NBI magnifying endoscopic classification using crystal violet staining

NBI magnifying imaging with crystal violet (CV-NBI magnifying imaging) makes recognition of micro-vascular pattern and grandular structure in the gastric mucosa better. NBI image emphasizes micro-vascular structure in mucosal surface. Magnification endoscopy with crystal violet staining delineates surface grandular structure better than without it. Crystal violet stained epithelium is clearly observed as cobalt green with NBI imaging. In the classification of CV-NBI magnification findings, 71% of differentiated type lesion was classified into ILL (intralobular loop pattern), and the rest (29%) was diagnosed as FNP (fine network pattern) which was originally advocated by Nakayoshi, et al. ILL is the new category of magnifying endoscopy. ILL corresponded mainly to differentiated-type adenocarcinoma, but it also includes undifferentiated-type adenocarcinoma. Corkscrew pattern is corresponding well to undifferentiated-type adnocarcinoma (Nakayoshi, et al). CV-NBI magnifying classification is considered to be related to tissue characterization in gastric cancer.     

Growth rate of lung cancer recognized as small solid nodule on initial CT findings

Introduction

To study the characteristics of lung cancer, appearing as small solid nodules on initial computed tomography (CT) findings, and to determine an appropriate follow-up duration so as to differentiate between malignancy and benign tumor.

Methods

We analyzed the records of 34 patients who had undergone surgical resection of lung cancer, which appeared as small solid nodules on initial CT findings. We studied the CT findings, volume doubling times (VDT), follow-up durations, pathological and clinical findings.

Results

VDT is classified as follows: (1) slow growth group (SGG), with a VDT of more than 700 days and (2) rapid growth group (RGG), with a VDT of less than 700 days. The median VDT of the SGG was 1083 days, and the RGG was 256 days (p < 0.01). The median duration for follow-up of the SGG was 1218 days, and 179 days for the RGG. A statistical difference was noted in the follow-up durations (p < 0.01). There were no statistical differences in the preoperative thin-section CT (TSCT) findings, or in the pathological findings. The RGG included more patients with smoking histories. The CT findings of RGG tended to reveal changed in base lung field such as emphysema, and lung fibrosis.

Conclusions

Generally, lung cancer appearing as small solid nodules on initial CT findings grew rapidly, but there were some cases which displayed slow growth patterns. These cases required follow up for over two years, before diagnosis was possible. We concluded the appropriate maximum followup duration is three years.     

Involvement of actin filament in the generation of Ca2+ mobilizing messengers in glucose-induced Ca2+ signaling in pancreatic β-cells

Glucose is a metabolic regulator of insulin secretion from pancreatic β-cells, which is regulated by intracellular Ca(2+) signaling. We and others previously demonstrated that glucose activates CD38/ADP-ribosyl cyclase (ADPR-cyclase) to produce two Ca(2+) second messengers, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP). Although F-actin remodeling is known to be an important step in glucose stimulated insulin secretion, the role of actin cytoskeleton in regulating Ca(2+) signaling in pancreatic β-cells remain to be solved. Here, we show that actin filaments are involved in the activation of CD38/ADPR-cyclase in pancreatic β-cells. Glucose induces a sequential formation of cADPR and NAADP. Pretreatment with jasplakinolide, an actin polymerizing agent, or a myosin heavy chain IIA (MHCIIA) blocker, blebbistatin, inhibited glucose-induced CD38 internalization, an essential step for cADPR formation. Blocking actin disassembly with jasplakinolide also abrogates glucose-induced cADPR and NAADP formation and sustained Ca(2+) signals. These results indicate that actin filaments along with MHCIIA play an important role in CD38 internalization for the generation of Ca(2+) mobilizing messengers for glucose-induced Ca(2+) signaling in pancreatic β-cells.