|
1. |
IMMUNOLOGICAL STABILITY OF AN ELAPID VENOM,TROPIDECHIS CARINATUS, AND ITS RELEVANCE TO THE CLINICAL DETECTION OF SNAKE VENOM |
|
Australian Journal of Experimental Biology and Medical Science,
Volume 61,
Issue 5,
1983,
Page 489-495
JJ Morrison,
JH Pearn,
AR Coulter,
WJ Halliday,
Preview
|
PDF (1389KB)
|
|
摘要:
SummaryUsing immunological techniques, cases of human snake‐bite can be proven and individual snake species identified, A series of experiments is described, to test the antigenic stability and physical properties of an Elapid venom, venom properties which will have implications in field use. transport, or the laboratory procedures relating to the immunological characterization of Australian snake venoms. Using venom from the Elapid,Tropidechis carinatus, we have demonstrated significant immunological stability at a temperature of 37° for 48 h at least, and for 24 h at least when incubated continuously with skin, muscle, and fat homogenates; the venom is stable at 56° for 2 h at least. No loss of venom occurs over the pH range 7‐10; at ph ranges10 only 30% of venom is detected after 30 min incubation. Sonication (10 min at 100 watts) does not destroy immunological properties of the venom; 10 freeze‐thaw cycles result in some 9% loss of immunologically detectable activity. Venom is adsorbed significantly on to dacron swabs, only 13% of the applied dose being detected after 48 h incubation at 28°. Sixty‐seven percent of applied venom can be recovered from the skin of human volunteers 6 h after a simulated bite. The venom of this Elapid is antigenically robust. With the currently available sensitive assays, venom from human skin should still be detected in material kept without special preparation under field conditions for up to 2 days at least.
ISSN:0004-945X
DOI:10.1038/icb.1983.46
出版商:Nature Publishing Group
年代:1983
数据来源: WILEY
|
2. |
GROWTH OF ORGAN‐CULTURED FOETAL MOUSE PANCREAS GRAFTS IN SYNGENEIC DIABETIC AND NON‐DIABETIC RECIPIENTS |
|
Australian Journal of Experimental Biology and Medical Science,
Volume 61,
Issue 5,
1983,
Page 497-508
TE Mandel,
Preview
|
PDF (3015KB)
|
|
摘要:
SummaryOrgan‐cultured foetal mouse pancreatic islets can reverse streptozotocininduced diabetes in syngeneic mice. Tissue from one donor is enough to produce and maintain euglycaemia in each recipient, but even smaller amounts of donor tissue may be sufficient and less than one third of a foetal pancreas frequently suffices. Insulin extracted from grafts removed after some monthsin situshows that their insulin content is proportional to the amount of tissue transplanted, and suggests that the grafted foetal islets have a finite capacity for growth. In organ culture some loss of potential islet tissue may occur, and larger grafts are obtained when small pieces of tissue are cultured, thereby minimizing losses of tissuein vitro. The growth of the graftin situalso depends on the diabetic state of the host, and greater and more prolonged mitotic activity is seen in grafts in diabetic than in non‐diabetic recipients, A degree of hyperglycaemia in the recipient may enhance graft growth.
ISSN:0004-945X
DOI:10.1038/icb.1983.47
出版商:Nature Publishing Group
年代:1983
数据来源: WILEY
|
3. |
A COMPARISON OF EPSTEIN‐BARR VIRUS‐SPECIFIC T‐CELL IMMUNITY IN RHEUMATOID ARTHRITIS AND OSTEOARTHRITIS PATIENTS |
|
Australian Journal of Experimental Biology and Medical Science,
Volume 61,
Issue 5,
1983,
Page 509-516
DJ Moss,
A Klestov,
S Burrows,
RG Kane,
Preview
|
PDF (482KB)
|
|
摘要:
SummaryThe level of Epstein‐Barr virus (EBV)‐specific T‐cell‐mediated immunity in 20 rheumatoid arthritis (RA) patients was compared with 16 age‐and sex‐matched osteoarthritis (OA) patients using the regression of EBV‐transformation assay. The results show that the level of EBV‐specific T‐cell immunity in RA patients is significantly depressed compared with OA patients (P<.001) or healthy laboratory controls (P<.001). In contrast, lymphocytes from RA and OA patients showed a similar ability to act as a responder population in the mixed leucocyte reaction. It is unlikely that the difference in EBV‐specific immunity is due to a general T‐cell defect in RA patients since there was no correlation between EBV‐specific T‐cell immunity and mixed leucocyte reactivity. There was no correlation between EBV‐specific T‐cell immunity and any of the indicators of disease activity nor was there any difference in the anti‐EBV antibody titre between both groups of patients. These results indicate that RA patients are deficient in the EBV‐specific cytotoxic T‐cell precursor population and may explain some of the reported observations of the involvement of EBV in this disease.
