自体细胞因子诱导杀伤细胞治疗HBV感染肝硬化患者的临床观察及护理

目的观察自体细胞因子诱导杀伤细胞（CIK细胞）治疗HBVDNA阳性肝硬化患者的近期疗效。方法33例HBVDNA阳性肝硬化患者给予CIK细胞治疗，在体外培养前后以及回输体内后检测CD3^＋、CD3^＋CD4^＋、CD3^＋CD8^＋、CD3^＋CD56^＋、CD25^＋细胞以及mDC和pDC。比较治疗前后病毒学指标及肝脏功能的变化。结果培养结束以及回输体内后，CD3^＋细胞、CD3^＋CD8^＋细胞、CD3^＋CD56^＋细胞较培养前显著升高，mDC和pDC在回输后也明显增高。12例患者HBVDNA阴转，4例患者拷贝数下降大于2个log。在14例HBeAg阳性患者中有10例阴转，2例出现HBeAb转换。肝脏功能较治疗前有所好转。所有患者均能耐受治疗。结论ClK细胞可明显提高免疫效应细胞数量，具有一定的抗病毒效果，毒副作用低，对患者伤害小，安全性高，不良反应小，经过护理干预，患者的症状和体征得到改善，取得了显著疗效。     

Subcutaneous panniculitis complicating pancreatic acinar cell carcinoma

Acinar cell carcinoma of the pancreas is rare and can occur with the unusual presentation of arthritis and panniculitis that mimic erythema nodosum. We report a case and review the available literature regarding this rare condition of erythema nodosum and panniculitis associated with bilateral ankle and feet pain, which has rendered the patient virtually wheelchair‐bound.     

Engraftment of bone marrow cells into normal unprepared hosts: effects of 5-fluorouracil and cell cycle status

Bone marrow from animals treated with 5-fluorouracil (5FU) competes equally with normal marrow when assessed in vivo in an irradiated mouse, but shows markedly defective engraftment when transplanted into noncytoablated hosts. Using Southern Blot analysis and a Y-chromosome specific probe, we determined the level of engraftment of male donor cells in the bone marrow, spleen, and thymus of unprepared female hosts. We have confirmed the defective engraftment of marrow harvested 6 days after 5FU (FU-6) and transplanted into unprepared hosts and shown that this defect is transient; by 35 days after 5FU (FU-35), engraftment has returned to levels seen with normal marrow. FU-6 marrow represents an actively cycling population of stem cells, and we hypothesize that the cycle status of the stem cell may relate to its capacity to engraft in the nonirradiated host. Accordingly, we have evaluated the cycle status of engrafting normal and FU-6 marrow into normal hosts using an in vivo hydroxyurea technique. We have shown that those cells engrafting from normal marrow and over 70% of the cells engrafting from FU-6 marrow were quiescent, demonstrating no killing with hydroxyurea. We have also used fluorescent in situ hybridization (FISH) analysis with a Y-chromosome probe and demonstrated that normal and post-5FU engraftment patterns in peripheral blood were similar to those seen in bone marrow, spleen, and thymus. Altogether these data indicate that cells engrafting in normal, unprepared hosts are dormant, and the defect that occurs after 5FU is concomitant with the induction of these cells to transit the cell cycle.     

Basis of CTLA-4 function in regulatory and conventional CD4(+) T cells

CTLA-4 proteins contribute to the suppressor function of regulatory T cells (Tregs), but the mechanism by which they do so remains incompletely understood. In the present study, we assessed CTLA-4 protein function in both Tregs and conventional (Tconv) CD4(+) T cells. We report that CTLA-4 proteins are responsible for all 3 characteristic Treg functions of suppression, TCR hyposignaling, and anergy. However, Treg suppression and anergy only required the external domain of CTLA-4, whereas TCR hyposignaling required its internal domain. Surprisingly, TCR hyposignaling was neither required for Treg suppression nor anergy because costimulatory blockade by the external domain of CTLA-4 was sufficient for both functions. We also report that CTLA-4 proteins were localized in Tregs in submembrane vesicles that rapidly recycled to/from the cell surface, whereas CTLA-4 proteins in naive Tconv cells were retained in Golgi vesicles away from the cell membrane and had no effect on Tconv cell function. However, TCR signaling of Tconv cells released CTLA-4 proteins from Golgi retention and caused activated Tconv cells to acquire suppressor function. Therefore, the results of this study demonstrate the importance of intracellular localization for CTLA-4 protein function and reveal that CTLA-4 protein externalization imparts suppressor function to both regulatory and conventional CD4(+) T cells.     

