The ecological cause of the higher accumulation of 90Sr and 137Cs in the food of northern inhabitants

PURPOSE: To quantify S-antigen-specific (S-Ag) T cells in the retina after adoptive transfer, and to evaluate their role in the initiation and progress of destructive ocular inflammation in experimental autoimmune uveoretinitis (EAU). METHODS: Lewis rats were administered 10 x 10(6) S-Ag-specific T cells from the SP35 cell line or 10 x 10(6) concanavalin A-stimulated syngeneic spleen cell lymphoblasts labeled with lipophilic PKH26 fluorescent dye immediately before intravenous inoculation. Labeled cells in each retina were counted at various times from 4 to 120 hours after cell transfer by fluorescence microscopic analysis of each dissociated retina. Recipient eyes were examined within the same period by light and confocal microscope. RESULTS: SP35 T cells showed a biphasic distribution in the retina. The first peak of 160 cells/retina was noted at 24 hours. A steady decline of labeled cells at 48 and 72 hours was followed by a rapid increase at 96 and 120 hours. Concanavalin A-stimulated, control-labeled cell populations showed an identical peak at 24 hours but a persistent decline thereafter; only two or three T cells were present in each retina at 120 hours. Concurrent inoculation of SP35 cells and nonspecific T cell blasts did not produce more SP35 cells than control cells in the retina at any time. Microscopic analysis showed mononuclear cell infiltration of the iris, ciliary body, and aqueous humor at 48 hours, which intensified rapidly and persisted through 120 hours. Retinal inflammation did not begin until 80 hours. Mononuclear cell adherence to vascular endothelium and perivascular macrophage infiltration of the innermost layers progressed to edema, and profound destructive inflammation and loss of retinal stratification were observed at 120 hours. CONCLUSIONS: There is no evidence of a blood-ocular or blood-retinal barrier to activated T cell blasts. Autologous S-Ag does not provoke a more rapid entry of specific T cells at that site. The data confirm that anterior segment inflammation precedes retinal inflammation, even though S-Ag-specific T cells were present in the retina within a few hours after cell transfer. Because S-Ag is clearly present in the retina, delay in antigen presentation at that site may account for the temporal difference between retinal and anterior segment inflammation.     

Sweat gland carcinoma of the foot: a review and patient report

PURPOSE: To determine the accuracy of applanation tonometry in patients with corneas thinned by photorefractive keratectomy, and to correlate corneal changes with tonometric readings. METHODS: The intraocular pressure was measured with Goldmann applanation tonometry in 87 patients who underwent photorefractive keratectomy before and 1, 6 and 12 months after treatment. The treatments ranged from -1.5 to -14 diopters (mean=-7.6+/-4.1 diopters) and the fellow eyes were used as controls. RESULTS: In the treated eyes the intraocular pressure before surgery ranged from 11 to 26 mmHg (mean=17.7+/-2.8 mmHg). One month after surgery it ranged from 5 to 22 mmHg (mean=11.9+/-2.7 mmHg) with a significant underestimation (P=1x10(-33)). Six months after surgery it ranged from 6 to 22 mmHg (mean=12+/-3 mmHg) with a significant underestimation (P=5x10(-30)). Twelve months after surgery it ranged from 8 to 22 mmHg (mean=12.7+/-2.7 mmHg) with a significant underestimation (P=5x10(-31)). CONCLUSIONS: A correcting factor should be applied when using applanation tonometry to measure intraocular pressure in patients who have undergone PRK.     

Functional characterization of transforming growth factor beta type II receptor mutants in human cancer

We recently identified missense mutations at amino acid residues 526 and 537 located within the highly conserved subdomain XI of the transforming growth factor beta type II receptor (TbetaR-II) serine-threonine kinase in two human squamous carcinoma cell lines. These cell lines are resistant to transforming growth factor beta-mediated inhibition of growth. Moreover, treatment with transforming growth factor beta fails to increase the levels of type 1 plasminogen activator inhibitor and fibronectin synthesis. To test the effects of the mutations on receptor function, mutant TbetaR-II cDNAs were expressed in TbetaR-II-deficient T47D cells. Cyclin A promoter activity was reduced by 50% in cells expressing wild-type TbetaR-II but increased 2-fold in cells transfected with either of the two mutant receptors. Conversely, plasminogen activator inhibitor type 1 promoter activity was increased 6-fold in cells transfected with wild-type receptor but not with either of the two mutant receptors. Moreover, the activity of both mutant serine-threonine kinases was strongly reduced compared to that of the wild-type receptor. Thus, the amino acid residues at positions 526 and 537 seem to be essential for kinase function and signaling activity of the TbetaR-II.     

