Qualitative and quantitative aspects of drinking water supply in Sardinia, Italy. A descriptive analysis of the ordinances and public notices issued during the years 2010-2015.

BACKGROUND: The aim of the study is to analyze the regional district ordinances and the warnings regarding qualitative and quantitavive drinking water abnormalities discovered by the Sardinian Municipalities and the Water Managing Authority between 2010 and 2015 in order to describe and identify the causes leading to an interruption or a limitation of the drinking water supply. METHODS: We carefully reviewed all ordinances and warnings of non-potable water and service interruption published between 2010 and 2015 by the websites of 377 Sardinian Municipalities and by the main regional newspapers, the Water Managing Authority and the Regional Health Trusts. RESULTS: From 2010 to 2015, 738 warnings/ordinances regarding drinking water supply limitation or interruption were issued. The warnings involved more than half (n. 191, 50.7%) of the 377 Sardinian Municipalities. Considering that these Municipalities included the main Sardinian cities we estimated that 80.3% of the population was affected by the issue. During the 6 years we observed a progressive increase of Municipalities involved beginning with 25 and reaching up 110 in 2014. The initial 29 warnings rose to 256 in 2014 along with an increased number of abnormal values, parameters and standards of the drinking water. Regarding the ordinances issued by the 191 Mayors we noticed that the legal limits were exceeded in 23 cases. Among those, we underline the abnormal levels of chlorites and trihalomethanes (22% of cases), the turbidity, the abnormal concentration of total chemical substances and the abnormal level of coliforms, Escherichia coli, manganese, aluminum, nitrites and iron. CONCLUSIONS: According to our observations, the Sardinian drinking water supply system is affected by a major inconvenience and the data suggest that qualitative abnormalities are mainly due to water purification treatments used in addition to the poor water supply network in existence. Considering these results, a cooperation between all Authorities involved would be desirable in order to analyze official data and provide a careful evaluation of population exposure and real risks related to the level of every parameter considered.

[Functioning tumors of the adrenal cortex in children. Clinical and therapeutic considerations on 11 cases]. / Tumores funcionantes de la corteza suprarrenal en niños. Consideraciones clínicas y terapéuticas en once casos.

In the last 20 years, eleven children with adrenocortical functional tumors were treated in the National Children Hospital of Costa Rica. There were nine females and two males and their ages ranged from nine months to 14 years. Eleven patients had features of virilism, five had stigmas of Cushing's syndrome and three hyperaldosteronism. The clinical diagnosis was established given the symptoms, hormonal tests and radiological and imagenological studies. The histologic diagnosis was carcinoma in six by clinical picture in one, and were adenoma in four. Three patients had regional and distant metastases. Four patients with carcinoma were treated by surgery and five received chemotherapy, two of them in presurgical stage, and four received radiotherapy. Two patients with carcinoma are alive and had no evidence of tumor recurrence ten and six years after diagnosis. Five are dead, two of them after partial response to chemotherapy. The four patients with adenoma were cured by complete surgical tumor resection, furthermore one of them received chemotherapy because there was not sure of his histologic benign condition. It is necessary more studies in use of chemotherapy in treatment of this tumors but in our experience CFM, VCR, Epi and Actin is a regimen that appears to be an active combination for the treatment in presurgical stage of adrenal cortical carcinoma.

Increased basal glucose production and utilization in children with recent obesity versus adults with long-term obesity.

To characterize the abnormalities of glucose homeostasis and insulin action early in the course of human obesity, we studied in vivo glucose kinetics in seven children who were recently massively overweight. At time of study they were gaining weight at a rate of 13.5 +/- 1.4 kg/yr. They were compared with six age-matched control subjects. Six adults with long-term obesity and five normal adults were studied in parallel. The obese children and adults were normoglycemic and hyperinsulinemic. We found that glucose production and utilization were remarkably higher in obese children (295 +/- 18 mg/min; 7.6 mg.kg-1 lean body mass.min-1) than in control children (129 +/- 13 mg/min; 4.4 mg.kg-1 lean body mass.min-1, P less than .01) and obese adults (151 +/- 8 mg/min; 3.1 +/- 0.3 mg.kg-1 lean body mass.min-1, P less than .01). Obese adults had normal rates of glucose production and utilization. Insulin- and non-insulin-mediated glucose uptake, estimated with somatostatin-induced suppression of endogenous insulin secretion, contributed almost equally to the excess glucose utilization observed in the obese children. When studied with the euglycemic-hyperinsulinemic clamp, obese children could not increase glucose disposal to the same extent as normal children and were not able to adequately suppress their endogenous glucose production. Recently obese children are therefore characterized by an increased basal glucose turnover rate and an already established insulin resistance of the liver and probably the skeletal muscles.

Risk of ketosis during intensive insulin therapy in pre-school-age diabetic children.

