Hydrocephalus induced by immunological blockage of the subcommissural organ–Reissner's fiber (RF) complex by maternal transfer of anti-RF antibodies

Stenosis of the cerebral aqueduct seems to be a key event for the development of congenital hydrocephalus. The causes of such a stenosis are not well known. Overholser et al. in 1954 (Anat Rec 120:917-933) proposed the hypothesis that a dysfunction of the subcommissural organ (SCO) leads to aqueductal stenosis and congenital hydrocephalus. The SCO is a brain gland, located at the entrance of the cerebral aqueduct, that secretes glycoproteins into the cerebrospinal fluid that, upon release, assemble into a fibrous structure known as Reissner's fiber (RF). By the permanent addition of new molecules to its rostral end, RF grows and extends along the aqueduct, fourth ventricle, and central canal of the spinal cord. The immunological blockage of the SCO-RF complex has been used to test Overholser's hypothesis. The following was the sequence of events occurring in pregnant rats that had been immunized with RF glycoproteins: the mother produced anti-RF antibodies and transferred them to the fetus through the placenta and to the pup through the milk, and the antibodies reached the brain of the fetus and pup and blocked the SCO-RF complex. This resulted in a permanent absence of RF that was followed by stenosis of the cerebral aqueduct, and then by the appearance of hydrocephalus. The latter was patent until the end of the 6-month observation period. The chronic hydrocephalic state appeared, in turn, to induce new alterations of the SCO. It is concluded that a selective immunological knock out of the SCO-RF complex leads to hydrocephalus.     

Central effects of aldosterone infused into the rat subcommissural organ region

D-Aldosterone (5 ng/microliter/h) was infused for 6 days into the region of the subcommissural organ (SCO) of conscious, adult male Sprague-Dawley rats. Aldosterone increased urinary sodium loss and the sodium/potassium ratio. Although probably central in origin, these effects still occurred when cannulae were displaced up to 1 mm from the targeted SCO placement. Aldosterone decreased adrenal medullary cross-sectional area without affecting cell density. This effect was highly dependent on proper cannula placement and was not observed when the cannula tip was not in contact with the cerebrospinal fluid of the pineal recess over the rostral two-thirds of the SCO. We conclude that aldosterone increases sodium excretion by an action in the SCO and/or adjacent structures. We also postulate a negative trophic relationship between mineralocorticoids and the adrenal medulla mediated by the SCO.     

Isolation of rhinoviruses and coronaviruses from 38 colds in adults

Nasal washings were collected from 27 normal adults during 38 naturally acquired colds. The washings were exhaustively tested using tissue cultures, organ cultures and electron microscopy. Washings yielding no identifiable agent were inoculated into human volunteers, and further specimens obtained from the latter were examined by the same techniques in vitro. Viruses were identified in association with 25 of the original 38 colds (65.7%). Fifteen were rhinoviruses (39.5%), seven coronaviruses (18.4%), two were para-influenza viruses, and one was influenza virus. Use of organ cultures and of volunteers significantly increased the isolation rate. No agent was cultivated from the remaining 13 specimens, although tests in volunteers showed that cold-producing agents were present in five of them (13%). Three specimens gave doubtful results in volunteers, and five others, all collected within a period of six weeks in December and January, apparently contained no infectious agent.     

Selective accumulation of monoclonal antibodies against neurospecific enolase in brain tissue of rats with middle cerebral artery occlusion

Preparations of I¹²⁵-labeled monoclonal antibodies against neurospecific enolase and mouse plasma IgG1 were injected intravenously to rats immediately after unilateral occlusion of the middle cerebral artery. Radioactivity of I¹²⁵-labeled monoclonal antibodies against neurospecific enolase in the brain tissue progressively increased, reached a maximum by the 48th hour, and remained practically unchanged after 72 h. At the same time radioactivity of labeled IgG1 in the brain tissue and radioactivity of both preparations in the blood, liver, spleen, kidneys, heart, and lungs decreased over 72 h. Selective accumulation of I¹²⁵-labeled monoclonal antibodies against neurospecific enolase was less significant in the brain tissue of the contralateral hemisphere and cerebellum not exposed to ischemia.Translated from Byulleten Eksperimentalnoi Biologii i Meditsiny, Vol. 138, No. 10, pp. 388–392, October, 2004     

