Biomedical subjects

L L Phillips

Publications and source records attributed to L L Phillips.

At least 37 records · Page 2Linked to original sources

PubMed1994

Muscarinic cholinergic receptor binding in rat brain following traumatic brain injury.

Recent evidence suggests that excessive activation of muscarinic cholinergic receptors (mAChRs) contributes significantly to the pathophysiological consequences of traumatic brain injury (TBI). To examine possible alterations in mAChRs after TBI, the affinity (Kd) and maximum number of binding sites (Bmax) of mAChRs in hippocampus, neocortex, brain stem and cerebellum were determined by [3H]QNB binding. Three groups of rats were examined: 1 h post-TBI (n = 21), 24 h post-TBI (n = 21) and sham-injured rats (n = 21). Kd values were significantly higher in hippocampus and brain stem at 1 but not 24 h post-TBI compared with sham-injured controls (P < 0.05). Kd values did not significantly differ in neocortex and cerebellum at 1 or 24 h post-TBI compared with sham-injured controls. Bmax values did not significantly differ in any brain areas at 1 or 24 h post-TBI compared with sham-injured controls. These results show that TBI significantly decreases the affinity of mAChRs in hippocampus and brain stem at an early stage post-TBI, which may contribute to desensitization of mAChRs after TBI. The findings of no change in Bmax values are consistent with a transient elevation in ACh concentrations after TBI.

Animals↗

PubMed1994

Increase of c-fos and ras oncoproteins in the denervated neuropil of the rat dentate gyrus.

When the entorhinal cortical input to the rat dentate gyrus is destroyed, the process of sprouting and synaptogenesis begins within the denervated dendritic laminae. The present study used immunohistochemical methods to determine whether there was an increase in the oncoproteins c-fos and ras within the denervated neuropil of the dentate gyrus during this period of terminal growth and synapse formation. Animals were prepared for immunolabeling one, three, six and 30 days after unilateral lesion of the entorhinal cortex. Rats were perfused with paraformaldehyde fixative and brain sections were incubated with antibodies to either c-fos or ras oncoprotein. Qualitative light microscopic analysis showed a marked increase in both c-fos and ras proteins over the denervated zone at three days postlesion when compared to both the intact contralateral control and the naive control. At one- and six-day postlesion intervals there was also an increase in labeling over the denervated neuropil with each oncoprotein; however, the intensity of label was reduced relative to that of the three-day time interval. No increase in labeling over the denervated zone was visible for either antibody at 30 days postlesion. The high level of both c-fos and ras labeling in the denervated molecular layer was confirmed with Western blot analysis of dissected molecular layers from lesioned and contralateral control hippocampi. Controls for antibody and method specificity showed that the labeling was specific for c-fos and ras proteins. The high level of c-fos labeling over the denervated molecular layer was uniform with scattered punctate sites of reaction product interspersed in the neuropil. Glial cell bodies in the neuropil contained the highest levels of c-fos oncoprotein. The granule cell nuclei showed an apparent reduction in the level of c-fos labeling at one, three and six days postlesion when compared with the nuclear staining of naive control cases. At 30 days postlesion, high levels of labeling over the denervated zone were not visible and c-fos localization had returned to the typical predominant nuclear sites seen in controls. Ras oncoprotein localization was diffuse in the cell processes of the molecular layer, with intermittent glial labeling within the denervated zone. No cell nuclei labeling was observed with antibodies to ras protein. These results show that both c-fos and ras oncoproteins are increased within the denervated neuropil of the dentate gyrus during sprouting and synapse formation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

Combined fluid percussion brain injury and entorhinal cortical lesion: a model for assessing the interaction between neuroexcitation and deafferentation.

