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Objective@#To investigate the ultrastructural features of muscle in patients with mitochondrial encephalomyopathy for its diagnosis and differential diagnosis.@*Methods@#The clinical data of 27 mitochondrial encephalomyopathy patients who underwent left or right biceps brachii muscle biopsy at Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University from July 2006 to August 2017 were analyzed retrospectively. The muscle biopsy specimens were examined underlight microscope and transmission electron microscope.@*Results@#There were 27 patients (17 males, 10 females) with an age range of 12 to 62 years (mean 29 years). The age of onset ranged from 3 to 38 years. The course of disease ranged from 1 month to 24 years. Twenty-two cases presented with lactic acidosis and stroke-like episodes (MELAS) syndrome, four with myoclonic epilepsy with ragged red fibers (MERRF) syndrome, and one with chronic progressive paralysis of extraocular muscle (CPEO) syndrome. Skeletal muscle biopsy showed abundant ragged red fibers and strongly SDH-reactive vessel. Genetic studies showed 17 of 22 cases of MELAS syndrome had A3243G mutation, and the other 5 cases had no abnormality. A8344G mutation was found in 3 of 4 cases of MERRF syndrome. No single or multiple mtDNA mutations were found in the single case of CPEO. Transmission electron microscopy of all 27 cases showed diffuse proliferation of mitochondria between the myofibrils and beneath the sarcolemma, with increased spacing between muscle cells. Seven cases showed numerous glycogen and four showed subsarcolemmal lipid droplets, 13 cases showed unusual mitochondrial morphology, including mitochondrial electron-dense substances and paracrystal line inclusions ("parking lot" change)in eight cases.@*Conclusions@#Transmission electron microscopy shows significant differences in ultrastructural pathological changes among different patients with mitochondrial encephalomyopathy. Some patients with mild clinical symptoms have increased mitochondrial number, increased metabolism of glycogen and lipid droplets, while others with severe clinical symptoms have abnormal mitochondrial morphology. Typical crystalloid inclusions are found in mitochondria, which are of great value in the diagnosis of this disease.
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Objective To investigate the effects of rolipram on neurofunction and the ultrastructure of the spinal cord in rats with spinal cord contusion.Methods Thirty adult,female Sprague-Dawley (SD) rats received spinal cord contusion at the T10 level.They were then randomited into an experimental group and a control group immediately after the operation.Rats in the experimental group received subcutaneous injections of 0.25mg/kg of rolipram twice daily for two weeks.Control rats received the same dosage of 0.9% sodium chloride solution on the same schedule.The rats'functional recovery was evaluated using the open-field locomotion rating scale of Basso,Beattie and Bresnahan (BBB score),once a week within the 1st month after spinal cord injury (SCI),and once every two weeks subsequently.The morphology of the spinal cord tissue around the lesion site was observed under the light microscope with HE staining at the 8th week postoperation,and the ultrastructure of the spinal cord was observed under the transmission electron microscope at the 2nd,4th and 8th week postoperation.Results At the 2nd and 3rd week after SCI the experimental group exhibited significandy greater improvement in average BBB scores than the control group.However,the average BBB scores in the experimental and control groups were not significantly different at 8 weeks after SCI.Under the light microscope,cavities were observed in the posterior dorsal column near the SCI in both the experimental and control groups.However thick,condensed glial scars in the injured area were observed only in the control group.The density of glial cells decreased more in the experimental group than in the control group.Transmission electron microscopy revealed that,compared with the control group,inflammatory edema was attenuated and fewer axons were damaged at the 2nd week postoperation in the experimental group.That group also showed less axon degeneration as well as more angiogenesis at the 4th and 8th week.Conclusion Rolipram can reduce secondary neuron degeneration,inhibit gliosis and the formation of glial scars,and promote angiogenesis.
