Surgical considerations in the treatment of pes planus.
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Ankle↗
Biomedical subjects
S D Smith
Publications and source records attributed to S D Smith.
Clinical and biologic characterization of T-cell neoplasias with rearrangements of chromosome 7 band q34.
In T cell malignancy, rearrangements of chromosome 14 have been observed with a break in the band that contains the alpha chain gene for the T cell receptor (TCR). Because the beta chain TCR gene is in chromosome band 7q34, we searched for and report finding specific rearrangements of 7q34 exclusively in T cell malignancies. The rearrangements were reciprocal translocations between 7q34 and other points: 1p34, 9q32, 9q34, 15q22, and 19p13. The malignancies containing a 7q34 translocation were either T cell acute lymphoblastic leukemias or T cell lymphoblastic lymphomas that had similarities in clinical, enzyme, immunologic, and cellular characteristics. Hybridization using a probe to the beta-TCR gene disclosed unique rearrangements consistent with clonality in every case. A common pattern with chromosome breakpoints involving TCR genes may be emerging in T cell neoplasia.
Adenosine Deaminase↗
Adnexal torsion: five-year experience at Tampa General Hospital.
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Adnexal Diseases↗
Idiotype as a tumor-specific marker in childhood B cell acute lymphoblastic leukemia.
Immunoglobulin (Ig) or idiotype (Id) is a tumor-specific target in those B cell malignancies that express this molecule on their surface. We explored the biology of B cell acute lymphoblastic leukemia (B cell ALL) using Id as a tumor marker. In this report we describe the development of anti-Id monoclonal antibodies (MAB) for two children with B cell ALL. These reagents were used retrospectively to study tumor kinetics and to detect residual disease after chemotherapy. In both cases serum Id values were strikingly high at diagnosis (1.2 mg/mL and 10.8 mg/mL), suggesting that the tumor cells were relatively mature B cells capable of significant antibody production. In both patients the serum Id levels fell with the institution of therapy and confirmed that the patients were in remission. Increasing serum Id predicted relapse four months before conventional methods in patient 1, and Id proved to be a more sensitive measure of tumor burden than Southern blot analysis of rearranged Ig genes in bone marrow samples. Surprisingly, low levels of Id were redetected in the second patient just before completing therapy and have persisted for over a year despite the absence of clinical evidence of recurrent disease. Thus, serum Id levels reflect tumor burden during initial therapy but may not necessarily predict tumor progression after a complete clinical remission.
Adolescent↗
Absence of cell surface LFA-1 as a mechanism of escape from immunosurveillance.
During studies of T-cell recognition of autologous tumour cells, a number of tumour cell lines derived from patients with lymphoma proved to be poor stimulators of both autologous and allogeneic T-cell responses. Analysis of the tumour cell surface molecules indicated that expression of the lymphocyte-function-associated antigen, LFA-1, was lacking, whereas normal leucocytes from these patients expressed normal levels of LFA-1. Examination of other lymphoid tumours revealed that most high grade lymphomas, but not most low or intermediate grade lymphomas, do not express the LFA-1 molecule. Furthermore, in an initial survey, the tumours from 5 of 7 patients with non-relapsing large cell lymphomas expressed LFA-1 whereas only 3 of 18 patients with relapsing lymphomas had tumours that did so. These findings suggest that tumour cells lacking surface LFA-1 cannot initiate an effective immune response in vivo. This lack of immunogenicity might contribute to escape from immunosurveillance.
Antigens, Surface↗
Analysis of DNA surrounding the breakpoints of chromosomal translocations involving the beta T cell receptor gene in human lymphoblastic neoplasms.
DNA containing breakpoints of two different t(7;9) chromosomal translocations was cloned from the T lymphoblastic tumor cell lines SUP-T1 and SUP-T3. Sequence analysis of DNA from the t(7;9)(q34;q34.3) translocation of SUP-T1 revealed that chromosome 9 DNA had recombined with DNA 5' to rearranged D-J regions in the beta T cell receptor gene of chromosome 7. Restriction analysis and hybridization studies using DNA fragments cloned from the t(7;9)(q34;32) translocation of SUP-T3 confirmed that beta T cell receptor DNA is also joined to the DNA of chromosome 9 in these cells. Using hybridization probes for the two breakpoints, several other cases of T lymphoblastic tumors were shown to possess DNA rearrangements near the 9q34.3 and 9q32 sites. Hybridization with the 9q34.3 probe detected multiple transcripts in SUP-T1 RNA and small amounts of larger transcripts in T cells lacking the t(7;9)(q34;q34.3) translocation. This work directly demonstrates that the beta T cell receptor locus may frequently be involved in chromosomal translocations within T lymphoblastic neoplasms.
Chromosome Mapping↗
JCAH accreditation provides competitive edge.
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Accreditation↗
Establishment and characterization of a common acute lymphoblastic leukemia cell line with a deletion of chromosome 3 band q26.
