[Epidemiological characteristics and spatio-temporal distribution of pulmonary tuberculosis cases reported in students from Guizhou Province, 2011-2020].

Objective: To analyze the trend of epidemiological characteristics and spatiotemporal distribution of pulmonary tuberculosis (PTB) among smear-positive or other types of students in Guizhou Province from 2011 to 2020, and to provide a reference for improving prevention and control measures. Methods: Data were collected from the Chinese Information System's Notifiable Disease and Tuberculosis Management Information System for disease control and prevention, the Joinpoint 4.9.1.0 software was used to analyze the trend of registration rate; the ArcGIS 10.6 software was used to construct a ring map and to perform spatial autocorrelation analysis; the SaTScan 9.7 software was used for spatial-temporal scan statistics. Results: A total of 32 682 student PTB cases were reported in Guizhou Province from 2011 to 2020, including 5 949 (18.20%) smear-positive cases. Most cases occurred from high school students of 16 to 18 years old (43.99%, 14 376/32 682); the annual average registered rate was 36.22/100 000, the highest in 2018 (52.90/100 000), and the registration rate showed an increasing trend. Meanwhile, a similar trend of registration rate was observed among smear-positive or other types of students. The spatialtemporal heterogeneity was found that the "high-high" clustering patterns of smear-positive or other types were aggregated in Bijie City. Six spatialtemporal clusters with statistically significant (all P<0.001) were detected among smear-positive or other cases, respectively. Conclusions: Upward trend with spatial- temporal clusters of PTB cases reported in students from Guizhou Province from 2011 to 2020. Surveillance should be strengthened for high school students, and regular screening should be conducted in high-risk areas to control the source of infection and reduce the risk of transmission.

Zinc glycine chelate absorption characteristics in Sprague Dawley rat.

This study was conducted to investigate absorption characteristics of zinc glycine chelate (Zn-Gly) by evaluating tissues zinc status and the expression of zinc transporters in rats. A total of 24 male rats were randomly allocated to three treatments and administered either saline or 35 mg Zn/kg body weight from zinc sulphate (ZnSO4 ) or Zn-Gly by feeding tube separately. Four rats per group were slaughtered and tissues were collected at 2 and 6 h after gavage respectively. Our data showed that Zn-Gly did more effectively in increasing (p < 0.05) serum zinc levels, and the activities of serum and liver alkaline phosphatase (ALP) and liver Cu/Zn superoxide dismutase (Cu/Zn SOD) at 2 and 6 h. By 2 h after the zinc load, the mRNA and protein abundance of intestinal metallothionein1 (MT1) and zinc transporter SLC30A1 (ZnT1) were higher (p < 0.05), and zinc transporter SLC39A4 (Zip4) lower (p < 0.05) in ZnSO4 compared to other groups. Zinc transporter SLC39A5 (Zip5) mRNA expression was not zinc responsive, but Zip5 protein abundance was remarkably (p < 0.05) increased in ZnSO4 2 h later. Overall, our results indicated that in short-term periods, Zn-Gly was more effective in improving body zinc status than ZnSO4 , and ZnSO4 did more efficiently on the regulation of zinc transporters in small intestine.

Effects of hypoxia on proliferation and osteogenic differentiation of periodontal ligament stem cells: an in vitro and in vivo study.

Changes in oxygen concentration may influence various innate characteristics of stem cells. The effects of varying oxygen concentration on human periodontal ligament stem cells (HPDLSCs) has not been explored, particularly under hypoxia-related conditions. First, HPDLSCs were cultured from the periodontium of human teeth using the outgrowth method. STRO-1 and CD146 expression of HPDLSCs was investigated by flow cytometry. To detect the multilineage differentiation capacities of HPDLSCs, osteogenic-like and adipogenic-like states were induced in cells. Next, HPDLSCs (passage 3) were exposed to normal oxygen (21% O2) or hypoxia (2% O2) conditions for 7 days and cell proliferation was evaluated. After culture in osteogenic medium for 7 days, osteoblastic differentiation was evaluated by semi-quantitative reverse transcription-polymerase chain reaction analysis to detect 3 osteoblastic markers: core-binding factor a 1/runt-related transcription factor 2, osteocalcin, and osteopontin. In addition, each cell group was incubated with a hydroxyapatite/tricalcium phosphate carrier and transplanted subcutaneously into the back of immunocompromised mice to investigate transplantation differences in vivo. HPDLSCs were isolated, cultured, and successfully identified. After exposure of HPDLSCs to hypoxia for 7 days, the proliferation rate was increased and showed higher osteogenic differentiation potential compared to control cells. After 12 weeks of transplantation, hypoxia-treated HPDLSCs differentiated into osteoblast-like cells that formed bone-like structures. These results suggest that oxygen concentrations affect various aspects of HPDLSC physiology and that hypoxia enhances osteogenic differentiation both in vivo and in vitro. Oxygen concentration may be a critical parameter for HPDLSCs during expansion and differentiation.