ISSN:0004-945X
DOI:10.1038/icb.1983.48
出版商:Nature Publishing Group
年代:1983
数据来源: WILEY
|
4. |
STABILIZATION OF ISLET ALLOGRAFTS BY TREATMENT OF RECIPIENTS WITH ULTRAVIOLET IRRADIATED DONOR SPLEEN CELLS |
|
Australian Journal of Experimental Biology and Medical Science,
Volume 61,
Issue 5,
1983,
Page 517-527
Michael Agostino,
Stephen J Prowse,
Kevin J Lafferty,
Preview
|
PDF (2475KB)
|
|
摘要:
SummaryCulture of mouse pancreatic islets in an oxygen‐rich atmosphere before transplantation facilitates long‐term allograft survival without the use of immunosuppression. A comparison of the capacity of ultraviolet (UV) irradiated and live spleen cells of donor origin to induce allograft rejection showed that UV‐irradiated spleen cells were not immunogenic: live spleen cells were immunogenic and their injection triggered allograft rejection. Following treatment with irradiated spleen cells from about day 30 post‐transplantation, recipient animals were able to withstand subsequent challenges with 106and 107viable donor spleen cells. Untreated animals rejected their graft when challenged with 106donor spleen cells. That is. treatment with UV‐irradiated cells stabilized the islet allograft by inducing a state of tolerance. Subsequent transplantation of stabilized animals with uncultured thyroids of both donor origin and from a third party strain demonstrated that the tolerance was specific.In vitrotest of immune reactivity showed this tolerance was not due to the deletion of antigen reactive cells.
ISSN:0004-945X
DOI:10.1038/icb.1983.49
出版商:Nature Publishing Group
年代:1983
数据来源: WILEY
|
5. |
CELL‐MEDIATED IMMUNE RESPONSE TO ROSS RIVER VIRUS IN MICE: EVIDENCE FOR A DEFECTIVE EFFECTOR CELL RESPONSE |
|
Australian Journal of Experimental Biology and Medical Science,
Volume 61,
Issue 5,
1983,
Page 529-540
JG Aaskov,
DA Dalglish,
CEA Davies,
M Tucker,
MD Donaldson,
Preview
|
PDF (2939KB)
|
|
摘要:
SummarySpleen cells recovered from mice during a primary infection with Ross River virus showed a virus‐specific proliferative response when challengedin vitro. The majority of the proliferating cells were T‐lymphocytes. In contrast, there was liltle detectable migration inhibition factor produclion by these spleen cells and little or no virus‐specific cytotoxic activity. Sub‐cutaneous challenge with virus elicited a weak delayed type hypersensitivity reaction.
