[Use of M-mode echocardiography in the diagnosis of tricuspid stenosis].
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Adolescent↗
Biomedical subjects
J Forman
Publications and source records attributed to J Forman.
[Conduction disorders and aneurysms of the sinus of Valsalva].
A series of 15 sinus of Valsalva aneurysms (SVA) admitted between 1961 and 1981 was reviewed to analyse associated conduction defects. It comprised 11 men and 4 women; the mean age was 31 years (range 16 to 53). The diagnosis of SVA was made at the time of rupture (4 cases), during investigation of associated cardiac disease (8 cases), at surgery (1 case) and during advanced conduction disorders (2 cases). All patients underwent catheterisation and angiography. Endocavitary electrophysiological studies were performed in 3 patients. Eight out of 15 patients had conduction defects which comprised: incomplete right bundle branch block (2 cases), atrioventricular block (AVB) (6 cases). Endocavitary investigation of 3 of the 6 AVB showed conduction defects at several levels: sino atrial, suprahisien, intrahisian and infrahisian blocks (1 case); transient complete AVB with 1 degree and 2 degree intrahisian block (1 case); complete AVB, six years after correction of SVA, due to infrahisian block (1 case). Thirteen of the 15 patients underwent surgery; none of the 9 cases of SVA without conduction defects before surgery developed conduction defects. Four of the 6 cases of AVB required permanent pacing; there was 1 postoperative death. One patient was not operated. These conduction defects were caused by the close relationship of the SVA to the intracardiac conduction pathways. The right anterior was the most commonly affected sinus. The investigation of AV conduction should be systematic in cases of SVA, and, conversely, the finding of AVB in young patients should alert the physician to the possibility of a SVA.
Adolescent↗
[Dissection of the ascending aorta after aortic valve replacement].
Three patients who underwent aortic valve replacement had dissection of the ascending aorta 7 months, 2 years and 15 years after surgery. This is a rare complication of aortic valve replacement (11 reported cases). Its incidence estimated from the literature would appear to be less than 1% of all aortic valve replacements. It occurs in both cases of stenosis and regurgitation (4 aortic regurgitations, 2 aortic stenosis, 5 mixed aortic valve disease) and is seen in ball and cage (7 cases), tilting disc (3 cases) and bioprosthesis (1 case). Six of these patients had hypertension. The role of the initial surgery for valve replacement in secondary aortic dissection is discussed. Aortic clamping and cannulation can cause immediate dissection but may also damage the aortic wall, leading to the risk of secondary dissection. An aneurysm of the ascending aorta was observed in 5 Cases at surgery; in 3 cases, the aorta was dilated without true aneurysm; in 3 other cases the aorta was considered to be macroscopically normal. The integrity aorta is sometimes difficult to confirm and a macroscopically normal of the aorta may have fragile aortic walls, especially in cases of aortic regurgitation due to valvular dysplasia and forms frustres of Marfan's syndrome, and are associated with a risk of secondary dissection. The appearances of the aorta at aortic valve replacement influence the choice of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
H-2L-restricted recognition of viral antigens In the H-2d haplotype, anti-vesicular stomatitis virus cytotoxic T cells are restricted solely by H-2L.
H-2d-encoded gene products were analyzed as restriction antigens for anti-vesicular stomatitis virus (VSV) cytotoxic T lymphocytes (CTL). Cold target competition experiments revealed that VSV recognition was H-2D region-restricted; H-2K-end-restricted recognition of VSV could not be demonstrated. That VSV is not recognized in the context of K-region-encoded gene products is also supported by the observation that H-2dm1 and H-2dm2 mice, strains that contain H-2Kd but have an alteration in H-2L and/or H-2D/L, are nonresponders in the CTL assay. Two different lines of evidence eliminated H-2Dd, H-2Md, and H-2Rd as the restriction antigens: (a) H-2dm2-VSV inhibitors that express H-2Dd and H-2Md did not block the lysis of P815-VSV targets by Balb/c anti-VSV killer cells, and (b) a hybridoma specific for H-2Dd failed to inhibit killer cell activity in this same effector/target combination. However, two monoclonal antibodies specific for H-2Ld but not H-2Rd completely blocked anti-VSV cytotoxic activity. Taken together, in the H-2d haplotype, anti-VSV CTL recognize VSV solely in the context of the H-2Ld molecule. This is the first demonstration of the exclusive use by a mouse stain of the H-2L molecule only for H-2-restricted recognition, and thus supports the notion that H-2L plays a major role in restricting antigen specific recognition. Finally, the fact that an anti-H-2Ld monoclone completely blocked an H-2dm2 anti-BALB/c CTL response indicates that H-2R, a molecule absent in H-2dm2 anti-BALB/c CTL response indicates that H-2R, a molecule absent in H-2dm2 but not BALB/c, does not sensitize H-2 alloreactive CTL.
