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Biomedical subjects

Y Lin

Publications and source records attributed to Y Lin.

At least 649 records · Page 36Linked to original sources
PubMed1989

Gastric gastrinoma.

Two patients with Zollinger-Ellison Syndrome were diagnosed and treated in PUMC Hospital, the primary tumors were found in the stomach. On sectioning of the gastrectomized specimens, 85 tumors ranging from 0.1 to 1.0 cm in diameter were disclosed in Case 1, and a large ulcero-infiltrative carcinoma-like tumor in Case 2. Both tumors had already metastasized to regional lymph nodes and/or liver. Tumor cells in both cases exhibited gastrin, NSE, GH and hCG alpha immunoreactivity immunocytochemically, and abundant neurosecretory granules of 100-250 nm in diameter under electron microscope. The clinicopathological, immunocytochemical and ultrastructural findings of tumors from these two cases met the criteria of primary malignant gastrinoma of the stomach.

Adult↗
PubMed1989

Study on environmental health strategy after earthquake.

The first task in prevention of diseases after an earthquake is to quickly provide an adequate source of safe drinking water. Otherwise, the incidence of infectious intestinal diseases in the disaster area residents will increase rapidly. Additional health measures, such as disinfecting drinking water, protecting the water source, and treating disaster area residents, must be taken at the same time. The sensory test of meat is a useful index of meat decomposition levels. Corpse alkali is a kind of toxic chemical, and personal protective measures must be taken in handling corpses. In general, all of these measures are important not only for achieving the goal of "no severe epidemic after strong earthquake disaster" in the affected areas, but also for enriching knowledge of disaster medicine.

Cadaver↗
PubMed1989

[A case report of sacral chordoma].

Sacrococcygeal chordoma is one of the retrorectal tumors. Relative rarity and anatomical location of this may lead to difficulty in diagnosis and surgical treatment. We report a case of sacrococcygeal chordoma successfully treated by high sacral resection by a posterior approach, in which the co-operative efforts of gastroenterological surgeons and an orthopedic surgeon were employed. A 64-year-old man with a long term continued vague anal pain was referred to our hospital. Digital rectal examination revealed an elastic hard mass presacrally. Plain sagittal radiograph, CT, barium enema showed a retrorectal mass and sacral destruction. Diagnosis was confirmed histologically by the specimen taken by open biopsy. Surgical resection was carried out in prone position with the buttocks elevated. The skin incision was upward arched transverse. The lower sacral vertebrae, including S3, were removed en block with the tumor. Bilateral S3 sacral nerve roots were preserved. Postoperative disturbances of the urination and defecation were not seen. High dose radiation therapy, 80 Gray, was done after surgery. Radiation ulcer of the skin was treated by free skin graft, but radiation proctocolitis was not seen. Now he is free from the disease.

Biopsy↗
PubMed1989

Natural cytotoxic activity is not necessarily mediated by the release of tumour necrosis factor.

Natural cell-mediated cytotoxicity is mediated by a family of effector cells that express cytolytic activities distinct from those generally attributed to B cells, T cells and macrophages; it includes both natural killer (NK) and natural cytotoxic (NC) activities. There is now convincing evidence to show that NC activity, but not NK activity, is mediated by tumour necrosis factor (TNF). Further, it has been argued that it is the release of TNF, as a freely diffusible factor, that causes NC-mediated target lysis. Here, we present evidence that the admixture of NC-sensitive target cells and spleen cells, under conditions that result in NC-mediated target cell lysis, does not necessarily result in the release of freely diffusible TNF into the culture medium. Also, it is demonstrated that the procedures used do not result in inactivation or loss of significant amounts of TNF during the assay period, which might account for our failure to detect free TNF. These results suggest that NC activity is mediated by either a membrane-associated TNF activity, similar to that described for some of the lytic activity of activated macrophages, or by the release of TNF that is capable of acting only over a very short distance.

Animals↗
PubMed1989

[Electrophysiological study on the atrophied pectoralis major muscle after modified radical mastectomy].

