Key insights on multisector community partnerships from real-world efforts to address social determinants of health.

PURPOSE: To better understand and inform how multisector community partnerships (MCPs) perform meaningful work to prevent chronic disease and advance health equity by addressing social determinants of health (SDOH). METHODS: We conducted a rapid retrospective evaluation of SDOH initiatives implemented within the past three years by 42 established MCPs across the United States. The mixed methods evaluation included document review and coding of available outcomes data, virtual discussions, and Prevention Impacts Simulation Model (PRISM) analysis. RESULTS: All 42 MCPs built community capacity for addressing SDOH through new or strengthened data systems, leveraged resources, or engaged residents, for example. Most MCPs (N = 38, 90%) reported contributions to community changes that promote healthy living. More than half of the MCPs (N = 22) reported health outcomes data for their SDOH initiatives, including improved health behaviors and clinical outcomes. Based on reach data provided by 27 MCPs, PRISM analysis results suggest that sustained initiatives could save over $633 million in productivity and medical costs cumulatively through 20 years. CONCLUSIONS: With sufficient technical assistance and funding resources, MCPs are a key component of the public health strategy to address SDOH.

Health Departments' Role in Addressing Social Determinants of Health in Collaboration With Multisector Community Partnerships.

Multisector community partnerships (MCPs) are key component of the public health strategy for addressing social determinants of health (SDOH) and promoting health equity. Governmental public health agencies are often members or leaders of MCPs, but few studies have examined the role of health departments in supporting MCPs' SDOH initiatives. We engaged 42 established MCPs in a rapid retrospective evaluation to better understand how MCPs' SDOH initiatives contribute to community changes that promote healthy living and improved health outcomes. As part of this work, we gained insights into how health departments support MCPs' SDOH initiatives, as well as opportunities for enhanced collaboration. Results indicate that health departments can support MCPs' SDOH initiatives through the provision of funding and technical assistance, data sharing, and connecting community organizations with shared missions, for example. Findings can be used to inform the development of funding opportunities and technical assistance for MCPs and health department partners.

Improving Older Adult Health by Operationalizing State Plans on Aging and Health Improvement.

The COVID-19 pandemic, a growing aging population, and inconsistent equity in aging have prompted more public health departments and agencies that focus on older adult services to establish partnerships to improve older adult health. To develop a model for strengthening and better aligning public health-aging partnerships, the Association of State and Territorial Health Officials (ASTHO) and Trust for America's Health engaged the Georgia Division of Aging Services (DAS) and Georgia Department of Public Health (DPH) to participate in a pilot project. ASTHO conducted an intensive qualitative analysis of Georgia's State Health Improvement Plan and State Plan on Aging to systematically assess shared priorities and differences. Through facilitated discussions about the results, prioritization, and planning, DAS and DPH developed an action plan with 2 priority areas to collaborate on and further their partnership. This process can be replicated by other jurisdictions seeking to enhance public health-aging collaboration.

Sphenopalatine ganglion pulsed radiofrequency treatment in 30 patients suffering from chronic face and head pain.

This study evaluated the efficacy of sphenopalatine ganglion pulsed radiofrequency (SPG-PRF) treatment in patients suffering from chronic head and face pain. Thirty patients were observed from 4 to 52 months after PRF treatment. The primary efficacy measures were the reduction in oral medication use, including opioids, time-to-next-treatment modality for presenting symptoms, duration of pain relief, and the presence of residual symptoms. Secondary objectives included the evaluation of adverse effects and complications. All data were derived from patient charts, phone conversations, and clinical follow-up visits. Fourteen percent of respondents reported no pain relief, 21% had complete pain relief, and 65% of the patients reported mild to moderate pain relief from SPG-PRF treatment. Sixty-five percent of the respondents reported mild to moderate reduction in oral opioids. None of the patients developed significant infection, bleeding, hematoma formation, dysesthesia, or numbness of palate, maxilla, or posterior pharynx. A large-scale study of SPG-PRF for the treatment of face and head pain has not been previously reported. Our results suggest that a prospective, randomized, controlled trial study to confirm efficacy and safety of this novel treatment for chronic head and face pain is justified.

Pulmonary vascular responses to ma huang extract.

