Synthesis, Structure, Characterization, and Calculation of a Noncentrosymmetric Fluorine-Containing Indium Iodate, Ba[InF₃(IO₃)₂

PARP1 Impedes SIRT1-Mediated Autophagy during Degeneration of the Retinal Pigment Epithelium under Oxidative Stress.

Retinitis pigmentosa (RP) is a group of clinically and genetically heterogeneous retinal degenerative hereditary diseases that cause severe vision impairment and often blindness.They are characterized by dysfunction and loss of retinal pigment epithelial (RPE) cells and photoreceptor cells.Sodium iodate (NaIO3) is an antimetabolite known to selectively damage RPE.The RP induced by NaIO3 resemble patchy loss of RPE in human RP, and has been frequently used to establish a RP model.The RP models induced by NaIO3 can be established in a variety of experimental animals.Among those models, the RP model induced by one injection of NaIO3 is most commonly used.The NaIO3-induced RP animal models can be manipulated in terms of onset age and disease progression.Moreover, RPE cells in some animals have a self-regenerative potential under specific conditions.Therefore, this model is relevant in the study of RP pathogenesis, drug or stem/progenitor cell therapy and regenerative medicine.There have been many reports on researches and application of NaIO3-induced RP models, we summarized recent progress in this model. Key words: Retinitis pigmentosa; Sodium iodate; Disease models, animal

Objective To study the influence of low-iodine diet on the expression of homeobox gene Nkx-6.1 and Nkx-6.2 in rat cerebrum tissue, and to explore the possible molecular mechanism of cerebrum development retardation caused by low-iodine. Methods Twenty female Wistar rats were randomly equally divided into two groups: low-iodine group and control group, both fed with low-iodine diet as low as 13.66 μg/kg determinated by spectrophotometry in Tianjin Institute of Endocrinology and the former with deionized water, the later 200 μg/L potassium iodate. Thyroid hormone level was detected using chemiluminescence immunoassay 3 months later and they were mated with male rats normally fed. Rats of 16-day pregnancy, new-born and 20th days old were detected the content of Nkx-6.1 and Nkx-6.2 mRNA in the cerebrum tissue by real-time fluorescence quantitative PCR 0.61), (3.28±0.80)pmol/L] were lower than the control group[(1.04±0.06), (39.42±14.68)nmol/L, (4.83±0.33), day pregnancy, new-born and 20th days old of control group was (1.90±0.23)×10-3,(1.86±0.40)×10-4, (1.11± 0.27)×10-4(F=827.58, P<0.01), Nkx-6.1 mRNA expression level gradually decreased along with aging(all P<0.05). The intra-group difference was significant (F=297.25, P<0.01) and the Nkxr.1 mRNA expression level during 16 days of pregnancy was the highest(P<0.01). It was higher in the control group than in the low-iodine group during 16 days of pregnancy (t=10.14, P<0.01) as well as in the low-iodine group than in the in 16-day pregnancy, new-born and 20th days old of control group was respectively(1.03±0.19)×10-2, (1.33± 0.10)×10-3, (8.79±0,87)×10-3, and that of low-iodine group was (0.31±0.03)×10-2, (1.53±0.13)×10-3, (7.51±0.86)×10-2. The intra-group difference was significant(F=1293.02,1065.83, all P<0.01). Nkx-6.2 expression level during 20th days old was the highest(P<0.01) and that of newborn was the lowest(P<0.01). The Nkx6.2 mRNA expression level in control group were higher than the low-iodine group during 16-day pregnancy and 20th days old(t=14.35, 4.05, all P<0.01). It was higher in the low-iodine group than in the control group during newboru(t=4.78, P<0.01). Conclusions The difference in the expression of Nkx-6.1 and Nkx-62 is highly related to the brain development retardation caused by low-iodine. Key words: Genes; homeobox; Polymerase chain reaction; Developmental disabilities; brain