Sensitivity of mouse,rat, and human embryonic lungs to the action of nitrosomethylurea in organ culture

In response to the direct action of nitrosomethylurea (NMU) in a concentration of 0.05 mg/ml on organ cultures of embryonic lungs of strain A mice, Wistar rats, and man, a varied degree of degenerative changes and hyperplastic proliferation of the epithelium developed in the cultures. In the early stages of the experiment the toxic effect of the cultures predominated. Tissue of rat embryonic lungs was most sensitive to the toxic action of NMU, mouse lung tissue least sensitive. The frequency of hyperplastic proliferation, on the other hand, was highest in cultures of mouse lungs and lowest in cultures of rat lungs. During culture the sensitivity of the human and rodent embryonic lungs to the toxic action of NMU decreased when the substance was repeatedly added to the nutrient medium. Meanwhile an increase in the survival of the experimental cultures was observed compared with the intact control.Department of Carcinogenic Agents, Oncologic Scientific Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR L. M. Shabad.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 84, No. 9, pp. 349–352, September, 1977.     

Interaction between the septal area and the subfornical organ in the control of water intake induced by thirst-eliciting procedures

Rats bearing lesions in the septal area followed by lesions in the subfornical organ were submitted to various thirst-eliciting procedures. The rats with hyperdipsia induced by lesions of the septal area drank more water than either during the control period or after lesion of the subfornical organ under the same thirst-eliciting or angiotensin-liberating stimuli (polyethyleneglycol, isoproterenol, water deprivation and ligation of the inferior vena cava). The overdrinking elicited by lesions in the septal area was blocked after lesion of the subfornical organ. Neither hypovolemia, nor hypotension or water deprivation could elicit increased water intake in animals whose subfornical organ had been destroyed. Animals with lesions in the subfornical organ showed decreased water intake after cellular dehydration. The results obtained suggest that the subfornical organ acts as a more important structure than the septal area in the regulation of water intake elicited by angiotensin, with two opposite effects: a direct one facilitating water intake, and an indirect one inhibiting the septal area. The septal area has an inhibitory effect on the subfornical organ and on water intake.     

器官培养在研究人食管上皮癌变中的应用

将组织块置于明胶海绵上,摇摆器官培养,4～6周后成人食管粘膜仍保持良好的结构形态,具有活跃生长的上皮细胞和良好的腺体结构;将组织块贴壁,静置外植块—细胞培养,成人食管粘膜和胎儿食管组织块可存活2～3个月,提供大量生长旺盛的上皮细胞。成人食管癌旁粘膜培养利于观察细胞癌前改变,可能较易于诱发癌变;胎儿食管具有正常背景,利于研究细胞癌变的全过程.二者配合可组成研究人食管上皮癌变的完整体外实验系统。     

Human liver stem cell-derived extracellular vesicles reduce injury in a model of normothermic machine perfusion of rat livers previously exposed to a prolonged warm ischemia

Livers from donors after circulatory death (DCD) are a promising option to increase the donor pool, but their use is associated with higher complication rate and inferior graft survival. Normothermic machine perfusion (NMP) keeps the graft at 37°C, providing nutrients and oxygen supply. Human liver stem cell-derived extracellular vesicles (HLSC-EVs) are able to reduce liver injury and promote regeneration. We investigated the efficacy of a reconditioning strategy with HLSC-EVs in an experimental model of NMP. Following total hepatectomy, rat livers were divided into 4 groups: (i) healthy livers, (ii) warm ischemic livers (60 min of warm ischemia), (iii) warm ischemic livers treated with 5 × 10⁸ HLSC-EVs/g-liver, and (iv) warm ischemic livers treated with a 25 × 10⁸ HLSC-EVs/g-liver. NMP lasted 6 h and HLSC-EVs (Unicyte AG, Germany) were administered within the first 15 min. Compared to controls, HLSC-EV treatment significantly reduced transaminases release. Moreover, HLSC-EVs enhanced liver metabolism by promoting phosphate utilization and pH self-regulation. As compared to controls, the higher dose of HLSC-EV was associated with significantly higher bile production and lower intrahepatic resistance. Histologically, this group showed reduced necrosis and enhanced proliferation. In conclusion, HLSC-EV treatment during NMP was feasible and effective in reducing injury in a DCD model with prolonged warm ischemia.