we employed a ventral intrahippocampal kainic acid model of TLE in mice, which exhibits profound behavioral deficits associated with chronic epilepsy. We demonstrate a loss of PV interneurons and dysfunction of the remaining PV interneurons in the BLA of chronically epileptic mice. Furthermore, we demonstrate altered principal neuron function and impaired coordination of BLA network and behavioral states in chronically epileptic mice. To determine whether the loss of PV interneurons contributes to these altered network and behavioral states, we partially ablated PV interneurons in the BLA by stereotaxically injecting AAV-Flex-DTA into the BLA of PV-Cre mice. Loss of PV interneurons in the BLA is sufficient to alter behavioral states, such as increasing avoidance behaviors and impairing fear learning. These data suggest that compromised inhibition in the BLA in chronically epileptic mice may contribute to behavioral deficits, suggesting a novel mechanism contributing to comorbid anxiety and epilepsy

Neuropeptide Y receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

Neuropeptide Y (NPY) receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Neuropeptide Y Receptors [156]) are activated by the endogenous peptides neuropeptide Y, neuropeptide Y-(3-36), peptide YY, PYY-(3-36) and pancreatic polypeptide (PP). The receptor originally identified as the Y3 receptor has been identified as the CXCR4 chemokine recepter (originally named LESTR, [137]). The y6 receptor is a functional gene product in mouse, absent in rat, but contains a frame-shift mutation in primates producing a truncated non-functional gene [83]. Many of the agonists exhibit differing degrees of selectivity dependent on the species examined. For example, the potency of PP is greater at the rat Y4 receptor than at the human receptor [61]. In addition, many agonists lack selectivity for individual subtypes, but can exhibit comparable potency against pairs of NPY receptor subtypes, or have not been examined for activity at all subtypes. [125I]-PYY or [125I]-NPY can be used to label Y1, Y2, Y5 and y6 subtypes non-selectively, while [125I][cPP(1-7), NPY(19-23), Ala31, Aib32, Gln34]hPP may be used to label Y5 receptors preferentially (note that cPP denotes chicken peptide sequence and hPP is the human sequence)

Neuropeptide Y receptors in GtoPdb v.2023.1

Neuropeptide Y (NPY) receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Neuropeptide Y Receptors [158]) are activated by the endogenous peptides neuropeptide Y, neuropeptide Y-(3-36), peptide YY, PYY-(3-36) and pancreatic polypeptide (PP). The receptor originally identified as the Y3 receptor has been identified as the CXCR4 chemokine recepter (originally named LESTR, [139]). The y6 receptor is a functional gene product in mouse, absent in rat, but contains a frame-shift mutation in primates producing a truncated non-functional gene [84]. Three-dimensional structures have been determined for subtype active receptors Y1, Y2 and Y4 [211, 114] and inactive antagonist bound Y1 and Y2 receptors [240, 210]. Many of the agonists exhibit differing degrees of selectivity dependent on the species examined. For example, the potency of PP is greater at the rat Y4 receptor than at the human receptor [62]. In addition, many agonists lack selectivity for individual subtypes, but can exhibit comparable potency against pairs of NPY receptor subtypes, or have not been examined for activity at all subtypes. [125I]-PYY or [125I]-NPY can be used to label Y1, Y2, Y5 and y6 subtypes non-selectively, while [125I][cPP(1-7), NPY(19-23), Ala31, Aib32, Gln34]hPP may be used to label Y5 receptors preferentially (note that cPP denotes chicken peptide sequence and hPP is the human sequence)