大鼠黑质毁损程度的行为学评价

本研究通过观察黑质毁损大鼠的行为学变化及其与毁损程度的相关性,评价开野实验作为毁损程度观察指标的可行性。采用6-羟基多巴胺(6-OHDA)单侧一点注射毁损大鼠黑质致密区(SNC)多巴胺(DA)能神经元,采用开野实验和阿朴吗啡(APO)诱导旋转实验,观察术后1、3、5、7、14、21 d行为学变化;利用Nissl染色和免疫组织化学方法观察各时间点黑质形态学变化。结果显示:毁损侧黑质DA能神经元逐渐减少;开野实验中旋转、探究、后肢站立和穿梭行为在术后1 d即有显著改变(与对照组比较P<0.05),其中,旋转行为与毁损程度呈正相关(r=0.471,P<0.01),探究、后肢站立和穿梭行为与毁损程度呈负相关(r分别为-0.719、-0.589、-0.594,P<0.01);术后14 d毁损比例超过80%,APO诱导旋转实验阳性。因此开野实验可作为毁损早期反映大鼠脑内DA耗竭程度的敏感的行为学观察指标。     

血清超敏C反应蛋白水平及TC/HDL比值与冠脉次全闭塞病变的关系

目的:探讨血清超敏C反应蛋白(hs-CRP)水平及总胆固醇/高密度脂蛋白比值(TC/HDL)与冠心病次全闭塞病变的关系。方法:冠心病冠脉次全闭塞病变组89例,非次全闭塞病变117例为对照组,测定两组血清hs-CRP水平,计算TC/HDL比值,比较两组间差异。以Logistic回归分析血清hs-CRP水平、TC/HDL比值是否能独立预测冠心病次全闭塞病变,并计算其相对危险度(以OR值表示)。结果:次全闭塞病变组hs-CRP水平(5.22±2.88mg/L)明显低于对照组(9.15±6.56mg/L),P<0.01,TC/HDL比值(4.51±1.37)明显高于对照组(3.75±0.75),P<0.01。Logistic回归分析表明hs-CRP≤5mg/L(OR=3.26,P<0.01)、TC/HDL比值≥4(OR=2.88,P<0.01)可独立预测次全闭塞病变。结论:低血清hs-CRP水平及高TC/HDL比值是冠心病冠脉次全闭塞病变的独立预测因素。     

Generator study of brainstem auditory evoked potentials by a radiofrequency lesion method in rats

Summary The generators of brainstem auditory evoked potentials (BAEPs) in rats were investigated experimentally. Discrete lesions of the brainstem auditory pathway were made unilaterally using a stereotaxic radiofrequency coagulation method, and the BAEPs were recorded before and after the lesions to observe the alterations. The waves of the BAEPs were affected by the lesions as follows: (1) all of the BAEP waves were attenuated or eliminated by a lesion of the auditory nerve; (2) wave II was abolished or attenuated in amplitude following a lesion of the cochlear nucleus; (3) marked reduction or abolition of wave III occurred with some effect on waves IV and V following lesions of the superior olivary complex; (4) the following trough in the wave III was significantly attenuated by lesions of the lateral lemniscus that were associated with inconsistent changes in waves IV and V; (5) no waves were affected significantly by a lesion of the inferior colliculus. The method of radiofrequency lesion using stereotaxic localization proved to be a simpler and more rapid procedure for determining the generators of BAEPs in animals than other surgical lesion methods.     

A Small Aneurysmal Bone Cyst Restricted to the Cortical Bone of the Femur Resembling So-called Subperiosteal Giant Cell Tumor or Subperiosteal Osteoclasia

We report a 16-year-old Japanese girl with a cystic lesion restricted to the cortical bone under the periosteum of the diaphysis of the left femur. Roentgenograms showed a long, oval translucent lesion in frontal view and an eccentric erosive lesion in lateral view. Computed tomography showed a distinct intracortical lesion. The lesion, which was excised en bloc , measured 3×2×2 cm. The outer layer of the cortical bone was eroded eccentrically. From the margin of the eroded bone, thin fragile bony tissue and preserved periosteum extended like the roof of a dome. Multicystic structures, filled with blood, were lined with fibrous granulation and occasional giant cells. Histologically, this lesion falls within the category of aneurysmal bone cyst. However this case is of a rare type, since the lesion was relatively small, and showed a very specific intracortical location, in marked contrast to typical aneurysmal bone cyst. Additionally, this lesion is similar to so-called subperiosteal giant cell tumor or subperiosteal osteoclasia described in the literature. Acta Pathol. Jpn. 39: 539∼544, 1989.     

