Objective To explore the changes of the total antioxigenic capacity (T-AOC) of the plasma and red blood cells (RBC) in the acute pulmonary edema rats induced by acute formaldehyde inhalation. Methods SD rats were randomly dived into the formaldehyde group and control group, then were exposed to formaldehyde and physical saline vapor respectively in a chamber for 2 hours, the actions and vital signs were observed. After treatment the rats were taken out the chamber, 5 hours later, the T-AOC of the red blood cells and plasma were measured and the body, lungs and heart were weighted, the lung /heart weight index and lungs/body weight index were calculated, the pathological examination was done. Results Compare with the control group, the lung weight, lung/body weight index, lung /heart weight index and the T-AOC of the plasma increased, the T-AOC of RBC and body weight decreased significantly(P

Background and purpose:Thyroglobulin antibody (TgAb) is often positive in papillary thyroid carcinoma (PTC) patients. This study aimed to investigate the effect of TgAb on radioiodine ablation efficacy in PTC patients.Methods:A total number of 329 PTC patients with no distant metastasis were included and classified into 2 groups[G1 group (>115 U/mL,n=84) and G2 group (<115 U/mL,n=245)], G2 group was further divided into 2 subgroups[S1 (>40 U/mL,n=31) and S2 (<40 U/mL,n=214)], before131I ablation. The median follow-up time was 24 months after a total or subtotal thyroidectomy and subsequent131I ablation. The efficacy in terms of131I ablation success rates (IBR) between two groups were compared and the influencing factors were analyzed according to criteria posed by 2015 American Thyroid Association Guidelines, then the effect of131I dose on IBR was also explored.Results:Female and younger age were more prevalent in patients with high TgAb (P<0.05). The G1 group presented lower IBR over the G2 group (35.7%vs 72.7%,P=0.000). Moreover, S1 group also presented lower IBR over S2 group (54.8%vs 75.2%,P=0.017), indicating the adverse effect from high titer TgAb on IBR. No matter high or low dose, the G1 group presented lower IBR (34.1%vs 71.9%, 37.2%vs 73.2%;P=0.000). However, IBR did not differ in G1 or G2 group either with high or low dose131I (P>0.05). TgAb was the only adverse indicator correlating with IBR in multi-logistic regression analysis (P=0.018).Conclusion:TgAb could negatively affect131I ablation efficacy, while increasing the dose of131I failed to improve the success rate in such cases.

131 I-metabolizing genes are markers for differentiation of thyroid carcinoma.The loss or down-regulation of these genes represents progression of dedifferentiation,which results in low 131 I uptake and suggests a poor prognosis.The mechanism of dedifferentiation of DTC is important for treatment.This article reviews the mechanism of dedifferentiation from 131I radiation damage,gene mutation,tumor markers and protein.

During 131Ⅰ therapy or the natural course of DTC,2％ to 5％ of them will gradually no longer be sensitive to 131Ⅰ therapy and lead to radioactive iodine-refractory DTC (RAIR-DTC).Recent studies found that alterations of critical molecular targets in main signal transduction pathways could decrease the iodine-trapping function of thyroid carcinoma,such as BRAFV600E mutation,followed by negative 131 Ⅰ-whole body scan (WBS) and discounted efficacy.This article reviews novel diagnostic and therapeutic modalities for RAIR-DTC.

Atrioventricular Block ; complications ; Child ; Electromyography ; instrumentation ; methods ; Female ; Histiocytic Necrotizing Lymphadenitis ; complications ; Humans ; Research Report ; Thrombocytopenia ; complications

