Biomedical subjects
Publications and source records attributed to C Y Li.
The causal mechanisms of reflex sympathetic dystrophy are not limited purely to sympathetic hyperactivity, but sympathetic blockade and physical therapy are still the mainstays of current treatment modalities. We reported a case of reflex sympathetic dystrophy over the left lower leg, who was successfully treated with repeated lumbar sympathetic blocks and physical therapy.
BACKGROUND: Benzene is a widely distributed environmental contaminant known to cause leukemia, particularly acute nonlymphocytic leukemia, and perhaps other hematologic neoplasms and disorders. Few epidemiologic studies, however, have been able to address relationships between the extent of benzene exposure and the level of risk. PURPOSE: A large cohort study was carried out in China to evaluate the risks of developing specific hematologic neoplasms and selected related disorders in relationship to quantitative estimates of occupational benzene exposure. METHODS: A cohort of 74828 benzene-exposed and 35805 unexposed workers employed from 1972 through 1987 in 12 cities in China was identified and followed to determine the incidence of hematologic neoplasms and related disorders. Estimates of benzene exposure were derived from work histories and available historic benzene measurements. Existing pathologic material and supporting medical records were reviewed to establish diagnoses of disease. Relative risks (RRs) (i.e., ratios of incidence rates for specific hematologic neoplasms and related disorders in the benzene-exposed group to incidence rates in the unexposed group) were determined by use of Poisson regression analysis, with stratification by age and sex. RESULTS: For workers historically exposed to benzene at average levels of less than 10 parts per million (ppm), the RR for all hematologic neoplasm combined was 2.2 (95% confidence interval [CI] = 1.1-4.2), and, for the combination of acute nonlymphocytic leukemia and related myelodysplastic syndromes, the RR was 3.2 (95% CI = 1.0-10.1). For individuals who were occupationally exposed to benzene at constant levels of 25 ppm or more, the RR for the combination of acute nonlymphocytic leukemia and related myelodysplastic syndromes was 7.1 (95% CI = 2.1-23.7). Workers with 10 or more years of benzene exposure had an RR of developing non-Hodgkin's lymphoma of 4.2 (95% CI = 1.1-15.9), and the development of this neoplasm was linked most strongly to exposure that had occurred at least 10 years before diagnosis (i.e., distant exposure) (P for trend = .005, two-sided). In contrast, the risk for the combination of acute nonlymphocytic leukemia and related myelodysplastic syndromes was significantly increased among those with more recent benzene exposure (P for trend = .003, two-sided), but it was not linked to distant exposure (P for trend = .51, two-sided). CONCLUSIONS: The results of this study suggest that benzene exposure is associated with a spectrum of hematologic neoplasms and related disorders in humans. Risks for these conditions are elevated at average benzene-exposure levels of less than 10 ppm and show a tendency, although not a strong one, to rise with increasing levels of exposure. The temporal pattern of benzene exposure appears to be important in determining the risk of developing specific diseases.
Extracellular recordings were made in the striate cortex in awake, behaving monkeys to test the influence of the eye position on cellular activity. Two monkeys (Macaca mulatta) were trained to fixate a small spot at 25 different eye positions. About half (52%) of the studied neurones showed a selective gaze field (GF). The cells' activities increased significantly when the monkey fixated at this field of view. For the majority of these neurones, GFs were located at the contralateral field of view with respect to the hemisphere from which responses were recorded, and were usually found a few degrees peripheral to the related receptive field. Eye position-dependent neurones were found at different depths of cortex, but mostly in the superficial layers. The results indicate that some neurones in striate cortex may code information about eye position and could contribute to target localization in a head-centred coordinate system by combining retinal and afferent eye position signals.
In order to gain a better understanding of the role of p53 in radiation-induced mitotic failure, apoptosis and mutagenesis, we introduced the HPV16 E6 gene via a retroviral vector into the TK6 human lymphoblast cell line which expresses wild type p53. Abrogation of p53 function by E6 resulted in a delayed and reduced apoptotic response and a moderate increase in the frequency of mutations at the thymidine kinase (tk) locus following gamma-irradiation, but failed to alter radiosensitivity. The apoptotic response of the E6-transduced line was intermediate between that of wild type TK6 and the WTK1 cell line. WTK1 is derived from the same parental cell line as TK6 but expresses mutant p53. The spontaneous and gamma-ray-induced mutation frequencies in E6-transduced TK6 cells, although higher than that of the parental TK6 cell line, were still much lower than that of the WTK1 line. No effect on apoptosis, radiosensitivity or mutability was observed when the HPV16 E6 gene was introduced into the WTK1 cells. These results indicate that p53 does not regulate the radiosensitivity of TK6 cells through the apoptotic pathway. Furthermore, the previously observed enhanced radioresistance and mutability in WTK1 cells must be attributed to a more complex mechanism than p53 status alone.
