Takedown of Glenn shunts in adults with congenital heart disease with polytetrafluoroethylene grafts: technique and long-term follow-up.
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Adult↗
Biomedical subjects
G S Kopf
Publications and source records attributed to G S Kopf.
Molecular biology in the modern work-up of the infertile male: the time to recognize the need for andrologists.
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Ciliary Motility Disorders↗
Regulation of protein tyrosine phosphorylation during bovine sperm capacitation by a cyclic adenosine 3'5'-monophosphate-dependent pathway.
Mammalian sperm capacitation, defined as an obligatory maturational process leading to the development of the fertilization-competent state, results from a poorly understood series of morphological and molecular events. We report here that ejaculated bovine sperm, incubated under conditions that support capacitation in vitro, display a reproducible pattern of protein tyrosine phosphorylations that are regulated by a cAMP-dependent pathway. The appearance of these tyrosine phosphorylated proteins correlated temporally with the time course of capacitation induced by heparin, and these phosphorylations displayed a similar heparin concentration dependence. Glucose, which inhibits capacitation, inhibited these protein tyrosine phosphorylations in media containing heparin. The biologically active cAMP analogues (dibutyryl cAMP [db-cAMP], 8-bromo cAMP, sp-cAMPS) and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX) induced the same protein tyrosine phosphorylation patterns as seen with heparin. Moreover, these cAMP agonists could overcome the inhibition of the heparin-induced tyrosine phosphorylations by glucose. In contrast, Rp-adenosine-3',5'-cyclic monophosphorothioate (Rp-cAMPS), a protein kinase A (PK-A) antagonist, blocked the capacitation-associated increases in protein tyrosine phosphorylation. This cAMP regulation of the protein tyrosine phosphorylation pattern is mediated by PK-A since N-[2-(p-bromocinnamylamino) ethyl]-5-isoquinolinesulfonamide-dihydrochloride (H89), another inhibitor of PK-A, inhibited the heparin-induced protein tyrosine phosphorylation pattern in a concentration-dependent manner in either the absence or presence of db-cAMP, IBMX, and glucose. These data support a model for sperm capacitation that includes protein tyrosine phosphorylation as an important regulatory pathway, and a role for cAMP/PK-A in the regulation of this pathway leading to capacitation. These studies are the first to report a unique interrelationship between tyrosine kinase/phosphatase and cAMP signaling pathways at the level of PK-A in bovine sperm capacitation.
1-Methyl-3-isobutylxanthine↗
Spontaneous activation of ovulated mouse eggs: time-dependent effects on M-phase exit, cortical granule exocytosis, maternal messenger ribonucleic acid recruitment, and inositol 1,4,5-trisphosphate sensitivity.
With increasing time after ovulation, mammalian eggs become more sensitive to agonists of activation in vitro or may undergo spontaneous activation in vivo. We have tested the hypothesis that postovulatory eggs undergo time-dependent cell cycle and cytoplasmic changes that result in a partially activated state, accounting for their time-dependent susceptibility to activate. In vivo changes in key activation markers in mouse eggs were quantified at 13, 16, and 22 h post-hCG (1, 4, and 10 h postovulation). Spontaneous activation was first detected at 16 h, with a 20-25% decrease in the activities of histone H1 and mitogen-activated protein (MAP) kinases and with 3% of eggs undergoing both anaphase onset and a partial loss of cortical granules. By 22 h, more than 60% of eggs were in anaphase, H1 and MAP kinase activities had decreased 40-50%, the extent of zona pellucida modification had increased, and proteins normally synthesized after fertilization had appeared. Pronuclear formation in response to inositol 1,4,5-trisphosphate injection increased dramatically from 10% at 13 h to about 40% and 90% at 16 h and 22 h, respectively. The partial decreases (less than those after fertilization) in H1 and MAP kinase activities provide a likely biochemical basis for the increased sensitivity of eggs to agonists, seen over time, that results in pronuclear formation. Also, all of these time-dependent changes caution against the use of mouse eggs > 16 h after hCG administration in studying the mechanism of normal fertilization and have implications for animal and human in vitro fertilization.
