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Z Chen

Publications and source records attributed to Z Chen.

At least 1,621 records · Page 90Linked to original sources

Effect of strychnine on the cutaneous responsiveness of wide-field cerebral neurons after depression by pentobarbital.

A small dose of pentobarbital administered intravenously to a chloralose-anesthetized cat rendered pericruciate wide-field neurons unresponsive to cutaneous stimulation without altering the responsiveness of small-field neurons. Under this condition, topical application of strychnine, which is known to markedly enhance the responses of small-field neurons, was found to restore the responsiveness of the wide-field neurons, but only to stimulation of the topographically focal cutaneous site. Wide-field responsiveness returned only after the effect of pentobarbital had disappeared and the cortex returned to its normal chloralose condition. This result is consistent with the idea that small-field neurons have excitatory synaptic connections with the wide-field neurons in their immediate neighborhood.

Animals↗

Gm allotypes in blacks with systemic lupus erythematosus.

Serum samples were collected from 328 healthy American Blacks and from 61 American Blacks with systemic lupus erythematosus (SLE). Sera were typed for the Gm1,2,3,5,6,13,17, and 21 allotypes as well as for the Km(1) allotype. The frequency of Gm phenotype 1,17;5,6,13 was significantly increased in the SLE patients (p = 0.0001, RR = 3.19, EF = 0.29). Our data suggest the existence of at least two immunoglobulin allotype associated genes that somehow interact to increase susceptibility to SLE in Blacks. To our knowledge, this is the first report of an association of Gm and SLE in Blacks.

Black People↗

The in vitro synthesis and degradation of prostaglandins during the development of bleomycin-induced pulmonary fibrosis in hamsters.

Subsequent to optimization of conditions for enzyme assay, we examined the in vitro synthesis and degradation of prostaglandins by the lung during the development of bleomycin-induced pulmonary fibrosis in hamsters. It was found that the microsomal protein content on a per lung basis was significantly increased to 144, 129, 134, and 121% of control (2.3 mg protein/lung) at 4, 7, 14 and 21 days post-treatment, respectively. The synthesis of PGD2 was significantly elevated to 10.2, 10.8, and 12.5 nmoles/lung at 7, 21 and 28 days, respectively, as compared to the control value of 5.6 nmoles/lung. Significant increases in PGF2 alpha synthesis from the control value of 3.3 nmoles/lung to 5.2, 8.2 and 5.5 nmoles/lung were found at 4, 7 and 21 days post-treatment, respectively. The synthesis of PGE2 also showed significant increases above the control value of 6.1 nmoles/lung to 10.5, 12.2 and 11.0 nmoles/lung at 7, 21 and 28 days post-treatment, respectively. Similarly, the synthesis of 6-keto-PGF1 alpha was significantly increased to 7.4, 7.5 and 8.6 nmoles/lung at 7, 21 and 28 days post-treatment, respectively, as compared to the control value of 4.4 nmoles/lung. The synthesis of TxB2 was also significantly increased from the control value of 3.9 nmoles/lung to 7.5 and 6.4 nmoles/lung at 7 and 21 days post-treatment, respectively. Accompanying the increased synthesis of prostaglandins in general, the in vitro degradation of PGF2 alpha was significantly increased from the control value of 71.1 nmoles/lung to 173.5, 131.7 and 143.3 nmoles/lung at 2, 4 and 7 days after bleomycin treatment, respectively. We conclude that bleomycin-induced pulmonary fibrosis leads to changes in prostaglandin synthesis and degradation possibly as a result of an accompanying inflammatory response and resident cellular proliferation.

6-Ketoprostaglandin F1 alpha↗

Erythroleukemia cells: variants inducible for hemoglobin synthesis without commitment to terminal cell division.