Two patients with chronic natural killer cell lymphocytosis (CNKL) and associated bone marrow granulomas (BMGs) are described. The increases in the peripheral blood of both the proportion (64 and 74%) and absolute number (2,000/microL and 4,700/microL) of NK cells have persisted for more than 1 and 3 years. One patient was asymptomatic with thrombocytopenia and neutropenia, and the other presented with fever of unidentified origin, which has since responded to a nonsteroidal anti-inflammatory agent. Bone marrow examination in both patients showed loose aggregates of epithelioid histiocytes similar to the noncaseating granulomas seen in other diseases. An unusual feature, however, was the presence of many scattered, large mononuclear histiocytes that were morphologically similar to atypical megakaryocytes. Extensive clinical and laboratory studies did not reveal an established cause for the BMGs. BMGs may be associated with CNKL, with the unusual feature of scattered, atypical mononuclear histiocytes.
Explore the source record for details and available documents.
PURPOSE: To evaluate the effects of ketamine on the activity and protein expression of inducible nitric oxide synthase (iNOS) induced by lipopolysaccharide (LPS) in rat alveolar macrophages. METHODS: Pulmonary alveolar macrophages isolated from Wistar-Kyoto rats were used. After incubation of macrophages with ketamine (1, 10, or 100 microM) and LPS (1 microgram.ml-1) for 24 hr, the cell-free medium was removed for measuring the nitrite and tumour necrosis factor-alpha (TNF-alpha) levels by Griess reaction and ELISA kit, respectively. The harvested macrophages were also used to determine the activity of iNOS by using the conversion of [3H]-L-arginine to [3H]-L-citrulline method. In addition, the protein expression of iNOS was detected by Western blot analysis. RESULTS: In rat alveolar macrophages, (i) ketamine (1 to 100 microM) caused a dose-dependent suppression of the production of nitrite and TNF-alpha induced by LPS and (ii) ketamine (100 microM) inhibited the activity (46.5 +/- 4.8%, P < 0.05) and protein expression (35 +/- 11%, P < 0.05) of iNOS in response to LPS. CONCLUSION: These results show that ketamine inhibits the activity and expression of iNOS in LPS-activated alveolar macrophages, which may be associated with the reduction of the release of TNF-alpha following LPS treatment.
In a prospective study of 93 consecutive untreated patients with B-cell chronic lymphocytic leukemia, we examined the clinical relevance of surface immunoglobulin (sIg) heavy chain (HC) and light chain (LC) isotypes, CD11c or CD25 expression, and the presence of trisomy 12 by fluorescence in situ hybridization (FISH). Careful morphologic evaluation was performed to exclude patients with other forms of chronic lymphoid leukemias, including mantle cell lymphoma, prolymphocytic leukemia, and leukemia phase of lymphoma. In addition, clonally restricted sIg and CD5 surface determinant were expressed in all patients. Clinical presentation, including blood cell counts, clinical stage, and organomegaly, did not correlate with any of the measured variables. After a median follow-up period of 3 years, the particular HC or LC isotype or CD11c expression did not correlate with either disease progression or treatment-free survival. However, trisomy 12 and CD25 expressions were both associated with accelerated disease progression and a shorter treatment-free survival time. Our results confirm the adverse prognostic significance of trisomy 12 expression in chronic lymphocytic leukemia and suggest that CD25 expression may have an unfavorable clinical impact.
This study examines the effect of intergenerational exchange on nursing home admissions among functionally disabled older adults in Taiwan. A group of 317 nursing home residents were randomly selected from all nursing homes in Taipei, the capital of Taiwan. In addition, two community groups were randomly selected as multiple controls in the study. The results showed that intergenerational exchange has a statistically significant effect on nursing home admission after controlling for sociodemographic characteristics and health status. The odds of being admitted into a nursing home was lower for those elderly who provided instrumental assistance to their families before they were disabled. The adjusted relative risk estimate was 0.2 (95% CI = 0.1 - 0.6). It shows that the instrumental assistance the elderly provided to the family before they became disabled was reciprocated when they needed ADL assistance. This finding provides strong support for the social exchange theory.
