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.     

Peripheral arterial occlusive disease: P-31 MR spectroscopy of calf muscle

The effect of a graded exercise protocol on phosphorus-31 magnetic resonance (MR) spectroscopy of calf skeletal muscle in nine healthy (control) subjects and 16 patients with symptomatic peripheral arterial occlusive disease (PAOD) was assessed. Ankle-brachial pressure indexes were obtained in all 16 patients, and 10 patients underwent peripheral arteriography. Temporal profiles of pH and the inorganic phosphorus (Pi) index were calculated from the spectra. A Pi-index recovery rate constant was calculated for each subject. Arteriograms were graded by calculating the runoff resistance in the limb of interest. The pH profiles during exercise did not differ significantly between the PAOD patients and control subjects. The Pi-index recovery rate constant in the PAOD patients was significantly (P less than .01) smaller than in the control subjects. There was no significant correlation between recovery rate and the ankle-brachial pressure indexes, but there was a strong negative correlation between recovery rates and angiographic resistance grades, with smaller recovery rate constants in patients with increased arterial resistance. It is concluded that P-31 MR spectroscopy shows promise as a direct measure of tissue perfusion.     

自身免疫性肝炎大鼠模型外周血淋巴细胞亚群变化与褪黑素的影响

目的:观察褪黑素对自身免疫性肝炎大鼠模型外周血淋巴细胞亚群的影响方法:实验于2004-10/2006-10在解放军第一二三医院南京军区肝病中心实验室完成。①实验材料:Wistar大鼠,雄性,3月龄,体质量(230±20)g,购自上海斯莱克实验动物有限责任公司。褪黑素:美国Sigma公司产品,临用前以无水乙醇溶解,再加生理盐水配制,使乙醇浓度为0.1%,置4℃冰箱保存备用。②实验方法:采用弗氏完全佐剂加肝细胞特异性脂蛋白法制作大鼠自身免疫性肝炎模型。将建模成功大鼠随机分为模型对照组、褪黑素注射组及猪促肝细胞生长素注射组,每组20只。褪黑素注射组褪黑素2mg/kg腹腔注射,1次/d,猪促肝细胞生长素注射组2mg/kg猪促肝细胞生长素腹腔注射,1次/d,模型对照组与正常对照组均用含0.01%乙醇的生理盐水腹腔注射。③实验评估:60d后检测各组大鼠外周血淋巴细胞亚群浓度。结果:①CD4 细胞≤39.5只,均为褪黑素注射组动物,肝炎组织活动性指数≤8分。22只CD4 细胞>39.5%动物中,4只肝炎组织活动性指数≤8分,其中2只为褪黑素注射组动物,2只为模型对照组动物。18只肝炎组织活动性指数>8分,均为模型对照组动物。②18只CD4 细胞≤39.5%褪黑素注射组动物中,17只肝纤维化指数≤4分,1只肝纤维化指数4分;22只动物CD4 细胞>39.5%,2只肝纤维化指数≤4分,为模型对照组动物,20只肝纤维化指数>4分,褪黑素注射组2只,模型对照组18只。③CD4 细胞≤39.5%,肝组织血管病变均为1级,>39.5%时,2级以上血管病变为90.9%。18只CD4 细胞≤39.5%褪黑素注射动物血管病变为1级。22只CD4 细胞百分比>39.5%,2只血管病变为1级,为模型对照动物,17只血管病变为2级,褪黑素注射组2只,模型对照组15只。3只血管病变为3级,为模型对照动物。④CD4 细胞≤39.5%时,83.3%血管内皮细胞生长因子表达呈弱阳性,CD4 细胞>39.5%时,81.8%血管内皮细胞生长因子表达呈强阳性,提示CD4 细胞与血管内皮细胞生长因子表达有关。⑤模型对照组外周血CD4 细胞数和CD4 /CD8 比值均明显高于其他组(P<0.05),CD8 细胞与其他组无明显差异(P>0.05)。褪黑素注射动物与猪促肝细胞生长素注射动物相比,无明显差异(P>0.05)。结论:褪黑素对自身免疫性肝炎模型大鼠外周血CD4 细胞有较强的抑制作用。     

Anorectal hamartoma in a neonate: a unique anorectal mass

Neonates presenting with perineal masses are uncommon. When encountered, most perineal masses are anorectal malformations, sacrococcygeal teratomas, rectal prolapse, or duplication cysts.We present an otherwise healthy newborn with a patent anal canal and a pedunculated anal mass. The mass was initially believed to be a prolapsed rectal duplication cyst. Further evaluation for concomitant congenital abnormalities was negative. The patient underwent mass excision at the bedside under local anesthesia. Histopathologic evaluation revealed benign hamartoma.This case is presented because of its rarity, unique presentation, and simplicity of management.     

A journey to continence: a case study of overactive bladder syndrome

Overactive bladder is a problem that many women experience and suffer with in silence for years. This is a case study about one such woman. Anna had problems with incontinence for more than five years when she sought treatment. This article presents the story of her journey and perseverance to achieve control of her bladder.     

