Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “APES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources

Further data about venous channels in South African Plio-Pleistocene hominids.

Original data about venous channels in South African Plio-Pleistocene hominids are discussed. To assess possible changes in blood volume flow of fossil hominids, we test whether dimensions of three extracranial venous foramina were different between Australopithecus africanus and Australopithecus (Paranthropus) robustus. Moreover, providing further data about the small sample of South African Plio-Pleistocene hominids, we also attempt to re-analyse the incidence of divided hypoglossal canals and four emissary foramina in a very large sample of extant African apes representing all ages, species and subspecies, in A. africanus and in "robust australopithecines". Up to now, only very poor data on extracranial dimensions of venous foramina were available for fossil hominids. However, this topic provides interesting information about the modifications of volume flow during human evolution. Assuming that in fossil hominids, as in humans, dimensions of condylar and mastoid foramina, as well as those of jugular foramina, depended on volume flow through them, we conclude, first, that volume flow through internal jugular veins was comparable in South African australopithecines, extant chimpanzees and humans, and second, that, in comparison with the extant less-encephalized chimpanzees (presumably reflecting the ancestral condition), volume flow was higher through condylar veins in A. (P.) robustus. This increase was responsible for a significantly greater amount of blood drainage from the brain (and consequently an increased arterial blood supply). We support the view that encephalization was the prevailing functional explanation for volume flow increase through condylar veins in A. (P.) robustus, in comparison with its ancestor with its presumably more ape-like degree of encephalization. Considering the incidence of emissary canals and foramina, significant differences between A. africanus, "robust australopithecines" and all the extant African ape species, were tested statistically. Concerning the condylar canal, we did not find differences between "robust australopithecines" and extant African apes. Concerning the incidence of divided hypoglossal canals, mastoid canals, parietal and occipital foramina, no difference was found between extant African apes, A. africanus and "robust australopithecines". High frequencies of either condylar or mastoid canals cannot be regarded as a "pongid condition". Moreover, we did not find convincing data to support the hypothesis that mastoid emissary veins (partly representing a putative "radiator" for cooling the brain) were selected in A. africanus, in comparison with "robust australopithecines".

Adult↗

Mutations affecting a regulated, membrane-associated esterase in Salmonella typhimurium LT2.

Mutations at the apeA locus in Salmonella typhimurium lead to loss of a soluble enzyme ("protease I") that hydrolyzes the chromogenic endoprotease substrate N-acetyl phenylalanine beta-naphthyl ester. We have isolated pseudorevertants of S. typhimurium apeA mutations that have regained the ability to hydrolyze this compound. These pseudorevertants contain mutations (apeR) that lead to overproduction of a membrane-bound esterase different from protease I. The apeR locus is phage P1 cotransducible with ilvC (83 map units) and is unlinked to apeA. Mutations at still another locus, apeE, lead to loss of the membrane-associated esterase. The apeE locus is P1 cotransducible with purE (12 map units). In an apeE-lacZ operon fusion strain, an apeR mutation increases the level of beta-galactosidase approximately 60-fold. We propose that apeR encodes a repressor of apeE. The evidence available suggests that the ApeE protein is not a protease.

Esterases↗

Induction of an ATP-polymerizing enzyme in TMV-infected tobacco and its homology to the human 2'-5' A synthetase.

Several reports have indicated that tobacco carries an enzyme (APE) that, in the presence of poly (rI):(rC), polymerizes ATP to oligoadenylates. This paper demonstrates that the tobacco APE system comprises several proteins (estimated sizes: 32, 42, 67, and 84 +/- 10% kD). Only one of these proteins (the "67-kD" form) binds to poly (rI):(rC). This APE form has been purified by affinity chromatography on a synthetic ds-RNA column. Four tobacco proteins, including the purified one, crossreact with antibodies against the human enzyme, 2'-5' A synthetase. The ATP-binding capacity of some of these proteins has also been demonstrated. The amount of plant oligoadenylates obtained by polymerizing ATP with the purified APE form allows, for the first time, their direct analysis by TLC. The TLC analysis indicated that the oligomer produced by APE is not identical to the 2'-5' oligoadenylate. The appearance of the 2'-5' A-related proteins correlates with the build up of TMV infection, and the pattern of their stimulation and turnover was established. Nucleic acid hybridization indicates homology of tobacco DNA and RNA sequences with cloned cDNA of the human 2'-5' A synthetase gene. The stimulation in tobacco, upon TMV infection, of mRNA species homologous to the above human cDNA has been demonstrated. The analogy between the plant and the human system is discussed.