OBJECTIVE: To test the hypothesis that ma huang induces a pressor response in the pulmonary vascular bed of the cat by activating alpha(1)-adrenergic receptors DESIGN: Prospective vehicle-controlled study. SETTING: Research laboratory at Texas Tech University School of Medicine, Lubbock, TX. SUBJECTS: Intact chest preparation; adult mongrel cats. INTERVENTIONS: The effects of phentolamine, a nonselective alpha receptor blocker, and prazosin, an alpha(1) selective antagonist, were investigated on pulmonary arterial responses to ma huang, phenylepherine, norepinephrine, and U-46619, a thromboxane A(2) mimic. MEASUREMENTS AND MAIN RESULTS: Lobar arterial perfusion pressure was continuously monitored, electronically averaged, and recorded with constant flow in the isolated left lower lobe vascular bed of the cat. Phentolamine and prazosin significantly reduced vasoconstrictor pulmonary perfusion pressure increases induced by ma huang. CONCLUSIONS: Ma huang has significant vasopressor activity in the pulmonary vascular bed of the cat mediated predominantly by alpha(1)-adrenergic receptor activation.

Noncompetitive antagonist binding sites in the torpedo nicotinic acetylcholine receptor ion channel. Structure-activity relationship studies using adamantane derivatives.

We used a series of adamantane derivatives to probe the structure of the phencyclidine locus in either the resting or desensitized state of the nicotinic acetylcholine receptor (AChR). Competitive radioligand binding and photolabeling experiments using well-characterized noncompetitive antagonists such as the phencyclidine analogue [piperidyl-3,4-(3)H(N)]-N-[1-(2-thienyl)cyclohexyl]-3,4-piperidine ([(3)H]TCP), [(3)H]ethidium, [(3)H]tetracaine, [(14)C]amobarbital, and 3-(trifluoromethyl)-3-(m-[(125)I]iodophenyl)diazirine ([(125)I]TID) were performed. Thermodynamic and structure-function relationship analyses yielded the following results. (1) There is a good structure-function relationship for adamantane amino derivatives inhibiting [(3)H]TCP or [(3)H]tetracaine binding to the resting AChR. (2) Since the same derivatives inhibit neither [(14)C]amobarbital binding nor [(125)I]TID photoincorporation, we conclude that these positively charged molecules preferably bind to the TCP locus, perhaps interacting with alphaGlu(262) residues at position M2-20. (3) The opposite is true for the neutral molecule adamantane, which prefers the TID (or barbiturate) locus instead of the TCP site. (4) The TID site is smaller and more hydrophobic (it accommodates neutral molecules with a maximal volume of 333 +/- 45 A(3)) than the TCP locus, which has room for positively charged molecules with volumes as large as 461 A(3) (e.g., crystal violet). This supports the concept that the resting ion channel is tapering from the extracellular mouth to the middle portion. (5) Finally, although both the hydrophobic environment and the size of the TCP site are practically the same in both states, there is a more obvious cutoff in the desensitized state than in the resting state, suggesting that the desensitization process constrains the TCP locus. A plausible location of neutral and charged adamantane derivatives is shown in a model of the resting ion channel.

Analysis of responses to valerian root extract in the feline pulmonary vascular bed.

OBJECTIVES: This study was undertaken to investigate pulmonary vascular response to valerian (Valeriana officinalis) in the feline pulmonary vasculature under constant flow conditions. DESIGN: In separate experiments, the effects of NG-L-nitro-L-arginine methyl ester (L-NIO), a nitric oxide synthase inhibitor, glibenclamide, an adenosine triphosphate (ATP)-sensitive potassium (K+) channel blocker, meclofenamate, a nonselective cyclooxygenase (COX) inhibitor, bicuculline, a GABA(A) receptor antagonist, and saclofen, a GABA(B) antagonist, were investigated on pulmonary arterial responses to various agonists in the feline pulmonary vascular bed. These agonists included valerian, muscimol, a GABA(A) agonist, SKF-97541 a GABA(B) agonist, acetylcholine (ACh), and bradykinin, both inducers of nitric oxide synthase, arachidonic acid, a COX substrate, and pinacidil, an ATP-sensitive K+ channel activator, during increased tone conditions induced by the thromboxane A2 mimic, U46619. SETTINGS/LOCATION: Laboratory investigation. SUBJECTS: Mongrel cats of either gender. INTERVENTIONS: Injections of the abovementioned agonists and antagonists were given. OUTCOME MEASURES: Baseline pulmonary tone, responses to the agonists, and responses to the agonists after injections of antagonists were all measured via a pulmonary catheter transducer and recorded. RESULTS: Valerian root extract is a potent smooth muscle dilator in the feline pulmonary vascular bed. The vasodilatory effects of valerian root extract were unchanged after the administration of L-NIO, glibenclamide, and meclofenamate. These effects were ablated, however, by both saclofen and bicuculline. The ability of saclofen and bicuculline to modulate the dilatory effects of valerian root extract was not statistically different. CONCLUSIONS: The vasodilatory effects of valerian root extract are mediated by a nonselective GABA mechanism.