The presence of Mycoplasma hominis in isolates of Trichomonas vaginalis impacts significantly on DNA fingerprinting results.

The genetic characterization of Trichomonas vaginalis (Protista: Trichomonadidae), the causative agent of trichomoniasis in humans, is central to understanding the epidemiology, treatment, drug resistance, and virulence as well as the diagnosis and control of this parasite. Various molecular approaches, including DNA fingerprinting, have been employed for this purpose, and random amplification of polymorphic DNA (RAPD) continues to be utilized. However, little attention has been paid to the fact that some T. vaginalis populations can harbor symbiotic Mycoplasma hominis and/or other agents, which could cause artifacts in the RAPD results. In the present study, we demonstrate clearly that the presence of M. hominis from T. vaginalis isolates impacts significantly on RAPD results and on the subsequent analyses and interpretation of data sets. Moreover, symbiotic M. hominis displays an isolate-to-isolate variability in RAPD profile before elimination, suggesting a variability of M. hominis infection.

Symbiosis of Mycoplasma hominis in Trichomonas vaginalis may link metronidazole resistance in vitro.

Fourteen of 28 Trichomonas vaginalis isolates collected from patients in Guangzhou, China from 2003 to 2004 were found to be naturally infected with Mycoplasma hominis, as determined by PCR using specific primers. In vitro metronidazole sensitivity assay of the 28 isolates revealed four displaying low susceptibility [minimum lethal concentration (MLC)= approximately 13-25 microg/ml] and another four displaying high resistance (MLC=50-100 microg/ml). The overwhelming majority of these resistant isolates (7/8) were mycoplasma-infected. The mean of MLCs of mycoplasma-infected isolates is approximately 10-fold higher than the mean of noninfected isolates (p=0.029). Sequence analyses of PCR-amplified small subunit-large subunit rRNA interspacer regions (ITS1/5.8S/ITS2) revealed that 23 of the 28 samples are identical, the remaining five being separable into two groups, each with a single point mutation. These internal transcribed spacer sequence variants are associated neither with mycoplasma infection nor with drug resistance. In contrast, random amplified polymorphic DNA analyses of DNAs using 10 different primers showed that the drug-resistant isolates are clustered together in association with mycoplasma infection, albeit more loosely. Taken together, the results obtained from this study suggest that in vitro metronidazole resistance of T. vaginalis is related to mycoplasma infection of this protozoan.

A point mutation in the albumin gene in a Chinese patient with familial dysalbuminemic hyperthyroxinemia.

Familial dysalbuminemic hyperthyroxinemia (FDH) is an autosomal dominant disorder characterized by euthyroid hyperthyroxinemia. However, FDH has not been reported in Chinese or African patients. Here, we report the first case of FDH in a Chinese patient. A 69-year-old Chinese man was found to have increased serum total T(4) concentrations (198-242nmol/l; normal range 58-148nmol/l) and free T(4) concentrations (>58pmol/l; T(4) analog method, normal range 9-28pmol/l). Serum total T(3) and TSH concentrations were normal. The patient was misdiagnosed as hyperthyroid and was later suspected to have a TSH-producing tumor by the finding of a pituitary microadenoma, which was eventually proven to be a non-functional pituitary 'incidentaloma'. Electrophoretic analysis of the patient's serum proteins demonstrated enhanced albumin binding of [(125)I]T(4). Serum free T(4) concentrations were normal (16-19pmol/l, normal range 9-26pmol/l) when a two-step method was used. Direct sequencing of the albumin gene showed a guanine to adenosine transition in the second nucleotide of codon 218, resulting in a substitution of histidine (CAC) for the normal arginine (CGC) in one of the two alleles in the patient. The point mutation was further confirmed by HphI digestion of exon 7 of the albumin gene. The patient's son was not affected. Our studies demonstrated that the point mutation of the albumin gene in a Chinese patient with FDH was similar to that found in western white families, but differed from that in a Japanese family in whom a guanine to cytosine transition at the same position was found.

Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein.

In 1948, Wolff and Chaikoff reported that organic binding of iodide in the thyroid was decreased when plasma iodide levels were elevated (acute Wolff-Chaikoff effect), and that adaptation or escape from the acute effect occurred in approximately 2 days, in the presence of continued high plasma iodide concentrations. We later demonstrated that the escape is attributable to a decrease in iodide transport into the thyroid, lowering the intrathyroidal iodine content below a critical inhibitory threshold and allowing organification of iodide to resume. We have now measured the rat thyroid sodium/iodide symporter (NIS) messenger RNA (mRNA) and protein levels, in response to both chronic and acute iodide excess, in an attempt to determine the mechanism responsible for the decreased iodide transport. Rats were given 0.05% NaI in their drinking water for 1 and 6 days in the chronic experiments, and a single 2000-microg dose of NaI i.p. in the acute experiments. Serum was collected for iodine and hormone measurements, and thyroids were frozen for subsequent measurement of NIS, TSH receptor, thyroid peroxidase (TPO), thyroglobulin, and cyclophilin mRNAs (by Northern blotting) as well as NIS protein (by Western blotting). Serum T4 and T3 concentrations were significantly decreased at 1 day in the chronic experiments and returned to normal at 6 days, and were unchanged in the acute experiments. Serum TSH levels were unchanged in both paradigms. Both NIS mRNA and protein were decreased at 1 and 6 days after chronic iodide ingestion. NIS mRNA was decreased at 6 and 24 h after acute iodide administration, whereas NIS protein was decreased only at 24 h. TPO mRNA was decreased at 6 days of chronic iodide ingestion and 24 h after acute iodide administration. There were no iodide-induced changes in TSH receptor and thyroglobulin mRNAs. These data suggest that iodide administration decreases both NIS mRNA and protein expression, by a mechanism that is likely to be, at least in part, transcriptional. Our findings support the hypothesis that the escape from the acute Wolff-Chaikoff effect is caused by a decrease in NIS, with a resultant decreased iodide transport into the thyroid. The observed decrease in TPO mRNA may contribute to the iodine-induced hypothyroidism that is common in patients with Hashimoto's thyroiditis.

Effects of iodine repletion on thyroid morphology in iodine and/or selenium deficient rat term fetuses, pups and mothers.

It has been suggested that selenium deficiency aggravates the iodine-induced thyroid inflammation and necrosis in iodine-deficient Wistar rats and possibly in man. Studies were carried out to determine whether large amounts of iodine given to iodine-deficient pregnant Sprague-Dawley rats with or without selenium deficiency would induce inflammation and necrosis in their term fetal thyroids. Iodine deficiency was induced in the dams by a low iodine diet or perchlorate in the drinking water and iodine excess was achieved by iodinated drinking water during pregnancy or daily subcutaneous injections of iodine from days 20 to 22 of pregnancy, 1 day after perchlorate was discontinued. Studies were also carried out in 30-day-old pups whose nursing mothers were iodine-deficient (perchlorate) with or without selenium deficiency from conception onward. The administration of iodine restored the morphologic changes in the thyroid induced by iodine deficiency, irrespective of selenium status, toward normal without inflammatory changes or necrosis. Possible explanations for these unexpected findings are discussed.

Restoration of cyclic adenosine monophosphate-stimulated chloride channel activity in human cystic fibrosis tracheobronchial submucosal gland cells by adenovirus-mediated and cationic lipid-mediated gene transfer.