Adenine Nucleotides↗

Internalization and shedding of Lym-1 monoclonal antibody following interaction with surface antigens of a cultured human B cell lymphoma.

Modulation of surface antigens of Raji Burkitt's lymphoma cells by monoclonal antibody Lym-1 was investigated by flow cytometry and radioimmunoassay (RIA). Raji cells, treated with antibody conjugated with FITC, became bright green as determined by FACS and the FITC-labeled Lym-1 remained associated with target cells for up to 48 hr after incubation at either 4 or 37 degrees C. Lym-1 antibody linked with biotin also bound to Raji cells and rendered these cells highly reactive with avidin-phycoerythrin (APE). However, the APE fluorescence intensity measured by FACS decreased substantially when Raji cells were cultured at 37 degrees C for 1 hr prior to APE exposure but not when incubation was carried out at 4 degrees C, indicating a disappearance of antibody from the surface of the metabolically active cells. This process was time dependent with a total loss of surface-bound biotinylated antibody occurring over a period of approximately 2 hr. Raji cells exposed to both fluoresceinated and biotinylated Lym-1 in a double labeling experiment became positive to both reagents. The flow cytometric profile was not altered when these cells were incubated for 1 hr at 4 degrees C followed by reaction with APE. However, they failed to react with APE when the 1-hr incubation took place at 37 degrees C despite the fact that they remained FITC positive, suggesting that the antibody with its fluorescent label had entered the cells. Utilizing 131I-labeled Lym-1 it was determined that approximately 50% of initially bound antibody had dissociated from the cells within the first 2 hr of incubation at 37 degrees C, although the remainder persisted with targets for up to 48 hr. The HPLC protein profile indicated that the radioactivity found in the culture supernatants and cytoplasm was associated with whole antibody, degradation products, and Ig complexes with antigen. Therefore, the present findings suggest that Lym-1 Ig molecules react with cell surface antigens and are rapidly internalized and shed, resulting in the disappearance of antibody from the surface membrane of Raji cells.

Antibodies, Monoclonal↗

Anthrylvinyl-labeled phospholipids as membrane probes: the phosphatidylcholine-phosphatidylethanolamine system.

The phase behavior of mixtures of phosphatidylcholine (PC) with phosphatidylethanolamine (PE) identical or differing in their fatty acid composition has been investigated by using the steady-state fluorescence anisotropy of anthrylvinyl-labeled PC and PE (APC and APE) as well as of the non-lipid probe 1,6-diphenyl-1,3,5-hexatriene (DPH) to detect temperature-dependent changes in multilayer liposomes. APC, but not APE, was able to detect the pretransition of dimyristoyl-PC. The phospholipid probes APC and APE showed the main phase transition of their unlabeled disaturated analogues at temperatures almost identical with those revealed by differential scanning calorimetry, whereas the onset of the PE phase transition recorded by DPH was several degrees higher. In PC-PE mixtures with high content of PE the phase transitions shown by APC and APE were broader than those recorded by DPH. Comparison of phase diagrams constructed on the basis of fluorescence anisotropy and calorimetric data led to the conclusion that in biphasic PE and PC-PE systems DPH tends to partition into solid regions, whereas the anthrylvinyl-labeled phospholipids distribute more evenly between coexisting phases or prefer fluid domains. The use of anthrylvinyl phospholipid probes made it possible to demonstrate that PEs and PCs identical in their fatty acids are not miscible completely, not only below but also well above Tm of the higher melting component. Generally, APC and APE fluorescence anisotropy measurements correctly reflect headgroup-dependent phase segregations in mixtures of PC with PE, but may lead to ambiguous conclusions if demixing is caused by differences in the hydrocarbon chains.