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ObjectiveTo investigate the morphological and ultrastructural characteristics of pancreatic stellate cells (PSCs) in a chronic pancreatitis murine model.MethodsSprague-Dawley rats were divided into experimental group (n=12) and control group (n=12).The experimental group was fed with a high-fat diet (HFD) for 16 weeks whereas the control group received regular rat feed.Pathologic changes in the pancreas were observed by several morphological studies including a Sirius Red staining method,as well as immunostaining for desmin and a smooth muscle actin (a-SMA).TEM and immunoelectron microscopy were performed to study the ultrastructure of the PSCs.Results The number of desmin and α-SMA positive cells significantly increased in the HFD groups compared to the control group.The quiescent and activated PSC cells both coexisted in the pancreas in the HFD group.ConclusionsThe morphology and ultrastructural study of pancreatic stellate cells may be helpful for further functional studies on chronic pancreatic fibrosis.
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ObjectiveTo investigate the impacts of neural stem cells (NSCs) transplantation on spinal pathology and ultrastructure after spinal cord injury (SCI) in rats and probe into the protective role of tacrolimus (FK506) on neural regeneration.MethodsCompressive SCI at T8 was induced in the adult SD rats,which were randomly assigned to the control group,FK506 group,NSCs group and NSCs + FK506 group.The differences of neural regeneration in each group were compared at days 7,14,28 and 56 after injury by motor evoked potentials ( MEP),HE staining,immunohistochemical staining,ultrastructure observation and image analysis of the myelinated fiber. ResultsThe MEP latency in the NSCs + FK506 group was significantly shorter than that in other groups at day 28 ( P < 0.05 ).HE staining revealed that only local necrosis presented in the NSCs + FK506 group at day 56.More BrdU and NF-200 positive cells were detected with immunohistochemical staining in the other three groups as compared with the control group.Moreover,the positive cells in the NSCs + FK506 group also outnumbered the FK506 group and NSCs group.Electron microscope scan showed edema under the membrane of large myelin sheath in the control group,and classic new myelin sheath and neuraxis in the NSCs + FK506 group at day 56.The regeneration of the nerve fiber in the NSCs + FK506 group was better than that of other three groups (P <0.01 ).ConclusionAfter NSCs transplantation for SCI rats,the early combination use of FK506 can improve the pathology and ultrastructure of the regenerative nerve fiber and is conducive to nerve regeneration.
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ObjectiveTo investigate the curative effect of neural stem cells (NSCs) transplantation combined with monosialotetrahexosyl ganglioside (GMi) in treatment of acute spinal cord injury in rats.MethodsCompressive spinal cord injury model at T8 segment was established in the adult SD rats that were then randomly divided into three groups, ie, control group, NSCs transplantation group and NSCs + GM1 group.Continuous observation was performed at 1,2, 4 and 8 weeks.Functional neurological recovery of the injured spinal cord was evaluated with motor function scale, pathology, transmission electron microscopy and somatosensory evoked potential (SEP).ResultsThe motor function of the lower extremities was recovered at different degrees in three groups.While the motor function recovery level of the animals and the positive staining cells of the calcitonin gene-related peptide (CGRP) in the NSCs + GM1 group were higher than those in the other two groups at 4 and 8 weeks (P < 0.01).Compared with control group and NSCs group, focal necrosis and small vessel regeneration were observed only in the center of the injured segment in the NSCs + GM1 group at 8 weeks.Electron microscope scan showed edema under the membrane of the large myelin sheath in the control group, much intact myelin sheath, well-differentiated neurons and many kinds of synapse vesicles in the NSCs + GM1 group.The latent period of SEP was shortened markedly in the NSCs + GM1 group two weeks after transplantation (P <0.05).The latent period shortening was apparent in the NSCs group at 4 and 8 weeks after transplantation but was still longer than that in the control group.ConclusionsTransplantation of neural stem cells combined with use of GM1 can protect the nervous tissues after spinal cord injury, when GM1 reconstructs the spinal cord through promoting differentiation of the transplanted stem cells and linking with the host cells.
