Akihiko Nakashima

Asplenia and polysplenia syndrome.

This report described the morphological characteristics of seven cases of asplenia syndrome and three of polysplenia syndrome. Each syndrome has been characterized by a tendency for symmetric development of normally asymmetric organs, with varying degrees of cardiovascular anomalies. These latter anomalies are usually present in asplenia syndrome to a greater extent than in polysplenia syndrome. While, as observed in our material, the conotruncal anomalies were present more commonly in cases with asplenia, and absence of inferior vena cava with azygos continuation was seen specifically in all the cases with polysplenia. This evidence implied the presence of some pathogenetic distinction between the two syndromes. ACTA PATHOL. JPN. 32: 505∼511, 1982.

Inhibition of Intimal Hyperplasia After Balloon Injury by Antibodies to Intercellular Adhesion Molecule-1 and Lymphocyte Function–Associated Antigen-1

BACKGROUND Although intercellular adhesion molecule-1 (ICAM-1) is known to be expressed in balloon-injured arteries, it remains unknown whether ICAM-1 plays a role in the progression of intimal hyperplasia (IH) induced by balloon injury. METHODS AND RESULTS We examined the ICAM-1 expression in rat carotid arteries at 1, 2, 5, 7, 10, and 14 days after injury by immunohistochemistry. Medial smooth muscle cells (SMC) expressed ICAM-1 intensely at 1 to 2 days after injury. The regenerating endothelial cells expressed ICAM-1 more than did those of intact carotid arteries. To investigate the effects of monoclonal antibodies (MAbs) on IH, we examined the intima/ medial ratio of arteries at 2 weeks after injury in five treatment groups: nonimmune IgG, anti-membrane glycoprotein MAb, anti-lymphocyte function-associated antigen-1 (LFA-1) MAb, anti-ICAM-1 MAb, and anti-ICAM/LFA-1 MAb. Treatments were administered intravenously into rats for 6 consecutive days after injury. MAb against LFA-1 alone or membrane glycoprotein had no effect on IH. The intima/media ratios in anti-ICAM-1 MAb-treated and anti-ICAM-1/LFA-1 MAb-treated animals were significantly less than those in nonimmune IgG-treated and anti-membrane glycoprotein MAb-treated animals (P < .05). CONCLUSIONS Balloon injury induced or upregulated the ICAM-1 expression on vascular SMC and on regenerating endothelial cells. MAb against ICAM-1 or ICAM-1/LFA-1 attenuated IH. These results suggest that ICAM-1 may play a role in the progression of IH after injury in rats.

Renal Denervation Prevents Intraglomerular Platelet Aggregation and Glomerular Injury Induced by Chronic Inhibition of Nitric Oxide Synthesis

Nitric oxide (NO) inhibits platelet adhesion and aggregation in vitro. In vivo, chronic inhibition of NO synthesis induces nephrosclerosis and hypertension. Although the pathophysiological mechanism of this glomerular injury has not been clarified, sympathetic nerve activation, a potent procoagulant stimulus elicited by NO inhibition, may play a role. To investigate the role of renal sympathetic nerves in the development of renal injury induced by NG-nitro-L-arginine methyl ester (L-NAME), a specific NO synthesis inhibitor, we examined renal histological changes in four groups of Sprague-Dawley rats: (1) sham operated, vehicle treated; (2) sham operated, L-NAME treated; (3) denervated, vehicle treated, and (4) denervated, L-NAME treated. Following renal denervation or sham operation, L-NAME was administered orally for 4 weeks. Chronic NO inhibition induced platelet aggregation and erythrocyte stasis in the glomerular capillary lumen accompanied by electron-microscopic glomerular injury. Renal denervation abrogated platelet aggregation and glomerular injury in L-NAME-treated animals. Thus, chronic NO synthesis inhibition induced intraglomerular platelet aggregation and glomerular injury, which was attenuated by renal nerve denervation. These results suggest that intrinsic NO may have an antithrombotic effect in the glomeruli and may play a protective role in the progression of glomerular injury possibly mediated by renal sympathetic nerves.

SHP-1 expression in primary central nervous system B-cell lymphomas in immunocompetent patients reflects maturation stage of normal B cell counterparts.

SHP‐1 is an important negative regulator involved in signaling through receptors for cytokine/growth factors, and differential patterns of SHP‐1 expression in several types of B‐cell lymphomas closely resemble the patterns seen in their normal B cell counterparts. In an effort to elucidate the origin of primary central nervous system lymphomas (PCNSL), the present study assessed 32 cases of PCNSL. Tumors were subclassified according to WHO classification and were evaluated by immunohistochemistry for expression of antigens associated with germinal center (GC) (CD10, Bcl‐6) and non‐GC stages (SHP‐1, CD138). Twenty‐nine cases showed diffuse large‐cell centroblastic morphology, whereas three cases showed diffuse large‐cell immunoblastic morphology. The immunophenotypes of PCNSL were as follows: SHP‐1+/Bcl‐6–/CD10–/CD138– (12 of 32 cases); SHP‐1+/Bcl‐6+/CD10–/CD138– (15 of 32 cases); SHP‐1+/Bcl‐6+/CD10+/CD138– (two of 32 cases); SHP‐1+/Bcl‐6–/CD10+/CD138– (one of 32 cases); and SHP‐1–/Bcl‐6–/CD10–/CD138– (two of 32 cases). These results indicate that PCNSL might be distinct lymphomas that originate from a late germinal center to an early postgerminal center.

Familial Amyloidosis A Histopathological Study

Four autopsy cases of familial amyloidosis were reported. The ages of the patients ranged from 37 to 51 years consisting of 3 males and 1 female. They all complained of neurological symptoms.

MORPHOLOGIC STUDY ON AORTA DOT STAINED WITH EVANS BLUE IN NORMAL AND HYPERCHOLESTEROLEMIC RABBITS

When a normal rabbit is injected Intravenously with Evans blue, focal blue areas showing strong permeability appear in a region of the aortic arch and in a region distal to the orifice of the aortic branches. These blue areas consist of the dot stained area but are not homogeneous blue area.