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Biomedical subjects

D Stern

Publications and source records attributed to D Stern.

At least 145 records · Page 8Linked to original sources

Sclerosing peritonitis. Possible early diagnosis by computerized tomography of the abdomen.

Sclerosing peritonitis (SP) has come to be recognized as a serious complication of peritoneal dialysis (PD). However, diagnosis is often established at a late stage of the disease and at laparotomy. The use of computerized tomography (CT) of the abdomen in 2 patients, clinically suspected of suffering from SP, revealed loculated ascites, adherent bowel loops, bowel lumenal narrowing, and thickening of the peritoneal membrane. Such radiological changes in patients on PD seem highly consistent with a diagnosis of SP. We feel that CT of the abdomen may help in attaining an early, correct, and noninvasive diagnosis of SP. We recommend that CT of the abdomen be performed in any patient on chronic PD who has clinical manifestations suggestive of SP. Early diagnosis of SP can lead to early cessation of PD and hopeful recovery of the peritoneal membranes and space.

Female↗

The other side.

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Humans↗

Faulty sternotomy and complications after median sternotomy.

In 11 of 55 patients with complications of median sternotomy, a paramedian sternotomy has been detected by computed tomography or at reparative operation. The thin side of the sternum is easily broken by the closing wires, this being the cause of instability and probably dehiscence and consequent infection and osteomyelitis. Most of the 11 patients in this group had some other predisposing risk factors, such as obesity, prolonged aortic cross-clamp time, and prolonged respiratory assistance. We suggest that, if a paramedian sternotomy is diagnosed at the primary operation, special closure techniques should be undertaken. Each patient with early dehiscence of a median sternotomy should undergo a computed tomographic examination. If a paramedian sternotomy is proved, simple reclosure is inadvisable. Sternectomy and closure with muscle flaps are then indicated.

Humans↗

[A combination of dihydroergotamine and acetylsalicylic acid--prevention of postoperative thromboembolic complications. Clinical study in orthopedics].

202 patients undergoing surgery involving the lower limbs were given antithrombotic treatment for at least 21 days, or until they had regained full mobility. Following subcutaneous prophylaxis with a combination of heparin and dihydroergotamine, two oral regimens were compared in a controlled and randomized prospective study. The first treatment consisted of a combination of acetylsalicylic acid (ASA) and dihydroergotamine (DHE), and the second of acenocoumarol. The radiofibrinogen uptake test was carried out in high-risk patients (i.e. those undergoing hip surgery) to detect deep-vein thrombosis. No statistically significant difference was found between the two groups. However, the ASA/DHE combination enjoyed better patient acceptance and was much easier to use.

Acenocoumarol↗

High-speed photography of excimer laser ablation of the cornea.

We have used laser-based high-speed photography to investigate excimer laser ablation of the cornea. Photographs of the ablation plume were obtained 500 ns to 150 microseconds after incidence of a 193- or 248-nm excimer laser pulse on the surface of the cornea. Ejection of material from the cornea begins on a time scale of nanoseconds and continues for 5 to 15 microseconds following the excimer pulse. At 193 nm the ablation plume resembles a burst of smoke, and individual particles are too small to be optically resolved with our apparatus. At 248 nm the plume resembles a spray of larger, discrete droplets. Material is ejected from the cornea at supersonic velocity but decelerates rapidly; the velocity for the first 500 ns following the excimer pulse averages 400 m/s at 193 nm. Plume size and velocity increase with increasing fluence.

Animals↗

Computed tomographic investigation of serosal and intramural gastrointestinal pathology.

Various cases are presented demonstrating the role of computed tomography (CT) in the assessment of serosal and bowel wall pathology. Reference is made to the morphology of the lesions. Illustrative examples of tumors, secondary malignant dissemination, irradiation injury to the gut, and intramural gas associated with ulcerative colitis, are all illustrated.

Aged↗

Directionality of dental trait frequency between human second deciduous and first permanent molars.

