Temporal trends and spatial distribution of research topics in anthropogenic marine debris study: Topic modelling using latent Dirichlet allocation.

The release of anthropogenic marine debris (AMD) is one of the major environmental challenges of our time. In this study, a topic model called latent Dirichlet allocation (LDA) was used to infer the research topics about AMD to provide the whole picture of the research area. The results of the LDA showed that the AMD research topics are mostly applied topics and belong to interdisciplinary or transdisciplinary research areas. Furthermore, the analysis of the temporal trends of the topics showed that topics related to such as plastic pollution exhibit an upward trend, whereas those dealing with the spatiotemporal dynamics and distribution patterns of marine debris showed a downward trend. The analysis of topic distribution over countries showed that research is scarce in landlocked countries. The findings of this study can be used as a map for the area of AMD study by various stakeholders related to marine debris issues.

Elevation of soluble CD307 (IRTA2/FcRH5) protein in the blood and expression on malignant cells of patients with multiple myeloma, chronic lymphocytic leukemia, and mantle cell lymphoma.

CD307 is a differentiation antigen expressed in B-lineage cells. One soluble and two membrane-bound forms have been predicted and an enzyme-linked immunosorbent assay (ELISA) for soluble CD307 established. Our goal was to determine if CD307 is expressed on the surface of cells from patients with multiple myeloma (MM), chronic lymphocytic leukemia (CLL), mantle cell lymphoma (MCL) and other B-cell malignancies and if soluble CD307 levels are elevated in the blood of patients with these B-cell malignancies. Cells and blood were collected from patients. Expression of CD307 was measured by flow cytometry and blood levels of soluble CD307 by ELISA. High soluble CD307 levels were detected in 21/43 (49%) of patients with MM, 36/46 (78%) with CLL and 9/24 (38%) with MCL. Soluble CD307 levels correlated with plasma cell percentages in bone marrow aspirates in MM and total white blood cells in CLL. CD307 on the cell membrane was detected by flow cytometry in 8/8 MM, 23/29 CLL and 4/5 MCL samples. Because CD307 is present on malignant cells from patients with MM, CLL and MCL, CD307 may be a useful therapeutic target for the treatment of these diseases.

MUC13 interaction with receptor tyrosine kinase HER2 drives pancreatic ductal adenocarcinoma progression.

Although MUC13, a transmembrane mucin, is aberrantly expressed in pancreatic ductal adenocarcinoma (PDAC) and generally correlates with increased expression of HER2, the underlying mechanism remains poorly understood. Herein, we found that MUC13 co-localizes and interacts with HER2 in PDAC cells (reciprocal co-immunoprecipitation, immunofluorescence, proximity ligation, co-capping assays) and tissues (immunohistofluorescence). The results from this study demonstrate that MUC13 functionally interacts and activates HER2 at p1248 in PDAC cells, leading to stimulation of HER2 signaling cascade, including ERK1/2, FAK, AKT and PAK1 as well as regulation of the growth, cytoskeleton remodeling and motility, invasion of PDAC cells-all collectively contributing to PDAC progression. Interestingly, all of these phenotypic effects of MUC13-HER2 co-localization could be effectively compromised by depleting MUC13 and mediated by the first and second EGF-like domains of MUC13. Further, MUC13-HER2 co-localization also holds true in PDAC tissues with a strong functional correlation with events contributing to increased degree of disorder and cancer aggressiveness. In brief, findings presented here provide compelling evidence of a functional ramification of MUC13-HER2: this interaction could be potentially exploited for targeted therapeutics in a subset of patients harboring an aggressive form of PDAC.

Y box-binding protein-1 binds preferentially to single-stranded nucleic acids and exhibits 3'-->5' exonuclease activity.

