Robin Medical (United States)

Context:Large local health departments (LHDs) serve diverse, high-need communities and are uniquely positioned to influence public health policy and practice locally, regionally, and nationally.Objective:The purpose of this study is to investigate policy engagement as a reported training need in the 2024 Public Health Workforce Interests and Needs Survey within large LHDs, highlighting gaps and opportunities to strengthen policy capacity.Design:Cross-sectional analysis of 2024 Public Health Workforce Interests and Needs Survey data using descriptive statistics and weighted logistic regression.Setting:Large LHDs, serving populations of 250 000 or more, across the US.Participants:Study sample included 24 121 responses from individuals working in large LHDs.Main Outcome Measures:Descriptive and regression-based statistics for training needs, self-identified skill-building interests, and predictors of reporting a policy engagement training need.Results:Nearly 40% of staff at large LHDs reported a training need in policy engagement, the only domain to show an increase in need since 2021. Women had significantly higher odds of reporting a policy training need (odds ratios [OR] = 1.67; P < .001), as did supervisors (OR = 2.09; P < .001) and managers (OR = 1.78; P < .001) compared to nonsupervisors, while those with master’s (OR = 0.64; P < .001) or doctoral degrees (OR = 0.40; P < .001) had lower odds compared to bachelor’s-level staff.Conclusions:Large LHDs are well positioned to advance public health policy given their scale and connection to local communities. Targeting policy engagement training to workforce segments with the highest reported need offers a strategic opportunity to strengthen policy capacity across the US public health workforce.

To describe the strength of a cross-sector and multi-university collaboration in co-designing an extended nursing placement innovation in rural and remote Australia. Registered nurses are Australia's largest health workforce. Short-duration placements can limit nursing student exposure to rural and remote practice, impacting student capacity to tailor and contextualise their practice, navigate complex inequities, establish a sense of belonging and consider rural practice post-registration. Extended nursing placements have been recommended to address these challenges, but there are no guidelines governing their development and limited resources to support implementation. Methods adopted in program development included the following: (1) collaboration establishment; (2) co-defining challenges confronting nurse education in these contexts; (3) co-developing guiding principles; (4) co-designing a new approach to nurse education, the Extended Nursing Placement Program (ENPP); and (5) the co-contribution of stakeholders to program design, implementation and evaluation. Regional stakeholders include a NSW and Victorian Local Health District/Service, three Aboriginal health services and the Royal Flying Doctor Service of Australia. University participants include two metropolitan universities, a University Department of Rural Health and final-year Bachelor of Nursing students. Program implementation in Semester 1 of 2022 with seven final-year nursing students. The authors propose that the adoption of collaborative approaches can contribute to re-framing student nurse education and the development of a rural-ready nursing workforce. These approaches can provide regions and universities with the opportunity to avoid student churn whilst promoting the attainment of skills required to work, live and thrive in these locations.

Introduction: Stroke and other neurologic diseases may disproportionately affect persons in rural areas, and stroke-related mortality in rural counties has increased in recent years. Little is known about distribution and trends in neurologists and telestroke services in rural vs urban counties in the US. Methods: Volume and age distribution of neurologists in each county were determined using the AMA Physician Masterfile for each year 2010-2018. Neurologist density (per 100,000 persons) was estimated based on county-level population data. Telestroke units per county were identified using Area Health Resource files. Counties were classified as large metropolitan, medium or small metropolitan, or rural based on CDC WONDER designations. Results: From 2010-2018, mean (SD) neurologist density in rural counties decreased from 6.3 (21.6) to 5.9 (18.7) per 100,000 persons. A majority of rural counties experienced little to no change (0-5 per 100,000) in neurologist density over time. In contrast, neurologist density increased in large metropolitan counties from 31.1 (42.7) to 37.8 (52.1) per 100,000 and in medium/small metropolitan counties from 29.3 (67.8) to 32.2 (74.9) per 100,000. Over time, 42% of large metropolitan and 27% of medium/small metropolitan counties experienced &gt;10 per 100,000 longitudinal increases in neurologist density. The proportion of younger neurologists (&lt;35 or 35-44 years) appeared to increase in urban counties, while the proportion of older neurologists (≥65 years) relatively increased in rural counties. In 2018, telestroke units were available in 51%, 37%, and 18% of large metropolitan, medium/small metropolitan, and rural counties, respectively. Conclusions: Neurologist density has decreased in rural counties in the US, with a relative aging of existing neurologists in these settings. Four out of 5 rural counties do not have telestroke units. These data underscore the need to improve access to neurology in rural areas.