Dental traits were scored for second deciduous molars (dm2) and first permanent molars (M1) on casts of the dental arches of children aged 7-11 years. The children were from four different ethnic groups. The overall frequency of traits differed between the groups but the relative frequency of expression of traits in the two teeth showed a similar pattern. Traits such as continuous oblique ridge, Carabelli cusp, Y pattern and 7th cusp, that appear in the early stages of development, were more frequent in dm2 than in M1. Wrinkling, occlusal tubercles and marginal ridge cusps were more frequent in M1; these appear later. Thus the relative frequency of traits in these teeth reflects their ontogenetic history.

Child↗

Cloned bovine aortic endothelial cells synthesize anticoagulantly active heparan sulfate proteoglycan.

Cloned bovine aortic endothelial cells were cultured with [35S]Na2SO4 and proteolyzed extensively with papain. Radiolabeled heparan sulfate was isolated by DEAE-Sephacel chromatography. The mucopolysaccharide was then affinity fractionated into two separate populations utilizing immobilized antithrombin. The heparan sulfate, which bound tightly to the protease inhibitor, represented 0.84% of the mucopolysaccharide mass, accounted for greater than 99% of the initial anticoagulant activity, and exhibited a specific activity of 1.16 USP units/10(6) 35S-cpm. However, the heparan sulfate that interacted minimally with the protease inhibitor constituted greater than 99% of the mucopolysaccharide mass, represented less than 1% of the starting biologic activity, and possessed a specific anticoagulant potency of less than 0.0002 USP unit/10(6) 35S-cpm. An examination of the disaccharide composition of the two populations revealed that the high-affinity heparan sulfate contained a 4-fold or greater amount of GlcA----GlcN-SO3-3-O-SO3 (where GlcA is glucuronic acid), which is a marker for the antithrombin-binding domain of commercial heparin, as compared with the depleted material. Cloned bovine aortic endothelial cells were incubated with [35S]Na2SO4 as well as tritiated amino acids and completely solubilized with 4 M guanidine hydrochloride and detergents. The double-labeled proteoglycans were isolated by DEAE-Sephacel, Sepharose CL-4B, and octyl-Sepharose chromatography. These hydrophobic macromolecules were then affinity fractionated into two separate populations utilizing immobilized antithrombin. The heparan sulfate proteoglycans which bound tightly to the protease inhibitor represented less than 1% of the starting material and exhibited a specific anticoagulant activity as high as 21 USP units/10(6) 35S-cpm, whereas the heparan sulfate proteoglycan that interacted weakly with the protease inhibitor constituted greater than 99% of the starting material and possessed a specific anticoagulant potency as high as 0.02 USP unit/10(6) 35S-cpm. The high-affinity heparan sulfate proteoglycan is responsible for more than 85% of the anticoagulant activity of the cloned bovine aortic endothelial cells. Binding studies conducted with 125I-labeled antithrombin demonstrated that these biologically active proteoglycans are located on the surface of cloned bovine aortic endothelial cells.

Animals↗

Tumor necrosis factor/cachectin interacts with endothelial cell receptors to induce release of interleukin 1.

Tumor necrosis factor/cachectin (TNF) has been implicated as a mediator of the host response in sepsis and neoplasia. Recent work has shown that TNF can modulate endothelial cell hemostatic properties, suggesting that endothelium is a target tissue for TNF. This led us to examine whether endothelial cells have specific binding sites for TNF and augment the biological response to TNF by elaborating the inflammatory mediator, IL-1. Incubation of 125I-recombinant human TNF with confluent, cultured human umbilical vein endothelial cells resulted in time-dependent, reversible, and saturable binding. Binding was half-maximal at a TNF concentration of 105 +/- 40 pM, and at saturation 1,500 molecules were bound per cell. Heat-treated TNF, which is biologically inactive, did not bind to endothelium. In addition to surface binding, TNF induced the elaboration of IL-1 activity by endothelial cells in a time-dependent manner. Generation of IL-1 activity required protein synthesis and was half-maximal at a TNF concentration of 50 +/- 20 pM. IL-1 activity from TNF-treated endothelium could be adsorbed by an immobilized antibody to IL-1. Heat-treated TNF was ineffective in eliciting endothelial cell IL-1. These data indicate that TNF can bind specifically to endothelium and initiate a cascade of inflammatory and coagulant events on the vessel surface potentially central to the host response to neoplasia and sepsis.