In human airways, the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) is predominantly expressed in serous cells of the tracheobronchial glands. Despite considerable evidence that submucosal glands are important contributors to the pathophysiology of CF lung disease, most attempts at CFTR gene transfer have primarily targeted airway surface epithelial cells. In this study, we systematically evaluated CFTR gene transfer into cultures of immortalized CF human tracheobronchial submucosal gland (6CFSMEO) cells using adenovirus and cationic lipid vectors. We found that the efficiency of adenovirus-mediated gene transfer was comparable in 6CFSMEO and CFT1 cells (a surface airway epithelial cell line isolated from a subject with CF). So was the ranking order of adenovirus vectors containing different enhancers/promoters (CMV >> E1a approximately phosphoglycerokinase), as determined by both X-Gal staining and quantitative measurement of beta-galactosidase activity. Further, we provide the first demonstration that cationic lipids mediate efficient gene transfer into 6CFSMEO cells in vitro. The transfection efficiency at optimal conditions was higher in 6CFSMEO than in CFT1 cells. Finally, either infection with adenoviral vectors or transfection with cationic lipid:plasmid DNA complexes encoding CFTR significantly increased chloride (Cl-) permeability, as assessed using the 6-methoxy-N-(3-sulfopropyl)-quinolinium (SPQ) fluorescence assay, indicating restoration of functional CFTR Cl- channel activity. These data show that although the mechanisms of transfection may be different between the two cell types, 6CFSMEO cells are as susceptible as CFT1 cells to transfection by adenoviral and cationic-lipid gene transfer vectors.

Ammonium persulfate: a new and safe method for measuring urinary iodine by ammonium persulfate oxidation.

The chloric acid method is most commonly used to obtain accurate and reproducible measurements of iodine and removes interfering substances. Unfortunately, chloric acid is a potential hazard requiring an explosion proof hood among other precautions. We have developed a simple, convenient, and economic method for measuring urinary iodine using 1 mol/L ammonium persulfate, a non-explosive, non-hazardous chemical, as the oxidizing reagent. The oxidation procedure can be completed in 30 minutes at a temperature of 91-95 degrees C. The iodine in the urine is then measured by a modification of the traditional colorimetric method of Sandell-Kolthoff. 110 urine samples collected from a mixed population of healthy males and females, ranging in age from 6 to 79 years and living in the United States were analyzed for iodine content by two methods: the proposed ammonium persulfate method and the chloric acid method. The ammonium persulfate method has an intra assay CV of 9.1% at 0.42 +/- 0.04 micromol/L (mean +/- SD), 7.8% at 1.46 +/- 0.11 micromol/L and 4.0% at 3.54 +/- 0.14 micromol/L. The inter assay CV is 10.2% at 0.46 +/- 0.05 micromol/L and 7.9% at 3.27 +/- 0.26 micromol/L. Recovery of iodine added to urine in vitro was 107%, 94% and 97% for 0.42 micromol/L, 0.77 micromol/L and 3.64 micromol/L, respectively. The lower limit of detectability was 0.0034 microgI. Values for iodine in 110 urines measured by the reference chloric acid method ranged from 0.06 to 8.03 micromol/L and by the ammonium persulfate method from 0.05 to 7.4 micromol/L. The persulfate method (y) correlated extremely closely with the reference chloric acid method (x) by the Pearson correlation (y = 0.923x + 0.810 micromol/L, and r = 0.994, Syx = 1.841). In conclusion a new, safe, simple method for measuring urinary iodine is described which uses ammonium persulfate as the oxidizing agent for the removal of interfering substances.

The effect of recombinant human thyrotropin (rhTSH) on thyroid function in mice and rats.

