A Scanning Electron Microscopy Study of Human Spleen: Relationship Between the Microcirculation and Functions

This paper reviews scanning electron microscope (SEM) observation of the circulatory system of the human spleen, based on our findings on freeze-cracked surfaces and vascular casts of the spleen. Central arteries ran straight in the white pulp without branching out follicular arteries and became penicillar arteries in the red pulp. Some penicillar arteries returned to the marginal zone. Some of their branches ended by opening there, whereas others passed through the marginal zone, entered the white pulp and became follicular arteries. Some of them took the shape of an arteriolar-capillary bundle . Most of the follicular capillaries ended opening into the marginal zone. The penicillar arteries usually ran straight or gently curved among the sinuses of the red pulp and opened into cordal spaces. Occasional arteries formed a labyrinthine structure of arterial channels which directly connected with thin sinuses. This study reveals that three different modes of arterial terminals are available in the human spleen: (1) arterial openings in the marginal zone which seem significant for presentation of antigens to the white pulp, (2) openings into the cords of Billroth which facilitate culling and pitting of blood cells, and (3) direct connections with sinuses (closed circulation) which account for the physiologically known quick blood flow through the spleen

Hemorrhagic infarction at 33 days after birth in a healthy full-term neonate

Intraparenchymal hemorrhage in the full-term neonate rarely occurs more than 2 weeks after birth, and its definitive cause remains unclear. In the present report, a case of a patient with intraparenchymal hemorrhage occurring 33 days after birth is described. Histological examination of the brain tissue obtained during hematoma evacuation through craniotomy showed hemorrhagic infarction. Patent foramen ovale may have been present and this may have led to spontaneous paradoxical cerebral embolism followed by hemorrhagic infarction

Emerin plays a crucial role in nuclear invagination and in the nuclear calcium transient.

Alteration of the nuclear Ca2+ transient is an early event in cardiac remodeling. Regulation of the nuclear Ca2+ transient is partly independent of the cytosolic Ca2+ transient in cardiomyocytes. One nuclear membrane protein, emerin, is encoded by EMD, and an EMD mutation causes Emery-Dreifuss muscular dystrophy (EDMD). It remains unclear whether emerin is involved in nuclear Ca2+ homeostasis. The aim of this study is to elucidate the role of emerin in rat cardiomyocytes by means of hypertrophic stimuli and in EDMD induced pluripotent stem (iPS) cell-derived cardiomyocytes in terms of nuclear structure and the Ca2+ transient. The cardiac hypertrophic stimuli increased the nuclear area, decreased nuclear invagination, and increased the half-decay time of the nuclear Ca2+ transient in cardiomyocytes. Emd knockdown cardiomyocytes showed similar properties after hypertrophic stimuli. The EDMD-iPS cell-derived cardiomyocytes showed increased nuclear area, decreased nuclear invagination, and increased half-decay time of the nuclear Ca2+ transient. An autopsied heart from a patient with EDMD also showed increased nuclear area and decreased nuclear invagination. These data suggest that Emerin plays a crucial role in nuclear structure and in the nuclear Ca2+ transient. Thus, emerin and the nuclear Ca2+ transient are possible therapeutic targets in heart failure and EDMD. © The Author(s) 2017