Hereditary complement (C6) deficiency associated with systemic lupus erythematosus, Sjögren's syndrome and hyperthyroidism.

Results of clinical, serologic and histologic studies documenting an association between hereditary C6 deficiency and a connective tissue disease are provided. The propositus had systemic lupus erythematosus with prominent discoid features, Sjögren's syndrome and hyperthyroidism. Serum C6 was undetectable by radial immunodiffusion and hemolytic assays. Serologic and typing studies performed on 9 family members suggested an autosomal codominant transmission. No correlation with a specific HLA phenotype was established.

Aflatoxin carryover and clearance from tissues of laying hens.

A feeding trial was conducted to determine the levels of aflatoxins deposited in the tissues of hens fed a diet contaminated with 3310 micrograms AFB1/kg and 1680 micrograms AFB2/kg for 4 wk. At the end of aflatoxin feeding, the livers were pale, enlarged and haemorrhagic and the ovaries were significantly smaller than those from control hens and contained only small ova. Only a small fraction of the aflatoxins consumed was deposited in the tissues, either as the original compounds or as their metabolites, which were widely distributed in all tissues. The highest levels of aflatoxins were detected in the gizzard, kidneys and liver, with average total concentrations of less than 3 micrograms/kg. The lowest residue levels were detected in the breast, blood serum and leg, with breast muscle having a total concentration of less than 0.1 microgram/kg. Two days after removal of the contaminated feed, aflatoxin residues in all tissues had decreased markedly, with no aflatoxins being detected in the heart or spleen. No aflatoxin residues were detected in the breast, leg, gizzard and ovaries of hens killed 8 days after withdrawal, or in the kidneys and blood at 16 days. However, one of seven hens had measurable amounts of AFB2 in the liver 32 days after withdrawal. Although few residues were detected in most tissues after 8 days on the aflatoxin-free diet, variation existed between tissues and between individual hens in the amount of time required to achieve tissue clearance.

Aflatoxin deposition and clearance in the eggs of laying hens.

Hens fed a diet containing 3310 micrograms of AFB1 and 1680 micrograms of AFB2 per kg feed for 28 days showed a significant decrease in egg production and egg weights by wk 3 and 4 of feeding, respectively. Transfer of aflatoxins to the eggs occurred rapidly, reaching maximum levels after 4-5 days, and remained relatively constant throughout aflatoxin feeding. The mean values for combined residue levels in eggs were less than 0.5 microgram/kg. Levels of AFB2, AFM1 and AFM2 were similar in yolk and albumen while levels of B1 and B2a were higher in the yolk. Upon removal of the aflatoxin-containing diet, residues in eggs decreased rapidly. Clearance of aflatoxin residues from the albumen occurred faster than from the yolk. Thus, no residues were detected in the albumen and in the yolk after 5 and 7 days of withdrawal, respectively. No aflatoxin residues could be recovered from whole eggs after feeding the aflatoxin-free diet for 4 days.

Broiler aflatoxicosis with recovery after replacement of the contaminated diet.

Broiler chickens were fed a diet containing 2057 and 1323 micrograms/kg feed of aflatoxins B1 and B2, respectively, for 35 d. Effects of aflatoxins on growth, food consumption, efficiency of food utilisation and manifestations of aflatoxicosis were compared with control birds at the end of the feeding trial and at 1, 2, 4, 8 and 16 d after replacing the contaminated feed. No difference in food consumption was observed between the controls and the aflatoxin-fed chickens, but efficiency of food utilisation was decreased from 2.2 for the controls to 2.4 g food/g gain for the group fed aflatoxins. Aflatoxins caused depressed growth and enlargement of the kidney, liver, heart and gall bladder. Haemorrhagic spots were present on the surface of the muscles and some of the livers. Most livers from aflatoxin-fed birds were pale and infiltrated with lipid. After withdrawal of the food containing aflatoxins, all apparent gross lesions of aflatoxicosis disappeared, with no evidence of any lesions 8 d after removal of the contaminated diet.

Tissue deposition and clearance of aflatoxins from broiler chickens fed a contaminated diet.

A study was conducted to determine aflatoxin levels in the tissues of broiler chickens that had been fed a diet containing 2057 micrograms aflatoxin B1 and 1323 micrograms aflatoxin B2/kg for 35 days. Results showed that aflatoxins were deposited in all tissues. The highest levels of aflatoxins were present in the gizzards, livers and kidneys. There was evidence that the high levels of aflatoxins B1 and B2 in the gizzards might have been caused by contamination by the gizzard contents during the slaughtering process. After feeding the aflatoxin-contaminated diet for 35 days, mean values for the combined aflatoxins were less than 3 micrograms/kg of tissue. Four days after withdrawal of the aflatoxin-contaminated ration, there were no detectable amounts of aflatoxins in any of the tissues. The results indicate that broiler chickens rapidly clear aflatoxins from their tissues once they are transferred to an aflatoxin-free diet.

Inherited complement component deficiencies in membranoproliferative glomerulonephritis.