In order to clarify the cause of the atrophy of the pectoral muscles after modified radical mastectomy, twenty patients who had had the operation at Nagasaki Chuo National Hospital 40 days to 2 years prior to this study, were investigated by electromyography. Of 20 subjects, 11 had the operation to preserve the pectoralis major muscle and 9 had the operation to preserve both the pectoralis major and minor muscles. The results were as follows: 1) Electromyography revealed some damages to the pectoral nerves in 16 cases of 20 (80%). In 12 cases, development of fibrillation potentials was observed at rest, while motor unit potentials disappeared during voluntary contraction. These findings suggest the damage to the nerves including neutrotomy. 2) The regions with macroscopic muscular atrophy remarkably coincided with those with neurogenic changes on electromyography. This suggests that the atrophy of the pectoralis major after modified radical mastectomy might be mainly caused by the damage to the pectoral nerves. 3) The mastectomy preserving only the pectoralis major tends to cause damage to nerves innervating the sternocostal part of the pectoralis major more frequently than the mastectomy preserving both the pectoralis major and minor muscles. The abdominal part was frequently damaged irrespective of the types of the operation.

Action Potentials↗
PubMed1988

The construction and characterization of a biologically active recombinant IL-2 containing a lysine-rich C-terminal extension.

A polylysine extended gibbon IL-2 (IL-2-L) was constructed by the addition of a lysine-rich oligopeptide, Gly3-(Lys-Lys-Asp)3-Leu-Glu to the C terminus of gibbon IL-2 by using rDNA technology. The bioactivity of the hybrid molecule was comparable to that of normal human rIL-2 in assays measuring T cell proliferation, and in generation of lymphokine-activated killer cells from PBL. Furthermore, the addition of the lysine-rich segment made the molecule more amenable to the chemical derivatization of amino groups. After biotinylation, IL-2-L retained a greater proportion of its bioactivity than normal rIL-2. In addition, biotinylated IL-2-L was capable of simultaneously binding to cell surface IL-2R and streptavidin. Thus, the addition of the lysine-rich oligopeptide facilitated the generation of an active form of biotinylated IL-2 which acts as a bridge between IL-2R-positive cells and avidin-coupled reagents and affinity supports. Such a selective means of labeling and binding IL-2-responsive cells may have great practical utility for IL-2-based immunotherapy.

Amino Acid Sequence↗
PubMed1988

Glutathione monoethyl ester can selectively protect liver from high dose BCNU or cyclophosphamide.

Normal Swiss Webster mice were treated with monocrotaline or high doses of three antitumor alkylating agents (BCNU, cyclophosphamide, or mitomycin C), all of which have been connected with hepatic veno-occlusive disease at our clinic. Prior administration of WR-2721 did not improve the survival of monocrotaline-treated animals. Glutathione (GSH) improved the survival of these animals to a small degree. Glutathione monoethyl ester (GSHet) almost completely protected animals from the toxicity of monocrotaline. Pretreatment with WR-2721 produced moderate increases in survival at the highest doses of BCNU, and at the lower BCNU doses none of the animals pretreated with WR-2721 died before they were killed on day 150. Pretreatment with GSHet gave good protection from BCNU toxicity at the highest dose of the drug, and there were no deaths in the groups of animals treated with GSHet 1 hour before BCNU. On a multiple dose schedule, GSH provided some protection from cyclophosphamide toxicity; GSHet gave a very good level of protection from cyclophosphamide. In none of these treatment groups were lesions suggestive of hepatic or pulmonary venoocclusive disease identified. In all three experimental protocols (monocrotaline, BCNU, and cyclophosphamide), there was a consistent decrease in hepatic toxicity after GSHet pretreatment; this was not observed in GSH- or WR-2721-pretreated animals. There was no evidence of protection of the FSaIIC fibrosarcoma growing in C3H mice as assayed by tumor growth delay or tumor cell survival in groups treated with two different doses of GSHet 1 hour before each drug injection compared to those treated with the BCNU or cyclophosphamide alone, or BCNU with cyclophosphamide. Pretreatment with GSHet did not alter the toxicity of these drugs to bone marrow. GSHet appears to be an effective protector of critical normal tissue and does not appear to protect tumor.

Amifostine↗
PubMed1988

Characterization of murine IL-1 beta. Isolation, expression, and purification.

