自拟通便方联合针刺治疗便秘临床观察

目的：观察探讨针刺联合通便方对阴虚津亏型便秘患者的临床疗效。方法阴虚津亏型便秘患者40例,按就诊先后顺序随机分为治疗组（通便方联合针刺）和对照组（通便方）,每组20例。对照组单纯采用通便方治疗,治疗组在对照组基础上加用针刺,7 d 为1个疗程,共计2个疗程。观察两组患者治疗后临床疗效及临床症状评分情况。结果两种方法均能有效缓解便秘临床症状（P ﹤0.05）,但治疗组在改善排便间隔时间、排便费力程度、排便不尽感及紧迫感、腹痛腹胀症状较对照组均有优势（P ﹤0.05）,且治疗组临床疗效优于对照组（P ﹤0.05）。结论针刺联合中药口服治疗慢性功能性便秘,通过建立以多层次、立体的治疗方案,从根本上调整了机体阴阳失衡的状态,疗效显著,值得推广。     

In vitro hemopoiesis in human micro long-term bone marrow cultures recharged with either allogeneic,T-cell-depleted allogeneic,or syngeneic bone marrow cells

Summary The production of granulocyte-macrophage colony-forming cells (GM-CFC) and the proliferation period in human long-term bone marrow cultures are inferior to murine cultures. There is also evidence that recharge of the cultures after establishing confluent stromal layers will not greatly improve myelopoiesis. Data in the literature indicate that PHA-responsive T lymphocytes persist for up to 5 weeks in human but not in murine long-term marrow cultures. We therefore analyzed the effects of recharging micro long-term bone marrow cultures with bone marrow cell samples depleted by T lymphocytes. Depletion was performed in a complement-mediated cytotoxicity assay by applying the monoclonal antibody CAMPATH-1. Our data show that regardless of whether T cells were removed only at recharge, at both initiation and recharge, or only at initiation, obvious enhancement could neither be achieved in the GM-CFC production nor in the proliferation period. Furthermore, no advantage was seen when using syngeneic marrow cells. We conclude that in allogeneic long-term marrow cultures hemopoiesis is not limited by immunological incompatibilities.     

A safeguard eliminates T cell receptor gene-modified autoreactive T cells after adoptive transfer

By transfer of T cell receptor (TCR) genes, antigen specificity of T cells can be redirected to target any antigen. Adoptive transfer of TCR-redirected T cells into patients has shown promising results. However, this immunotherapy bears the risk of autoreactive side effects if the TCR recognizes antigens on self-tissue. Here, we introduce a safeguard based on a TCR-intrinsic depletion mechanism to eliminate autoreactive TCR-redirected T cells in vivo. By the introduction of a 10-aa tag of the human c-myc protein into murine (OT-I, P14) and human (gp100) TCR sequences, we were able to deplete T cells that were transduced with these myc-tagged TCRs with a tag-specific antibody in vitro. T cells transduced with the modified TCR maintained equal properties compared with cells transduced with the wild-type receptor concerning antigen binding and effector function. More importantly, therapeutic in vivo depletion of adoptively transferred T cells rescued mice showing severe signs of autoimmune insulitis from lethal diabetes. This safeguard allows termination of adoptive therapy in case of severe side effects.     

Cytomegalovirus infection in recipients of related and unrelated donor bone marrow transplants: no evidence of increased incidence in patients receiving unrelated donor grafts

Recent reports suggest an increased incidence of cytomegalovirus (CMV) infection in recipients of unrelated donor (UD) bone marrow transplantation (BMT).
In this study we have collated the incidence of CMV infection and disease in sequential UD ( n  = 119) and related donor (RD; n  = 79) BMT performed in a single institution over a 7-year period. Low-risk patients (CMV seronegative recipient and donor) accounted for 51% of UD BMT ( n  = 61) and 62% of RD BMT ( n  = 49), with CMV excretion documented in one RD BMT only. The remaining high-risk patients received identical prophylaxis regimens with aciclovir and intravenous immunoglobulin (IVIG). Two groups consisting of 58 UD BMT (median age 9.0 years, range 0.7–45.3 years) and 30 RD BMT (median age 13.6 years, range 1.6–47.6 years) were analysed. CMV reactivation/re-infection was documented in 15 UD BMT (26%) and 10 RD BMT (33%) ( P  = 0.72), and CMV disease in four UD BMT (8%) and four RD BMT (13%) ( P  = 0.533). In this series the risk of CMV excretion and disease following UD BMT was similar to that following RD BMT.     