Chemical Phenomena↗

Autoantibodies to kininogen-phosphatidylethanolamine complexes augment thrombin-induced platelet aggregation.

Autoantibodies to the zwitterionic phospholipid (PL), phosphatidylethanolamine (PE), have been described in patients with thrombotic disease. We have reported that certain anti-PE antibodies (aPE) are not specific for PE, but are directed to PE-binding plasma proteins, high molecular weight kininogen (HK) and low molecular weight kininogen (LK). Kininogens bind to platelets and inhibit thrombin-induced platelet aggregation. This inhibition is specific for thrombin because kininogens do not inhibit platelet aggregation induced by adenosine diphosphate (ADP), collagen or calcium ionophore. To date, a platelet kininogen receptor has not been described. We recently reported that purified kininogens bind to purified PE in vitro. This opens the possibility that kininogens can bind to platelets by virtue of exposed PE in the platelet membrane. We thus questioned if aPE can recognize platelet bound kininogens and negate their antithrombotic property. Our experiments support this possibility by demonstrating that exogenously added kininogen-dependent IgG aPE markedly increased thrombin-induced platelet aggregation in vitro but did not alter ADP-induced aggregation. In contrast, kininogen independent IgG aPE which recognized PE per se did not augment thrombin-induced platelet aggregation. These data support a hypothesis that kininogen dependent aPE may cause thrombosis in vivo due to disruption of the normal antithrombotic effects of kininogen.

Animals↗

Prostacyclin synthesis elicited by cholinergic agonists is linked to activation of M2 alpha and M2 beta muscarinic receptors in the rabbit aorta.

This study was conducted to investigate the subtypes of muscarinic receptors involved in the action of cholinergic agents on prostacyclin synthesis in the rabbit aorta. Prostacyclin production measured as 6-keto-PGF1 alpha was assessed after exposing the aortic rings to different cholinergic agents. Acetylcholine (ACh) (M1 and M2 agonist) (1-10 microM) and arecaidine proparagyl ester (APE) (M2 selective agonist) (1-10 microM) enhanced 6-keto-PGF1 alpha output in a concentration-dependent manner. A selective M1 receptor agonist, McN-A-343, at 1 microM-1 mM did not alter 6-keto-PGF1 alpha output. ACh- and APE induced increases in 6-keto-PGF1 alpha output were attenuated by the M1/M2 antagonist atropine (0.1 microM), M2 alpha antagonist (AF-DX 116), (0.1-1.0 microM), and by selective M2 beta antagonist, hexahydro-sila-difendiol (HHSiD) (0.1-1.0 microM), but not by the M1 antagonist pirenzepine (1.0 microM). 6-Keto-PGF1 alpha output elicited by ACh- or APE was not altered by the adrenergic receptor antagonists phentolamine and propranolol or by the nicotinic receptor blocker hexamethonium. Similarly, the arachidonic acid- or norepinephrine induced 6-keto-PGF1 alpha accumulation was not altered by these muscarinic receptor antagonists. Indomethacin, a cyclooxygenase inhibitor, prevented arachidonic acid, ACh- or APE induced 6-keto-PGF1 alpha output. Removal of the endothelium abolished the production of 6-keto-PGF1 alpha elicited by ACh, APE, bradykinin, and calcium ionophore A 23187, but not that induced by angiotensin II, K+ or norepinephrine. These data suggest that vascular prostaglandin generation elicited by cholinergic agonists is mediated via activation of M2 alpha and M2 beta but not M1 muscarinic receptors, which are most likely located on the endothelium.

6-Ketoprostaglandin F1 alpha↗

Myoglobin stratifies short-term risk in acute major pulmonary embolism.

