A linguistic crisis? Maybe. A linguistic crises? Definitely not!
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Humans↗
Biomedical subjects
C S Jenkins
Publications and source records attributed to C S Jenkins.
Acquired von Willebrand syndrome: from pathophysiology to management.
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Hematologic Neoplasms↗
Salpingitis isthmica nodosa: a review of the literature, discussion of clinical significance, and consideration of patient management.
OBJECTIVES: To examine and discuss the pathology, diagnosis, incidence, and patient profile of salpingitis isthmica nodosa and to question its natural history, propose management strategies, and identify areas of promising research. DESIGN: Over 50 studies were reviewed, evaluated, and compared to offer the clinician a foundation on which to generate treatment plans. RESULTS: Salpingitis isthmica nodosa is diagnosed by the pathological presence of isthmic diverticula and may be suggested by characteristic changes on hysterosalpingogram. Its incidence in healthy, fertile women ranges from 0.6% to 11%, but it is significantly more common in the setting of ectopic pregnancy and infertility. There are no studies, retrospective or prospective, that clearly dictate appropriate therapy. CONCLUSION: Given its progressive nature and probable deleterious effects on fertility, we propose that microtubal surgery be the definitive treatment for qualified women who have salpingitis isthmica nodosa.
Fallopian Tubes↗
Mobilization of calla-positive lymphoblasts during treatment with granulocyte colony-stimulating factor.
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Adult↗
Psychopathology of chronic haemodialysis: is it a behavioural cognitive continuum?
Neuropsychiatric complications of chronic renal haemodialysis cover a wide gamut of clinical syndromes. These pictures can be diagnostically classified as non-psychotic and psychotic-like syndromes. On the basis of a review of the literature, some nosological precisions are formulated, and a hypothesized cognitive-behavioural psychopathological continuum is presented. The hypothesis postulates that a central cognitive disturbance, due to multiple organic aetiopathogenic factors, results in a step-wise decline, initially disguised as an affective, neurotic or personality disorder, and further deteriorating into the well-known "dialysis dementia", with a variety of other clinical presentations in between. Additional research in the biological and psychosocial areas is needed to verify different aspects of these conditions, their validity in the context of the authors' hypothesis, and their relevance to the overall "quality of life" of chronic haemodialysis patients.
Cognition Disorders↗
Fibronectin synthesis and degradation in human fibroblasts with aging.
Fibronectin was measured in early and late passaged human skin fibroblasts utilizing immunoprecipitation and polyacrylamide gel electrophoresis. A progressive increase in the rate of fibronectin and total cellular protein synthesis per cell was observed by late passaged human diploid fibroblasts. The absolute protein concentration increased in the late passaged fibroblasts. There was no significant difference in the [3H]leucine incorporation into fibronectin or total cellular protein/mg protein. The turnover of fibronectin and total cellular protein did not differ between early and late passaged fibroblasts. The transport of fibronectin to the cell membrane was similar in late passaged fibroblasts. The increased fibronectin synthesis in senescent fibroblasts appeared to correlate with the general increase in rate of protein synthesis/cell.
Cell Survival↗
Platelet cytoskeleton alpha-actinin in normal and thrombasthenic platelets: distribution and immunologic characterization.
