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PubMed2005

[The research progress of accelerating tendon healing and preventing tendon adhesion].

OBJECTIVE: To study the status quo of the methods and materials for accelerating the tendon healing and preventing the tendon adhesion as to provide an essential reference for future research and clinical application. METHODS: The recent articles on methods of accelerating tendon healing and preventing tendon adhesion were extensively reviewed. RESULTS: Tendon healing was decided by the co-effects of both endogenous and exogenous ways, and the former was more important. It was affected by the tendon sheath, vincula tendinum and synovial fluid as well. Tendon adhesion was mostly caused by excessive participation of exogenous healing factors and serious damage of the situations around the tendon. Tendon healing was accelerated by methods like repairing, reconstruction of peri-tendon tissues, electric stimulation, physiotherapy, adding herbs or growth factors, and gene intervention. Tendon adhesion was reduced or prevented by methods like the restoration of tendon sheath, using substitutions, adding herbs/drugs, and improving suturing techniques. CONCLUSION: Via the appropriate methods and techniques combining the Chinese traditional and modern medicine, tendon healing can be accelerated and the quality of tendon healing can be improved.

Animals↗

PubMed2006

[Quantitative analysis of psychometric indicators among 40-55 years old accelerant Georgian men and women of normal physical development].

Determination of individual characteristics of a human being causes much interest. Furthermore, you can seldom come across the studies about determination of psychological categories of accelerants. The aim of the present work was to determine quantitative analysis of psychometric indicators among 40-55 years old accelerant Georgian men and women of normal physical development for given age scales as well as to determine personal characteristics of each person to be researched. On the basis of conducted research we may shape out, that older Georgian women are characterized with phlegmatic temperament and introversive character. They are observed to have average degree of logic and verbal intellect; constitutional types of mid exciting, conflicting and static mood. While elder Georgian men have sanguine temperament, they are characterized with extroversive character, average degree of logic intellect, plastic-dynamic and constitutional-stable mood; they are considered to be harmonic and dynamic constitutional types. We have also established that Georgian accelerant men are observed to have phlegmatic temperament, extroversion, average mathematical intellect and conflicting and static mood. Accelerant Georgian women displayed phlegmatic temperament, extroversion, average logic intellect, and conflicting and static mood. But still they were observed, though seldom, to have harmonic and dynamic character.

Adult↗

PubMed2006

An accelerated method for the detection of extended-spectrum beta-lactamases in urinary isolates of Escherichia coli and Klebsiella pneumoniae.

We prospectively studied an accelerated phenotypic method by incorporating the double disk synergy test in the standard Kirby-Bauer disk diffusion susceptibility testing, to evaluate a protocol for the rapid detection of extended-spectrum beta-lactamases (ESBL) in urinary isolates of Escherichia coli (E. coli) and Klebsiella pneumoniae (K. pneumoniae). All ESBL-positive isolates were confirmed by the standard Clinical Laboratory Standards Institute (CLSI) confirmatory disk diffusion method. Between November 2004 and December 2005, a total of 6988 urine specimens were analyzed of which, 776 (11%) showed significant growth. They included E. coli in 577 cases (74%) and K. pneumoniae in 199 (25.6%). Of these, 63 E. coli (8%) and 15 K. pneumoniae (7.5%) were positive for ESBL by the accelerated and CLSI methods. Compared to the standard CLSI method, the accelerated method reduced the ESBL detection time from two days to one day. We conclude that the accelerated ESBL detection technique used by us in this study is a reliable and rapid method for detecting ESBL in urinary isolates of E. coli and K. pneumoniae.

Escherichia coli↗

PubMed1991

Peak aortic blood acceleration: a possible indicator of initial left ventricular impairment in patients with coronary artery disease.

In 25 patients undergoing diagnostic cardiac catheterization, a catheter-tip electromagnetic velocity transducer was used to evaluate maximum velocity and acceleration of blood in the ascending aorta. All patients underwent a complete haemodynamic evaluation, including high-fidelity recording of intraventricular pressures and calculation of the derived indices, left ventriculography and coronary angiography. Nineteen patients with critical coronary stenoses were divided according to the presence of signs of left ventricular dysfunction, while the control group consisted of six subjects with chest pain, but without cardiac abnormalities detectable by cardiac catheterization. Maximum aortic acceleration was significantly lower in coronary patients (378 +/- 130 vs 562 +/- 82 in the control group P less than 0.01) and also in the selected subgroup of coronary patients with normal haemodynamic and angiographic indices of left ventricular systolic function (310 +/- 102 vs 562 +/- 82, P less than 0.01). No relationship could be observed between maximal blood acceleration and left ventricular peak systolic pressure, +dP/dt, left ventricular end-systolic volume index and ejection fraction. Our results suggest that maximal blood acceleration from the left ventricle may detect an initial myocardial impairment in patients with definite coronary artery disease but with normal conventional indices of left ventricular function. The clinical interest of this index, however, is limited by overlapping values in patients with and without coronary artery disease and the inability of a further separation of ischaemic patients in accordance with the severity of left ventricular impairment and the extension of coronary artery involvement.

