Light and electron microscopic studies on rat arterial lesions induced by experimental arterial contraction

Summary Experimental contraction was produced in the rat mesenteric arteries and the arterial segments were studied morphologically. When the rat mesenteric artery was exposed in physiological saline solution at 37° C and 2–3 mg of methoxamine hydrochloride (10 mg/ml) was dripped onto it, intense contraction was observed for about 30 min but elevation in blood pressure was slight. During the contraction, numerous vacuoles were seen in the medial smooth muscle cells of the arterial segments, and these vacuoles were shown electron microscopically to have double unit membranes, indicating that they were formed by herniation of a part of the adjacent smooth muscle cell body. In the arteries 1–6 h after the end of the contraction, cellular, nuclear and vacuolar membranes and myofilaments of the medial muscle cells were partially lost. 12–24 h after the contraction the arteries exhibited necrosis and desquamation of endothelial cells and platelet adhesion. In the media, smooth muscle cells were completely deprived of cell membranes, myofilaments, nuclei, intracytoplasmic organelles other than mitochondria, and vacuolar membranes. The cytoplasm was filled with fine granular and granulo-vesicular material, and fibrin insudation was observed in these severely damaged cells. Arterial contraction may be an important factor in the induction of arterial lesions.     

妊娠合并重型肝炎40例临床分析

目的:总结妊娠合并重型肝炎的病因、诊断、治疗及预后,探讨其治疗的特殊性,降低孕产妇病死率.方法:对40例重型肝炎孕妇的临床资料进行回顾性分析.结果:①34例发生于妊娠晚期;②病原学检查HBV感染28例,HEV感染5例,7例原因未明;③并发症多见,合并肝性脑病19例、肝肾综合征17例、妊娠期高血压疾病13例、产后出血22例;④3例抗病毒治疗患者均存活,6例行人工肝辅助支持系统(ALSS)治疗者存活5例.1999～2003年,2004～2006年,两组的母婴病死率分别与1984～1988年,1989～1993年,1994～1998年3组比较,差异均有统计学意义(P均＜0.05);⑤孕产妇死亡率45.0%,围生儿死亡率48.39%.结论:HBV感染是妊娠合并重型肝炎的主要原因,常需与妊娠期急性脂肪肝等病鉴别.产后出血是导致病情加重的重要因素,多种并发症的出现是预后凶险的信号.积极综合治疗和及时终止妊娠是改善预后的关键,抗病毒治疗和ALSS治疗是提高生存率的有力手段.     

Morphogenesis of plasmatic arterionecrosis as the cause of hypertensive intracerebral hemorrhage

Summary The morphogenesis of the vascular lesions, which were considered to be the immediate cause of hypertensive intracerebral hemorrhage, was morphologically studied in autopsy cases. The direct cause of the hemorrhage was the rupture of the intracerebral microaneuysms resulted from the plasmatic arterionecrosis. The arterionecrosis was predominantly present in the intracerebral arteries of approximately 150 µ diameter, especially in the external branches of the arteriae corporis striati mediae in the putamen, and characterized by medial smooth muscle cell loss, blood plasma insudation in the intima, histolysis of the internal elastic lamina and intimal collagenous fibers, fibrin deposition (fibrinoid degeneration) in the intima, and luminal dilatation. The morphogenesis of the arterionecrosis was the development of histolysis as well as fibrinoid degeneration caused by blood plasma insudation in the wall of the intracerebral arteries with preceding necrosis and loss of medial smooth muscle cells and subsequent fibrous intimal thickening with dilated lumina. Intracerebral microaneurysms were also formed by the plasmatic arterionecrosis in a narrow sense, in which histolysis due to blood plasma insudation had occurred, but fibrin (fibrinoid substance) deposition in the intima had not yet arisen.     

MORPHOGENESIS OF ARTERIOSCLEROSIS

The basic process in the morphogenesis of arteriosclerosis consists of proliferation and insudation in the intima, and varied combinations of these two processes produce various types of arteriosclerotic lesions.
The morphogenesis of atherosclerosis is considered to be as follows: Atheroma is formed by the infiltration of blood plasma lipids into the intima of the large and medium-sized arteries having cellulofibrous intimal thickening, which grows with age. As the result, proliferation advances especially in the upper layer of the intima. There were two types of atheroma formation.
Arteriosclerosis of the small arteries and arterioles is produced by various combinations of insudation and proliferation in the small arteries and arterioles where the intimal thickening does not occur with age, or only to a slight degree, if any.
In order to elucidate the mechanism of the proliferation and insudation in the intima, animal experiments were carried out. On the basis of the experimental results, possible causes of the proliferation (cellulofibrous intimal thickening) and the insudation (blood plasma infiltration) were discussed. ACTA PATH. JAP. 18 :75–82, 1968.     

