Comparison of dermoscopic features between congenital and acquired acral melanocytic nevi in Korean patients.

BACKGROUND: The dermoscopic patterns of acral melanocytic nevi (AMNs) are crucial in differentiating them from acral melanoma. Several studies have reported the dermoscopic patterns of acquired acral melanocytic nevi (AAMNs). However, few have investigated the dermoscopic patterns of congenital acral melanocytic nevi (CAMNs). OBJECTIVE: To compare the clinical and dermoscopic features of CAMNs and AAMNs. METHODS: The present study included 43 patients with CAMNs and 40 with AAMNs. We reviewed their medical records as well as their clinical and dermoscopic findings. RESULTS: Congenital acral melanocytic nevis were more asymmetrical than AAMNs (P = 0.002) and presented more frequently as comma-shaped (P = 0.005). Regarding dermoscopic findings, globular pattern (55.8%) was the most common feature of CAMNs, while parallel furrow pattern (37.5%) was the most common feature of AAMNs. The presence of fibrillar, globular, and parallel ridge patterns, and diffuse multi-component pigmentation differed significantly between the groups (P < 0.05). Furthermore, CAMNs showed melanoma-specific dermoscopic patterns, such as parallel ridge (18.6%) and diffuse multi-component pigmentation (25.6%). CONCLUSION: The dermoscopic patterns of CAMNs and AAMNs differed markedly. In terms of dermoscopic patterns, CAMNs resembled acral melanoma more often than AAMNs did.

Efficacy of polymers from spontaneous carotenoid oxidation in reducing necrotic enteritis in broilers.

This study evaluated the preventive effect of the spontaneous oxidation of ß-carotene (OxC-beta) in broiler chickens with necrotic enteritis by Clostridium perfringens taking into consideration various parameters including clinical signs, body weight, intestinal lesion severity, and bacterial enumeration. The mean body weight of the OxC-beta treatment groups increased significantly (P < 0.05) compared to that of the C. perfringens challenge group. Intestinal lesion scores due to C. perfringens infection were significantly alleviated by OxC-beta treatment (P < 0.05), and the number of clostridial bacteria in intestine was reduced by OxC-beta in a dose-dependent manner. OxC-beta in feed contributes to the prevention of necrotic enteritis in commercial broiler chicken, and has a positive effect in improving productivity.

Vitamin E and selenium levels are within normal range in pigs diagnosed with mulberry heart disease and evidence for viral involvement in the syndrome is lacking.

Mulberry heart disease (MHD) in pigs is characterized by lesions of acute haemorrhagic myocarditis and myocardial necrosis. The objectives of this study were to determine the levels of vitamin E and selenium and 13 other trace minerals in heart and liver tissues and to determine the prevalence of certain viral infections in heart tissues from MHD-affected and MHD-unaffected pigs and the vitamin E and selenium concentration in feed samples from selected farms with MHD. Based on the pathological examination, 114 pigs were separated into MHD lesion-negative (L-NEG) (n = 57) and MHD lesion-positive (L-POS) (n = 57) groups. Seventy-three samples (40 L-NEG and 33 L-POS) were subjected to chemical analysis, and 66 (32 L-NEG and 34 L-POS) were subjected to PCR detection for viral pathogens. Lower (P < 0.05) levels of myocardial copper, lower (P < 0.05) levels of hepatic magnesium and higher (P < 0.05) levels of myocardial and hepatic sodium were detected in the L-POS cases. Although lower (P < 0.05) levels of hepatic selenium were detected in L-POS group, all were within the normal range. Analysis of feed samples (n = 22) revealed that selenium levels in all the samples were above the legal limit (0.3 ppm) for pigs. Vitamin E levels in all feed samples were above 20 IU/kg. Among the 66 pigs subjected to PCR detection, there were 19, 4, 13, 8, 2 and 1 animals positive for porcine circovirus type 2, porcine reproductive and respiratory syndrome virus, pan-herpes virus, porcine enterovirus, pan-pestivirus and porcine parvovirus, respectively. Clear evidence of viral association with L-POS was lacking.