Animals↗
The Qa2 subregion controls the expression of two antigens recognized by H-2-unrestricted cytotoxic T cells.
B6.KI mice were immunized with spleen cells from B6.K2, a Qa2-subregion congenic strain. Cytotoxic T cells were generated that recognize two target antigens controlled by this region. One of the target antigens is Qa-2. This was demonstrated by the findings that pretreatment of target cells with monoclonal anti-Qa-2 antibody blocked lysis of target cells, and Qa-2 target antigens and serological determinants had a concordant distribution on a panel of B10.W (wild) mice. The gene controlling the Qa-2 target antigen is not polymorphic because B6.K2 and three strains of Qa-2(+) B10.W mice express the same antigens, as determined by a CTL cold target competition assay. Anti-Qa-2 CTL were H-2 unrestricted because effector cells lysed Qa-2(+) targets irrespective of their H-2 haplotype, including five B 10.W strains, and lysis was not inhibited by pretreating target cells with anti-H-2 sera. The Qa2 subregion does not act as a restricting locus for anti-minor-H antigen CTL. A second target antigen was detected that was associated with the expression of the Qa-5 determinant. However, CTL activity could not be blocked by pretreating target cells with monoclonal anti-Qa-5. Therefore, the CTL target antigen may be expressed on a Qa-5(-) molecule. Although the Qa-5 associated CTL specificity is only detected on H-2D(b) strains, it is unlikely that CTL recognition is H-2 restricted because anti-H-2(b) sera has no effect in blocking this reactivity. Qa-2 and H-2 class I antigens share a similar structure and serve as target antigens for unrestricted CTL. However, unlike class I H-2 genes, Qa-2 neither restricts antigen-specific CTL nor is polymorphie. Therefore, it is likely that Qa-2 and H-2 are derived from a common ancestral gene and have evolved to serve different functions.
Animals↗
Helper activity is required for the in vivo generation of cytotoxic T lymphocytes.
B6.T1a(a) (Qa-1(a)) mice that are primed in vivo and restimulated in vitro with Qa-1 congenic spleen cells from B6 (Qa-1(b)) animals are unable to generate anti-Qa-1(b) cytotoxic T lymphocytes (CTL). This nonresponsive pattern was observed regardless of the route of immunization or the time of testing in vitro. Although B6.T1a(a) mice are nonresponders to Qa-1(b) when presented on B6 cells, these mice can generate anti-Qa-1(b) CTL when primed in vivo with Qa-1 and H-Y alloantigens (females primed with B6 male cells) or Qa-1 and minor-H- alloantigens (primed with sex-matched A.BY cells). Therefore, the inability to generate anti-Qa-1(b) CTL is due to a lack of helper or accessory antigens on B6 immunizing cells obligatory during in vivo priming, rather than an absence of anti-Qa-1(b) CTL precursors (CTL-P). Demonstration that the additional determinants required during in vivo priming actually function as carrier or helper determinants was shown by the requirement for linked recognition of Qa-1 and the helper determinants (H-Y) in vivo, and the fact that H-Y was not present on susceptible target ceils. Animals primed in vivo with H-Y only could not generate anti-Qa-1 CTL activity when challenged in vitro with both Qa-1 and H-Y, indicating that recognition of the helper determinant causes in vivo priming of CTL-P rather than generating helper activity that might activate unprimed CTL-P in vitro. Whereas unprimed peripheral CTL-P require the presence of both Qa-1 (CTL) and H-Y (helper) determinants for successful in vivo priming, helper determinants were not required in vitro because primed CTL-P from B6.T1a(a) mice could be driven to CTL in vitro using sex-matched B6 stimulator cells. The generation of anti-Qa-1(b) CTL is under immune response (Ir) gene control because F(1) mice, obtained by crossing responder A/J with nonresponder B6.T1a(a) animals, generated CTL to the Qa-1(b) alloantigen when presented on B6 spleen cells. Progeny testing of backcross mice further demonstrated that the Ir gene(s) is linked to the H-2 complex. These data indicate that an H-2-linked Ir gene controls the recognition of helper determinants required for CTL priming in vivo. These helper determinants can be distinguished from CTL determinants and both must be recognized together for successful priming of CTL-P.