Animals↗
Minimally invasive coronary artery bypass grafting: initial Connecticut experience.
We report the initial Connecticut experience with minimally invasive coronary artery bypass grafting. This procedure allows bypass grafting to the left anterior descending coronary artery utilizing the internal mammary artery as the conduit. The procedure is minimally invasive because it is performed through a mini-thoracotomy incision in the fourth anterior intercostal space and it is conducted without the use of cardiopulmonary bypass. The procedure has been applied to 13 patients operated between February and October 1996. All but one patient selected were poor candidates for conventional coronary artery bypass surgery because of advanced age (6), chronic renal failure/dialysis/kidney transplant (4), redo status with vulnerable grafts (1), severe peripheral vascular disease (6), severe chronic obstructive pulmonary disease (4). All patients survived operation and were discharged in good condition. Mean postoperative intubation time was seven hours and mean hospital stay was 4.5 days despite the very high pre-existing comorbidity of these patients. All patients are alive at the current follow-up time. Two patients required a conventional bypass procedure for occlusion of the minimally invasive graft, the first because of diffuse disease in the target artery and the second attributable to the technical limitations of minimally invasive coronary artery bypass grafting; both tolerated the subsequent procedure well. All patients are now angina-free. All four grafts studied by routine postoperative angiography were widely patent. Routine post-operative exercise nuclear imaging was normal in an additional patient. This procedure of minimally invasive coronary artery bypass grafting offers significant advantages compared to the conventional bypass procedure (short hospital stay, quick recovery, and, especially, avoidance of cerebrovascular accidents caused by the heart-lung machine). This minimally invasive procedure is expected to apply to a growing percentage of patients. The procedure, especially vis-à-vis angioplasty, may well offer the superior long-term patency of the mammary conduit achieved with a modest initial "investment" in hospital stay, costs of medical care, and discomfort and disability. A prospective, randomized trial comparing angioplasty and minimally invasive coronary artery bypass grafting is warranted.
Aged↗
Effects of calcium-BAPTA buffers and the calmodulin antagonist W-7 on mouse egg activation.
Results of numerous experiments indicate that the transient rise in intracellular Ca2+ following sperm-egg fusion is essential for the subsequent events that constitute egg activation. Some events of egg activation, e.g., cortical granule exocytosis, however, appear more sensitive to intracellular Ca2+ than other events, e.g., cell cycle resumption. To examine if specific events of egg activation have different thresholds for Ca2+, we manipulated buffered intracellular Ca2+ concentrations by microinjecting Ca2+-BAPTA buffers and then examined the effect on the cortical granule exocytosis, recruitment of maternal mRNAs, and cell cycle resumption. We find that whereas cortical granule exocytosis occurs over a narrow threshold range of injected free Ca2+ concentrations between 0.5 and 1.0 microM, recruitment of maternal mRNAs is only partially stimulated at injected free Ca2+ concentrations of 2.5 microM, and no evidence for cell cycle resumption was observed (up to 2.5 microM Ca2+). Although the Ca2+- and phospholipid-dependent protein kinase, protein kinase C, is implicated in aspects of egg activation, calmodulin is also a potential target for the transient increase in Ca2+ that occurs following fertilization. Whereas incubation of eggs in the presence of the calmodulin antagonist W-7 followed by insemination does not block cortical granule exocytosis, cell cycle resumption, as assessed by the metaphase-to-anaphase transition, a decrease in histone H1 kinase activity and the time course for the emission of the second polar body are significantly delayed/inhibited.
Animals↗
Regulation of protein tyrosine phosphorylation in human sperm by a calcium/calmodulin-dependent mechanism: identification of A kinase anchor proteins as major substrates for tyrosine phosphorylation.