2-Chlorodeoxyadenosine (2-CdA) is a purine nucleoside analogue with therapeutic activity in low-grade lymphoproliferative disorders. In addition, 2-CdA has a potent myelosuppressive effect, and it has been shown to be toxic to malignant myeloid cells both in vitro and in vivo. In this pilot study we treated nine patients who had advanced myelofibrosis with myeloid metaplasia (MMM) and progressive hepatomegaly or symptomatic thrombocytosis after therapeutic splenectomy. 2-CdA was administered at 0.05-0.1 mg/kg/d for 7 d for one to five treatment cycles. A reduction in liver size associated with marked improvement in fatigue and control of thrombocytosis and leucocytosis was achieved in seven of the nine patients (78% response rate). In four of the seven responding patients the reduction in liver size was durable (4-28 months) and was associated with a decrease in serum alkaline phosphatase levels. However, no patient had improvement in anaemia, and two of the seven initially responding patients have since died of acute leukaemia or progressive disease. Improvement in bone marrow fibrosis was noted in two of five available post-treatment marrow examinations. Toxicity was mainly myelosuppression, which was severe in two patients. 2-CdA may be considered a palliative therapeutic agent after splenectomy in noncytopenic patients with MMM who have progressive hepatomegaly or extreme thrombocytosis.
Guillain-Barré syndrome in northern China occurs in two forms: acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). AMAN and AIDP have an immunologic basis, and some cases are associated with preceding Campylobacter jejuni infection. The distribution of allelic forms of the histocompatibility genes HLA-DPB1, DQB1, DRB1, DRB3, DRB4, and DRB5 was examined by DNA-based technology in 34 control, 12 AIDP, and 31 AMAN cases. In AIDP patients, the DRB1*1301 allele showed a significant increase (18% vs. 0%, P = .055). In AMAN patients, alleles DRB1*1301-03 and DRB1*1312, taken collectively, were increased (19% vs. 0%, P = .009), but by itself, the DRB1*1301 allele was not increased, as in AIDP patients. With a larger number of persons, more definitive statements will be possible; however, the differential distribution of DR13 allelic forms between AIDP and AMAN cases may suggest that there are different immunologic mechanisms operating at the molecular level of these diseases.
To evaluate the feasibility of acute leukemia typing on routinely processed bone marrow biopsy specimens, 72 cases of previously established acute leukemia covering the spectrum of 17 known subtypes were studied immunohistochemically. Most leukemic myeloblasts were positive for myeloperoxidase in 16 (84%) of 19 cases of acute myeloid leukemia, M1-M4, and M6. Most leukemic cells in 11 of 12 M4 and M5 cases were positive for CD68 (PG-M1). All six M6 cases stained with hemoglobin. Leukemic megakaryoblasts in three of four M7 cases were positive for factor VIII-related antigen. Almost all leukemic cells of 8 T-lineage acute lymphoblastic leukemia (ALL) and 19 B-lineage ALL cases were positive for CD3 and CD79a (HM57), respectively. Staining with CD20 (L26) was positive in the more differentiated B-lineage ALL cases and strongest in L3. Immunohistochemical typing of acute leukemia is possible for most types using this panel of cell lineage-specific antibodies.
The demonstration of tartrate-resistant acid phosphatase (TRAP) activity has long been a cornerstone in the diagnosis of hairy cell leukemia (HCL). Recently a monoclonal antibody to this enzyme has been developed that can be used in an immunoperoxidase method on paraffin-embedded tissues. By using a peroxidase-labeled streptavidin biotin method, paraffin sections of B5 and formalin-fixed tissue from 86 cases of HCL (41 bone marrow, 36 spleen, 9 liver) were stained with the antibody to TRAP and compared against staining for CD20 (L26) and DBA.44 (DAKO, Carpinteria, Calif). In addition, 193 specimens (127 bone marrow, 42 lymph node, 19 spleen, 5 other) from a variety of neoplastic and nonneoplastic hematologic conditions were stained using the monoclonal antibody to TRAP. For comparison, these cases were also stained with DBA.44. In the cases of HCL, 80 of 86 specimens were immunoreactive for TRAP. While the antibody to TRAP generally stained less than 50% of the hairy cells, CD20 and DBA.44 stained 90% and 50% to 60% of hairy cells, respectively. Two of three cases of marginal zone lymphoma showed weak immunoreactivity to the TRAP antibody. Two specimens from a patient with Gaucher's disease and 8 of 13 cases of mastocytosis also showed positivity to the TRAP antibody in the macrophages and mast cells, respectively. In contrast, staining for DBA.44 was positive in 3 of 9 cases of B-cell large cell lymphoma, 1 of 4 cases of mantle cell lymphoma, and in the paraimmunoblasts of 1 of 7 cases of small lymphocytic lymphoma. Only HCL was TRAP and DBA.44 positive. This antibody to TRAP is a useful addition to the diagnosis of HCL but should be used in conjunction with CD20 and DBA.44. The use of this antibody to determine minimal residual disease after chemotherapy was not addressed.