Background and purpose: Neck lymph node metastasis, most of which presents in central neck compartment, is common in patients with papillary thyroid carcinoma (PTC). The objective of this study was to investigate the relationship between the number of dissected central neck lymph nodes and clinical outcome after radioactive iodine (RAI) ablation in pN1a PTC with no more than 5 lymph nodes involvement. Methods: A total of 167 PTC patients who had 1-5 proven metastatic lymph nodes according to postoperative pathological diagnosis were retrospectively analyzed, all of whom underwent total or near total thyroidectomy and central lymph node dissection. After a median follow-up period of 26 months, the clinical outcome of each patient was evaluated as excellent response (ER), indeterminate response (IDR), bio-chemical incomplete response (BIR), or structural incomplete response (SIR) according to the new American Thyroid As-sociation guidelines. The accumulative ER rate (ERn) was calculated in patients with different numbers of dissected lymph nodes (ERn was defined as the proportion of patients who achieved ER with the dissected lymph node number of ≤n). The relationship between the number of dissected central neck lymph nodes and ERn were investigated. Results: As the increase in the number of dissected central neck lymph nodes,there was also an overall increase in ERn, especially when n rose from 1 to 10. The values of ER1, ER5, ER10 and ER30 were 25.0%, 66.7%, 74.7% and 79.1%, respectively. Besides, the proportion of patients who achieved ER was higher in those with 10 or more dissected lymph nodes than in those with less than 10 (85.7% vs 73.3%, P=0.05). In the multivariate logistic regression analysis, both the dissected central lymph node number of ≥10 (OR=2.720, 95%CI: 1.052-7.033, P=0.039) and the level of preablation stimulated thyroglobulin (OR=0.955, 95%CI: 0.926-0.984, P=0.003) were shown to contribute independently to ER. Conclusion: As the increas-ing number of dissected central neck lymph nodes, the percentage of pN1a PTC patients that achieved ER after RAI ablation generally rises. In pN1a PTC patients with no more than 5 lymph nodes involvement, a central compartment dissection with 10 or more lymph nodes might help them achieve ER after RAI ablation.

Objective:To evaluate the biochemical and structural changes of apatinib in patients with progressive radioactive iodine-re-fractory differentiated thyroid cancer (RAIR-DTC). Methods:The participants (n=10) were followed up since March 2016. Treatment ef-fect was evaluated in using both biochemical [thyroglobulin (Tg) and thyroglobulin antibody (Tg-Ab)] and structural responses (target lesions, TL). Adverse events were also recorded over time. Results:The median follow-up was 7.9 months. The Tg level declined rapid-ly within 6 weeks after apatinib treatment, and the average decline ranged from 60%to 90%, indicating the immediate biochemical re-sponse of apatinib in progressive RAIR-DTC. The Tg level tended to stabilize thereafter. However, the Tg level rebounded by 4%–135%when withdrawal was performed for 3–14 days. The number of TLs decreased rapidly within 8 weeks, and the average decreased ranged from 40%to 60%, indicating the presence of rapid structural responses. Thereafter, the number of TLs continued to stabilize. TLs, in contrast to Tg, were not significantly affected by drug withdrawal. The rate of change in Tg (Tgvn) was positively correlated with the rate of change in TL (TLvn) [TLvn=0.17×Tgvn+0.50 (r=0.56, P<0.05)]. The apatinib dose was adjusted due to adverse events, which could be relieved after 3 to 14 days of withdrawal. Apatinib can effectively control the disease even at a reduced dose of 250 mg/d. Conclusion:Apatinib treatment showed a fast and sustainable biochemical and structural responses. Tg could be regarded as an objec-tive indicator. Tgvn is positively correlated with TLvn, and the response of Tg is more sensitive than that of TLs.