The subcellular localization of alpha-actinin (Mr 100,000) in human skeletal muscle is restricted to the Z line, in which it is believed to anchor actin filaments. Recently, this protein was identified in normal and thrombasthenic human platelets by its antigenic cross-reaction with antibodies to chicken gizzard alpha-actinin. In our study, the biochemical interaction between purified platelet alpha-actinin and striated muscle F-actin was examined by electron microscopy of negatively stained preparations. Like its muscle counterpart, platelet alpha-actinin promotes the cross-linking and bundling of actin filaments. Antibodies prepared to human platelet alpha-actinin cross-reacted with chicken gizzard alpha-actinin as shown by immunoelectrophoresis and the western blotting technique. Immunoblots prepared with normal and thrombasthenic platelets with antibodies to human platelet alpha-actinin revealed that this protein is susceptible to proteolysis. Extracts of freshly drawn platelets showed a protein band of 100 K. When the platelet extracts were incubated at 37 degrees C for various times, the immunoblots showed protein bands of 100 and 80 K. The proportion of the 80 K protein band increased with incubation time. This proteolysis can be prevented by chelating agents such as EDTA or the protease inhibitor leupeptin. Indirect immunofluorescent studies of human skin fibroblasts with antibodies to chicken gizzard actin and human skeletal muscle, chicken gizzard, and platelet alpha-actinin revealed the staining pattern characteristic of each protein. The distribution of alpha-actinin in normal and thrombasthenic platelets was assessed by ferritin-labeled immunoelectron microscopy. Ferritin particles were found in the cytoplasm immediately below the membrane and in some granules. There was no labeling associated with the mitochondria.
Actinin↗
The effect of the extracellular matrix on the detachment of human endothelial cells.
Human umbilical vein endothelial cells can be serially passaged by supplementing medium with a partially purified growth factor. Cell-substratum detachment of early and late passage endothelial cells was examined using trypsin, collagenase, or homocysteine. Late-passage cells detached more rapidly than early passage cells under all conditions tested. The rate of detachment was dependent upon the specific agent used. Protease-mediated detachment was most rapid, occurring over minutes, in contrast to homocysteine-induced detachment, which occurred over hours. When detached cells were collected and replated in the absence of the detaching agent, these cells reattached, spread, and continued to proliferate. No significant difference was observed in the rate of adhesion of either early or late passage cells to a gelatin matrix. When early or late-passage endothelial cells were plated and grown to confluence on a matrix synthesized by the opposite cell type, the rate of protease-mediated cell detachment resembled the cell type from which the matrix was derived. The ease of endothelial cell detachment was determined by the origin of the extracellular matrix. Examination of the extracellular matrices from early and late passage cells revealed significant differences in the amounts of glycosaminoglycans and sulfated proteins present. These studies demonstrate the importance of the endothelial cell extracellular matrix in protease-mediated cell detachment. The rate of cell detachment was controlled by the extracellular matrices are not altered by the endothelial cells.
Cell Adhesion↗
Platelet cytoskeleton: immunofluorescence studies on thrombin-activated platelets.
Cytoskeletal proteins were isolated from chicken gizzard smooth muscle and from platelets and antibodies prepared against them. It was shown by indirect immunofluorescence technique that actin, alpha-actinin, and vinculin are not present on the surface of platelets. Physiologic concentrations of thrombin (0.04 to 0.5 U/ml) that induce platelet aggregation and release in the presence of calcium from freshly isolated platelets do not induce platelet changes resulting in the availability of the cytoskeleton to antibodies. Because the F(ab')2 fragments of anti-cytoskeletal proteins IgG do not inhibit thrombin-induced aggregation of platelets, the direct role of these proteins in thrombin-induced platelet aggregation, as with ADP and collagen, may be rejected. However, when freshly isolated platelets are treated with thrombin (1 U/ml), antibodies to actin, alpha-actinin, and vinculin stained the platelets; therefore, this demonstrates that thrombin at this high and probably nonphysiologic concentration induces a reorganization of the membrane components with the subsequent exposure of the proteins of the cytoskeleton. We demonstrate interaction between isolated actin and alpha-actinin but not vinculin with fibronectin. After stimulation of platelets by thrombin, certain cytoskeletal proteins may interact with subendothelial fibronectin and thereby promote and consolidate platelet adhesion.
Animals↗
Platelet cytoskeleton: immunofluorescence studies on ADP and collagen-activated platelets.