The short term accumulation of axonally transported organelles in the region of localized lesions of single myelinated axons

Summary Myelinated axons were isolated from the sciatic nerve ofXenopus laevis and were subjected to localized (<30 m wide) lesions. In axons which were bathed in a 0.12 M potassium glutamate solution there was very little local reaction to the lesion and optically-detectable particles undergoing axoplasmic transport accumulated immediately adjacent to, and mostly distal to, the lesion. Preparations fixed for electron microscopy at times up to 3 h following the lesion showed that the axoplasmic changes about the lesion were asymmetrical. Large organelles predominated on the distal side of the lesion; these were mostly dense lamellar bodies (DLB) with mean dimensions, as determined from thin sections, of 0.48 by 0.19 m. Multivesicular bodies, mitochondria, and a variety of smaller membrane bounded bodies also appeared in the particle accumulation distal to the lesion. Analysis of these results led to the conclusion that DLB were transported up to the lesion and represent the majority of the optically detectable particles which are transported in the retrograde direction. Small vesicles and tubules were the commonest structures which accumulated proximal to the lesion. The time course of this accumulation was consistent with the hypothesis that these structures are particulate bodies which move in the orthograde direction at about 1.5 m/s.Incidental findings which are also of significance to the study of axonal transport were: large particulate material may reverse its direction of movement at an axonal obstruction, and organelles which accumulate on either side of a lesion do so in rows which are associated with microtubules.     

Gastric collision tumor of large cell neuroendocrine carcinoma and adenocarcinoma – A case report

Large cell neuroendocrine carcinomas (LCNECs) of the stomach are rare and represent only a small percentage of all gastric endocrine tumors. Here we report a case of a rare combination of gastric LCNEC concurrent with gastric adenocarcinoma. A 50-year-old man presented with heartburn sensation for 2 weeks. An endoscopic evaluation revealed a relatively well-demarcated ulcerative elevated lesion at the lower body of the stomach. Grossly, the gastric mass was a 5×4.5 cm-sized ulcerative fungating lesion. Microscopically, two separated lesions were recognized. The main lesion showed neuroendocrine morphology, such as nests and trabeculae. Most of the tumor cells had large, vesicular nuclei with prominent eosinophilic nucleoli, variable amounts of eosinophilic cytoplasm, and immunoreactivity for synaptophysin and chromogranin A. The other lesion was a well-differentiated adenocarcinoma of early gastric cancer type IIa located adjacent mucosa of the main lesion. We diagnosed this lesion as gastric LCNEC concurrent with focal adenocarcinoma, collision type.     

Transmucosal potential difference in experimental colitis in rats

Colon transmucosal potential difference (TPD), macro- and microscopic lesions, myeloperoxidase activity, and leukotriene levels were studied after the induction of experimental colitis in the rat. Forty-three male Wistar rats were subjected to the instillation of 200 mg/ml 2,4,6-trinitrobenzenesulfonic acid (TNB) solution through a rectal cannula. TPD measurements were made at different distances from the anus before and 24 h and one, two, three, and four weeks after lesion induction. Leukotriene B₄ levels were assayed by intracolonic dialysis 24 h and one, two, three and four weeks after lesion induction. Macro- and microscopic evaluations were made of the bowel lesions, and myeloperoxidase activity was assayed. The mean basal TPD was ?46.06 mV at 1 cm from the anus, and +10.86 mV in the proximal colon. Twenty-four hours after lesion induction the values proved markedly positive. This was correlated with an abrupt increase in LTB₄ levels and myeloperoxidase activity. After one week the TPD values exhibited a greater electronegativity, returning to basal values by the fourth week after lesion induction. This coincided with an improved macroscopic lesion index, LTB₄ levels, and myeloperoxidase activity. In conclusion, TPD is a useful indicator of acute colonic lesions and correlates well with LTB₄ and myeloperoxidase assays. Moreover, the parameter is able to delimit lesion evolution, reflecting possiblead integrum restoration of the bowel mucosa.     