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Objective To examine ultrastructural features of the arteriole responsible for intracerebral hemorrhage or the perforating branches artery around hematoma in patients with hypertensive intracerebral hemorrhage and explore the mechanism of hypertensive intracerebral hemorrhage. Methods Twelve hypertensive patients with CT proved intracerebral hemorrhage underwent operation. The small artery specimens were obtained through cortex fistula and their ultrastructures were observed under the electron microscope. Results Twelve specimens including 4 cases of duty arteriolae and 8 cases of perforating branch arteriolae were collected, Different degrees of degeneration were observed in three layers of the arteriola in all 12 specimens. Changes in endothelial cells included endothelial cell necrosis, collapse, or fallen of from endomembrane, accompanied by degeneration of internal elastic membrane, such as uneven thickness, absence of intermittent and medial smooth muscle cell necrosis. Myofilaments in the cytoplasm were condensed to form a high electron-dense cytoplasm. No micro-aneurysm was observed. Conclusions The pathological changes of cerebral small artery walls load-bearing layer in hypertensive patients include internal elastic layer rupture, smooth muscle layer of degeneration, decreased elasticity and increased fragility. Small artery walls may rupture, resulting in bleeding under the condition of rapid dynamic changes of blood flow.
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@#Objective To observe the pathology in temporal lobe cortexes and hippocampus in protopathic intractable temporal lobe epileptics.Methods The cortexes of spike foci in temporal lobe and hippocampus were obtained from 9 cases with protopathic intractable temporal lobe epilepsy who accepted operation.The samples were observed under the transmission electron microscope.Results The ultrastructure changes in spike focus of temporal lobe cortexes are similar to those in hippocampus.It is common that neurons were pycnotic and decreased.Astrocytes were hydropic and degenerative.Gliosis were found in some cases.The number of synapses increased or decreased in different cases and positions.Blood-brain barriers were destroyed because foot processes of astrocytes around capillaries were edematous.Conclusion Neuronal loss,gliosis and synaptic reorganization which occur in epileptic hippocampus and maybe also in epileptic temporal lobe cortexes destroy the balance between excitatory and inhibitory neurotransmission.The abnormalities probably associate with protopathic intractable temporal lobe epileptic seizures.
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@#ObjectiveTo investigate the changes of ultrastructure of global cerebral ischemia and reperfusion damage in rats.MethodsSix adult male Wistar rats were randomly divided into the ischemia group (n=3), and sham injury group (n=3). Global cerebral ischemia and reperfusion model were established with Pulsinelli's method. Cortical ultrastructure changes were investigated on the first hour after reperfusion.ResultsIn the ischemia group, different degrees of pyconosis neurons, abnormal organell and microtube of neurons were observed. In addition, glial cell and microvessels were damaged in ischemia group, but that in sham injury group were not demaged.ConclusionCortical neurons, neuroglia cells, cytoskeleton and blood-brain barrier changed at early stage of reperfusion damage.
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BACKGROUND: Craniocerebral injury can cause a series of visceral complications, among which cardiovascular complication is paid special attention.OBJECTIVE: To investigate the effects of craniocerebral injury on changes of circulatory and local angiotensin Ⅱ (Ang Ⅱ ) and local angiotensin Ⅱ receptor 1 (AT1) in the heart.DESIGN: Randomized controlled experiment taking animals as subjects.SETTING: Beijing Tiantan Hospital, and the College of Basic Medicine,Capital University of Medical Sciences.MATERIALS: The experiment was conducted at the Central Laboratory of Capital University of Medical Sciences and the Central Laboratory of Beijing Tiantan Hospital from 2003 to 2004. Totally 40 healthy male Wistar rats were divided randomly into craniocerebral injury group and control group with 20 in each group.METHODS: Rats in craniocerebral injury group were treated with weightdrop method to establish the model of craniocerebral injury, while rats in control group received no impact. Twenty-four hours after hitting, 10 rats in each group were selected to assay their Ang Ⅱ and AT1; the other 10 in each group were selected to observe their myocardial forms.myocardium of rats assayed with light microscope after hematoxylin-eosin staining and transmission electron microscope.It was significantly higher in craniocerebral injury group than in control ity: It was obviously higher in craniocerebral injury group than in control Ⅱ and AT1: The area of positive reactant and gray value in craniocerebral toxylin-eosin staining: Strong acidophil staining was found on myocardial cellular plasma in craniocerebral injury group. The results showed that cytoplasm shrank obviously; muscle fiber broke, decreased or disappeared.Focal hydropic degeneration, lysis or necrosis was observed in myocardium.Ultrastructural pathological observation revealed pathological damage of myocardium.CONCLUSION: Craniocerebral injury in rats can cause myocardial damage, and changes of angiotensin system may be one of the factors.