Immunofluorescence studies reveal that platelet changes induced by adenosine diphosphate and collagen do not include the reorganization of the cytoskeleton in such a way as to expose actin, alpha-actinin, or vinculin. However, when such platelets were made permeable by saponin, these cytoskeletal proteins were present. In studies with collagen, fluorescence was observed along the fibers at areas of platelet adhesion and where no platelets were seen by phase microscopy. No fluorescence was observed with collagen treated with platelet-poor plasma. Scanning electron microscopy of collagen samples treated with platelet-rich plasma revealed a fibrillar meshwork with single platelets, platelet aggregates, and nodular structures that were smaller in size than individual platelets. These nodular structures may represent remnants of platelets still attached to the collagen after platelet detachment has occurred. These tenacious collagen-platelet membrane-binding sites have associated with them cytoplasmic alpha-actinin and vinculin, proteins that have been proposed by others to anchor actin filaments to the plasma membrane.
Adenosine Diphosphate↗
Antibodies against platelet membrane glycoproteins. III. Effect on thrombin-and bovine Von Willebrand factor-induced aggregation.
Glycocalicin has been proposed as the common platelet receptor for both ristocetin-human VIIIR:WF and thrombin-induced platelet aggregation. Platelets which have lost glycocalicin do not respond to either ristocetin-human VIIIR:WF or bovine VIIIR:WF. Using antibodies to the platelet membrane glycoproteins Ia and Ib, IIb and IIIa, and glycocalicin we show that the Fab' fragments of anti-glycoproteins Ia and Ib and anti-glycocalicin IgG totally inhibited bovine VIIIR:WF-induced platelet aggregation, while those from anti-glycoproteins IIb and IIIa IgG were without effect. Thrombin-induced platelet aggregation was strongly inhibited by the Fab' fragments of anti-glycoproteins Ia and Ib IgG and anti-glycocalicin IgG, indicating that these glycoproteins play a major role in thrombin-platelet interaction. Fab' fragments of anti-glycoproteins IIb and IIIa IgG inhibited thrombin-induced platelet aggregation to a lesser extent implying that these glycoproteins are also somehow involved in the platelet response to thrombin perhaps as fibrinogen receptors. The data presented here give further support to the proposal that ristocetin-human VIIIR:WF and bovine VIIIR:WF share a common receptor on the platelet surface and indicate that this structure plays an important role in thrombin-induced platelet responses.
Antibodies↗
The effectiveness of progressive relaxation in chronic hemodialysis patients.
An experimental group of 38 patients on chronic hemodialysis were presented a 30-min, self-instructional, color videotape on progressive relaxation (PR) exercises; and a control group of 23 patients viewed a neutral videotape. Both groups were given the State-Trait Anxiety Inventory while on the dialysis machine, before and after the actual viewing. The experimental group significantly reduced its state anxiety level while the control group remained the same. Patients who reported higher levels of state anxiety and experienced tension more frequently tended to achieve the greater benefit from the program. It is postulated that PR can be a useful resource to overcome the sometimes severe anxiety related to the stresses of chronic hemodialysis.
Adult↗
Antibodies against platelet membrane glycoproteins. II. Influence on ADP- and collagen-induced platelet aggregation, crossed immunoelectrophoresis studies and relevance to Glanzmann's thrombasthenia.
In Glanzmann's thrombasthenia glycoproteins IIb and IIIa are missing or strongly reduced and aggregation to ADP, collagen and thrombin is impaired. Antibodies against glycoproteins IIb and IIIa did not entirely induce a thrombasthenia-like state in normal platelets. However, they did strongly inhibit collagen-induced aggregation and inhibited the second wave of aggregation induced by ADP. Crossed immunoelectrophoresis studies using Triton X-100 extracts of whole platelets with these antibodies gave a single immunoprecipitate. This immunoprecipitate was absent when similar studies were carried out with thrombasthenic platelets. Platelet antibodies gave a number of immunoprecipitates with normal platelets and differences were observed with thrombasthenic platelets, the most notable of which was a marked reduction in one of the major immunoprecipitates. These results provide further evidence that glycoproteins IIb and IIIa are involved in the latter stages of platelet aggregation.
Adenosine Diphosphate↗
Antibodies against platelet membrane glycoproteins. I. Crossed immunoelectrophoresis studies with antibodies that inhibit ristocetin-induced platelet aggregation.
