US hospital engagement in cross-sector partnerships for population health improvement in socioeconomically distressed counties.

OBJECTIVES: This study identifies the internal characteristics of hospitals located in counties with poor socioeconomic conditions that develop collaborative partnerships with a wide range of community organizations, including non-health organizations. STUDY DESIGN: Cross-sectional study that conducted Chi-square and logistic regression analyses. METHODS: Chi-square tests and logistic regression analyses were performed in this cross-sectional research to identify the internal hospital characteristics associated with non-health sector partnership development for hospitals located in U.S. counties in the worst quartile of performance across three socioeconomic conditions. The 2015 American Hospital Association Population Health Survey provided data on hospitals' collaborative arrangements and internal characteristics, including hospital size, teaching status, ownership type, and system affiliation (n = 1,238). The 2014 County Health Rankings were used to identify counties in the worst quartile of performance on educational attainment, unemployment, and child poverty. RESULTS: Chi-square analyses show that larger hospitals, teaching hospitals, hospitals that belong to a system, and not-for profit hospitals are significantly and positively correlated with non-health sector collaborative partnerships across one or more of the county indicators of poor socioeconomic conditions. Logistic regression results show that the only significant internal hospital characteristic associated with such partnerships is hospital size, in counties with poor educational attainment and those with high child poverty. CONCLUSION: Larger hospitals are more likely to have the resources and strategic perspectives to address community health in counties with poor socioeconomic conditions.

Multidisciplinary Approach in the Treatment of Resistant Hypertension.

With its high prevalence and the eminent number of undetected or poorly controlled patients, the management of arterial hypertension is still a challenging task. Uncontrolled blood pressure is the major adjustable risk factor for cardiovascular end organ damage for coronary heart disease, heart failure, stroke, and renal disease. Patients with resistant hypertension often need a multidisciplinary approach in order to control their blood pressure sustainably. In cooperation with hypertension specialists, the underlying cause for therapy resistance should be evaluated. Pseudohypertension, white coat hypertension, and non-adherence need to be addressed. The medication can often be optimized and simplified. Reducing the number of pills per day can enhance the drug-adherence remarkably. The multidisciplinary evaluation of secondary causes of hypertension includes an endocrinological work-up, ruling out relevant sleeping disorders, and renal diagnostics. If there are no causative treatments possible and pharmacological and non-pharmacological measurements are not sufficient to control the blood pressure, one has to consider multidisciplinary approaches bringing nurses, pharmacists, dieticians, physiotherapists, social workers, psychologists, and community health workers onboard. Utilizing various strategies might improve medication management, patient follow-up, adherence, and self-management. Interventional therapy such as renal renervation, baroreflex activation therapy, or carotid body modulation is the final option that can be discussed with interventional active colleagues. However, large randomized controlled trials proving a benefit of these interventional therapies are still missing. The use of these still experimental approaches should be restricted to randomized controlled trials accordingly.

Chronic p38 mitogen-activated protein kinase inhibition improves vascular function and remodeling in angiotensin II-dependent hypertension.

INTRODUCTION: An excess of angiotensin II (Ang II) causes hypertension and vascular injury. Activation of mitogen-activated protein kinase p38 (p38-MAPK) plays a substantial role in Ang II-dependent organ damage. Recently, we showed that p38-MAPK activation regulates the pressor response to Ang II. This study evaluates the effect of chronic p38-MAPK inhibition in Ang II-dependent hypertension. MATERIALS AND METHODS: C57Bl/6J mice were infused with Ang II for 14 days and either treated with the p38-MAPK inhibitor BIRB796 (50 mg/kg/day) or the vehicle as the control. We assessed vascular function in the aorta and isolated perfused kidneys. RESULTS: Chronic p38-MAPK inhibition did not alter blood pressure at the baseline, but attenuated Ang II-induced hypertension significantly (baseline: 122 ± 2 versus 119 ± 4 mmHg; Ang II: 173 ± 3 versus 155 ± 3 mmHg; p < 0.001). In addition, BIRB796 treatment improved vascular remodeling by reducing the aortic media-to-lumen ratio and decreasing the expression of the membrane metalloproteinases (MMP) MMP-1 and MMP-9. Moreover, renal vascular dysfunction induced by chronic Ang II infusion was significantly ameliorated in the BIRP796-treated mice. Acute p38-MAPK inhibition also improved vascular function in the aorta and kidneys of Ang II-treated mice, highlighting the important role of p38-MAPK activation in the pathogenesis of vascular dysfunction. CONCLUSIONS: Our findings indicated there is an important role for p38-MAPK in regulating blood pressure and vascular injury, and highlighted its potential as a pharmaceutical target.

