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Biomedical subjects

L Xu

Publications and source records attributed to L Xu.

At least 577 records · Page 32Linked to original sources

Very low rates of hip fracture in Beijing, People's Republic of China the Beijing Osteoporosis Project.

One third of the world's hip fractures are said to occur in Asia, mostly in China. However, there have as yet been no validated studies of hip fracture rates in China. The authors estimated the incidence of hip fractures in Beijing, People's Republic of China, and took several steps to validate the estimates. All 76 Beijing hospitals reported all 1988-1992 admissions that had been coded as 820 (hip fracture) or 821 (other femoral fracture) according to the International Classification of Diseases, Ninth Revision. The authors then compared a random sample of the reports with original medical records, and discovered that 70% of intertrochanteric hip fractures had been miscoded as "other femoral fractures." The authors retrained all hospital staffs to provide corrected reports. Revised reports missed only 13% of the hip fracture cases recorded in operating room logs of 11 randomly selected hospitals. To validate hospital-based estimates of hip fracture rates, the authors interviewed a random sample of 2,113 Beijing women aged 50 years or more (97% response rate); all but 4% of past fractures and all seven hip fractures had been treated in hospitals. Finally, the authors surveyed the 27 hospitals in the counties surrounding Beijing. No Beijing residents had been treated for hip fracture outside of the city. Based on the 1990 China census, age-standardized rates of hip fracture (per 100,000) in Beijing-87 for women, 97 for men-were much lower than those seen in Hong Kong in 1985 (353 for women, 181 for men) or in US Caucasians (510-559 for women, 174-207 for men). From 1988 to 1992, the rates in Beijing increased 34% in women and 33% in men. The authors conclude that hip fracture rates in Beijing are among the lowest in the world but may be rising rapidly.

Adult↗

The merlin tumor suppressor localizes preferentially in membrane ruffles.

Merlin is a tumor suppressor whose inactivation underlies the familial schwannomas and meningiomas of neurofibromatosis 2 and their sporadic counterparts. It bears striking similarity to the ERM proteins, ezrin, radixin and moesin, members of the protein 4.1 superfamily that link proteins in the cytoskeleton and the plasma membrane. We have generated polyclonal and monoclonal antibodies that detect merlin as an approximately 66 kD protein in many different cell types. Using indirect immunofluorescence we have for the first time visualized endogenous merlin and localized it to the motile regions, such as leading or ruffling edges, in human fibroblast and meningioma cells. Merlin co-localizes with F-actin in these motile regions but is not associated with stress fibers. Merlin does not localize to the same structures as either ezrin or moesin in human meningioma cells, suggesting a function distinct from these ERMs. Thus, merlin is associated with motile regions of the cell and its participation in these structures may be intimately involved in control of proliferation in Schwann cells and meningeal cells.

Actins↗

Participation of nucleoside-diphosphate kinase in muscarinic K+ channel activation does not involve GTP formation.

Agonist-bound muscarinic receptors open atrial K+ channels through a GTP-dependent pathway mediated by the G protein Gk. However, nucleotides other than GTP are also able to support channel activity, even in the absence of agonists. This process was proposed to be mediated by nucleoside-diphosphate (NDP) kinase, which would transfer phosphate from nucleotide triphosphates to the GDP bound to Gk, producing Gk-GTP without the need for receptor-induced GDP-GTP exchange. We examined the effect of antibodies to NDP kinase on the ATP-supported activity of atrial muscarinic K+ channels and the corresponding GIRK1/CIR channels expressed in HEK 293 cells. Inhibitory antibodies reduced ATP-induced channel openings, but this effect displayed an absolute requirement for agonist and was also seen with antibodies that do not inhibit the enzyme. Both types of antibodies also reduced agonist-dependent channel activity in the presence of GTP, ruling out a role for NDP kinase in GDP rephosphorylation. Channel activity was not affected by the antibodies in preparations where ATP-induced muscarinic channels are not under tight receptor control, namely pertussis toxin-treated atrial patches and membranes from cells expressing KACh channel subunits. Thus, participation of NDP kinase in this pathway requires activated receptors and has a function distinct from phosphate transfer between nucleotides.

Adenosine Triphosphate↗

Synaptonemal complex (SC) component Zip1 plays a role in meiotic recombination independent of SC polymerization along the chromosomes.

