No abstract

No abstract

A 79-year-old female patient with hepatitis C virus-related liver cirrhosis was diagnosed as having hepatocellular carcinoma (HCC) with a diameter of 2.0 cm. She refused therapy for HCC. Nine months after the diagnosis, she developed dermatomyositis when the HCC enlarged to a diameter of 6.0 cm. She underwent therapy for dermatomyositis, and then transcatheter arterial chemoembolization for HCC. Although the manifestations of dermatomyositis improved and entire tumor necrosis was achieved, she died of pneumonia 2 mo after the treatment of HCC. HCC and/or chronic hepatitis C virus infection might be involved in the pathogenesis of dermatomyositis.

Patients with cough variant asthma (CVA) and classic asthma are frequently among subjects who present at clinics complaining of a chronic persistent cough. To reveal the features of CVA, we examined the differences in the clinical appearance between CVA and classic asthma. Ten CVA subjects and 11 classic asthmatics were enrolled in the study; they were recruited among patients who presented at the National Minamiokayama Hospital complaining of a chronic cough. The number of eosinophils in peripheral blood was 256 ± 45.8/µl in CVA and 400 ± 123/µl in classic asthma. Eosinophils represented 67% of the cells of sputum in CVA and 82% in classic asthma. Bronchial responsiveness to methacholine was Dmin 1.37 ± 0.56 U in CVA and 0.71 ± 0.46 U in classic asthma. There was no significant difference in these three parameters. There was only a significant difference in v̇25 between CVA and classic asthma, 80.0 ± 6.9 and 52.2 ± 10.0%, respectively. Eosinophil inflammation was almost the same in both CVA and classic asthma.

Human lifespan continues to extend as an unprecedented number of people reach their seventh and eighth decade of life, unveiling chronic conditions that affect the older adult. Such skin conditions include senile purpura, seborrheic keratoses, pemphigus vulgaris, bullous pemphigoid, diabetic foot wounds, and skin cancer. Current methods of drug testing prior to clinical trials require the use of pre-clinical animal models, which are often unable to adequately replicate human skin response. A reliable model for aged human skin is needed. Current challenges in developing an aged human skin model include the intrinsic variability in skin architecture from person-to-person. An ideal skin model would incorporate innate functionality such as sensation, vascularization, and regeneration. The advent of 3D bioprinting allows us to create human skin equivalent for use as clinical-grade surgical graft, for drug testing, and other needs. In this review, we describe the process of human skin aging and outline the steps to create an aged skin model with 3D bioprinting using skin cells (i.e., keratinocytes, fibroblasts, and melanocytes). We also provide an overview of current bioprinted skin models, associated limitations, and direction for future research.