人卵巢组织中HBV DNA和HBV cccDNA的表达与HBV宫内感染的相关性研究

目的研究人卵巢组织中乙型肝炎病毒(HBV)DNA、HBV共价闭合脱氧核糖核酸(cccDNA)表达与HBV宫内感染的相关性。方法采用荧光定量聚合酶链反应方法(FQ-PCR)检测33例HBV DNA阳性孕妇卵巢组织中的HBV DNA和HBV cccDNA。采用化学发光法检测相应33例婴儿出生当日和1月龄外周血血清乙型肝炎病毒标志物(HBVM),FQ．PCR法检测婴儿血清HBVDNA含量。结果33例卵巢组织中HBVDNA和HBV cccDNA总阳性率为51．52%(17/33)。婴儿宫内感染率为12．12%(4/33,4例均为肝功能正常的孕妇)。婴儿母亲卵巢组织中HBVDNA和HBV cccDNA均阳性时,宫内感染率比HBVDNA、HBV cccDNA均阴性时显著升高(P<0．05)。宫内感染婴儿较非宫内感染婴儿母亲卵巢组织中HBV cccDNA的表达水平和阳性率明显升高(P<0．01和P<0．05)。结论HBV可感染人卵巢组织并在其中复制,且有可能通过卵细胞垂直传播至子代。     

Paradoxical response in a patient with non-small cell lung cancer who received nivolumab followed by anti-Mycobacterium tuberculosis agents

Anti-programmed cell death-1 (PD-1) agents enhance the antitumor immunoresponse. A number of reports have indicated that patients with malignancies who receive anti-PD-1 agents are at risk for tuberculosis (TB) infection. In this report, we present a patient with non-small cell lung cancer who developed pulmonary tuberculosis while receiving the anti-PD-1 agent nivolumab, and who subsequently demonstrated a paradoxical response (PR) 10 days after initiation of anti-MTB treatment. We suggest that anti-PD-1 agents not only induce the development of pulmonary TB, but also development of PR after anti-MTB treatment, through upregulation of the immune response. Furthermore, based on their radiological and immunological similarity, we speculate that the schema of development of PR closely resembles that of pseudoprogression in non-small cell lung cancer patients after anti-PD-1 treatment.     

ROLE OF LYSOSOMES IN CORONARY ARTERY LESIONS OF HYPERTENSIVE RATS

Electron microscopically the role of acid phosphatase (acid P) positive lysosomes in the pathoǵenesis of intramyocardial coronary artery lesions of hypertensive rats with bilaterally constricted renal arteries was studied. At 3 postoperative weeks, acid P positive lysosomes were increased in endothelial cells of the coronary arteries, but at 5 weeks and thereafter, they were decreased in number. In the intima, intimal smooth muscle cells with acid P positive lysosomes appeared at 3 postoperative weeks, but their number remained small as late as 9 postoperative weeks. The internal elastic lamina was fraǵmented into amorphous masses from 3 postoperative weeks, at 5 weeks and thereafter the fraǵmentation and disruption became severer, and at 9 weeks the lamina disappeared because of marked disruption. At 3 postoperative weeks, acid P positive extracellular lysosomes were observed in the ǵaps of the fraǵmented internal elastic lamina. At 5 weeks and thereafter, extracellular lysosomes and attenuated processes of medial smooth muscle cells with lysosomes were seen extending through the ǵaps of the fraǵmented internal elastic lamina. Necrosis of these extendinǵ cell processes and lysosomes remaininǵ after the necrosis were observed. The findinǵs suǵǵested that the fraǵmentation and lytic chanǵe of the internal elastic lamina observed in hypertensive rat intramyocardial coronary arteries might be induced by extracellular lysosomes discharǵed not only from endothelial cells and intimal smooth muscle cells but also from the extendinǵ processes of medial smooth muscle cells into the gaps of the internal elastic lamina. ACTA PATHOL. JPN. 36: 1529-1536, 1986.     

An electron microscopic study of plasmatic arterionecrosis in the human cerebral arteries

Summary An electron microscopic study of the intracerebral arteries from 9 hypertensive cases was performed in order to elucidate the morphogenesis of the plasmatic arterionecrosis which was considered to be the direct cause of hypertensive intracerebral hemorrhage. In the preceding stage of the arterial lesions, marked necrosis of medial smooth muscle cells and increase of basement membrane-like substance in the intima and media were observed. The lumina of these arteries were slightly dilated. The dilatation and hemodynamic factors were supposed to cause endothelial injury resulting in blood plasma insudation into the intima through the opened spaces between endothelial cells. The insudated blood plasma dispersed and dissolved the basement membrane-like substance, collagen and elastic fibers in the arterial wall, leading to the development of the plasmatic arterionecrosis.This study was supported by a Grant-in-Aid for Scientific Research of the Japanese Ministry of Education (No. 857052).