We have previously shown that Y box-binding protein-1 (YB-1) binds preferentially to cisplatin-modified Y box sequences. Based on structural and biochemical data, we predicted that this protein binds single-stranded nucleic acids. In the present study we confirmed the prediction and also discovered some unexpected functional features of YB-1. We found that the cold shock domain of the protein is necessary but not sufficient for double-stranded DNA binding while the C-tail domain interacts with both single-stranded DNA and RNA independently of the cold shock domain. In an in vitro translation system the C-tail domain of the protein inhibited translation but the cold shock domain did not. Both in vitro pull-down and in vivo co-immunoprecipitation assays revealed that YB-1 can form a homodimer. Deletion analysis mapped the C-tail domain of the protein as the region of homodimerization. We also characterized an intrinsic 3'-->5' DNA exonuclease activity of the protein. The region between residues 51 and 205 of its 324-amino acid extent is required for full exonuclease activity. Our findings suggest that YB-1 functions in regulating DNA/RNA transactions and that these actions involve different domains.

Transcription factor Y-box binding protein 1 binds preferentially to cisplatin-modified DNA and interacts with proliferating cell nuclear antigen.

The Y-box binding protein (YB-1) binds to inverted CCAAT box sequences that are present in the promoter region of many genes. We previously showed that YB-1 is overexpressed in human cancer cell lines that are resistant to cisplatin and that the depletion of YB-1 by transfection of a vector expressing YB-1 antisense RNA increases the sensitivity of human cancer cells to cisplatin. To determine whether YB-1 can bind to cisplatin-modified DNA, we fused YB-1 cDNA to glutathione S-transferase (GST) cDNA and purified the resulting GST fusion protein. When we tested the fusion protein with unmodified or cisplatin-modified oligonucleotides, we found that GST-YB-1 bound more strongly to cisplatin-modified oligonucleotides, as did GST fusion proteins of high mobility group 1 (HMG1), HMG2, and xeroderma pigmentosum group A protein. When we assayed the ability of proliferating cell nuclear antigen (PCNA) to interact with the GST fusion proteins, we observed binding to YB-1 but not to HMG1, HMG2, or xeroderma pigmentosum group A. Subsequent experiments demonstrated that YB-1 and PCNA interact directly via the COOH-terminal region of YB-1. Using immunochemical coprecipitation methods, we observed binding of YB-1 and PCNA in vivo. These results suggest that YB-1 can function as a recognition protein for cisplatin-damaged DNA and that it may be important in DNA repair or in directing the cellular response to DNA damage.

Transcriptional activation of the human HMG1 gene in cisplatin-resistant human cancer cells.

The nonhistone chromosomal protein, high mobility group 1 (HMG1), which is ubiquitously expressed in higher eukaryotic cells, preferentially binds to cisplatin-modified DNA. The observation that HMG1 is overexpressed in cisplatin-resistant human cancer cells suggests that cisplatin resistance may be closely associated with HMG1. To decipher the mechanism of HMG1 overexpression in cisplatin-resistant cells, we isolated two overlapping genomic DNA clones containing the entire human HMG1 gene. These clones, which span approximately 15 kb of contiguous DNA, include 5 kb of the 5' flanking region as well as the entire coding sequence. We sequenced 1500 bp upstream of the first exon. The segment proximal to the transcription initiation site did not contain a TATA box but did possess an activating transcription factor site, an activator protein-2 site, one CCAAT box, and two CCAAT-binding transcription factor/nuclear factor-1 (CTF/NF-1) sites. HMG1 promoter activity was 3-10-fold higher in cisplatin-resistant KB-CP20 cells than in parental KB cells. An in vivo footprint experiment showed several differences of dimethyl sulfate modifications between KB and KB-CP20 cells in the area around the CTF/NF-1 sites. In addition, electrophoretic gel mobility shift assays showed that binding of a nuclear factor from cisplatin-resistant cells to the CTF/NF-1 site was significantly higher than the binding of the same factor from parental cells. Semiquantitative reverse transcription-PCR and Western blot analysis also showed that expression of CTF/NF-1 was 3-20-fold higher in the resistant cell line than in its parental counterpart. These findings suggest that, in cisplatin-resistant cells, the expression of HMG1 gene product is enhanced at the transcriptional level and that this probably occurs through the enhanced expression of the CCAAT binding factor, CTF/NF-1.

