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The Coronavirus disease 19 (COVID-19) pandemic has disrupted both transportation and health systems. While about 40% of Americans have delayed seeking medical care during the pandemic, it remains unclear to what extent transportation is contributing to missed care. To understand the relationship between transportation and unmet health care needs during the pandemic, this paper synthesizes existing knowledge on transportation patterns and barriers across five types of health care needs. While the literature is limited by the absence of detailed data for trips to health care, key themes emerged across populations and settings. We find that some patients, many of whom already experience transportation disadvantage, likely need extra support during the pandemic to overcome new travel barriers related to changes in public transit or the inability to rely on others for rides. Telemedicine is working as a partial substitute for some visits but cannot fulfill all health care needs, especially for vulnerable groups. Structural inequality during the pandemic has likely compounded health care access barriers for low-income individuals and people of color, who face not only disproportionate health risks, but also greater difficulty in transportation access and heightened economic hardship due to COVID-19. Partnerships between health and transportation systems hold promise for jointly addressing disparities in health- and transportation-related challenges but are largely limited to Medicaid-enrolled patients. Our findings suggest that transportation and health care providers should look for additional strategies to ensure that transportation access is not a reason for delayed medical care during and after the COVID-19 pandemic.

Since March 2020, COVID-19 transportation system disruptions have altered how Americans access routine health care. This report examines current knowledge about disparities in transportation and access to health care for people with various health conditions and health care needs. We highlight evidence related to end-stage kidney disease, pregnancy, cancer, mental health and substance use, disabilities, multiple chronic conditions, and preventive care to discuss population-specific transportation needs and challenges, COVID-19 health risks, and impacts of transportation system disruption on health outcomes during the pandemic. The report concludes with policy recommendations for how leaders in transportation, public health, and health care can improve transportation access to care during the COVID-19 pandemic.

OBJECTIVE: To develop a conceptual framework and preliminary item bank for childbirth-specific patient-reported outcome (PRO) domains. DATA SOURCES: Women, who were U.S. residents, ≥18 years old, and ≥20 weeks pregnant, were surveyed regarding their childbirth values and preferences (V&P) using online panels. STUDY DESIGN: Using community-based research techniques and Patient-Reported Outcomes Management Information System (PROMIS® ) methodology, we conducted a comprehensive literature review to identify self-reported survey items regarding patient-reported V&P and childbirth experiences and outcomes (PROs). The V&P/PRO domains were validated by focus groups. We conducted a cross-sectional observational study and fitted a multivariable logistic regression model to each V&P item to describe who wanted each item. PRINCIPAL FINDINGS: We identified 5,880 V&P/PRO items that mapped to 19 domains and 58 subdomains. We present results for the 2,250 survey respondents who anticipated a vaginal delivery in a hospital. Wide variation existed regarding each V&P item, and personal characteristics, such as maternal confidence and ability to cope well with pain, were frequent predictors in the models. The resulting preliminary item bank consisted of 60 key personal characteristics and 63 V&P/PROs. CONCLUSIONS: The conceptual framework and preliminary (PROMIS® ) item bank presented here provide a foundation for the development of childbirth-specific V&P/PROs.

PurposeTo evaluate whether exposure to MyFamilyPlan-a web-based preconception health education module-changes the proportion of women discussing reproductive health with providers at well-woman visits.DesignCluster randomized controlled trial. One hundred thirty participants per arm distributed among 34 clusters (physicians) required to detect a 20% change in the primary outcome.SettingUrban academic medical center (California).ParticipantsEligible women were 18 to 45 years old, were English speaking, were nonpregnant, were able to access the Internet, and had an upcoming well-woman visit. E-mail and phone recruitment between September 2015 and May 2016; 292 enrollees randomized.InterventionIntervention participants completed the MyFamilyPlan module online 7 to 10 days before a scheduled well-woman visit; control participants reviewed standard online preconception health education materials.MeasuresThe primary outcome was self-reported discussion of reproductive health with the physician at the well-woman visit. Self-reported secondary outcomes were folic acid use, contraceptive method initiation/change, and self-efficacy score.AnalysisMultilevel multivariate logistic regression.ResultsAfter adjusting for covariates and cluster, exposure to MyFamilyPlan was the only variable significantly associated with an increase in the proportion of women discussing reproductive health with providers (odds ratio: 1.97, 95% confidence interval: 1.22-3.19). Prespecified secondary outcomes were unaffected.ConclusionMyFamilyPlan exposure was associated with a significant increase in the proportion of women who reported discussing reproductive health with providers and may promote preconception health awareness; more work is needed to affect associated behaviors.