Laboratory studies suggest that excessive neuroexcitation and deafferentation contribute to long-term morbidity following human head injury. Because no current animal model of traumatic brain injury (TBI) has been shown to combine excessive neuroexcitation and significant levels of deafferentation, we developed a rat model combining the neuroexcitation of fluid percussion TBI with subsequent entorhinal cortical (EC) deafferentation. In this paradigm, moderate fluid percussion TBI was induced in each rat, followed 24 h later by bilateral EC lesion (BEC). Six conditions were examined: (1) fluid percussion TBI followed 24 h later by bilateral EC lesion (TBEC), (2) fluid percussion TBI (TBI), (3) bilateral EC lesion (BEC), (4) sham fluid percussion TBI (SHAM), (5) TBI followed 24 h later by unilateral EC lesion (TUEC), and (6) unilateral EC lesion (UEC). The first four groups were assessed for motor (with beam-balance and beam-walk testing) and cognitive deficits (with the Morris water maze) and hippocampal morphology (with immunocytochemistry and electron microscopy). The TUEC and UEC groups were assessed for cognitive deficits alone. Motor deficits were greater in the TBEC injury than in TBI or sham alone; however, no significant difference was observed between the TBEC and BEC conditions in motor performance. Cognitive deficits were of a greater magnitude in the combined TBEC injury model relative to each individual insult. These cognitive deficits appeared to be additive for the two experimental injuries, BEC deafferentation producing deficits intermediate between TBI and TBEC insults. Morphologic analysis of the dentate gyrus molecular layer at 15 days after TBEC showed that the distribution of synaptophysin-positive presynaptic terminals was distinct from that observed after either TBI or BEC alone. Specifically, the laminar pattern of presynaptic rearrangement induced by BEC lesion did not occur after TBEC injury. The present results show that axonal injury and its attendant deafferentation, when coupled with traumatically induced neuroexcitation, produce an enhancement of the morbidity associated with TBI. Moreover, they indicate that this model can effectively be used to study the interaction between neuroexcitation and synaptic plasticity.

Animals↗

PubMed1992

Expression of c-fos in the hippocampus following mild and moderate fluid percussion brain injury.

An oncoprotein mediator of gene expression, c-fos, was evaluated in the central fluid percussion model of traumatic brain injury (TBI). Since hippocampal CA1 neurons are particularly vulnerable to TBI, we hypothesized that TBI may produce pathobiologic changes in CA1, in part, by alterations in gene expression through c-fos. Sprague-Dawley rats were subjected to mild (1.0 atm) or moderate (2.1 atm) fluid percussion TBI or sham injury. At 15 min, 1 h, and 24 h after injury (or sham injury), sections from middorsal hippocampus were immunostained with antibodies to c-fos, and c-fos-positive CA1 neurons were counted. As predicted, c-fos was localized in the nuclei of CA1 pyramidal neurons. However, the intensity of label was not equal over all CA1 neurons. Cells with high-intensity c-fos label were more prevalent after mild TBI. The number of c-fos-labeled CA1 neurons was increased at 15 min after both mild and moderate TBI relative to paired sham controls. Counts of c-fos-positive neurons remained significantly elevated at 1 h postinjury only after mild TBI. By 24 h postinjury, the number of c-fos-positive cells at both injury levels was not different from sham controls. No difference was observed between the number of c-fos-positive cells in naive and sham controls. However, label intensity was slightly less in the naive cases. These results suggest that the pathobiologic changes at early intervals following mild or moderate TBI may involve c-fos alteration of gene expression and that c-fos expression may be differentially regulated as a function of injury level.

Animals↗

PubMed1991

Biphasic cellular response to transection in the newt optic nerve: glial reactivity precedes axonal degeneration.

Morphological interactions between axons and glia within the lesioned newt optic nerve were studied at time periods prior to the onset of Wallerian degeneration. Optic nerves were transected 0.5 mm from the eye, animals were killed at 5, 10, 20 and 30 min post-lesion, and the intracranial half of the tract was examined with light and electron microscopy. A sequence of structural changes was observed within the time interval 5-30 min post-lesion. Over the first 20 minutes these changes primarily involved the endogenous neuroglia; there was a displacement of glial nuclei from the center to the periphery of the nerve and an increase of 50-100% in glial cytoplasmic and nuclear area. Nuclei of reactive glia were euchromatic and surrounded by a high density of Golgi, vesicles, mitochondria and filaments, the last of which extended throughout the expanded glial processes. Optic axons appear intact at 20 min post-lesion except for some separation between the axolemma and myelin sheath in some of the myelinated fibres. By 30 min post-lesion both myelinated and non-myelinated fibres were found in various stages of lysis. Many of the expanded glial processes contained a population of vesicles aggregated adjacent to the glial plasmalemma. Profiles of infolded glial membranes suggested the opening of such vesicles into the extracellular space around degenerating axons. We conclude that, after optic nerve injury, there are very rapid reactive changes in glia and axons, with the changes in glia preceding the degenerative events in axons.

Animals↗

PubMed1991

Combination of in situ hybridization and immunocytochemistry to detect messenger RNAs in identified CNS neurons and glia in tissue culture.