Background: Fundamental advances in stroke care will require pooling imaging phenotype data from multiple centers, to complement the current aggregation of genomic, environmental, and clinical information. Sharing clinically acquired MRI data from multiple hospitals is challenging due to inherent heterogeneity of clinical data, where the same MRI series may be labeled differently depending on vendor and hospital. Furthermore, the de-identification process may remove data describing the MRI series, requiring human review. However, manually annotating the MRI series is not only laborious and slow but prone to human error. In this work, we present a recurrent convolutional neural network (RCNN) for automated classification of the MRI series. Methods: We randomly selected 1000 subjects from the MRI-GENetics Interface Exploration study and partitioned them into 800 training, 100 validation and 100 testing subjects. We categorized the MRI series into 24 groups (see Table). The RCNN used a modified AlexNet to extract features from 2D slices. AlexNet was pretrained on ImageNet photographs. Since clinical MRI are 3D and 4D, a gated recurrent unit neural network was used to aggregate information from multiple 2D slices to make the final prediction. Results: We achieved a classification accuracy (correct/total cases) of 99.8%, 98.5% and 97.5% on the training, validation and testing set, respectively. The averaged F1-score (percent overlap between predicted cases and actual cases) over all categories were 99.8% 98.2% and 94.4% on the training, validation and testing set. Conclusion: We showed that automated annotation of MRI series by repurposing deep-learning techniques used for photographic image recognition tasks is feasible. Such methods can be used to facilitate high throughput curation of MRI data acquired across multiple centers and enable scientifically productive collaboration by researchers and, ultimately enhancing big data stroke research.

Dietary sodium stimulates renal excretion of sodium long before the sodium is enterally absorbed. Moreover, intravenously administered sodium does not stimulate as large an excretory response as sodium taken by mouth. We previously showed that sodium stimulates an increase in gastrin mRNA and protein in stomach G-cells via PPAR-α and dopamine D1 receptor (D 1 R). Studies have shown that PKA pathway is important in the regulation of PPAR-α activity, and PKA is also involved in the D 1 R pathway. Thus, we hypothesized that D 1 R may regulate PPAR-α through PKA in human G-cells in response to sodium. Human G-cells were treated with 8-Br-cAMP, a cell-permeable second messenger analog, and Rp-cAMP (RPCA), a PKA inhibitor. Image analysis showed there was more PPAR-α in the nucleus with 8-Br-cAMP treatment, and less PPAR-α in the nucleus with RPCA treatment. Therefore, PKA is involved in regulating PPAR-α (VEH, 1194±74; 8-Br-cAMP, 1490±44; RPCA, 740±75; 8-Br-cAMP+ RPCA, 1037±54; VEH vs 8-Br-cAMP, P&lt;0.01; 8-Br-cAMP vs 8-Br-cAMP+ RPCA, P&lt;0.001; one-way ANOVA, n=13). Moreover, gastrin mRNA was increased by 8-Br-cAMP stimulation while the increase was blocked by RPCA (VEH, 1.01±0; 8-Br-cAMP, 1.32±0.07; RPCA, 0.82±0.08; 8-Br-cAMP+ RPCA, 0.9±0.05; VEH vs 8-Br-cAMP, P&lt;0.05; 8-Br-cAMP vs 8-Br-cAMP+ RPCA, p&lt;0.01; one-way ANOVA, n=3). Gastrin protein level was also increased by 8-Br-cAMP treatment with image analysis (VEH, 1.14±0.01; 8-Br-cAMP, 1.28±0.01; RPCA, 1.17±0.01; 8-Br-cAMP+ RPCA, 1.38±0.03; VEH vs 8-Br-cAMP, P&lt;0.01; one-way ANOVA, n=3). These data indicate that PKA is involved in the D 1 R and PPAR-α pathways to regulate G-cell gastrin expression stimulated by sodium.

