The effect of supplementing layer diets with shark cartilage or chitosan on egg components and yolk lipids.

1. An experiment was designed to evaluate the effects of the addition of shark cartilage (SC) or chitosan (CH) to layer diets on egg component weights, yolk lipids and hen plasma lipids. 2. Hy-Line laying hens (80) were used during a 56 d feeding trial. Treatments were: basal diet (BD), BD + 20 g/kg SC, BD + 30 g/kg SC, BD + 20 g/kg CH and BD + 30 g/kg CH. Eggs were analysed on d 14, 28, 42 and 56. 3. Egg weight and egg component weights were not affected by these treatments throughout the experimental period. 4. After 14d of experimental feeding, cholesterol levels were higher in eggs from birds given BD + 20 g/kg CH and BD + 30 g/kg CH than in those from birds given BD. 5. Furthermore, eggs from hens given BD + 20 g/kg SC or BD + 20 g/kg CH were higher in palmitic and stearic acids and lower in oleic acid than those from birds fed on BD. After 56 d feeding, however, palmitic and stearic acid contents in eggs from hens given any of the supplemented diets were lower than in those from hens given BD, and oleic acid in eggs from hens given BD + 20 g/kg SC, BD + 30 g/kg SC and BD + 30 g/kg CH was higher than in those from birds fed on BD. 6. Plasma cholesterol and triacylglycerol levels were not significantly affected by dietary treatment. 7. Shark cartilage or chitosan at up to 30 g/kg in layer diets did not affect egg component weights (yolk, white and shell) and total lipid contents. During the period from 42 to 56d of experimental feeding, diets containing up to 30 g/kg chitosan reduced egg yolk contents of cholesterol, palmitic and stearic acids and increased the content of oleic acid.

[Evolutive aspects of post-transfusion hepatitis C. Review of 175 cases]. / Aspectos evolutivos da hepatite C pós-transfusional. Revisão de 175 casos.

Hepatitis C virus is the main agent responsible for post-transfusion hepatitis. Progression to chronic hepatitis, cirrhosis and hepatocellular carcinoma is very common. The aim of this study was to evaluate the frequency, timing and factors related to progression of hepatitis C. One hundred seventy five patients with chronic post-transfusion hepatitis C were grouped in a cirrhosis group (n = 92) and a non-cirrhosis group (n = 83). The medium time of development to cirrhosis was 11 +/- 6 years. Patients with cirrhosis were older at the time they received transfusion, used more alcohol and had longer times of evolution. The prognosis was worse in the cirrhosis group with a mortality rate of 28.4% and 9.1% of evolution towards hepatocellular carcinoma, comparing with 5.5% and 0% in the non-cirrhosis group respectively. It is shown that post-transfusion hepatitis C is slowly developing progressive disease which progress is much more rapidly in elderly patients and patients with others factors of liver damage.

Aspectos evolutivos da hepatite C pós-transfusional: revisão de 175 casos / Evolutive aspects of post-transfusion hepatitis C: review of 175 cases

O vírus da hepatite C é o principal responsável pela hepatite pós-transfusional e sua progressão para hepatite crônica, cirrose e carcinoma hepatocelular é muito comum. A fim de avaliar frequência, tempo e fatores relacionados à progressão da hepatite C, estudamos 175 pacientes com hepatite C pós-transfusional. Estes foram divididos em 2 grupos com cirrose (n = 92) e sem cirrose (n = 83). O tempo médio de desenvolvimento de cirrose foi de 11 ± 6 anos. Pacientes com cirrose eram mais velhos à época da transfusão, apresentavam maior prevalência de alcoolismo e tinham tempo de evolução mais longo. O prognóstico foi pior no grupo com cirrose com 28,4% de mortalidade e 9,1% de carcinoma hepatocelular, comparados a 5,5% e 0% no grupo sem cirrose, respectivamente. Concluímos que a hepatite C pós-transfusional é uma doença progressiva, que se agrava com o passar do tempo, progridindo mais rapidamente em idosos e pacientes com outros fatores de agressão hepática.

Hepatitis C virus is the main agent responsible for post-transfusion hepatitis. Progression to chronic hepatitis, cirrhosis and hepatocellular carcinoma is very common. The aim of this study was to evaluate the frequency, timing and factors related to progression of hepatitis C. One hundred seventy five patients with chronic post-transfusion hepatitis C were grouped in a cirrhosis group (n = 92) and a non-cirrhosis group (n = 83). The medium time of development to cirrhosis was 11 +/- 6 years. Patients with cirrhosis were older at the time they received transfusion, used more alcohol and had longer times of evolution. The prognosis was worse in the cirrhosis group with a mortality rate of 28.4% and 9.1% of evolution towards hepatocellular carcinoma, comparing with 5.5% and 0% in the non-cirrhosis group respectively. It is shown that post-transfusion hepatitis C is slowly developing progressive disease which progress is much more rapidly in elderly patients and patients with others factors of liver damage.

Identification of aluminium fractions in serum using the techniques of high performance liquid chromatography, ultrafiltration and Zeeman atomic absorption spectrometry.