Structural basis for the regulation of UDP-N-acetyl-alpha-D-galactosamine: polypeptide N-acetylgalactosaminyl transferase-3 gene expression in adenocarcinoma cells.

The UDP-N-acetyl-alpha-D-galactosamine: polypeptide N-acetylgalactosaminyl transferase-3 (Gal NAc-T3) gene, a member of the Gal NAc transferase gene family, is expressed in a tissue-specific manner. To elucidate the function of this gene, we have focused on the molecular mechanism underlying regulation of gene expression. We have cloned Gal NAc-T3 cDNA and used it to show that Gal NAc-T3 mRNA is expressed in tumor cell lines derived from secretory epithelial tissue adenocarcinomas but not in cell lines derived from bladder and epidermoid carcinomas. Using a polyclonal antibody to Gal NAc-T3, we observed protein expression in adenocarcinoma but not non-adenocarcinoma cell lines, and in breast carcinoma cells but not in normal breast tissue. We used Gal NAc-T3 cDNA to isolate three overlapping genomic clones containing the 5'-portion of the human Gal NAc-T3 gene, and we sequenced 1.6 kb around the first exon. A transient expression assay using the luciferase gene showed that promoter activity was much higher in MCF-7 cells than in KB cells. In vivo footprint experiments showed significant protection of a distal GC box, an NRF-1 site, and an AP-2 site in MCF-7 cells. A novel stem and loop structure extending from nucleotide -103 to nucleotide -165 and contiguous to these transcription factor binding sites seemed to be functional in regulating Gal NAc-T3 gene transcription, and a KMnO4 footprint experiment showed that this stem and loop structure could be formed in vivo. We also observed dimethyl sulfate hypersensitive sites in the untranslated region around nucleotide +50 in MCF-7 but not in KB cells. These findings indicate that Gal NAc-T3 gene expression is regulated by multiple systems, including transcription factor binding sites and a stem-and-loop structure, and that this regulation is restricted to cell lines derived from epithelial gland adenocarcinomas but not cells derived from nonsecretory epithelial tissue carcinomas. In addition, our immunohistochemical results suggest that our anti-Gal NAc-T3 antibody may be useful for diagnostic purposes in the early stages of breast cancer.

Direct interaction of p53 with the Y-box binding protein, YB-1: a mechanism for regulation of human gene expression.

The Y-box binding protein, YB-1, belongs to a family of multifunctional proteins which regulate gene expression on both transcriptional and translational levels. The tumor suppressor gene p53 displays growth suppressive properties by regulating gene expression through transcriptional regulation. We now demonstrate that YB-1 directly interacts with p53 using an in vitro pull-down assay. Using immunochemical co-precipitation methods, we also found that the two proteins are bound in vivo. Deletion analysis showed that three independent domains of YB-1, one at the N-terminal and two at the C-terminal, interact with p53. Conversely, a 14 amino acid sequence at the C-terminal of p53 was required for its interaction with YB-1. Gel mobility shift assays showed that the interaction of YB-1 with p53 stimulated the sequence-specific DNA binding of p53 to its consensus sequence. By contrast, this interaction inhibited the binding of YB-1. Using a p53-responsive p21 promoter linked to a reporter gene, it can be shown that antisense expression of YB-1 inhibits the induction of this promoter by p53 in transient transfection assays. These findings delineate a straightforward mechanism for gene expression through p53-YB-1 interaction.

Structure and functional analysis of the human STAT3 gene promoter: alteration of chromatin structure as a possible mechanism for the upregulation in cisplatin-resistant cells.