One cDNA clone encoding a truncated murine IL-1 beta (M IL-1 beta) sequence was isolated from a murine macrophage cDNA library. We reconstituted the coding sequence of the 152-residue mature protein and expressed it in Escherichia coli. rM IL-1 beta was purified to homogeneity and characterized by oligonucleotide and NH2-terminal sequence analysis. Purified rM IL-1 beta exhibited biologic activity equivalent to 7.8 x 10(7) units/mg in the murine thymocyte proliferation assay and 9.9 x 10(3) units/mg in the human gingival fibroblast PGE2 production assay, indicative of species specificity. The isoelectric point of rM IL-1 was found to be 8.85. The circular dichroism spectrum revealed that the secondary structure of M IL-1 is indistinguishable from that of the human protein. Receptor binding studies indicated the rM IL-1 bound to murine EL-4.1 thymoma cells in a specific and dose-dependent fashion with an affinity of 32 pM. Competition binding data suggested that murine and human IL-1 compete for a single class of receptor. Antisera were generated in rabbits against both murine and human IL-1. Results of ELISA binding and antisera neutralization assays indicated that there are common antigenic sites between the two IL-1 beta molecules. These domains are of functional importance because they are capable of mediating the neutralization of biologic activity.

Amino Acid Sequence↗
PubMed1988

Effect of mycoplasmas on natural cytotoxic activity and release of tumor necrosis factor alpha by spleen cells.

It has been reported that mycoplasma-infected cells are more sensitive to lysis by natural cytotoxic (NC) effector cells and that splenic NC cells release tumor necrosis factor (TNF-alpha) when they lyse sensitive target cells. Here we showed that spleen cells released TNF-alpha when they were incubated with NC-sensitive cells that were infected with mycoplasmas or when they were incubated with mycoplasmas alone, but did not release TNF-alpha when incubated with NC-sensitive cells that were not infected with mycoplasmas. Thus, in the presence of mycoplasmas, spleen cell cultures contain both NC effector cells and free TNF-alpha. Because NC-sensitive cells are also sensitive to free TNF-alpha, when mycoplasma-infected cells were incubated with spleen cells, they were lysed by the combination of NC cells and free TNF-alpha. When NC-sensitive cells that were not infected with mycoplasmas were incubated with spleen cells, they were lysed only by NC effector cells and thus appeared to be less sensitive than mycoplasma-infected cells. These results also suggested that the release of TNF-alpha may be part of a host protective response to mycoplasmas.

Animals↗
PubMed1988

Inhibition of tumour necrosis factor and natural cytotoxic cell lytic activities by a spleen cell-elaborated factor.

Natural cytotoxic (NC) cell lytic activity is mediated by tumour necrosis factor (TNF), a protein with potent cytolytic activity on certain target cells. TNF also appears to mediate a wide range of other important biological activities (e.g. interferon-like anti-viral activity, induction of granulocyte-monocyte colony-stimulating factor, mediation of endotoxin-induced shock). Evidence is presented here that spleen cells from normal, untreated mice produce a factor(s) that inhibits both NC and TNF cytolytic activity. The factor(s) has a molecular weight greater than 10,000. Since indomethacin inhibits production by spleen cells of the NC/TNF inhibitory factor, it is suggested that prostaglandins are involved in the regulation of its production. Additionally, these studies indicate that the factor(s) does not function by inactivation of either NC effectors or TNF molecules, or by inhibition of the binding of NC cells or TNF to targets. Instead, the data suggest that the factor(s) acts on the targets rendering them refractory to TNF binding. Moreover, since the factor(s) acts slowly and requires protein synthesis in the target to function, it appears that the inhibitory activity is mediated via de novo-synthesized proteins from the target cells. At present, it is not known whether such a factor functions in vivo, although it is conceivable that its in vivo role is to modulate the pathological potential of TNF by protecting certain cells from NC or TNF lysis.

Animals↗
PubMed1988

[A case report of the effective arterial infusion for advanced recurrence breast cancer with 5-FU, ADM, CDDP and OK-432].

