C3 Deposition in IgA Nephropathy in Children and Adolescents

The aim of this study was to assess the significance of C3 deposition in IgA nephropathy in children and adolescents. One hundred and two patients aged 5–21 years (57 male and 45 female) were studied. The findings of C3 deposition were classified into 8 groups by immunofluorescent (IF) pattern and intensity as follows: group MC3+ (N = 12): mesangiocapillary pattern and 3+ in intensity; group MC2+ (N = 13): mesangiocapillary and 2+; group MC1 + (N = 4): mesangiocapillary and 1 +; group M3+ (N = 11): mesangial and 3+; group M2+ (N = 24): mesangial and 2+; group M1 + (N=18): mesangial 1 +; group S (N = 12): only segmentally positive; and group N (N = 8): negative. Histological changes were scored semiquantitatively as an activity index (cellular proliferation, necrosis, interstitial cell infiltration, and cellular crescents) and a chronicity index (mesangial sclerosis, segmental and global glomerular sclerosis, fibrous crescents, adhesion and tubulo-interstitial change). IF findings were scored semiquantitatively and laboratory findings were also studied. The following results were obtained: 1) The scores of total activity index in MC groups were higher than in the M, S or N groups, and the greater the degree of C3 deposition, the higher the score; 2) Such result was not evident in the chronicity index; 3) High IF scores of IgG and IgM were found in the MC3+ and MC2+ groups; 4) Hematuria was more severe in MC3+ and MC2+ than in other groups, and proteinuria was more prominent in the MC than other groups. Thus the degree of C3 deposition was parallel with histological activity and urinary findings.     

Effect of temperature in focal ischemia of rat brain studied by 31P and 1H spectroscopic imaging

³¹P, ¹H and lactate spectroscopic imaging was used to evaluate the effects of hypothermia on focal cerebral ischemia produced by middle cerebral artery occlusion. The effects on high energy phosphate metabolism, pH, lactate and NAA were investigated in 24 spontaneously hypertensive rats subjected to either permanent or transient ischemia. Under either normothermic (37.5°C) or hypothermic (32°C) conditions, with permanent 6-h occlusion, there was little difference between groups in either the NMR measurements or the volume of infarction. In animals that underwent 3 h of ischemia followed by 12 h of reperfusion, the ischemic changes in lactate, pH, NAA, and high-energy phosphate returned toward control values, and there was a protective effect of hypothermia (infarct volume of 211 ± 26 and 40 ± 14 mm³ in normothermic and hypothermic groups, respectively). Thus, hypothermia did not ameliorate the changes in lactate, pH, NAA, or high energy phosphate levels occurring during ischemia, however, during reperfusion there was an improvement in both the recovery of these metabolites and pathological outcome in hypothermic compared with normothermic animals.     

Measurement of γ-enolase release, a new method for selective quantification of neurotoxicity independently from glial lysis

We have developed a sensitive enzymatic-immunoassay to quantify the level of gamma-enolase (a specific neuronal enzyme) which is released from cultured cells after exposure to various toxins. We show that this method can estimate selectively neuronal cell death without significantly interfering with glial cell death. Indeed, no gamma-enolase is released when glial cells are killed with free-radical producing agents. Experiments comparing the levels of neuronal cell death induced by NMDA or free-radical producing drugs, performed either by measuring gamma-enolase release or using the classical fluorescein diacetate method, yielded similar results. In addition to selectively follow neuronal death in a mixed population of neurons and glial cells, this method provides a way of determining the cell death kinetics from a single culture dish, since enolase can be measured on small samples taken from the culture medium. Finally, we propose these two methods as being complementary and useful neuronal and other cellular death indexes and also to understand the complex problem of glial influence on neuronal survival or death.     

The prevalence of the markers of viral hepatitis B and delta among the population in regions differing in the level of morbidity]

From two regions differing by the levels of incidence of hepatitis B, 2019 blood serum specimens from normal population were examined for markers of HBV infection. In Moscow, among 1040 samples examined HBsAg was found in 2.0%, anti-HBs in 10.0%, anti-HBc in the absence of HBsAg and anti-HBs in 4.5%. In the Osh Province of Kirgizstan, among 979 subjects examined the same markers were found in 10.3%, 22.4%, and 14.0%, respectively. In this area, HBsAg was detected most frequently among infants (14.9% in infants under 1 year), in whom HBs-antigenemia was combined with the presence of HBeAg in 54.5% and with anti-HBc-IgM in 69.2%. Antibody to delta antigen (anti-delta) was found in 24 (25.8%) out of 93 HBsAg-positive subjects in the Osh Province but in none of 21 subjects with HBs-antigenemia in Moscow.     

Effects of age and turpentine-induced inflammation on the activity of ceruloplasmin from blood of CFY rats

The activity of ceruloplasmin (CP) increased 3-fold in rat blood between 1 week and 20 months of age, but the difference in CP activity of adult and old rats was only 14%, which still is statistically significant (p less than 0.01). The increase in NaCl and KCl concentrations in vitro resulted in the same exponential decrease in activities of CP from both young and old animals. Turpentine-induced inflammation caused an increase in blood CP levels in both young (52%) and old (25%) animals compared to age-matched controls (p less than 0.001 and p less than 0.01, respectively). These results indicate that the antioxidant activity of CP is maintained as a function of age in rat blood, which is beneficial for preventing the increase in lipid peroxidation.     

Ocular manifestations of malignant disease.

Systemic malignancies may produce a variety of ocular manifestations, reflecting both direct infiltration of ocular tissue by neoplastic cells and secondary phenomena related to tumour-induced physiological disturbances. The diagnosis and significance of these often neglected aspects of clinical oncology are discussed.