The vast majority of studies to determine the biological activity of recombinant human thyrotropin (rhTSH) have been carried out in the mouse. We have recently reported that 0.1 mg of rhTSH IM (one-ninth the dose given in thyroid cancer patients) given to normal subjects elicits a brisk rise in serum thyroxine (T4), triiodothyronine (T3), and thyroglobulin (Tg) concentrations. In contrast, in initial studies in the rat, a low dose of rhTSH failed to increase serum T4 or T3 concentrations. The present study was, therefore, carried out to determine the biological activity of rhTSH in euthyroid and in T3-treated, TSH-suppressed rats and mice. Doses of rhTSH based on body weight were used and resulted in similar serum human thyrotropin (hTSH) concentrations in the two species. Euthyroid and TSH-suppressed mice responded briskly to rhTSH administration. In contrast, serum T4 did not increase after rhTSH administration in euthyroid rats. In TSH-suppressed rats, the increase in serum T4 was similar to that observed in TSH suppressed mice. These observations suggest that rhTSH more readily displaces endogenous TSH from the mouse than from the rat thyroid TSH receptor, because equal responses were observed when endogenous TSH was suppressed.

Circulating iodide concentrations during and after pregnancy.

Early, indirect studies suggested that an important aspect of thyroid economy during pregnancy was a decline in plasma or serum inorganic iodide (PII) concentrations, but there is little information concerning circulating iodide concentrations as assessed by direct measurement. The present study was undertaken to determine the relationship between gestation and serum iodide concentrations as assessed by direct measurement of PII. PII concentrations, urinary iodide levels, and other parameters of thyroid economy were measured during the first, second, and third trimesters and after delivery in 16 women. Mean serum T4 concentrations were significantly higher in all 3 trimesters than those after delivery. Serum free T4 index concentrations were significantly higher in the first trimester than during later periods of gestation or after delivery, but serum TSH concentrations were not depressed in the first trimester. Serum thyroglobulin concentrations were similar during pregnancy and after delivery. There was wide variability in PII and urinary iodide concentrations during and after pregnancy, but there was no trend for PII concentrations to be depressed during pregnancy. Pregnancy, at least in iodine-sufficient regions, does not have an important influence on circulating concentrations of iodide.

Efficiency of cationic lipid-mediated transfection of polarized and differentiated airway epithelial cells in vitro and in vivo.

Systematic analysis of a large number of different cationic lipids has led to the identification of novel structures (GL-67) and formulations of cationic lipid:plasmid DNA (pDNA) complexes that facilitate high levels of gene expression in lungs of mice. However, despite significant improvement in gene transfer activity, we show here that the efficiency of GL-67-mediated gene transduction of intact airway epithelia is still relatively low. Administration of GL-67:pCF1-CFTR (encoding the cystic fibrosis transmembrane conductance regulator) complexes into the nasal epithelium of cystic fibrosis (CF) transgenic mice resulted only in marginal correction of the ion transport defects. Measurements of nasal potential differences (PD) showed no correction of the sodium (Na+) transport defect, and only partial restitution of the chloride (Cl-) transport defect was achieved in a small proportion of the animals after perfusion of the nasal epithelium with the complexes. Furthermore, in contrast to results obtained following instillation of GL-67:pDNA complexes into the lungs of mice, perfusion of GL-67:pDNA into the nasal epithelium resulted only in a moderate enhancement of gene transduction activity relative to that attained with naked pDNA alone. To determine the basis for this low efficiency of transfection, a series of studies was conducted to identify some of the barriers governing cationic lipid-mediated gene transfer to the airway epithelium. We show here that the transfection activity of GL-67 was affected by the polarization, differentiation, and proliferative state of the cells. Diminished transfection activity was observed with nonmitotic, highly polarized and differentiated airway epithelial cells. This observed reduction in gene expression with nonmitotic cells was determined to be due in part to inefficient nuclear translocation of the pDNA from the cytoplasm. Together these data indicate that much improvement in the ability of cationic lipids to transfect polarized and differentiated airway epithelial cells is a necessary prerequisite for effective cationic lipid-mediated gene therapy of airway diseases such as CF.

Partial restoration of cAMP-stimulated CFTR chloride channel activity in DeltaF508 cells by deoxyspergualin.