Animals↗
[Non-invasive study of aortic insufficiency by Doppler echocardiography].
The possibilities of diagnosis and quantification of aortic regurgitation by pulsed Doppler analysis of blood flow in the aortic arch were examined in 60 patients aged between 9 and 67 years old. Aortic flow curves were recorded from the suprasternal area with the sample volume positioned at the junction of the horizontal part of the aortic arch and the descending aorta. Normal flow curves are characterised by an anterograde systolic wave with a brief proto-diastolic reflux. In aortic regurgitation holodiastolic reflux is observed. An index of regurgitation may be calculated from the ratio of the amplitude of end diastolic reflux measured on the R wave of th ECG and the maximal amplitude of anterograde systolic flow. This ratio eliminates the factor related to the incident angle between the ultrasound beam and the direction of blood flow. The values of this ratio were compared to the semi quantitative assessment of aortic regurgitation from ascending aortic angiography. The only false negatives were observed in patients with negligible regurgitation (grade I). One false positive result was obtained in a patient in whom it was difficult to obtain the recording and in whom the value of the ratio was very low (0,02). Global specificity was 91 p. 100 and sensitivity was 82 p. 100. The sensitivity for average or severe regurgitation was 100 p. 100. The correlation coefficient between the Doppler index or regurgitation and the semi quantitative angiographic estimation was 0,69. In patients with pure aortic regurgitation the correlation reached 0,85 (p less than 0,001). The differences between the different groups then became highly significant.
Adolescent↗
[Doppler echocardiographic diagnosis and evaluation of tricuspid regurgitation].
The reliability of pulsed Doppler echocardiography in the diagnosis and quantification of tricuspid regurgitation was assessed by analysis of blood flow in the inferior vena cava in 28 patients. The inferior vena caval flow was sampled in the retrohepatic portion of the vessel from the subxiphoid region. Recordings from 10 normal patients were used to define criteria of normality. This was characterised by two anterograde components (one systolic and one diastolic); atrial contraction gave rise to an end diastolic retrograde component. In tricuspid incompetence, retrograde systolic blood flow was recorded. A Doppler index was calculated from the ratio of the maximal amplitude of systolic reflux to the maximal amplitude of anterograde diastolic flow. In the absence of tricuspid regurgitation, this index approximated 0. The average of this ratio over 10 consecutive beats was compared with the semi quantitative assessment of tricuspid regurgitation from selective right ventricular angiography. There were no false positive results, specificity was, therefore, 100 p. 100. Six minimal regurgitations were not detected: sensitivity was therefore 74 p. 100. All moderate and severe regurgitations were detected, and the sensitivity for these cases was 100 p. 100. There was a close correlation (R = 0,89, p less than 0,01) between the Doppler index and the degree of regurgitation assessed by selective right ventricular angiography.
Adolescent↗
Cytotoxic T cells specific for antigens expressed on surface immunoglobulin-positive cells.
C.B-20 mice were immunized with splenocytes or B leukemia cells (BCL1) from Ig H chain allotype congenic strains. Spleen cells from these immunized mice were rechallenged in vitro to generate H-2-restricted cytotoxic T cells that were specific for target antigens controlled by genes linked to the Ig H chain locus. The anti-Ig H cytotoxic T cells detected an antigen(s) expressed only on surface Ig+ cells. Thus, T cell lymphoblasts, eight BALB/c myeloma cell lines, and a T cell lymphoma were not lysed by the effector cells. In contrast, B cell lymphoblasts and the surface Ig+ BCL1 cells were sensitive to lysis. A surface Ig- hybridoma (which secretes the IgM from the BCL1 cells) generated by fusing BCL1 cells to X63 myeloma cells was not killed by the effector cells. These data indicate that cytotoxic T cells specific for antigenic determinants on either surface IgM+ or IgD+ or on a molecule that is coordinately expressed on IgM+ or IgD+ cells can be generated and that such cells might play a role in regulating the growth of normal B cells or surface Ig+ tumor cells in vivo.
Alleles↗
Role of glycosylation in the H-2-restricted cytolysis of virus-infected cells.
