A Japanese multi-institutional collaborative study of antigen-positive red blood cell (RBC) transfusions in patients with corresponding RBC antibodies.

BACKGROUND AND OBJECTIVES: It is sometimes difficult to obtain antigen-negative red blood cells (RBCs) for patients with antibodies against RBCs. However, the frequency and severity of the adverse reactions have not been well elucidated. Here, we conducted a multi-institutional collaborative study to clarify the background, frequency and clinical significance of antigen-positive RBC transfusions to patients with the respective antibodies. MATERIALS AND METHODS: The survey included the background of patients, antigens on RBCs transfused, total amount of antigen-positive RBCs transfused, results from antibody screen and direct antiglobulin tests, specificity of antibodies, adverse reactions and efficacies. All antibodies were surveyed regardless of their clinical significance. RESULTS: In all, 826 cases containing 878 antibodies were registered from 45 institutions. The main reasons for antigen-positive RBC transfusions included 'negative by indirect antiglobulin test' (39%) and 'detection of warm autoantibodies' (25%). In 23 cases (3% of total), some adverse reactions were observed after antigen-positive RBC transfusion, and 25 antibodies (9 of 119 clinically significant and 16 of 646 insignificant antibodies) were detected. Non-specific warm autoantibodies were detected in 9 cases, anti-E in 5 cases, 2 cases each of anti-Lea , anti-Jra or cold alloantibodies, and 1 case each of anti-Dib , anti-Leb or anti-P1. Other antibodies were detected in 2 further cases. Five (22%) of these 23 cases, who had anti-E (3 cases) or anti-Jra (2 cases), experienced clinically apparent haemolysis. CONCLUSIONS: Adverse reactions, especially haemolysis, were more frequently observed in cases with clinically significant antibodies than those with clinically insignificant antibodies (P < 0·001).

Plasmapheresis for the Treatment of Anti-M Alloimmunization in Pregnancy.

Intrauterine transfusion is the standard antenatal treatment for a fetus with severe anemia. Plasmapheresis is an alternative treatment for cases with a history of severe hemolytic disease of the fetus and newborns at less than 20 weeks of gestation. There is only one previous report of plasmapheresis for the anti-M alloimmunization in pregnancy, and we report here on the successful treatment of plasmapheresis for anti-M alloimmunization. A woman with a history of intrauterine fetal death at 24 weeks of gestation due to severe fetal anemia caused by anti-M alloimmunization received plasmapheresis once or twice a week from 14 weeks of gestation onward. An intrauterine blood transfusion was conducted at 28 weeks, and a cesarean section was performed at 31 weeks. The infant had anemia and jaundice but was discharged at day 46. Plasmapheresis may delay the development of fetal anemia and reduce the risk of early and repeat intrauterine transfusion in cases of anti-M alloimmunization in pregnancy.

A healing period increases mini-implant stability in growing rats.

We assessed the stability of orthodontic mini-implants in young rats. Male rats with mean ages of 6 weeks (n = 16) and 20 weeks (n = 16) were divided into four groups (n = 8 each). In the 6- and 20-week immediate-loading groups, immediately after placement, mini-implants were exposed to an experimental traction force for 2 weeks. In the 6- and 20-week healing groups, the force was applied for 2 weeks after a 6-week healing period. Right tibiae served as the test limbs and the left tibiae as controls. A Periotest device was used to measure mini-implant mobility after traction, and Tukey's test was used to compare Periotest values among groups. The results showed significantly greater mobility in the 6-week immediate-loading group than in the 20-week immediate-loading and 6- and 20-week healing groups, and significantly less mobility in the 6-week healing group than in the 20-week immediate-loading group (P < 0.05). Mini-implants were stable during the healing period. The results indicate that mini-implants can be used for orthodontic anchorage in juvenile patients if the duration of healing is sufficient.

Longitudinal quantitative evaluation of the mid-palatal suture after rapid expansion using in vivo micro-CT.