Anti-inflammatory effect of jeongshintang through suppression of p38 activation in human astrocytoma, U373MG cells.

Jeongshintang (JST) is a Korean herbal prescription, which has been successfully used for cerebral diseases. However, the anti-inflammatory effect of JST on Alzheimer's disease (AD) is still not fully understood. In this study, we investigated the effects of JST in attenuating the inflammatory response induced by interleukin (IL)-1beta plus beta-amyloid [1-42] fragment (A beta) in the human astrocyte cell line, U373MG. The production of IL-6, IL-8, and prostaglandin (PG)E2 was significantly increased by IL-1beta plus A beta (1-42) in a time-dependent manner (P < 0.05). JST significantly inhibited the IL-1beta plus A beta (1-42)-induced IL-6, IL-8, and PGE2 production at 24 h (P < 0.05). Maximal inhibition rate of IL-6, IL-8, and PGE2 production by JST was about 54.40%, 56.01%, and 44.06% respectively. JST (0.01-1 mg/ml) also attenuated the expression of cyclooxygenase (COX)-2 and activation of p38 MAPK induced by IL-1beta and A beta (1-42). These results demonstrated that JST has an anti-inflammatory effect, which might explain its beneficial effect in the treatment of various neurodegenerative diseases such as AD.

Characterization of the humoral immune response of experimentally infected and vaccinated pigs to swine influenza viral proteins.

The value of serologic tests for diagnosis of swine influenza virus (SIV) infection has been diminished by the emergence of new subtypes and by antigenic drift within subtype. The intensive use of vaccination also has complicated interpretation of serology results. Serologic assays are needed that can detect infection regardless of subtype or antigenic variation and that can differentiate antibody induced by infection from that induced by vaccination. In this study, the antibody responses to specific viral proteins in pigs infected by or vaccinated for SIV were characterized by Western immunoblot. Both IgM and IgG against hemagglutinin, nucleoprotein, NS1 and NS2 were detected in experimentally infected pigs by 7 days post inoculation (DPI). IgG against these proteins was still detectable at the end of the study (28 DPI). In contrast, IgG against neuraminidase and M1 was not detected until 14 DPI and no IgM against these proteins was detected. In vaccinated pigs, no antibody against NS1 was detected while antibody responses to other proteins were identical to those in exposed pigs. In conclusion, nucleoprotein may be a suitable antigen for use in a subtype-unrestricted serologic assay. NS1 protein may be suitable for a serologic assay that differentiates between infected and vaccinated pigs.

Role of p27(Kip1) in cAMP- and TGF-beta2-mediated antiproliferation in rabbit corneal endothelial cells.

PURPOSE: To determine whether p27(Kip1) plays a role in antiproliferation mediated by antimitogens (cAMP and TGF-beta2) in rabbit corneal endothelial cells (CECs). METHODS: Cell proliferation was assayed using a colorimetric method to determine the number of viable cells. Subcellular localization of cell cycle-regulatory proteins was determined by immunofluorescent staining, and expression of the proteins was analyzed by immunoblot analysis. RESULTS: When cells were treated with cAMP or TGF-beta2, serum-mediated cell proliferation was inhibited in a dose-dependent manner. Simultaneous treatment of the two antimitogens did not show a synergistic effect on inhibition of cell growth. Expression of cell cycle-regulatory proteins, such as cyclin-D1, cyclin-E, cdk2, cdk4, p21(Cip1), and p27(Kip1) was determined using immunofluorescent staining. A strong nuclear staining was observed for p27(Kip1). The other proteins were not stained or were only very faintly stained. Treatment of cells with either cAMP or TGF-beta2 did not change the staining potential of any proteins other than p27(Kip1), but all cells were positive for nuclear p27(Kip1) when treated with either TGF-beta2 or cAMP. In contrast, mitogen (FGF-2)-containing medium decreased the number of p27(Kip1)-positive cells. When the expression level of p27(Kip1) was determined using immunoblot analysis in the cells treated either with FGF-2 alone or with a concomitant treatment with FGF-2 and cAMP for 24 hours, FGF-2 markedly decreased the p27(Kip1) level, and cAMP prevented the decrease in p27(Kip1) level induced by FGF-2. No such phenomenon occurred during a short-term exposure of cells to either FGF-2 or cAMP or to a combination of the two. When cells were stained for phosphorylated p27(Kip1), FGF-2 markedly enhanced the staining of phosphorylated p27(Kip1) in nuclei, whereas both cAMP and TGF-beta2 prevented the phosphorylation of p27(Kip1). CONCLUSIONS: These findings suggest that both antimitogens upregulate the expression of p27(Kip1) as they prevent the decrease of the p27(Kip1) level mediated by mitogen. Furthermore, cAMP and TGF-beta2 may inhibit the G(1)-to-S transition by blocking phosphorylation of p27(Kip1), which is a prerequisite for nuclear export of the inhibitor molecule for degradation.