Zip1 is a yeast synaptonemal complex (SC) central region component and is required for normal meiotic recombination and crossover interference. Physical analysis of meiotic recombination in a zip1 mutant reveals the following: Crossovers appear later than normal and at a reduced level. Noncrossover recombinants, in contrast, seem to appear in two phases: (i) a normal number appear with normal timing and (ii) then additional products appear late, at the same time as crossovers. Also, Holliday junctions are present at unusually late times, presumably as precursors to late-appearing products. Red1 is an axial structure component required for formation of cytologically discernible axial elements and SC and maximal levels of recombination. In a red1 mutant, crossovers and noncrossovers occur at coordinately reduced levels but with normal timing. If Zip1 affected recombination exclusively via SC polymerization, a zip1 mutation should confer no recombination defect in a red1 strain background. But a red1 zip1 double mutant exhibits the sum of the two single mutant phenotypes, including the specific deficit of crossovers seen in a zip1 strain. We infer that Zip1 plays at least one role in recombination that does not involve SC polymerization along the chromosomes. Perhaps some Zip1 molecules act first in or around the sites of recombinational interactions to influence the recombination process and thence nucleate SC formation. We propose that a Zip1-dependent, pre-SC transition early in the recombination reaction is an essential component of meiotic crossover control. A molecular basis for crossover/noncrossover differentiation is also suggested.

Chromosomes, Fungal↗

A CBP integrator complex mediates transcriptional activation and AP-1 inhibition by nuclear receptors.

Nuclear receptors regulate gene expression by direct activation of target genes and inhibition of AP-1. Here we report that, unexpectedly, activation by nuclear receptors requires the actions of CREB-binding protein (CBP) and that inhibition of AP-1 activity is the apparent result of competition for limiting amounts of CBP/p300 in cells. Utilizing distinct domains, CBP directly interacts with the ligand-binding domain of multiple nuclear receptors and with the p160 nuclear receptor coactivators, which upon cloning have proven to be variants of the SRC-1 protein. Because CBP represents a common factor, required in addition to distinct coactivators for function of nuclear receptors, CREB, and AP-1, we suggest that CBP/p300 serves as an integrator of multiple signal transduction pathways within the nucleus.

Animals↗

Expression of a protective gene-prolongs survival of T cells in human immunodeficiency virus-infected patients.

The resistance of acquired immunodeficiency syndrome (AIDS) to traditional drug therapy has prompted a search for alternative treatments for this disease. One potential approach is to provide genetic resistance to viral replication to prolong latency. This strategy requires the definition of effective antiviral genes that extend the survival of T cells in human immunodeficiency virus (HIV)-infected individuals. We report the results of a human study designed to determine whether a genetic intervention can prolong the survival of T cells in HIV-infected individuals. Gene transfer was performed in enriched CD4+ cells with plasmid expression vectors encoding an inhibitory Rev protein, Rev M10, or a deletion mutant control, deltaRev M10, delivered by gold microparticles. Autologous cells separately transfected with each of the vectors were returned to each patient, and toxicity, gene expression, and survival of genetically modified cells were assessed. Cells that expressed Rev M10 were more resistant to HIV infection than those with deltaRev M10 in vitro. In HIV-infected subjects, Rev M10-transduced cells showed preferential survival compared to deltaRev M10 controls. Rev M10 can therefore act as a specific intracellular inhibitor that can prolong T-cell survival in HIV-1-infected individuals and potentially serve as a molecular genetic intervention which can contribute to the treatment of AIDS.

Acquired Immunodeficiency Syndrome↗

Identification of defensin-1, defensin-2, and CAP37/azurocidin as T-cell chemoattractant proteins released from interleukin-8-stimulated neutrophils.