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BACKGROUND: Quiet a number of researches has reported the morphological changes of global ischemic reperfusion model. However, there are few reports on the ultrastructural changes of cortex in early reperfusion, especially the change of blood brain barrier.OBJECTIVE: To explore the changes of brain cortex neurons, glial cells and blood brain barrier in order to provide reliable evidence for clinical treatment.DESIGN: A randomized and controlled trial.SETTING: Department of Neurosurgery, Departnent of Anesthesia and Electron Microscope Room of Beijing Tiantan Hospital.MATERIALS: The experiment was conducted to 6 Wistar rats in Beijing Neurological Surgery Research Institute of Capital University of Medical Sciences during February 2003 to February 2004. The rats were randomly divided into two groups with one of ischemia-reperfusion group and sham operation group with 3 rats in each group.INTERVENTIONS: To prepare global ischemic reperfusion model of rats. Brain was removed from ischemic group in one hour of reperfusion and from sham operation group one hour after the operation. Electronic microscope technique was used to observe the ultrastructural changes of cortex.MAIN OUTCOME MEASURES: Ultrastructural changes of cortex.RESULTS: The neurons of cortex shrank to certain degree in the early stage of ischemic reperfusion(1 hour) . The glial cells were swollen with dissolved chromosome in nucleus and unclear nuclear membrane. The foot protrusions around blood vessel slightly swelled and separated from basement membrane. Mircro-tubes were partially dissolved.CONCLUSION: In early stage of reperfusion injury, the cortex neurons, glial cells, cellular framework and blood brain barrier already changed which suggested that the protective treatment such as reducing brain edema, protecting blood brain barrier should start as early as possible.
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@#ObjectiveTo detect the ultrastructure of neural stem cells (NSCs) cultured in vitro .MethodsNSCs separated from the cortex of 17—19 days Wistar rat fetus were cultured and induced to differentiate in vitro. Electron microscopes were used to visualize the ultrastructure of these cells before and after differentiation.ResultsNSCs had the similar cellular size, morphology and intracellular structures pre-differentiation. Cells were able to proliferate via mitosis. The nucleus/cytoplasm ratio was very high. The nucleus was poly-morphological. Cells had very little cytoplasm and no mature organelles. After differentiation, several processes protruded out from cellular surface. Cells became flat shape, the volume of cytoplasm increased dramatically and various kinds of mature organelles appeared in the cytoplasm. Cells differentiated into two kinds of cells,neural cells and glial cells,with quite different morphology and intracellular structure. ConclusionNSC is one kind of original cells which can be induced to differentiate into mature neural cells and glial cells.