We conducted a case-control study, using matching on date of birth, sex, and date of diagnosis, in northern Taiwan to evaluate the risks of adult leukemia, brain tumors, and female breast cancers in relation to residential exposure to 60-Hertz (Hz) magnetic fields. Cases were persons with newly diagnosed cancers reported to the cancer registry between 1987 and 1992, and controls were persons with cancers sites other than those previously suspected of being associated with magnetic fields. Magnetic fields in the residences occupied by the study subjects at the time of diagnosis were estimated from high-voltage transmission lines. The results were based on the separate analysis of 870 cases of leukemia, 577 brain tumors, and 1,980 female breast cancers. We estimated the risk of leukemia among those exposed to magnetic fields of > 0.2 microtesla (microT), relative to the risk among those exposed to fields of < 0.1 microT; the odds ratio was 1.4 [95% confidence interval (CI) = 1.0-1.9]. For distance < 50 meters relative to > or = 100 meters, the relative risk was 2.0 (95% CI = 1.4-2.9). For brain tumors and female breast cancers, the odds ratios were close to unity.
OBJECTIVES: To reassess the risk of leukaemia associated with residential exposure near high voltage transmission electric lines of 49 kV and above in view of the recent publications. METHODS: Through a review of papers considering the risk of leukaemia among people living near high voltage transmission lines, the combined risks of leukaemia were calculated for distances < or = 50 m and < or = 25 m and for exposures at 2 mG, 3 mG, 4 mG, and 10 mG. RESULTS: The combined analysis of the contributive studies indicated an estimate of risk (odds ratio (OR)) for exposure > or = 2 mG of 1.3, 95% confidence interval (95%CI) 1.0 to 1.7. The ORs increased with exposures at 3 mG, 4 mG, and 10 mG. The risks were also increased for distances of 50 and 25 m from the lines. CONCLUSIONS: This meta-analysis tends to confirm the presence of an association between exposure to magnetic fields and leukaemia among people who reside in the vicinity of high voltage transmission electric lines of > or = 49 kV. There is consistency across studies. Measures of exposure used in the studies were either distance from the lines or calculated fields estimated from pertinent line features. The results apply to adults as well as to children.
PURPOSE: The International Prognostic Factor Index has been shown to predict the outcome of patients with predominantly B-cell lymphomas classified using traditional classifications, including the Working Formulation, but its prognostic importance has not been tested in a cohort of patients with exclusively T-cell lymphomas. This study was conducted to evaluate the prognostic significance of the International Prognostic Factor Index in patients with peripheral T-cell lymphoma (PTCL). PATIENTS AND METHODS: Seventy-eight patients (48 men and 30 women) with PTCL seen at a single institution between 1985 and 1995 were included in the analysis. The morphology and immunocytochemistry of all the original biopsy specimens were reviewed by a single pathologist and classified using the Revised European-American Lymphoma (REAL) classification. The International Prognostic Factor Index, as well as clinical and biochemical parameters, were evaluated by univariate and multivariate analyses to determine their association with patient outcome. RESULTS: The International Prognostic Factor Index strongly predicted survival when all patients were included in the analysis (P < .001). For patients < or = 60 years, the age-adjusted International Index significantly predicted long-term survival (P = .0218). For patients older than 60 years, the age-adjusted International Index also significantly predicted survival (P = .002). Liver involvement (P = .006) and bone marrow involvement (P = .014) were also significant prognostic factors in the univariate analysis, but only the International Index remained significant in the multivariate analysis (P = .001). CONCLUSION: The International Prognostic Factor Index, which significantly predicts outcome in patients with aggressive/intermediate-grade B-cell lymphomas, has similar prognostic importance in patients with PTCL.
Clinical, electrodiagnostic, and pathologic studies indicate that the Guillain-Barre syndromes (GBSs) include both primary demyelinating and primary axonal forms. The axonal forms are usually thought to have a poorer prognosis, with less chance for rapid or complete recovery. In northern China, epidemics of one axonal form, acute motor axonal neuropathy (AMAN), occur annually in the summer. Autopsy studies in some fatal cases have demonstrated wallerian-like degeneration of motor roots and motor fibers in the peripheral nerves. Recovery of such patients would require axonal regeneration along the entire length of the nerve fiber. In a 2-year prospective study of GBS at a single hospital in northern China, 42 patients were classified as having either AMAN (32 patients), acute inflammatory demyelinating polyneuropathy (AIDP) (8 patients), or as undetermined (2 patients) by electrodiagnostic criteria. Their recoveries were monitored clinically. The recovery times of AMAN and AIDP patients were similar: the median time to regain the ability to walk 5 meters with assistance was 31 days for patients classified as having AMAN and 32 days for those classified as having AIDP. These rapid recovery times are incompatible with severe wallerian degeneration of the ventral roots and motor nerve fibers. The rapid recoveries observed in AMAN patients could be explained by relatively quickly reversible immune-mediated changes at nodes of Ranvier in motor fibers, by degeneration and regeneration of intramuscular motor nerve terminals, or both.
Explore the source record for details and available documents.