Adult↗

PubMed1991

Chronic rejection of rat aortic allograft. II. Administration of cyclosporin induces accelerated allograft arteriosclerosis.

Rat aortic allografts immunosuppressed with cyclosporin--but not with azathioprine or steroids--develop an early inflammatory lesion in the subendothelial space. This "endothelialitis" is followed by an influx of proliferating smooth muscle cells into the intima, resulting in intimal thickening and accelerated arteriosclerosis. Administration of azathioprine and steroids largely ameliorates the development of the accelerated lesion. Similar endothelialitis and accelerated arteriosclerosis have been observed previously in the autopsy material of cardiac transplant recipients. Our results confirm the suggestion that the development of accelerated allograft arteriosclerosis is most likely linked to cyclosporin administration.

Animals↗

PubMed1977

[Acceleration of the initial stages of thrombin clearance in the bloodstream of rats during stress].

In a stress due to 30-min immobilization, the initial stages of the thrombin clearance in the blood flow of rats are considerably accelerated. Thus, in 5 min after i.v. administration of thrombin I131, The blood relative radioactivity in experimental rats decreases by about 40% while in the control animals--by 20%. The same stress against the background of exogenous ACTH leads to a still greater acceleration of the thrombin clearance and the blood relative radioactivity within the 5 min decreases by 55%. The accelerated clearance of the thrombin I131 from the blood during immobilization and combination of the latter with ACTH administration is followed by its accumulation in the liver and its reduction in the lungs. The activating effect of ACTH on the thrombin I131 clearance is not, apparently, mediated through activation of the adrenal glucocorticoid function as the clearance initial stages are not accelerated after hydrocortisone administration. The clearance depends on the heparin contents in the blood: binding of endogenous heparin with protamine--sulphate leads to abolishing of the stress activating effect, and the speed of clearance in immobilized animals decreases to basal level of control animals.

Adrenocorticotropic Hormone↗

PubMed1987

The pathogenesis of accelerated fibrinolysis in liver cirrhosis: a critical role for tissue plasminogen activator inhibitor.

The pathogenesis of accelerated fibrinolysis in liver cirrhosis was investigated by comparing the results of specific assays for tissue plasminogen activator (tpa) antigen, tpa activity, tpa inhibitor, and alpha-2 plasmin inhibitor (a2PI) in 12 patients with cirrhosis and markedly accelerated fibrinolysis (dilute whole blood clot lysis time (DWBCLT) less than two hours), in nine patients with cirrhosis and moderately accelerated fibrinolysis (DWBCLT two to four hours), and in nine patients with cirrhosis and normal fibrinolysis (DWBCLT greater than four hours). Mean tpa antigen was markedly increased in all three groups, but no correlation was observed between overall fibrinolytic activity as measured by the DWBCLT and the level of tpa antigen. In contrast, there was a significant correlation between overall fibrinolytic activity and tpa activity and an equally significant correlation between fibrinolytic activity and decreased tpa inhibition. Mean a2PI activity was significantly lower than normal in groups 1 and 2 but was normal in group 3. The pathogenesis of accelerated fibrinolysis in liver cirrhosis thus appears to depend critically on the capacity of plasma inhibitors to inhibit increased circulating tpa antigen. Reduced a2PI also appears to play a role.

Antigens↗

PubMed1989

[The accelerated phase of Chediak-Higashi syndrome].

We have retrospectively analysed the clinical and biological features as well as the outcome of 18 accelerated phases having occurred in 11 patients with the Chediak-Higashi syndrome. This complication is very frequent and is characterized by a multi-visceral lymphohistiocytic infiltration with hemophagocytosis leading to pancytopenia, a bleeding disorder secondary to low fibrinogen level, hypertriglyceridemia and hemodilution. The accelerated phase of the Chediak-Higashi syndrome is identical to the manifestations of familial erythrophagocytic lymphohistiocytosis and of the viral-associated hemophagocytic syndrome. The outcome was invariably fatal before the use of etoposide (VP 16) in association with steroids and intrathecal methotrexate. Complete remission with this management regimen was observed in 7/7 cases. However, remissions were only transient. HLA identical bone marrow transplantation appeared to be the only therapeutic strategy capable of curing the disease (3/3 patients). Non transplanted patients relapsed and died as well as one patient who received a HLA non identical bone marrow transplantation. Due to the frequency and the severity of the accelerated phase of the Chediak-Higashi syndrome, HLA identical bone marrow transplantation should be proposed as early as possible after the onset of the accelerated phase.