Reports that interleukin-8 (IL-8) induces the infiltration of neutrophils followed by T-cells into injection sites led us to postulate that by stimulation of neutrophil degranulation IL-8 may cause the release of factors with chemoattractant activity for T-lymphocytes. Extracts of human neutrophil granules were chromatographed to isolate and purify T-lymphocyte chemoattractant factors. Two major peaks of T-cell chemotactic activity were purified by C18 reversed phase high pressure liquid chromatography (HPLC). The first peak was resolved further by C4 reversed phase HPLC and yielded an active fraction shown by NH2-terminal amino acid sequence analysis to contain defensins HNP-1, HNP-2, and HNP-3. Purified defensins HNP-1 and HNP-2 (kindly provided by Dr. R. I. Lehrer, UCLA) were also potent chemoattractants for human T-cells, while HNP-3 was inactive. The second peak of T-cell chemoattractant activity was also further purified to homogeneity by C4 reversed phase HPLC and identified by NH2-terminal sequence analysis as CAP37/azurocidin, a protein with sequence homology to serine proteases. 0.1 100 ng of defensins and 1.0 100 ng/ml CAP37 were able to stimulate in vitro T-cell chemotaxis. Neutrophil activating factors, i.e. IL-8, phorbol 12-myristate 13-acetate/ionomycin, and formylmethionylleucylphenylalanine each induced the release of CAP37 and defensins from neutrophil granules. Subcutaneous administration of defensins or CAP37/azurocidin into BALB/c mice resulted in a moderate neutrophil and mononuclear cell infiltrate by 4 h, which was greater by 24 h at the site of injection. Additionally, subcutaneous injection of defensins into chimeric huPBL-SCID mice resulted in significant infiltration by human CD3+ cells within 4 h. These results identify the antimicrobial proteins, CAP37/azurocidin and defensins HNP-1 and HNP-2, as potent neutrophil-derived chemoattractants for T-cells. These proteins represent primordial antimicrobial peptides which may have evolved into acute inflammatory cell-derived signals that mobilize immunocompetent T-cells and other inflammatory cells.

Amino Acid Sequence↗

Exogenous mouse mammary tumor virus (MMTV) infection induces endogenous MMTV sag expression.

The mouse mammary tumor virus (MMTV) superantigen (Sag) protein is involved in the transmission of milk-borne MMTV from virus-infected milk in the gut to the target mammary gland tissue. Using an RT-PCR assay for in vivo MMTV infection, BALB/c or C3H mice nursed on C3H MMTV-infected mothers showed sag mRNA expression in intestine, spleen, and thymus as early as 1 day after infection, whereas uninfected BALB/c control animals had approximately 10- to 30-fold lower sag expression. Further fractionation experiments with small intestine indicated that sag expression occurred in gut-associated lymphoid cells. Restriction enzyme digestion of PCR products indicated that the sag mRNA detected was derived from the endogenous MMTVs, and sequencing analysis confirmed that the PCR products were derived from endogenous MTv-6. Expression of C3H-specific mRNA was detectable in BALB/cfC3H or C3H tissues by RNase protection or by RT-PCR. Endogenous MMTV sag expression was low in spleen and undetectable in thymocytes of C3H MMTV-infected C57BL/6 mice, a strain resistant to C3H MMTV tumorigenesis and defective for MHC class II I-E molecules. The RT-PCR assay for sag mRNA appears to measure the Sag-induced stimulation previously predicted for milk-borne MMTV infection. Together these data suggest that exogenous MMTV sag expression is minimal, but sufficient to rapidly stimulate transcription of endogenous MMTV sag mRNA in B- and T-cells in an MHC class II I-E-dependent manner. The endogenous sag expression on maternal lymphocytes may increase the number of proliferating T-cells available for milk-borne MMTV infection.

Animals↗

Placental lactogen-I variant utilizes the prolactin receptor signaling pathway.

Placenta lactogen-I variant (PL-Iv) is a member of a family of proteins expressed by the rat placenta with characteristics similar to prolactin (PRL). In this report, we present the molecular cloning, chromosomal localization, and heterologous expression of PL-Iv. Nucleotide sequence analysis of the PL-Iv cDNA clone predicted a precursor protein of 223 amino acids, including a 28-amino acid signal sequence. The PL-Iv gene was localized to chromosome 17 of the rat genome, which also carries other members of the PRL gene family. PL-Iv heterologously expressed in Chinese Hamster ovary (CHO) cells exhibited similar immunoreactive and electrophoretic characteristics with PL-Iv produced by the rat placenta. N-terminal sequencing verified the identity and purity of the recombinant PL-Iv species and the site of cleavage of the signal peptide from the mature secreted PL-Iv species. Recombinant PL-Iv was shown to bind to ovarian and liver PRL receptors, stimulate the proliferation of Nb2 lymphoma cells, and activate Jak2. Each of these actions is consistent with PL-Iv utilizing the PRL receptor signal transduction pathway.