Platelet membrane glycoproteins have been isolated by lectin-affinity chromatography and antibodies prepared against them. Platelets that have lost glycocalicin no longer respond to ristocetin-human VIIIR:WF, bovine VIIIR:WF, or to glycocalicin or glycoproteins Ia and Ib antibodies but are still agglutinated by glycoproteins IIb and IIIa antibodies. Glycoproteins Ia and Ib and glycocalicin antibodies, IgG and Fab' fragments, inhibited ristocetin-human VIIIR:WF-induced aggregation of fixed, washed platelets and of platelets in plasma while glycoproteins IIb and IIIa antibodies were without effect. Cross immunoelectrophoretic studies showed that glycocalicin was present on whole platelets in only trace amounts. Glycocalicin antibodies, however, recognized a slower migrating component. Platelets incubated in an EDTA-free medium no longer respond to ristocetin-human VIIIR:WF. Membranes isolated from such platelets contained glycocalicin which cross-reacted with a remnant of the slower migrating component. Glycoproteins Ia and Ib antibodies gave more complex patterns but it was possible to identify the slower moving component recognized by the glycocalicin antibodies. These results show that glycocalicin is not normally found as such on whole platelets but is present as a precursor which is most likely glycoprotein Ib. On degradation of this precursor, glycocalicin is released from the membrane and VIIIR:WF-receptor activity is lost.
Animals↗
Human blood platelet membrane glycoproteins. Resolution in different polyacrylamide gel electrophoretic systems.
The separation of the major platelet membrane glycoproteins of normal subjects and subjects with well defined platelet membrane glycoprotein abnormalities have been examined using four different polyacrylamide gel electrophoretic techniques (continuous and discontinuous). The mobilities of the resolved glycoprotein bands have been correlated with the glycoprotein nomenclature proposed for the conventional sodium dodecyl sulphate-phosphate buffer system. Since the glycoprotein distribution varies depending on the system used, the merits of each method should be considered before application to a specific problem.
Acetates↗
Spontaneous platelet aggregation in cerebrovascular disease II. Further characterisation of the platelet defect.
A group of 186 patients with Transient Ischaemic Attacks (TIA) or cerebral infarction (CI) was found to demonstrate in vitro Spontaneous Platelet Aggregation (SPA) in 39% of those studied. Of the 176 normal subjects studied the incidence on in vitro SPA was found to be 5%. Further investigation of the phenomenon of SPA revealed that: 1. it is associated with ADP-hyperaggregability, i. e. the threshold concentration to induce second wave aggregation is decreased; 2. it is dependant on the increase in pH which occurs in platelet-rich plasma stirring in an aggregometer while concurrent ADP-hyperaggregability is independant of this change in pH; 3. it is associated with malondialdehyde production and the release of endogenous 5-hydroxytryptamine; and that 4. in addition Km and Vmax values for [14c]-5HT incorporation are normal; and that 5. no gross abnormalities of the platelet membrane glycoproteins were apparent although occasionally glycoprotein III was found to be increased. This study demonstrates abnormal platelet behaviour in patients with TIA and CI where the enzyme system involved in thromboxane production is sufficiently stimulated, by stirring alone, to induce aggregation of platelets and the release reaction. Acetylsalicylic acid abolishes SPA and prolongs the bleeding time with similar characteristics as has been described for normal individuals. Plasma beta-thromboglobulin levels are significantly increased in the patients studied. However, no correlation was established with the incidence of in vitro SPA.
Adenosine Diphosphate↗
Acquired factor XII Deficiency in a patient with nephrotic syndrome.
A patient with nephrotic syndrome and an acquired factor XII deficiency associated with a factor XII-like procoagulant activity in the urine was investigated. The urinary protein with procoagulant activity was isolated and comparative investigations revealed similar properties to plasma factor XII. It is suggested that the acquired coagulation defect may result from an insufficient biosynthetic capacity to compensate for the loss of factor XII in the urine.
Adult↗