Deletion of the codon encoding phenylalanine 508 (DeltaF508) is the most common mutation in cystic fibrosis (CF) and results in a trafficking defect. Mutant DeltaF508-CF transmembrane conductance regulator (CFTR) protein retains functional activity, but the nascent protein is recognized as abnormal and, in consequence, is retained in the endoplasmic reticulum (ER) and degraded. It has been proposed that this retention in the ER is mediated, at least in part, by the cellular chaperones heat shock protein (HSP) 70 and calnexin. We have investigated the ability of deoxyspergualin (DSG), a compound known to compete effectively for binding with HSP70 and HSP90, to promote trafficking of DeltaF508-CFTR to the cell membrane. We show that DSG treatment of immortalized human CF epithelial cells (DeltaF508) and cells expressing recombinant DeltaF508-CFTR partially restored cAMP-stimulated CFTR Cl- channel activity at the plasma membrane. Although there are several possible explanations for these results, one simple interpretation is that DSG may have altered the interaction between DeltaF508-CFTR and its associated chaperones. If this is correct, agents capable of altering the normal functioning of cellular chaperones may provide yet another means of restoring CFTR Cl- channel activity to CF subjects harboring this class of mutations.

Dehydroepiandrosterone sulfate does not prevent spontaneous and iodine-induced lymphocytic thyroiditis and diabetes mellitus in the BB/Wor rat.

Chronic feeding of dehydroepiandrosterone (DHEA) and its sulfated metabolite, dehydroepiandrosterone sulfate (DHEAS), has previously been reported to decrease hyperglycemia, obesity, cancer, and autoantibody generation in a number of animal models and to increase muscle mass and physiological and psychological well-being in elderly humans, although these latter studies remain controversial. The present study was carried out to determine whether large amounts of DHEAS given orally would prevent the occurrence of spontaneous and iodine-induced autoimmune lymphocytic thyroiditis (LT) and/or spontaneous insulin-dependent diabetes mellitus (DM) in male and female BB/Wor rats. DHEAS was administered by gavage (44 mg/rat/day) or in the chow (133 mg/rat/day) to LT- and DM-prone rats from 30 to 120 days of life; some of these rats also received iodine in the drinking water to enhance the incidence and intensity of LT. Onset of DM requiring protamine zinc insulin and its maintenance dose were assessed. Rats were killed at 90 or 120 days of age and blood, thyroid, adrenals, pancreases, testes, and ovaries were removed. Serum glucose, DHEA, DHEAS, thyroxine (T4), tri-iodothyronine (T3) and thyrotropin (TSH) concentrations were measured in all rats in both experiments. Serum DHEAS concentrations were 10-fold higher in the rats given the steroid by gavage or in the diet compared with levels in control rats. DHEAS administered over a prolonged period of time had no significant effect on body weight, incidence and severity of DM, incidence and intensity of spontaneous and iodine-induced LT, and thyroid, pancreas and testes weights but did significantly decrease adrenal and ovarian weights. Serum T4, T3, and TSH concentrations were similar in control and DHEAS-treated rats. In conclusion, DHEAS did not prevent the occurrence of iodine-induced or spontaneous autoimmune LT or spontaneous DM in the BB/Wor rat, at variance with its reported immunosuppressive effects in other animal models.

The effect of nicotine on thyroid function in rats.

Very recently, it has been reported that subclinical hypothyroidism is more severe and peripheral markers of hypothyroidism are more pronounced in women with subclinical or overt hypothyroidism who smoke. Increased concentrations of the known goitrogen thiocyanate, generated from cigarette smoke, have been the major explanation for the decreased thyroid function in these women but do not explain the reported increased peripheral markers of hypothyroidism. There are no data on the effect of the other major product of cigarettes, nicotine, on thyroid function in vivo. The present studies were therefore performed to determine the effects of large doses of nicotine infused for 7 days on thyroid function, outer-ring 5'deiodinase activity (5'D-I), and hepatic malic enzyme activity (a measure of thyroid hormone action) in euthyroid, subclinically hypothyroid (hemithyroidectomized), and L-thyroxine (L-T4)-treated thyroidectomized rats. Nicotine infusion had no effect on serum T4, triiodothyronine (T3), thyrotropin (TSH), and cholesterol concentrations, intrathyroidal metabolism of 125I, liver and kidney 5'D-I activity, and hepatic malic enzyme activity in euthyroid and subclinically hypothyroid rats. Nicotine administration also did not affect serum T3, TSH, or cholesterol concentrations, liver and kidney 5'D-I activity, and hepatic malic enzyme activity in L-T4-treated thyroidectomized rats. These studies provide strong evidence that nicotine is not responsible for the observed adverse effects of smoking on the thyroid in humans.