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<p><b>OBJECTIVE</b>To observe sulfhydryl compound variation in the injury of pancreatic cells and the effects of external sulfhydryl compounds on cytoprotection.</p><p><b>METHODS</b>Male Wistar mice were divided randomly into three groups: groups A and B served as animal models (retrograde duct infusion with 5% sodium taurocholate), in group A, 45 animals were treated with normal saline therapy, in group B, 45 animals were treated with Tiopronin therapy; and group C, 15 animals, were designated as normal control. Animals were killed at 2, 4, 6, 12 and 24 h, and pancreatic tissue was analyzed for total sulfhydryl (TSH), nonprotein sulfhydryl (NPSH) and malondialdehyde (MDA). Histopathology, serum amylase (Sam) and C reactive protein (CRP) were assessed as well.</p><p><b>RESULTS</b>Levels of Sam and CRP increased in both group A and group B, with corresponding pathological changes of acute nerotic pancreatitis (ANP). Levels of TSH, NPSH and protein sulfhydryl (PSH) in group A decreased markedly during pancreatitis (P < 0.01), but MDA increased significantly (P < 0.01). The depletion of NPSH in group B was markedly ameliorated at 4 h or 6 h, when Tiopronin was prophylactically administered (P < 0.05), after which the level of MDA showed very little increase when compared to group A (P < 0.01). Histopathological damage was attenuated to a certain extent, in regards to serum amylase and CRP.</p><p><b>CONCLUSIONS</b>All sulfhydryl compounds decreased significantly during ANP; external sulfhydryl compound could protect the pancreatic cells most likely as a type of scavengers of oxygen free radicals, which are critically involved in the pathophysiology of ANP. Sulfhydryl plays an important role in the action of pancreatic cytoprotection.</p>
Subject(s)
Animals , Male , Rats , Acute Disease , Amylases , Blood , C-Reactive Protein , Cytoprotection , Lipid Peroxidation , Necrosis , Pancreatitis , Drug Therapy , Pathology , Rats, Wistar , Sulfhydryl Compounds , Physiology , Tiopronin , Therapeutic Uses摘要
<p><b>OBJECTIVE</b>To investigate the role of hypertension in the pathogenesis of cerebral aneurysms in rats.</p><p><b>METHODS</b>Twenty spontaneous hypertensive rats (SHR) and 10 Wistar-Kyoto rats (WKY) were included in this observational study. Animals were fed with normal diet and drinking water. No experimental modifications were undertaken in either group. They were sacrificed at one year of age, the bifurcations of the circle of Willis were dissected and longitudinal serial sections were prepared for light microscopic and transmission electron microscopic study.</p><p><b>RESULTS</b>In the SHR group, 2 of the 20 rats formed an aneurysm respectively at the bifurcations of the basilar artery. As revealed by electron microscopy, injury at the bifurcation of the artery first occurred on the steeper side of the intimal pad. Furthermore, loss of endothelial cells, small depressions on the intima, disruptive internal elastic lamina and lymphocytes or red blood cells infiltration were noted at the steeper side of the intimal pad. No significant changes were observed in WKY group.</p><p><b>CONCLUSIONS</b>Cerebral aneurysms can form spontaneously in SHR without ligation of the common carotid artery and without a diet containing beta-aminoproprionitrile. Long-standing systemic arterial hypertension is one of the etiological factors that contributes to aneurysm formation in SHR rats.</p>
Subject(s)
Animals , Male , Rats , Cerebral Arteries , Pathology , Hypertension , Intracranial Aneurysm , Pathology , Rats, Inbred SHR , Rats, Inbred WKY摘要
<p><b>OBJECTIVE</b>Electrolytic detachable coils (EDC) have been the main embolic materials for intracranial aneurysms. Liquid aneurysmal embolic materials represented by cellulose acetate polymer (CAP) are still in controversy. In this research, the embolization results and pathological reactions after embolization of canine aneurysmal models with EDC or CAP were observed and compared.</p><p><b>METHODS</b>The canine aneurysmal models constructed by anastomosis of venous pouches were randomly grouped. The aneurysms were respectively occluded with CAP and electrolytic detachable coils that was named by Wu electrolytic detachable coil (WEDC) and made by us. Angiogram follow-ups were performed at 24-hour, 2-week, and 2-month after embolization. The occluded aneurysms were dissected in each stage for light microscopic, electron microscopic, and histochemical research.</p><p><b>RESULTS</b>The effect of embolization was significantly better with WEDC than that with CAP (chi2 = 5. 56, P < 0.05). Post-embolized complications such as aneurysm rupture and stenosis of parent arteries could only be found in CAP group. Pathological research showed that CAP mass could packed the aneurysms more densely than coils. Acute chemical damage of aneurysmal wall and inflammatory cell infiltration was prominently found in early stage after CAP-embolization. Organization of thrombus inside aneurysms and formation of endothelial tissue over the orifices of aneurysmal necks could be found in both groups 2 months after embolization. But parts of coils might be exposed outside endothelial layer.</p><p><b>CONCLUSIONS</b>EDC are still the most safe, efficient, and reliable instruments to embolize aneurysm. CAP should be improved further to solve the problem of strong chemical corrosion and difficulty in control before it is widely used.</p>
