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Biomedical subjects

E V Potter

Publications and source records attributed to E V Potter.

At least 19 recordsLinked to original sources

Unilateral renal vein occlusion in rats.

To study the relationship of renal vein thrombosis to membranous glomerulonephritis with the nephrotic syndrome, we attempted to simulate the former by occluding to 0.5 mm one renal vein in rats. Although increased proteinuria did occur during the first 3 days after such occlusion, there was little difference from control animals in the amount of proteinuria thereafter, up to 46 days, and no evidence of membranous glomerulonephritis by light, immunofluorescent, or electron microscopy.

Animals↗

Factor VIII-related antigen in occluded human arteries and grafts.

Direct immunofluorescence was used to determine the disposition of factor VIII-related antigen (VIIIR:Ag) in occluded arteries and grafts from patients undergoing reconstructive operation. The presence of VIIIR:Ag on the luminal surface of these vessels was equated with their endothelialization according to the work of others. In 12 of the 20 arteries examined, stain for VIIIR:Ag was absent or markedly reduced from the luminal surfaces, and in six more it was only present focally. The adventitial capillaries were brightly stained in most of these specimens. Both of two saphenous vein grafts and all of six Dacron grafts stained for VIIIR:Ag along their luminal surfaces and in the adventitial capillaries as brightly as normal arteries. However, all of eight Gore-tex grafts had little or no stain for VIIIR:Ag along their luminal surfaces, and the capillaries of the adventitia were not as plentiful as those in the normal arteries and Dacron grafts. With one exception, the Gore-tex grafts had become occluded less than 1 year after implantation, while the Dacron grafts had remained patent for 2 to 8 years. Thus many of the diseased arteries and the short-lived Gore-tex grafts were characterized by relative absence of VIIIR:Ag from their luminal surfaces, presumably reflecting the loss or absence of endothelialization.

Adult↗

Skin infections and immunoglobulin A in serum, sweat, and saliva of patients recovered from poststreptococcal acute glomerulonephritis or acute rheumatic fever and their siblings.

Differences in hygienic habits and base-line secretory immunoglobulin (Ig) A which might have contributed to the prevalence of skin infections and/or absence of increased serum IgA values were sought in patients with poststreptococcal acute glomerulonephritis (nephritis) in contrast to patients with acute rheumatic fever in Trinidad by studying patients and their siblings after the patients had recovered from these diseases. The overall history of skin infections was similar at this time in all groups, although they had been much more common in patients with nephritis and their families at the time of acute illness. The recovered nephritis patients bathed slightly less often than the other individuals, used a cream or lotion after bathing rather than coconut oil, and tended to sweat less than the others, but none of these differences was statistically significant. Neither were significant differences demonstrated in amounts of IgA and IgG in serum and saliva of recovered nephritis patients and their siblings compared to recovered rheumatic fever patients and their siblings, while only small amounts of IgA and IgG were present in any sweat, and probably had been transuded rather than secreted. These studies suggest that the lower serum IgA titers in patients with nephritis compared to patients with rheumatic fever in Trinidad do not reflect basic differences in serum IgA or secretory IgA as measured in saliva, and that IgA is not secreted by the eccrine glands.

Adolescent↗

Serum immunoglobulin A and antibody to M-associated protein in patients with acute glomerulonephritis or rheumatic fever.

Serum immunoglobulin A (IgA) was markedly increased in 80% of 50 patients with acute rheumatic fever in Trinidad in contrast to 20% of 63 patients with acute glomerulonephritis, whereas serum IgG was increased in nearly all of both groups. Since total antibody to M-associated protein (MAP) (assessed by complement fixation) is the only antibody as yet consistently found to be of higher titer in patients with acute rheumatic fever than in patients with acute glomerulonephritis in Trinidad, it was measured and the titers were related to serum levels of IgA. The titers of total antibody to MAP were greater than or equal to 40 in 58% of the rheumatic fever patients, 43% of the nephritis patients, and 8% of well school-children. However, its presence in rheumatic fever patients did not correlate directly with amounts of serum IgA present (r = 0.0507). Moreover, titers of total antibody to MAP related equally well to enzyme-linked immunosorbent assay indicated amounts of IgG antibody (r = 0.3939) and IgA antibody (r = 0.3054) to MAP in rheumatic fever patients but not in nephritis patients (r = 0.0301 for IgA antibody and 0.6909 for IgG antibody to MAP), whereas they related best to IgM antibody to MAP in the school-children (r = 0.4204).