We have developed a technique in which immunofluorescence is combined with in situ hybridization using cDNA and RNA probes to assess the expression and distribution of messenger RNAs (mRNA) by neurons and neuroglia in tissue cultures of the rat dentate gyrus. The probes used in this study include a cDNA probe for ribosomal RNA (rRNA) and an RNA probe (cRNA) for glial fibrillary acidic protein (GEAP), an intermediate filament protein subunit expressed by astrocytes in the central nervous system. Both ubiquitous (tubulin) and cell type-specific (MAP-2 and GEAP) antibodies were used to identify neurons and neuroglia in culture. Using this procedure, the mRNA for rRNA was found in the cell bodies and large processes of MAP-2-positive neurons and throughout the cytoplasm of GEAP-positive flat astrocytes. In process-bearing astrocytes, GEAP mRNA is concentrated in the cell body, although some hybridization also occurred in astrocyte cell processes. With this combined in situ hybridization-immunofluorescence technique, the expression and distribution of an mRNA can be examined in different immunocytochemically identified cell types under identical culture and hybridization conditions. It is also possible to determine if there is a differential subcellular distribution of an mRNA in a single cell and if the distribution of the mRNA reflects the distribution of the protein itself. Finally, this technique can be utilized to verify the specificity of probes for cell type-specific mRNAs and to determine appropriate hybridization conditions to produce a specific signal.

Animals↗

PubMed1990

Prolonged memory impairment in the absence of hippocampal cell death following traumatic brain injury in the rat.

Prolonged neurological dysfunction that results from an insult to the brain is often attributed to irreversible structural damage such as loss of neurons or axonal degeneration. For example, following cerebral ischemia even partial hippocampal CA1 neuronal loss has been proposed to be sufficient to result in deficits in hippocampal dependent spatial memory. This study examined if hippocampal CA1 neuronal loss and/or axonal injury was necessary to produce prolonged spatial memory deficits resulting from traumatic brain injury (TBI). Prior to TBI Sprague-Dawley rats were trained on an 8-arm radial maze, a task sensitive to detecting specific lesions of the hippocampus or its extrinsic connections. Following a mild, moderate, or sham injury, rats were tested for working and reference memory for 25 days. After 25 days of maze testing, histological cell counts were made from consistent coronal sections of the mid-dorsal hippocampus. Rats subjected to mild or moderate TBI manifested working memory deficits for 5 and 15 days, respectively, after injury in the absence of overt (all brain regions) or quantitative (CA1 only) evidence of neuronal death. The number of CA1 pyramidal neurons of representative sections of the mid-dorsal hippocampi for injured maze-deficit rats and sham control rats were: 1626 (S.E.M. = +/- 66) and 1693 (S.E.M. = +/- 69) per 10(6) micron2, respectively. Additionally, no overt evidence of axonal injury was observed in any forebrain structure including major intrinsic or extrinsic connecting hippocampal pathways. These data strongly suggest that mild to moderate TBI is capable of producing prolonged spatial memory deficits in the rat without evidence of either neuronal cell death in the intrinsic hippocampus or overt axonal injury in hippocampal pathways.

Animals↗

PubMed1990

Excitatory amino acid receptor subtype binding following traumatic brain injury.

Sprague-Dawley rats were subjected to a moderate level (2.2 atm) of traumatic brain injury (TBI) using fluid percussion. Injured animals were allowed post-trauma survival periods of 5 min, 3 and 24 h. Regional glutamate receptor subtype binding was assessed with quantitative autoradiography in each group for N-methyl-D-aspartate (NMDA), quisqualate and kainate receptor subpopulations at approximately the -3.8 bregma level and compared to a sham control group. [3H]glutamate binding to the NMDA receptor was significantly (P less than 0.05) decreased at 3 h post-TBI in the hippocampal CA1 stratum radiatum, the molecular layers of the dentate gyri and the outer (layers 1-3) and inner (layers 5 and 6) overlying neocortex. NMDA receptor binding was significantly reduced in layers 5 and 6 of the neocortex at all post-trauma survival times but no further differences were seen in the hippocampi. No significant changes were observed with [3H]AMPA binding to quisqualate receptors and [3H]KA binding was significantly reduced only in layers 5 and 6 of the neocortex at 24 h after TBI. These data further confirm the pathological involvement of the NMDA receptor complex in brain regions selectively vulnerable to moderate levels of TBI in this model.

Animals↗

PubMed1990

Protein synthesis in the neuropil of the rat dentate gyrus during synapse development.