Differential activity of TGF-beta2 on the expression of p27Kip1 and Cdk4 in actively cycling and contact inhibited rabbit corneal endothelial cells.

PURPOSE: To determine whether TGF-beta2 exerts inhibitory action in a density dependent manner in primary, first passage, and second passage corneal endothelial cells (CEC). METHODS: Fifty percent confluent cultures were used for actively cycling cells and monolayers were used as contact inhibited cultures. Half of the experiments were performed in cells treated with TGF-beta2 at 10 ng/ml for 24 h. Subcellular localization of cyclin dependent kinase 4 (Cdk4), p27Kip1 (p27), and phosphorylated p27 (pp27) was determined by immunofluorescent staining followed by confocal laser microscopic analysis. Expression of proteins were analyzed by immunoblotting. RESULTS: Before colocalization between Cdk4 and p27 was studied, the two proteins were respectively stained, either in growing cells for the presence of Cdk4 or in contact inhibited cultures for the presence of p27. Nuclear Cdk4 was observed in FGF-2 treated cells while nuclear staining of Cdk4 was lost in mitogen deprived or TGF-beta2 treated cells. On the other hand, a strong positive staining of nuclear p27 was observed in growth down regulated conditions, which was completely lost in growth up regulated conditions. When cells were double stained with Cdk4 and p27 antibodies, actively cycling cells contained nuclear Cdk4. Less than 10% of the primary cells were positive for Cdk4 staining, whereas all of the second passage CEC contained nuclear Cdk4. Conversely, p27 was not detected in actively cycling cells in either primary or passaged cells. Contact inhibited cells demonstrated nuclear p27 staining in all cells, but only a few cells were positive for nuclear Cdk4. Nuclear Cdk4 was absent when the actively cycling cells were treated with TGF-beta2, whereas TGF-beta2 did not induce the expression of nuclear p27 in the same cultures. In contact inhibited cells, TGF-beta2 did not affect the staining profiles of p27. In the first passage CEC, TGF-beta2 slightly increased the number of cells that were positive for nuclear Cdk4. When the effect of TGF-beta2 at the level of protein synthesis was determined, TGF-beta2 markedly downregulated Cdk4 synthesis and slightly upregulated p27 synthesis in actively cycling cells. On the other hand, TGF-beta2 did not exert the same effect on Cdk4 synthesis in contact inhibited cells as it did on actively cycling cells. Contact inhibited cells contained a high level of p27, and TGF-beta2 slightly upregulated p27 synthesis in these cells. When phosphorylated p27 was determined to be present, the nuclei of both actively cycling and contact inhibited cells contained phosphorylated p27 in the nuclei, regardless of the passage numbers. TGF-beta2 inhibited phosphorylation of p27 in actively cycling cells, but it had no effect on phosphorylation of p27 in contact inhibited cells. CONCLUSIONS: These data suggest that Cdk4 and p27 expression is density dependent, and TGF-beta2 exerted its activity on actively cycling cells. In these cells, TGF-beta2 downregulated Cdk4 expression and prevented the phosphorylation of p27, which is a prerequisite for nuclear export of the inhibitor molecule for degradation. Thus, TGF-beta2 inhibits the G1/S transition while it maintains p27 in an active form in the nuclei during the exponential growth cell stage.