Animals↗

Liver injury model in mice induced by a cellular immunologic mechanism--delayed-type hypersensitivity-induced liver injury to picryl chloride and phenotype of effector cell.

Liver injury was induced in BALB/c mice by local delayed-type hypersensitivity (DTH) to picryl chloride (PC1). Distinct changes of biochemical parameters were observed including the elevation of serum alanine and aspartate aminotransferases, increase of liver lipid peroxides, as well as decrease of serum alkaline phosphatase. Damage was confirmed by histopathological findings such as hepatocellular necrosis, granulocyte infiltration, and fatty degeneration. The liver injury was passively transferred into naive syngeneic mice by infusing spleen cells from immune mice. The capacity of the splenocytes to induce liver injury in recipient mice was almost completely abolished by pretreatment of the cells with anti-Thy 1.2 or anti-CD4, but not anti-CD8 antibody. These findings suggest that the production of liver injury by a local DTH mechanism is possible and the subpopulation of T cells, Thy-1.2+, L3T4+, and Lyt-2- cells, is at least one of the effector cells that mediate the injury.

Animals↗

Prevalence of herpesviridae and hepatitis B virus DNA in the liver of patients with non-A, non-B fulminant hepatic failure.

Members of the herpes virus family and hepatitis B virus (HBV) have been implicated as etiologic agents in non-A, non-B (NANB) fulminant hepatic failure (FHF), but the frequency of infection with these agents has not been established using appropriate controls. To examine this issue, we studied 50 NANB FHF patients and 104 liver transplant recipients from North America and Europe. Hepatic DNA was analyzed by polymerase chain reaction (PCR) for evidence of Epstein-Barr virus (EBV), cytomegalovirus (CMV), herpes simplex virus I (HSV I) and II (HSV II), varicella-zoster virus (VZV), and human herpes virus-6 (HHV-6) nucleic acid sequences. The prevalence of HBV was assessed in North American subjects only. HSV I, HSV II, VZV, and HHV-6 viral sequences were not observed in any samples. Three of 50 FHF (6%) and 14 of 104 control patients (13%) were positive for CMV DNA. Two of 50 FHF (4%) and 10 of 104 control patients (10%) had EBV DNA, and HBV DNA was observed in 3 of 10 North American FHF patients (30%) and 3 of 59 controls (5%) without serum markers for HBV infection. The finding of HBV DNA in the liver of seronegative controls from North America but not Europe suggests that occult hepatitis B sequences in patients with NANB FHF may simply reflect geographic differences. The majority of cryptogenic FHF cases cannot be attributed to infection with herpes viruses or HBV.

Adolescent↗

IL-8-Induced T-Lymphocyte Migration: Direct as Well as Indirect Mechanisms

Although IL-8 has been reported to be a chemoattractant for T cells in vivo and in vitro, this has been a controversial issue. By using freshly purified human T cells (>90% CD3(+)), we demonstrated consistent T-cell migration in response to recombinant human IL-8 in vitro. However, highly purified T cells, when incubated at 37°C for more than 12 h or cultured overnight in the presence of anti-CD3 antibody, showed a markedly reduced capacity to migrate in response to IL-8. This reduction in chemotaxis was associated with a decrease in binding of 125I-IL-8 to T cells. Northern blots showed that freshly purified T cells expressed both IL-8 receptor type A and type B transcripts. Steady-state levels of mRNA for IL-8RA and IL-8RB in T cells were progressively reduced with time by incubation of the cells at 37°C with or without anti-CD3. The inability of cultured T cells to migrate in response to IL-8 accounts for the contradictory published reports on this issue. In vivo administration of IL-8 in rats resulted in the infiltration at the injection site of neutrophils followed by T cells, and this later T-cell infiltration was reported to be partially blocked by selective depletion of neutrophils. These observations raised the possibility that IL-8 may trigger neutrophils to release a factor(s) that may also participate in the T-cell recruitment. Neutrophil granule proteins, defensins, and CAP37/azurocidin released upon stimulation of cells by IL-8 were shown to induce human T-cell migration in vitro. Subcutaneous injection of defensins into SCID mice engrafted with human PBL resulted in significant infiltration by human CD3(+) T lymphocytes. These results indicate that IL-8 is able not only to act directly and induce migration of T lymphocytes that express IL-8 receptors, but also to act indirectly by activating neutrophils to release additional T-cell chemoattractants.