The role of the eicosanoids in the development of a postischemic shock reaction

The role of eicosanoids as one of the main shock mediators was demonstrated in experiments anesthetized dogs with modeled postischemic shock using premedication with indometacin and/or quercetin. Preliminary administration of the eicosanoid biosynthesis inhibitors has prevented reperfusion hemodynamics disturbances during 3 hours after the beginning of an extremity reperfusion. The presented results confirm vascular endothelium injury in the investigated areas, which caused disbalance in the necessity-flow balance in working organs. Therefore, a damage in the endotheliocytes function is the first and, probably, a leading factor in development of the postischemic disturbances of circulation.     

The protective reaction of the myocardium to ischemic damage

The morphological and functional consequences of epinephrine-induced myocardial infarction were studied in normo- (Wistar) and hypertensive (ISIAH) rats. After experimental myocardial infarction there was an irreversible transition to the "worn-out" stage or "plastic damage" to the myocardium. Thus, myocardial hibernation in ISIAH rats anticipates and determines the development of myocardial stunning, i.e., irreversible myocardial damage, whereas in the normotensive animals, the protective effect of hibernation is fully shown. The ontogenetic features of myocardial response of ISIAH rats to hypoxia promote transformation of adaptive hibernation and stunning to maladaptive pathological changes causing hypoxic alterations.     

Mutational analysis of N-RAS and GAP-related domain of the neurofibromatosis type 1 gene in chronic myelogenous leukemia

RAS mutations can be detected in a variable number of patients with myeloproliferative disorders such as myelodysplastic syndromes and acute myeloid leukemia, but are rare events in chronic myelogenous leukemia in chronic phase. However, there is good evidence supporting the involvement of RAS signalling pathway in CML and this could be due to alterations in RAS activity regulatory proteins. The neurofibromatosis (NF1) gene down-regulates the RAS signal transduction pathway through the inhibitory function of its GAP-related domain (GRD) on RAS protein. The loss or alteration of neurofibromin (the NF1 protein) may produce a disfunction similar to point mutations in the RAS gene resulting in the permanent stimulation of the RAS signal transduction pathway. Mutations involving the GRD region of the NF1 gene (GRD-NF1) have been described in a variety of tumors such as colon carcinoma and astrocytoma. Germline mutations and deletions in the NF1 gene, as seen in neurofibromatosis type 1, are also associated with certain myeloid disorders. In the present work, we sought to identify mutations in the codons 12/13 and 61 of RAS gene and in the Lys-1423 codon of GRD-NF1, which are well known hot spots in these genes, in a group of 36 adults and ten children with chronic myelogenous leukemia in chronic phase and blast crisis. Using the PCR-SSCP and the allele-specific restriction assay (ASRA) techniques, we were not able to observe any RAS or NF1 detectable mutation. These findings suggest that RAS and GRD-NF1 mutations are not involved either in chronic phase or in the progression to blast crisis in chronic myelogenous leukemia in adults and children.     

Complex assessment of inhacort effectiveness in bronchial asthma

AIM: To investigate efficiency of inhacort in long-term (6 months to 2 years) treatment of bronchial asthma (BA). MATERIALS AND METHODS: 67 inpatients and 65 outpatients with moderate BA were divided into two groups. 96 patients of group 1 had received standard combined treatment without glucocorticosteroids (GCS), 36 patients of group 2 had received GCS. Inpatients were given inhacort in a dose 1000 micrograms/day, outpatients took inhacort in a daily dose 500 micrograms/day. The examination scheme included assessment of external respiration function (ERF), blood hydrocortisone, sputum rheology and diagnosis of candidosis. RESULTS: Inhacort treatment has reduced frequency of asphyxia attacks 2.5-fold 30 and 25% of the patients stopped taking sympathomimetics and GCS, respectively. None of the patients had asphyxia as a status. ERF, sputum viscosity improved, hydrocortisone secretion was unchanged. Only 3.8% of the patients developed oral candidosis. CONCLUSION: Inhacort in a dose 1 mg controls BA. 73% of the patients treated outpatiently had no need in hospitalization.