Ionizing radiation potentiates the induction of nitric oxide synthase by interferon-gamma (Ifn-gamma) or Ifn-gamma and lipopolysaccharide in bnl cl.2 murine embryonic liver cells: role of hydrogen peroxide.

The effects of ionizing irradiation on the nitric oxide (NO) production in murine embryonic liver cell line, BNL CL.2 cells, were investigated. Various doses (5-40 Gy) of radiation made BNL CL.2 cells responsive to interferon-gamma alone for the production of NO in a dose-dependent manner. Small amounts of lipopolysaccharide (LPS) or tumor necrosis factor-alpha (TNF-alpha) synergized with IFN-gamma in the production of NO from irradiated BNL CL.2 cells, even though LPS or TNF-alpha alone did not induce NO production from the same cells. Immunoblots showed parallel induction of inducible nitric oxide synthase (iNOS). NO production in irradiated BNL CL.2 cells by IFN-gamma or IFN-gamma plus LPS was decreased by the addition of catalase, suggesting that H(2)O(2) produced by ionizing irradiation primed the cells to trigger NO production in response to IFN-gamma or IFN-gamma plus LPS. Furthermore, the treatment of nongamma-irradiated BNL CL.2 cells with H(2)O(2) made the cells responsive to IFN-gamma or IFN-gamma plus LPS for the production of NO. This study shows that ionizing irradiation has the ability to induce iNOS gene expression in responsive to IFN-gamma via the formation of H(2)O(2) in BNL CL.2 murine embryonic liver cells.

Identification of a putative DEAD-box RNA helicase and a zinc-finger protein in Candida albicans by functional complementation of the S. cerevisiae rok1 mutation.

We identified two novel genes, CHR1 and CSR1, of the fungal pathogen Candida albicans, by functional complementation of the Saccharomyces cerevisiae rok1 mutation. The Rok1 protein is a member of the DEAD protein family of ATP-dependent RNA helicases. ROK1 is required for cell cycle progression and also for rRNA processing. The CHR1 gene product of 578 amino acids is highly homologous to the Rok1 protein (54% identity) and is considered to be a putative DEAD-box RNA helicase. We predict that the CSR1 gene encodes a 73 kDa protein of 612 amino acids with five zinc-finger motifs at the C-terminal region. CHR1 or CSR1 on a high-copy number plasmid showed a slow-growth phenotype in a condition where the ROK1 expression is turned on from the GAL1 promoter. This result is consistent with the lethality caused by the ROK1 overexpression. We conclude that CHR1 encodes a functional homologue of Rok1 protein and CSR1 is a heterologous suppressor of the rok1 mutation.

Human basophils express CD22 without expression of CD19.

BACKGROUND: Even modern automatic cell counters cannot count basophils precisely. Therefore, we need a rapid, accurate, precise, and easy method for counting basophils. METHODS: Using flow cytometry, basophils (CD22+/CD19-) and B cells (CD22+/CD19+) were counted. Within a large lymphocyte light scatter gate, % basophils (G%baso) and % B cells (G%B) were determined from the total count. Another method of analysis was to make two regions (R1 for basophils and R2 for B cells) and to determine in those the % basophils (R1%baso) and % B cells (R2%B) without gating. The flow cytometric basophil counts of the blood of 21 normal controls and 43 chronic myelogenous leukemia (CML) patients were compared with manual basophil count (Ma%baso) and basophil count by Coulter electronic cell counter (Hialeah, FL) (Auto%baso). CD22+/CD19- cells were sorted by a FACSCalibur (Becton Dickinson, San Jose, CA). RESULTS: The G%baso of all samples was 4.66 +/- 5.35%, and R1%baso was 4.23 +/- 4.88%, and they were well-correlated (r = 0.996, P < 0.001). The G%B of all samples was 1.55 +/- 1.68%, and R2%B was 1.59 +/- 1.67%, and they were also well-correlated (r = 0.993, P < 0.001). Their correlation was better in normal controls than in CML. G%baso was well-correlated to Ma%baso (r = 0.827) and Auto%baso (r = 0.806), and R1%baso was well-correlated to Ma%baso (r = 0.831) but showed poor correlation to Auto%baso (r = 0.734). Auto%baso revealed the poorest correlation to Ma%baso (r = 0.692). The sorted CD22+/CD19- cells were all basophils (99.48 +/- 0.30%), and they revealed CD13, CD33, and dim CD45 expression, whereas CD3, CD14, CD16, and HLA-DR were not detected on them. CONCLUSIONS: We discovered a specific marker combination to identify basophils (CD22+/CD19-), and we suggest that flow cytometric analysis using these markers is an easy, reliable, and accurate method of basophil counting.

