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Y Qin

Publications and source records attributed to Y Qin.

135 records · Page 8Linked to original sources

Somatostatin analogue RC-160 inhibits the growth of transplanted colon cancer in rats.

The effect of somatostatin analogue RC-160 on the growth of DHD/K12 rat colon cancer has been investigated in vivo as well as in vitro. Twenty syngeneic BDIX rats with s.c. implanted tumors were divided randomly into 2 groups. The rats from each group received a daily s.c. injection of either RC-160 (100 micrograms/kg/day) or injection vehicle as control for 37 days starting from the day of tumor inoculation. Tumor volumes were measured every 3-4 days. At the end of the treatment, the mean tumor volume was 504.5 +/- 97.0 mm3 in the control group and 177.8 +/- 60.5 mm3 in the RC-160 treated group (p less than 0.01). The tumor volume doubling time was calculated to be 11 days in the control group and 13.5 days in the RC-160 group, respectively. The tumor growth delay time was 18 days. Using bromodeoxyuridine labelling in vivo, the mean labelling index in the tumors was decreased by 35% (p less than 0.01) after RC-160 treatment. Total protein and total DNA contents in the tumors were decreased by 70.1% (p less than 0.05) and 68.7% (p less than 0.05), respectively. The data indicate that somatostatin analogue RC-160 inhibits the growth of DHD/K12 colon cancer in vivo. In 2 studies in vitro, DHD/K12 cells were cultured for 72 hr with RC-160 and natural somatostatin-14 (S-S-14) at concentrations ranging from 62.5 ng/ml to 2,000 ng/ml. Tumor-cell growth was measured spectrophotometrically by the crystal violet staining assay. No direct effect on tumor cell growth in vitro was observed with either RC-160 or S-S-14, possibly because of the loss of somatostatin receptors in previous passages of the DHD/K12 cell line.

Adenocarcinoma↗

Preproenkephalin messenger RNA-containing neurons in striatum of patients with symptomatic and presymptomatic Huntington's disease: an in situ hybridization study.

Previous studies have revealed a loss of enkephalin immunoreactivity in the terminals of striatal neurons projecting to the external globus pallidus in patients with early grades of Huntington's disease (HD). To assess the status of the perikarya of striatal enkephalinergic neurons, we performed in situ hybridization histochemistry with a radiolabeled RNA probe complementary to preproenkephalin messenger RNA. We studied postmortem brain tissue of 6 patients with symptomatic HD, 7 control subjects, and 2 presymptomatic carriers of the HD allele. There was a significant reduction in the areal density of striatal neurons expressing preproenkephalin messenger RNA in the patients with symptomatic HD, but the level of labeling in the remaining cells was not altered compared with the control subjects. In the specimens from presymptomatic individuals, there was no reduction of areal density of preproenkephalin messenger RNA-containing neurons in the striatum, despite the fact that loss of enkephalin immunoreactivity in the external globus pallidus had been previously demonstrated in the same brains. The results correlate with the previous demonstration of depleted enkephalin immunoreactive terminals in the external globus pallidus in patients with symptomatic HD. They also suggest that the early loss of enkephalin immunoreactivity observed in the external globus pallidus of presymptomatic carriers of the HD allele is not related to a generalized death of striatal enkephalinergic neurons early in the course of the disease.

Adolescent↗

[Determination of hydrocortisone and methylprednisolone in plasma by reversed-phase HPLC].

A sensitive and rapid method for the simultaneous measurement of both hydrocortisone (HC) and methylprednisolone (MP) using dexamethasone (DX) as the internal standard was presented. High-performance liquid chromatograph Model 344 (Beckman, USA) with a 254 nm wavelength UV detector and reversed-phase Ultrasphere ODS (5 microns) column was used. Sample was extracted with ethyl acetate and the organic layer was evaporated to dryness under an air stream in a 37 degrees C water bath. The residue was dissolved in 30 microliters mobile phase and 20 microliters injected. The mobile phase of methanol and 0.01 mol/L acetate buffer (pH 3.0) (64:36) was pumped at 1.0 ml/min through the column. The detector was operated at 0.005 aufs. The retention time for HC, MP and DX was 5.43 min, 7.7 min and 11.5 min, respectively. Standard curve was linear in the concentration range of 0.02 to 1.28 mg/L for HC and 0.05 to 12.8 mg/L for MP. Sensitivity was 1 ng for HC and 1.5 ng for MP; extraction recovery 76-83%; within day CV less than 4%, and inter-day CV less than 6% for both steroids.

Animals↗

Suppression of experimentally induced autoimmune encephalomyelitis by cytolytic T-T cell interactions.

