PCV16 Smoking Related Costs in the United States

Smoking is a high-risk behavior that affects the health and economic welfare of society. Thus, it is important to quantify the economic burden smoking places on social institutions in the United States.
OBJECTIVE: The purpose of this review paper is to analyze smoking cost studies and to provide estimates that represent the economic costs of smoking from different perspectives of society, and as a whole.
METHODS: Current Contents (1996–), Health Star (1970–), and Medline (1966–) databases were searched through the use of pertinent subject headings and key words: tobacco use, smoking, cost, and economics. The internet was utilized to identify potential sources of epidemiological and cost information on smoking. Recent cost-of-illness studies using different methodologies: human capital, incidence, and prevalence were chosen for review based on their relevance.
RESULTS: Preliminary results indicate that the published cost studies available underestimate the "true" costs of smoking. The most current articles approximate annual direct medical costs to health care payers of $50 billion (1993); inflating to 1997 equals $59 billion or $1,200 per smoker. Although the latest cost studies do not attempt to estimate indirect costs, past studies have found indirect costs to be 1.5–2 times the direct costs. Therefore, using direct and indirect costs we estimate total smoking costs to be $150 billion (1993); inflating to 1997 equals $176 billion or $3,500 per smoker.
CONCLUSION: Quantifying the cost of smoking is a difficult task due to tobacco use infiltrating many aspects of life and the dependency of cost on perspective. Cost-of-illness studies provide cost estimation data which can be useful in aiding decision-makers who are allocating health care resources.     

Human fibroblast tissue factor is inhibited by lipoprotein-associated coagulation inhibitor and placental anticoagulant protein but not by apolipoprotein A-II

Studies of proteins that inhibit tissue factor activity have generally been conducted using either an extracted tissue homogenate ("thromboplastin") or tissue factor protein reconstituted into phospholipid vesicles rather than with tissue factor expressed in cell membranes (its physiological environment). In the present study, a human fibroblast cell strain was used to evaluate the effects of lipoprotein associated coagulation inhibitor (LACI), placental anticoagulant protein (PAP), and apolipoprotein A-II (apo A-II) on human tissue factor in cell membranes. LACI was tested from 7.8 to 500 pmol/L on fibroblasts cultured at cell densities ranging from 3,500 to 9,925 cells/well, and caused a progressive inhibition of tissue factor activity. PAP was tested from 3.9 nmol/L to 1 mumol/L at cell densities ranging from 4,500 to 15,400 cells/well and caused up to 83% inhibition of tissue factor activity. Inhibition by these proteins appeared to be influenced by cell density as well as whether the cells were intact or disrupted. Apo A-II, up to 1 mumol/L, did not inhibit the tissue factor activity of intact or disrupted fibroblasts at any cell density examined even though it did inhibit the activity of tissue factor in phospholipid vesicles. Of these inhibitors of tissue factor-dependent activation of factor X, LACI was the most effective in suppressing the generation of factor Xa activity. The effects obtained with apo A-II are clearly dependent on the nature of the tissue factor preparation with which it is tested. The disparity between the inhibitory effect of apo A-II on the activity of tissue factor reconstituted into lipid vesicles and the absence of effect on the activity of tissue factor remaining in cell membranes serves to reemphasize the necessity of reexamining results obtained with model systems using as nearly physiological reagents as possible.     

Quantitative evaluation of liver-specific promoters from retroviral vectors after in vivo transduction of hepatocytes

Hepatic gene therapy could be used to treat a number of inherited blood diseases such as hemophilia or thrombophilia. Although liver-directed retroviral transduction can result in long-term gene expression in vivo, the low level of protein production has limited its clinical application. We reasoned that the insertion of liver-specific promoters into retroviral vectors would increase gene expression in vivo. The 347- bp human alpha 1-antitrypsin (hAAT), the 810-bp murine albumin (mAIb), the 490-bp rat phosphoenolpyruvate carboxykinase (rPECK), and the 596- bp rat liver fatty acid binding protein promoters were inserted into a Moloney murine leukemia retroviral backbone containing the hAAT reporter gene. Vectors that produced appropriately sized RNA and hAAT protein in vitro were tested in vivo by transducing regenerating rat livers. Long-term serum expression of the hAAT reporter gene was normalized to retroviral transduction efficiency as determined by using a polymerase chain reaction-based assay of genomic DNA from transduced rat livers. The hAAT, mAIb, and rPEPCK promoters were, respectively, 35- , 8-, and 0.02-fold as strong as the previously studied constitutive Pol-II promoter. We conclude that the hAAT promoter resulted in the highest expression from a retroviral vector and may result in therapeutically significant expression of other clinically significant blood proteins.     