The protein kinase C (PKC) family of serine/threonine kinases functions downstream of nearly all membrane-associated signal transduction pathways. Here we identify PKC-[alpha] as a fundamental regulator of cardiac contractility and Ca[sup.2+] handling in myocytes. Hearts of Prkca-deficient mice are hypercontractile, whereas those of transgenic mice overexpressing Prkca are hypocontractile. Adenoviral gene transfer of dominant-negative or wild-type PKC-[alpha] into cardiac myocytes enhances or reduces contractility, respectively. Mechanistically, modulation of PKC-[alpha] activity affects dephosphorylation of the sarcoplasmic reticulum Ca[sup.2+] ATPase-2 (SERCA-2) pump inhibitory protein phospholamban (PLB), and alters sarcoplasmic reticulum Ca[sup.2+] loading and the Ca[sup.2+] transient. PKC-[alpha] directly phosphorylates protein phosphatase inhibitor-1 (I-1), altering the activity of protein phosphatase-1 (PP-1), which may account for the effects of PKC-[alpha] on PLB phosphorylation. Hypercontractility caused by Prkca deletion protects against heart failure induced by pressure overload, and against dilated cardiomyopathy induced by deleting the gene encoding muscle LIM protein (Csrp3). Deletion of Prkca also rescues cardiomyopathy associated with overexpression of PP-1. Thus, PKC-[alpha] functions as a nodal integrator of cardiac contractility by sensing intracellular Ca[sup.2+] and signal transduction events, which can profoundly affect propensity toward heart failure., Author(s): Julian C Braz [1, 2]; Kimberly Gregory [2]; Anand Pathak [2]; Wen Zhao [2]; Bogachan Sahin [3]; Raisa Klevitsky [1]; Thomas F Kimball [1]; John N Lorenz [4]; Angus [...]

Objectives. The percentages of cesarean deliveries attributable to specific indications (breech, dystocia, fetal distress, and elective repeat cesarean) were computed for 1985 and 1994. Methods. Data were derived from the 1985 and 1994 National Hospital Discharge Surveys. Results. Dystocia was the leading indication for cesarean delivery in both years. In comparison with 1985, cesareans performed in 1994 that were attributable to dystocia and breech presentation increased, those attributable to fetal distress did not change significantly, and elective repeat cesareans declined. Conclusions. Studying indications for cesareans can be useful for hospitals, clinicians, and researchers in determining strategies to lower primary and repeat cesarean rates. (Am J Public Health. 1998;88:1384-1387)

Aggregate databases are increasingly being used to evaluate appropriateness of care, and, for cesarean sections, Anderson and Lomas' International Classification of Diseases, 9th Revision (ICD-9), coding hierarchy is a widely used tool. The aim of this study was to assess the validity of the hierarchy and expand its applicability to repeat cesareans. Hospital records of 1885 singleton cesareans were reviewed. Clinical indications and ICD-9 hierarchical codes were concordant for 83% of primary and 86% of repeat cesareans; modification allowed elective repeat cesareans to be distinguished from indicated procedures. The Anderson and Lomas ICD-9 hierarchy is a valid tool for assessing indications for cesarean. The current modification improves its clinical utility and expands its application to repeat procedures. (Am J Public Health. 1995; 85:1143-1146), A change in the codes used to identify the indications for cesarean section could increase the accuracy of the data. Current codes list repeat cesarean, breech presentation, lack of progress, fetal distress, and 'other' as possible indications. The codes for 1,885 cesareans performed at Cedars Sinai Medical Center during 1992 were compared with cesarean indications as recorded in case notes. Notes agreed with the code for 83% of the 1,242 first cesareans. However, accuracy of coding would be improved if failed induction of labor, malpositioned baby, and overly large baby were coded in the 'lack of progress' category. The repeat cesarean code should be broken down into the same categories as first cesareans so that elective cesareans can be distinguished from medically indicated cesareans. This would result in agreement between notes and code in 85% of cases. Adding three specific contraindications to labor after a prior cesarean would further improve the discrimination of the codes.