[Safety aspects of parenteral iron supplementation therapies in patients with chronic kidney disease]. / Sicherheitsaspekte parenteraler Eisentherapien bei Patienten mit chronischer Niereninsuffizienz.

Iron deficiency often occurs in patients with chronic kidney disease and can be effectively treated with parenteral supplementation of iron. In these patients, prompt application of iron therapy can help to reduce the dependence of erythropoietin-stimulating agents and effectively treat anemia. Correct evaluation of iron metabolism in CKD patients can be difficult. Duration of and response to therapy should always be considered while planning parenteral supplementation of iron. The main safety aspects of parenteral iron preparations relate to their possible anaphylactic potential and the potential induction of oxidative stress due to the release of free iron. However, parenteral iron supplementation is usually safe and without major side effects. Regarding current data, none of the iron preparations is showing definitive superiority. Although uncommon, iron preparations containing dextran can lead to severe side effects, therefore these preparations appear to have an inferior safety profile. Due to limited data, a comparison of third-generation iron preparations with previous preparations is not possible. Recently, for the first time, the third generation iron preparation ferumoxytol has been directly compared to iron sucrose. From this data and others, it remains unclear whether third generation iron preparations show safety-relevant superiority.

[Primay hyperaldosteronism--diagnostic and treatment]. / Primärer Hyperaldosteronismus--Diagnostik und Therapie.

Primary hyperaldosteronism (PHA) is characterized by an increased Aldosterone synthesis which is independent of the Renin-Angiotensin-Aldosterone-System (RAAS). The prevalence of PHA in patients who present in specialized hypertension centers is approx. 10 %. Besides patients with the classical symptoms known as "Conn-Trias" (hypertension, hypokalemia, metabolic alkalosis), the more frequent normokalemic patients with PHA also show a worse outcome compared to patients with essential hypertension. Identifying these patients is an important task in the evaluation of hypertension since targeted treatment options are available. Screening for PHA using the Aldosterone-Renin-Ratio (ARR) should be performed in patients with hypokalemic, severe or resistant hypertension. In addition, young patients with early onset of severe hypertension and/or positive family history should be screened. A positive screening result should be followed by a confirmatory test. The saline infusion test is the preferred clinical test for confirming a suspected PHA since it is accessible and time efficient. Other confirmatory tests are not used on a regular basis. After any confirmatory test, CT- or MRI-imaging and adrenal vein sampling (AVS) is used in order to differentiate between a unilateral adenoma, a bilateral hyperplasia or another cause of PHA. CT or MRI usually cannot discriminate smaller tumors form hyperplasia. Therefore AVS is used to detect lateralization of autonomous aldosterone production. Lateralization of aldosterone production indicates a unilateral adenoma. In these cases, laparoscopic adrenalectomy is the therapeutic option of choice with a hypertension cure rate of up to 60 %. If no lateralization is detectable, bilateral hyperplasia as the underlying cause of PHA is likely. Pharmacological inhibition of the mineralocorticoid receptor is the preferred treatment option in these cases. If Spironolactone is not well tolerated, Eplerenone and potassium-sparing diuretics should be prescribed. Often, however, in order to fully control hypertension, additional antihypertensive therapy is necessary.

BH3-only proteins are tail-anchored in the outer mitochondrial membrane and can initiate the activation of Bax.

During mitochondrial apoptosis, pro-apoptotic BH3-only proteins cause the translocation of cytosolic Bcl-2-associated X protein (Bax) to the outer mitochondrial membrane (OMM) where it is activated to release cytochrome c from the mitochondrial intermembrane space, but the mechanism is under dispute. We show that most BH3-only proteins are mitochondrial proteins that are imported into the OMM via a C-terminal tail-anchor domain in isolated yeast mitochondria, independently of binding to anti-apoptotic Bcl-2 proteins. This C-terminal domain acted as a classical mitochondrial targeting signal and was sufficient to direct green fluorescent protein to mitochondria in human cells. When expressed in mouse fibroblasts, these BH3-only proteins localised to mitochondria and were inserted in the OMM. The BH3-only proteins Bcl-2-interacting mediator of cell death (Bim), tBid and p53-upregulated modulator of apoptosis sensitised isolated mitochondria from Bax/Bcl-2 homologous antagonist/killer-deficient fibroblasts to cytochrome c-release by recombinant, extramitochondrial Bax. For Bim, this activity is shown to require the C-terminal-targeting signal and to be independent of binding capacity to and presence of anti-apoptotic Bcl-2 proteins. Bim further enhanced Bax-dependent killing in yeast. A model is proposed where OMM-tail-anchored BH3-only proteins permit passive 'recruitment' and catalysis-like activation of extra-mitochondrial Bax. The recognition of C-terminal membrane-insertion of BH3-only proteins will permit the development of a more detailed concept of the initiation of mitochondrial apoptosis.