Journal Article↗

Structure and analysis of phospholipase D gene from Ricinus communis L.

Phospholipase D (PLD; EC 3.1.4.4) has been proposed to play a pivotal role in various cellular processes, but molecular understanding of this enzyme is rather limited. This report describes the nucleotide sequence, structure, and genomic organization of a PLD gene from castor bean (Ricinus communis L. cv. Hale). The PLD gene was isolated from a castor bean genomic library using the PLD cDNA as a hybridization probe. Sequence comparison with the PLD cDNA revealed that the PLD gene consisted of four exons and three introns, one of which interrupts the 5'-untranslated region. Southern blot analysis indicated that the cloned PLD gene was present as a single-copy gene, and yet there were other PLD or PLD-related sequences in the castor bean genome.

Ricinus communis↗

The effect of concurrent Pseudomonas or Xanthomonas exposure on adherence of Acanthamoeba castellanii to soft contact lenses.

BACKGROUND: Approximately 85% of Acanthamoeba-contaminated contact lens systems in asymptomatic patients have concurrent bacterial contamination. Pseudomonas aeruginosa and Xanthomonas maltophilia are common contact lens contaminants; we investigated the effect of coincubation of Acanthamoeba adherence to contact lenses. METHODS: A. castellanii, 1 x 10(5) organisms/ml, was coincubated with P. aeruginosa or X. maltophilia, 1 x 10(8) CFU/ml in phosphate-buffered saline. Sterile, unworn polymacon, etafilcon A or lidofilcon contact lens were investigated. The experimental groups were: (I) lenses exposed to bacteria for 1 h, then Acanthamoeba for 2 h; (II) lenses exposed concurrently to bacteria and Acanthamoeba for 2 h; (III) Acanthamoeba coincubated with bacteria for 24 h, then lenses exposed for 2 h; (IV) lenses exposed to Acanthamoeba for 2 h (control). RESULTS: For all experimental groups, Acanthamoeba adherence was greater to lidofilcon than to polymacon and etafilcon. For both P. aeruginosa and X. maltophilia, neither group I nor group II displayed greater Acanthamoeba adherence than group IV. Group III exhibited significantly less adherence than group IV for lidofilcon and polymacon. The decrease in group III adherence reflected an overall decrease in Acanthamoeba trophozoite concentration. CONCLUSION: Short bacteria/Acanthamoeba coincubation times did not result in increased Acanthamoeba adherence. Twenty-four-hour coincubation resulted in decreased adherence for Pseudomonas and unchanged adherence rates for Xanthomonas. This model suggests that Pseudomonas or Xanthomonas co-contamination does not necessarily facilitate quantitative Acanthamoeba contact lens adherence.

Acanthamoeba↗

Molecular detection of bean common mosaic and bean common mosaic necrosis potyviruses and pathogroups.

Partial nucleotide sequences of selected isolates of bean common mosaic virus (BCMV) and bean common mosaic necrosis virus (BCMNV) were determined. Based on these sequences and previously published sequence data, a reverse transcription, polymerase chain reaction (RT-PCR) in combination with restriction endonuclease analyses, was developed for molecular detection of BCMV, BCMNV and some viral pathogroups (PG). Specific detection of the two viruses was accomplished by constructing two virus-specific primer pairs that amplified a PCR product specific for each virus. By application of RT-PCR, four BCMV-PG-V isolates were differentiated from isolates of BCMV pathogroups I, II, IV and VII. Distinction of two BCMNV pathogroups (PG-III and PG-VI) was achieved by restriction enzyme XbaI digestion of BCMNV PCR products. However, no combination of tested restriction enzymes distinguished all five recognized BCMV pathogroups. A primer pair Dts/Uny15 proved to be specific for BCMV pathogroup PG-V. Thus, by a combination of RT-PCR and restriction enzyme analyses, it was possible to differentiate both viruses, two pathogroups of BCMNV, and one pathogroup of BCMV from the others.

Amino Acid Sequence↗

Focal adhesion kinase as a marker of invasive potential in differentiated human thyroid cancer.

