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Biomedical subjects

J G Johnson

Publications and source records attributed to J G Johnson.

At least 73 records · Page 4Linked to original sources

Improving the operating room to increase revenues.

Hospitals often overlook the potential to increase revenues by improving operating rooms and attracting additional surgery. Administrators should respond to surgeons' dissatisfaction with services despite limitations and ambiguities imposed by the surgical suite's chain of command. Directors of surgery can overcome formal authority problems by establishing informal relationships with the chiefs of surgery and anesthesia. Monthly reports to administration on quality and performance standards can avoid difficulties and prompt timely solutions. Satisfied surgeons will increase admissions by directing elective surgery patients to the hospital. Administrators can conduct interviews with all surgical personnel or use questionnaires to identify problems, potential new surgeons, and suggestions for improvement. Other tasks are to analyze each surgical section's functions, accumulate data by specialty and surgeon to plan daily schedules, evaluate organization and staffing, and evaluate instrumentation and supplies. Block scheduling and surgical acuity systems help establish controls in these areas. Feedback systems ensure that personnel remain sensitive to surgeons' needs. A nurse should be assigned to each surgeon to communicate information about patients, and surgeons should be encouraged to complete forms after each surgery to identify deficiencies in procedures. Other incentives for surgeons include favorable OR scheduling arrangements, purchase of special equipment, and package pricing for certain procedures.

Anesthesia Department, Hospital↗

Long-term captopril therapy: evolving hemodynamic effects.

Nine patients with resistant hypertension received captopril for 12 months. Five received captopril alone, four required additional therapy. In the former, mean blood pressure fell from 109 +/- 4.2 mm Hg to 84 +/- 7.5 mm Hg (P less than 0.025) after seven days. A rise to 101 +/- 19 mm Hg was noted at six and 12 months. Total peripheral resistance fell at seven days but returned to levels above control at six and 12 months. Cardiac index was 3.21 +/- 0.55 liters/min/m2 before treatment, 3.27 +/- 0.56 liters/min/m2 at seven days, and 2.17 +/- 4.0 liters/min/m2 (P less than 0.025) at 12 months. However, forearm blood flow rose from subnormal levels during the 12 months of observation, suggesting a persistent effect on the arterioles of the extremities. Plasma converting enzyme activity was significantly reduced at seven days but was above control levels at six and 12 months. However, plasma renin activity remained elevated, and plasma aldosterone concentration was significantly reduced. The fall in mean blood pressure was not related to the change in plasma converting enzyme activity in patients receiving captopril alone (five patients) or with diuretic (two patients). In the presence of beta-adrenergic blockade and volume depletion (two patients), changes in mean blood pressure appeared to be related to changes in converting enzyme activity. The data suggest that patients with essential hypertension whose blood pressure was not adequately controlled by previous medications may initially respond to captopril with a fall in blood pressure and total peripheral resistance. However, in certain individuals, these effects diminish with time despite addition of diuretics and beta-adrenergic receptor blocking agents.

Adult↗

Identification of surface proteins on viable Plasmodium knowlesi merozoites.

Viable merozoites of Plasmodium knowlesi were isolated and the proteins that were labeled on intact merozoites by lactoperoxidase-catalyzed radioiodination were identified. Sodium dodecyl sulfate polyacrylamide gel electrophoresis and autoradiography of Triton soluble extracts of labeled merozoites demonstrated eight major bands ranging in apparent molecular weight from 150,000 D to 22,000 D. Exposure of intact merozoites to trypsin (10 microgram/ml) for 10 min resulted in the loss of the two highest molecular weight proteins (150,000 D and 105,000 D) and the appearance of two new bands at 70,000 D and 62,000 D. Trypsin treatment under these conditions also removed the receptor(s) for merozoite attachment to erythrocytes. Therefore, these high molecular weight proteins are candidates for the merozoite component that attaches to erythrocytes. There was no evidence that the labeled membrane components were serum or erythrocyte membrane components, two potential contaminants in the preparation. Anti-rhesus erythrocyte antibody did not precipitate labeled merozoite proteins. Furthermore, the immunoprecipitation of labeled merozoite proteins by rhesus anti-merozoite serum was not inhibited by erythrocyte ghosts.

Animals↗

Determinants on surface proteins of Plasmodium knowlesi merozoites common to Plasmodium falciparum schizonts.

In this report and (R. Schmidt-Ullrich, L. H. Miller, and D. F. H. Wallach. Manuscript in preparation.), we have demonstrated that malaria proteins on the surface of merozoites and infected erythrocytes cross-react between at least two primate malarias, Plasmodium knowlesi and P. falciparum. Sera from five Gambian adults who were highly immune to P. falciparum were used as a reagent to study the cross-reactivity between P. falciparum schizonts and surface proteins on P. knowlesi merozoites. Although the sera bound to the surface of viable, intact P. knowlesi merozoites, the sera did not block invasion of rhesus erythrocytes. 125I-lactoperoxidase-labeled surface proteins on merozoites formed complexes with the antibody. All major protein bands seen in the electrophoresis of the original Triton extract were bound by the immune sera. Because Gambians have never been exposed to P. knowlesi malaria, the antibodies that reacted with P. knowlesi merozoites must be directed against antigens of another parasite such as P. falciparum. We tested this hypothesis by competition for antibody in a Gambian serum between Triton-extracted antigens from P. falciparum schizont-infected erythrocytes and from surface-labeled P. knowlesi merozoites. P. falciparum inhibited the reaction, thus indicating cross-reaction between antigens in P. falciparum schizonts and P. knowlesi merozoites.