Objective To evaluate the impact of low-dose 131I therapy and high-dose 131I therapy on the clinical outcome in PTC patients coexisting with Hashimoto's thyroiditis (HT).Methods A total of 140 non-distant metastatic PTC patients (16 males,124 females,age range:16-66 years) from July 2010 to December 2014 were enrolled in this retrospective study.Patients concurrent with HT (n=84,group A) were divided into low-dose group (1 110 MBq,n=56,group A1) and high-dose group (5 550 MBq,n=28,group A2) according to 131I ablation dose.Patients without HT (n =56) were enrolled as control group (group B),and received 1 110 MBq of 131I.The thyroid remnant ablation outcome was evaluated according to 131I diagnostic whole-body scan (Dx-WBS),neck ultrasonography (US),serum Tg and TgAb level 6-8 months after 131I ablation therapy.The successful ablation rates were compared by x2 test.Kruskal-Wallis rank sum test was also used.Results There were no significant differences among the 3 groups in terms of both clinicopathological features and postoperative remnant thyroid (H:0.203-2.944,x2:0.271-0.970,all P＞0.05).When negative Dx-WBS and US were deemed as successful ablation criterion,complete ablation rate was found significantly more in group B (94.6％,53/56) than that in group A1 (82.1％,46/56;x2=4.264,P＜0.05),but no significant difference was found between group A2 (85.7％,24/28) and group A1 (x2 =0.318,P＞0.05).When combining negative sTg (sTg＜1 μg/L,TgAb＜46 kU/L) with the above 2 criterions to assess remnant ablation outcome,group B also had a higher successful rate to achieve complete ablation (85.7％,48/56) compared with group A1 (75.6％,34/45),but without statistical significance (x2=2.978,P＞0.05),and no difference was observed between group A2 (12/15) and group A1 (x2=1.320,P＞ 0.05).Conclusion Non-distant metastatic PTC patients coexisting with HT has undesirable 131I ablation outcome compared with those without HT,increasing 131I dose is unhelpful to enhance efficiency of remnant ablation for PTC patients with HT.

Objective: To explore the protective roll of ifbroblast growth factor 21 (FGF21) in endoplasmic reticulum stress (ERS) induced rat's H9c2 cardiomyocyte apoptosis with its mechanism. Methods: pcDNA4 was used as gene vector, pcDNA4-FGF21 plasmid was constructed and transfected into rat's H9c2 myocardiocytes for 48 h. ERS model was established by 10 μM tunicamycin (TM) induction for 24 h. The experiment was conducted in 4 groups:①Control group,②TM group, the cells were treated by TM,③pcDNA4-FGF21+TM group,④pcDNA4+TM group. The expressions of FGF21, protein kinase R-like ER kinase (PERK) and c-Jun N-terminal kinases (JNK) mediated apoptosis pathway related protein were measured by Western blot analysis; cell survival rate was examined by CCK-8 method and apoptosis rate was detected by TUNEL technique. Results: pcDNA4-FGF21 vector was successfully constructed and overexpressed in H9c2 myocardiocytes. Compared with Control group, TM group and pcDNA4+TM group had up-regulated endogenous FGF21 expression, increased PERK and JNK mediated apoptosis pathway related protein expression; reduced cell survival rate and elevated apoptosis rate. Compared with TM group and pcDNA4+TM group, pcDNA4-FGF21+TM group had down-regulated PERK and JNK mediated apoptosis pathway related protein expression; increased cell survival rate and decreased apoptosis rate. Conclusion: FGF21 overexpression can reduce ERS induced apoptosis rat's H9c2 myocardiocytes which might be partly related for inhibiting PERK and JNK mediated signal transduction of apoptosis pathway.

Objective To investigate the effects of ketamine on anoxia-reoxygenation(A/R)induced glutamate release from cerebral cortex neurons.Methods Primary cultured neurons obtained from cerebral cortex of fetal Wistar rats(16-18 d)were randomly divided into 3 groups:Ⅰcontrol group;ⅡA/R group andⅢketamine pretreatment+I/R group.The control group was not subjected to A/R while A/R group was exposed to anoxic air(95% N_2+5% CO_2)for 5 h followed by 24 h reoxygenation.In groupⅢdifferent doses of ketamine were added to the culture media before anoxia and the final ketamine concentrations were 1,20 and 100?mol?L~(-1) respectively.The extracellular glutamate concentration was detected at the end of 24 h reoxygenation.Results The extracellular glutamate concentration was significantly higher after 24 h reoxygenation in A/R group than in control group.Ketamine 20 and 100?mol?L~(-1) significantly inhibited glutamate release from the neurons induced by A/R in a dose-dependent manner.Conclusion Ketamine can inhibit glutamate release from neurons induced by A/R in a dose-dependent manner.