* Context.--Managing the quality of point-of-care testing (POCT) is a continuing challenge. Advances in testing technologies and the development of specialized informatics for POCT have greatly improved the ability of hospitals to manage their POCT program. Objectives.--To present the evolving role of technology improvement, informatics, and program management as the key developments to ensure the quality of POCT. Data Sources.--This presentation is based on a review of the literature and on our experiences with POCT at the Massachusetts General Hospital (Boston). Conclusions.--Federal and state regulations, along with accreditation standards developed by the College of American Pathologists and The Joint Commission, have established guidelines for the performance of POCT and have provided a strong incentive to improve the quality of testing. Many instruments for POCT have incorporated advanced design features to prevent analytic and operator errors. This, along with the development of connectivity standards and specialized data management software, has enabled remote review of test data and electronic flow of information to hospital information systems. However, documentation of manually performed, visually read tests remains problematic and some POCT devices do not have adequate safeguards to prevent significant errors. In the past 2 decades the structure of a successful POCT management program has been defined, emphasizing the role of POCT managers working in conjunction with a pathology-based medical director. The critical skill set of POCT managers has also been identified. The POCT manager is now recognized as a true specialist in laboratory medicine. (Arch Pathol Lab Med. 2011; 135:1405-1414; doi: 10.5858/arpa.2011-0157-RA), The development of technologies to perform laboratory testing at the point of care (POC) has created unique opportunities to increase the operational efficiency of clinical services and in some cases, [...]

Since 2000, the U.S. Preventive Services Task Force (USPSTF) has issued eight clinical recommendation statements on screening for sexually transmitted infections. This article, written on behalf of the USPSTF, is an overview of these recommendations. The USPSTF recommends that women at increased risk of infection be screened for chlamydia, gonorrhea, human immunodeficiency virus, and syphilis. Men at increased risk should be screened for human immunoodeficiency virus and syphilis. All pregnant women should be screened for hepatitis B, human immunodeficiency virus, and syphilis; pregnant women at increased risk also should be screened for chlamydia and gonorrhea. Nonpregnant women and men not at increased risk do not require routine screening for sexually transmitted infections. Engaging in high-risk sexual behavior places persons at increased risk of sexually transmitted infections. The USPSTF recommends that all sexually active women younger than 25 years be considered at increased risk of chlamydia and gonorrhea. Because not all communities present equal risk of sexually transmitted infections, the USPSTF encourages physicians to consider expanding or limiting the routine sexually transmitted infection screening they provide based on the community and populations they serve. [ABSTRACT FROM AUTHOR]

Abstract: Objective: The histidine-rich Ca-binding protein (HRC) is a Ca-storage protein in cardiac sarcoplasmic reticulum. Recent transgenic studies revealed that this protein inhibits the maximal rates of sarcoplasmic reticulum Ca-transport, leading to cardiac dysfunction. In view of the role of sarcoplasmic reticulum Ca-cycling in myocardial ischemia/reperfusion injury, we designed this study to gain further insight into the role of HRC during ischemia/reperfusion. Methods and results: The transgenic mouse model with cardiac-specific overexpression of HRC was utilized and cardiac contractile parameters were assessed before and after ischemia/reperfusion injury by Langendorff perfusion. After a 20-min stabilization period, the hearts were subjected to 40 min of global ischemia, followed by 60 min of reperfusion. We found that although transgenic (TG) hearts showed depressed cardiac function (25%) compared to wild types (WTs) at baseline, they exhibited better recovery of left ventricular developed pressure (86.6±2.6% in TGs vs. 58.3±4.0% in WTs of pre-ischemic values, P <0.05) and higher rates of contraction and relaxation after ischemia/reperfusion than WTs. This improvement was accompanied by smaller infarcts (23.1±1.7% in TGs vs. 41.1±2.5% in WTs of infarct region-to-risk region ratio, P <0.05) and lower creatine kinase release. Notably, the extent of apoptotic cell death was significantly attenuated, as evidenced by decreased DNA fragmentation, upregulation of the antiapoptotic protein Bcl-2, and downregulation of the active caspases (3, 9 and 12) following ischemia/reperfusion in TG hearts, compared with WTs. Extension of these studies to an in vivo model of 30-min myocardial ischemia, via coronary artery occlusion, followed by 24-h reperfusion, showed that the infarct region-to-risk region ratio was 9±0.9% in TGs, compared with 20.4±2.9% in WTs (P <0.05). Conclusions: Our findings suggest that increased cardiac HRC expression protects against ischemia/reperfusion injury in the heart, resulting in improved recovery of function and reduced infarction. [Copyright &y& Elsevier]