Subject(s)
Animals , Dogs , Female , Male , Biocompatible Materials , Cellulose , Embolization, Therapeutic , Methods , Follow-Up Studies , Intracranial Aneurysm , Therapeutics , Random Allocation , Tungsten摘要
<p><b>OBJECTIVES</b>To investigate the findings of magnetic resonance (MR) imaging and histopathology in early postoperative normal brain, and to define the correlation between MR images and histopathology.</p><p><b>METHODS</b>Thirty-six New Zealand rabbits weighing 2.0 to 3.0 kg were divided into 10 groups according to different postoperative days: 1 to 10 days. A partial resection of the parietooccipital region was performed under usual aseptic conditions after the animals were anesthetized intravenously with 3% pentobarbital (30 mg/kg). MR imaging procedures consisted of pre- and postcontrast scanning and were carried out on postoperative days 1 to 10. Brain tissue samples were prepared for examination immediately after MR scanning. Histopathological examination was done under light both and electron microscopes. The findings of MR imaging were compared with histopathologic findings.</p><p><b>RESULTS</b>Surgical margin contrast enhancement on MR images could be seen 24 hours after surgery. The degree of contrast enhancement increased gradually up to 5 days postoperation, and no remarkable changes were present from days 5 to 10. Disruption of the blood brain barrier (BBB) was the main cause of contrast enhancement during the first 3 postoperative days. After that period, the mechanism responsible for contrast enhancement was the formation of neovascularity and a broken BBB. An increase in the amount of neovascularity played a predominant role in contrast enhancement in normal postoperative brain tissue.</p><p><b>CONCLUSIONS</b>The features of enhanced MR images present at the surgical margin followed a typical time course during the early postoperative period. The role of neovascularity and BBB disruption in the formation of contrast enhancement at the surgical margin varies with time. Knowledge of the features of contrast enhancement in postoperative MR images of normal brain can help in differentiating benign changes from residual malignant glioma.</p>
Subject(s)
Animals , Rabbits , Brain , Pathology , General Surgery , Dura Mater , Pathology , Edema , Pathology , Magnetic Resonance Imaging , Methods , Microscopy, Electron摘要
Objective To investigate the manifestations of MR imaging and histopathology of early postoperative normal brain, and to define the correlation between MRI and histopathology. Methods Thirty six New Zealand rabbits weighing 2.0 to 3.0 kg were divided into 10 groups according to the different postoperative days: 1 to 10 day. Six animals were in groups 3, 5, 7, 10, and 2 were in the other groups. A partial resection of the parietooccipital region was performed under the usual aseptic conditions after the animals were anesthetized intravenously with 3% pentobarbital (30 mg/kg). MR imaging procedures consisted of pre and postcontrast scanning were carried out on postoperative 1 to 10 day respectively. Brain tissue samples were obtained to be prepared for examinations immediately after MR scanning. Histopathological study was made under microscope and electron microscope. The findings of MRI were compared with pathology findings. Results (1) Surgical margin contrast enhancement on MR images could be seen 24 hours after surgery. (2) The degree of contrast enhancement increased gradually before 5 days postoperatively, and no remarkable changes were present from 5 to 10 days. (3) The disruption of blood brain barrier(BBB) is the main cause of contrast enhancement during the postoperative 3 days. After that period, mechanism responsible for contrast enhancement is the formation of neovascularity and broken BBB, an increase in the number of neovascularity play a predominant role in the contrast enhancement in normal postoperative brain tissue. Conclusion The characteristics of enhanced MRI present at the surgical margin followed a typical time course during the early postoperative period. The role of neovascularity and BBB disruption in the formation of contrast enhancement at surgical margin vary with time. Knowledge of the characteristics on postoperative MR images of the normal brain can help in differentiating benign changes from malignant gliomas residual.