Allosterically linked noncompetitive antagonist binding sites in the resting nicotinic acetylcholine receptor ion channel.

Previous studies have established the presence of overlapping binding sites for the noncompetitive antagonists (NCAs) amobarbital, tetracaine, and 3-trifluoromethyl-3-(m-[(125)I]iodophenyl) diazirine ([(125)I]TID) within the ion channel of the Torpedo nicotinic acetylcholine receptor (AChR) in the resting state. These well-characterized NCAs and competitive radioligand binding and photolabeling experiments were employed to better characterize the interaction of the dissociative anesthetics ketamine and thienylcycloexylpiperidine (TCP) with the resting AChR. Our experiments yielded what appear to be conflicting results: (i) both ketamine and TCP potentiated [(125)I]TID photoincorporation into AChR subunits; and (ii) ketamine and TCP had very little effect on [(14)C]amobarbital binding. Nevertheless, (iii) both ketamine and TCP completely displaced [(3)H]tetracaine binding (K(i)s approximately 20.9 and 2.0 microM, respectively) by a mutually exclusive mechanism. To reconcile these results we propose that, in the resting ion channel, TCP and ketamine bind to a site that is spatially distinct from the TID and barbiturate locus, while tetracaine bridges both binding sites.

An analysis of responses to levosimendan in the pulmonary vascular bed of the cat.

UNLABELLED: Calcium-sensitizing drugs, such as levosimendan, are a novel class of drug therapy for heart failure. We investigated the hypothesis that levosimendan is a pulmonary vasodepressor mediated through inhibition of phosphodiesterase, adenosine triphosphate (ATP)-dependent potassium channels, or both. We investigated responses to the calcium sensitizer levosimendan in the pulmonary vascular bed of the cat under conditions of controlled pulmonary blood flow and constant left atrial pressure when lobar arterial pressure was increased to a high steady level with the thromboxane A(2) analog U-46619. Under increased-tone conditions, levosimendan caused dose-related decreases in lobar arterial pressure without altering systemic arterial and left atrial pressure. Responses to levosimendan were significantly attenuated, although not completely, after the administration of U-37883A, a vascular selective nonsulfonylurea ATP-sensitive K(+)-channel-blocking drug. Responses to levosimendan were not significantly different after the administration of the nitric oxide synthase inhibitor L-N(5)-(1-iminoethyl)-ornithine or the cyclooxygenase inhibitor sodium meclofenamate or when lung ventilation was interrupted. These data show that levosimendan has significant vasodilator activity in the pulmonary vascular bed of the cat. They also suggest that pulmonary vasodilator responses to levosimendan are partially dependent on activation of ATP-sensitive K(+) channels and independent of the synthesis of nitric oxide, activation of cyclooxygenase enzyme, or changes in bronchomotor tone in the pulmonary vascular bed of the cat. IMPLICATIONS: Calcium-sensitizing drugs, such as levosimendan, are a novel class of drug therapy for heart-failure treatment. The lung circulation affects both right- and left-sided heart failure. Levosimendan decreased lobar arterial pressure via a partial K(+)(ATP) (potassium channel sensitive to intracellular adenosine triphosphate levels)-dependent mechanism. These data suggest that, in addition to calcium-sensitizing activity, levosimendan decreases pulmonary resistance, which may also aid in the treatment of heart failure.