BACKGROUND: Concentrations of cardiac troponins can be elevated in acute pulmonary embolism (APE) indicating myocardial injury. Although concentration of myoglobin (MYO) increases after myocardial damage, even before detectable rise of cardiac troponin levels occurs, MYO was not evaluated in APE. Therefore, we assessed prevalence and prognostic significance of myoglobin in major APE. METHODS: We studied 46 patients (30 women, aged 61.9+/-17.8 years) with major APE defined with right ventricular dilatation. On admission serum myoglobin, and cardiac troponin T (cTnT) were measured. Serum MYO concentrations >58 ng/ml for women, and >72 ng/ml for men were considered abnormal. CTnT>0.01 ng/ml was regarded to indicate myocardial injury. RESULTS: MYO levels exceeding sex specific norms were found in 21/46 (45.7%) of patients, while detectable cTnT was found in 24/46 (52.1%) of patients. Seven patients died during hospitalization. Elevated MYO significantly predicted in-hospital mortality (OR 25, 95% CI 1.3-474.2), while increased cTnT concentration did not affect the survival. Among clinical and echocardiographic variables only older age indicated worse prognosis (OR 1.6, 95% CI 1.06-2.41). CONCLUSIONS: Myoglobin levels are elevated in serum on admission in almost half of patients with major APE. Elevated myoglobin level, marker of myocardial injury, is a powerful predictor of increased risk of fatal outcome in major pulmonary embolism.

Aged↗

Little foot and big thoughts--a re-evaluation of the Stw573 foot from Sterkfontein, South Africa.

The part of the fossil assemblage Stw573 consisting of some medial foot bones was initially reported by Clarke & Tobias (Science 269 (2002) 521). They found it to have both ape- and human-like qualities, being human-like proximally and ape-like distally. We have undertaken a re-examination of this pedal assemblage using a multivariate analysis; while we also found ape- and human-like qualities, they are in direct conflict with the original findings of Clarke and Tobias. We report an essentially ape-like morphology proximally and a human-like morphology distally; the talus and navicular were found to be ape-like and the medial cuneiform human-like. We also undertook a morphometric analysis of the medial cuneiform from the fossil assemblage OH8, as this was not included in the original OH8 study of Kidd et al (J Hum Evol 31 (1996) 269); this cuneiform was found to have a human-like morphology. Thus, the medial column findings from the two assemblages are very similar. This finding, coupled with the re-evaluation of the stratigraphy at Sterkfontein (Am J Phys Anthrop 119 (2002) 192), suggests that the two may have been contemporaneous. We also note that three broad patterns of modification have been identified, equating to proximal-distal lateral-medial (cranio-caudal) and dorsal plantar (posterior-anterior). It has not escaped our notice that these patterns are each controlled by specific genes or growth factors; we thus see a morphometric expression of our developmental past.

Animals↗

Antinociceptive, anti-inflammatory and antidiabetic properties of Hypoxis hemerocallidea Fisch. & C.A. Mey. (Hypoxidaceae) corm ['African Potato'] aqueous extract in mice and rats.

In order to scientifically appraise some of the anecdotal, folkloric, ethnomedical uses of Hypoxis hemerocallidea Fisch. & C.A. Mey. (Hypoxidaceae) corm ['African Potato'], the present study was undertaken to examine the antinociceptive, anti-inflammatory and antidiabetic properties of the corm's aqueous extract (APE) in mice and rats. The antinociceptive effect of APE was evaluated by 'hot-plate' and 'acetic acid' analgesic test methods in mice; while the anti-inflammatory and antidiabetic effects of the plant's extract were investigated in rats, using fresh egg albumin-induced pedal (paw) oedema, and streptozotocin (STZ)-induced diabetes mellitus models. Morphine (MPN, 10 mg/kg), diclofenac (DIC, 100 mg/kg) and chlorpropamide (250 mg/kg) were used as reference drugs for comparison. H. hemerocallidea corm aqueous extract (APE, 50-800 mg/kg i.p.) produced dose-dependent, significant (P < 0.05-0.001) antinociceptive effects against thermally- and chemically-induced nociceptive pain stimuli in mice. The plant extract (APE, 50-800 mg/kg p.o.) also significantly (P < 0.05-0.001) inhibited fresh egg albumin-induced acute inflammation, and caused dose-related, significant (P < 0.05-0.001) hypoglycaemia in normal (normoglycaemic) and diabetic rats. The results obtained in this study suggest that the antinociceptive effects of the plant's extract are peripherally- and centrally-mediated. The findings of this experimental animal study indicate that H. hemerocallidea corm aqueous extract (APE) possesses antinociceptive, anti-inflammatory and antidiabetic properties; and thus lend pharmacological support to folkloric, anecdotal uses of 'African Potato' in the treatment and/or management of painful, arthritic inflammatory conditions, as well as in the management and/or control of type-2 diabetes mellitus in some parts of southern Africa.