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Objective To study on the ultrastructural characteristic of segments of photoreceptors from neonatal retinas for supporting donor retina choice of retinal transplantation. Methods Photoreceptors from neonatal calf and adult calf were analysed by scanning electron microscopy and transmission electron microscopy. Results Segments of photoreceptors from neonatal calf appeared the mushroom pattern, in which, distal end of outer segment which was ball shaped formed the head with mushrooms appea rance, and the inner segments along with some of outer segments formed the body with mushrooms appea rance. Within the outer segment, plasma membranes of adjacent evaginations form a disk subsequently. The array of most disks were vertical to the entire length of segments, but some were parallel and slope to. Owing to the incomplete formation, some rim of disk near distal end of outer segment revealed step shaped appearance. The distal end of outer segment displays some processes consisted of membranous discs, much vesicular material and mitochondria, much rough endoplasmic reticulum (RER) and numerous polysomes. Segments of photoreceptor connected with outer nuclear layer via the external limiting membrane. Conclusion The typical morphological structures of outer segments suggest the immature and strong gowth ability of photoreceptors of the retina of neonatal calf, and therefore the competence for donor material of retinal transplantation.
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Objective To investigate the CT manifestations of follicular thyroid adenoma.Methods CT manifestations of follicular thyroid adenoma proved by operation and pathology in 19 cases were analyzed retrospectively.Results Of 19 cases,5 cases were male and 14 cases were female,the average age was 36.6 years old.There were single focus in 17 and multiple focus in 2.All lesions were round or round-like.The lesions were homogeneous low density with smooth clear edges on plain CT scans.2 cases showed calcification in tumor.All cases had slight enhancement on contrast-enhanced CT scans.Conclusion CT manifestations of follicular thyroid adenoma are mostly typical which appear round or round-like,with clear smooth edges and most of which can be correctly diagnosed.
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The purpose of this experiment is to study the destiny of cancer cells and changes of lymph node after lymphatic metastasis.Ehrlich ascitic carcinoma cells were injected intradermally into the right footpad of mice. We try to estabilish a model about lymphatic metastasis in the popliteal lymph node.The lymph nodes of the drainage area were taken out at different time intervals and examined by light microscopy, transmission electron microscopy as well as scanning electron microscopy. Onehour after the injection cancer cells were found in the popliteal lymph node. Mitotic figures of cancer cells were discovered in fifth hours and the tumor cells had reached to second lymph node——lumber lymph node or parailiac lymph node. The metastasis were formed in 24 hours after injection. The tumor cells first migrated in the subcapsular sinus of lymph node, then they entered the intermediate and medullary sinuses. Besides, the lymph nodes showed active reactionary proliferation, hyperplasia of histocytes and enlargement of germinal centers after three days. There were many small lymphocytes assuming the form of active amebae, surrounding the postcapillary venules. Degeneration and necrosis of cancer cells was observed at same time.Under the electron microscope many lymphocytes were observed to adhere closely to the cancer cell and their Golgi apparatus and mitochondria were accumulated towards the cell memberane opposing the cancer cell, as if some substance were released to it.This experimental result showed that lymph node probably prosess ability to defend metastasis of cancer cells.