Fluorine intake of a Tibetan population.

Measurements of food consumption of randomly selected families and fluorine levels in food and beverages were used to calculate the fluorine intake of Tibetan people living in nomadic or semi-nomadic areas of the region and regularly consuming brick tea both as a beverage and in food. The fluorine intake of these groups (children 5.49-7.62 mg day; adults 10.43-14.48 mg/day) was much higher than that of members of a Han population living in the region (children 1.44 mg/day; adults 2.54 mg/day). The amounts of fluorine consumed by the Tibetan inhabitants are at least twice the WHO suggested limit (2 mg/day). Tea plants are rich in fluorine, and the highest levels are found in older leaves which are used to make brick tea. We conclude that brick tea is the major source of fluorine intake by the Tibetan population studied.

Comparison of the effects of propylthiouracil and selenium deficiency on T3 production in the rat.

Selenium deficiency and propylthiouracil (PTU) treatment both decrease hepatic type I T4 5'-deiodinase activity (5'D-I), which is considered to be an important regulator of the serum T3 derived from peripheral T4 to T3 conversion (T3 neogenesis). The effects of PTU treatment or a selenium-deficient diet on T4 and T3 kinetics were compared in thyroid-ablated rats infused with stable T4 to determine whether PTU treatment is a more potent inhibitor of T3 neogenesis than selenium deficiency and to compare the degree of inhibition of T3 production with the degree of inhibition of 5'D-I. PTU treatment and selenium deficiency (Se-) did not affect the T3 MCR (control, 46.0 +/- 2.5; PTU, 41.7 +/- 2.8; Se-, 41.1 +/- 4.0 ml/h.100 g BW), but did reduce serum T3 concentrations by 29% and 25%, respectively (control, 58.7 +/- 2.6; PTU, 41.5 +/- 1.0; Se-, 43.9 +/- 2.7 ng/dl; P < 0.01 for PTU or Se- vs. control) and the T3 production rate by 35% and 32%, respectively (control, 26.6 +/- 1.0; PTU, 17.3 +/- 2.0; Se-, 18.0 +/- 1.9 ng/h.100 g BW; P < 0.01 for PTU or Se- vs. Control). PTU treatment and selenium deficiency significantly increased serum T4 concentrations by 36% and 32%, respectively, due to a decrease in T4 MCR (control, 1.4 +/- 0.1; PTU, 1.1 +/- 0.1; Se-, 1.1 +/- 0.04 ml/h.100 g BW; P < 0.05 for PTU or Se- vs. control). Assuming that the concentration of T4 available for T3 neogenesis is proportional to the serum T4 concentration, the increase in serum T4 concentrations caused by PTU treatment or Se- would probably have proportionally increased the rate of T3 neogenesis. Based on these considerations, the apparent decrease in T3 neogenesis in the PTU-treated animals was 52%. This is less than the 79% and 67% inhibition of 5'D-I noted, respectively, in the liver and kidneys of these rats. Similarly, the apparent decrease in T3 neogenesis in the Se- rats was 48%, again less than the 85% and 64% inhibition of 5'D-I in their liver and kidneys, respectively. These studies suggest that PTU and Se- have similar effects on T3 neogenesis. The more potent effects of these treatments on liver and kidney 5'D-I activities than on T3 neogenesis suggest that the activities of these enzymes in these tissues are not the only important determinants of the serum T3 that is derived from nonthyroidal sources.

Serum iodothyronine concentrations in intestinally decontaminated rats treated with a 5'-deiodinase type I inhibitor 6-anilino-2-thiouracil.

