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J Z Yin

Publications and source records attributed to J Z Yin.

7 recordsLinked to original sources

[Estrogen secretion and cellular source of ovarian epithelial tumors].

This paper studies the estrogen secretion of ovarian epithelial tumors in postmenopausal women by using the radioimmunoassay method to measure the concentration of estradiol (E2) in peripheral and ovarian venous blood, using the immunohistochemical method (ABC) to locate the cell position of E2 in tumor tissue, and observing the clinical symptoms of the patients. The results demonstrated that epithelial ovarian tumors in postmenopausal women can secret E2 and the secretory function of mucinous tumor is most active in epithelial ovarian tumors; the E2 produced by the tumors is not only from the stromal cells of the tumors, but mainly from the epithelial cells of the tumors. The secretory function of E2 is usually manifested in "the subclinical condition", but sometimes it may show clinical symptoms. So, epithelial ovarian tumors should be considered when women have the symptom of postmenopausal uterine bleeding.

Adenocarcinoma, Mucinous↗

Microvascular decompression for trigeminal neuralgia.

Of 42 patients undergoing a microvascular decompression for trigeminal neuralgia with a follow-up of 4 to 7 years, 32 (76.19%) had no postoperative recurrence of neuralgic pain, 4 (9.52%) had a minor recurrence and 6 (14.29%) had a major recurrence. It was considered that the neuralgic recurrence might be due to some possibly missed pathogenic vessel during operation or a new compression of the trigeminal nerve root occurring after operation.

Adult↗

[Evaluation of long-term results of vidian neurectomy in the treatment of perennial rhinitis].

Vidian neurectomies by transnasal and transseptal approaches were performed on 21 patients with perennial rhinitis and with a follow-up of 5 years. The results showed that sneezing and watery rhinorrhea relapsed in 85.7% of the operated series and 66.7 per cent in one year after operation. The causes of recurrence were discussed and analysed. We consider that symptoms of sneezing and watery rhinorrhea are induced by a series of factors so that the efficacy of single vidian neurectomy needs further evaluation.

Adult↗

Effect of various adjuvants on the antibody response of mice to pneumococcal polysaccharides.

Adjuvant effects on the serum antibody response to pneumococcal polysaccharide (pps) types 3 and 14 were studied in BALB/c mice. First, dose responses were established for the two pps types and were found to be entirely different. High (5 micrograms) and low (0.005 microgram) doses of pps 3 induced antigen-specific unresponsiveness and suppression, while 0.1 microgram induced an optimal response. The secondary response to a single dose of killed pneumococci or 0.1 microgram of pps 3 injected 2 weeks later was not higher than the primary response. Nu/Nu, athymic BALB/c mice showed high but not low dose tolerance to pps 3. In contrast, no convincing evidence for high dose tolerance to pps 14 was obtained: 25 micrograms of pps 14 induced an optimal response, whereas 0.2-0.5 microgram induced antigen-specific suppression. Secondary anti-pps 14 IgM and IgG responses, even after optimal primary doses, were only slightly higher than primary responses to a single dose of killed bacteria. Athymic BALB/c mice showed lower IgG antibody responses than euthymic mice to pps 14. Injection of detoxified endotoxin (D-LPS) 2-4 days after antigen enhanced both primary and secondary responses and reversed high dose tolerance induction. Injection of D-LPS also at least partially prevented the induction of low dose tolerance as did injection of interleukin-1, but normuramyl dipeptide (nor-MDP) failed to affect the responses to pps 3 and 14. Coupling of muramyl tripeptide to pps 3 rendered the pps more immunogenic. Administration of emulsified pps in squalene arlacel, particularly with nor-MDP incorporated in the mixture, appeared to induce a better 7S antibody response than did pps in saline, but these serum antibody levels were not sustained at a high level. Pretreatment with IgD or simultaneous injection of IgD with pps 14 enhanced both primary and secondary responses. The response to pps 3 was only slightly enhanced and low dose tolerance was not prevented by pretreatment with IgD.

Acetylmuramyl-Alanyl-Isoglutamine↗

Prevention by a platelet-derived factor (platelet factor 4) of induction of low dose tolerance to pneumococcal polysaccharides.