Effect of Brain Lesions and Chlorpromazine on Accumulation and Disappearance of Catecholamines Formed in vivo from 14C-Tyrosine

Rats were subjected to a unilateral stereotaxic lesion at the level of the mesencephalic-hypothalamic junction where the nigro-striatal dopamine (DA) pathway is known to pass. Between 6 and 18 h after the lesion the level of DA in the striatum on the same side was increased by about 50 per cent. Between 18 and 48 h after the lesion the content of DA declined to 15 per cent of that of the contralateral striatum and stayed at this low level during the following 6 days. The content of noradrenaline (NA) tended to be increased 24 h after the lesion but no change was found on the following days. The accumulation and disappearance of ¹⁴C-DA formed from ¹⁴C-tyrosine in the striatum 12–24 h after the nigral lesion were decreased on the lesion side in comparison with the contralateral side. The accumulation and disappearance of ¹⁴C-NA did not differ between the 2 sides. Chlorpromazine accelerated both accumulation and disappearance of ¹⁴C-DA in the striatum on the side contralateral to the lesion but not in the striatum of the lesion side. In animals with a unilateral lesion above the DA pathway, in the posterior thalamus, chlorpromazine accelerated the accumulation of ¹⁴C-DA on both sides. The accumulation of ¹⁴C-XA in the striatum was increased by chlorpromazine on the intact side following both types of lesions. The disappearance of ¹⁴C-NA, however, was not influenced by the drug. The results are taken as evidence that chlorpromazine accelerates DA turnover in the striatum by activating the nerve impulse flow in the nigro-striatal DA pathway.     

脊髓压迫性损伤大鼠海马和脊髓内BDNF的表达变化

目的探讨脑源性神经营养因子(BDNF)在脊髓压迫性损伤后的表达变化及作用。方法用自行设计的方法制作脊髓压迫模型,免疫荧光检测BDNF在星形胶质细胞、神经元和上下行轴突的表达;WB检测BDNF在大鼠海马及脊髓的表达。结果随着时间延长,受损部位的BDNF+-GFAP荧光强度逐渐增强;BDNF+-Tuj1荧光强度逐渐减弱;受损部位相邻上下段的BDNF+-NF200比受损部位的明显增强。海马和脊髓受损中心相邻的上、下段的BDNF蛋白表达在损伤后1d达到峰值,然后逐渐下降(P0.05);而脊髓受损中心的BDNF蛋白表达逐渐下降(P0.05)。结论脊髓损伤后,BDNF的表达下调,随伤后时间呈一定规律变化,是引起受损部位神经元表达下降的原因之一。     

Reconstruction of the glial environment of a photochemically induced lesion in the rat spinal cord by transplantation of mixed glial cells

Summary It is becoming increasingly apparent that the astrocytic environment is critical to the normal development and functioning of the CNS, and that acute injury to the spinal cord causes destruction of glial cells in addition to neurones and axons. The aims of this study were to assess the viability of reconstructing the astrocytic environment of a cystic spinal cord lesion by transplantation of glial cells and to examine the effect of the transplanted cells on meningeal cell invasion and revascularisation of the lesion and on axonal regeneration. Neonatal rat and kitten mixed glial cells and the CG-4 rat O-2A progenitor cell line were transplanted into a lesion produced in the dorsal funiculus of the rat spinal cord by photochemical infarction. The animals were killed 4 weeks after injury, their cords examined with light and electron microscopy and compared with control animals that were injected with medium alone. Transplantation of all three preparations resulted in increased numbers of astrocytes in the area of Wallerian degeneration cranial to the lesion and within the cyst. Mixed glial cell cultures prepared from neonatal rat forebrain contained cells within vitro characteristics of type-1 astrocytes, and produced dense clusters of astrocytes that were surrounded by meningeal cells, resulting in a fragmented environment in the cyst. In contrast, glial cell cultures prepared from kitten forebrain and the CG-4 cell line produced cells that filled the cyst with a loose network of fine processes and reduced meningeal cell infiltration of the lesion. The CG-4 cell line significantly increased the density of blood vessels in the centre of the lesion and the number of spared axons present dorsal to the lesion, but none of the preparations significantly increased the number of axons regenerating at the caudal end of the lesion. We conclude that O-2A progenitorderived astrocytes are more suitable for reconstruction of the glial environment of a cystic lesion in the rat spinal cord than type-1 like astrocytes and would therefore be the cell of choice to engineer to produce factors that promote axonal regeneration.     

