Rapid discharges from the myocardium extendingfrom the left atrium onto the pulmonary vein (PV) have been shown to initiate AF, and AF may be eradicated by the catheter ablation within the PV. However, if there is any difference in the distribution patterns of the myocardial sleeve onto the PV between the subjects with and without AF is to be determined. Twenty-one autopsied hearts were examined. Eleven patients previously had AF before death and another 10 patients had normal sinus rhythm as confirmed from the medical records including ECGs before death. After exposing the heart, the distance to the peripheral end of the myocardium was measured from the PV-atrial junction in each PV. Then, the PVs were sectioned and stained and the distal end of myocardium and the distribution pattern were studied. The anteroposterior diameter of the left atrium was also measured. In 74 of 84 PVs, the myocardium extended beyond the PV-atrial junction. The myocardium was localized surrounding the vascular smooth muscle layerforming a myocardial sleeve. The peripheral end of the myocardial sleeve was irregular and the maximal and minimal distances were measured in each PV. The myocardium extended most distally in the superior PVs compared to the inferior ones and the maximal distance to the peripheral end was similar between the AF and non-AF subjects (8.4 +/- 2.8 vs 8.7 +/- 4.4 mm for the left superior and 6.5 +/- 3.5 vs 5.1 +/- 3.9 mm for the right superior PV, respectively). A significant difference was found in the maximal distance in the inferior PVs: 7.3 +/- 4.6 vs 3.3 +/- 2.8 mm for the left (P < 0.05) and 5.7 +/- 2.4 vs 1.7 +/- 1.9 mm for the right inferior PV (P < 0.001) in the subjects with and without AF, respectively. The diameter of left atrium was slightly dilated in AF patients but insignificantly (4.1 +/- 0.1 vs 3.6 +/- 0.1 cm, P > 0.07). The myocytes on the PV were less uniform and surrounded by more fibrosis in patients with AF compared to those without AF. In conclusion, the myocardium extended beyond the atrium-vein junction onto the PVs. The distribution patterns of the myocardium was almost similar between subjects with and without AF, but the histology suggested variable myocytes in size and fibrosis in patients with AF.

AimWe aimed to investigate the effect of resveratrol (Rsv) on expression of genes regulating triglyceride (TG) accumulation and consumption in differentiated 3T3-L1 preadipocytes.Methods3T3-L1 preadipocytes were cultured in DMEM supplemented with 10% fetal calf serum. Upon reaching confluence, cells were induced to differentiate for 4 days, cultured for 10 days for TG accumulation, and then incubated with Rsv (0, 25 or 50 μM) for 3 days. TG accumulation was analyzed by Oil Red-O staining. To understand how Rsv regulates TG accumulation and consumption, changes in gene and protein expressions of several factors associated with free fatty acid (FFA) uptake and β-oxidation were investigated by real-time RT-PCR and Western blot. For further elucidation of underlying mechanisms, we also investigated gene expressions using Sirtuin1 (Sirt1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) siRNA.ResultsRsv dose dependently enhanced Sirt1 expression and reduced TG accumulation. Rsv-induced reduction of TG accumulation was abolished by inhibition of Sirt1 and PGC1α. Rsv also enhanced expressions of genes involved in FFA uptake [peroxisome proliferator-activated receptor-gamma (PPARγ) and lipoprotein lipase] and in β-oxidation regulation [PGC1-α and carnitine palmitoyl-transferase 1a (CPT1a)]. All these effects were abolished by Sirt1 inhibition.ConclusionThe present results suggest that Rsv may augment synthesis and oxidation of fatty acid, and possibly increases energy utilization efficiency in adipocytes through activation of Sirt1. The present study may provide meaningful evidence supporting the efficacy of Rsv in the treatment of obesity.

Carcinomas of the gallbladder can be grossly divided into two types: carcinoma in adenoma (CIA) and carcinoma without adenoma (CWA). The histogenesis of both types of gallbladder carcinoma (CIA and CWA) was investigated in association with metaplastic changes in 35 early carcinomas larger than 5 mm in diameter and 16 microcar‐cinomas up to 5 mm in largest diameter. In five early ClAs and two micro‐CIAs, the carcinoma was surrounded by the adenoma, and the areas of both carcinoma and adenoma mainly showed gastric‐type metaplasia (GM). On the other hand, 90% of the other 30 early CWAs showed GM and/or intestinal‐type metaplasia (IM) in the tumor, and all of them were surrounded by GM and/or IM. Seven of the other 14 micro‐CWAs showed GM and/or IM in the tumor as well as in the surrounding mucosa, and had non neoplastic metaplastic glands underneath the carcinoma tissue. The remaining seven micro‐CWAs showed no or only mild metaplasia in the tumor and were surrounded by proper mucosa without metaplasia. From these data, it is concluded that carcinoma of CIA possibly arises from adenoma mainly with GM, and that CWA originates either from the upper part of the metaplastic mucosa or from the proper mucosa of the gallbladder. In addition, some CWA may undergo secondary metaplastic changes during tumor growth. Acta Pathol Jpn 39: 235–244, 1989.

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We present herein a case of a patient who was clinically diagnosed as having a granulocyte-colony stimulating factor (G-CSF)-producing tumor on the basis of the close correlation of the hematological parameters with the tumor status and his high serum G-CSF level. A 76-year-old male patient underwent transthoracic radical esophagectomy for advanced carcinoma of the lower esophagus. His leukocyte count and serum G-CSF level were markedly high at 24 260/μl and 134 pg/ml, respectively, before the operation. By immunohistochemical staining of the resected tumor, focal but obvious expression of G-CSF was demonstrated in the cytoplasm of cancer cells, and neutrophilic infi ltration was histologically observed in adjacent struma of the tumor invasion front. After surgery, the leukocyte count decreased to a nearly normal level but increased again when the disease recurred in the pleura and lymph nodes 5 months later. Although palliative chemoradiotherapy decreased the leukocyte count to a normal level transiently, leukocyte count again markedly increased when metastatic disease occurred. The leukocyte count reached 78 060/μl the day before the patient died.

Type 2 diabetes mellitus (T2DM) is associated with an increased risk of bone fractures without reduction of bone mineral density. The cholesterol oxide 7-ketocholesterol (7KCHO) has been implicated in numerous diseases such as atherosclerosis, Alzheimer's disease, Parkinson's disease, cancer, age-related macular degeneration and T2DM. In the present study, 7KCHO decreased the viability of MC3T3-E1 cells, increased reactive oxygen species (ROS) production and apoptotic rate, and upregulated the caspase-3/7 pathway. Furthermore, these effects of 7KCHO were abolished by pre-incubation of the cells with N-acetylcysteine (NAC), an ROS inhibitor. Also, 7KCHO enhanced the mRNA expression of two endoplasmic reticulum (ER) stress markers; CHOP and GRP78, in MC3T3-E1 cells. Pre-incubation of the cells with NAC suppressed the 7KCHO-induced upregulation of CHOP, but not GRP78. In conclusion, we demonstrated that 7KCHO induced apoptosis of MC3T3-E1 cells associated with ROS generation, ER stress, and caspase-3/7 activity, and the effects of 7KCHO were abolished by the ROS inhibitor NAC. These findings may provide new insight into the relationship between oxysterol and pathophysiology of osteoporosis seen in T2DM.