The Sequential Relation Between Changes in Catastrophizing and Changes in Posttraumatic Stress Disorder Symptom Severity

Catastrophizing has been discussed as a cognitive precursor to the emergence of posttraumatic stress disorder (PTSD) symptoms following the experience of stressful events. Implicit in cognitive models of PTSD is that treatment-related reductions in catastrophizing should yield reductions in PTSD symptoms. The tenability of this prediction has yet to be tested. The present study investigated the sequential relation between changes in a specific form of catastrophizing—symptom catastrophizing—and changes in PTSD symptom severity in a sample of 73 work-disabled individuals enrolled in a 10-week behavioral activation intervention. Measures of symptom catastrophizing and PTSD symptom severity were completed at pre-, mid-, and posttreatment assessment points. Cross-sectional analyses of pretreatment data revealed that symptom catastrophizing accounted for significant variance in PTSD symptom severity, β = .40, p < .001, sr = .28 (medium effect size), even when controlling for known correlates of symptom catastrophizing, such as pain and depression. Significant reductions in symptom catastrophizing and PTSD symptoms were observed during treatment, with large effect sizes, ds = 1.42 and 0.94, respectively, ps < .001. Cross-lagged analyses revealed that early change in symptom catastrophizing predicted later change in PTSD symptoms; early changes in PTSD symptom severity did not predict later change in symptom catastrophizing. These findings are consistent with the conceptual models that posit a causal relation between catastrophizing and PTSD symptom severity. The clinical implications of the findings are discussed.     

Constitutive production of leukemia differentiation, colony- stimulating, erythroid burst-promoting, and pluripoietic factors by a human hepatoma cell line: characterization of the leukemia differentiation factor

Conditioned medium (CM) obtained from a human hepatoma cell line, SK- HEP-1, contains colony-stimulating factors (CSFs) active on murine and human bone marrow-derived granulocyte and macrophage colony-forming units (CFU-GM) and a factor capable of inducing granulocyte-macrophage differentiation (GM-DF) of murine myelomonocytic leukemic cells WEHI- 3B(D+) and human promyelocytic leukemic cells HL-60 when assayed in semisolid agar cultures. The human active granulocyte-macrophage colony- stimulating factor (GM-CSF) for day 7 CFU-GM and the GM-DF for WEHI- 3B(D+) and for HL-60 are not separable by acrylamide agarose column chromatography, eluting at an apparent molecular weight between 20,000 and 35,000 daltons, or by isoelectric focusing (isoelectric point, pH 5.4). In addition, SK-HEP-1 CM contains erythroid burst-promoting activity (BPA) and a factor that promotes the growth of human mixed colonies. SK-HEP-1 cells, which grow as an adherent monolayer, appear not to be endothelial or monocytic in origin since by immunofluorescent staining they are negative for Ia (HLA-DR), monocyte antigen 1 and 2, lysozyme, and factor VIII-related antigen. Positive immunofluorescent staining for keratin and fibronectin suggests the possibility that SK- HEP-1 is an epithelial cell line. Constitutive production of GM-DF as well as other hematopoietic activities including GM-CSF, erythroid BPA, and an activity that promotes the growth of human mixed colony progenitors by a human epithelial tumor cell line, SK-HEP-1, suggests that this cell line is a valuable resource for both large-scale production of these factors and the cloning of the gene(s) that code for these regulators.     

Estimating health care delivery system value for each US state and testing key associations

ObjectiveTo estimate health care systems'' value in treating major illnesses for each US state and identify system characteristics associated with value.Data sourcesAnnual condition‐specific death and incidence estimates for each US state from the Global Burden Disease 2019 Study and annual health care spending per person for each state from the National Health Expenditure Accounts.Study designUsing non‐linear meta‐stochastic frontier analysis, mortality incidence ratios for 136 major treatable illnesses were regressed separately on per capita health care spending and key covariates such as age, obesity, smoking, and educational attainment. State‐ and year‐specific inefficiency estimates were extracted for each health condition and combined to create a single estimate of health care delivery system value for each US state for each year, 1991–2014. The association between changes in health care value and changes in 23 key health care system characteristics and state policies was measured.Data collection/extraction methodsNot applicable.Principal findingsUS state with relatively high spending per person or relatively poor health‐outcomes were shown to have low health care delivery system value. New Jersey, Maryland, Florida, Arizona, and New York attained the highest value scores in 2014 (81 [95% uncertainty interval 72‐88], 80 [72‐87], 80 [71‐86], 77 [69‐84], and 77 [66‐85], respectively), after controlling for health care spending, age, obesity, smoking, physical activity, race, and educational attainment. Greater market concentration of hospitals and of insurers were associated with worse health care value (p‐value ranging from <0.01 to 0.02). Higher hospital geographic density and use were also associated with worse health care value (p‐value ranging from 0.03 to 0.05). Enrollment in Medicare Advantage HMOs was associated with better value, as was more generous Medicaid income eligibility (p‐value 0.04 and 0.01).ConclusionsSubstantial variation in the value of health care exists across states. Key health system characteristics such as market concentration and provider density were associated with value.     

DA8 Evaluating Health Outcomes and Pharmacoeconomic Literature

In 1997, the United States Pharmacopeia (USP) established an Ad Hoc Outcomes/Cost Effectiveness Advisory Panel to consider the development of specifications for compiling, indexing, and evaluating outcomes research/cost-effectiveness literature on a disease-specific basis. Such a resource could be used to support pharmaceutical therapy choice decision making by a variety of potential users. The USP had developed a protype health outcomes and pharmacoeconomic annotated registry of the literature on the disease state, congestive heart failure. Other organizations have established and are marketing pharmacoeconomic and health outcome literature registries, with two examples being the HEED database (OHE-IFPMA Database Ltd.) and the University of York NHS Centre for Reviews and Dissemination (DARE).
OBJECTIVE: To share experiences and to identify the needs of decision makers for outcome/pharmacoeconomic information and to discuss whether they are being met by currently available literature sources. Decision makers include health care practitioners, managed care organizations, third party payers, industry and governments.
WORKSHOP FORMAT: The USP congestive heart failure protype literature registry will be described and compared to currently available pharmacoeconomic/outcome databases. Participants will share their assessment of the currently available abstracting service/databases and determine if there is a role for further developments.
DESIRED OUTCOME: To determine if there is a need for a collaborative approach among interested parties to make relevant health outcome/pharmacoeconomic information more accessible to the drug therapy decision makers in a format that is "user friendly."     

Mesoatrial shunts for Budd-Chiari syndrome and inferior vena cava thrombosis: angiographic and hemodynamic evaluations

When inferior vena caval obstruction complicates the Budd-Chiari syndrome, conventional portosystemic shunts are not possible. The mesoatrial shunt has been devised to enable portal and sinusoidal decompression in these patients. Findings in 12 patients with Budd-Chiari syndrome and inferior vena caval obstruction in whom a mesoatrial shunt was performed are reported. Preoperative inferior vena cavography with pressure measurements is essential to determine the appropriate shunt procedure. Postoperatively, shunt patency is assessed with superior mesenteric arterial portography. Where possible, transvenous catheterization of the shunt is performed to confirm patency and assess hemodynamic function.