In order to ascertain the distribution of aluminium in normal and occupationally exposed sera, size-exclusion chromatography using two fractionation techniques was applied: gel filtration (Sephadex G-100 SF) and HPLC (TSK G4000 SW). For each of the techniques, protein profiles obtained for control and exposed sera did not differ and aluminium was found to be associated with the same fractions. Ultrafiltration of sera using Centricon concentrators having a nominal cut-off of M(r) = 10,000 confirmed the presence of high molecular mass and ultrafiltrable low molecular mass aluminium complexes in serum. Absolute quantitation and relative distribution of aluminium in the aforementioned complexes in original and spiked sera were determined using Zeeman atomic absorption spectrometry. It was found that the relative distribution of aluminium between high molecular mass and low molecular mass fractions was 79.1% and 19.6% in controls, compared to 91.3% and 8.7% in exposed sera, which is highly significant for both high molecular mass (p < 0.026) and low molecular mass (p < 0.004). After spiking both control and exposed sera with 400 micrograms/l of Al, the distribution changed. The percentage of the aluminium bound to high molecular mass increased from 79.1% to 98.9% for controls, and from 91.3% to 98.4% for exposed sera, confirming the affinity of high molecular mass proteins, especially transferrin for aluminium. On the other hand, the percentage of aluminium bound to low molecular mass decreased after spiking to 1.12% for controls and to 1.6% for exposed sera. These differences were not statistically significant. This suggests that at high concentrations of total aluminium in serum, the percentage of the aluminium bound to the low molecular mass is lower but the absolute quantity of aluminium circulating as the low molecular mass complex is increased. This low molecular mass aluminium complex is thought to play an important role in intracellular accumulation of aluminium.

Elastase binding capacity of alpha 2-macroglobulin and its association with glucocorticoid concentration in southern African black patients with hepatocellular carcinoma.

Thirty-three Southern African black patients with hepatocellular carcinoma (HCC) (7 women) and 43 black control individuals (14 women), all in the age group 18-45 years, were investigated for plasma alpha 2-macroglobulin (alpha 2M) elastase binding capacity (EBC). Cortisol levels were measured in 15 (3 women) of the HCC patients and 10 (5 women) of the control subjects. A significant difference in EBC was found between the HCC patients and the control subjects (P < 0.001). A significant difference was also found in cortisol levels between the two groups (P < 0.001). A significant correlation between EBC and cortisol levels was obtained (r = 0.57; P < 0.042). The significant increase in EBC of alpha 2M in HCC patients could be due to an increase in circulating cortisol.

Ethnic differences in the occurrence of the M1(ala213) haplotype of alpha-1-antitrypsin in asthmatic and non-asthmatic black and white South Africans.

An ethnic study of 175 individuals, comprising 65 black and 110 white South Africans, has shown a conclusive difference in the frequency of the M1(ala213) haplotype of alpha 1-antitrypsin (P < 0.00001). The M1(ala213) haplotype occurred more frequently in the black group. In the latter group, the frequency of the M1(ala213) haplotype was the same in both controls (0.55) and asthmatics (0.53). However, there was a significant difference in the frequencies (0.19 and 0.36) for the respective white groups (P < 0.01), the frequency of the M1(ala213) haplotype being much higher in the asthmatics. Apart from the above differences, there was also a difference in the elastase-inhibitory capacities of the homozygote phenotypes M1(val213) vs M1(ala213) (P < 0.0001), this capacity being lower in the latter phenotype. We conclude that the occurrence of the M1(ala213) allele of alpha 1-antitrypsin differs in various ethnic groups and may play a role in asthma.

Differences in elastase-binding activity of alpha 1-protease inhibitor and alpha 2-macroglobulin for asthma patients and control subjects with various alpha 1-protease inhibitor phenotypes.

Forty-two adult patients with asthma and 30 control subjects were investigated for elastase-binding capacities of alpha 1-protease inhibitor and alpha 2-macroglobulin in plasma. The binding activities of alpha 1-protease inhibitor and alpha 2-macroglobulin in asthmatic patients with the M phenotype for the alpha 1-protease inhibitor differed in their relationship to the values in control subjects with the same phenotype [less alpha 1-protease inhibitor for asthmatics (35.1 +/- 1.8) than for controls (42.9 +/- 2.0 kU/L) (P < 0.001); more alpha 2-macroglobulin for asthmatics (6.9 +/- 0.3) than for control subjects (5.9 +/- 0.4 kU/L) (P < 0.03)]. In contrast, the patients with a deficiency allele (S, V, or Z) for alpha 1-protease inhibitor had lower activities of both alpha 1-protease inhibitor [22.1 +/- 0.1 vs 42.9 +/- 2.0 kU/L (P < 0.001)] and alpha 2-macroglobulin [4.6 +/- 0.6 vs 5.9 +/- 0.4 kU/L (P < 0.001)] than did the control subjects with the M phenotypes. The relevance of the results to the pathogenesis of asthma is discussed.

[Prevalence of antibodies to hepatitis C (anti HCV) in blood donors in Rio de Janeiro, Brazil. Its relation to ALT and anti HBC]. / Prevalência do anticorpo contra hepatite C (anti VHC) em doadores de sangue no Rio de Janeiro, Brasil. Sua relação com ALT e anti HBC.

UNLABELLED: We have studied 933 volunteer blood donors from May to July, 1990. After a interview and screening tests for syphilis, Chagas disease, malaria and HIV, they underwent an enzyme immunoassay for HBsAg, anti HBc and anti HCV antibodies. Alanine aminotransferase (ALT) serum levels were determined by auto analyser. Most blood donors were male with mean age of 33 years (19-65). Anti HCV prevalence was 3.1% (29 from 933 blood donors). Among anti HCV+, blood donors, 44.8% (13/29) had ALT 40 UI/L, 31% (9/29) were anti HBc+ and 17.2% (5/29) had both surrogate markers simultaneously. From 109 donors with ALT 40 UI/L, 13 (11.9%) were anti HCV+, while among 153 anti HBc+ donors, the anti HCV was 5.8%. CONCLUSIONS: 1) we found a higher anti HCV prevalence among our blood donors than previous published reports from other countries; 2) our data show that surrogate assays do not adequately identify anti HCV blood donors, 41.4% of them would not have been excluded by anti HBc and ALT tests alone; 3) there were a correlation between anti HCV positivity with a sample to cutoff optical density ratio equal or greater than 4 and elevated ALT serum levels.