Analgesics↗

Frequency and timing of scaphoid-centrale fusion in hominoids.

Fusion between the os centrale and the scaphoid has played a central role in many functional and phylogenetic interpretations of hominoid evolution. In particular, scaphoid-centrale fusion shared among African apes and humans has been interpreted as an adaptation in knuckle-walkers, an exaptation in hominins, and has been offered as evidence for a knuckle-walking origin of bipedalism. However, discrepancies in the literature concerning the taxa in which this scaphoid-centrale fusion occurs, as well as the timing and/or frequency of this fusion, have confounded the significance of this trait. This study provides an historical review of the literature on scaphoid-centrale fusion in primates and the first formal investigation into the timing and frequency of this character among primates, with a focus on extant hominoids. Results indicate that there is a significant difference in the timing and frequency of scaphoid-centrale fusion in African apes and humans compared to Asian apes, suggesting that prenatal or early postnatal fusion among hominines is a synapomorphy. Scaphoid-centrale fusion does not occur randomly within primates. Instead, only Homininae and some members of Lemuroidea show consistent and ontogenetically early fusion of these carpals. The consistent occurrence of this trait within only two primate clades and a clear heterochronic trend in timing and frequency of scaphoid-centrale fusion among hominines suggest that this character is primarily phylogenetically controlled. We could not falsify the hypothesis that scaphoid-centrale fusion in African apes is indeed related to midcarpal stability in knuckle-walking, but neither were we able to find direct biomechanical or kinematic evidence to support this hypothesis. A more definitive answer to the question of the functional significance of scaphoid-centrale fusion will have to await more detailed analyses of great ape wrist kinematics.

Africa↗

Hemodynamic effects of sildenafil interaction with a nitric oxide donor compound in a dog model of acute pulmonary embolism.

Sildenafil attenuates acute pulmonary embolism (APE)-induced pulmonary hypertension. However, the hemodynamic effects of sildenafil in combination with other vasodilators during APE have not been examined yet. In the present study, we examined the hemodynamic effects of combined diethylenetriamine/nonoate (DETA-NO, 1microMol kg(-1), i.v.) and sildenafil (0.25mg/kg, i.v.) in an anesthetized dog model of APE. Plasma nitrite/nitrate (NO(x)) and cyclic GMP concentrations were determined using an ozone-based chemiluminescence assay and a commercial enzyme immunoassay, respectively. We found that this dose of DETA-NO did not attenuate APE-induced pulmonary hypertension. However, significant decreases in mean pulmonary artery pressure were observed 15, 30 and 45min after the administration of sildenafil alone or after the combined administration of DETA-NO and sildenafil (all P<0.05). No significant differences among groups were observed in the respiratory parameters. While DETA-NO significantly increased NO(x) concentrations by approximately 4microM, cyclic GMP concentrations increased only when sildenafil was administered (all P<0.05). These results show that the combined administration of 1microMol kg(-1) of DETA-NO and sildenafil is not advantageous compared with sildenafil alone, thus suggesting that sildenafil alone produced maximum attenuation of APE-induced pulmonary hypertension, as far as the NO-cGMP pathway is concerned.

Animals↗

l-Arginine attenuates acute pulmonary embolism-induced oxidative stress and pulmonary hypertension.