It was previously shown that human or mouse serum, and platelet factor 4 (PF4) prepared from human platelet releasate, counteracts nonspecific immunosuppression induced in mice by injection of concanavalin A or syngeneic gamma-irradiated lymphoma cells. The present studies show that PF4 prepared from normal mouse or human serum by absorption to heparin-agarose and elution between 0.5 and 1.5 M NaCl is also active in this respect. The ability of PF4 to counteract antigen-specific suppression of the antibody response to pneumococcal polysaccharide (pps) was now studied. PF4 derived from human or mouse serum as well as recombinant PF4 interferes with induction of antigen-specific low dose tolerance when they are injected at the same time as a low dose (0.2 microgram) of type 14 pps 3 days before an optimal immunizing dose (25 micrograms). Furthermore, injection of platelet releasate at the time of an optimal primary immunizing dose of pps type 14 enhances the secondary response to killed bacteria injected 2 weeks later, but not the primary response itself. Both effects are interpreted as due to interference with antigen-specific suppressor cell induction during primary immunization. Injection of PF4 is much less effective in reversing low dose tolerance to an optimal immunizing dose (0.1 microgram) of type 3 pps induced by injection of 0.005 microgram of this antigen. Differences in the mechanism of tolerance induction for the two pps types that might be responsible for this are discussed.

Animals↗

Studies on immunity in hybridoma-bearing mice. A. Immune response to antigens. II. inhibition of production of anti-dinitrophenyl antibodies in mice which have rejected the B 53 anti-dinitrophenyl-producing IgE hybridoma.

When BALB/c mice, which had rejected the anti-dinitrophenyl (DNP) IgE-producing hybridoma B 53, were immunized with DNP proteins, they produced much less anti-DNP antibodies than control (normal) mice. The anti-DNP plaque-forming cell (PFC) number was much less when spleen cells from mice immunized with DNP proteins were treated with sera of mice which had rejected the hybridoma B 53 than the PFC number from the same spleen cells not treated by the sera. The sera of mice which had rejected the hybridoma B 53 contained an inhibitor which was adsorbed and eluted from an anti-mouse immunoglobulin column and also a mouse anti-DNP IgG2a column. The inhibition of PFC was hapten-reversible. In Western blotting the eluates from the anti-DNP IgG2a column reacted as well with the blotted anti-DNP IgE B 53 as an anti-idiotypic antibody to anti-DNP IgE B 53. These criteria establish that the inhibitor in the sera of the mice which had rejected the B 53 tumor was an anti-idiotypic antibody of the type which mimics the epitope (DNP) of the immunizing antigen.

Animals↗

Protease-induced immunoregulatory activity of platelet factor 4.

Intravenous injection of human or mouse serum or platelet material secreted from appropriately stimulated platelets ("releasate") together with antigen alleviates the immunosuppression in SJL/J mice induced by injection of irradiated lymphoma cells or in (CB6)F1 mice induced by injection of concanavalin A. We now report that injection of releasate from 10(6) human platelets restores plaque-forming cells to the unsuppressed number; greater amounts increase responses further. Immunoregulatory activity is released from platelets exposed to thrombin in parallel with other alpha-granule components. Heparin-agarose absorbs activity. Purified platelet factor 4 (PF4) has activity; beta-thromboglobulin and platelet-derived growth factor have little or none. Activity in serum is neutralized by goat anti-human PF4. An enzymatic step is necessary for production of immunoregulatory activity. Releasates boiled immediately after platelet aggregation with 250 nM A23187 or those produced by adding A23187 in the presence of 100 microM serine protease inhibitor (p-amidinophenyl)methanesulfonyl fluoride (APMSF) are ineffective, whereas releasates boiled or mixed with APMSF after incubation for 60 min are active. Activity is generated by incubating a mixture of heparin-absorbed releasate (as enzyme source) and heparin-agarose eluate of releasate made in the presence of APMSF (as substrate source). The enzymatic step does not alter the heparin-neutralizing activity of PF4. Apparently a secreted platelet protease converts PF4 to a form with immunoregulatory activity.

Animals↗