BACKGROUND: The FAK gene encodes a 125-kDa tyrosine kinase (p125FAK) involved in signal transduction pathways used in cell adhesion, motility, and anchorage-independent growth. Because thyroid carcinomas have a wide variability in their propensity for invasion and metastasis, we studied the expression of FAK in a variety of thyroid tissues. METHODS: We synthesized a recombinant N-terminal fragment of the human FAK protein and developed a specific polyclonal antisera. Using Western blot analysis, we assessed the levels of p125FAK expression in 30 human thyroid tissue samples from 27 patients that included paired normal and malignant specimens. Levels of FAK protein in individual tumors were quantitated by densitometric scanning of the immunoblots, and the results were correlated with tumor histology and biologic behavior. RESULTS: The levels of FAK expression were directly correlated with thyroid carcinomas demonstrating the most aggressive phenotypes. The highest levels of p125FAK were seen in follicular carcinomas and tumors associated with distant metastatic foci. In contrast, neoplastic thyroid tissues with limited invasive potential, such as papillary carcinomas, follicular adenomas, and other nonmalignant thyroid lesions, showed minimal p125FAX expression. CONCLUSIONS: Overexpression of FAK may be part of a mechanism for invasion and metastasis of thyroid cancer. Furthermore, the levels of p125FAK may serve as a marker of biologic behavior in this disease.

Adenocarcinoma, Follicular↗

Dietary marine lipids suppress continuous expression of interleukin-1 beta gene transcription.

n-3 Polyunsaturated fatty acids abundant in marine lipids suppress certain inflammatory and immune reactions, and dietary marine lipid supplements have antiinflammatory effects in experimental and human autoimmune disease. Previous work by other investigators demonstrated that dietary marine lipid supplements suppressed production of cytokines from stimulated human peripheral blood mononuclear cells ex vivo. The present study further documents the ability of n-3 fatty acids to inhibit cytokine formation, and in part defines the mechanism of the inhibition of production of interleukin-1 beta (IL-1 beta) by dietary n-3 fatty acid. Female BALB/c mice were each fed a fat-free balanced diet to which was added either a refined fish oil (FO) preparation as a source of n-3 fatty acid, or beef tallow (BT), which consisted primarily of saturated and monoenoic fatty acids. After ingesting the experimental diets for periods ranging from 3 to 12 wk. spleen cell preparations were stimulated ex vivo with either lipopolysaccharide (LPS) or phorbol 12-myristate 13-acetate (PMA), and proIL-1 beta mRNA (IL-1 beta mRNA) was measured by northern analysis. Levels of IL-1 beta mRNA in both LPS- and PMA-stimulated cells from BT-fed mice were elevated to a greater extent than in cells from FO-fed mice, at most concentrations of LPS and PMA. Stability of LPS-stimulated mRNA levels after actinomycin D was similar for BT and FO groups, indicating that lower levels of IL-1 mRNA with FO groups was related to suppressed IL-1 gene transcription and not due to accelerated transcript degradation. Nuclear run-on transcription assays revealed a more transient expression of the IL-1 beta gene in LPS-stimulated spleen cells from FO-fed mice compared to cells from BT-fed mice. We conclude that dietary marine lipids reduce transient expression of the IL-1 beta gene in stimulated splenic monocytic cells. Preliminary results from nuclear run-on transcription assays indicate that n-3 fatty acids may not change the initial rate of gene transcription but may promote more rapid shutting down of transcription of this gene after induction than do alternative lipids.

Animals↗

Dibutyl phthalate purged autologous bone marrow transplant in the treatment of leukemia.

It has been proved that di-N-butyl phthalate (DBP) is singular in killing leukemic cells selectively or accelerating the deterioration of residual leukemic cells in long-term marrow culture in vitro. Based on this principle, the DBP-purged autologous bone marrow transplant has been applied to the treatment of a group of 14 patients suffering from acute nonlymphocytic leukemia. After 5-10 days of in vitro co-culture of marrow cells with DBP at a concentration of 50 micrograms/ml, the recovery of total nucleated cells and the amount of CFU-GM were 67.5% and 68.1%, respectively. In all patients, the reconstitution of hematopoiesis was observed after pre-conditioning and transfusion of purged marrow cells. Among these, two patients had a relapse, two patients died from complications of transplant, one patient died from non-leukemic disease, and the others are all alive and free of disease; the mean survival time as calculated recently was 15 months. These preliminary clinical data support that marrow culture in the presence of DBP is a safe and effective measure for treating leukemia in purged autologous bone marrow transplant.

Adolescent↗