Dynamics of Cytotoxic T Lymphocyte Precursors in Vivo Assessed by Change in the Radiation Sensitivity

The dynamics of cytotoxic T lymphocyte precursors (CTL-p) in mice injected with allogeneic spleen cells (SC) was studied with special reference to changes in their radiation sensitivity. Whole-body 400 rad X-ray irradiation of allo-SC-primed and unprimed mice virtually abolished the capacity of their SC to proliferate and to generate CTL in primary or secondary mixed leucocyte culture (MLC). However, the impaired ability of SC to generate CTL in the primary MLC was restored by interleukin 2 (IL-2). This showed that helper cells whose activity was replaceable with IL-2 (IL-2-producing cells) were functionally more radiation-sensitive than CTL-p in unprimed mice. In contrast, the radiation-impaired activity in secondary MLC was not restored by IL-2, suggesting that memory CTL-p in allo-SC-primed mice were unexpectedly sensitive to radiation. The D37 values determined from the percentage of residual CTL-p activity of SC in bulk cultures 1 day after irradiation were 525 rad for virgin CTL-p and 75 rad for memory CTL-p. Further studies demonstrated that the radiation-sensitive memory CTL-p were generated from relatively radiation-resistant precursors, largely independent of radiation-sensitive IL-2-producing cells and of cellular proliferation. The mean frequency of CTL-p in SC measured by limiting dilution assay was not significantly increased by the priming. This supports our conclusion that the development of the memory CTL-p activity in allo-SC-primed mice did not depend on clonal expansion. Whole-body 400 rad-irradiation reduced the frequency of CTL-p in SC from unprimed mice to 1/2-1/3 and that in SC from allo-SC-primed mice to 1/8-1/15. This supports the view that the majority of radiation-resistant virgin CTL-p functionally mature to radiation-sensitive memory CTL-p without cellular proliferation in allo-SC-primed mice.     

Multiple pulmonary nodules after recovery from chickenpox in a patient with chronic lymphocytic leukaemia

Abstract A 61-year-old woman with chronic lymphocytic leukaemia (CLL) was found to have multiple pulmonary nodules on an annual chest radiograph 4 months after recovery from chickenpox. To exclude the metastatic carcinoma, an open lung biopsy was performed. Histological examination disclosed isolated necrotic nodules surrounded by some lymphocytes and a few giant cells. These histological findings were compatible with healed varicella pneumonia and the DNA of varicella-zoster virus (VZV) was detected by polymerase chain reaction (PCR) method. We report a case of asymptomatic pulmonary involvement of VZV infection in a patient with CLL.     

Cerebral Hyperperfusion Syndrome following the Excision of a Mycotic Aneurysm with Superficial Temporal Artery-to-Middle Cerebral Artery Bypass: Case Report

The authors report a rare case of cerebral hyperperfusion syndrome (HPS) following the excision of a mycotic aneurysm with superficial temporal artery-to-middle cerebral artery (STA-MCA) bypass. A 74-year-old woman with infective endocarditis presented with progressive cerebral infarction and subarachnoid hemorrhage due to a mycotic aneurysm, which was excised with a STA-MCA bypass. Postoperatively, the patient developed HPS that was considered to be exacerbated by a previous ischemic event. Therefore, cerebral hemodynamics should be evaluated before bypass surgery to prevent subsequent hyperperfusion.     

Reactivity of stage-specific monoclonal antibody 1G7 with metacyclic trypomastigotes of Trypanosoma cruzi strains: lytic property and 90 000 mol. wt surface antigen polymorphism

Eleven strains of Trypanosoma cruzi, originating from a variety of vertebrate and invertebrate hosts in distinct geographical regions, were examined for the reactivity of metacyclic stages with the monoclonal antibody 1G7. Trypomastigotes of five strains were susceptible to complement-dependent 1G7-mediated lysis. Higher levels of 1G7 bound to metacyclics of lysis-susceptible strains as compared to lysis-resistant isolates. Excluding Y and CL strains, 1G7 reacted with metacyclics of all T. cruzi isolates by binding to a 90,000 mol. wt surface polypeptide. A 90,000 mol. wt protein lacking the 1G7-specific epitope but immunologically related to the 90,000 mol. wt antigen of other T. cruzi isolates is present in Y and CL strains. The intensity of the 90,000 mol. wt band, detected by surface iodination of metacyclics or in immunoblots using the monoclonal antibody 1G7 or the monospecific antiserum to 90,000 mol. wt protein, varied among different strains and also a discrete variation was observed in its molecular weight. The overall analysis reveals a polymorphism of the 90,000 mol. wt protein, which is ubiquitous among the different T. cruzi isolates.     

Enhanced arterial intimal thickening after balloon catheter injury in diabetic animals accompanied by PDGF β-receptor overexpression of aortic media

Abstract. Cultured aortic smooth muscle cells (SMC) of diabetic rats and rabbits, which overexpress platelet-derived growth factor (PDGF) β -receptor compared with controls, have a unique phenotype. In this study we report on the PDGF β -receptor overexpression in aortas of diabetic animals and the increased intimal thickening of carotid arteries in diabetic rabbits after balloon catheter injury compared with that in controls. In diabetic aortas with no treatments of balloon catheter injury, intimal thickening was not observed in spite of the overexpression of PDGF β -receptor, indicating that the growth property of medial SMC in diabetic aortas was changed before the intimal thickening could take place. PDGF is known to be the main contributor to the intimal thickening induced by balloon catheter injury, which is one of several forms of arterial injuries. Intimal thickening after balloon catheter injury in diabetic rabbits increased compared with that in controls. These results imply that PDGF β -receptor overexpression of SMC in medial layers plays an important role in intimal thickening in the formation of advanced diabetic macroangiopathy.