Enteric bacteria have been postulated to have a role in thyroid economy by promoting the hydrolysis of thyroid hormone conjugates of biliary origin, thus permitting the absorption and recycling of thyroxine (T4) and triiodothyronine (T3). An enterohepatic circulation of T3 might be more pronounced under conditions in which type I iodothyronine deiodinase activity (5'D-I) is inhibited, because this augments the accumulation of T3 sulfate conjugates in bile. This potential of increased gut reabsorption of T3 might explain, at least in part, the failure of serum T3 values to decrease appreciably when marked reductions in peripheral 5'D-I activity are induced by selenium deficiency or 6-anilino-2-thiouracil (ATU) administration. Thus, studies were performed to determine the effect of intestinal decontamination, in the absence and in the presence of 5'D-I inhibition, on plasma T4 and T3 concentrations. Groups of adult male rats received either enteric antibiotics or no antibiotics for 12 days and then, in half of the rats in each group, treatment for 10 days with ATU, a 5'D-I inhibitor that does not affect thyroid hormone synthesis. The activity of intestinal arylsulfatase and arylsulfotransferase, enzymes that catalyze hydrolysis of thyroid hormone conjugates, was reduced markedly by approximately 87% in rats that received antibiotics, regardless of whether or not they also received ATU. The ATU treatment markedly inhibited liver 5'D-I activity in antibiotic-treated as well as in non-antibiotic-treated rats (control = 399 +/- 32 U/mg protein (mean +/- SEM); ATU = 152 +/- 17: antibiotics = 351 +/- 29; antibiotics + ATU = 130 +/- 10; p < 0.01) and significantly increased plasma T4 and T3 sulfate (T4S, T3S) concentrations (control: T4S = 2.8 +/- 0.4 and T3S = 6.7 +/- 1.3 ng/dl; ATU: T4S = 6.2 +/- 1.4 and T3S = 10.6 +/- 2.1 ng/dl; antibiotics: T4S = 1.8 +/- 0.2 and T3S = 3.6 +/- 1.0 ng/dl; antibiotics + ATU: T4S = 6.8 +/- 0.7 and T3S = 9.7 +/- 1.8 ng/dl; p < 0.05). The ATU treatment was associated with a significant increase in plasma T4 and rT3 concentrations but did not affect plasma T3 concentrations, and intestinal decontamination did not alter these ATU-associated effects on circulating thyroid hormones. These results suggest that anaerobic enteric bacteria in the rat do not have an important role in recycling of thyroid hormones, either under normal conditions or in circumstances where 5'D-I activity is markedly reduced, and that increased gut absorption of T3 from T3S cannot explain the near-normal serum T3 values found when peripheral 5'D-I activity is markedly decreased.

Ammonium persulfate: a safe alternative oxidizing reagent for measuring urinary iodine.

The chloric acid method is most commonly used to obtain accurate and reproducible measurements of iodine and remove interfering substances. Unfortunately chloric acid is a potential hazard, requiring an explosion-proof hood, among other precautions. We have developed a simple, convenient, and economic method for measuring urinary iodine by using 1 mol/L ammonium persulfate, a nonexplosive, nonhazardous chemical, as the oxidizing reagent. The oxidation procedure can be completed in 30 min at a temperature of 91-95 degrees C. The iodine in the urine is then measured by a modification of the traditional colorimetric method of Sandell and Kolthoff. Urine samples (110) collected from a mixed population of healthy males and females, ranging in age from 6 to 79 years and living in the US, were analyzed for urine iodine content by two methods: the proposed ammonium persulfate method and the chloric acid method. The ammonium persulfate method has an intraassay CV of 9.1% at 0.42 +/- 0.04 micromol/L (mean +/- SD), 7.8% at 1.46 +/- 0.11 micromol/L, and 4.0% at 3.54 +/- 0.14 micromol/L. The interassay CV is 10.2% at 0.46 +/- 0.05 micromol/L, and 7.9% at 3.27 +/- 0.26 micromol/L. Recovery of iodine added to urine in vitro was 107%, 94%, and 97% for 0.42 micromol/L, 0.77 micromol/L and 3.64 micromol/L, respectively. The lower limit of detectability was 0.0034 microgram of iodine. Values for iodine in 110 urines measured by the reference chloric acid method ranged from 0.06 to 8.03 micromol/L and by the ammonium persulfate method from 0.05 to 7.4 micromol/L. The persulfate method (y) correlated extremely closely with the reference chloric acid method (x) by the Pearson correlation (y = 0.923x + 0.810 micromol/L, and r = 0.994, Sy/x = 1.841).