This paper describes the establishment and characterization of a new cell line (SUP-B7) which was established from a child with "common" acute lymphoblastic leukemia. The SUP-B7 cells (and the patient's tumor) have been characterized by cytochemical staining, monoclonal antibodies, enzyme analyses, gene rearrangement studies, and karyotype analysis. The SUP-B7 cells are periodic acid-Schiff positive, common acute lymphoblastic leukemia antigen positive, and terminal deoxynucleotidyl transferase positive, and they lack the Epstein-Barr virus genome. In addition, the SUP-B7 cells lack cytoplasmic and surface immunoglobulins, and the immunoglobulin gene rearrangement studies showed rearranged heavy chain genes with germ line light chain genes. Concordance between the cell line and the patient's tumor was established by the immunoglobulin gene rearrangement studies. Using Southern blot analysis of the DNA from the patient's tumor and the SUP-B7 cells, there was comigration of the bands representing the rearranged immunoglobulin heavy chain gene. In addition, the SUP-B7 cells possess a single chromosome abnormality: del(3)(q26q28), with the chromosome breakpoint at or near the transferrin receptor gene. Since the SUP-B7 cell line is concordant with the patient's malignancy and since these cells possess a single chromosomal abnormality, the SUP-B7 cell line may be a useful tool in determining the biological significance of the chromosome deletion: del(3)(q26q28).
Antigens↗
Relationship between the c-myb locus and the 6q-chromosomal aberration in leukemias and lymphomas.
Deletions of the long arm of chromosome 6 (6q-) are frequently found in hematopoietic neoplasms, including acute lymphoblastic leukemias, non-Hodgkin lymphomas and (less frequently) myeloid leukemias. The c-myb proto-oncogene has been mapped to region 6q21-24, which suggests that it could be involved in the 6q- aberrations. By means of in situ chromosomal hybridization on cells from six hematopoietic malignancies, it was demonstrated that the c-myb locus is not deleted, but is retained on band q22, which is consistently bordered by the chromosomal breakpoints in both interstitial and terminal 6q- deletions. The deletion breakpoints were located at some distance from the myb locus since no rearrangement of c-myb sequences was found. In one case, however, amplification of the entire c-myb locus was detectable. Furthermore, in all cases tested that carry 6q- deletions, myb messenger RNA levels were significantly higher than in normal cells or in malignant cells matched for lineage and stage of differentiation but lacking the 6q- marker. These results indicate that 6q- deletions are accompanied by structural and functional alterations of the c-myb locus and that these alterations may be involved in the pathogenesis of leukemias and lymphomas.
Chromosome Deletion↗
Left-handedness and immune disorders in familial dyslexics.
We examined the frequency of left-handedness, various immune disorders, and comparison disorders in 87 dyslexics and 86 nondyslexics from 14 extended dyslexic families. These families were participants in our genetic linkage studies of dyslexia, which found linkage to chromosome 15 in some families but not others. In the present study, we found a significant elevation of both autoimmune and allergic disorders in the dyslexics only, but no elevation in mixed- or left-handedness in either group. Moreover, the frequency of immune disorders was not higher in the mixed- or left-handed subjects. There was also no elevation in the comparison disorders, which argues against an overreporting bias. The elevation of immune disorders did not vary with linkage status, arguing against a common cause for dyslexia and immune disorders. These findings are discussed in light of Geschwind's hypothesis of a testosterone-mediated association within families between left-handedness, immune disorders, and dyslexia.
Autoimmune Diseases↗
Cat-eye syndrome with different marker chromosomes in a mother and daughter.
Except for atypical eye findings in the daughter, a mother and daughter with bisatellited marker chromosomes had abnormalities consistent with cat-eye syndrome. The mother's marker chromosome (mar number 1) is derived from one 22 and another acrocentric, possibly also a 22; the daughter's marker (mar number 2) may be an iso-dicentric, inv-dup (22) derivative of mar number 1. The mother has a tertiary trisomy translocation chromosome composed of at least one and perhaps two copies of 22pter----q11.2, whereas the daughter clearly has a secondary trisomy 22pter----q11.2 isochromosome, confirming this region as a cause of cat-eye syndrome. Results of hybridization using a unique sequence probe localized to 22q11 are consistent with the interpretation that both ends of both marker chromosomes are derived from 22.
Abnormalities, Multiple↗
Calcium cyclotron resonance and diatom mobility.
The hypothesis that movement of biological ions may be predicted by cyclotron resonance theory applied to cell membranes is tested in these experiments. Diatoms (Amphora coffeaeformis) were chosen as the biosystem since they move or don't move, depending on how much calcium is transported across the membrane. The experiments demonstrate that a particular ion (calcium) is apparently moved across the cell membrane in response to the DC and AC values of magnetic flux densities (B) and the frequency derived from the cyclotron resonance theory. A clear resonance is shown and a rather sharp frequency response curve is demonstrated. The experiments also show a dose response as the AC value of the flux density is varied, and that odd harmonics of the basic cyclotron frequency are also effective.