STAT3 is involved in the signal transduction activated by various cytokines and growth factors. We found that the STAT3 gene is overexpressed in cisplatin-resistant cells. We isolated a genomic fragment containing the 5'-portion of the human STAT3 gene using a bubble PCR method. Using the bubble PCR product as a probe, one genomic clone was isolated. The nucleotide sequence of the first exon and the 1800 base pairs (bps) preceding it was determined. The promoter region of the human STAT3 gene is highly homologous to the corresponding region of the mouse STAT3 gene; several potential factor binding sites such as CRE/ATF, SBE, and GC boxes are also well conserved between human and mouse. A transient expression assay using the luciferase reporter gene showed that the sequence from -403 to +102 possesses maximal promoter activity, and transcription of the STAT3 gene was significantly higher in cisplatin-resistant cells than in parental cisplatin-sensitive cells. Deletion of the region between -261 and -167 resulted in significant loss of promoter activity in both parental and cisplatin-resistant cells. In vivo footprint analysis revealed several protein bindings; however, no significant differences were observed between drug-sensitive and drug-resistant cells. MNase digestion revealed that several open or active nucleosomes were only detected in cisplatin-resistant cells. These results suggest that STAT3 promoter function in a highly structured chromatin environment requires a complex interaction of several transcriptional factors.

Cloning and characterization of the umu operon responsible for inducible mutagenesis in Escherichia coli.

In Escherichia coli, radiation and chemically inducible mutagenesis requires a functional umuC gene product. The umuC mutants are defective in mutagenesis and slightly sensitive to DNA damaging agents. A chromosomal fragment that complemented the umuC mutations for UV mutability and UV resistance was cloned into miniF vector plasmid pMF3 by a shotgun method. A restriction map of the hybrid plasmid was constructed. Further subcloning, Tn1000 insertion inactivation, and complementation tests revealed that there are two genes, umuD and umuC in the former umuC region. The gene products of umuD and umuC were identified by the maxicell method to be proteins with Mr of 18 000 and 46 000, respectively. The two genes comprise an operon, and the transcriptional direction is from umuD to umuC. A plasmid carrying an umuC'-lac'Z gene fusion was constructed in vitro to study the regulation of the umu operon. It was shown that the umu operon is inducible by UV and chemical mutagens, and is regulated by the recA and lexA genes.

Expression of Th1 and Th2 cytokine mRNAs in freshly isolated peripheral blood mononuclear cells of a patient with cutaneous paragonimiasis.

Using semiquantitative reverse transcriptase polymerase chain reaction, we examined the levels of various cytokine mRNAs of freshly isolated peripheral blood mononuclear cells (PBMCs) from a cutaneous paragonimiasis patient in the course of successful treatment with praziquantel administration. The pre-treatment levels of Th2 cytokines such as interleukin (IL)-4, IL-5, IL-10 and IL-13 mRNAs in PBMCs of the patient were much higher than those of healthy controls. The levels of IL-4, IL-5 and IL-13 mRNAs slightly elevated on day 2 of the treatment and then declined to the control levels on day 25. The IL-10 mRNA level rapidly decreased after the chemotherapy. In contrast, the mRNA levels of interferon (IFN)-gamma, a Th1 cytokine, remained in the control levels during the course. Peripheral eosinophil counts and levels of total IgE and eosinophil cationic protein in the sera correlated well with the levels of these Th2 cytokine mRNAs. These results suggested the major role of Th2 cytokines in clinical manifestation of human helminthic infection.

Spectra of base substitution mutations induced in Escherichia coli by tritiated water and the decay of incorporated tritiated thymidine.