Signal transduction pathways regulate various aspects of mammalian sperm function. When human sperm were incubated in a medium supporting capacitation, proteins became tyrosine-phosphorylated in a time-dependent manner. This phosphorylation was inhibited by genistein, a protein tyrosine kinase inhibitor. Phosphorylation was also reduced when sperm were incubated either in the presence of increasing concentrations of extracellular Ca2+ or in a medium containing the Ca2+ ionophore A23187. This Ca2+-induced dephosphorylation was calmodulin-dependent, suggesting that calcineurin was involved. In this regard, the calcineurin inhibitor deltamethrin inhibited the Ca2+ ionophore-induced dephosphorylation. A limited number of Mr 80,000-105,000 polypeptides were the most prominent phosphotyrosine-containing proteins present in human sperm. Unlike mouse sperm, which contains a tyrosine-phosphorylated isoform of hexokinase, a phosphotyrosine-containing hexokinase in human sperm was not detected. Most of the tyrosine-phosphorylated proteins were Triton X-100-insoluble and were localized to the principal piece of the flagellum, the region where the cytoskeletal fibrous sheath is found. Prominent phosphotyrosine-containing proteins of Mr 82,000 and 97,000 were identified as the human homologues of mouse sperm AKAP82, the major fibrous sheath protein, and pro-AKAP82, its precursor polypeptide, respectively. These proteins are A Kinase Anchor Proteins, polypeptides that sequester protein kinase A to subcellular locations. Taken together, these results suggest that protein tyrosine phosphorylation may be part of a signal transduction cascade(s) regulating events pertaining to capacitation and/or motility in mammalian sperm and that an interrelationship between tyrosine kinase and cAMP signaling pathways exists in these cells.
Alkaloids↗
Regulation of nuclear envelope assembly/disassembly by MAP kinase.
Mouse eggs arrested in metaphase II display high levels of cdc2/cyclin B1 and MAP protein kinase activities. Following fertilization there is a time-dependent decrease in the activity of each of these protein kinases. The decline in cdc2/cyclin B1 protein kinase correlates with the resumption of meiosis and the emission of the second polar body and precedes the decline in MAP kinase activity, which correlates temporally with the formation of the male and female pronuclear envelopes. These results suggest that high levels of MAP kinase activity are incompatible with the presence of a pronuclear envelope. To test this possibility, we expressed in mouse eggs a constitutively active form of MAP kinase kinase (MEK) whose only known target is p42/p44 MAP kinase. We show that following fertilization cdc2/cyclin B1 kinase activity declines and a second polar body is emitted. The endogenous MAP kinase remains active, however, and no pronuclear envelopes form. Thus, high levels of MAP kinase activity by itself in mouse eggs appear incompatible with the presence of a pronuclear envelope.
Animals↗
Properties and localization of a tyrosine phosphorylated form of hexokinase in mouse sperm.
Mouse sperm possess a phosphotyrosine-containing hexokinase type 1 (HK1) that is associated with the plasma membrane fraction of these cells (Kalab et al., 1994; J. Biol Chem 269:3810-3817). This apparent plasma membrane association appears unique, since somatic HK1 is normally cytoplasmic or bound to the outer mitochondrial membrane via contact sites with a voltage-dependent anion channel (porin) through a porin-binding domain. In male germ cells, three cDNA clones have been described that encode unique HK1 isoforms (HK1-sa, HK1-sb, HK1-sc) that do not contain porin binding domains (Mori et al., 1993: Biol Reprod 49:191-203). This suggests that these proteins might not be localized to the outer mitochondrial membrane and could have alternative functions in germ cells and/or sperm. We demonstrate in the mouse that male germ cells and sperm could potentially express four HK1 isoforms (HK1-sa, HK1-sb, HK1-sc, and the somatic HK1). At the protein level, at least one of the HK1 isoforms becomes phosphorylated on tyrosine residues during spermatogenesis. Treatment of sperm membrane fractions to dissociate the phosphotyrosine-containing HK1 (pY-mHK1) yields results demonstrating that pY-mHK1 has properties of an integral membrane protein. Indirect immunofluorescence using a monoclonal antibody to HK1 demonstrates specific staining both in the head and tail regions of sperm. Surface biotinylation of intact sperm followed by precipitation with either polyclonal HK1 antiserum or with avidin-Sepharose suggests that pY-mHK1 possesses an extracellular domain. These results suggest that mouse sperm contain at least one HK1 isoform that is present on the sperm head, has an extracellular domain, and behaves as an integral membrane protein.