Previous studies have shown that there are dramatic accumulations of polyribosomes under developing synapses on dendrites of CNS neurons. The present study was designed to evaluate what types of proteins might be synthesized by the synapse-associated polyribosomes. Hippocampal slices from rat pups sacrificed at 4, 7, 10, 12, 14, and 21 days after birth as well as slices from adult animals were incubated in a modified Eagle's medium containing 3H-leucine. After a 30 min exposure to radiolabeled amino acids, the slices were microdissected, separating the dendritic enriched molecular layer from the cell bodies of the dentate gyrus and the hippocampus proper. The level of protein synthetic activity was assessed by comparing the incorporation in cell body and dendritic laminae. Polypeptides present in each dissected zone were separated electrophoretically on 1D SDS-polyacrylamide gels according to their molecular weight and the newly synthesized proteins were analyzed through gel fluorography. The overall level of 3H-amino acid incorporation into protein (measured as cpm/microgram protein) was higher than that of the adult at all postnatal ages. When the entire slice was analyzed, the maximum incorporation was at 12 days after birth. In the dissected subregions of the slice the peak protein synthetic activity in cell-body-enriched regions of dentate gyrus and hippocampus proper was at 4-7 days postnatal, declining between 7 and 21 days to values comparable to the adult. By contrast, protein synthesis in the molecular layer of the dentate gyrus did not peak until 12 days after birth, decreasing toward adult rates after 14 days. The overall pattern of Coomassie stained polypeptides present in the dentate molecular layer was comparable at all ages examined. Moreover, one-dimensional gel analysis showed no qualitative differences in the proteins that were synthesized in the three dissected zones across ages.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1990

Increases in mRNA for cytoskeletal proteins in the denervated neuropil of the dentate gyrus: an in situ hybridization study using riboprobes for beta-actin and beta-tubulin.

Following destruction of entorhinal cortical (EC) input to the dentate gyrus there is an increase in protein synthesis within the denervated dendritic laminae. The present study utilized in situ hybridization to determine whether there were increases in the messenger RNAs (mRNAs) for beta-actin and beta-tubulin within the denervated neuropil of the dentate gyrus during the time of increased protein synthesis. Animals were prepared for in situ hybridization 2-21 days after a unilateral lesion of the EC. Brain sections were hybridized with either 3H or 35S-labeled riboprobes prepared from chick beta-actin and chick beta-tubulin mRNA. Analysis of light microscopic autoradiograms revealed increases in the mRNAs for beta-actin and beta-tubulin within the denervated neuropil between 6 and 8 days postlesion when compared to the intact dentate gyrus of the contralateral side. Labeling over the granule cell body layer was comparable on the two sides for both probes. Increases in both mRNAs were also observed in the scar tissue at the lesion site. These results suggest that local protein synthesis within the denervated neuropil of the dentate gyrus involves, in part, an increase in the production of actin and tubulin.

Actins↗

PubMed1990

The process of reinnervation in the dentate gyrus of adult rats: time course of increases in mRNA for glial fibrillary acidic protein.

The present study evaluates the time course of increased expression of the mRNA for glial fibrillary acidic protein (GFAP) within the dentate gyrus and hippocampus after unilateral lesions of the entorhinal cortex. Levels of GFAP mRNA were evaluated by dot blot hybridization of mRNA isolated from the hippocampus and quantitative in situ hybridization. For dot blot hybridization, RNA was isolated from pooled hippocampi obtained from animals killed at 12 hr, 1, 2, 4, 6, 8, 10, 14, and 30 d postlesion. A separate set of animals killed at 2, 4, 6, 8, 10, 12, 14, and 32 d were prepared for in situ hybridization. The dot blot analyses of mRNA isolated from the hippocampus revealed that on the side ipsilateral to the lesion, the levels of GFAP mRNA increased rapidly, reaching a peak at 2 d postlesion. The increases were not evident by 12 hr postlesion, but by 24 hr, levels of GFAP mRNA were 5-fold higher than control, and by 48 hr, the levels were over 6-fold higher than control. The levels of GFAP mRNA decreased after 2 d postlesion. At 4 and 6 d postlesion the levels were about 2-fold higher than control. At later postlesion intervals, mRNA levels were comparable to the control. At 2 d postlesion, the levels of GFAP mRNA were also increased about 2-fold over control levels on the contralateral side. After 2 d, the levels of GFAP mRNA on the contralateral side were comparable to the control. In situ hybridization revealed a complex pattern of changes in the levels of GFAP. At 2 d postlesion, the levels of GFAP mRNA increased dramatically throughout the hippocampus bilaterally. The increases were most pronounced in the denervated portions of the neuropil; however, the levels of GFAP mRNA were also substantially elevated in laminae that do not receive direct projections from the entorhinal cortex. GFAP mRNA levels were also increased in other areas that receive projections from the entorhinal cortex, including the septum, lateral-dorsal thalamus, and entorhinal cortex contralateral to the lesion. In addition, GFAP mRNA levels were increased in regions bordering the ventricles throughout the brain, and over the surface of the tectum. After 2 d postlesion, the increases in the levels of GFAP mRNA were for the most part restricted to areas containing terminal degeneration. The generalized increases throughout the hippocampus were no longer apparent. Areas bordering the ventricles continued to exhibit higher labeling than in control animals, but this effect was not as prominent as at 2 d postlesion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