Limitations in transplantation of astroglia-biomatrix bridges to stimulate corticospinal axon regrowth across large spinal lesion gaps

Regrowth of injured axons across rather small spinal cord lesion gaps and subsequent functional recovery has been obtained after many interventions. Long-distance regeneration of injured axons across clinically relevant large spinal lesion gaps is relatively unexplored. Here, we aimed at stimulating long-distance regrowth of the injured corticospinal (CS) tract. During development, an oriented framework of immature astrocytes is important for correct CS axon outgrowth. Furthermore, a continuous growth promoting substrate may be needed to maintain a CS axon regrowth response across relatively large spinal lesion gaps. Hence, we acutely transplanted poly(d,l)-lactide matrices, which after seeded with immature astrocytes render aligned astrocyte-biomatrix complexes (R. Deumens, et al. Alignment of glial cells stimulates directional neurite growth of CNS neurons in vitro. Neuroscience 125 (3) (2004) 591–604), into 2-mm long dorsal hemisection lesion gaps. In order to create a growth promoting continuum, astrocyte suspensions were also injected rostral and caudal to the lesion gap. During 2 months, locomotion was continuously monitored. Histological analysis showed that astrocytes injected into host spinal tissue survived, but did not migrate. None of the astrocytes on the biomatrices survived within the lesion gap. BDA-labeled CS axons did not penetrate the graft. However, directly rostral to the lesion gap, 120.9 ± 38.5% of the BDA-labeled CS axons were present in contrast to 12.8 ± 3.9% in untreated control animals. The observed anatomical changes were not accompanied by locomotor improvements as analyzed with the BBB and CatWalk. We conclude that although multifactorial strategies may be needed to stimulate long-distance CS axon regrowth, future studies should focus on enhancing the viability of cell/biomatrix complexes within large spinal lesion gaps.     

A pharmaco-fMRI study on pain networks induced by electrical stimulation after sumatriptan injection

The unilateral 6-hydroxydopamine (6-OHDA) lesion of the medial forebrain bundle induces hemiparkinsonism in rats and is a well established animal model of Parkinson’s disease. In this study, we assessed the spontaneous activity of substantia nigra pars reticulata (SNr) neurons in unilateral 6-OHDA- or sham-treated rats. Extracellular single cell recordings revealed a bilaterally decreased firing rate in short-term 6-OHDA-lesioned rats (8–10 weeks post lesion) while no rate differences were evident in long-term lesioned animals (5–8 months post lesion) in vivo under chloral hydrate anaesthesia. However, firing pattern of the SNr neurons (indicated by interspike interval (ISI) histogram parameters: coefficient of variation, skewness and kurtosis) was significantly altered only after long-term lesion: 53.8 % of the recorded cells in the ipsilateral 6-OHDA-lesioned SNr fired in a bursting pattern (compared to 5.9–16.7 % in contralateral SNr or sham controls). Additionally, behavioural effects of the lesion were assessed 4 weeks post lesion by the forelimb adjusting stepping test. A decreased number of adjusting steps with the contralateral forepaw, as well as an increased performance with the ipsilateral paw was found for the 6-OHDA-lesioned rats as compared to sham controls. Furthermore, stepping values were negatively correlated with the ISI parameters after long-term lesion, while there were no correlations with the short-term groups. Firing rate was not correlated regardless of the time frame. In conclusion, long-term changes in firing pattern may represent a neuronal correlate of the 6-OHDA-induced hemiparkinsonism and may be useful for the interpretation of 6-OHDA-induced motor deficits and compensatory mechanisms as well.     

The pathology of the end-stage osteoarthritic lesion of the knee: potential role in cartilage repair