The influence of trisomy 21 on the incidence and severity of congenital heart defects in patients with duodenal atresia

Duodenal atresia is associated with a wide variety of congenital malformations. Trisomy 21 occurs in approximately one-thirds of infants with duodenal atresia. Congenital heart disease in patients with trisomy 21 and duodenal atresia is well known. However, the frequency and spectrum of congenital heart defects in infants with duodenal atresia and a normal karyotype has not been outlined in the literature. Therefore, we conducted a retrospective chart review to clarify our knowledge about this population. Retrospective review of the medical record was performed on patients with duodenal atresia/stenosis from January 1995 to September 2007. Demographic data included birth weight and gestational age. Variables of interest included cardiac defects and karyotype. Surgical repair for duodenal and cardiac malformations were reviewed. Ninety-four patients with duodenal atresia/stenosis were identified. Average gestational age was 36 weeks and birth weight was 2,536 g. Trisomy 21 was identified in 39 (41%) patients. Overall, 37 patients (39.3%) had a congenital heart defect. Defects were identified in 24 (61.5%) patients with trisomy 21, when compared to 13 (23.6%) patients with a normal karyotype. Of the patients with congenital heart defects and trisomy 21, 11 (28.2%) required operative repair compared to the 6 (10.9%) patients with a defect and normal karyotype. Therefore, in patients with duodenal atresia, the presence of trisomy 21 carries a relative risk of 2.61 for congenital heart defects, and relative risk of 2.59 for open heart surgery. In patients with duodenal atresia, the presence of trisomy 21 carries a 2.5-fold increased risk of cardiac defect and the same increased risk for repairing a cardiac defect.     

L-精氨酸对糖尿病大鼠心肌缺血再灌注损伤的影响

目的:观察糖尿病大鼠心肌缺血再灌注时血管紧张素Ⅱ、胰岛素样生长因子1、醛固酮、细胞间黏附分子1和自由基代谢的变化及L-精氨酸对其的影响。方法:实验于2005-02/2006-06在江苏大学医学院机能学实验室完成。①实验分组:腹腔注射链脲佐菌素制作糖尿病大鼠模型,30只大鼠造模成功。按随机数字表法分为3组(n=10):心肌缺血再灌注组:开胸结扎冠脉,造成心肌缺血,60min后放松再灌注60min;L-精氨酸治疗组:于手术前4周灌胃L-精氨酸250mg/(kg·d),然后重复心肌缺血再灌注组操作;假手术组:完成操作后只穿线不结扎,观察2h作为对照。实验结束时心室取血6mL,摘取心脏,留取左心室心肌组织。②实验评估:检测大鼠血浆血管紧张素Ⅱ、醛固酮和血清胰岛素样生长因子1含量及心肌细胞间黏附分子1蛋白表达。检测大鼠血清、心肌组织超氧化物歧化酶、谷胱甘肽-过氧化物酶活性、丙二醛含量及心肌线粒体Na ,K -ATP酶、Mg2 -ATP酶、Ca2 -ATP酶活性。结果:30只大鼠全部进入结果分析。①与假手术组相比,心肌缺血再灌注组血浆血管紧张素Ⅱ、醛固酮含量明显升高(P<0.05～0.01),血清胰岛素样生长因子1含量降低(P<0.05);L-精氨酸治疗4周后血浆血管紧张素Ⅱ、醛固酮含量低于心肌缺血再灌注组(P<0.05～0.01),血清胰岛素样生长因子1含量高于心肌缺血再灌注组(P<0.05)。②与假手术组相比,心肌缺血再灌注组血清、心肌丙二醛含量明显升高(P<0.05),血清、心肌超氧化物歧化酶和谷胱甘肽-过氧化物酶活性明显降低(P<0.05￣0.01);用L-精氨酸治疗4周后血清、心肌丙二醛含量低于心肌缺血再灌注组(P<0.05￣0.01),血清、心肌超氧化物歧化酶和谷胱甘肽-过氧化物酶活性高于心肌缺血再灌注组(P<0.05～0.01)。③与假手术组相比,心肌缺血再灌注组心肌线粒体Na ,K -ATP酶、Mg2 -ATP酶、Ca2 -ATP酶活性明显降低(P<0.05),心肌细胞间黏附分子1蛋白表达明显升高(P<0.01);用L-精氨酸治疗4周后心肌线粒体Na ,K -ATP酶、Mg2 -ATP酶、Ca2 -ATP酶活性明显高于心肌缺血再灌注组(P<0.05),心肌细胞间黏附分子1蛋白表达低于心肌缺血再灌注组(P<0.05)。结论:血管紧张素Ⅱ、醛固酮和胰岛素样生长因子1可能共同参与了糖尿病心肌缺血再灌注的发生,细胞间黏附分子1蛋白表达与糖尿病心肌损伤关系密切。L-精氨酸通过减少细胞间黏附分子1蛋白表达,起心肌保护作用。糖尿病心肌缺血再灌注时存在自由基代谢异常,补充L-精氨酸后,可通过提高超氧化物歧化酶、谷胱甘肽-过氧化物酶和ATP酶活性,降低丙二醛水平,减轻自由基损伤,改善心肌组织功能。