A 42-year-old female visited our hospital because of left breast tumor and left arm swelling with severe pain. She had had right radical mastectomy and bilateral oophorectomy at 27 and 29 years of age, respectively. On admission, she had a hard mass, which seemed to be a severe invasion of the chest wall, on her left breast with a severe nipple ulcer. We inserted a catheter operatively through the thyrocervical truncus to the subclavian artery for the arterial infusion therapy. She was administered 250 mg of 5-FU daily, and 10 mg of ADM, 10 mg of CDDP, 10 KE of OK-432, every other week. During 70 days, 10,000 mg of 5-FU, 50 mg of ADM, 50 mg of CDDP and 50 KE of OK-432 were administered. As soon as the breast tumor became smaller, showed some mobility and the nipple ulcer healed, we carried out left mastectomy and axillary lymph node dissection. Pathological findings showed severe degeneration and necrosis of cancer cells. Lymphocytes surrounded necrotic tissue, and there was a follicular pattern of invasion. This phenomenon was considered to result from the promotion of cellular immunological reaction by OK-432.

Adult↗
PubMed1987

Natural cytotoxic cells and tumor necrosis factor activate similar lytic mechanisms.

The lytic activity of natural cytotoxic (NC) cells has several characteristics which clearly distinguish it from other cell-mediated lytic activities and from most soluble cytolytic factors. An exception is the lytic activity mediated by tumor necrosis factor (TNF). In this paper, we report a detailed comparison of NC and TNF lysis of target cells which are used as prototype NC targets or TNF targets, and show that the two cytolytic activities have very similar, if not identical, lytic mechanisms. We present data showing that target cells which are NC-sensitive are also TNF-sensitive and that target cells which are NC-resistant are also TNF-resistant. Moreover, cells selected either in vivo or in vitro for NC resistance are selected for TNF resistance, and cells selected for TNF resistance are selected for NC resistance. The analysis of the kinetics of 51Cr release mediated by NC cells or by TNF show that both activities affect similar kinetics, in that there is no cell lysis for several hours after targets and effectors first interact. However, NC and TNF lytic activities can be distinguished. By using the cell lines 10ME or B/C-N as targets, it can be shown that whereas NC-mediated lysis is dependent on protein synthesis, TNF-mediated lysis is not. We also show that targets which are resistant to NC-mediated lysis because they express a protein synthesis-dependent resistance mechanism also require protein synthesis to resist TNF-mediated lysis, suggesting that the same resistance mechanism protects cells against both NC cells and TNF. Together, these data strongly support the hypothesis that NC cells and TNF activate the same lytic mechanism within target cells and that TNF may mediate the lytic activity of NC effector cells.

Animals↗
PubMed1987

Analysis of demand conditions associated with stereotypy.

Possible escape/avoidance functions of stereotypic behavior were investigated in a classroom setting using functional academic tasks. A 6-year-old boy's stereotypic mouthing was assessed during high vs low response activities, familiar vs novel activities and avoidance vs partial-avoidance conditions. Results showed that stereotypy occurred at higher rates during more difficult activities (i.e. those that were novel or required a greater number of responses), and when stereotypy was allowed to effect a delay in instructional demands. Treatment procedures based on these analyses were implemented by the classroom teacher and shown to be effective.

Avoidance Learning↗
PubMed1987

Transcriptional activity of the gibbon ape leukemia virus in the interleukin 2 gene of MLA 144 cells.

The gibbon ape leukemia virus (GALV)-infected T-cell line, MLA 144, constitutively makes the lymphokine, interleukin 2 (IL 2), without stimulation by antigen or mitogen. This line contains two GALV insertions in the IL-2 gene: one in the 3' untranslated region of the gene and one 1200 bp 5' to the gene. It is likely that one or both of these viral insertions is(are) involved in activation of IL-2 expression. We investigated the ability of sequences within the LTR of MLA 144 cells (GALV-MLA) to act as transcriptional elements and have demonstrated here the presence of cis-acting sequences in the GALV LTR capable of enhancing transcription of the GALV promoter as well as two heterologous promoters, SV40 early and IL-2. The results indicate that insertion of the enhancer element(s) alone is not sufficient to activate IL-2 expression but can enhance levels of IL-2 expressed from the activated gene.

Animals↗