Cells, Cultured↗

Participation of endothelial cells in the protein C-protein S anticoagulant pathway: the synthesis and release of protein S.

The protein C-protein S anticoagulant pathway is closely linked to the endothelium. In this paper the synthesis and release of the vitamin K-dependent coagulation factor protein S is demonstrated. Western blotting, after SDS PAGE of Triton X-100 extracts of bovine aortic endothelial cells grown in serum-free medium, demonstrated the presence of protein S. A single major band was observed at Mr approximately 75,000, closely migrating with protein S purified from plasma absent from cells treated with cycloheximide. Metabolic labeling of endothelial cells with [35S]methionine confirmed de novo synthesis of protein S. Using a radioimmunoassay, endothelium was found to release 180 fmol/10(5) cells per 24 h and contain 44 fmol/10(5) cells of protein S antigen. Protein S released from endothelium was functionally active and could promote activated protein C-mediated factor Va inactivation on the endothelial cell surface. Warfarin decreased secretion of protein S antigen by greater than 90% and increased intracellular accumulation by almost twofold. Morphological studies demonstrated intracellular protein S was in the Golgi complex, concentrated at the trans face, rough endoplasmic reticulum, lysosomes, and in vesicles at the periphery. In contrast, protein S was not found in vascular fibroblasts or smooth muscle cells. A pool of intracellular protein S could be released rapidly by the calcium ionophore A23187 (5 microM). This effect was dependent on the presence of calcium in the culture medium and could be blocked by LaCl3, which suggests that cytosolic calcium flux may be responsible for protein S release. These results demonstrate that endothelial cells, but not the subendothelial cells of the vessel wall, can synthesize and release protein S, which indicates a new mechanism by which the inner lining of the vessel wall can contribute to the prevention of thrombotic events.

Animals↗

Activation of coagulation releases endothelial cell mitogens.

Recent studies have indicated that endothelial cell function includes elaboration of growth factors and regulation of coagulation. In this paper we demonstrate that activated coagulation Factor X (Factor Xa), a product of the coagulation mechanism generated before thrombin, induces enhanced release of endothelial cell mitogens, linking these two functions. Mitogenic activity generated by cultured bovine aortic endothelial cells in response to Factor Xa included platelet-derived growth-factor-like molecules based on a radioreceptor assay. Effective induction of mitogens by Factor Xa required the integrity of the enzyme's active center and the presence of the gamma-carboxyglutamic acid-containing domain of the molecule. Factor Xa-induced release of mitogens from endothelium occurred in serum-free medium and was not altered by hirudin or antibody to Factor V, indicating that it was a direct effect of Factor Xa and was not mediated by thrombin. Elaboration of mitogenic activity required only brief contact between Factor Xa and endothelium, and occurred in a time-dependent manner. Generation of enhanced mitogenic activity in response to Factor Xa was unaffected by the presence of actinomycin D and was not associated with increased hybridization of RNA from treated cells to a v-sis probe. Release of mitogenic activity was dependent on the dose of Factor Xa, being half-maximal at 0.5 nM and reaching a maximum by 5 nM. Radioligand binding studies demonstrated a class of endothelial cell sites half-maximally occupied at a Factor Xa concentration of 0.8 nM. The close correspondence between the parameters of Factor Xa-induced mitogen release and Factor Xa binding suggests these sites may be related. When Factor X was activated on the endothelial cell surface by Factors IXa and VIII, the Factor Xa formed resulted in the induction of enhanced release of mitogenic activity. These data suggest a mechanism by which the coagulation system can locally regulate endothelial cell function and vessel wall biology before thrombin-induced release of growth factors from platelets.