Impaired sarcoplasmic reticulum (SR) Ca release has been suggested to contribute to the depressed cardiac function in heart failure. The release of Ca from the SR may be regulated by the ryanodine receptor, triadin, junctin, calsequestrin, and a histidine-rich, Ca-binding protein (HRC). We observed that the levels of HRC were reduced in animal models and human heart failure. To gain insight into the physiological function of HRC, we infected adult rat cardiac myocytes with a recombinant adenovirus that contains the full-length mouse HRC cDNA. Overexpression (1.7-fold) of HRC in adult rat cardiomyocytes was associated with increased SR Ca load (28%) but decreased SR Ca-induced Ca release (37%), resulting in impaired Ca cycling and depressed fractional shortening (36%) as well as depressed rates of shortening (38%) and relengthening (33%). Furthermore, the depressed basal contractile and Ca kinetic parameters in the HRC-infected myocytes remained significantly depressed even after maximal isoproterenol stimulation. Interestingly, HRC overexpresssion was accompanied by increased protein levels of junctin (1.4-fold) and triadin (1.8-fold), whereas the protein levels of ryanodine receptor, calsequestrin, phospholamban, and sarco(endo)plasmic reticulum Ca-ATPase remained unaltered. Collectively, these data indicate that alterations in expression levels of HRC are associated with impaired cardiac SR Ca homeostasis and contractile function. [ABSTRACT FROM AUTHOR]

Proposes a general model whereby up to 10 levels of signaling by G-protein-coupled receptors can be present based on the influences of desensitization and genetic variation on coupling. Expression of four receptors in Chinese hamster fibroblasts at equivalent levels; Relative effects of genetic modifications and those of short term agonist-promoted desensitization on receptor function.

Summarizes the U.S. Preventive Services Task Force's (USPSTF) recommendation on screening for glaucoma and the supporting scientific evidence, and updates the 1996 recommendations contained in the "Guide to Clinical Prevention Services," 2nd edition. Explanations of the ratings and of the strength of overall evidence; Discussion and recommendations of other groups.

Depressed cardiac Ca cycling by the sarcoplasmic reticulum (SR) has been associated with attenuated contractility, which can progress to heart failure. The histidine-rich Ca-binding protein (HRC) is an SR component that binds to triadin and may affect Ca release through the ryanodine receptor. HRC overexpression in transgenic mouse hearts was associated with decreased rates of SR Ca uptake and delayed relaxation, which progressed to hypertrophy with aging. The present study shows that HRC may mediate part of its regulatory effects by binding directly to sarco(endo)plasmic reticulum Ca-ATPase type 2 (SERCA2) in cardiac muscle, which is confirmed by coimmunostaining observed under confocal microscopy. This interaction involves the histidine- and glutamic acid-rich domain of HRC (320-460 aa) and the part of the NH(2)-terminal cation transporter domain of SERCA2 (74-90 aa) that projects into the SR lumen. The SERCA2-binding domain is upstream from the triadin-binding region in human HRC (609-699 aa). Specific binding between HRC and SERCA was verified by coimmunoprecipitation and pull-down assays using human and mouse cardiac homogenates and by blot overlays using glutathione S-transferase and maltose-binding protein recombinant proteins. Importantly, increases in Ca concentration were associated with a significant reduction of HRC binding to SERCA2, whereas they had opposite effects on the HRC-triadin interaction in cardiac homogenates. Collectively, our data suggest that HRC may play a key role in the regulation of SR Ca cycling through its direct interactions with SERCA2 and triadin, mediating a fine cross talk between SR Ca uptake and release in the heart.

Impaired sarcoplasmic reticulum (SR) Ca release has been suggested to contribute to the depressed cardiac function in heart failure. The release of Ca from the SR may be regulated by the ryanodine receptor, triadin, junctin, calsequestrin, and a histidine-rich, Ca-binding protein (HRC). We observed that the levels of HRC were reduced in animal models and human heart failure. To gain insight into the physiological function of HRC, we infected adult rat cardiac myocytes with a recombinant adenovirus that contains the full-length mouse HRC cDNA. Overexpression (1.7-fold) of HRC in adult rat cardiomyocytes was associated with increased SR Ca load (28%) but decreased SR Ca-induced Ca release (37%), resulting in impaired Ca cycling and depressed fractional shortening (36%) as well as depressed rates of shortening (38%) and relengthening (33%). Furthermore, the depressed basal contractile and Ca kinetic parameters in the HRC-infected myocytes remained significantly depressed even after maximal isoproterenol stimulation. Interestingly, HRC overexpresssion was accompanied by increased protein levels of junctin (1.4-fold) and triadin (1.8-fold), whereas the protein levels of ryanodine receptor, calsequestrin, phospholamban, and sarco(endo)plasmic reticulum Ca-ATPase remained unaltered. Collectively, these data indicate that alterations in expression levels of HRC are associated with impaired cardiac SR Ca homeostasis and contractile function.