T-cell depletion and autologous stem cell transplantation in the management of tumour stage mycosis fungoides with peripheral blood involvement

Nine patients with tumour stage mycosis fungoides (MF) have been entered into a pilot study of T-cell depletion and autologous stem cell transplantation (SCT). Eight patients had detectable rearrangements of the T-cell receptor (TCR) gamma-gene demonstrated by polymerase chain reaction (PCR)/single-stranded conformation polymorphism (SSCP) in the peripheral blood. The median age was 47 years and the median duration of disease before SCT was 61 months; Peripheral blood progenitor cells were mobilized using high-dose etoposide (1.6 g/m2) and granulocyte colony-stimulating factor (G-CSF). The apheresis products underwent rigorous T-cell depletion with immunomagnetic methods. Double CD34-positive and CD4/CD8-negative selection achieved a median reduction of 3.89 log of T cells. All nine patients have been transplanted. Conditioning included carmustine (BCNU), etoposide and melphalan (BEM) in seven patients and total body irradiation plus etoposide or melphalan in two. Eight patients engrafted promptly and one patient died of septicaemia. All survivors entered complete remission. Seven patients have relapsed at a median of 7 months (2-14) post SCT. However, most patients have relapsed into a less aggressive stage, which has responded to conventional therapy. Four out of seven evaluable patients had detectable TCR rearrangements in the T-cell depleted graft. A T-cell clone was also detected in the peripheral blood before relapse in four cases. Autologous SCT is feasible, safe and can result in complete remission in a significant proportion of patients with tumour stage mycosis fungoides. Despite a short relapse-free survival, most patients achieved good disease control at the time of relapse.     

Fludarabine-based cytoreductive regimen and T-cell-depleted grafts from alternative donors for the treatment of high-risk patients with Fanconi anaemia

Eighteen consecutive patients aged 5·5–24 years with Fanconi anaemia and diagnoses of aplastic anaemia ( n  = 8), myelodysplastic syndrome ( n  = 4), acute myeloid leukaemia ( n  = 6), received allogeneic haematopoietic stem cell transplants from alternative donors. All patients had been transfused, 13 had previously been treated with androgens and 14 had a history of infection. Donors were related human leucocyte antigen (HLA) mismatched for eight patients, unrelated HLA mismatched for seven patients and unrelated HLA matched for three patients. Cytoreduction included single dose total body irradiation (450 cGy), fludarabine (150 mg/m²) and cyclophosphamide (40 mg/kg). Immunosuppression included antithymocyte globulin and tacrolimus. Grafts were granulocyte colony-stimulating factor-mobilized, CD34⁺ T-cell-depleted peripheral blood stem cells in 15 patients and T-cell-depleted marrows in three. All 18 patients engrafted with 100% donor chimaerism; only one patient developed graft-versus-host disease (GVHD). With a median follow-up of 4·2 years, 13/18 patients were alive, 12 of these were disease-free. Five-year overall survival and disease-free survival were 72·2% and 66·6% respectively. Immune reconstitution was achieved at approximately 6 months post-transplant for most patients. These are encouraging results of T-cell-depleted transplants from alternative donors using fludarabine-based cytoreduction in 18 high-risk patients with Fanconi anaemia, with no evidence of rejection and minimal GVHD.     

