Educational and health services innovation to improve care for rural Hispanic communities in the USA.

BACKGROUND: Access to comprehensive and quality healthcare services is difficult for socioeonomically disadvantaged groups in rural regions. Barriers to health care for rural Latinos include lack of insurance, language barriers and cultural differences. For the Latino immigrant population in rural areas, barriers to access are compounded. HEALTH NEEDS OF RURAL AREAS: THE CASE OF WALHALLA, SC: The town of Walhalla, South Carolina, USA, is a rural community located in Oconee County, the northwest corner of the state. Disparities exist between rural and urban residents in several health categories, and these disparities illustrate the need to provide competent, appropriate and affordable healthcare to rural populations. The Hispanic population of Oconee has dramatically increased in the past decade, and the majority of these immigrants have no health insurance and have limited access to health services. DESIGNING A PROGRAM TO FIT THE COMMUNITY--THE "WALHALLA EXPERIENCE": The purpose of the Accessible and Culturally Competent Health Care Project (ACCHCP) is to provide care for underserved populations, in Oconee County, South Carolina while providing rural educational opportunities for health services students. Funded by the Health Resources and Services Administration of DHHS, the program is designed to offer culturally appropriate, sensitive, accessible, affordable and compassionate care in a mobile clinic setting. In this interdisplinary program, nurse practitioners, health educators, bilingual interpreters, medical residents and Clemson University students and professors all played key roles. Women in the community also serve as promotoras or lay health advisors. The program is unique in using educational initiatives and innovative strategies for bringing health care to this underserved community and offers important information for rural healthcare initiatives targeting minority groups. This article reports on the challenges and successes in the development and implementation of the ACCHCP program in Walhalla, South Carolina.

Are postoperative complications related to resident sleep deprivation?

This real-world study compares the outcome of surgery and the sleep-deprivation status of the resident surgeon. Residents who operated the day after a 24-hour on-call period were considered sleep deprived; all other resident surgeons were considered non-sleep-deprived. We retrospectively reviewed data on 6,371 surgical cases and identified 351 postoperative complications. The complication data were analyzed using logistic regression analysis, with outcome being the presence or absence of surgical complications. No statistically significant change in complication incidence was noted when the resident surgeon was sleep deprived.

Increased prostacyclin and thromboxane A2 formation in human varicose veins.

Increased urinary metabolites of the antiaggregatory vasodilator prostacyclin (PGI2) and the proaggregatory vasoconstrictor thromboxane A2 (TXA2) have been reported in deep vein thrombosis; however, the tissue(s) of origin is uncertain. Because little is known about the formation of PGI2 or TXA2 from its common precursor, prostaglandin (PG) endoperoxide H2 (PGH2), by varicose veins, we determined the formation of 6-keto-PGF1 alpha (the stable metabolite of PGI2), TXB2 (the stable metabolite of TXA2), and PGE2. Segments of normal saphenous vein and varicose vein (nine and six patients, respectively) were incubated with 10 microM [14C]PGH2 for 2 min at 37 degrees C; products were separated by thin-layer chromatography. Surface area and mass of normal and varicose vascular segments were 19.5 +/- 0.8 versus 18.8 +/- 0.6 mm2 and 11.6 +/- 1.4 versus 10.7 +/- 0.7 mg, respectively. Formation of 6-keto-PGF1 alpha and TXB2 by the segments of varicose vein was significantly increased over that of normal vein: 157 +/- 14 versus 243 +/- 17 pmole of 6-keto-PGF1 alpha (P less than 0.005) and 22 +/- 3 versus 35 +/- 5 pmole of TXB2 (P less than 0.01). The formation of PGE2 by segments of varicose vein was not significantly different from that of normal vein (201 +/- 9 vs 219 +/- 11, respectively). Deoxyribonucleic acid (DNA) content of normal and varicose vein was 1.69 +/- 0.12 and 1.51 +/- 0.13 mg per gram of tissue, respectively. The data suggest that the increased PGI2 formation may reflect increased activity or content of PGI2 synthase. The increase in TXA2 formation may reflect increased productivity or an increased presence of residual platelets or microemboli.

Prostacyclin and thromboxane A2 formation by atherosclerotic carotid artery: comparison with normal aorta, saphenous vein, and platelets.

Prostacyclin (PGI2) and thromboxane A2 (TxA2) formation by whole-tissue segments of nine carotid endarterectomy specimens (CES), five normal aortic specimens (NAS), six saphenous vein specimens (SVS), and four platelet samples were determined by incubation with 10 mumol/L 1-14C-radiolabeled prostaglandin endoperoxide H2 (PGH2), and in other experiments with and without 10 mumol/L of CGS 13080, a TxA2 synthase inhibitor. PGI2 formation (expressed as picomoles 6-keto-PGF1 alpha/2-min incubation per sample) by nonatheromatous proximal intima of CES (307 +/- 23, mean +/- standard error) and distal intima of CES (260 +/- 22) was not statistically different; however, it was greater than atheromatous transitional plaque (159 +/- 13 pmol) (p less than 0.01) and ulceration regions (140 +/- 15 pmol) (p less than 0.01) of CES, NAS (204 +/- 16 pmol) (p less than 0.01), and SVS (165 +/- 9 pmol) (p less than 0.01). TxA2 formation (expressed as picomoles TxB2/2-min incubation per sample) by CES ulceration (51 +/- 2 pmol) was low but greater than proximal (17 +/- 2 pmol) (p less than 0.01), distal (19 +/- 3 pmol) (p less than 0.01), and transitional (23 +/- 3 pmol) (p less than 0.01) regions. TxA2 formation by NAS and SVS was not detected (less than 10 pmol). CGS 13080 inhibited TxA2 formation by CES below the limits of detection. Incubation of 1.9 x 10(5) intact platelets with 10 mumol/L of PGH2 formed a quantity of TxA2 equal to that of CES ulceration.(ABSTRACT TRUNCATED AT 250 WORDS)