Acute Disease↗

Streptococcal neuraminidase and acute glomerulonephritis.

We examined the hypothesis that streptococcal neuraminidase may alter host serum immunoglobulin G so that autoantibodies are formed which lead to immune complexes and acute glomerulonephritis. We confirmed the observation that T-type 4 and T-type 12 streptococci (both associated with acute glomerulonephritis) are the most likely of many types studied to produce neuraminidase. However, we did not find this enzyme to be produced by any of 23 streptococcal strains isolated from patients with nephritis, whereas it was produced by two strains from patients with rheumatic fever and by one strain from a patient with scarlet fever. Also, we were unable to find direct or indirect evidence of increased neuraminidase activity in the sera of six patients with acute glomerulonephritis when they were compared with the sera of six patients with acute rheumatic fever and with those of six normal subjects.

Acute Disease↗

Fibronectin in von Willebrand's disease and thrombasthenia: role in platelet aggregation.

Fibronectin is involved in cell-cell and cell-substratum adhesion processes. Since von Willebrand's disease and thrombasthenia are characterized, respectively, by platelet-substratum and platelet-platelet adhesion anomalies, we investigated the state of fibronectin in platelets and plasma of these two disorders as well as the role of plasma fibronectin in platelet aggregation. The levels of platelet and plasma fibronectin in three cases of von Willebrand's disease and in three cases of thrombasthenia did not show statistically significant differences as compared with the normal controls. Immunofluorescent staining intensity and patterns of disease-derived and normal platelets, studied with anti-fibronectin antibodies, were similar. Furthermore, 125I-labeled protein A binds to anti-fibronectin-treated platelets from the two diseases investigated in the same fashion as in normal controls. No role for plasma fibronectin was detected in platelet aggregation induced by ADP, thrombin, collagen, epinephrine, and arachidonic acid. Thus our results do not indicate a direct quantitative role of fibronectin in the adhesion anomalies encountered in these diseases. However, fibronectin may still be important to platelet adhesion and normal hemostasis processes through interactions with the plasma von Willebrand factor and the membrane glycoproteins IIb and III, which have been shown to be deficient in von Willebrand's disease and thrombasthenia, respectively.

Blood Platelets↗

Some immunofluorescent observations on factor VIII/von Willebrand factor in dogs.

Factor VIII/von Willebrand factor (vWF) was sought by immunofluorescence in or on canine platelets and blood vessels. None was found on normal canine platelets and little was present in normal canine arteries, veins and capillaries compared with normal human blood vessels. However, free granules of vWF were scattered in platelet-rich canine plasma and occasional granules appeared on small clumps of platelets when ristocetin or collagen was added to the plasma. When the same platelets were suspended in human plasma and ristocetin or collagen was added, more clumps were formed and more vWF (human) was associated with these clumps. When thrombin was added to canine platelets in either canine or human serum, more solid, small clumps of platelets were formed and stained with anti-vWF sera. When thrombin was added to canine platelets in either canine or human plasma, a single large clot was formed which stained brightly for vWF.

Animals↗

Extracellular factors, blood group antigens, and bacteriophage of nephritogenic and nonnephritogenic strains of M-type 12 streptococci.

Strains of M-type 12 streptococci from 18 patients with acute glomerulonephritis and 18 patients with uncomplicated pharyngitis were analyzed for in vitro production of streptolysin O, diphosphopyridine nucleotidase, hyaluronidase, streptokinase, streptolysin S, proteinase, hyaluronic acid, and fibrinogen-precipitating factor. In addition, relations to blood group antigens, lysogeny, and susceptibility to bacteriophage were determined. No significant differences were found between strains from nephritic and nonnephritic patients. By not indicating a role in the pathogenesis of poststreptococcal acute glomerulonephritis for any of the factors studied, these observations diminish the probability that these factors are of specific importance in this disease and thus direct our attention elsewhere.