Protein synthesis by rat hippocampal slices maintained in vitro.

The present study evaluates protein synthesis in rat hippocampal slices maintained in vitro. Transverse slices of hippocampus were prepared from both adult rats and rat pups during postnatal development and incubated in a gassed (95% O2/5% CO2) balanced salt medium containing 5 nM 3H-leucine. The time course of 3H-leucine incorporation into TCA-precipitable protein was determined using slices removed from the media after 5, 10, 20, 30, 40, 60, and 120 min of incubation. The pattern of 3H-amino acid incorporation was evaluated by fixing slices with paraformaldehyde, embedding the slices in plastic, and sectioning the slices end on and en face for autoradiographic analysis. Biochemical analysis of 300 and 400 micron slices revealed that incorporation of leucine into protein proceeds at a constant rate. The autoradiographic analysis revealed that in adult hippocampal slices of 300-600 micron thickness there was complete penetration of 3H-leucine with no indication of a gradient in the extent of incorporation throughout the slice. The pattern of grain density within 300-600 micron slices matches that previously reported after in vivo injections of radiolabeled amino acid, where grain density is highest over neuronal cell bodies and lower over the laminae that contain dendritic processes and axons (Phillips et al: Mol Brain Res 2:251-261, 1987). Hippocampal slices of 200, 800, and 1,000 micron thickness showed irregular labeling. Slices of 200 micron were filled with pyknotic nuclei and vacuoles and exhibited patchy labeling. In 800 micron slices there were isolated areas of good preservation within the slice core, but these areas exhibited little incorporation. Relative to the 300-600 micron slices, there was a higher number of pyknotic nuclei and a much deeper layer of necrosis along the cut edges. Slices of 1,000 micron thickness showed poor preservation throughout and low levels of incorporation. Biochemical studies revealed a much higher rate of incorporation in the slices prepared from postnatal animals. Autoradiography of the slices from developing rats revealed that penetration was excellent and incorporation appeared to be greater as judged by an overall higher grain density. We believe that rat hippocampal slices provide a good in vitro model of protein metabolism that will be useful for studies of protein synthesis in isolated cell body and dendritic laminae and for the evaluation of whether protein synthesis in particular laminae is regulated by synaptic activity.

Amino Acids↗

PubMed1988

Protein synthesis and processing in cytoplasmic microdomains beneath postsynaptic sites on CNS neurons. A mechanism for establishing and maintaining a mosaic postsynaptic receptive surface.

Recent studies have shown that protein synthetic machinery consisting of polyribosomes and associated membranous cisterns is selectively localized beneath synaptic sites on neurons. In the present paper, the role of this machinery in neuronal function will be considered. We will: 1. Summarize the studies that characterize the polyribosomes and define their associations with membranous cisterns. Taken together, these observations suggest the existence of a system for the synthesis and posttranslational processing of proteins at individual synaptic sites; 2. Review the evidence that the protein synthetic machinery is particularly prominent during the initial formation of synaptic contacts (during early development), and during lesion-induced synaptogenesis in mature animals. These observations have led to the hypothesis that the polyribosomes produce proteins that play a role in the formation of the synaptic junction; 3. Review evidence that supports the hypothesis that there is a local synthesis of protein within dendrites, as well as local glycosylation; 4. Describe the evidence suggesting that at least some of the protein constituents of the synaptic junction itself are synthesized locally; and 5. Describe our studies that reveal a mechanism for selective dendritic transport of RNA; this transport mechanism permits the delivery of RNA to postsynaptic sites throughout the dendritic arbor. We will advance the hypothesis that neurons position protein synthetic machinery together with the mRNA's that are appropriate for particular synapses beneath synaptic contact regions. At the synaptic site, this machinery could then direct the synthesis of particular proteins that are critical for synapse formation or maintenance. The positioning of protein synthetic machinery at postsynaptic sites permits a rapid local regulation of the production of key proteins by events at individual synapses.