[Expert consensus statement on interventional renal sympathetic denervation for hypertension treatment]. / Interventionelle renale Sympathikusdenervation zur Behandlung der therapieresistenten Hypertonie.

This commentary summarizes the expert consensus and recommendations of the working group 'Herz und Niere' of the German Society of Cardiology (DGK), the German Society of Nephrology (DGfN) and the German Hypertension League (DHL) on renal denervation for antihypertensive treatment. Renal denervation is a new, interventional approach to selectively denervate renal afferent and efferent sympathetic fibers. Renal denervation has been demonstrated to reduce office systolic and diastolic blood pressure in patients with resistant hypertension, defined as systolic office blood pressure ≥ 160 mm Hg and ≥ 150 mm Hg in patients with diabetes type 2, which should currently be used as blood pressure thresholds for undergoing the procedure. Exclusion of secondary hypertension causes and optimized antihypertensive drug treatment is mandatory in every patient with resistant hypertension. In order to exclude pseudoresistance, 24-hour blood pressure measurements should be performed. Preserved renal function was an inclusion criterion in the Symplicity studies, therefore, renal denervation should be only considered in patients with a glomerular filtration rate > 45 ml/min. Adequate centre qualification in both, treatment of hypertension and interventional expertise are essential to ensure correct patient selection and procedural safety. Long-term follow-up after renal denervation and participation in the German Renal Denervation (GREAT) Registry are recommended to assess safety and efficacy after renal denervation over time.

PTH-receptors regulate norepinephrine release in human heart and kidney.

Recent data suggests that chronic renal failure and hyperparathyroidism are associated with sympathetic overactivity. Since peptide hormones are known to modulate norepinephrine (NE) release by activating prejunctional receptors, this study investigates whether parathyroid hormone fragment (1-34) (hPTH(1-34)) increases neuronal NE release in human heart and kidney. Using specific PTH-receptor agonists and antagonists, this study furthermore highlights functional differences between PTH1 and PTH2 receptors. Human atrial and renal tissues were incubated with [(3)H]-NE and superfused. Three electrical stimulations (5Hz, 1min) induced a stable [(3)H]-NE release which was taken as an index of endogenous NE release. RT-PCR with specific primers for PTH1- and PTH2-receptor was performed in heart and kidney. hPTH(1-34) (0.01-0.1µmol/L) and a stable analog of its second messenger cAMP (8-bromo-cAMP) increased [(3)H]-NE release in human atria. This facilitatory effect of PTH was also observed in human renal cortex. The PTH1-receptor antagonist (D-Trp(12), Tyr(34))-pTH-(7-34) (0.5µmol/L) abolished the effect of hPTH(1-34). This data was verified using isolated perfused mouse kidneys. Tuberoinfundibular peptide of 39 residues (TIP-39) (0.1nmol/L-0.1µmol/L) decreased [(3)H]-NE release in atria. PTH1- and PTH2-receptor expressions were demonstrated in human heart and kidney. Moreover, a splice variant of the PTH2-receptor was detected in human kidney. In conclusion, PTH is able to facilitate NE release in human atria and renal cortex by activation of PTH1-receptors. The highly increased PTH levels that can be observed in chronic renal failure might be one contributor for the elevated sympathetic nerve activity and the associated cardiovascular mortality in patients with end stage renal disease.

Chronic treatment with angiotensin-(1-7) improves renal endothelial dysfunction in apolipoproteinE-deficient mice.