Animals↗
Sperm from mice carrying two t haplotypes do not possess a tyrosine phosphorylated form of hexokinase.
Mouse sperm contain a tyrosine phosphorylated form of hexokinase type 1 (HK1; Kalab et al., 1994: J Biol Chem 269:3810-3817) that has properties consistent with an integral plasma membrane protein. Furthermore, this tyrosine phosphorylated form of HK1 has an extracellular domain and HK1 is localized to both the head and flagellum of nonpermeabilized cells (Visconti et al., 1995c). We have characterized HK1 in mature sperm from sterile tw32/tw5 mice (mutant sperm) that have defects in motility and sperm-egg interaction (Johnson et al., 1995: Dev Biol 168:138-149). Immunoprecipitation of mouse sperm extracts with an antiserum made against purified rat brain HK1 demonstrates the presence of HK1 in mutant sperm. Various biochemical and immunofluorescence assays indicate that at least a portion of the HK1 present in these cells is an integral membrane protein with an extracellular domain located on the sperm head and flagellum. However, immunoblot analysis with anti-phoshotyrosine antibodies demonstrates that HK1 in mutant sperm is not tyrosine phosphorylated. Northern blot and RT-PCR analysis does not indicate any obvious abnormalities in the transcription of somatic or germ cell-specific HK1 isoforms in mutant testes, and RFLP analysis of recombinant mice indicates that no genes specifying HK1 isoforms are located on chromosome 17. We have mapped the locus responsible for the lack of tyrosine phosphorylation of HK1 mutant sperm to the most proximal (to the centromere) of the four inversions within the t haplotype. A male sterility factor is located in this same inversion (Lyon, 1986: Cell 44:357-363). Since the mutant sperm are unable to complete fertilization, there could be a relationship between sterility and the lack of tyrosine phosphorylation of HK1 in these mutant sperm.
Animals↗
G protein gene expression during mouse oocyte growth and maturation, and preimplantation embryo development.
Fertilization in mammals initiates "egg activation," a series of events leading to embryo development. The signal transduction events that occur as a result of sperm-egg interactions and that initiate egg activation may be analogous to a ligand-receptor-effector pathway, but the details of this signaling pathway are poorly understood. Several lines of evidence support a role for guanine nucleotide-binding regulatory proteins (G proteins) in mammalian egg activation. Prior to initiating studies to examine further the role of specific G proteins in sperm-induced mouse egg activation, we needed to define the complement of G proteins expressed in the egg. Using a reverse transcription-polymerase chain reaction (RT-PCR) assay, the relative levels of mRNAs encoding specific G protein alpha, beta, and gamma subunits were determined in meiotically incompetent oocytes, fully-grown competent oocytes, metaphase II-arrested eggs, one-, two-, and eight-cell embryos, and blastocysts. mRNA transcripts representing all of the heterotrimeric G protein families were present at all of the stages examined, and all underwent significant changes in their patterns of expression. The following heterotrimeric G protein mRNA transcripts were present in oocytes, eggs, or preimplantation embryos: G alpha q family (q, 11, and 14), G alpha 12 family (12 and 13), G alpha i family (i1, i2, i3, t2, z, and s), beta subunits 1, 2, 4, and 5, and gamma subunits 2, 3, 5, and 7. A recently described large molecular weight G protein, G alpha h (Nakaoka et al., 1994: Science 264:1593-1596), was also present, G alpha 15, G alpha t1, G alpha olf, G alpha oA, G beta 3, G gamma 1, and G gamma 8 mRNA transcripts were not detected using this method. The most common pattern of expression observed was a maturation-associated decrease followed by an increase after the two-cell stage. Some transcripts, however, were expressed at low levels until the eight-cell to blastocyst stages, whereas others were expressed at high levels in the oocyte but following maturation declined and remained at a low level throughout preimplantation development.