Animals↗

Factors affecting the ability of isolated Plasmodium knowlesi merozoites to attach to and invade erythrocytes.

Plasmodium knowlesi merozoites were prepared by the polycarbonate sieving method of Dennis, Mitchell, Butcher & Cohen (1975). Merozoite function was assayed by their attachment to and invasion of rhesus erythrocytes at 37 degrees C. The early merozoites from the culture chamber were the most invasive, although maximum numbers of merozoites appeared later. Merozoites were most stable when incubated at room temperature (23 degrees C). At 37 and 0 degrees C invasiveness rapidly declined to zero. Attachment was rapidly lost at 37 degrees C but was retained at 0 degrees C. Attachment was unchanged in the pH range 6.8--7.9 but invasion was reduced at pH 7.9. The presence of L-fucose, D-galactose, D-glucose, D-mannose, N-acetyl-D-galactosamine or N-acetyl-D-glucosamine did not reduce invasion. Attachment and invasion were greatly reduced or abolished by the presence of 2.5 mM EDTA or EGTA, by lactoperoxidase-catalysed iodination of the merozoites, or by treatment of the merozoites with trypsin at a concentration of 1 micrograms/ml or greater for 10 min at 23 degrees C.

Animals↗

Selective cleavage of variant surface glycoproteins from Trypanosoma brucei.

Two conformationally distinct regions were revealed by tryptic cleavage of six undenatured variant surface glycoproteins purified from clones of Trypanosoma brucei. Within 5 min, the native glycoproteins (65,000 mol.wt.) were cleaved, yielding a large N-terminal fragment (48,000-55,000 mol.wt. depending on the variant) together with one or more C-terminal fragments. After 30-60 min incubation, further breakdown of the large fragment occurred in some variants. The ultimate large product (40,000-52,000 mol.wt.) was very resistant to further degradation by trypsin (in the absence of denaturation). The distinction between N-terminal and C-terminal domains may be significant in relation to the organization and function of these glycoproteins on the trypanosome surface.

Amino Acids↗

Interaction between cytochalasin B-treated malarial parasites and erythrocytes. Attachment and junction formation.

We have previously demonstrated that invasion of erythrocytes (RBCs) by malaria merozoites follows a sequence: recognition and attachment in an apical orientation associated with widespread deformation of the RBC, junction formation, movement of the junction around the merozoite that brings the merozoite into the invaginated RBC membrane, and sealing of the membrane. In the present paper, we describe a method for blocking invasion at an early stage in the sequence. Cytochalasin-treated merozoites attach specifically to host RBCs, most frequently by the apical region that contains specialized organelles (rhoptries) associated with invasion. The parasite then forms a junction between the apical region and the RBC. Cytochalasin blocks movement of this junction, a later step in invasion. Cytochalasin-treated (Plasmodium knowlesi) merozoites attach to Duffy-negative human RBCs, although these RBCs are resistant to invasion by the parasite. The attachment with these RBCs, however, differs from susceptible RBCs in that there is no junction formation. Therefore the Duffy associated antigen appears to be involved in junction formation, not initial attachment.

Animals↗

True hermaphroditism with peripheral blood and gonadal karyotyping.

Eight documented cases of true hermaphroditism have been seen in the reproductive endocrine unit at the Medical College of Georgia since 1969. There was histologic evidence of both ovarian and testicular tissue in all cases. Seven patients had peripheral blood karyotypes: 6 had normal 46,XX peripheral blood karyotypes, and 1 patient had a normal 46,XY blood karyotype. Four of the 7 patients studied had chromosomal analysis of 1 or both gonads. Five gonads were karyotyped as 46,XX and 1 revealed a mosaic gonadal pattern of 46,XX/46,XY. The clinical features, anatomic findings, and cytogenetic studies of these patients are reviewed. Discordant findings in peripheral blood and gonadal chromosomes are discussed.

Adolescent↗

Carbohydrate composition of variant-specific surface antigen glycoproteins from Trypanosoma brucei.

The carbohydrate of variant-specific surface antigen glycoproteins from bloodstream forms of 13 cloned variants of Trypanosoma brucei was analyzed by gas-liquid chromatography. The glycoproteins contained from 6 to 17% carbohydrate by weight, and all contained the same 4 sugars: mannose, galactose, glucose, and glucosamine (probably as N-acetylglucosamine). The glycoprotein from variant 048, strain 427 contained (+20%) 11 mannose, 4 galactose, 4 glucose, and 5 glucosamine residues/mole of glycoprotein (molecular weight 65,000). Glucose was an intergral component of the glycoproteins, not dissociable by sodium dodecyl sulphate, 8 M urea, or 1 M acetic acid. Some of the glucose was dissociated by trichloroacetic acid. Most of the glycoproteins formed precipitin with concanavalin A in Ouchterlony double diffusion, but none formed such bands with wheat germ agglutinin or Ricinus communis lectin (molecular weight 120, 000).