BACKGROUND AND PURPOSE: ApolipoproteinE-deficient [apoE (-/-)] mice, a model of human atherosclerosis, develop endothelial dysfunction caused by decreased levels of nitric oxide (NO). The endogenous peptide, angiotensin-(1-7) [Ang-(1-7)], acting through its specific GPCR, the Mas receptor, has endothelium-dependent vasodilator properties. Here we have investigated if chronic treatment with Ang-(1-7) improved endothelial dysfunction in apoE (-/-) mice. EXPERIMENTAL APPROACH: ApoE (-/-) mice fed on a lipid-rich Western diet were divided into three groups and treated via osmotic minipumps with either saline, Ang-(1-7) (82 µg·kg(-1) ·h(-1) ) or the same dose of Ang-(1-7) together with D-Ala-Ang-(1-7) (125 µg·kg(-1) ·h(-1) ) for 6 weeks. Renal vascular function was assessed in isolated perfused kidneys. KEY RESULTS: Ang-(1-7)-treated apoE (-/-) mice showed improved renal endothelium-dependent vasorelaxation induced by carbachol and increased renal basal cGMP production, compared with untreated apoE (-/-) mice. Tempol, a reactive oxygen species (ROS) scavenger, improved endothelium-dependent vasorelaxation in kidneys of saline-treated apoE (-/-) mice whereas no effect was observed in Ang-(1-7)-treated mice. Chronic treatment with D-Ala-Ang-(1-7), a specific Mas receptor antagonist, abolished the beneficial effects of Ang-(1-7) on endothelium-dependent vasorelaxation. Renal endothelium-independent vasorelaxation showed no differences between treated and untreated mice. ROS production and expression levels of the NAD(P)H oxidase subunits gp91phox and p47phox were reduced in isolated preglomerular arterioles of Ang-(1-7)-treated mice, compared with untreated mice, whereas eNOS expression was increased. CONCLUSION AND IMPLICATIONS: Chronic infusion of Ang-(1-7) improved renal endothelial function via Mas receptors, in an experimental model of human cardiovascular disease, by increasing levels of endogenous NO.

Proapoptotic signalling through Toll-like receptor-3 involves TRIF-dependent activation of caspase-8 and is under the control of inhibitor of apoptosis proteins in melanoma cells.

Toll-like receptor-3 (TLR3), a member of an immune recognition receptor family, is widely expressed in tumour cells and has been shown previously to have the capacity to not only activate immune signalling pathways, but also to exert proapoptotic activity in some cells. We show here that HaCaT human keratinocytes are susceptible to apoptosis induction by the TLR3 ligand poly I:C, and use these cells as a model to analyse the apoptotic signalling pathway. Although the BH3-only protein Noxa was transcriptionally induced by poly I:C and translocated to mitochondria, RNAi experiments showed that the BH3-only proteins Noxa, Bim and Puma were individually dispensable for poly I:C-induced apoptosis. Instead, poly I:C-induced activation of caspase-8 via TLR3 and its adapter TRIF was required for apoptosis. In human melanoma cell lines poly I:C failed to induce apoptosis unless protein synthesis was blocked. Significantly, sensitisation towards poly I:C-dependent caspase-8 activation and apoptosis in melanoma cells was also achieved by the synthetic Smac mimetic/inhibitor of apoptosis protein (IAP) antagonist, LBW242, or by specific downregulation of cIAP1 by siRNA. Inactivation of caspase-8 by CrmA overexpression reduced poly I:C/LBW242-induced apoptosis. These results indicate that the proapoptotic activity of TLR3/TRIF/caspase-8 in melanoma cells is under the control of IAPs, and the use of novel Smac mimetics might be a feasible approach to target melanoma.

N-cadherin engagement provides a dominant stop signal for the migration of MDA-MB-468 breast carcinoma cells.

The development of a primary tumor as such is not the main cause of death, but is rather the spreading of metastases, which causes over 90% of deaths in cancer patients. This largely depends on the ability of tumor cells to migrate away from the tumor and relocate at other areas of the body. Cell migration is known to be regulated by various extracellular signal substances such as neurotransmitters. However, before single tumor cells can start to invade into distant tissue, they have to dissociate from the primary tumor. This requires the disruption of cell-cell contacts, which are provided by a plethora of adhesion molecules like the family of cadherins. Using our well, established three-dimensional collagen-based cell migration assay, we show that engagement of N-cadherin results in a significant decrease of the spontaneous and the norepinephrine-induced migration of MDA-MB-468 breast carcinoma cells, which was due to an increase in the average break length. Moreover, this N-cadherin driven influence on the migratory activity is intracellularly integrated via multiple signaling pathways. Our results show that the impact of N-cadherin on the locomotion of MDA cells involves the activation of the adenylyl cyclase and the phosphatidylinositol-3-kinase (PI3K), but is independent of the protein kinase C (PKC) alpha. In summary, we provide evidence that the engagement of N-cadherin provides a stop signal for breast carcinoma cell migration, and accordingly the use of anti-N-cadherin antibodies or soluble ligands might be a tool to inhibit metastasis formation in E-cadherin negative but N-cadherin positive tumors.

