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Thyroid hormones, thyroxin ([T.sub.4]) and 3,5,3'-triiodothyronine ([T.sub.3]), Of maternal origin, are available to the mammalian embryo early in development. However, after the onset of fetal thyroid function, they are of both fetal and maternal origin. Maternal [T.sub.4] has a protective effect on the fetal brain in cases of congenital hypothyroidism. In severe iodine deficiency, maternal [T.sub.4] is low, although [T.sub.3] is normal; the developing embryo is markedly [T.sub.4]-deficient; and [T.sub.3] deficiency increases with gestational age. In contrast to mechanisms in the hypothyroid fetus from a normal mother, the low [T.sub.4] of the iodine-deficient mother prevents any protective effects on the fetal brain. Thyroid hormone deficiency of the iodine-deficient fetus, including the brain, is more severe and prolonged than it is in the cases of maternal or fetal thyroid failures. These findings may help to explain the relationship between severe maternal hypothyroxinemia and the severe central nervous system damage of the neurological endemic cretin. Am J Clin Nutr Suppl 1993;57:280S-5S

Monitoring of water sources is a major concern worldwide. Wireless sensor networks (WSN) may be used for this monitoring. However, current systems employ mainly physical sensors for variables such as temperature, pressure, humidity and light. Wireless chemical sensors networks (WCSNs) for environmental monitoring are scarce due to the lack of autonomy of conventional sensors. This paper presents results of a WCSN for monitoring pH based on ion selective field effect transistors (ISFETs). Sensing nodes employ a human interface required for in situ calibration of chemical sensors. Unlike most studies, our work evaluates the network employing chemical measurements and wireless network metrics. Results show zero packet losses by using a time division multiple access (TDMA) protocol. The network allows wireless communication within 300m including attenuation from buildings and trees. Therefore, the system presented in this paper is suitable for long range applications with unobstructed line of sight. pH measurements present a standard deviation below 1%, showing high repeatability. When compared to a commercial pH meter, difference in measurements is below 5%. As a consequence, accuracy is adequate for the application. Measurements also presented high stability during 3h of continuous measurement.

Iodine deficiency induces multiple intrathyroidal autoregulatory changes leading to an increased triiodothyronine (T3) production and secretion, at the expense of thyroxine (T4). It is characterized by low serum T4, normal or slightly elevated T3, and as a consequence of the latter, normal thyrotropin (TSH). Tissues are also hypothyroxinemic, but their T3concentrations are mostly normal and ensure clinical euthyroidism, except for those that depend to a high degree on local generation from T4by extrathyroidal mechanisms involving the iodothyronine deiodinases isoenzymes. Thus, unless iodine deficiency is so severe and chronic that intrathyroidal and extrathyroidal mechanisms are no longer sufficient to maintain a normal T3in most tissues, individuals are clinically and biochemically euthyroid, but some tissues may be selectively hypothyroid (i.e., the brain). In adults both the intrathyroidal and the extrathyroidal mechanisms reacting to the iodine deficiency are fully operative even when the latter is mild. They contribute jointly to the maintenance of elevated or normal T3in those tissues deriving most of it from the plasma, until iodine deficiency becomes very severe. Those depending to a large extent from local generation from T4, mostly by an interplay between type 2 iodothyronine deiodinase (D2) and type 3 (D3), may already be T3-deficient (and hypothyroid) with mild iodine deficiency. Therefore, thyroid status of the iodine-deficient individual not only depends on the degree of iodine shortage, but is mostly tissue-specific, and is difficult to define for the individual as a whole: elevated, normal, and low concentrations of T3are found simultaneously in different tissues of the same animal, even with severe deficiencies. Most effects of iodine deficiency are reversed in the adults with an adequate iodine prophylaxis, but the absence of T4during early fetal life leads to irreversible brain damage (neurologic cretinism). Thyroid hormones of maternal origin are available to the embryo early in development and continue contributing to fetal thyroid hormone status, even after onset of fetal thyroid secretion. In the case of congenital hypothyroidism and normal maternal T4, the transfer of the latter, together with increased D2 activity, protects the fetal brain from T3deficiency, even when it may be insufficient to maintain euthyroidism in other fetal tissues. Practically all of the T3found in the fetal brain is derived locally from T4, and not from circulating T3. In the case of severe iodine deficiency, both the embryo and the mother are T4-deficient; therefore, the fetal brain is exposed to T3-deficiency, both before and after onset of fetal thyroid function. This leads to irreversible alterations and damage to the central nervous system (i.e. abnormal corticogenesis). Moreover, because intrathyroidal autoregulatory mechanisms are not yet operative in the fetus, both T4and T3continue to be very low until birth, and the fetus is not only hypothyroxinemic, similar to its mother, but also clinically and biochemically hypothyroid.

Maternal diabetes influences fetal pancreas development. As there are some controversial reports, we studied the morphometric changes of the fetal insular pancreas and insulin immunostain of beta cells as well as the proliferative activity of insular cells in 21-day-old fetuses from control, diabetic, and insulin-treated diabetic pregnant rats. Streptozotocin was injected into 7-day-pregnant rats (controls were not injected). Some rats were either left untreated (diabetic) or injected with insulin. Animals were killed at 21 days of gestation. Fetal pancreas were fixed in toto for the morphometry and immunohistochemistry studies using anti-insulin, anti-Ki-67 and anti-proliferating cell nuclear antigen (PCNA) antibodies. Diabetic status was determined by measuring maternal and fetal serum glucose and insulin levels. The morphometric studies showed hyperplasia of the diabetic fetal insular tissue which had not been normalized by insulin therapy. Diabetes caused an increase of both insulin-positive and insulin-negative cells. The increase in insulin-positive cells was not corrected by insulin treatment, although the number of non-beta cells became normal. The nuclear area in beta cells increased in diabetic rats but was not corrected by insulin. The cytoplasmic area decreased in diabetic rats and was normalized by insulin administration. Diabetes increased the expression of the nuclear antigen Ki-67 in fetal insular pancreas, and insulin treatment returned it to the normal state. Maternal diabetes leads to hyperstimulation of fetal beta cells, with increased proliferative activity. Insulin administration to the dams corrects some of the changes observed. Anat. Rec. 251:173–180, 1998. © 1998 Wiley-Liss, Inc.