Adrenal Cortex Hormones↗

PubMed1989

Age-related changes in the temporomandibular joint of the senescence accelerated mouse. SAM-P/3 as a new murine model of degenerative joint disease.

Age-related changes of the condyle of the temporomandibular joint (TMJ) in strains of Senescence Accelerated Mouse (SAM) were investigated. With advancing age, all strains of SAM showed degenerative joint disease initiated by degenerative changes such as eg, roughness, fissure, and erosion on the condylar surface. These degenerative changes were in concert with an active remodeling that can lead to deformation of the condyle. Moreover, the short-lived SAM-P (accelerated senescence prone mouse) strains developed these degenerative changes earlier than did the SAM-R (accelerated senescence resistant mouse) strains. Thus, development of degenerative joint disease in SAM was closely related not only to chronological age but also to the accelerated senescence phenomenon. Of the SAM-P series, the SAM-P/3 strain was the first to manifest degenerative changes (approximately 50% at 7 to 9 months of age and 100% over 12 months of age) and thereafter showed the highest incidence of severe changes with overt deformity. As a model of degenerative joint disease, this strain of SAM should prove useful.

Aging↗

PubMed1989

Allograft heart accelerated atherosclerosis: evidence for cell-mediated immunity in pathogenesis.

The problem of accelerated atherosclerosis in the allograft heart continues to adversely effect the long term survival of transplant patients. Most traditional risk factors influencing atherogenesis do not appear to play an important role in accelerated atherosclerosis. Additional causative factors proposed in recent years are not without controversy. An immune-mediated endothelial damage by cytotoxic B-cell antibodies as the initial injury in the induction of accelerated atherosclerosis has not been confirmed on morphologic grounds. This study is based on six cases (four autopsies and two explanted hearts) from transplant patients whose hearts were examined at different post-transplantation intervals (24 h to 14 mo). Our morphologic findings of a segmental coronary vasculitis involving primarily the outer two-thirds of the media and adventitia suggest that the early vascular manifestations may reflect tissue rejection similar to that seen in the myocardium. Furthermore, our findings from the medium size coronary arteries are suggestive of a cell-mediated immune injury probably directed against the smooth muscle cells of the media. Although the end result (occlusive coronary lesion) may reveal some morphologic similarities in both naturally occurring atherosclerosis and accelerated atherosclerosis, the pathogenetic mechanisms involved in these two conditions may differ.

Adult↗

PubMed1987

The acceleration of Na+,K+-ATPase activity by ATP and ATP analogues.

Since Na+,K+-ATPase (EC 3.6.1.3) of pig kidney modified with a fluorescent sulfhydryl reagent, N-[p-(2-benzimidazolyl) phenyl]maleimide, at Cys-964 of the alpha-chain showed ATP-dependent, reversible, and dynamic fluorescence changes (Nagai, M., Taniguchi, K., Kangawa, K., Matsuo, S., Nakamura, S., and Iida, S. (1986) J. Biol. Chem. 261, 13197-13202), we studied the conformational change during Na+,K+-ATPase reaction using the modified enzyme. The addition of K+ to the enzyme increased the fluorescence intensity to 2% in the presence of 160 mM Na+ and 3 mM Mg2+ (K0.5 = 16.4 mM). Addition of low concentrations of ATP immediately increased the intensity to 3.2% (K0.5 less than 0.1 microM) to accumulate fully K+-bound enzyme in the presence of 43 mM K+ with Na+ and Mg2+, but further addition of higher concentrations of ATP diminished the increase (K0.5 = 120 microM). After exhaustion of ATP, the fluorescence intensity decreased to -0.4% (K0.5 = 0.3 microM) and -2% (K0.5 = 20 microM), respectively, in the presence of low and high concentrations of ADP produced from ATP. High concentrations of ATP accelerated Na+,K+-ATPase activity with a simultaneous increase in the amount of ADP-sensitive phosphoenzyme irrespective of the modification. Adenylyl imidodiphosphate and ADP accelerated Na+,K+-ATPase activity in the presence of 2.7 microM ATP by decreasing the extent of the fluorescence without affecting the amount of phosphoenzyme, irrespective of the modification. These data suggest that Na+,K+-ATPase activity was accelerated due to the acceleration of the breakdown of K+-bound enzyme by high concentrations of ATP and ATP analogues.