The role of the oligosaccharide portions of cell surface glycoproteins in the susceptibility of virus-infected cells to H-2-restricted cytolysis was investigated by using the antibiotic tunicamycin (TM). TM inhibits the addition of sugars to the polypeptides of glycoproteins. TM treatment of P815 cells before and during infection with vesicular stomatitis virus (VSV) inhibited glycosylation of proteins and reduced by about 50% the lysis of infected P815 cells by VSV-immune, H-2-identical killer cells. In contrast, TM treatment had a modest inhibitory effect on cytolysis of P815 cells by alloimmune effector cells. TM treatment did not inhibit the surface expression of either H-2 or VSV glycoprotein. Thus, glycosylation of H-2 and/or viral glycoprotein is a prerequisite for the lysis of infected cells by H-2-identical, VSV-immune cytotoxic cells.
Animals↗
Antigen-presenting cells that induce anti-H-2K T-cell responses: differences in stimulator-cell requirements for induction of proliferation and cell-mediated lympholysis.
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Animals↗
Are allogeneic and associative recognition coincident T cell paradigms?
T lymphocytes are obsessed with cell surface molecules encoded by genes of the MHC, particularly class I (K/D) gene products. In one paradigm, T cells recognize and are activated by allodisparate class I antigens (allogeneic recognition); in another paradigm, T lymphocytes recognize viral antigens or haptens in the context of syngeneic class I determinants (associative recognition). Whether these paradigms are coincident, or even overlapping, is unresolved. We have studied neonatal tolerance induction among the H-2Kb parent strain and several of its class I mutants as a means of analyzing the fine discrimination potential of T cell recognition. Neonatal C57BL/6 animals were rendered tolerant of Kb mutant antigens; bm1, bm3, bm5, or bm8. Similar panels of mutant mice were rendered tolerant neonatally of the parent Kb antigen. When fully tolerant, mature animals were challenged with third-party grafts bearing related Kb alloantigenic disparities, they proved to be highly discriminant. Kb animals tolerant of bm1 or bm3 always rejected third-party grafts bearing bm3 and bm1 antigens, respectively. Similarly, the majority of Kb animals tolerant of bm5 or bm8 (and vice versa) were able to distinguish accurately the tolerated antigen from third-party antigens, rejecting grafts bearing the latter. Since associative recognition involving these antigens has been found to be at least partially degenerate and since neonatally tolerant animals nonetheless remain highly discriminant of these same antigenic variations, it is tempting to conclude that associative and allogeneic recognition address different aspects of T cell function.
Animals↗
Cell membrane antigens recognized by anti-viral and anti-trinitrophenyl cytotoxic T lymphocytes.
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Animals↗
Mechanisms for generating cell membrane antigens that are recognized by cytotoxic T lymphocytes.
Studies with many viruses have revealed that viral specific protein synthesis is an obligatory step in generating antigens on target cells for antiviral cytotoxic T lymphocytes. This has been most clearly demonstrated with DI particles, virions that are structurally complete but lack infectious RNA. Adsorption of such particles onto target cell membranes does not render these cells susceptible to lytic attack by antiviral effector cells, unless some viral protein synthesis transpires. However, some viruses, such as Sendai virus, circumvent the requirement for viral protein synthesis via fusion of the viral envelope with the target cell membrane, a process mediated by a specialized fusion protein. Once inserted into the lipid bilayer, it is likely that viral components and self H-2 noncovalently associate so that the complex can be recognized by antiviral cytotoxic T cells. This idea is supported by the demonstration that viral proteins and H-2 containing membrane proteins, incorporated into reconstituted membrane vesicles or liposomes are recognized by cytotoxic T cells. These data further show that native rather than altered viral and H-2 molecules are the moieties recognized. Associations between antigen and H-2 have been detected by a variety of techniques and in some cases are not random but selective; that is, viral antigens perferentially associate with some H-2 alleles and not others. In summary, these findings indicate that although viral antigens are present in the mature virions, these components are not recognized by antiviral killer cells until integrated into the plasma membrane. This may be achieved either through direct fusion of the viral envelope with the target cell or following viral protein synthesis and insertion of viral antigens into the plasma membrane.
Animals↗
Influence of IgH V-region genes on the growth kinetics of a murine B cell leukemia (BCL1).