The risk of ketosis and its relationship to the mode of insulin therapy were studied in a subset of pre-school-age diabetic children. These five children, who initially responded poorly to standard in-hospital diabetes management, were selected for a program of intensified therapy directed at achieving more stable blood glucose control. Optimized conventional therapy was first employed for 16 +/- 5 mo and did not improve substantially blood glucose level or stability. During this period, there was an average of almost one episode of ketonuria per patient per month, and three diabetic ketoacidosis episodes were observed. Because of its limited efficacy, the treatment was then changed to continuous subcutaneous insulin infusion. This mode of therapy had a rapid favorable effect on blood glucose control, with no concomitant increase of the frequencies of ketonuria or diabetic ketoacidosis, most of which occurred during the first months of insulin pump therapy. Deliberate cessation of either conventional or subcutaneous insulin infusion therapy for 7 h under close in-hospital control resulted in similar metabolic changes: a slight nonconstant increase of blood glucose, and an abrupt rise of blood 3-hydroxybutyrate to 3 mM, with massive ketonuria. The management of these young diabetic children with insulin pump therapy was thus not associated with an increased frequency or an accelerated rate of development of ketosis. However, the possible failures originating from the infusing device and the rapid increase of ketosis in young ages require special vigilance from the parents, based on twice-daily urine testing for ketones and appropriate insulin supplementation.

Frequency of hypoglycemia in children with adrenal insufficiency.

The frequency of hypoglycemia in 165 children with primary adrenal insufficiency, 118 of whom had Congenital Adrenal Hyperplasia and 47 Addison's Disease, was 18%. Half of the hypoglycemic episodes occurred in the neonatal period. Hypoglycemia was isolated in 13 children, revealing the disease in 4 newborns with Congenital Adrenal Hypoplasia and in a boy with 11 B Hydroxylase deficiency. Basal plasma cortisol levels were significantly lower in those of subjects who experienced hypoglycemia (47.1 +/- 28.6 ng/ml vs. 106.0 +/- 86.6 ng/ml, p less than 0.001). A significant correlation (p less than 0.001) was found between the plasma concentration of glucose and cortisol at time of hypoglycemia.

Effects of hypopituitarism and growth hormone replacement therapy on the production and utilization of glucose in childhood.

Glucose metabolism during fasting was investigated in 10 children aged 1.5 month-11.5 yr with deficiency of GH with or without other pituitary hormone deficiencies. After 10-16 h of fasting, mean plasma glucose was 56 +/- 4 (SEM) mg/dl, the result of decreased hepatic production of glucose (3.3 +/- 0.3 mg kg-1 min-1) insufficient to match glucose utilization (3.6 +/- 0.4 mg kg-1 min-1). The diminution of plasma glucose and of glucose production was similar whether ACTH deficiency was present (3.2 +/- mg kg-1 min-1) or not (3.5 +/- 0.6 mg kg-1 min-1). These results indicate that the lack of GH was the primary cause of hypoglycemia. Fasting plasma alanine (212 +/- 41 mumol/liter) and lactate (1222 +/- 136 mumol/liter), the main gluconeogenic substrates, were normal and did not correlate with the decrease of hepatic glucose release. Both plasma FFA (552 +/- 35 microM) and beta-hydroxybutyrate (654 +/- 158 microM) were in the low normal range, and neither correlated with the rate of glucose utilization. hGH replacement therapy resulted in a normalization of fasting plasma glucose concentration (78.5 +/- 6 mg/dl, P less than 0.005) and hepatic glucose production (6.1 +/- 1.2 mg kg-1 min-1). No significant changes occurred in the plasma concentrations of gluconeogenic or lipid substrates. These results, together with the known stimulatory effects of GH on carbohydrate-induced insulin secretion and storage of hepatic glycogen, suggest that the changes in glucose production in untreated and GH treated patients reflect the degree of hepatic glycogen replenishment.

Comparison between the radiosensitivity of human, mouse and chicken fibroblast-like cells using short-term endpoints.

We have performed a comparative study of the radiosensitivity of fibroblastic cell lines from three different animal species: human, mouse and chicken. Endpoints reflecting short term responses were utilized: colony forming ability (CFA), DNA single strand break (SSB) repair and repair of potentially lethal damage (PLD). Regardless of the criterion employed, the response to radiation varies from one species to another. According to our survival curves, chicken cells appear to be more radioresistant than those of human and mouse. SSB repair is apparently absent in murine cells, partial in chicken cells and complete in human cells. This lack of correlation between survival curves and SSB repair demonstrates that survival of irradiated cells does not depend only (or at all) on the repair of SSB. The repair of PLD is much more efficient in human and chicken cells than in murine cells.

Changes in RNA synthesis during the life span of human fibroblasts in vitro.

The prolongation of the life span of human fibroblasts in vitro by hydrocortisone seem to be associated with its stimulatory action on ribosome synthesis. The sustaining effect of the hormone on the latter remains, after withdrawal of hydrocortisone, for a time which is dependent on the age of the cells. When hydrocortisone is removed from cultures that have grown beyond the life span of the controls, the cells die within two passages. Hence, the events leading to the growth decline took place in spite of the presence of the hormone which does not seem to prevent the aging process but rather to delay it. The results could be compatible with either the error hypothesis or the theory which explains aging by an increased binding of histones to DNA with the subsequent blocking of genetic information.

Relationship between cell kinetic changes and metabolic events during cell senescence in vitro.

Cell kinetic studies performed throughout the lifespan of fibroblasts with a limited lifespan in vitro have led to the conclusion that although division slows down, almost all cells are able to divide until the last subcultivation. The prolongation of the division cycle is primarily due to the impariment of mechanisms preceding DNA synthesis and mitosis. An attempt was made to distinguish between primary and secondary changes and to correlate the findings concerning cell kinetics with alterations observed at the molecular level. A decline in protein synthesis was the first modification detected. The two parameters that are always present during cell senescence in vitro, i.e., and increase in cell volume and a decrease in saturation density could be due respectively to a change in cell permeability and a decline in ribosome synthesis. The latter could also be the step responsible for the limited potential of division.