[Umbilical cord stromal cells (UCSC). Cells featuring osteogenic differentiation potential]. / Umbilical Cord Stromal Cells (UCSC). Zellen mit osteogenem Differenzierungspotenzial.

The identification of appropriate cell types is necessary to establish cell-based therapies in regenerative medicine. These cell types must (1) be available in an appropriate amount, (2) be easy to obtain, (3) be sufficiently expandable in vitro, and (4) fit to or at least be able to differentiate into the required cell type. Since the umbilical cord is available without any intervention and represents a notable amount of tissue, we consider it to be a promising source for isolating cells for cell-based therapies. This study demonstrates that umbilical cord stromal cells (UCSC), the connective tissue cells of the umbilical cord, can be isolated in sufficient quantities and be well expanded. UCSC feature phenotypic plasticity and thus are functionally similar to stem cells. UCSC can be differentiated into cells with osteoblastic properties (expression of alkaline phosphatase, formation of bone nodules). It is concluded that the umbilical cord should no longer be regarded as valueless tissue and be unthinkingly discarded. Instead, it should be considered a valuable resource for the isolation of potent cells for cell-based therapies, especially for treatment of bone defects.

Regulation of the estrogen-responsive pS2 gene in MCF-7 human breast cancer cells.

To understand how hormones and antihormones regulate transcription of estrogen-responsive genes, in vivo footprinting was used to examine the endogenous pS2 gene in MCF-7 cells. While the consensus pS2 estrogen response element (ERE) half site was protected in the absence of hormone, both the consensus and imperfect ERE half sites were protected in the presence of estrogen. 4-Hydroxytamoxifen and ICI 182,780 elicited distinct footprinting patterns, which differed from those observed with vehicle- or with estrogen-treated cells suggesting that the partial agonist/antagonist and antagonist properties of 4-hydroxytamoxifen or ICI 182,780, respectively, may be partially explained by modulation of protein-DNA interactions. Footprinting patterns in and around the TATA and CAAT sequences were identical in the presence and in the absence of estrogen suggesting that the basal promoter is accessible and poised for transcription even in the absence of hormone. In vitro DNase I footprinting experiments demonstrated that the estrogen receptor bound to the pS2 ERE and that adjacent nucleotides were protected by MCF-7 nuclear proteins. These findings indicate that transcription of the pS2 gene is modulated by alterations in protein binding to multiple sites upstream of the basal promoter, but not by changes in protein-DNA interactions in the basal promoter.

Evaluation of a computerized contraceptive decision aid for adolescent patients.

Recent efforts to involve patients more actively in therapeutic decisions have suggested the relevance of computer-based interventions at clinic visits. This paper presents a longitudinal, experimental study evaluating a computer-based contraceptive decision aid in Chicago and Madison family planning clinic visits. Patient interviews at three time points evaluated patient acceptance by and program impact on 949 young women. Both Chicago and Madison patients reported high acceptance. The program resulted in improved short-term knowledge and confidence in oral contraceptive (OC) efficacy for Chicago and Madison patients. In addition, compared to their control group, Madison experimental group patients had higher OC knowledge 1 year after the initial visit and a trend for fewer pregnancies (P < 0.074). Compared to their control group, a higher percent of the Chicago experimental group patients adopted OC's after stating their intention to do so at the initial visit. Exposure to the computer program had no observable impact on the number of months on the oral contraceptive for Chicago or Madison patients. Overall findings suggest the usefulness of informatics tools as a supplement to patient-provider interactions.

PIP: This paper presents findings of a longitudinal, experimental study which evaluated the effect of a computer-based contraceptive decision aid, the Aid for Contraceptive Decision-Making Program, as a supplement to family planning clinic visits by adolescent patients. Patient interviews at three time points evaluated patient acceptance by and program impact on 949 young women in Chicago and Madison family planning clinics. Both Chicago and Madison patients reported high acceptance. The program also resulted in improved short-term knowledge and confidence in oral contraceptive (OC) efficacy for Chicago and Madison patients. Furthermore, the Madison experimental group patients had higher OC knowledge 1 year after the initial visit and a trend for fewer pregnancies (P 0.074) as compared to their control group. While a higher percentage of the Chicago experimental group patients adopted OCs after stating their intention to do so at the initial visit as compared to the control group. However, exposure to the computer program had no observable impact on the number of months on the OC for Chicago and Madison patients. Overall findings implicate the usefulness of informatics tools as a supplement to patient-provider interactions.