Anästhesie bei Nierentransplantation

Ohne Zusammenfassung     

A STUDY OF NEUROKININS AND OTHER OEDEMA-INDUCING MEDIATORS AND MECHANISMS IN THERMAL INJURY

1. Mechanisms involved in the plasma extravasation observed following thermal injury of rat dorsal skin were investigated. 2. Heat applied to the dorsal skin of anaesthetized rats by a temperature-controlled skin heater (1 cm diameter) for 5 min induced temperature-dependent plasma protein extravasation a. 48–48.5°C, measured for up to 4 h following initiation of heat. 3. A tachykini. NK₁ receptor antagonist (SR140333), a bradykinin B₂ receptor antagonist (HOE 140) and a cyclooxygenase inhibitor (indomethacin), when given as cotreatments prior to the selected measurement period, markedly suppressed oedema formation observed over 0–1 h (P < 0.05) but not that observed over 3–4 h after injury. 4. These results indicate that although neurokinins, bradykinin and cyclo-oxygenase products may be important for the early response to thermal injury, they do not appear to play an important role in the ongoing oedem. response. 5. Neutrophils accumulate at the inflammatory site by 4h after thermal injury. Therefore, the effect of depletion of circulating neutrophils by a rat anti-neutrophil antiserum on oedema formation over the 0–4 h period was investigated. The results show that oedema formation was similar in control and antineutrophil-treated rats. 6. In conclusion, the data from the present study indicate that neuropeptides as well as other vasoactive mediators play a role in the acute plasma extravasation observed after thermal injury, but not in the ongoing inflammatory injury. Neutrophils, despite their presence at sites of thermal injury, do not appear to be involved in mediating the oedema formation observed up to 4 h after thermal injury.     

Einfluss von niedrigem Alkalimetallgehalt im Atemkalk auf Compound-A-Bildung w?hrend Low-flow-Narkosen mit Sevofluran

Nach bisherigem Kenntnisstand ist der Gehalt an Alkalimetallhydroxiden in Atemkalken wesentlich für die Bildung von Compound A (CpA) aus Sevofluran (Sevo) verantwortlich. Insbesondere das Kaliumhydroxid (KOH), weniger das Natriumhydroxid (NaOH), reagiert im Laborversuch stark mit Sevofluran. Mit dieser klinischen Studie sollte untersucht werden, ob die Verwendung eines KOH-freien Atemkalks w?hrend Niedrigflussnarkosen (0,8 l/min Frischgasfluss) mit Sevofluran bei laparoskopischen Cholezystektomien tats?chlich zu einer Verminderung der CpA-Exposition führt. In die Studie wurden 30 Patienten eingeschlossen. Bei jeweils 15 Patienten wurde entweder Sodasorb (SO) oder KOH-freier Soda Lime (SL) verwendet. Von der SO-Gruppe mussten 3 Patienten auf Grund von technischen Problemen bei der CpA-Messung ausgeschlossen werden. Neben demographischen Daten wurden Vital- und Beatmungsparameter sowie die Konzentrationen von Sevofluran und Kohlendioxid dokumentiert. Die durchschnittlichen endtidalen Sevoflurankonzentrationen betrugen 1,94±0,17 (SO) bzw. 1,97±0,15 (SL) Vol.-%, die Gesamtexposition gegenüber Sevofluran 1,52±0,36 (SO) und 1,64±0,47 (SL) MAC-h (n. s.). Die maximale inspiratorische CpA-Konzentration war in der SL-Gruppe signifikant h?her (19,6±2,8 vs. 11,7±4,1 ppm, p<0,001). Der alleinige Verzicht auf KOH in NaOH-haltigen Atemkalken führt daher nicht zwangsl?ufig zu einer Verminderung von CpA.