Animals↗
Temporal patterns of gene expression of G1-S cyclins and cdks during the first and second mitotic cell cycles in mouse embryos.
Cell-cycle progression in somatic cells is regulated by a family of cyclins and cyclindependent kinases (cdks) that form specific complexes as a function of cell-cycle progression. However, the transcript abundance of G1-S cyclins and cdks during the meiotic and mitotic cell cycles of mammalian embryos has not been previously reported. Using a reverse transcription-polymerase chain reaction (PCR) assay that detects changes in either mRNA abundance or polyadenylation state, we examined the relative levels of gene expression for the G1-S cyclins and cdks, as well as for p21, p27, and the retinoblastoma (Rb) gene in mouse oocytes, metaphase II-arrested eggs, and 1-2-cell embryos. The PCR products for cyclins D1, D3, and A, as well as cdk4, p21, and Rb, displayed similar levels in meiotically incompetent and competent oocytes, as well as in metaphase II-arrested eggs. The levels of PCR products for cyclin D2, p27, and two forms of cdk2 were similar in meiotically incompetent and competent oocytes but decreased during oocyte maturation. Finally, the level of PCR products for cyclin E and cdk2 gradually decreased during the progression from meiotically incompetent oocytes to metaphase II-arrested eggs. When the levels of PCR products for the G1-S regulatory genes were evaluated during the first and second mitotic cell cycles, four main patterns were found: 1) steady levels for cyclin A; 2) steady levels followed by a 2-3-fold increase during the G2 phase of the second mitotic cell cycle for cyclins D1, E, cdk2, and p21; 3) a transient increase during the S and/or G2 phases of the first mitotic cell cycle for p27, cyclin D3, and the two forms of cdk2; and 4) higher levels during the first cell cycle and then a decrease with lower levels during the second mitotic cell cycle for cyclin D2 and Rb. cdk4 expression displayed a combination of patterns 2 and 3. The increase in the amount of PCR product for the cdk4 gene during the first mitotic cell cycle was due to polyadenylation, whereas the increase in the amount of PCR product for cdk4, cdk2, and cyclins D1 and E in the second mitotic cell cycle was a product of activation of the embryonic genome.
Amanitins↗
Maturation of mouse oocytes in serum-free medium.
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Animals↗
Cycloheximide-induced activation of mouse eggs: effects on cdc2/cyclin B and MAP kinase activities.
Fertilization of metaphase II-arrested mouse eggs results in resumption of meiosis and a decrease in both cdc2/cyclin B kinase and MAP kinase activities; the decrease in cdc2/cyclin B kinase activity precedes the decrease in MAP kinase activity. Cycloheximide treatment of metaphase II-arrested mouse eggs also results in resumption of meiosis but bypasses the fertilization-induced Ca2+ transient. However, it is not known if cycloheximide treatment results in the same temporal changes in cdc2/cyclin B kinase and MAP kinase activities that are intimately associated with resumption of meiosis. We report that cycloheximide-treated mouse eggs manifest similar temporal changes in the decrease in both cdc2/cyclin B kinase and MAP kinase activities that occur following fertilization, although cortical granule exocytosis is not stimulated. The decrease in cdc2/cyclin B kinase activity, however, does not seem to be required for the decrease in MAP kinase activity, since the decrease in MAP kinase activity still occurs in cycloheximide-treated eggs that are also incubated in the presence of nocodazole, which inhibits cyclin B degradation and hence the decrease in cdc2/cyclin B kinase. Following removal of these drugs, cdc2/cyclin B kinase activity remains high, MAP kinase activity increases to levels similar to that in the metaphase II-arrested eggs, and a spindle(s) forms with the chromosomes aligned on a metaphase plate. Results of these experiments suggest that some other protein with a relatively short half-life, e.g. cmos, a known upstream activator of MAP kinase, may be responsible for events leading to the decrease in MAP kinase activity.