ISSN:0004-945X
DOI:10.1038/icb.1983.50
出版商:Nature Publishing Group
年代:1983
数据来源: WILEY
|
6. |
FAILURE TO MODIFY ANTI‐P2 REACTIVITY IN LONG‐TERM (P1 × P2)F1→P1 RADIATION CHIMERAS BY TOTAL LYMPHOID CELL ABLATION: IMPLICATIONS FOR THE ROLE OF THYMIC ANTIGEN‐PRESENTING CELLS |
|
Australian Journal of Experimental Biology and Medical Science,
Volume 61,
Issue 5,
1983,
Page 541-544
RB Ashman,
PF Gallagher,
Preview
|
PDF (239KB)
|
|
ISSN:0004-945X
DOI:10.1038/icb.1983.51
出版商:Nature Publishing Group
年代:1983
数据来源: WILEY
|
7. |
THE EFFECT OF CEREBRAL ISCHEMIA ON THE ULTRASTRUCTURE OF THE HYPOTHALAMO‐NEURO‐HYPOPHYSIAL SYSTEM OF THE MONGOLIAN GERBIL. THE SUPRAOPTIC AND PARAVENTRICULAR NUCLEI |
|
Australian Journal of Experimental Biology and Medical Science,
Volume 61,
Issue 5,
1983,
Page 545-556
Andrzej Loesch,
Preview
|
PDF (3185KB)
|
|
摘要:
SummaryThe results of ultrastructural studies of thc nucleus supraopticus (SON) and n. paraventricularis (PVN) of male mongolian gerbils subjected to experimental cerebral ischemia induced by 10 min bilateral occulsion of the common carotids are reported. Marked alterations concerned endocrine neurons. some neurosecretory axons and synaptic terminals as well as astroglia cells. Basing on the electron density of cytoplasmic ground, two varieties of endocrine neurons, that is ‘light’ and ‘intermediate’, were designated in both SON and PVN nuclei. These findings suggest that during cerebral ischemia the SON and PVN neurons become activated (Golgi complex and granular endoplasmic reliculum enlargement) and that they represent different phases of secretory cycle of a single cell type. However, in SON nucleus some neurons were probably damaged because they had the appearance of decidedly ‘dark’ cells. With respect to some neurosecretory axons, the finding of externally lying lamellar whorls indicates ischemic injury of the axons. Similar significance may be attributed to some synaptic terminals which showed an increased polymorphism of synaptic vesicles and vesicular aggregation. There was marked swelling of perivascular astroglia cells and change of their cytoplasm in both SON and PVN nuclei. Moreover, the swollen astroglia cells contacted those ‘dark’ neurons in SON nucleus. The present study indicates that SON and PVN nuclei are highly sensitive to application of cerebral ischemia. At the same time perivascular injury may suggest involvement of astroglia cells in the production of subsequent changes in the SON and PVN neuropil.
ISSN:0004-945X
DOI:10.1038/icb.1983.52
出版商:Nature Publishing Group
年代:1983
数据来源: WILEY
|
8. |
THE EFFECT OF CEREBRAL ISCHEMIA ON THE ULTRASTRUCTURE OF THE HYPOTHALAMO‐NEURO‐HYPOPHYSIAL SYSTEM OF THE MONGOLIAN GERBIL. THE NEUROHYPOPHYSIAL AXONS AND PITUICYTES |
|
Australian Journal of Experimental Biology and Medical Science,
Volume 61,
Issue 5,
1983,
Page 557-568
Andrzej Loesch,
Preview
|
PDF (3215KB)
|
|
摘要:
SummaryThe results of ultrastructural studies of the neurohypophysial axons atid pituicytes of male mongolian gerbils subjected to experimental cerebral ischemia induced by 10 min bilateral occlusion of the common carotids are reported. In gerbils with cerebral ischemia some neurohypophysial axons were well preserved and, as regards ultrastructural organization, did not differ from the control animals. Some axons showed ultrastructural changes. They were characterized by depletion of dense cored neurosecretory granules and the appearance of optically empty vesicles. These suggest the increased secretion of neurohypophysial hormones. Moreover, the findings of intra‐axonal large multilamellar bodies and externally lying tightly arranged lamellar whorls (similar to myelin sheath) were linked with simultaneous obliteration of the primary structure of certain axons. The neurohypophysis of the animals subjected to cerebral ischemia revealed the presence of ‘light’ (‘fibrillar’) and ‘dark’ pituicytes. The ‘light’ cells were characterized by large Golgi complex and the presence of fine fibrilles or fibrillar bundles which occupied a large cytoplasmic area of the cell body or of the processes. The finding of accumulated fibrilles suggests the ischemia damage of the cells. The ‘dark’ cells revealed the presence of dense cytoplasmic ground and the lobulated nucleus. In these cells ribosomes were predominant. The mitochondria were swollen in both varieties of pituicytes, arbitrarily designated here as ‘light’ (‘fibrillar’) and ‘dark’. The results of the present study, therefore, indicate a functional susceptibility of neurosecretory axons and pituicytes to haemodynamic disturbances associated with bilateral cerebral ischemia.