Reduced glutathione concentration in erythrocytes of patients with acute and chronic viral hepatitis

SUMMARY. Reduced glutathione (GSH), the main intracellular mechanism that protects against oxidative stress, is the subject of considerable interest in viral hepatitis. In patients with chronic hepatitis C, results reported from different centres are controversial, demonstrating either a reduction or an elevation of GSH concentration. The aim of this study was to evaluate the glutathione concentration in erythrocytes (normal range 2.45 ± 0.15 mmol l^?1) in patients with acute and chronic viral hepatitis. In 52 patients with acute viral hepatitis (hepatitis A virus (HAV), hepatitis B virus (HBV) and hepatitis C virus (HCV) infection) there was marked reduction of GSH at the beginning of the disease (0.79 ± 0.43 mmol l^?1. P < 0.001) with high alanine aminotransferase (ALT) activity (1549 ± 772.9 IU l^?1). In 37 patients with chronic HCV infection the mean value of GSH was below the normal range (1.92 ± 0.62 mmol l^?1. P < 0.001). In 60% of patients (n = 22), depletion of GSH was observed and 40% (n = 15) presented with a normal concentration of GSH. In 10 patients with chronic HBV infection the mean value of GSH was also below the normal range (1.93 ± 0.32 mmol l^?1, P < 0.001); in 80% of cases (n = 8) depletion of GSH was observed and 20% of patients (n = 2) had normal GSH concentrations. The ALT activity was not significantly different in patients with depleted and normal GSH concentrations (P > 0.05) in groups with chronic HBV and HCV infection.     

A COMPARATIVE STUDY OF T-CELL DEPLETED AND NON-DEPLETED MARROW TRANSPLANTATION FOR HEMATOLOGICAL MALIGNANCY

Sixteen patients with hematological malignancy received cyclophosphamide (120 mg/kg), fractionated total body irradiation (12 Gy), oral cyclosporin, and an HLA-identical sibling marrow transplant depleted of T cells by incubation with the monoclonal antibody anti-HuLy-m1 (CD2) and rabbit complement with (five patients) or without (11 patients) anti-HuLy-m8 (CD8). These 16 patients were compared historically to 84 patients with hematological malignancy receiving cyclophosphamide (120 mg/kg), fractionated total body irradiation (12 or 14 Gy), oral cyclosporin, and unmanipulated HLA-identical sibling marrow, for parameters of engraftment and graft-versus-host disease (GVHD). Graft failure occurred in one of the 16 T-cell depleted recipients and in one of the 84 non-depleted recipients. Engraftment was slightly but significantly slower in the T-cell depleted group and bacterial infections significantly more, frequent and severe than in the unmanipulated group. There was a suggestion that the severity of acute GVHD was reduced in those receiving T depleted marrow. Randomized trials will be necessary to determine if marrow T-cell depletion results in superior long-term leukemia-free survival.     

IMMUNOLOGICAL RECONSTITUTION IN A PATIENT WITH SEVERE COMBINED IMMUNE DEFICIENCY USING NON-SIBLING BONE MARROW DEPLETED OF T CELLS WITH HuLy-m1

Abstract An infant with severe immune deficiency received bone marrow from an HLA-A, -B, -DR matched, mixed leucocyte reaction non-reactive first cousin. The donor marrow was fractionated on a discontinuous Percoll gradient and before infusion was treated with the anti-human T lymphocyte antibody, HuLy-m1, and rabbit serum as a source of complement. Methotrexate was given during the following two weeks. A rise in the peripheral blood lymphocyte count, indicating engraftment, occurred six weeks after transplantation. There was no clinical evidence of graft versus host disease (GVHD). Engraftment has been sustained for one year and the patient is in normal health and has normal in vitro immunological function. In vitro treatment of human marrow with HuL-m1 allows stable engraftment and may be useful in attempting to diminish or prevent GVHD.     

Monoclonal gammopathy (IgA:λ) after autologous T-cell-depleted bone marrow transplantation in a patient with non-Hodgkin's lymphoma

Summary We report a case study of a patient suffering from T-lymphoblastic lymphoma, for whom autologous T-cell-depleted bone marrow transplantation was carried out. Low-dose cyclosporin A (CsA) was administered just after autologous bone marrow transplantation (ABMT) for induction of autologous graft-versus-host disease. Three months later, the lymphoma relapsed with marked monoclonal gammopathy of the immunoglobulin A type, which had not been seen before ABMT. It is suggested that the regrowth of the lymphoma cells was related to the maturation of B cells or the secretion of immunoglobulins from plasma cells, associated with some cytokines produced under the condition of an abnormal immunological circumstance after ABMT plus CsA.