Animals↗
Reoperative mitral valve surgery via right thoracotomy: decreased blood loss and improved hemodynamics.
BACKGROUND AND AIMS OF THE STUDY: Reoperative mitral surgery via sternotomy can be associated with significant complications, including excessive blood loss and injuries to the heart, great vessels and patent coronary artery grafts. The right antero-lateral thoracotomy offers excellent exposure with less risk from re-entry. MATERIALS AND METHODS: Between 1982 and 1992, 221 patients had repeat mitral valve procedures at our institution. Fifteen of these 221 underwent mitral valve replacement via right thoracotomy. Indications for surgery in each group included bioprosthetic valve failure, paravalvular leak and bacterial endocarditis. Fifteen patients having reoperative mitral valve surgery via right thoracotomy approach were compared with a control group of 33 patient who underwent surgery via repeat sternotomy. All thoracotomy patients underwent mitral replacement or repair with ventricular fibrillation without aortic cross-clamping. Operative time, cardiopulmonary bypass time, requirement for inotropic support, blood loss within the first six postoperative hours, number of blood units transfused, length of ICU stay, days to discharge, and 30-day survival were compared between the two groups. In addition, the preoperative PaO2/FiO2 (P/F) ratio was evaluated as a prognostic indicator. RESULTS: Bypass time (162 +/- 43 min thoracotomy group vs. 131 +/- 34 min sternotomy group), operative time (389 +/- 100 min thoracotomy group vs. 450 +/- 25 min sternotomy group), ICU stay (6 +/- 8 days thoracotomy group vs. 5 +/- 6 days sternotomy group), P/F ratio (352 +/- 142 thoracotomy group vs. 423 +/- 108 sternotomy group), and 30-day survival (93% thoracotomy group vs. 91% sternotomy group) were not found to be significantly different between groups. Of great significance was the reduction in blood loss (277 +/- 152 ml thoracotomy vs. 651 +/- 504 ml sternotomy, p < 0.05) and blood transfused (2.0 +/- 1.7 units thoracotomy vs. 6.5 +/- 3.3 units sternotomy, p < 0.01) with the thoracotomy approach. Also of significance was a reduction in frequency with which significant inotropic support was needed to separate from cardiopulmonary bypass (26% vs. 63%, p < 0.05). Despite decreased access to the heart for de-airing maneuvers, no cerebrovascular events whatsoever were noted with the thoracotomy approach. CONCLUSION: The right thoracotomy approach is recommended for redo mitral valve surgery. Despite these advantages, severe pulmonary dysfunction (as indicated by a P/F ratio less than 300) correlated with a prolonged hospital course in four thoracotomy patients; such patients should have repeat sternotomy.
Blood Loss, Surgical↗
Thromboembolic complications after Fontan operations.
BACKGROUND: Despite the increasing recognition of thromboembolic complications of the Fontan procedure, data characterizing such events are limited. The total cavopulmonary connection is believed to be less prone to this complication than other modifications of Fontan operations. We examined our experience with thromboembolism after Fontan operations to better characterize these events and their relation to the type of Fontan operation performed. METHODS AND RESULTS: We retrospectively identified 70 patients who underwent a Fontan operation between January 1978 and March 1994. Patients were divided into three groups: (1) total cavopulmonary connection, (2) atriopulmonary connection, and (3) conduit interposition. Fourteen patients (20%) developed a thromboembolic complication during a mean (+/- SD) follow-up of 5.2 +/- 4.7 years. The rate of thrombosis was similar in each group. The time from Fontan operation to thrombosis averaged 6.1 +/- 5.0 years. The overall rate of thromboembolic events was 3.9 per 100 patient-years. Twelve of the 14 thrombi were located within the venous circulation, 1 was in the left ventricle, and the location of 1 was undetermined. Six of the patients (43%) were asymptomatic, 3 (21%) presented with cerebrovascular events, and 5 (36%) presented with other symptoms. Thromboembolic events occurred from the perioperative period to 15 years after surgery. CONCLUSIONS: Thromboembolic complications occur frequently after the Fontan operation and its modifications and are a cause of significant morbidity. The time of presentation varies greatly. The rate of thrombosis appears to be similar in all modifications of the Fontan operation.