The biological effects of tritiated water and of [6-3H]thymidine or [methyl-3H]thymidine incorporated into DNA were compared with those induced by 60Co gamma rays. The killing efficiencies of tritiated water and the tritium-labeled bases were very similar, between 1.8 and 2.0 in terms of the RBE of 60Co gamma rays when compared with the absorbed dose to the bacterial nucleus. The frequency of His+ revertants induced by the decay of [6-3H]thymidine was 3.5 times higher than that induced by [methyl-3H]thymidine or tritiated water; these revertants were most often the result of A:T leads to G:C transitions. In comparison, the other treatments efficiently induced both transitions and transversions. The mutational spectrum resulting from the decay of tritiated water was also determined in the lacI forward-mutagenesis system of Escherichia coli. Transitions predominated at the low dose (2.5 krad), while both transitions and transversions were recovered after a high dose (18 krad). These results are very similar to those observed with 60Co gamma rays and are consistent with the hypothesis that mutagenesis resulting from the decay of [6-3H]thymidine is the result of a position effect, while mutagenesis resulting from the decay of [methyl-3H]thymidine and tritiated water is due to beta-particle ionization.

Endothelin effects on renal function and tubuloglomerular feedback.

Analysis of our data in conjunction with other recent literature allows the following conclusions regarding the role of endothelin in the tubuloglomerular feedback control mechanism and in the pathogenesis of acute ischemic renal failure: (1) Endothelin reduces nephron filtration rate in the nephrons with interrupted signal perception at the macula densa, in accord with preglomerular arteriolar constriction. Yet, the increase in filtration fraction in the whole kidney clearance study suggests a preferential postglomerular arteriolar constriction. Taken together, endothelin, which is a very potent renal vasoconstrictor, seems to constrict both preglomerular and postglomerular arterioles with a predominant constriction of the latter at the doses employed. (2) The endothelin-induced natriuresis is due to a fall in tubular reabsorption, reflecting a direct tubular action, possibly related to an elevation in blood pressure. (3) At the doses of endothelin used and under the present experimental conditions, changes in the magnitude of tubuloglomerular feedback (TGF) response or the feedback characteristic could not be detected. (4) No evidence was found for a participation of endothelin in the pathogenesis of acute postischemic renal failure, as evidenced by the absence of an improvement in glomerular filtration after treatment with endothelin antiserum.

Role of endogenous endothelin and nitric oxide in tubuloglomerular feedback.

To elucidate the roles of endogenous endothelin (ET) and nitric oxide (NO) in tubuloglomerular feedback (TGF), the effects of FR139317, a specific ET-A receptor antagonist, and NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor on TGF were studied in Sprague-Dawley rats. FR139317 (1.5 mg/kg/hr i.v.) reversed the systemic pressor and renal vasoconstrictor responses induced by ET-1 (2 nmol/kg/hr i.v.), but did not alter the early proximal flow rate (EPFR) reduction in response to a loop perfusion with an artificial tubular fluid at 40 nl/min (47 +/- 3 vs. 47 +/- 3% in controls). L-NNA (0.2 mg/kg + 2 micrograms/kg/min i.v.) had no effect on systemic blood pressure (BP), renal hemodynamics or EPFR measured at zero perfusion (31 +/- 2 vs. 31 +/- 2 nl/min in controls), but enhanced the EPFR reduction during loop perfusion to 77 +/- 3%. Loop perfusion with 10(-3) M L-NNA in perfusate also increased the EPFR reduction to 70 +/- 7%. In conclusion, inhibition of NO synthesis enhances the TGF-mediated reduction of nephron GFR. This indicates an active participation of endogenous NO in the control of afferent arteriolar tone. endogenous ET does not influence TGF via the ET-A receptor.

Is cerebral control of plasma [Na] a major determinant for systemic sodium balance?