l-Arginine is substrate for nitric oxide (NO) synthesis and produces pulmonary vasodilatory effects in patients with pulmonary hypertension and in hypoxic animals. We hypothesized that l-arginine would attenuate the increase in oxidative stress and the pulmonary hypertension observed during acute pulmonary embolism (APE). Using an isolated lung perfusion rat model of APE, we examined whether l-arginine (0, 0.1, 0.5, 3, and 10 mmol/L) attenuates the pulmonary hypertension induced by the injection of 6.6 mg/kg of 300 microm Sephadex microspheres into the pulmonary artery. Thiobarbituric acid reactive species (TBA-RS) and nitrite/nitrate (NO(x)) concentrations were measured in lung perfusate to assess oxidative stress and NO production. l-Arginine (0.5, 3, and 10 mmol/L) attenuated (all P<0.05) APE-induced pulmonary hypertension by about 50%. The protective effect of l-arginine was completely reversed by inhibition of NO synthesis with l-NAME (4 mmol/L). In addition, l-arginine (0.5-10 mmol/L) blunted the increase in TBA-RS observed after APE. NO(x) tended to increase only when l-arginine (10 mmol/L) was added to the lung perfusate of non-embolized lungs. Taken together, these findings suggest that l-arginine attenuates APE-induced pulmonary hypertension through antioxidant mechanisms involving increased NO synthesis.

Acute Disease↗

Membrane process for emulsified waste containing mineral oils and nonionic surfactants (alkylphenolethoxylate).

Using membrane processes we studied the improvement of the treatment of waste emulsified by mineral oils and alkylphenolethoxylate (APE) and investigated diatomaceous earth processing for comparison. A quantitative analysis of the mineral oils and APE using column chromatography was applied to assess these processes. Despite substantial rejection of the turbidity values of emulsified model waste, the percentages of mineral oil and APE rejections using microfiltration (MF) processes were 39-61% and 16-19%, respectively. In contrast, the ultrafiltration (UF) process could reject 97% for the mineral oils and 90% for APE. The diatomaceous earth adsorption processes reduced the mineral oils 40-49% and the APE, 8-14%, and therefore were inferior to the UF process for waste treatment. The average fluxes of both the MF and UF membranes until the volume reduction factor (VRF) reached a value of 5 were almost the same in the range of 8 x 10(-6)-14 x 10(-6) m3 m-2 s-1. For commercial application, decrease in the permeate flux by fouling needs to be resolved.

Adsorption↗

Enamel thickness, microstructure and development in Afropithecus turkanensis.

Afropithecus turkanensis, a 17-17.5 million year old large-bodied hominoid from Kenya, has previously been reported to be the oldest known thick-enamelled Miocene ape. Most investigations of enamel thickness in Miocene apes have been limited to opportunistic or destructive studies of small samples. Recently, more comprehensive studies of enamel thickness and microstructure in Proconsul, Lufengpithecus, and Dryopithecus, as well as extant apes and fossil humans, have provided information on rates and patterns of dental development, including crown formation time, and have begun to provide a comparative context for interpretation of the evolution of these characters throughout the past 20 million years of hominoid evolution. In this study, enamel thickness and aspects of the enamel microstructure in two A. turkanensis second molars were quantified and provide insight into rates of enamel apposition, numbers of cells actively secreting enamel, and the time required to form regions of the crown. The average value for relative enamel thickness in the two molars is 21.4, which is a lower value than a previous analysis of this species, but which is still relatively thick compared to extant apes. This value is similar to those of several Miocene hominoids, a fossil hominid, and modern humans. Certain aspects of the enamel microstructure are similar to Proconsul nyanzae, Dryopithecus laietanus, Lufengpithecus lufengensis, Graecopithecus freybergi and Pongo pygmaeus, while other features differ from extant and fossil hominoids. Crown formation times for the two teeth are 2.4-2.6 years and 2.9-3.1 years respectively. These times are similar to a number of extant and fossil hominoids, some of which appear to show additional developmental similarities, including thick enamel. Although thick enamel may be formed through several developmental pathways, most Miocene hominoids and fossil hominids with relatively thick enamel are characterized by a relatively long period of cuspal enamel formation and a rapid rate of enamel secretion throughout the whole cusp, but a shorter total crown formation time than thinner-enamelled extant apes.

Animals↗

[The gammagraphic diagnosis of acute pulmonary thromboembolism].