The amiloride-sensitive epithelial sodium channel (ENaC) localizes to the apical membrane of epithelial cells in distal nephron, playing an important role in regulating whole-body Na + homeostasis and blood pressure. We were the first to describe the presence of αENaC in human renal proximal tubule cells (hRPTC). Gene variants in αENaC have been shown to be associated with salt sensitivity of blood pressure (SS) . We also verified that the specific gene variant rs4764586 was significantly associated with SS (χ 2 =9.67, P=0.046). In our salt sensitivity clinical study, 11% participants (N=27/240) had a paradoxical increase in blood pressure (BP) (≥7-mm Hg) on a low NaCl diet, defined as inverse salt sensitive ( ISS ) as compared to salt resistant ( SR , 72%) and salt sensitive ( SS , 17%). The incidence of the minor allele αENaC rs4764586 in the ISS group was 2-fold of that in SR or SS ( ISS , 14.8%; SR , 7.0%; SS , 7.1%). Expression of αENaC protein in urine derived hRPTCs was significantly lower in ISS than in SR ( ISS , 0.55±0.01, n=3; SR, 0.97±0.12, n=3; SS, 0.87±0.12, n=3; one-way ANOVA, ISS vs SR p&lt;0.05), with the lowest in the homozygous variants (HV) of rs4764586 and highest in wild type. The heterozygous variant containing hRPTCs had an intermediate expression of αENaC (WT, 0.94±0.11, n=4; Heterozygous, 0.72±0.11, n=4; HV, 0.53, n=1). ENaC-like channels were demonstrated in hRPTCs using single-channel patch-clamp electrophysiology with a conductance of 10.5±0.7 pS and E rev 39.2±5.5 mV vs 10.3±0.8 pS in SR and ISS lines, respectively. However, in ISS baseline ENaC-like channel activity was too low to be recorded without trypsin in the pipette (Po = open probability), unlike SR . In contrast, ISS cells demonstrated a higher Po than SR cells in response to trypsin both immediately and after 4 minutes of activation, even though the number of channels recorded at 4 min after GigaOhm seal formation was lower in the ISS line compared to SR line (4.7±1.7 vs 1.75±0.5, p=0.042 in SR vs ISS lines). These results suggest that ISS phenotype may be related to impaired ENaC activity in the renal proximal tubule. The long-term physiologic consequences of the ISS phenotype remain to be determined

Cerebral venous thrombosis is associated with intracranial hemorrhage. The occurrence of brain bleeding complicates management and is associated with worse outcomes. We aimed to identify clinical and imaging risk factors for intracerebral hemorrhage. We hypothesized that higher clot burden would be associated with a higher risk of intracerebral hemorrhage. Methods: We performed a retrospective analysis of an international, multicenter cohort of patients with cerebral venous thrombosis who underwent CT within 2 weeks of symptom onset and who had a subsequent confirmed diagnosis of CVT on MRV, CTV or DSA. Clinical and imaging features were compared between patients with and without intracranial hemorrhage. Clot burden was assessed by counting the number of thrombosed venous sinuses and veins on confirmatory imaging. Results: We recruited 260 patients with cerebral venous thrombosis from 10 institutions in Europe and Mexico. The mean age was 42 and 74% were female. Intracranial hemorrhage was found in 102 (39%). Intracerebral hemorrhage occurred in 64 (63%), small juxtacortical hemorrhage in 30 (29%), subarachnoid hemorrhage in 24 (24%) and subdural hemorrhage in 11 (11%). Combinations of these types of hemorrhage occurred in 23 (23%). Intraparenchymal hemorrhages in multiple locations occurred in 6 (6%). Older age, presence of hematological disease and superior sagittal thrombosis involvement were significantly associated with presence of hemorrhage. The number of thrombosed venous sinuses was not associated with intracerebral hemorrhage (average number of sinuses/veins involved with hemorrhage 2.1 versus 1.9 without hemorrhage, p=0.4). Conclusion: The high rate of intracranial hemorrhage in cerebral venous thrombosis is not explained by widespread involvement of the venous sinuses. Superior sagittal sinus involvement is associated with the presence of intracranial hemorrhage.