Calcium↗
Beneficial effects of a hypertonic solution for resuscitation in the presence of acute hemorrhage.
Crystalloid solutions such as Ringer's lactate have become the standard for initial volume replacement after hemorrhage. Although the relative merits of blood, colloid, and crystalloid have been extensively studied, little attention has been directed toward determining the optimal composition of the crystalloid solution. Based on the beneficial properties of hypertonic lactated saline solution in burn resuscitation, we have extended its use to acute hemorrhage. Using an awake canine model analogous to the clinical situation, we compared hypertonic lactated saline solution with Ringer's lactate solution for resuscitation in the presence of acute blood loss. The hypertonic lactated saline solution group required less fluid to restore and maintain cardiac output and blood pressure while maintaining better urine output. Although the Ringer's lactate solution group had increased shunt function indicative of pulmonary dysfunction, the shunt function in the hypertonic lactated saline solution group did not differ from that in the control group. Serum sodium and osmolality values were higher in the hypertonic lactated saline solution group, but at no time did they approach toxic levels.
Acute Disease↗
Nifedipine is an antagonist to cyclotron resonance enhancement of 45Ca incorporation in human lymphocytes.
The incorporation of 45Ca in mixed human lymphocytes was measured following one-hour exposures of the cells to combined steady and periodic magnetic fields designed to probe for cyclotron resonance response in calcium incorporation. Measurements were made as a function of magnetic field frequency, up to 30 Hz, and as a function of magnetic field amplitude, up to 1.5 x 10(-4) Trms. The amplitude measurements demonstrated that the relative 45Ca uptake at resonance follows different mechanisms of interaction above and below 0.2 x 10(-4) Trms. After adjusting the magnetic field configuration for maximum incorporation, we then determined the effects of the calcium influx blocker nifedipine on 45Ca incorporation, with and without simultaneous exposure to this specific magnetic field combination. The presence of nifedipine in both unexposed and exposed cell suspensions resulted in decreased 45Ca uptake, presumably through the slow inward calcium channels. Evidence was found suggesting that nifedipine acts antagonistically to the 45Ca cyclotron resonance tuning signal.
Calcium↗
Challenges in pain management. Part 1. Diagnosis and treatment of temporomandibular joint disorders.
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Humans↗
Molecular analysis of TCRB and ABL in a t(7;9)-containing cell line (SUP-T3) from a human T-cell leukemia.
A translocation between chromosomes 7 and 9, t(7;9), has been described in cell lines derived from the malignant cells of children with acute T-cell lymphoblastic leukemia or lymphoma. Our cytogenetic analysis of one such cell line, SUP-T3, demonstrates that the breakpoints on chromosomes 7 and 9 lie within bands q36 and q34, respectively, corresponding to the location of the gene encoding the beta chain of the T-cell receptor, TCRB, and the gene homologous to the transforming gene of the Abelson murine leukemia virus, ABL. We investigated the role of these genes in the t(7;9). In situ chromosomal hybridization of TCRB and ABL probes to metaphase cells from SUP-T3 demonstrated that ABL is translocated from chromosome 9 to 7 and that all or part of TCRB is translocated from chromosome 7 to 9. Southern blot analysis revealed that both TCRB alleles were rearranged; however, it could not be determined whether the translocation breakpoint lies within this gene. Pulsed-field gel electrophoresis and Southern blot analysis were used to examine more than 500 kilobases of the ABL locus; we concluded that there are no rearrangements within 250 kb in either direction of the sequences homologous to v-abl. Additionally, no abnormal ABL protein was detected in an in vitro phosphorylation assay. These results indicate that, in SUP-T3, the breakpoint on chromosome 9 lies proximal to ABL and that the break results in no apparent alteration of the ABL protein. We therefore hypothesize that another gene on chromosome 9, at band q34, plays a role in this translocation. This study also demonstrates that pulsed-field gel electrophoresis is a powerful new tool for the analysis of human chromosomal translocations.
Abelson murine leukemia virus↗
Anesthetic management of tracheal esophageal fistula with distal tracheal stenosis.
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Anesthesia, General↗
In vitro susceptibility of Capnocytophaga species to antimicrobial agents.
A total of 33 clinical isolates of Capnocytophaga spp. were susceptible to 4-quinolone antimicrobial agents. The antipseudomonal penicillins tested were equally active against all isolates, as were cefuroxime, ceftriaxone, ceftizoxime, cefotaxime, latamoxef, and ceftazidime. Most isolates were resistant to trimethoprim, and some were resistant to aztreonam. Most regimens for the empirical treatment of septic episodes in immunocompromised patients are suitable for the treatment of Capnocytophaga spp. infections.
Anti-Bacterial Agents↗