Primary pulmonary artery sarcoma: modern diagnostic imaging methods and successful surgical treatment.

Primary pulmonary artery sarcoma is a rare tumor. We present a case report in which the presumptive diagnosis was made preoperatively with magnetic resonance imaging, Doppler color flow methods, and computer tomography. Surgical treatment was successful.     

Synergistic effect of 1,25-dihydroxyvitamin D3 and retinoic acid in inducing U937 cell differentiation.

We examined the effects of retinoic acid (RA), 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3), and its synthetic analogue, 22-oxa-1,25-(OH)2D3, on differentiation of U937 cells by studying the cellular growth, surface marker expression and cytosolic free Ca2+ concentration ([Ca2+]i). RA inhibited cellular growth but did not induce expression of Mo2 (CD14), a monocyte/macrophage specific surface marker. To the contrary, 1,25-(OH)2D3 did not inhibit cellular growth, but increased CD 14-positive cells. Simultaneous addition of 1,25-(OH)2D3 and RA had no additive effect on cellular growth inhibition or CD14 expression. With regard to [Ca2+]i, however, 5 days' incubation with either of them increased the basal [Ca2+]i level and induced U937 cells to respond to formyl-methionyl-leucyl-phenylalanine (FMLP). When the cells were incubated with both 10(-6) M RA and 10(-8) M 1,25-(OH)2D3, basal [Ca2+]i was higher and FMLP caused a greater increase in [Ca2+]i than when only RA or 1,25-(OH)2D3 was added. These data suggest that RA and 1,25-(OH)2D3 induce monocytoid differentiation in U937 cells through different pathways and act synergistically in the differentiation process. The 22-oxa-1,25-(OH)2D3 induced CD14 expression, basal [Ca2+]i increase and [Ca2+]i response to FMLP, but did not cause cellular growth inhibition in U937 cells, and in these points, 22-oxa-1,25-(OH)2D3 exhibited no significantly different effects from 1,25-(OH)2D3. Thus, 22-oxa-1,25-(OH)2D3 has the same potent activity as 1,25-(OH)2D3 in inducing differentiation of U937 cells.     

Outcomes in patients with interrupted aortic arch and associated anomalies: a 20-year experience.

OBJECTIVE: The surgical results for the repair of interrupted aortic arch (IAA) have evolved in recent years. We report our results for staged repair of this complex congenital malformation. METHODS: Sixty-five patients (mean age, 16.9+/-41.7 days) were diagnosed with IAA and referred for surgical therapy. The surgical management strategy at our institution between 1982 and 2005 has been one-stage complete repair (n=13) or staged repair (n=52) in selected patients. Non-complex patients (group I, n=51) had a ventricular septal defect (87%), aortopulmonary window (8%), and left ventricular outflow tract obstruction (27%). Group II (n=14) were patients with Taussig-Bing double outlet right ventricle (n=6) or truncus arteriosus (n=8). Method of staged repair of IAA was to transect and turn down the left carotid artery and anastomosis it to the descending aorta (n=41) or graft interposition (n=2) combined with a pulmonary artery (PA) banding followed in a few months by delayed ventricular septal defect (VSD) closure and PA de-banding. RESULTS: There were 5 early and 10 late deaths. The actuarial survival including early mortality was 92% at 1 year, 81% at 5 years, and 76% at 10 and 15 years. There was an 81% 15-year survival for children in group I compared with a 54% for children in group II (p<0.001). Risk factors for increased mortality by univariate analysis were as follows: (1) primary aortic anastomosis (p=0.03), (2) presence of complex anomalies (p=0.05), and (3) initial IAA repair performed before 1994 (p=0.05). Actuarial freedom from any type of aortic reoperation or intervention was 86% at 1 year, 69% at 5 years, and 60% at 10 and 15 years. Univariate and multivariate analyses identified no tested variables as risk factors for reoperation. The majority (86%) was in New York Heart Association (NYHA) class I, and 14% remained in NYHA class II. During the postoperative course there were no neurologic deficits, seizures, and growth disturbances in any patient. CONCLUSION: Staged repair of IAA using a left carotid artery turn down can be safely applied in IAA patients with and without other intracardiac anomalies with good results. Use of the left carotid artery for arch reconstruction did not result in any detectable neurological events or growth disturbances later in life. Associated anomalies played an important role in outcomes. The long-term probability for reoperation and/or reintervention remains high regardless of operative technique.     

Experimental focal cerebral ischemia produced by embolization with silicone cylinder in normotensive (NTR) and spontaneously hypertensive rats (SHR): comparison of neurological and pathological findings

A focal cerebral ischemic model was produced by occlusion of the intracranial main cerebral artery with a silicone cylinder in normotensive (NTR) and spontaneously hypertensive rats (SHR). Main cerebral artery could be successfully occluded in approximately 90%. The most frequent embolized site was the distal part of the internal cerebral artery (ICb) and less frequently the horizontal segment of the anterior cerebral artery (Al). Mortality rate of NTR with ICb occlusion (NTR-ICb) was 43% at 72 hours after embolization and that of SHR with ICb occlusion (SHR-ICb) was 67% at 24 hours after embolization. NTR-ICb showed neurological signs (i.e. circling movement, hemiparesis, poor response to pain stimuli) and histologically, showed infarction in the deep cerebral structures (i.e. thalamus, hypothalamus, hippocampus, and internal capsule) accompanied with mild disruption of blood-brain barrier (BBB). SHR-ICb showed more serious neurological signs and more severe cerebral infarction in the deep cerebral structures with severe disruption of BBB. In SHR-ICb, ischemic cerebral edema was more prominent which may deteriorate symptoms and pathological findings compared to NTR-ICb. This embolization model is proposed to be useful for studying the pathophysiology of focal cerebral ischemia, especially, early ischemic edema.     