Dimensions of risk behaviors among American Indian youth.

OBJECTIVE: To explore the covariation of risk behaviors in a national sample of American Indian reservation-based youth using listwise principal components factor analysis and to determine how these risk behaviors may vary by age and sex. DESIGN: Analysis of data from the National Indian Adolescent Health Survey, a validated anonymous self-report questionnaire of 162 items addressing various health domains. SETTING: The survey was administered nationally in more than 200 reservation-based schools. PARTICIPANTS: Thirteen thousand nine hundred twenty-three reservation-based American Indian or Alaska Native students in grade 7 through 12 representing more than 50 tribes. The listwise factor analysis sample included 7687 respondents with complete data. MAIN OUTCOME MEASURES: Item loading and factor correlations by age and sex for 30 risk behaviors across various health domains. RESULTS: Three risk behavior factors were fairly stable across sex and age: (1) the use of alcohol, tobacco, and other drugs; (2) risky sexual behavior, and (3) suicidal behaviors. Correlations between these and other factors suggested different strengths of relationships by sex and age. Other factors, including violence, truancy, and delinquency, showed differences in item loading on factors and correlations between factors. The use of tobacco, alcohol, and other drugs was most frequently associated with other risk behavior factors, and suicidal behaviors showed the next highest frequency of intercorrelations. CONCLUSIONS: There are sex and age differences in the covariation of risk behaviors, and suicidal behaviors should be further investigated to determine of our findings are unique to American Indian youth. Health interventions that focus categorically on 1 risk dimension should also emphasize substance use prevention and intervention. To prevent substance abuse among American Indian youth, research efforts need to focus on effective strategies for coping with social and psychological stressors.

The validity of self-reported condom use among adolescents.

BACKGROUND: Research and public health interventions designed to reduce the risk of sexually transmitted diseases (STDs) often are based on self-reported condom use. Yet, validation of self-reported condom use, in particular with adolescents, has rarely been described in the literature. METHODS: Baseline data were obtained from 540 adolescents, 13-21 years of age, enrolled in a 1-year longitudinal study of health beliefs, sexual behaviors, and STD acquisition. Of the 445 participants reporting to be sexually active, 404 (90.8%) agreed to a complete physical examination, including a genital examination, with STD screening after completing the self-administered written questionnaire. Participants' written self-report of condom use was compared to histories obtained by clinicians and laboratory diagnosis of acute STDs to assess validity of written self-report. RESULTS: Complete data were available for 321 females and 77 males of whom 52 females and 5 males had laboratory evidence of 63 infections. Although three individuals who had STDs reported to be consistent users of condoms, a significant association (P < 0.05) was found between those who reported more frequent condom use with the last two partners and the absence of STDs. CONCLUSION: In this group of adolescents, self-report of condom use with the last two partners was associated with the absence of an acute STD. This finding suggests that self-reported condom use is a valid indicator of risk for STDs, with implication for those working with adolescents clinically and in research contexts.

PIP: Although most research on sexually transmitted disease (STD) risk behavior surveillance and prevention is based on self-reports of condom use, there have been few attempts to assess the extent to which self-reports accurately reflect true behavior. To validate this methodology, baseline data were obtained from 540 US male and female adolescents 13-21 years of age enrolled in a 1-year longitudinal study of sexual behaviors and STDs. Of the 445 participants who reported they were sexually active, 398 underwent genital examination and STD screening. 52 females and 5 males had laboratory evidence of acute STDs. 15.2% of females and 32.3% of males reported consistent condom use with their most recent sexual partner. Although 3 young people with STDs had reported they were consistent condom users, a significant (p 0.05) inverse association was found between consistency of reported condom use with the last 2 sexual partners and the occurrence of an acute STD. This finding suggests that, even among adolescents, self-reported condom use is a valid indicator of STD risk.

Improving hospital discharge planning for elderly patients.

Hospital discharge planning has become increasingly important in an era of prospective payment and managed care. Given the changes in tasks, decisions, and environments involved, it is important to identify how to move such planning from an art to an empirically based decisionmaking process. The authors use a decision-sciences framework to review the state-of-the-art of hospital discharge planning and to suggest methods for improvement.