Animals↗

PubMed1987

Increases in ribosomal RNA within the denervated neuropil of the dentate gyrus during reinnervation: evaluation by in situ hybridization using DNA probes complementary to ribosomal RNA.

Previous studies have revealed that there are increases in the incorporation of [3H]amino acids into protein in the denervated neuropil of the dentate gyrus during periods of reactive synaptogenesis. The present study evaluates whether the increase in incorporation reflects an increase in protein synthetic machinery (ribosomes) in the denervated zone. We evaluated the distribution of ribosomal RNA (rRNA) in the denervated dentate gyrus 2-14 days after unilateral destruction of the entorhinal cortex using DNA probes complementary to rRNA for in situ hybridization. Animals with comparable lesions were injected with [3H]leucine 30 min prior to sacrifice and prepared for autoradiography in order to define the extent of protein synthesis within the denervated neuropil. Quantitative analyses revealed that the increases in [3H]leucine incorporation were accompanied by increases in labeling with the rRNA probe. In both cases, the increases were first apparent at 2 days postlesion, reached a peak on day 6, and then declined between 8 and 14 days postlesion. Plots of grain density across the neuropil revealed that the increases in rRNA, like the increases in amino acid incorporation, occurred selectively within the denervated portion of the neuropil. We propose that increased incorporation of protein precursor is the result of an increase in protein synthetic machinery within the denervated neuropil. These increases may reflect in part the increases that we have previously noted in polyribosomes under dendritic spines.

Animals↗

PubMed1984

Transfusion support in acquired coagulation disorders.

Transfusion support for acquired coagulation defects can be life-saving when used correctly. There should be laboratory evidence of such defects combined with clinical evidence of excessive bleeding. The laboratory values alone should not be treated except in preparation for an invasive procedure. Then plasma defects are best treated with fresh frozen plasma immediately before surgery since many of the factors have short half-lives. Platelet infusions are better withheld until the platelet-destroying features of some surgical procedures are completed, as in splenectomy or extracorporeal circulation.

Anticoagulants↗

PubMed1983

Bodian's silver method reveals molecular variation in the evolution of neurofilament proteins.

The recent demonstration that Bodian's silver method specifically stains mammalian neurofilament subunits (NFs), but not other intermediate filament proteins (IFs), provides a specific marker for the identification of neurofilament polypeptides. We have applied the Bodian stain to SDS-PAGE separated polypeptides in nervous tissues from 9 species, representing neuronal evolution in 4 major phyla: chordata, mollusca, arthropoda and annelida. Every species tested except the arthropod showed intense silver staining of a set of polypeptides, each subsequently identified as NFs by immunomethods. These results demonstrate that the affinity of NFs for Bodian's silver stain is conserved during the evolution of nervous systems in a diverse spectrum of animals. Further, considerable variation in the molecular weight of NF subunits was found among the 6 vertebrates studied. This variation suggests that the molecular weight of NFs has not been conserved during evolution, a quality which appears to be unusual for a structural protein.

Animals↗

PubMed1979

Coagulation studies of patients taking low-dose heparin during and after major gynecologic surgery.

In February, 1975, a prospective, randomized study of 75 patients undergoing major gynecologic surgery was undertaken. Patients were randomly assigned to three groups regardless of diagnosis and surgery contemplated. Coagulation studies were performed preoperatively and postoperatively in a control group, a receiving 2,000 U heparin/12 hr subcutaneously, and a third group receiving 5,000 U/12 hr via the same route. There was a statistically significant increase noted in fibrin degradation products in the group treated with 5,000 U heparin/12 hr as compared to the control group. Excessive bleeding intraoperatively or postoperatively was not encountered.

Antifibrinolytic Agents↗

PubMed1979

Procoagulant activity of ascitic fluid in hepatic cirrhosis: in vivo and in vitro.

Three cases of disseminated intravascular coagulation following infusion of ascitic fluid from the peritoneal cavity to the vascular system are reported in patients with hepatic cirrhosis. One of these was treated with intermittent drainage and infusion, and in the other two a LeVeen shunt was used. Studies on the ascitic fluid indicate the presence of a procoagulant material which would appear to be an activator of factor X. Preactivated factor X (Xa) from the fluid and/or a tissue factor activator of factor VII are additional possibilities.

Adult↗