Animals↗

Role of a sugar-lipid intermediate in colanic acid synthesis by Escherichia coli.

Membrane fractions from a lon strain of Escherichia coli but not a wild-type strain catalyze the incorporation of fucose from guanosine 5'-diphosphate-fucose into a lipid and into polymeric material. Both incorporation reactions specifically require only uridine 5'-diphosphate (UDP)-glucose. The sugar lipid was shown to be an intermediate in the synthesis of the polymer which was related to colanic acid. The sugar lipid had the structure (fucose3, glucose2)-glucose P-P-lipid. Its behavior on column and thin-layer chromatography, the rates of its hydrolysis in acid and base, and the response of its synthesis to inhibitors are all identical to the other sugar-lipid intermediates which have been shown to contain sugars attached to the C55-polyisoprenol, undecaprenol, by a pyrophosphate linkage. The membrane fractions from both the lon strain and the wild-type strain also catalyzed the incorporation of either glucose from UDP-glucose or galactose from UDP-galactose into a lipid fraction which was shown to contain the free sugar attached by a monophosphate linkage to an undecaprenol-like lipid. This lipid was isolated and its nuclear magnetic resonance spectra was identical to undecaprenol. The membrane fractions from both strains also incorporated glucose from UDP-glucose into glycogen and into a polymer that behaved like Escherichia coli lipopolysaccharide. Conditions were found where the incorporation of glucose could be directed specifically into each compound by adding the appropriate inhibitors.

Bacitracin↗

Malignant hypertension in blacks. Malignant intrarenal arterial disease as observed by light and electron microscopy.

Volhard and Fahr recognized that hypertensive intrarenal vascular disease could be divided into two groups corresponding to the clinical states of benign and malignant hypertension. Since that time, numerous papers on malignant hypertension, primarily dealing with European derived populations, have emphasized fibrinoid necrosis of small arteries and arterioles as the lesion of malignant hypertension, although some have also recognized a myxoid intimal lesion as characteristic. Today in the United States, however, a significant proportion of malignant hypertension occurs in blacks. In the present study, patients have lacked fibrinoid necrosis of arterioles and only rarely have had some atypical necrosis of small arteries. The prominent, but not pathognomonic, lesion in this series is a myxoid intimal thickening of small arteries consisting of smooth muscle cells, acid mucopolysaccharides, basement membrane-like materal, collagen, and other amorphous and unidentified material, probably plasma derived.

Adult↗

Treatment of patients with severe hypertension by inhibition of angiotensin-converting enzyme.

1. The results of the administration of the nona-peptide inhibitor (SQ 20,881) of the enzymatic conversion of angiotensin I into angiotensin II in twelve severe hypertensive patients are presented. 2. Administration of the compound was associated with a fall in blood pressure in ten of twelve patients. 3. Four patients had a normal plasma renin activity (PRA) with a range of 1.6-3.7 ng h-1 ml-1 and eight patients had a high PRA with a range of 5.0-74 ng h-1 ml-1. Two of the patients with normal PRA had no fall in blood pressure despite receiving 2 mg/kg of the compound. Two patients with normal PRA, however, did respond, thus indicating that a high PRA is not necessary for a response to the inhibitor compound. 4. It was found that haemodialysis or diuresis with frusemide enhanced the blood pressure response to the compound. 5. The presence of a measured low total blood volume was found to be associated with an exaggerated fall in blood pressure to a small dose of compound (0.125 mg/kg) in one patient.

Blood Pressure↗

Malignant hypertension due to musculo-mucoid intimal hyperplasia of intrarenal arteries. Absence of renal fibrinoid necrosis.

Severe essential hypertension in a subset of American black subjects is associated with marked stenosis of interlobular arteries and arterioles of the kidneys, observed by renal biopsy and binephrectomy specimens. The interlobular arterial stenosis is caused by marked thickening of the intima due mainly to the presence of smooth muscle cells, basement membrane material, and acid mucopolysaccharide. Because of this makeup, we propose the term "musculo-mucoid intimal hyperplasia" for this lesion. The media of these arteries appears maximally dilated, and by electron microscope displays degenerative changes of the smooth muscle cells. The arterioles are thickened, due mainly to hyalinization, but also due to the musculo-mucoid change (onionskin effect). The smooth muscle cells are degenerated and atrophic. These patients do not exhibit fibrinoid necrosis of the arteries, arterioles, and glomeruli, presumably because of the rapidity of the development of the arterial stenotic lesion. Accordingly, the glomeruli are destroyed by ischemia, and there is no evidence of glomerulitis (no "Kombinations" form of Fahr). A unifying hypothesis concerning renal hypertensive arterial disease is suggested by these studies. This hypothesis places the main emphasis for all the morphological expressions of the intrinsic visceral vasculature on changes involving the main functional unit of the vessel wall, the medical smooth muscle.

Acute Kidney Injury↗