ISSN:0004-945X
DOI:10.1038/icb.1983.53
出版商:Nature Publishing Group
年代:1983
数据来源: WILEY
|
9. |
RECEPTOR‐MEDIATED125I‐LABELLED INSULIN DEGRADATION IN THE RAT HEPATOCYTE. STUDIES USING CHLOROQUINE |
|
Australian Journal of Experimental Biology and Medical Science,
Volume 61,
Issue 5,
1983,
Page 569-579
Anne M Bonser,
Peter Garcia‐webb,
Chotoo I Bhagat,
Preview
|
PDF (2529KB)
|
|
摘要:
SummaryDegradation of insulin during incubation with target cells occurs via receptor‐mediated processes. In this study, receptor‐mediated degradation of125I‐labelled insulin was investigated in rat hepatocytes, using the agent chloroquine.Chloroquine increased specific cell‐associated125I‐labelled insulin at 37°. The increased radioactivity with chloroquine was intracellular (53.3 ± 1.2% of initially bound label was displaced by excess cold insulin; in control cells 67.0±2.1 % was displaced. P<0.005). The effect of chloroquine was prevented by adding label at 15° or by pre‐treatment with 5 mM KCN, 5 mM NaN3or 1 g/1 bacitracin, which indicated a post‐internalization site of action. Chloroquine had no effect on degradation of125I‐labelled insulin in buffer alone or in buffer previously incubated with cells. Specific studies of receptor‐mediated degradation at 37° showed that more125I‐labelled insulin remained associated with hepatocytes when chloroquine was present (P<0.0005 after 60 min). Analysis of chloroquine's effect on the intactness of125I‐labelled insulin released during processing of surface‐bound label at 37° showed that chloroquine‐sensitive mechanisms accounted for at least 50% of receptor‐mediated insulin degradation in rat hepatocytes.
ISSN:0004-945X
DOI:10.1038/icb.1983.54
出版商:Nature Publishing Group
年代:1983
数据来源: WILEY
|
10. |
STARVATION IN THE RAT: EFFECT ON PEPTIDES OF THE GUT AND BRAIN |
|
Australian Journal of Experimental Biology and Medical Science,
Volume 61,
Issue 5,
1983,
Page 581-587
A Shulkes,
Y Caussignac,
CB Lamers,
TE Solomon,
T Yamada,
JH Walsh,
Preview
|
PDF (416KB)
|
|
摘要:
SummaryThe effects of starvation on the tissue concehtrations of some peptides common to the gastrointestinal tract and the central nervous system have been examined. Groups of 6 rats were either fedad libitumor starved for up to 4 days and killed by decapitation. Antrum, fundus, duodenum, jejunum, ileum, colon, pancreas and brain were dissected, weighed and then frozen on dry ice. The tissues were extracted sequentially in boiling water and 3% acetic acid, centrifuged and the supernatants radioimmunoassayed for gastrin, cholecystokinin (CCK), vasoactive intestinal peptide (VIP), gastric inhibitory peptide (GIP) and soma‐tostatin. Each peptide was not assayed in each tissue. Starvation had no effect on the concentrations of peptides measured in the fundus (somatostatin and VIP), ileum (somatostatin, GIP, VIP) and colon (somatostatin, GIP, VIP). VIP concentration was increased in the jejunum and GIP was increased in both the duodenum and jejunum. Antral gastrin was the only peptide in the gastrointestinal tract to be decreased by food deprivation. Somatostatin concentration was approximately doubled in the antrum, duodenum, jejunum and pancreas. Brain VIP was unchanged. Brain somatostatin and CCK were significantly reduced by starvation. We conclude that starvation results in organ‐specific and hormone‐specific alterations in tissue concentrations of peptides of the gastrointestinal tract and the central nervous system.
ISSN:0004-945X
DOI:10.1038/icb.1983.55
出版商:Nature Publishing Group
年代:1983
数据来源: WILEY
|
|