The growth kinetics of an IgM-bearing B cell leukemia of BALB/c (Ig-1a) origin, designated BCL1, has been investigated in 2 allotype immunoglobulin (Ig) heavy (H) chain congenic strains, C.B-20 (Ig-1b) and C.AL-20 (Ig-1d), and an (H) chain recombinant strain, BAB-14 (Ig-1a/1b), that carries Ig-1a genes in the variable (V)-region and Ig-1b genes in the constant (C)-region. When large numbers (10(6) to 10(7)) of BCL1 cells were injected into these mice, leukemia, as measured by the appearance of leukemic cells in peripheral blood with subsequent mortality, did not occur in C.B-20, was delayed in C.AL-20, and progressed at the same rate in BAB-14 relative to BALB/c control mice. These results indicate that an immune response directed against an antigen encoded for by an H chain V region gene (idiotype or variable-region allotype) or linked gene (minor histocompatibility antigen) prevents the growth of the BCL1 leukemia in the C.B-20 mice. Tumor resistance appears to be due to T cell activity since adoptive transfer of such cells from C.B-20 tumor rejectors protected sublethally irradiation recipients from subsequent tumor challenge. Although H-2 restricted, anti-BCL1 cytotoxic cells were detected in C.B-20 mice challenged in vivo and restimulated in vitro with BCL1 cells, evidence is discussed that suggests that the resistance observed is not due to these effector cells. The resistance of allotype congenic mice to BCL1 was not absolute; a small inoculum (10(2)) was as lethal in C.B-20 and C.AL-20 as BALB/c mice. Thus, Ig-encoded cell surface antigens, although immunogenic, in no way ensure ultimate host survival.
Animals↗
[Left ventricular relaxation in myocardial diseases. Hemodynamic study].
Left ventricular relaxation as opposed to contraction, was studied by recordings of left ventricular pressure and its first derivation in primary hypertrophic cardiomyopathy without obstruction (25 cases, Group II) in primary dilated cardiomyopathy (33 cases, Group III) and in normal subjects (22 cases, Group I). Simultaneous recording of the pressure, the first derivation and intraventricular and intraaortic phonocardiogrammes showed the significance of certain features of the tracings and allowed a simplified protocol: ventricular relaxation was then defined from the pressure tracing (high fidelity recording) and its first derivation. The onset of isovolumic relaxation corresponded to the point of inflection on the descending part of the first derivation tracing, preceding its negative peak by an average of 0.02 s. The end of isovolumic relaxation corresponded to the crossing point of the atrial and ventricular pressure curves. In the absence of atrial pressure tracings the initial part of the rapid filling phase was included as far as the return of the first derivation tracing to its baseline (early diastole on the ventricular pressure tracing) as the duration of this period seemed remarkably constant (0.07 s). The parameters studied were: duration of isovolumic relaxation or the period defined above including the rapid filling phase; the average rate of fall of left ventricular pressure during this part of diastole; the value of the negative peak of the first derivation (dp/dt min); the rate of lengthening of the contractile elements at minimum dp/dt (dp/dt min/28P). Changes in relaxation were obvious in the pathological groups. The duration was increased and its average speed, dp/dt min, and dp/dt min/28 P were reduced. In the hypertrophic group, however, these changes seemed to be primary and contractility was usually unaffected. In dilated cardiomyopathy these changes could be considered secondary to decreased contractility. The hypothesis that changes in relaxation are specific for hypertrophic forms, and that changes in contractility are specific for dilated forms of primary cardiomyopathy may therefore be proposed.
Adolescent↗
[Mitral incompetence as presenting feature of idiopathic left ventricular aneurysm (author's transl)].
A further case of the exceptionally rare condition of idiopathic left ventricular aneurysm is reported in which the lesion was detected in a most unusual manner. The patient, a young 22-year-old negro woman, had been admitted for investigation of a mitral incompetence. The true diagnosis was established by angiography, which demonstrated a large multilobular left ventricular aneurysm, also communicating with the left auricle, this being the cause of the mitral incompetence. Surgical correction of the lesion suppressed the mitral leak without touching the normal mitral apparatus.
Adult↗
The use and limitations of serial plasma carcinoembryonic antigen (CEA) levels as a monitor of changing metastatic liver tumor volume in patients receiving chemotherapy.
Nine patients with liver-predominant or liver-only metastatic adenocarcinoma, who received hepatic intra-arterial and peripheral intravenous chemotherapy, were evaluated to determine if changes in plasma CEA accurately indicated changes in liver tumor volume as estimated from serial liver scan defect sizes, and if the two were quantitatively related. When selected periods of tumor remission or progression were studied during chemotherapy, the index of change of serial CEA values correlated positively (r = 0.764, P = 0.01) with the index of change of liver tumor volume in all 9 cases. Changes in absolute CEA values, however, aid not correlate significantly with changes in absolute liver tumor volumes when assessed either during these selected periods or throughout individual patient courses. Biologic and methodologic factors that influence the quantitative relation between liver tumor volume and plasma CEA are discussed.
Adenocarcinoma↗