Expression of thyroid stimulating hormone β splice variant in thyroid of mouse with autoimmune thyroiditis / 中华地方病学杂志

Objective To investigate the expression of marrow-derived thyroid stimulating hormone β (TSHβ) splice variant in thyroid of mouse with autoimmune thyroiditis induced by thyroglobulin(Tg) immunization,and to analyze whether TSHβ splice variant participated in the pathological process of autoimmune thyroiditis.Methods Using random number table,forty-eight mice(24 females and 24 males) of 7 to 8 weeks old with body mass 20 to 25 g were randomly divided into 4 groups(12 females and 12 males in each group) based on body weight and gender.The control group:fed with deionized water; the Tg-treated group(TG):fed with deionized water,and immunized subcutaneously with 0.1 mg Tg at 8 weeks old,boost immunized twice at 11 and 15 weeks old,respectively; the high iodine-treated group (HI):fed with deionized water containing 0.05％ sodium iodide (NaI); the Tg combined with HI group (TG + HI):fed with deionized water containing 0.05％ NaI,and immunized the same way as the TG group did.Peripheral blood was collected after 8 weeks treatment,which was used for determination of total tetraiodothyronine (TT4),free tetraiothyronine (FT4),total triiodothyronine (TT3) and free triiodothyronine (FT3) with chemiluminescence immunoassay (CIA); thyroid glands were collected to examine the expression of TSHβ splice variant with SYBR Green fluorescent quantitative real-time PCR,and frozen sections were HE stained for observation of histopathological changes of thyroid cells under light microscopy.Results Under naked eyes,the thyroid gland enlarged significantly,and looked dark red in HI and TG + HI groups.Under an optical microscope,thyroid follicular epithelial cells presented cuboidal,with abundant cytoplasm,presented abundant glial in follicular cavity,without lymphocyte infiltration in the control group; in TG group,the thyroid follicular epithelial cells presented cuboidal,with some single scattered lymphocytes; in HI group,colloid volume expansion appeared in thyroid follicles,thyroid follicular epithelial cells presented low cuboidal or flat,with few single scattered lymphocytes; in TG + HI group,most colloid accumulative large follicles presented in thyroid,thyroid follicular epithelial cells presented flat,some destructive thyroid follicular structure and infiltrating lymphocytes appeared.The differences of FT3,TT4,FT4 and TSHβ splice variant between groups were statistically significant(F =4.00,12.54,31.92,214.29,all P ＜ 0.05).Compared to the control group,the serum TT3(nmol/L:0.92 ± 0.07 vs.1.30 ± 0.33,t =-2.24),TT4(nmol/L:1.30 ± 0.33 vs.95.60 ± 14.10,t =-3.02),FT4(pmoL/L:54.07 ± 3.67 vs.154.80 ± 0.01,t =-54.87) and the thyroids' TSHβ(× 10-3:4.11±0.32 vs.8.38 ± 0.22,t =-19.11) were higher in TG group(all P ＜ 0.05) ; the serum TT4(nmol/L:67.75 ± 11.91 vs.45.50± 3.85,t =3.55,P ＜ 0.05) was lower in HI group; the serum FT4(pmol/L:54.07 ± 3.67 vs.139.46 ± 30.00,t =-5.65) and the thyroids' TSHβ splice variant (× 10-3:4.11 ± 0.32 vs.5.33 ± 1.47,t =-5.95) were higher in TG + HI group (all P ＜ 0.05).Conclusions High iodine has aggravated thyroiditis of BALB/c mice induced by Tg immunization; the level of thyroid TSHβ in mice with autoimmune thyroiditis is higher; all of these results indicated that TSHβ is involved in the pathogenesis of autoimmune thyroiditis.

Iodine deficiency up-regulates monocarboxylate transporter 8 expression of mouse thyroid gland / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Iodine deficiency is a major factor affecting thyroid auto-regulation, the quantity of iodine may greatly influence the synthesis of thyroid hormones (THs). It has long been believed that TH enters the cell through passive diffusion. Recent studies have suggested that several transporters could facilitate transportation of TH. The monocarboxylate transporter 8 (MCT8) was identified as a very active and specific TH transporter. The purpose of this study was to investigate whether iodine insufficient affected the expression of MCT8 in the thyroid gland.</p><p><b>METHODS</b>Sixty BALB/c mice were randomly divided into two groups: control group was fed with standard feed (iodine concentration of 300 µg/kg); while low-iodine (LI) group received iodine-insufficient feed (iodine concentration of 20-40 µg/kg). After 3 months, 10 mice of each group were sacrificed. The remaining 20 mice of each group were kept till 6 months. From the LI group, we randomly selected 15 mice and injected triiodothyronine (T3, 100 µg/kg body weight per day) intraperitoneally for 24, 48 or 72 hours (5 mice for each time-point). Then, all the mice were sacrificed. Mouse serum thyroxine (T4), T3, and thyroid-stimulating hormone (TSH) levels were determined by chemiluminescence immunoassay (CIA). The protein content or messenger RNA (mRNA) level of thyroid MCT8 was measured by Western blotting analysis or real time RT-PCR respectively. MCT8 subcellular location in thyroid tissues was probed with immunohistochemistry (IHC) assay.</p><p><b>RESULTS</b>We found that mouse serum T3 and T4 levels decreased and TSH level increased by the end of the third month. Consistent with these findings, there was significant goiter and hypothyroidism in the LI group. Meanwhile, the MCT8 mRNA increased to 1.36-fold of the level in the control group at the 3(rd) month. At 6(th) month, the serum T4 level in LI mice remained at a lower level, and MCT8 mRNA expression continued rising to nearly 1.60-fold compared with the control group. The protein content was also about 3 times higher than that in the control group. IHC results also revealed MCT8 was of higher expression and localized in the cytoplasm of thyroid follicular cells. After providing exogenous T3 to iodine deficient mice, the serum T3 and T4 gradually increased, whereas MCT8 mRNA and protein both started to decrease and returned to the same level as the control group.</p><p><b>CONCLUSION</b>There is a compensatory increase in thyroid MCT8 expression to enhance its capability to transport TH from thyroid to the blood circulation in iodine deficient mice.</p>

Medical Equipment Management and Benefit Analysis / 医疗卫生装备

Objective To investigate the method for benefit management of medical equipment. Methods By analyzing the actuality of equipment management, problems were founded and the solutions were discussed. Results The problems are the repeated purchase of medical equipment, less use in some equipments, dis- accordance among equipment, card and account. Conclusions In hospital, medical equipment play a crucial role in medical affairs, teaching and scientific research, and can bring prominent economic benefit. Enhancing the scientific management in medical equipment, emphasizing the details, procedure and scientific investigation in management can promote the using efficiency, ensure the reasonable match in equipment as much as possible in order to make the hospital sustainable development.