Anecdotal reports of complement component deficiencies in patients with immune complex disease led to a systematic study of the levels of seven complement components in serum specimens from 178 patients with glomerulonephritis and 163 normal subjects. Deficiencies were found with significantly higher frequency (22.7%) among 44 patients with membranoproliferative glomerulonephritis (MPGN) types I and III, than among the normal subjects (6.7%, P less than 0.002) or among 134 patients with other glomerulonephritides (5.2%, P less than 0.001). The component deficiencies in MPGN were partial in nine patients and subtotal in one. They could not be ascribed to acquired hypocomplementemia or to a nephrotic syndrome. They were present over long periods, were found in family members, and involved C2, C3, factor B, C6, C7, and C8. Six were presumably the result of null structural genes, two were associated with a structurally abnormal component, and two were of unknown cause. The results give evidence that partial deficiency of one or more complement components is a factor predisposing to MPGN.

An inherited defect in the C3 convertase, C3b,Bb, associated with glomerulonephritis.

The control of the amplification C3 convertase, C3b,Bb, of the serum complement system has been found to be defective in five members of a family spanning three generations. One of the five has membranoproliferative glomerulonephritis (MPGN) type III and another has mild idiopathic rapidly progressive glomerulonephritis. The defect is manifested by low serum concentrations of C3 and usually factor B with normal levels of the proteins which control the convertase, H and I. C3 nephritic factor (C3NeF) was not demonstrable. Enhanced C3 conversion was produced by the incubation of their serum at 37 degrees C for 30 min. This conversion was further accelerated by incubation after increasing the serum magnesium concentration by increments ranging from 0.25 to 1.9 mM. Incremental additions of H to serum depleted of H indicated that the amplification convertase of affected family members required more H for its inhibition than did that of normal subjects. This requirement was reduced by the addition of purified normal C3 but not by the addition of purified C3 of the propositus. It is postulated that affected family members are heterozygous for a gene producing an abnormal C3 which, as a constituent of the amplification convertase, C3b,Bb, confers resistance to H. Investigation of this apparently nephritogenic defect may provide insight into the pathogenesis of these glomerulonephritides.

Control of serum C3 levels by beta 1H and C3b inactivator.

In serum specimens from 50 normal adults, a high correlation was found between the sum of the levels of the control proteins of the C3b amplification loop, C3b inactivator and beta 1H, and the sum of the component proteins, C3 and factor B (R = 0.83), when the concentrations are expressed as percent of the normal adult level. The slope for this regression was 0.98 and the y intercept practically zero, indicating that under normal conditions, beta 1H + C3b inactivator = C3 + factor B +/- 35% (95% error of the prediction). Biological significance of the combined values was suggested by the fact that their equality was largely preserved in serum specimens from cord blood, from infants, and from patients with idiopathic nephrotic syndrome, malnutrition, chronic illness, and partial C3b inactivator deficiency even though, individually, control and component protein concentrations deviated from normal in many of these conditions and, as single proteins, did not correlate with each other as in normal subjects. On the other hand, C3 + factor B was disproportionately lower than beta 1H + C3b inactivator in subjects heterozygously deficient in C3 and in those with hypocomplementemic glomerulonephritis and was often disproportionately high in those with an acute-phase reaction. The data indicate that for meaningful interpretation of the serum C3 level, the concurrent levels of factor B, C3b inactivator, and beta 1H must be taken into consideration.

Rank and promotion of library faculty in a health sciences university.

One method of determining faculty rank and promotion of library personnel in a health sciences university setting is presented. The focus is on appointment and promotion policies and procedures for librarians as faculty. The promotion document stresses (1) superior teaching, (2) outstanding service to the institution, (3) academic achievement, and (4) professional growth and development. Criteria for appointment and promotion to specific ranks are given. Detailed promotion procedures and a timetable are also included. This method of determining rank and promotion of library faculty is now in operation at the Medical College of Georgia.

Disc electrophoresis of turkey serum alkaline phosphatase isoenzymes using polyacrylamide gel. 1. Procedure.

The isoenzymes of alkaline phosphatase in turkey serum were separated by disc electrophoresis using polyacrylamide gel as the supporting medium In this laboratory we have been unable to adapt polyacrylamide gel electrophoresis procedures for turkey serum that had been described by previous workers as successful in separating the isoenzymes of avian alkaline phosphatase. A rapid and repeatable procedure that yielded excellent resolution of alkaline phosphatase isoenzymes was devised. This procedure involved a step-by-step determination of the following: a suitable gel system, buffer system, staining procedure and sample preparation.

Disc electrophoresis of turkey serum alkaline phosphatase isoenzymes using polyacrylamide gel. 2. Turkey serum alkaline phosphatase zymograms.

The isoenzymes of alkaline phosphatase (akp) in turkey serum were separated by disc electrophoresis using polyacrylamide gel as the supporting medium Test subjects consisted of 103 turkeys maintained for the "Vibrator" condition at Michigan State University; and 46 female turkey of the Nicholas Broad Breasted White egg laying strain. Thirteen distinct akp bands were isolated. The 13 bands were observed to occur in 13 different patterns, each pattern being classified as a separate zymogram. Specific types of zymograms were detected for "Vibrator" birds vs. Nicholas strain; females vs, males; high intensity egg production vs. low intensity egg production and molting vs. laying.