Background: Prior studies have suggested race-ethnic differences in functional outcome, mortality, and use of comfort care after stroke, but have been limited by analysis of single stroke subtypes, lack of 3-month outcomes, and uncertainty whether delayed access to acute care was moderating response patterns. Methods: We analyzed all patients with final diagnoses of acute cerebral ischemia or intracranial hemorrhage enrolled within 2 hours of onset in the multicenter, prehospital NIH FAST-MAG trial. Self- or family-reported race-ethnicity was analyzed for relation to presenting stroke features, stroke subtype, and 3-month outcome. Results: Among 1616 hyperacute cerebrovascular disease patients (76.4% acute cerebral ischemia, 23.6% intracranial hemorrhage), race-ethnic frequencies were: white, non-Hispanic (W) - 55.5%, Hispanic (H) - 23.1%, Black (B) - 13.6%, Asian (A) - 8.4%. Ischemic vs hemorrhagic stroke differed by race-ethnicity, with hemorrhagic strokes more common in Hispanics (34.0%) and Asians (28.1%), compared with Whites (19.8%) and Blacks (17.8%), p = 0.0001. Age at time of stroke was highest in Whites (mean 73.1), vs H (65.5), B (63.5), A (66.9); and presenting severity (NIHSS) highest in A (mean 13.5) and H (12.7), vs W (10.7) and B (10.8). A greater dimorphic spread in 3 month outcomes was seen in W than in the other race-ethnic groups: Whites had more excellent (mRS 0-1) 3 month outcomes - W- 42.2%, B- 35.0%, H -28.4%, A-28.0%, p = 0.002; but Whites also had higher mortality by 3m - W-18.2%, A- 15.6%, H-13.0%, B-10.6%, p = 0.007. The race-ethnic difference in mortality was driven by hemorrhagic rather than ischemic strokes: ICH mortality - W-41.7%, A-19.4%, H-19.0%, B-18.2%; IS mortality: A-14.4%, W-13.5%, H-10.5%, B-9.4%. Conclusions: In this multicenter study of acute cerebrovascular disease in a diverse US region, notable race-ethnic differences included higher frequencies of hemorrhagic vs ischemic stroke among Hispanics and Asians; and more excellent, but also more fatal, 3 month outcomes among Whites. These patterns likely distinct different race-ethnic risk factor profiles shaping incident stroke type, as well as divergent sociocultural influences upon robust rehabilitation care and comfort care measures.

Background: Age is a major determinant of stroke outcome, but few studies have investigated whether the effect of age differs between men and women. Methods: Analysis of all patients enrolled in a multicenter acute stroke trial (FAST-MAG) presenting with acute cerebral ischemia and treated without intravenous thrombolysis. Effects of age and sex were evaluated for: 1) disability or death (modified Rankin Scale, mRS, 2-6); 2) reduced stroke-related quality of life (Stroke Impact Scale, SIS &lt; 80); and 3) mortality, unadjusted and adjusted for baseline NIHSS, ASPECTS, and 7 additional prognostic variables. Results: Among the 772 patients meeting entry criteria, age was 71.2, 44.0% were women, and presenting NIHSS 6.8. Overall, men were slightly younger than women (69.9 vs 73.0), without difference in initial NIHSS (6.4 vs 7.2), nor in 3m outcomes: mRS 2-6, 44.7% vs 50.2%, p=0.13; SIS&lt;80, 44.6% vs 44.1%, p=0.90; mortality 9.5% vs 9.7%, p=0.92. However, the sexes differed in age-functional outcome patterns. Among women, there were U-shaped relationships between age and rates of both mRS 2-6 (Figure) and SIS &lt;80. In contrast, among men, a much more attenuated U-shaped relationship was visualized, did not reach statistical significance. For both sexes, mortality showed a generally linear increase with age. Compared to those aged 40-64, mortality rates in the oldest old (age ≥85) were: women - HR 4.81 (95CI 0.98-23.39); men - HR 4.06 (95CI 1.17-14.14). Conclusions: The relationship between age and functional outcome in supportively treated acute cerebral ischemia patients differs between the sexes, with women but not men showing better outcomes in early senescence than either midlife or very late-life. This contrasting outcome profile may reflect sex-specific biological differences in ischemic stroke mechanism and neuroplasticity, cultural differences in social roles and support, or additional factors that merit further study.