The Impact of the Macroeconomy on Health Insurance Coverage: Evidence from the Great Recession

This paper investigates the impact of the macroeconomy on the health insurance coverage of Americans using panel data from the Survey of Income and Program Participation for 2004–2010, a period that includes the Great Recession of 2007–2009. We find that a one percentage point increase in the state unemployment rate is associated with a 1.67 percentage point (2.12%) reduction in the probability that men have health insurance; this effect is strongest among college‐educated, white, and older (50–64 years old) men. For women and children, health insurance coverage is not significantly correlated with the unemployment rate, which may be the result of public health insurance acting as a social safety net. Compared with the previous recession, the health insurance coverage of men is more sensitive to the unemployment rate, which may be due to the nature of the Great Recession. Copyright © 2013 John Wiley & Sons, Ltd.     

Liver-related events after direct-acting antiviral therapy in patients with hepatitis C virus-associated cirrhosis

Journal of Gastroenterology - Direct-acting antiviral (DAA) therapy enables a high rate of sustained virologic response (SVR) in patients with hepatitis C virus associated cirrhosis. However, the...     

Clinicopathologic evaluation of the trend toward histologically poor differentiation with submucosal invasion in superficial early colorectal adenocarcinomas

We examined differences in the degree of differentiation in intramucosal and submucosal areas of involvement in early colorectal adenocarcinomas of 131 patients and compared these findings with tumor morphology. In addition, K-ras and p53 protein expression was determined in cases where poorly differentiated adenocarcinoma was detected in the submucosa. We identified 6 patients with both intramucosal differentiated (well-to-moderately differentiated) adenocarcinoma and submucosal poorly differentiated adenocarcinoma (MwSp). The morphological tumor type was superficial in all MwSp cases. The observed MwSp adenocarcinomas had a significantly higher frequency of lymphatic invasion than the more common superficial type of adenocarcinoma. Genetic analysis of these MwSp lesions was carried out using the polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP) method to detect the presence of K-ras codon 12 point mutations, and an immunologic staining technique was used to identify the presence of p53 protein overexpression. The K-ras mutation rate was 33.3%, and the p53 overexpression rate was 66.7% for the MwSp adenocarcinomas. Our findings suggest that the rapidly reduced histologic differentiation observed in some of these superficial colorectal adenocarcinomas may play a role in their higher degree of invasiveness. Received: November 17, 1999 / Accepted: July 7, 2000     

Ala601-Thr type dysplasminogenaemia genetically diagnosed in patients with retinochoroidal vascular disorders

Dysplasminogenaemia has been reported in patients with retinochoroidal vascular disorders. The precise genetic defects of these cases, however, remain unclear because of the limitations of conventional diagnostic techniques. In this study, three patients with these diseases were investigated at the DNA level for the first time to define the molecular bases of these disorders. Polymerase chain reaction–restriction fragment length polymorphism analysis revealed that all three cases carried the same Ala601-Thr mutation. This defect may also play a role in the pathogenesis of circulation disorders in small local vessels because of reduced fibrinolytic activity due to decreased functional plasminogen levels.     

Transesophageal cross-sectional echocardiography

A transesophageal cardiac imaging system is described. This system employs hand-held mechanical sector and linear scanners each having a flexible tube and a small ultrasonic transducer contained within a small oil bag easily swallowed by adults. In the sector scanner, a small transducer in the esophagus rotates alternately and horizontal heart images are displayed. In the linear scanner, a small transducer in the esophagus moves up and down and vertical heart images are displayed. The system was evaluated in 31 adult subjects. In all subjects, stable high quality heart images were observed continuously from base to apex as the transducer was being withdrawn or advanced in the esophagus. In horizontal scans, entire heart images were observed at the level of the atrioventricular valves. In vertical scans, the bifurcation of the pulmonary artery could be observed clearly. There was little difference in the image quality among subjects.     

Mutation Analysis of the IL36RN Gene in 14 Japanese Patients with Generalized Pustular Psoriasis

Generalized pustular psoriasis (GPP) is a rare, potentially life threatening, and aggressive form of psoriasis, which is characterized by sudden onset with repeated episodic skin inflammation leading to pustule formation. Familial GPP is known to be caused by recessively inherited mutations in the IL36RN gene, which encodes interleukin 36 receptor antagonist (IL‐36Ra). In this article, we performed mutation analysis of the IL36RN gene in 14 Japanese patients with GPP, and identified mutations in two of these patients analyzed. One patient was compound heterozygous for mutations c.115+6T>C and c.368C>G (p.Thr123Arg), whereas the other carried compound heterozygous mutations c.28C>T (p.Arg10*) and c.115+6T>C in the IL36RN gene. Expression studies using total RNA from the patients’ skin revealed that the mutation c.115+6T>C resulted in skipping of exon 3, leading to a frameshift and a premature termination codon (p.Arg10Argfs*1). The protein structure analysis suggested that the missense mutation p.Thr123Arg caused misfolding and instability of IL‐36Ra protein. In vitro studies in cultured cells showed impaired expression of the p.Thr123Arg mutant IL‐36Ra protein, which failed to antagonize the IL‐36 signaling pathway. Our data further underscore the critical role of IL36RN in pathogenesis of GPP.