A case of unruptured anterior temporal artery aneurysm showing pupil-sparing oculomotor palsy

The authors report a case of unruptured anterior temporal artery aneurysm showing pupil-sparing oculomotor palsy. The patient was a 55-year-old male with the complaints of left blepharoptosis and diplopia. He had a history of tuberculous meningitis 9 years previously, and since then he suffered from paraparesis of lower extremities and bladder and bowel disturbance. Neurological examination on admission revealed left blepharoptosis and disturbance of medial and vertical movement of the left eye ball, but the pupils were isocoric with normal light reaction. Carotid angiography demonstrated that the left internal carotid artery was tortuous toward the medial side in the C2 portion, and the saccular aneurysm was present in the anterior temporal artery 3 mm distal from the middle cerebral artery. At operation it was revealed that the aneurysm which had a diameter of 17 mm located in the proximal portion of the anterior temporal artery, and compressed the dorsal aspect of the oculomotor nerve. A month after operation the left oculomotor palsy disappeared. There had been no report of the case of unruptured middle cerebral artery aneurysm causing oculomotor palsy. Pupil-sparing oculomotor palsy is characteristic of diabetic oculomotor palsy, and rare cases showing pupil-sparing oculomotor palsy are caused almost by aneurysms of the internal carotid-posterior communicating artery junction. Anatomical study revealed that the parasympathetic fibers which go to the pupil constrictor muscle were in the dorsomedial aspect of the oculomotor nerve in the subarachnoid portion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Light microscopy of GTP-binding protein (Go) immunoreactivity within the retina of different vertebrates

To examine species differences in the distribution pattern of guanosine triphosphate (GTP)-binding protein (Go) within the vertebrate retina, paraffin-embedded retinae from a number of vertebrate species, including the goldfish, frog, turtle, chicken, monkey, and human, were immunohistochemically stained with affinity-purified antibody against the alpha-subunit of Go. Go-immunoreactive products were found to be located in the neuropil, but not in the cell bodies of neurons, in the retina of all these species. However, some species differences were observed. In the frog, monkey and human, the inner plexiform layer (IPL) was homogeneously stained with this antibody, but in the goldfish, turtle and chicken, the IPL was heterogeneously stained. In the frog, chicken, turtle and human, the outer plexiform layer (OPL) was densely stained with this antibody, but in the goldfish and monkey, the OPL was rather faintly immunoreactive to the antibody. In the goldfish, monkey and human, the outer nuclear layer (ONL) was not immunoreactive to the Go-antibody, whereas in the frog, turtle and chicken, the ONL was immunoreactive to it. The implications of these species differences in Go localization in the vertebrate retina are discussed.     

在免眼中进行经瞳孔阈值下温热疗法的组织学效应和蛋白表达

目的：研究阈值下经瞳孔温热疗法（TTT）对视网膜组织学的效应。方法：对正常视网膜色素的兔眼进行TTT，通过1个810nm激光二极管产生直径为1．2mm能量为50mW的光斑，持续时间为15、30和60秒。4周后进行荧光血管造影并摘除眼球，通过电子显微镜和免疫组化染色来检查。     

Histopathological study on the effects of aging in myocardium of hypertrophied hearts

To clarify the effects of aging in myocardium of hypertrophied hearts, 555 autopsied hearts were studied histopathologically. Degrees of myocyte hypertrophy, disarrangement and fibrosis and lipofuscin deposits were estimated light-microscopically in tissue specimens taken from the anterior wall of the left ventricle. Myocyte hypertrophy was assigned to one of four classes from 0 to 3+ according to size. Other findings were estimated using the conventional three classes. All cases were divided according to heart weight, into the following groups: severe hypertrophy (Group I; more than 450 g for males and 400 g for females), mild hypertrophy (Group II; 450 greater than HW greater than 350 g for males and 400 greater than HW greater than 300 g for females) and no hypertrophy (Group III: less than 350 g for males and 300 g for females). Lipofuscin deposits increased with aging, but in Group I the increase was delayed in comparison to that in other groups. As a rule, myocyte size in the outer layer was equal to or smaller than that in the inner layer (outer-layer-selective atrophy). This was particularly true in pressure-overloaded hypertrophy and less so in volume-overloaded hypertrophy. Myocyte disarrangement was observed in the inner and median layers in the oldest group. Peri-vascular fibrosis became thick with aging, and perimysial fibrosis increased with age. The fibrotic process was accelerated in hypertrophied myocardium. As to the mode of hypertrophy, aging appears to result in a kind of myocardial asymmetry of layer-selective atrophy.(ABSTRACT TRUNCATED AT 250 WORDS)     

The relationship between cerebral white matter changes, mental function and blood pressure in normal elderly

The authors examined the relationship between cerebral white matter changes and mental function, blood pressure in 39 neurologically normal aged (21 males, 18 females, mean age 75.0 years) who had no latent lesions on MRI images. The severity of cerebral white matter changes was estimated by T1 value images on MRI and was measured in the bilateral frontal lobe on an axial slice at the level of the basal ganglia and in the bilateral anterior, middle, and posterior portions on axial slices at the level of the body of the lateral ventricle. Mental function was measured by the Hasegawa's dementia rating scale (HDS) and Kohs' block design test (Kohs' test). The severity of cerebral frontal white matter changes increased significantly with age (p less than 0.05). However there was no significant correlation between the severity of cerebral white matter changes and HDS, Kohs' test. The severity of frontal white matter changes correlated with the mean arterial blood pressure (p less than 0.02). These results suggest that the severity of cerebral white matter changes is not related with mental function in the normal elderly, and that the severity of frontal white matter lesions is related with mean arterial blood pressure.