The purpose was to explore whether there were any pathological characteristics of the end-stage osteoarthritic sclerotic lesion that have potential to participate in cartilage repair.Specimens harvested following total knee surgery were examined for gross pathology including staining with Safranin O. Multiple small sections of the lesion were placed in tissue culture for 6 weeks. Gross examination and photographic documentation was made at 3 and 6 weeks. At 6 weeks the specimens from culture were subject to histological examination. The pathology of the end-stage osteoarthritic lesion showed sclerotic bone, dead osteons, hypervascularity and scattered cartilaginous aggregates. Additional observations showed multiple pitting on the sclerotic surface, which histologically was related to three events; fragmentation of dead bone, ruptured blood vessels, and eroded aggregates. There were no pathological or biological changes in the specimens following the time in tissue culture.The in-depth pathological evaluation showed the end-stage osteoarthritic lesion to have certain features with potential to facilitate cartilage repair. The cartilaginous aggregates may be a participant in cartilage repair following surgery. The cartilaginous aggregates remained unchanged in the tissue culture absent the normal synovial joint chemical and physical environment and therefore further testing with a different experimental model would be necessary to establish these aggregates as a source of cartilage regeneration. The multiple small depressions in this lesion may have potential to be a “home” for therapeutics.     

The effect of riluzole and mannitol on cerebral oedema after cryogenic injury in the mouse.

A cryogenic lesion was produced under halothane anaesthesia in the mouse by placing a cotton swab soaked in liquid nitrogen onto the surface of the cranium. This provoked an oedematous lesion which developed within the hour after the insult and evolved over the following week. Treatment with mannitol at 3 g/kg i.v. caused a significant 22% reduction in oedema 1 h later, when administered immediately after lesion, but not when administered 23-h post lesion. Likewise riluzole (16 mg/kg, i.v.) significantly reduced oedema by 17% when administered immediately after lesion, or 13% (P < 0.05) when administered 23 h after lesion. Repeated doses (2 x 16 mg/kg, i.p.) of riluzole were also able to reduce oedema significantly (24%, P < 0.05) at 24 h post lesion. Riluzole, in four repeated doses of 8 mg/kg i.p. was also able to reduce lesion surface size by 16% (P < 0.05) 48 h after lesion.     

Prediction of Coronary Atherosclerotic Ostial Lesion with a Damping of the Pressure Tracing during Diagnostic Coronary Angiography

Purpose

When performing coronary angiography (CAG), diagnostic catheter intubation to the ostium can cause damping of the pressure tracing. The aim of this study was to determine the predictors of atherosclerotic ostial stenosis in patients showing pressure damping during CAG.

Materials and Methods

In total, 2926 patients who underwent diagnostic CAG were screened in this study. Pressure damping was defined as an abrupt decline of the coronary blood pressure with a blunted pulse pressure after engagement of the diagnostic catheter. According to CAG and intravascular ultrasound (IVUS), we divided damped ostia into two groups: atherosclerotic ostial lesion group (true lesion group) and non-atherosclerotic ostium group (false lesion group). Clinical and angiographic characteristics were compared between the two groups.

Results

The overall incidence of pressure damping was 2.3% (68 patients and 76 ostia). Among the pressure damped ostia, 40.8% (31 of 76 ostia) were true atherosclerotic ostial lesions (true lesion group). The true lesion group had more frequent left main ostial damping and more percutaneous coronary interventions (PCIs) performed on non-ostial lesions, compared to the false lesion group. On multivariate logistic regression analysis, left main ostial damping [hazard ratio (HR) 4.11, 95% confidence interval (CI) 1.24-13.67, p=0.021] and PCI on non-ostial lesion (HR 5.34, 95% CI 1.34-21.27, p=0.018) emerged as independent predictors for true atherosclerotic ostial lesions in patients with pressure damping.

Conclusion

Left main ostial damping and the presence of a non-ostial atherosclerotic lesion may suggest a significant true atherosclerotic lesion in the coronary ostium.     

Five myofibrillar lesion types in eccentrically challenged,unloaded rat adductor longus muscle—a test model