Animals↗

Regulation of growth hormone and somatomedin-C secretion in postmenopausal women: effect of physiological estrogen replacement.

To determine the effects of estrogen deficiency and replacement on GH secretion, we measured the 22-h GH secretory pattern and response to 1 h of light exercise in 16 normal postmenopausal women before and after treatment replacement with ethinyl estradiol (20 micrograms/day for 15 days). To determine whether the changes found were due to pituitary sensitization by estrogen, the response to synthetic GH-releasing hormone (GHRH; 1.0 microgram/kg, iv) was measured. To assess the biological effectiveness of GH in estrogen-treated women, somatomedin-C (Sm-C) responses to GHRH were measured. Pre- and postestrogen GH secretion rates, expressed as mean areas circumscribed by plasma GH values, were as follows: 22-h study, 1.4 +/- 0.1 (+/- SEM) vs. 2.0 +/- 0.3 ng/ml X h (P = 0.04; n = 5); during 1 h of exercise, 2.3 +/- 0.4 vs. 3.2 +/- 0.4 ng/ml X h (P = 0.03; n = 16); after GHRH-(1-40), 6.7 +/- 1.7 vs. 8.5 +/- 1.5 ng/ml X h (P = 0.12; n = 16). There also was a modest but significant increase in resting plasma GH (1.5 +/- 0.2 vs. 2.3 +/- 0.5 ng/ml (P = 0.039). Pre- and postestrogen plasma Sm-C concentrations were 0.56 +/- 0.08 and 0.32 +/- 0.03 U/ml, respectively (P = 0.006; n = 16). Thus, estrogen therapy increased spontaneous and exercise-induced GH secretion in postmenopausal women and reduced Sm-C levels. The mechanisms of GH elevation by estrogen may include both central effects and a negative feedback linkage to reduced plasma Sm activity.

Aged↗

Management of hypertension in twelve Oxfordshire general practices.

The general practice records of 2371 hypertensive patients on drug therapy in 12 practices were reviewed retrospectively. It was found that the mean systolic blood pressure of the patients had fallen by 29 mmHg and the mean diastolic pressure by 16 mmHg after one year of treatment and that there was a further reduction of 5 mmHg in the systolic pressure and 5 mmHg in the diastolic pressure at the most recent recording of blood pressure. Half of the patients had only a single blood pressure reading recorded before treatment was started and for 56% of the patients there was no record of smoking habit and for 69% no record of weight. Twenty-seven per cent of the patients suffered from mild hypertension, that is blood pressure less than 180/110 mmHg, and 56% were over 65 years of age. These results indicate the need for policies for selection of patients for treatment and for standards of recording. It is suggested that practices should review their results and undertake to treat elderly hypertensive patients and those with mild hypertension only when they can demonstrate that their policies are effective for young hypertensive patients and for those with moderate or severe hypertension.

Adult↗

Individual variation in enamel structure of human mandibular first premolars.

Nine human mandibular first premolars were examined to assess variation in external morphology and enamel structural organization within a tooth type. The relationship of enamel ultrastructure to gross dental morphology was also studied. The teeth were cut in the mesiodistal direction just lingual to the buccal cusp, and etched. Montages were constructed of the cut enamel surface photographed in the scanning electron microscope at 100 X magnification. Parameters were measured and correlation coefficients were calculated for the comparison of various odontometric features. The mesiodistal and buccolingual dimensions were highly correlated and the occlusal thickness of enamel was significantly correlated to crown height but not crown width. Hunter-Schreger bands were less pronounced in fossa areas than at lateral aspects, cusps, or ridges; these bands were directly related to the geometry of the tooth. It was concluded that within this tooth type, there is a large amount of individual variation not only in gross morphology but also in enamel ultrastructure. This result underscores the fact that interspecific comparisons must be made with care.

Bicuspid↗