Effectiveness of rotor off fraction in allogeneic murine bone marrow transplantation with complete disparity of major histocompatibility.

Counterflow centrifugal elutriation (CCE) has been a highly efficient physical method for separating T cells from bone marrow (BM) without impairing cell function and yield. To investigate the usefulness of CCE, the hematopoietic potential as well as the level of T cell contamination in rotor-off (R/O) fraction of BM was studied using a murine bone marrow transplantation (BMT) model [C3H/He (H-2k)-->BALB/C (H-2d)]. The total recovery of cells after CCE procedure was 71.4%. Morphologically, R/O fraction contained abundant mononuclear cells and a few lymphocytes. The numbers of colony forming unit for granulocyte/monocyte (CFU-GM), Sca-1+ cells, and T cells were compared among four fractions of CCE (fractions at flow rate of 17, 25, 28 mL/min, and R/O fraction). The number of CFU-GM per 10(5) nucleated cells in each fraction were significantly higher in R/O fraction (331.3 +/- 34.4) compared to unfractionated marrow (UM) (21.1 +/- 1.3) and fraction of 17 mL/min (FR 17) (23.7 +/- 2.2 ) (chi2 = 0.0044). Neither fraction of 25 mL/min (FR 25) nor fraction of 28 mL/min (FR 28) contained CFU-GM colonies. The concentration of Sca-1+ cells in R/O fraction was significantly higher (1.96-fold) than UM (p < 0.05), and 80.0 +/- 10.1% of Sca-1+ cells in UM were recovered in R/O fraction; 88.1% of Thy-1.2+ T cells were eliminated in R/O fraction (p < 0.05). Mice receiving UM after lethal irradiation (875cGy) suffered from severe graft-versus-host disease (GVHD) and all five died within 7 days after BMT procedure (Group A). Of interest, mice receiving mixture of R/O fraction with lymphocyte-rich fraction (FR 25 plus FR 28) to equalize T cell number as UM, developed severe GVHD and four out of five died (probability of survival; 20%) (Group B). Mice receiving R/O fraction had mild GVHD and four out of five survived for at least 90 days (probability of survival; 80%) (Group C). In group C, probability of survival (p = 0.0006) was higher, and severity of GVHD (p = 0.0043) and progression rate of GVHD (p = 0.02) was lower. In conclusion, the elutriated R/O fraction cells of BM have the advantages of stable engraftment and tolerable GVHD in murine allogeneic BMT with complete major histocompatibility disparity. This could be directly applicable to patients with high risk of GVHD and graft failure in upcoming clinical trials.

Acute lymphoblastic leukemia with maturation--a new entity with clinical significance.