To evaluate the role of volume expansion for prandial/postprandial natriuresis, we first determined spontaneous daily NaCl, H2O, and diet turnover and Evans blue and inulin spaces in male Wistar rats on various high-salt diets. Second, we measured the time course of Na and water clearance in chloralose/ketamine anesthetized rats over 270 minutes after a single intragastric Na load (0, 290.4, or 581 micromol/100 g body weight). Finally, similar measurements were made during and after a local [NaCl] increase in the left carotid artery supplying the brain for 60 minutes. Daily NaCl, H2O, and diet intake per rat was 2 to 74 mmol, 13 to 223 ml, and 1.5 to 33 g, respectively. Only inulin space and plasma [Na] correlated with daily Na uptake (X; regressions Y = 0.02X + 15.13, N = 99, r2 = 0.0716, P = 0.02; and Y = 141.7 + 0.1005X, N = 179, r2 = 0.104, P < 0.0001, respectively). Under chloralose/ketamine anesthesia, 86% to 102% of the total (i.v. plus i.g.) Na load and some 50% of the unilaterally administered intracarotid Na were excreted. Chloralose/ketamine anesthesia is thus suitable for studies on Na balance mechanisms. Plasma [Na] is under cerebral control. Because of its immediate onset, this mechanism might be the principal determinant of prandial and postprandial natriuresis and hence for the systemic Na balance.

Sodium balance and blood pressure response to salt ingestion in uninephrectomized rats.

The possible role of extracellular volume (ECV) expansion in prandial/postprandial natriuresis was evaluated in control, sham-operated (SO), and uninephrectomized (UNX) male Wistar rats fed a 0.64 (normal salt, NS) or 8 (high salt, HS) g% NaCl diet for seven days after UNX. We thus determined daily NaCl, diet, and water intake and Evans blue and inulin spaces on day 7. Finally, we determined Na and water clearance after a single i.g. Na load (581 micromol/100 g body weight) under chloralose/ketamine anesthesia in UNX and control HS rats. NaCl, diet, and water intakes were comparable beyond day 5. Plasma volume and ECV were similar in all groups. With NS diet, glomerular filtration rate (GFR) in UNX was compensated but lower than that of SO rats (0.55 vs. 0.74 ml/min per 100 g body weight). Blood pressure (BP) was 111 mm Hg in SO controls and 112 mm Hg in the UNX group. After oral Na loading, BP rose in both groups and remained higher in UNX (134 vs. 126 mm Hg at 15 minutes, 130 vs. 118 mm Hg at 225 minutes). Cumulative Na and water excretions were similar (513 and 610 micromol/100 g body weight, 1.97 and 2.35 ml/100 g body weight in SO and UNX, respectively). Chronically salt-loaded UNX rats seem to maintain dietary Na balance by mechanism(s) other than volume expansion.

Diurnal variation of hemodynamic indices in non-dipper hypertensive patients.

The purpose of this study was to elucidate the underlying mechanisms of blunted nocturnal blood pressure reduction in non-dipper hypertensive patients. We studied the diurnal variations in systemic hemodynamic indices and baroreflex sensitivity. In 45 subjects with essential hypertension (24 men; mean age, 49+/-1 years), intra-arterial pressure was monitored telemetrically. Non-dippers were defined as those with a nocturnal reduction of systolic blood pressure of less than 10% of daytime systolic blood pressure. Stroke volume was determined using Wesseling's pulse contour method, calibrated with indocyanine green dilution. Baroreflex sensitivity was calculated as deltapulse interval/deltasystolic blood pressure on spontaneous variations. The mean values of the hemodynamic parameters were calculated every 30 min. Twenty-six subjects were classified as non-dippers. Daytime blood pressure was not significantly different between dippers (149+/-4/87+/-3 mmHg) and non-dippers (147+/-3/82+/-2 mmHg), while the nighttime blood pressure was significantly reduced in dippers (131+/-3/77+/-2 mmHg) but not in non-dippers (145+/-3/80+/-2 mmHg). Nocturnal decreases in both cardiac index and stroke index were smaller in non-dippers (-12.0+/-1.2% and 1.5+/-1.0%) than in dippers (-17.5+/-1.4% and -2.2+/-1.1%). Baroreflex sensitivity significantly increased at nighttime both in dippers (6.5+/-0.6 to 8.0+/-0.7 ms/mmHg) and in non-dippers (5.1+/-0.3 to 6.4+/-0.4 ms/mmHg). Neither daytime nor nighttime baroreflex sensitivity was significantly different between the groups. We conclude that the hemodynamics of non-dipper essential hypertension are characterized by an inadequate nocturnal decrease in cardiac index and stroke index, suggestive of relative volume expansion or malsuppressed sympathetic activity.