New bone formation is known to occur between the opened palatal bones after rapid mid-palatal expansion (RME), although the time-dependent changes in the mid-palatal suture after RME have not been fully examined. Thus, we investigated time-dependent morphological changes in the mid-palatal suture using in vivo micro-computed tomography (mCT) and the expression of bone morphogenetic factors. RME was performed by inserting a 1.5-mm-thick circular metal ring between the maxillary incisors of rats, and morphological changes in the mid-palatal suture were investigated using in vivo mCT imaging after RME. Bone morphogenetic protein 2 (BMP-2) and insulin-like growth factor-I (IGF-I) expression in the suture were also examined using reverse-transcription polymerase chain reaction and immunohistochemistry. The bone volume of the mid-palatal suture decreased after RME to a minimum of -0.34mm(3) on day 12, then increased with bone formation over time and reached -0.13mm(3) on day 24. Significant increases in BMP-2 and IGF-I mRNA expression after RME were found on day 3 compared with day 0. By immunohistochemistry, BMP-2 and IGF-I were detected in osteoblasts on days 5 and 7, in endothelial cells of blood vessels, and fibroblasts on day 7. Expansion of the mid-palatal suture continues for 12 days after a single RME, and restoration requires more than 30 days. Additionally, BMP-2 and IGF-I may play important roles in the restoration process.

Osteoblasts stimulate osteoclastogenesis via RANKL expression more strongly than periodontal ligament cells do in response to PGE(2).

OBJECTIVE: Periodontal ligament cells (PDLs) produce prostaglandin E(2) (PGE(2)) in response to orthodontic force. PGE(2) is a potent osteoclast-inducing factor that induces the receptor activator of nuclear factor-κB ligand (RANKL). Some studies reported that PDLs express RANKL in response to mechanical stress, whereas another study reported that they do not. Based on an immunohistochemical study, RANKL expression is localized around the alveolar bone surface 3 days after tooth movement. However, ankylosed teeth cannot be moved by therapeutic mechanical stress, suggesting that PDLs play a major role in alveolar bone resorption. In this study, we compared the functional difference in osteoclastogenesis between human PDLs (HPDLs) and normal human osteoblasts (HOBs) as a direct effect of PGE(2) exposure. DESIGN: We examined the expression of RANKL, osteoprotegerin, and macrophage colony-stimulating factor after 48-h culture with or without PGE(2) (10(-11) to 10(-5)M) in HPDLs and HOBs. Then to confirm whether RANKL produced by PGE(2) treatment induces osteoclastogenesis or not, RAW264.7 cells were co-cultured on HPDLs or HOBs pretreated with 10(-6)M of PGE(2). RESULT: PGE(2) exposure increased significantly RANKL expression in HOBs compared with HPDLs. PGE(2) exposure significantly decreased osteoprotegerin expression in HPDLs compared with HOBs. The number of tartrate-resistant acid phosphatase staining osteoclast-like cells from RAW264.7 cells increased significantly by PGE(2) pretreatment in HOBs and was reduced by small interfering RNA knockdown of RANKL. CONCLUSION: These results suggest that osteoblasts strongly influence the stimulation of osteoclastogenesis via RANKL, induced by PGE(2) in periodontal tissues, compared with PDLs.

Defective human T-lymphotropic virus type 1 provirus in asymptomatic carriers.

Few studies have specifically examined defective provirus in asymptomatic human T-lymphotropic virus Type 1 (HTLV-1) carriers and its relation to proviral DNA loads (PVLs). To assess the significance of defective provirus in asymptomatic carriers, we examined PVLs in peripheral blood mononuclear cells of 208 asymptomatic HTLV-1 carriers. The mean PVLs determined using primers for the pol region were less than that for the pX region in these carriers. Analysis of seven carriers with high PVLs for the pX region but lower PVLs for the pol region showed that four had single nucleotide polymorphisms of proviral genomes for the pol region and three had HTLV-1-infected cells with defective provirus. Three carriers with defective provirus showed high PVLs at their initial screens, and PVLs increased after a 10- to 12-year interval in two carriers. Southern blot assay showed clonal expansion of HTLV-1-infected cells, and the predominant clones changed during the observation period. These data suggest that although HTLV-1-infected cells with defective provirus may have a growth advantage, the predominant clones of HTLV-1-infected cells do not always survive for many years in asymptomatic carriers.