Bacteriophages↗

Variations in serum complement following inulin infusion in man.

Complement levels were determined in 12 normal human volunteers while receiving intravenous infusions of inulin for determination of standard inulin clearances. Significant decreases in beta IC globulin and total hemolytic complement activity were observed when inulin was infused, but not following infusion of saline as a control. These effects were noted only when steady-state inulin levels were greater than 26 mg%, suggesting a dose-dependent response. No evidence of increased coagulation was noted as measured by fibrinogen and fibrin degradation products. Since C4 levels remained largely unchanged following inulin infusion, it was concluded that the results most likely occurred through activation of the alternate complement pathway.

Adult↗

Clinical healing two to six years after poststreptococcal glomerulonephritis in Trinidad.

To determine the incidence of chronic nephritis after poststreptococcal acute glomerulonephritis in Trinidad, 760 patients (41 adult) were examined two to six years after recovery from the illness, 344 being studied twice (four and six years). Only 1.8 per cent had persistent urine abnormalities on their last follow-up examination, and another 8.0 per cent had abnormalities that were transient or occurred only after the patient had assumed the lordotic position. In 1.4 per cent hypertension was present, whereas only one had azotemia. Both persistent urine abnormalities and hypertension increased in prevalence with age at onset of prior poststreptococcal glomerulonephritis but did not vary between sexes, races or epidemic versus endemic forms. Half the urine abnormalities present four years after recovery were absent two years later. Thus, poststreptococcal acute glomerulonephritis appears to have a low incidence of chronicity in Trinidad, with continuing resolution for more than four years.

Acute Disease↗

Tropical acute rheumatic fever and associated streptococcal infections compared with concurrent acute glomerulonephritis.

Ninety-three patients with acute rheumatic fever and 195 patients with acute glomerulonephritis were observed in Trinidad during an outbreak of scabies with a high incidence of secondary streptococcal infections. Clinical and laboratory manifestations of ARF were the same as those seen in temperate zones, except that antistreptolysin O titers were less markedly increased. The patients with ARF were similar to those with AGN in respect to sex, race, location of residence, and living conditions, but were older and had markedly fewer skin infections. Currently prevalent nephritogenic streptococcal strains never were isolated from patients with ARF even when M55 streptococci appeared and led to an epidemic of AGN.

Acute Disease↗

The families of patients with acute rheumatic fever or glomerulonephritis in Trinidad.

The families of 21 patients with acute rheumatic fever (ARF) and 44 patients with acute glomerulonephritis (AGN) in Trinidad were examined in their homes. The ARF and AGN families were equally large and crowded and they lived in the same largely rural areas. However, only 22% of the ARF family members had skin infections in contrast to 61% of the AGN family members. Sixty-eight per cent of skin infections in ARF families and 69% of skin infections in Agn families yielded group A streptococci. Throat cultures were positive in 19% of ARF family members and 25% of AGN family members. Thirty-two per cent of 51 group A strains isolated from ARF family members (29 from throat, 22 from skin) were M11 or "M41" strains which were associated with ARF during the study, while only 8% were M1, T4 (MNT or 60) or M55 strains which were associated with AGN. In contrast, 49% of 171 group A strains isolated from Agn family members (64 from throat, 107 from skin) were M1, T4 (MNT or 60) or M55 while only 10% were M11 or "M41." Serum antibody titers were similar in both groups: antistreptolysin-0 titers were not markedly increased in either while anti-hyaluronidase and/or antideoxyribonuclease-B titers were increased in both. Evidence of subclinical AGN was found equally often in both groups: 6% of each had abnormal urine and 4% of each had decreased serum complement while 2% of the ARF and 3% of the AGN family members had both abnormal urine and decreased serum complement.

Adolescent↗