We aimed to determine the prevalence of acute pulmonary embolism (APE) in our population and to establish the diagnostic reliability of pulmonary scintigraphy (PS), as well as the influence of the clinical context (CC). During a 2-year prospective study, patients were diagnosed by either pulmonary angiography or normal-perfusion PS. A diagnosis of APE was made in 73 (75%) of a total of 97 patients. In the group of 58 patients diagnosed by ventilation/perfusion (V/Q) PS, 33 were classified as "highly probably" having APE; 32 of these in fact had the syndrome (sensitivity 88%, specificity 94%). Combining the "highly probable" patients with the "highly suspected" patients diagnosed by ventilation/perfusion PS, we obtained a sensitivity of 51% and specificity of 100%. Ventilation scintigrams were unobtainable in 28 older patients with greater dyspnea and tachypnea, who were unable to perform the maneuvers. Of the 21 "highly probable" patients as assessed by PS, 19 were diagnosed as having APE (sensitivity 86%, specificity 85%). Combining the "highly probable" patients with the "highly suspected" group, we obtained a sensitivity of 32% and specificity of 100%. Normal perfusion PS excludes clinically relevant APE. "Intermediate" or "slight" probability PS results, even when combined with CC, have no diagnostic validity.

Acute Disease↗

Successful management of acute pulmonary embolism after surgery for lung cancer.

OBJECTIVE: Although many case reports of acute pulmonary embolism (APE) have been published, the literature dealing with the management of APE after resection of lung cancer is limited. This report describes seven cases of successful management of APE after surgery for lung cancer and discusses how to manage this problematic complication. METHODS: The medical charts of seven patients with APE after lobectomy and complete mediastinal lymphnode dissection were retrospectively reviewed. RESULTS: Six patients collapsed during their first attempt at walking after surgery in conjunction with a dramatic respiratory change. All these patients promptly underwent enhanced spiral computed tomography (CT) scanning. Bilateral clots were detected in all patients and one patient with a deep venous thrombus (DVT) in the femoral vein had a temporary inferior vena cava filter implanted. Non-surgical therapy was used for six patients: thrombolysis (systemic urokinase) and anticoagulant (heparin or argatroban) for four patients and only anticoagulant therapy started on the day after the operation using argatroban for two. There were no bleeding problems with these thrombolysis and/or anticoagulant therapies except in one case of hemorrhage induced by heparin usage on the day after the operation. None of the cases required allotransfusion in connection with these therapies. Thromboembolectomy was performed for one patient who was hemodynamically unstable due to massive embolism and primary atrial fibrillation. All patients were discharged from our hospital without major complications. CONCLUSIONS: Patients with pulmonary embolism after surgery for lung cancer can be treated aggressively with anticoagulants with/without fibrinolitics or even with pulmonary embolectomy on cardiopulmonary bypass, without excessive risk of bleeding complications. Enhanced spiral CT scanning was very helpful for making a simultaneous diagnosis of APE and DVT. The use of argatroban in conjunction with activated clotting time monitoring should be effective without causing bleeding problems during the early stages after pulmonary resection for lung cancer.

Acute Disease↗

Mechanism of DNA cleavage and substrate recognition by a bovine apurinic endonuclease.

The location of the phosphodiester bond cleaved by homogeneous Mg2+-dependent apurinic endodeoxyribonuclease (EC 3.1.25.2; APE) of bovine calf thymus has been determined by using a 21-mer oligonucleotide containing a single central apurinic site as a substrate. A single product of cleavage consistent with cleavage of the oligonucleotide 5' to the apurinic site, and leaving a 3' hydroxyl group, was identified. This enzyme is, therefore, a class II apurinic endonuclease. The substrate specificities of this enzyme have been determined by using a variety of natural and synthetic DNAs or oligonucleotides containing base-free sites. Calf thymus APE has an absolute requirement for a double-stranded DNA and requires an abasic site as a substrate. The presence of a base fragment such as a urea residue, an alkoxyamine group attached to the C'-1 position of the abasic site, or reduction of the C'-1 aldehyde abolishes the APE activity of this enzyme. Synthetic abasic sites containing either ethylene glycol, propanediol, or tetrahydrofuran interphosphate linkages are excellent substrates for bovine APE. These results indicate that APE has no absolute requirement for either ring-opened or ring-closed deoxyribose moieties in its recognition of DNA-cleavage substrates. The enzyme may interact with the pocket in duplex DNA that results from the base loss or with the altered conformations of the phosphodiester backbone that result from the abasic site.

Amines↗