Adolescent↗
Optimal timing of coronary artery bypass graft surgery after acute myocardial infarction.
BACKGROUND: To assess optimal timing for coronary artery bypass graft surgery (CABG) after an acute myocardial infarction (AMI), all patients undergoing CABG without associated procedures at our institution from January 1, 1991, to July 30, 1992, were reviewed. Patients were divided into three groups based on time from infarct to revascularization. The control group consisted of patients operated on for angina refractory to medical management. Relative risks (incident infarction group divided by incident control group) were established for need of vasopressors, new balloon to separate from bypass, perioperative myocardial infarction, and hospital mortality. METHODS AND RESULTS: One hundred sixteen patients underwent CABG within 6 weeks of infarction. In the experimental group, 58 patients underwent CABG for non-Q-wave infarction, and 58 patients underwent CABG for Q-wave infarction. In the control group, 255 patients underwent surgery for angina without infarction. Patients were analyzed by group relative to the time between infarction and CABG. Patients were analyzed between infarction and CABG and assigned to one of three groups. Group 1 patients were revascularized within 48 hours; group 2, between 3 and 5 days; and group 3, after 5 days. Significance was determined by Fisher's exact or Mantel-Haenszel chi 2 test where appropriate. Multivariate analysis was performed on statistics that were significant. All patients within all groups after Q-wave or non-Q-wave myocardial infarction had a significantly higher risk of needing an intra-aortic balloon pump and vasopressors to be weaned from bypass and a greater incidence of perioperative MI compared with control patients. Surgical mortality is highest immediately after Q-wave infarctions. CONCLUSIONS: Patients with non-Q-wave infarction may undergo CABG relatively safely at any time. Acceptable timing for CABG after Q-wave infarction is after 48 hours.
Aged↗
Identification and localization of integrin subunits in oocytes and eggs of the mouse.
Results of a recent study have implicated egg integrins in sperm binding to the egg plasma membrane (Blobel et al., 1991: Nature 356:248-252). In this report, immunoprecipitation was used to identify, and confocal immunofluorescence microscopy was used to localize, several different integrin subunits in mouse eggs. Antibodies to alpha 2, alpha 5, alpha v, and beta 1 subunits, as well as antibodies to the fibronectin receptor (FNR; alpha 5 beta 1 and/or alpha 3 beta 1) and vitronectin receptor (VNR; alpha v beta 3 and/or alpha v beta 5), detect polypeptides of the appropriate molecular weights following immunoprecipitation. beta 1 is localized preferentially to either the microvillar or amicrovillar membrane/cortical regions of eggs, and these asymmetric localizations depend on the antibody used. Proteins recognized by anti-FNR antibodies are localized preferentially to the amicrovillar membrane/cortical region. Germinal vesicle-intact oocytes display a symmetric plasma membrane distribution using beta 1 and FNR antibodies, and the asymmetric distribution develops as a consequence of oocyte maturation and is clearly observed by metaphase I. In contrast to the membrane localization of these integrin subunits, alpha 2, alpha 5, and VNR are predominantly localized in the cytoplasm of both oocytes and eggs. In the oocyte, each of these integrin subunits is uniformly distributed throughout the cytoplasm. Oocyte maturation is associated with a redistribution of alpha 5 and VNR, leading to an asymmetric cytoplasmic distribution with an increased localization towards the spindle. alpha v, which is localized in the plasma membrane/cortex of both oocytes and eggs, does not show such a change during oocyte maturation. Results of these experiments are discussed in the context of a role for integrins in mediating sperm plasma membrane-egg plasma membrane interactions leading to egg activation.
Animals↗