胆道解剖变异影像与临床手术对比4例

本文通过4例胆道解剖变异影像与临床手术对比分析,提出预防由于胆道解剖变异引起胆道损伤的方法．     

A comparative study of the phenotype and proliferative capacity of peripheral blood (PB) CD34+ cells mobilized by four different protocols and those of steady-phase PB and bone marrow CD34+ cells

Peripheral blood (PB) CD34+ cells from four commonly used mobilization protocols were studied to compare their phenotype and proliferative capacity with steady-state PB or bone marrow (BM) CD34+ cells. Mobilized PB CD34+ cells were collected during hematopoietic recovery after myelosuppressive chemotherapy with or without granulocyte- macrophage colony-stimulating factor (GM-CSF) or granulocyte colony- stimulating factor (G-CSF) or during G-CSF administration alone. The expression of activation and lineage-associated markers and c-kit gene product were studied by flow cytometry. Proliferative capacity was measured by generation of nascent myeloid progenitor cells (granulocyte- macrophage colony-stimulating factor; CFU-GM) and nucleated cells in a stroma-free liquid culture stimulated by a combination of six hematopoietic growth factors (interleukin-1 (IL-1), IL-3, IL-6, GM-CSF, G-CSF, and stem cell factor). G-CSF-mobilized CD34+ cells have the highest percentage of CD38- cells (P < .0081), but otherwise, CD34+ cells from different mobilization protocols were similar to one another in their phenotype and proliferative capacity. The spectrum of primitive and mature myeloid progenitors in mobilized PB CD34+ cells was similar to their steady-state counterparts, but the percentages of CD34+ cells expressing CD10 or CD19 were lower (P < .0028). Although steady-state PB and chemotherapy-mobilized CD34+ cells generated fewer CFU-GM at day 21 than G-CSF-mobilized and steady-state BM CD34+ cells (P < .0449), the generation of nucleated cells and CFU-GM were otherwise comparable. The presence of increased or comparable numbers of hematopoietic progenitors within PB collections with equivalent proliferative capacity to BM CD34+ cells is not unexpected given the rapid and complete hematopoietic reconstitution observed with mobilized PB. However, all four types of mobilized PB CD34+ cells are different from steady-state BM CD34+ cells in that they express less c-kit (P < .0002) and CD71 (P < .04) and retain less rhodamine 123 (P < .0001). These observations are novel and suggest that different mobilization protocols may act via similar pathways involving the down-regulation of c-kit and may be independent of cell-cycle status.     

Polyclonal antibodies against the NB1-bearing 58- to 64-kDa glycoprotein of human neutrophils do not identify an NB2-bearing molecule

The neutrophil-specific NB antigen system has been serologically characterized with human alloantisera. Two alleles, NB1 and NB2, have been described; however, there may be important quantitative or qualitative variation in the expression of NB1 and NB2. Human alloantibodies have been used to identify the 58- to 64-kDa glycoprotein (GP) on which NB1 antigen is located, but an NB2 antigen- bearing molecule has not yet been identified. To identify the NB2 molecule, human alloantibody to NB1 was used to isolate the 58- to 64- kDa NB1 GP, and rabbits were immunized with this GP. Two rabbit antisera were produced. Both antisera immunoblotted and immunoprecipitated the 58- to 64-kDa GP on which NB1 is located, but neither identified the molecule on which NB2 is located. The inability of two rabbit polyclonal antibodies specific for the NB1 molecule to react with the NB2-bearing molecule suggests that considerable differences may exist between these two molecules or that NB2 as currently defined is not related to NB1.     

A dichotomy between the expression of IgD on B cells and its requirement for triggering such cells with two T-independent antigens

The majority of adult B lymphocytes in the mouse bear two immunoglobulin isotypes, IgM and IgD (μ(+)δ(+) cells) (1). A small population of IgM-bearing cells lacks, or expresses very low levels of IgD (μ- predominant [μp] cells) (1). These cells are believed to constitute a less mature subset of B cells analogous to neonatal B cells (2). Based on the time during ontogeny when responses to T-independent (TI) and T-dependent (TD) antigens appear (3, 4) and the ability to block in vitro responses with anti- μ or anti-δ (5, 6, D. Mosier, personal communication), it has been suggested that the precursors of two TI-1 responses, trinitrophenyl (TNP)- Brucella (TNP-BA) and TNP-lipopolysaccharide (TNP-LPS) are μp cells (5, 6), whereas the precursor for a TD response, TNP-sheep erythrocytes (TNP-SRBC), bears both IgM and IgD (6). However, the possibility cannot be excluded that IgD is present on some or all of the TI precursors, but that it is not obligatory for triggering. In the present experiments we have examined the phenotypes of TI and TD precursors by treating cells with C’ and either anti-μ or anti-δ before stimulation with antigen. Our results suggest that the majority of B cells that respond to TNP-BA, TNP-LPS, and TNP-SRBC bear IgD, even though in the case of the two TI antigens, IgD is not required for triggering.     

Risk Modulation of Oral Pre Cancer and Cancer with Polymorphisms in XPD and XPG Genes in North Indian Population

Background: Environmental carcinogens cause DNA damages which if not repaired properly, may increase therisk of cancer. The Xerodermapigmentosum group D (XPD) and group G (XPG) genes are essential genes for DNArepair and alteration in DNA repair causes cancer. The present study aimed to evaluate the relationship between XPDand XPG polymorphisms and risk of oral pre cancer and cancer. Methods: Present study genotyped 302 samples oforal diseases and 300 controls for XPD (A/C) and XPG (G/C) polymorphisms with PCR-RFLP method. Results: Ourresult showed that compared to AA genotype frequency of AC and CC genotype for XPD(A/C) polymorphism weresignificantly lower among cases than in control and are associated with decreased risk of oral diseases (OR= 0.621and 0.603 respectively). In contrast with reference to GG genotype the frequency of CC genotype of XPG (G/C) wassignificantly higher in case than in control population (p value=0.004) and found to increase the risk of oral diseases(OR= 2.077). Particularly C allele for XPD A/C polymorphism was found to be associated with decreased risk of Lichenplanus and increased risk of ( OR = 0.470 and 1.541 respectively) oral cancer. While C allele of XPG G/C polymorphismsignificantly increased the risk of Oral Submucous Fibrosis and Leukoplakia (OR= 1.879 and 1.837 respectively) butnot of Lichen planus and oral cancer. In combined genotype analysis from the aforesaid polymorphisms presence of Callele for XPD (A/C) polymorphisms were found to decrease the risk of oral diseases. However, the same C allele wasobserved to increase the chance of having high stage disease (OR= 5.71) with nodal involvement (OR= 6.78) once thecancer been initiated. Conclusion: This work shows association of XPD (A/C), XPG (G/C) polymorphisms with thedevelopment of pre oral cancer as well as oral cancer and its clinical courses.