Adenosine Diphosphate↗

PubMed1988

Biochemical characterization of a factor produced by trypomastigotes of Trypanosoma cruzi that accelerates the decay of complement C3 convertases.

Infective- and vertebrate-stage trypomastigotes of Trypanosoma cruzi resist serum killing by the alternative complement pathway, whereas noninfective vector-stage epimastigotes, from which trypomastigotes derive, are serum-sensitive. This form of developmental preadaption is commonly observed in protozoan parasites, but its mechanisms are poorly understood. We have demonstrated previously that trypomastigotes spontaneously shed molecules which interfere with formation and accelerate the intrinsic decay of complement C3 convertases, a finding which may explain the evasion of complement lysis by trypomastigotes. We now describe the partial purification and characterization of the T. cruzi C3 convertase inhibitor from the supernatant of culture metacyclic and tissue culture trypomastigotes. Decay-accelerating activity for both classical and alternative pathway C3 convertases copurifies on anion-exchange fast protein liquid chromatography and chromatofocusing with 35S-labeled molecules of 87-93 kDa, pI 5.6-5.8. The labeled components are destroyed by papain and retained on concanavalin A-Sepharose, procedures which remove functional decay-accelerating activity from the supernatant. The 87-93-kDa components are immunoprecipitated by sera from patients chronically infected with T. cruzi, but not by antisera to any known regulatory proteins of the human complement cascade. Lytic activity for tissue culture trypomastigotes in chagasic sera is associated with antibody reactivity against the 87-93-kDa 35S-labeled components and with inhibition of decay-accelerating activity. The T. cruzi factor is the first developmentally regulated microbial complement inhibitor to be biochemically characterized.

Animals↗

PubMed1985

Acceleration of fibrinolysis by the N-terminal peptide of alpha 2-plasmin inhibitor.

When blood plasma containing the NH2-terminal 12-residue peptide (N-peptide) of alpha 2-plasmin inhibitor (alpha 2PI; alpha 2-antiplasmin) was clotted in the presence of calcium ions, the N-peptide and alpha 2PI were cross-linked to fibrin by activated coagulation factor XIII. The amount of N-peptide cross-linked to fibrin was proportional to the concentration of N-peptide present in plasma. On the other hand, the amount of alpha 2PI cross-linked to fibrin was decreased by the presence of N-peptide, and the decrease was in reverse relationship to the increase of cross-linking of N-peptide. Spontaneous fibrinolysis or fibrinolysis induced by tissue plasminogen activator was accelerated by the presence of N-peptide, and the acceleration was dependent on the concentrations of N-peptide and directly proportional to inhibition of alpha 2PI cross-linking exerted by N-peptide. The acceleration was more pronounced when the clot was compacted by platelet-mediated clot retraction or by a squeeze. Fibrinolysis of an alpha 2PI-deficient or a factor XIII-deficient plasma clot was not accelerated by N-peptide. These findings were substantiated in a purified system and support the previous proposal that alpha 2PI is cross-linked to fibrin at the glutamine residue that is next to the NH2-terminus of alpha 2PI, and this factor XIII-mediated cross-linking of alpha 2PI is significant in inhibition of physiologically occurring endogenous fibrinolysis.

Fibrin↗

PubMed1988

[Evaluation of the fetal movements and accelerations of fetal heart rate in twin pregnancy].

In twin pregnancy, the fetal heart rates (FHR) of each fetus and uterine contraction were recorded simultaneously on a single recording chart by two cardiotocographs and a linear multichannel recorder. In addition, with a new technique, FHR and fetal movement (FM) signal bursts for each fetus were recorded similarly on a single recording chart by two ultrasonic Doppler actographs and an electronic polyrecorder. Simultaneous nonstress tests were done for 32 sets of twins at 28 to 41 weeks' gestation. The observed acceleration number in every gestational week increased till 38 weeks and this result was similar to that in singletons. Completely synchronous acceleration patterns in the 2 fetuses were observed in 654 recordings (31.4%) and asynchronous acceleration patterns in 1,108 recordings (53.1%). Simultaneous FHR and FM signal burst recordings were performed in 7 twin pregnancies. In about half of the 1,535 recordings, the FM signal bursts were synchronous between 2 fetuses, whereas they were asynchronous in the other half. Synchronous FM bursts in each gestational week decreased with time. Neurological independency between the twins was suggested by the results. The synchronous appearance of FM signal bursts with FHR accelerations of 2 fetuses was more pronounced in a uniovular twin than in a biovular twin.