Does insulin resistance participate in an impaired glucose tolerance in primary aldosteronism?

It has been reported that glucose intolerance is occasionally found in primary aldosteronism. In this study, we measured insulin sensitivity by the euglycaemic hyperinsulinaemic glucose clamp technique and ability to release insulin by 75 g oral glucose tolerance test (OGTT) in primary aldosteronism. Seven patients with primary aldosteronism (PA) (53.7 +/- 3.4 years; mean +/- SEM) and eight normotensive subjects (NS) (57.5 +/- 2.6 years) were employed in this study. The two-hour euglycemic hyperinsulinaemic glucose clamp technique was performed in seven PA before adrenalectomy, six PA after adrenalectomy and eight NS. The 75 g OGTT was also done in five PA before and after adrenalectomy and eight NS. The mean rate of glucose infusion to maintain euglycemia for the last 30 minutes of the clamp technique was used as an indicator of insulin sensitivity (M-value). The total blood glucose levels during 75 g OGTT (area under the curves) (sigma blood glucose) were significantly higher in PA than those in NS, and the total insulin levels during 75 g OGTT (area under the curves) (sigma IRI) were significantly lower in PA than those in NS. After adrenalectomy in PA, blood glucose levels were significantly decreased and IRI were significantly increased compared with the normal range. There was a significant positive correlation (P < 0.05, r = 0.71) between serum potassium levels and IRI in PA which were determined before and after adrenalectomy. In PA, M-values (240.7 +/- 14.6 mg/m2/min) were significantly higher than those in NS (199.0 +/- 12.3 mg/m2/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Apheresis therapy for prolonged red cell aplasia after major ABO-mismatched bone marrow transplantation.

Two cases of leukemia were treated successfully with apheresis for delayed recovery of erythropoiesis due to antibody-mediated red cell aplasia after ABO-mismatched bone marrow transplantation (BMT). A 25-year-old female (ABO group O) underwent BMT from her brother (group A). Immunoadsorption using Biosynsorb A performed on day 146 after BMT followed by double filtration plasma pheresis (DFPP) reduced anti-A antibody titers from 1:32 to 1:2. Anemia improved dramatically within 2 weeks. A 49-year-old female (group O) underwent BMT from her mother (group A). She was treated with DFPP on day 131 after BMT. Anti-A antibody titers dropped from 1:16 to 1:1 and anemia improved gradually.

A case of Ki-1 positive anaplastic large cell lymphoma transformed from mycosis fungoides.

A case of cutaneous Ki-1 positive anaplastic large cell lymphoma which developed in the plaque stage of mycosis fungoides was described. A 73-year-old woman who had suffered from pruritic scaly eruptions over her entire body for more than two decades was admitted because of an ulcerated tumor measuring 45 x 55 x 15 mm and several satellite tumors on the buttock. All tumorous lesions were resected without recurrence to date. Histochemical study revealed that the tumor consisted of large anaplastic cells which were Ki-1 (CD30)-positive and LCA-negative. Some of the erythematous plaques contained LCA-positive, small-sized atypical lymphocytes. In other plaques which developed two years later, there were large Ki-1-positive atypical cells. In the specimens obtained from the tumor and the plaque, the same pattern of T-cell receptor gene rearrangements was detected. These findings indicate that both Ki-1 positive anaplastic cells in the tumor and atypical lymphoid cells in the plaques were derived from the same T cell clone.