Objective To observe the effects of subretinal transplantation of rat mesenchymal stem cells (rMSCs) on Sodium Iodate (SI)-induced retinal degeneration.Methods One hundred and twenty Brown-Norway (BN) rats were divided into three groups including SI injection group,rMSCs transplantation group and normal control group,each with 40 rats.The retinal degeneration was induced by caudal vein injection of SI.The retinal pigment epithelium(RPE)and neural retinal were evaluated by ocular fundus photograph,fluorescein fundus angiography (FFA),electroretinogram (ERG) and histological approach,and TUNEL(terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling).CM-Dilprelabeled primary rMSCs were transplanted into the subretinal space of Sl-induced rats.The survival,integration,and differentiation of rMSCs were observed between 14 day to 60 day after the transplantation.Results The rat retinal function was gradually reduced afterl4 days of SI injection,with a time-dependent manner.After the RPE cells were damaged,the outer segments of photoreceptors became disrupted and shortened until karyopyknosis.The nuclear morphology and positive TUNEL labeling indicated that the death of photoreceptor cells was apoptosis.After rMSCs transplantation,CM-DiI labeled donor cells were observed to be scattered in the subretinal space and expressed RPE cell markers.Average amplitude of bwave and Ops (oscillation potential) in ERG improved 27.80%,59.38% respectively after rMSCs transplantation.Conclusions Transplanted rMSCs can survive in subretinal space and differentiate into RPE cells,thus cure SI- induced retinal degeneration. Key words: Stem cells/cytology; Myeloid progenitor cells/transplantation; Mesenchymal stem cell transplantation/methods; Retinal diseases/diagnosis; Animals,laboratory

Dithiane Hydrolysis by a Polymer-Supported Iodate

目的 观察静脉注入碘酸钠后早期引起的兔眼图形视诱发电位(P-VEP)的改变,从而推测出视力的变化.方法 将10 mg/ml碘酸钠40 mg/kg从兔耳缘静脉注入体内.镜片矫正兔眼屈光不正,注药前及注药后3 h分别对兔右眼P-VEP进行检测(翻转棋盘格,分别对应的视角6'、3'、1.5').结果 注药后3 h,光感受器细胞未见明显损害,3 d后,外节中可以看到许多空泡样改变.注药前约50 ms可记录到一个正向的反应波(P100),注药后3 h此波明显下降或消失(配对t检验,P＜0.05).结论 静脉注入碘酸钠后3 h可以影响兔眼视力。

To investigate the effects of chronic mild and moderate iodine excess on thyroid oxidative injury and anti-oxidative ability of iodine deficiency and non-iodine deficiency Wistar rats. Four-week-old Wistar rats were fed with iodine deficient diet for three months to make iodine deficient goiter models, then divided randomly into three groups: iodine deficient control group (Group IDC) fed with double distilled water, iodine-supplement group I (Group IS I) fed with potassium iodate solutions with the iodine concentrations of 100 microg/L, and iodine-supplement group II (Group IS II), fed with potassium iodate solution with the iodine concentrations of 330 microg/L. Another four-week-old Wistar rats were fed with normal diet for three months, and then divided randomly into three groups: normal control group (NC) fed with double distilled water, iodine-excess group I (IEI) fed with potassium iodate solution with the iodine concentration of 300 microg/L, and iodine-excess group II (Group IEII), fed with potassium iodate solution with the iodine concentration of 660 microg/L. 1, 2, 4, 8, and 24 weeks after treatment samples of urine were collected to detect the median urine iodine (MUI), samples of plasma were collected from the hearts of 8-14 rats from each group and then rats were killed. Their thyroid glands were taken out to measure the wet weight and made into homogenate. Biochemical method was used to measure the activities of glutathione-peroxidase (GSH-P(X)) and superoxide dismutase (SOD) as well as the contents of malonyldialdehyde (MDA) and H2O2 in the homogenates of thyroid glands. The GSH-P(X) activity 2 weeks after treatment of Group IS II was significantly lower than that of Group IDC (P < 0.05), and the GSH-P(X) activity 4 weeks after treatment of Group IS I was significantly lower than that of Group IDC (P < 0.001). The activities of GSH-P(X) 4, 8, and 24 weeks after treatment of Groups IS I and IS II were all lower than those of Group C at the same time points significantly (P < 0.001, < 0.01, and < 0.05 respectively). The activities of SOD were decreased gradually in Groups IS I and IS II and were significantly lower than those of Group IDC since 8 weeks after treatment (P < 0.001 or < 0.05). The SOD activities in thyroid glands of Groups IEI and IEII since 8 weeks after treatment decreased significantly in comparison with Group NC (all P < 0.01 or < 0.001). The contents of H2O2 in thyroid glands of Groups IS I and IS II were significantly lower than those of Group IDC at different time points (P < 0.001, < 0.01, or < 0.05), and were significantly lower than those of Group NC 8 and 24 weeks after treatment (P < 0.001 or < 0.01). The contents of MDA in thyroid glands since 2 weeks after treatment of Group IEI were all significantly lower than those of Group IDC at the same time points (all P < 0.05), and the content of MDA in thyroid glands since 1 week after treatment of Groups IS II were all significantly lower than those of Group IDC at the same time points (all P < 0.05). Supplementation of 100 microg/L and 330 microg/L iodine on iodine deficiency Wistar rats may alleviate the oxidative injury but weaken the anti-oxidative protection of thyroid. The anti-oxidative protection of thyroid glands of non-iodine deficiency Wistar rats may also be weakened by supplementation of 300 microg/L and 660 microg/L iodine.