The diagnosis of 'ALL with maturation' (ALLm) is proposed. One hundred and one patients with untreated ALL were entered into this study. The diagnosis of ALLm was made when more than 20% of all nucleated elements in the bone marrow showed maturation beyond prolymphocytes by light microscopic examination. The mature-appearing leukemic cells showed the same immunophenotype to remaining lymphoblasts. The number of ALLm cases was 19 (18.8%). The mean age at presentation of ALLm was 29 +/- 18, older than that of 18 +/- 16 of the remaining typical ALL (ALLt) (P = 0.015). Remission was induced with daunorubicin, vincristine, prednisone and L-asparaginase. Only two of 19 ALLm patients achieved CR after 4 weeks induction chemotherapy. In contrast, 57 of 82 (69.5%) ALLt patients achieved CR after the same induction chemotherapy. There was no significant difference in immunophenotype of ALLm compared with ALLt. Labeling index of DNA topoisomerase IIalpha (TopoLI) was studied by immunohistochemistry. Initial TopoLI of ALLm (221 +/- 147) was much lower than that of ALLt (609 +/- 262, P = 0.005). Furthermore, the remaining leukemic cells after chemotherapy were not labeled with anti-DNA topoisomerase IIalpha. The P53 protein was expressed in nine of 18 ALLm cases (50.0%) and P-glycoprotein was not expressed in ALLm cases. Twelve of 19 ALLm cases were studied for carrying bcr/abl fusion by karyotyping and/or fluorescent in situ hybridization. Only two cases revealed bcr/abl fusion. In conclusion, ALLm is a separate entity of ALL which has a very poor clinical course and is independent of other prognostic factors. The morphologically mature leukemic cells are in resting GO phase.

Chromosomal numerical aberrations in gastric carcinoma: analysis of eighteen cases using in situ hybridization.

Paraffin-embedded tumor cells of 18 cases of gastric carcinoma were hybridized with digoxigenin-labeled repetitive DNA probes specific for the centromeric regions of chromosomes X, Y, 1, 2, 3, 4, 6, 7, 8, 9, 10, 11, 12, 15, 16, 17, 18, and 20. All cases demonstrated numerical chromosomal aberrations. The most exciting aberration, polysomy (five or more copies) of several chromosomes, was found in all cases except a case of mucinous adenocarcinoma, which showed trisomy 9 as the sole chromosomal numerical aberration. In nine cases of tubular adenocarcinoma, poorly-differentiated polysomies of several chromosomes were the consistent numerical aberration and monosomy 7, 18(2 cases each), 10, and 17(1 case each) were also found. In moderately-differentiated tubular adenocarcinoma all three cases also showed polysomies of several chromosomes. The total number of extra chromosomes (polysomy was counted as 5 copies) was higher in the intestinal type (mean 20.9) than in the diffuse type (mean 14.1). Regional lymph node metastasis, vein invasion, or perineural invasion was not related to any specific chromosomal numerical aberration in gastric cancer. Chromosomes X, 1, 2, 3, 4, 15, 17, and 20 had extra copies especially polysomy in most cases. However, chromosomes 7 and 18 revealed monosomy in many cases (31.3% and 33.3% respectively, and chromosome 9 and 11 revealed trisomy in 35.7% and 75% each. Numerically, the most conserved chromosome in gastric cancer was chromosome 12 (62.5%). By flow cytometry, two diploidy and 8 aneuploidy cases with the DNA indices from 1.30 to 1.85 were found.

The effect of HLA mismatching on graft survival in living-donor kidney transplants: Catholic Medical Center, 1984 to 1993.

This study focuses on the beneficial effect of HLA matching on long-term graft survival rates in CsA-treated living primary kidney transplants at Catholic Medical Center, 1984 to 1993. 1. An impressive 26% difference in kidney graft survival was observed at 5 years between recipients who received 0 and 2 HLA-DR mismatches (79% vs 53%). 2. Five-year kidney graft survival rates in the 0, 1, 2, and 3-HLA-B+DR mismatches were 87%, 76%, 77%, and 74%, respectively, which was significantly different from 54% survival rates in the 4-HLA-B+DR mismatch group. 3. The 5-year kidney graft survivals in the 0, 1, 2, HLA-DR-mismatched living-nonrelated donor group were 84%, 76%, and 39%, respectively, which were significant differences. 4. The 5-year kidney graft survivals in the 0, 1, 2, HLA-DR-mismatched living-related donor group were 75%, 79%, and 72%, respectively, which were not significant. 5. The effect of HLA-A, B, A+B, A+DR, and A+B+DR mismatches showed little difference among the groups with different mismatch numbers. In conclusion, better matching for the HLA-DR, B+DR antigens significantly improved kidney graft survivals in our CsA-treated primary living-donor transplant recipients.

Allogeneic bone marrow transplantation for the patients with hemopoietic stem cell disorders: CUMC experience.