Murine erythroleukemia cells (MELC) are virus-transformed erythroid precursors that appear to be blocked at an erythroid precursor stage comparable to the erythroid colony-forming unit (CFU-e). These cells are useful in examining factors regulating terminal differentiation. Induced MELC are characterized by a coordinated program of gene expression, including commitment to terminal cell division, accumulation of globin mRNAs and corresponding hemoglobins, and accumulation of several other proteins, including the chromatin-associated protein H1(0). Two cloned variant cell lines, DR10 and R1, have been developed from inducer-sensitive DS19 cells by selection for inducer resistance. DR10 and R1 cells fail to display commitment to terminal cell division when cultured with dimethyl sulfoxide (Me2SO), hexamethylene bisacetamide (HMBA), or butyric acid. Both cell lines are induced by all three agents to accumulate H1(0). DR10 cells are resistant to Me2SO-mediated accumulation of hemoglobin but are sensitive to HMBA- or butyric acid-mediated accumulation. R1 cells are resistant to Me2SO- and HMBA-mediated accumulation of hemoglobin but are sensitive to butyric acid-mediated accumulation. Both DR10 and R1 are commitment-negative MELC variants, displaying variable responses to inducers with respect to other features of terminal erythroid cell differentiation.

Acetamides↗

Further evidence for T cell abnormalities in chronic lymphocytic leukaemia of the B cell type.

Functional properties were studied in the purified T cell fraction of patients with chronic lymphocytic leukaemia of the B cell type (B-CLL). This analysis included the evaluation of T suppressor activity when investigated patients' T cells were co-cultured together with allogenic normal B and OKT4 enriched T cells in the presence of pokeweed mitogen (PWM). The Ig secreting cells (ISC) were assessed in a reverse haemolytic plaque assay (RHPA). Antibody-dependent cytotoxicity (ADCC) and natural killer activity (NK) were determined in a 51Cr release assay. Furthermore, purified T cells reactive with the monoclonal antibody HNK1, known to recognize most effector cells in ADCC and NK, were enumerated using an indirect immunofluorescence. Our results revealed increased T suppressor cell activity and markedly deficient NK activity in peripheral blood lymphocytes (PBL), T cell and T gamma cell fractions from B-CLL patients, whereas ADCC potential was only increased in T cells and T gamma cells. Accordingly, T cells were recognized by HNK1 in greater numbers in B-CLL patients than in healthy subjects. Our data suggest that there may be a link between our findings and the hypogammaglobulinaemia as well as the increased incidence of second neoplasias reported in CLL.

Aged↗

Inducer-mediated commitment of murine erythroleukemia cells to differentiation: a multistep process.

There are a number of agents which, when added to cultures of murine erythroleukemia cells (MELC), markedly increase the probability of commitment to express the characteristics of terminal erythroid differentiation, including loss of proliferative capacity and increased accumulation of globin mRNA and hemoglobin. Some characteristics of inducer-mediated commitment of MELC to terminal erythroid differentiation were examined by determining the effects of dexamethasone (an inhibitor of inducer-mediated MELC differentiation) and of hemin (an inducer of globin mRNA accumulation). Previously, it was shown that exposure of MELC to hexamethylene-bisacetamide (HMBA) leads to commitment, detectable within 12 hr. MELC cultured with both HMBA and dexamethasone do not express commitment. MELC transferred from culture with HMBA and dexamethasone to cloning medium without these agents express commitment to terminal erythroid differentiation, indicating that MELC retain a "memory" for some early HMBA-mediated changes leading to commitment which occur even in the presence of the inhibitory steroid. The kinetics of commitment in experiments in which exposure to HMBA is interrupted, or dexamethasone is added to the culture in HMBA, suggest that there is a rate-limiting step early in the commitment process. The memory for this step persists for more than one cell cycle. Addition of hemin to cultures with HMBA and dexamethasone initiated accumulation of globin mRNA but does not reverse the steroid-mediated inhibition of terminal cell division (that is, the cells retain their proliferative capacity). Inducer-mediated MELC commitment is associated with accumulation of the chromatin protein IP25; dexamethasone does not inhibit this accumulation. Accumulation of IP25 may be inducer-related, but it is not sufficient to cause expression of terminal erythroid differentiation.

Acetamides↗