Abstract For Abstract see ChemInform Abstract in Full Text.

THE NEUTRALIZE EXAMINATION OF THE SPICES REACTIVITY IN THE IODIZED SALT BY THE ADDITIVE OF THE FOOD ADDITIVES. Background: The potassiumiodate of the iodized salt in the mixture with some spices is bind in the form of the compounds, which are not available for the determination of the iodine by the chemical method. This is due to the reactivity of susbtances contained inspices, such as capsaicin in the chilli, and piperine in the paprika, which are responsible for the spiciness of the spices. Although ithasn't been studied, the configuration of the potassiumiodate in the spices is probably also not available for the human consumption. Where as the supplementation of iodized salt to recover the iodine deficiency is effective. The food additives mostly are the chemical substances, which have properties to keep or increase the quality of food. Objectives: The study was performed to investigate the effect of food additives to the reactivity of spices to the potassiumiodate of iodized salt. Material and Methods: The food additive was added to the iodized salt, and then mixed with the spice. Dissolved by the water incertain volume, filtered, and then determined the potassiumiodate content of the filtrate by the Yodometric method. The potassiumiodate content of the filtrate was compared with the potassiumiodate content of the salt. The result of percent comparisonis the recovery of potassiumiodate when mixed with food additive and spice. The recovery of potassiumiodate was done for the different potassiumiodate content of iodized salt. The study was using CaCO3, KH2P04, MgS04, Na2C03, NaHP04, K-citrate, benzoat acid, dan Na-benzoat as food additives, and the red chilli, hot chilli, pepper and coriander. Results: The reactivity of the pepper and coriander to the potassiumiodate of the iodized salt could be netralized by the addition of CaCO3, KH2P04, MgS04, Na2CO3, NaHP04, K-citrate, benzoic acid, dan Na-benzoic. But for the red chilli and hot chilli were not allof them, these were for CaC03 K-citrate, and benzoic acid. It was shown by the value of recovery of potassiumiodate contents of the iodized salt. The netralization properties of food addives were increased by the increasing of the potassiumiodate content of the iodized salt. Conclusions: The addition of some food additives into the iodized salt is able to prevent the iodate content of the salt from there activity of subtances in the spice. The addition of food additives also can pick up moisture of salt resulting preventation of the salt particles clumping together and so keep the product free flowing. Keywords: potassiumiodate, spices, iodized salt

Fate of intravenously injected iodate and periodate

The determination of iodine in feces.

A preparation of carrier-free iodate

The separation and determination of lead as iodate and its application to glass analysis

The Solubility of Thallous Iodate in Solutions of Sodium Mellitate¹

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Preparation of iodate of potash