Down-regulatory phenomena have been described in several experimental models of tissue-specific, T-cell-mediated autoimmunity. For example, resistance to active induction of experimental autoimmune encephalomyelitis (EAE) can be induced by pretreating animals with non-pathogenic inocula of autoantigen or effector cells. Moreover, animals that have recovered from one EAE episode are resistant to subsequent induction of EAE. In some models, resistance to EAE has been transferred with immune cells to naive recipients. These experiments, which were based on transfers of unseparated immune cell populations, are difficult to interpret. Immune suppression circuits are known to be complex and involve various distinct cellular subsets. To further complicate the issue, resistance to EAE can be transferred not only by suppressor cells, but also by encephalitogenic effector cells injected in 'subclinical' doses. We describe now the isolation of homogeneous T lymphocyte lines from the spleens of Lewis rats that had recovered from T-cell-mediated EAE (tEAE) caused by the MBP-specific T cell line S1. These spleen-derived T line cells express the CD8 phenotype and specifically respond to determinants on the inducing S1 line, but not to the autoantigen MBP. Furthermore, the anti-S1 cells selectively lyse the encephalitogenic S1 T line in vitro and efficiently neutralize their encephalitogenic capacity in vivo.

Animals↗

Firing characteristics of deep layer neurons in prefrontal cortex in rats performing spatial working memory tasks.

Single cells were recorded with 'tetrodes' in regions of the rat medial prefrontal cortex, including those which are targets of hippocampal afferents, while rats were performing three different behavioral tasks: (i) an eight-arm radial maze, spatial working memory task, (ii) a figure-eight track, delayed spatial alternation task, and (iii) a random food search task in a square chamber. Among 187 recorded units, very few exhibited any evidence of place-specific firing on any of the behavioral tasks, except to the extent that different spatial locations were related to distinct phases of the task. Furthermore, no prefrontal unit showed unambiguous spatially dependent delay activity that might mediate working memory for spatial locations. Rather, the cells exhibited diverse correlates that were generally associated with the behavioral requirements of performing the task. This included firing related to intertrial intervals, onset or end of trials, selection of specific arms on the eight-arm radial maze, delay periods, approach to or departure from goals, and selection of paths on the figure-eight track. Although a small number of cells showed similar behavioral correlates across tasks, the majority of cells showed no consistent correlate when recorded across multiple tasks. Furthermore, some units did not exhibit altered firing patterns in any of the three tasks, while others showed changes in firing that were not consistently related to specific behaviors or task components. These results are in agreement with previous lesion and behavioral studies in rats that suggest a prefrontal cortical role in encoding 'rules' (i.e. structural features) or behavioral sequences within a task but not in encoding allocentric spatial information. Given that the hippocampal projection to this cortical region is capable of undergoing LTP, our data lead to the hypothesis that the role of this projection is not to impose spatial representations upon prefrontal activity, but to provide a mechanism for learning the spatial context in which particular behaviors are appropriate.

Action Potentials↗

Comparison of the classical autoradiographic and the immunohistochemical methods with BrdU for measuring proliferation parameters in colon cancer.

In vivo labelling with bromodeoxyuridine (BrdU) was compared with 3H-thymidine (3HTdR) labelling for the study of cell proliferation in normal colon epithelium and in colon cancer tissue. Twenty-four BDIX rats with implanted subcutaneous tumors of DHD/K12 colon cancer cells were subdivided into 3 groups. Each rat received an intraperitoneal injection of either 5-bromo-2'deoxyuridine (50 mg/kg), or 3H-thymidine (1mCi/kg) or both precursors (double labelling). Immunoperoxidase staining with a monoclonal antibody to BrdU, or autoradiography were used. In the colonic crypts, similar patterns of spatial distributions of the labelled colonic epithelial cells were observed after each kind of labelling. The mean labelling indices (LI) by BrdU and by 3HTdR were similar in the normal colon as well as in the implanted tumors. The validity of BrdU labelling in vivo was further investigated by using BrdU+3HTdR double labelling technique. In the colonic crypts, the total BrdU labelled colonic epithelial cells were 11.85%, whereas the total 3HTdR labelled cells were 11.99% (p > 0.05). In the implanted tumors of colon cancer, the total BrdU and 3HTdR labelled cells accounted for 19.40% and 20.10% respectively of the colon cancer cells (p > 0.05). There was a close correlation between BrdU LI and 3HTdR LI in colonic epithelial cells (r = 0.99, p < 0.0001) as well as in colon cancer cells (r = 0.97, p < 0.001). There data indicate that the labelling index of BrdU is equivalent to that of 3HTdR not only in normal colonic epithelium but also in colon cancer. BrdU may thus be used for measuring proliferation parameters in cancer tissues.

Adenocarcinoma↗