Female↗

PubMedDate not supplied

[Tolerance to +G(z) acceleration in rhesus monkeys].

The procedure of Cosmos-1514 selection and training of rhesus-monkeys included +Gz acceleration tests. Two experimental series were performed. In the first experimental series (52 monkeys) acceleration tolerance was determined with respect to general health condition and behavioral responses of animals, electrocardiographic data (in three standard leads), heart rate and respiration rate. In the second experimental series acceleration tolerance was measured on the basis of blood pressure and flow velocity in the common carotid artery. Rhesus-monkeys exhibited noticeable individual variations in +Gz tolerance as well as in circulation responses to this exposure. The tests helped to select flight animals with a high level of acceleration tolerance.

Animals↗

PubMed1988

Fetal vibro-acoustic stimulation: magnitude and duration of fetal heart rate accelerations as a marker of fetal health.

The relationship between intrapartum fetal acid-base status and fetal heart rate (FHR) response to vibro-acoustic stimulation was investigated in 100 patients. Fetal heart rate responses were classified into three groups: acceleration of 15 or more beats per minute lasting 15 or more seconds, acceleration of ten or more beats per minute lasting 10 seconds but less than 15 beats per minute and 15 seconds, or no acceleration. The mean fetal scalp blood pH was 7.29 in both groups with acceleratory responses, and such responses were highly predictive (98-100%) of scalp pH 7.20 or above. The mean pH value for the no-acceleration group (7.22) was significantly lower than the mean pH value for both groups with an acceleratory response (P less than .05), and the lack of response to the stimulus detected 90-100% of fetuses with a pH below 7.20. This sensitivity was reduced to 45% in the detection of fetuses with pH less than 7.25.

Acid-Base Equilibrium↗

PubMed1986

[Prognostic significance of heart rate accelerations of the fetus in the first stage of labor].

The clinical data and the cardiotocograms of 232 low-risk-deliveries and that of 344 cases of high risk deliveries (98 premature deliveries, 102 cases with meconium stained amniotic fluid, 86 cases with EPH gestosis and 58 cases of fetal distress necessitating emergency cesarean section) have been studied. It is concluded that the fetal heart rate accelerations even in cases of high risk pregnancies and deliveries indicate a good fetal state and a good neonatal outcome. In the presence of both of decelerations and accelerations the fetal state is still good. In the presence of accelerations the low- and high risk deliveries (except the premature deliveries) have a similarly good prognosis. In the lack of accelerations the neonatal mortality, the frequency of resuscitations is higher, and the low Apgar-scores are commoner.

Asphyxia Neonatorum↗

PubMed1986

Role of ternary complexes, in which heparin binds both antithrombin and proteinase, in the acceleration of the reactions between antithrombin and thrombin or factor Xa.

Oligosaccharides (10-20 monosaccharide units) with high affinity for antithrombin, as well as larger high-affinity heparin fractions (having relative molecular masses between 6,000 and 21,500), all markedly accelerated the inhibition of Factor Xa by antithrombin. Moreover, all high-affinity oligosaccharides and heparins enhanced, to a similar extent, the amount of free proteolytically modified antithrombin cleaved at the reactive bond by Factor Xa. In contrast, a minimum high-affinity heparin size of approximately 18 monosaccharide units was required to significantly accelerate the inactivation of thrombin by antithrombin and to enhance the production of modified antithrombin by this enzyme. All high-affinity fractions studied had similar affinities for antithrombin, as determined by fluorescence titrations. In competition experiments, binary complexes of antithrombin with octadecasaccharide or larger high-affinity heparins, but not with smaller oligosaccharides, displaced inactivated 125I-thrombin from matrix-linked low-affinity heparin. Moreover, similar binary complexes with 3H-labeled octadecasaccharide or larger chains, but not with smaller oligosaccharides, were capable of binding to matrix-linked inactivated thrombin. These results indicate that simultaneous binding of antithrombin and thrombin to high-affinity heparin is a prerequisite to the acceleration of the antithrombin-thrombin reaction and that the minimum heparin sequence capable of binding both proteins comprises approximately 18 monosaccharide units. Similar complex formation apparently is not required for the acceleration of the antithrombin-Factor Xa reaction.

Animals↗