Sarcomere disruptions are observed in the adductor longus (AL) muscles following voluntary reloading of spaceflown and hindlimb suspension unloaded (HSU) rat, which resemble lesions in eccentrically challenged muscle. We devised and tested an eccentric contraction (ECCON) test system for the 14‐day HSU rat AL. Six to 7 hours following ECCON, ALs were fixed to allow immunostaining and electron microscopy (EM). Toluidine blue‐stained histology semithin sections were screened for lesion density (#/mm²). Serial semithin sections from the ECCON group were characterized for myosin immunointensity of lesions. Five myofibrillar lesion types were identified in histological semithin sections: focal contractions; wide A‐bands; opaque areas; missing A‐bands; and hyperstretched sarcomeres. Lesion density by type was greater for ECCON than NonECCON ALs (P ≤ 0.05; focal contractions and opaque regions). Lesion density (#‐of‐all‐five‐types/mm²) was significantly different (ECCON: 23.91 ± 10.58 vs. NonECCON: 5.48 ± 1.28, P ≤ 0.05; ECCON vs. SHAM: 0.00 ± 0.00; P ≤ 0.025). PostECCON optimal tension decreased (Poi‐drop, 17.84 ± 4.22%) and was correlated to lesion density (R² = 0.596), but prestretch tension demonstrated the highest correlation with lesion density (R² = 0.994). In lesions, the darkly staining A‐band lost the normally organized thick filament alignment to differing degrees across the different lesion types. Ranking the five lesion types by a measure of lesion length deformation (hypercontracted to hyperstretched) at the light microscopy level, related to the severity of thick filament registry loss across the lesion types at the electron microscopic level. This ranking suggested that the five lesion types seen in semithin sections at the light level represented a lesion progression sequence and paralleled myosin immunostaining loss as the distorted A‐band filaments spread across the hyperlengthening lesion types. Lesion ultrastructure indicated damage involved calcium homeostasis loss (focal contraction lesions) and “thick‐filamentcentering” failure of titin (wide A‐band lesions) in the early stages of lesion development. Anat Rec 254:39–52, 1999. © 1999 Wiley‐Liss, Inc.     

Adenomyolipoma of the uterus: a case report

Adenomyolipoma of the uterus is a rare, benign, polypoid lesion considered to be of hamartomatous origin or represent an unusual type of benign Müllerian mixed tumour with a heterologous element. The authors present a case of uterine adenomyolipoma and discuss its pathogenesis. A 62-year-old woman complained of lower abdominal pain and postmenopausal bleeding. Imaging techniques revealed a solid ovarian mass and a polypoid intrauterine lesion. The frozen section diagnosis of the ovarian mass was a thecoma. A total hysterectomy and bilateral salpingo-oophorectomy were performed. On gross examination a pedunculated, polypoid lesion of 7x4.5x3cm was found in the uterine cavity. Microscopically, the polypoid lesion contained both epithelial and mesenchymal elements. The epithelial elements were endometrial glands of various size, formed by proliferative endometrial cells. The mesenchymal elements were composed of endometrial stroma, smooth muscle and mature adipocytes. Both the epithelial and the mesenchymal elements showed a benign appearance, were intermingled with each other and periglandular stromal condensation was absent. The lesion had an irregular surface. Microscopic diagnosis was an adenomyolipoma. The peculiar shape and microscopic features of this lesion suggested that it was a variant of benign Müllerian mixed tumour.     

Malacoplakia of the thyroid gland

A case of malacoplakia of the thyroid gland is described in a 50-year-old Japanese woman. This lesion clinically mimicked a malignant neoplasm, and the true diagnosis of malacoplakia was made only after histologic examination; light microscopy revealed a granulomatous nodule with an accumulation of von Hansemann's histiocytes containing PAS-positive and von Kossa's-positive intracytoplasmic and extracytoplasmic inclusions known as Michaelis-Gutmann bodies. There were some foci consisting of neoplasm-like or hyperplastic residual follicles within the lesion. Electron microscopically, a small number of bacilliform organisms were demonstrated within the lesion. X-ray microanalysis of Michaelis-Gutmann bodies was performed and revealed the presence of phosphorus, calcium, iron, and chloride. It is suggested that the malacoplakic lesion may be associated with the hyperplastic or neoplastic follicular lesion, and bacterial infection could be important in the causation of malacoplakia of the thyroid gland.     

Various clinico-anatomic variants of heart lesions in lymphosarcoma

In 457 autopsies of cases with non-Hodgkin's malignant lymphoma tumour cardiac lesion was found in 43 (9.4%) observations; 5 of them with a combination of tumour with post infarctional myocardial sclerosis were excluded from the analysis. The clinical-anatomic data from 38 autopsies were divided into 3 groups: marked insignificant and only microscopically revealed tumour lesion of the myocardium. No correlations between the degree of morphological changes and clinical-electrographic picture were found. The distribution of some clinical and morphologic features of myocardial lesion depending on the histologic tumour type is presented according to "Working Formulation", 1982. Myocardial lesion was noted predominantly in non-Hodgkin's malignant lymphomas with a high degree of malignancy.