Bone marrow transplantation from an HLA-identical sibling is increasingly used as a curative therapy for patients with hemopoietic stem cell disorders including acute leukemia, chronic myelogenous leukemia and severe aplastic anemia. Between March 1983 and March 1991, we performed 86 cases of allogeneic bone marrow transplantation (BMT) for the patients with hemopoietic stem cell disorders: 25 acute myelogenous leukemia (AML); 15 acute lymphoblastic leukemia (ALL); 20 chronic myelogenous leukemia (CML); and 26 severe aplastic anemia (SAA). Ten out of 25 AML are in disease free survival (DFS). The causes of death were recurrence of leukemia (12), acute GVHD (3), sepsis (1) and veno-occlusive disease (1). Nine of 15 ALL are in unmaintained remission. Thirteen out of 20 CML are in DFS. Among 26 SAA, 21 are enjoying DFS, but 1 died of engraftment failure, 3 of graft rejection followed by cytomegalovirus (1) and aspergillus pneumonia (1). Comparing the survival between standard [less than or equal to CR1: 9/14 (64%)] and high risk [greater than or equal to CR1: 1/11 (9%)] AML, our data suggest that preparative regimen for high risk AML was not potent enough to eradicate the minimal residual disease in advanced AML. Although our cases are limited and the follow-up period is short, our result of ALL [overall: CCR (60%), standard risk (adult less than or equal to CR1, children less than or equal to CR2; 8/11 (73%) and high risk; 1/4 (25%)] and CML [overall: 65%, CP; 9/10 (90%), AP; 4/6 (67%), BP; 0/4 (0%)] are optimistic. It is of our interest that the incidence of death related with IP (1/33: 3%) and with AGVHD 94/33: 12%) were much less than that of other's observation but the explanation for this still remains to be clear.

[Is permanent survival of kidney allograft receivers in weak histo-incompatible combinations dependent on enhancement?]. / Ist permanentes Uberleben der Nierenallotransplantatempfänger bei schwach histoincompatiblen Kombinationen durch Enhancement bedingt?

To study the immunological status of indefinitely surviving recipients of histocompatible (minor histoincompatible) allografts we transplanted Fi or (Fi x LEW)F1-kidneys to LEW-rats. At the same time bilateral nephrectomy was performed. To examine the cellular immune response we carried out local GvHR, microcytotoxicity assay and allorosette-formation test with recipient cells. We also studied lymphocytotoxins in the serum of recipients. To detect a blocking serum factor we used allorosette-formation inhibition test and microcytotoxicity assay. A blocking serum factor could not be found. In spite of stimulation with donor specific skin graft the cellular immune response of prolonged surviving recipients was inhibited. Our results suggest that prolonged survival of minor histoincompatible renal allograft recipients was caused by suppression of cellular immune response.

Detection of serum-blocking factors by inhibition of allorosette formation in rats with long-surviving renal allografts following short-term postoperative ALS treatment.

Thirty-nine (LEW x BN)F1 kidneys were transplanted to LEW rats. Twenty-four untreated recipients survived for a mean time of 16.1 +/- 1.7 days (group 1). Fifteen recipients received 4 ml of antilymphocytic serum per rat (group 3). In the last group 10 recipients survived for more than 4 months. The spleen cells of these permanently surviving 10 rats were obtained by splenectomy and used in a graft-versus-host assay, and this assay showed that the reactivity of these cells was normal. Following splenectomy the animals were given an (LEW x BN)F1 skin allograft, followed 18 days by a second. After another 18 days (LEW x Buf)F1 "third party" skin allografts were transplanted to the same animals. Animals of group 2 rejected their first grafts with a mean survival time of 12.2 +/- 1.2 days, whereas the second grafts were rejected normally as were the third party grafts. Attempts were made to detect lymphocytotoxic antibodies and haemagglutinins before and after the transplantation of skin grafts and none could be found up to day 53. The sera of group 2 inhibited allorosette formation by 38%. This serum-blocking factor was donor specific. It is probable that the survival of the kidney transplants following antilymphocytic serum treatment was brought about by the development of blocking antibodies.