Ameloblastoma: current etiopathological concepts and management

Ameloblastoma is a benign odontogenic tumor of epithelial origin. It is locally aggressive with unlimited growth capacity and has a high potential for malignant transformation as well as metastasis. Ameloblastoma has no established preventive measures although majority of patients are between ages 30 and 60 years. Molecular and genetic factors that promote oncogenic transformation of odontogenic epithelium to ameloblastoma are strongly linked to dysregulation of multiple genes associated with mitogen‐activated protein kinase, sonic hedgehog, and WNT/β‐catenin signaling pathways. Treatment of ameloblastoma is focused on surgical resection with a wide margin of normal tissue because of its high propensity for locoregional invasion; but this is often associated with significant patient morbidity. The relatively high recurrence rate of ameloblastoma is influenced by the type of molecular etiological factors, the management approach, and how early the patient presents for treatment. It is expected that further elucidation of molecular factors that orchestrate pathogenesis and recurrence of ameloblastoma will lead to new diagnostic markers and targeted drug therapies for ameloblastoma.     

Involvement of Ca~(2+) activated K~+channels in receptor regulated sperm motility in rats

Involvement of Ca~(2+) activated K~+channels in receptor regulated sperm motility in rats     

The distinctive jaw and alveolar bone regeneration

The skeletal system is structurally and functionally unique. It can be referred to as connective tissue that lost its ability to resist mineralization as mineralization in any other connective tissues is heterotopic. In addition to providing support for muscular attachments, the skeletal system protects nerves and harbors the hematopoietic and mesenchymal stem cells within the bone marrow compartment. However, there are distinct phenotypic and functional differences between the orofacial skeleton compared to axial and appendicular skeleton. How different is the jaw bone from other non‐craniofacial bones? Interestingly, developmental, biological, and clinical outcomes point to distinctive features that make the jaw bone unique.     

White cell subsets in apheresis and filtered platelet concentrates

BACKGROUND: White cell (WBC)-reduced platelet concentrates (PCs) are defined by their absolute WBC count, a criterion which provides no information regarding the various WBC subsets contained in the PC. These heterogeneous cells are known to mediate different physiologic and pathophysiologic functions and account for distinct adverse transfusion responses. This study describes a method which allows the detection and quantification of these subsets and characterizes their presence in a variety of platelet components. STUDY DESIGN AND METHODS: Random-donor pooled PCs (RD PCs) and single-donor apheresis PCs (SD PCs) were studied. RD PCs consisting of 6 units of 2- to 3-day old PCs were randomly assigned to be filtered with one of four WBC-reduction filters from three different manufacturers (n=34). The residual WBCs were pelleted by centrifugation and isolated on a density gradient. The various WBC subsets were quantified by flow cytometry in unfiltered and filtered PCs using fluorescence and two-angle light scatter. SD PCs obtained with two manufacturer's systems and three processing protocols (n=30) were studied in like manner. RESULTS: WBC counts for non-WBC- reduced PCs averaged 3 × 10(8) in RD PCs and ranged from 8.6 to 9.6 × 10(6) per SD PC. Residual WBC counts in filtered PCs ranged from 2.3 × 10(4) to 2.2 × 10(5) and those in WBC-reduced SD PCs averaged 2.2 × 10(5) per unit. The data demonstrate significant phenotypic differences among PCs produced with various procedures. All SD PCs and two of four filtered RD PCs contained five WBC populations including granulocytes and monocytes, while RD PCs filtered with the remaining manufacturer's devices contained only lymphocytes. CONCLUSION: The data confirm that distinct phenotypic differences exist among PCs prepared with different devices and/or procedures. It is suggested that as for non-generic pharmaceuticals, the clinical benefits of these various PCs should be individually proved.