Water quality of swimming pools in Athens area

In this work a representative sample of 11 indoor and outdoor swimming pools were investigated with respect to critical physicochemical, health-related, microbiological and technical parameters. These pools were used either as competition (athletic) or as recreation pools. Useful correlations of the above parameters were deduced and properly attributed. Results were checked against well-established standards, such as DIN 19643, showing poor compliance with them in all parameters investigated. Thus, compliance for health-related parameters varied from 0 to 100%, for physical and chemical parameters from 20 to 100%, for microbiological parameters from 45 to 91% and for technical parameters from 27 to 36%. The most critical parameters implicated for poor water quality were Redox potential, turbidity and the appearance of certain opportunistic pathogens ( Staphylococcus aureus and Pseudomonas aeruginosa ). These were attributed to poor process design of pools and lack of sufficient vocational training of the technical personnel operating the water treatment installations.     

Nocturnal sleep and blood pressure in essential hypertension

Blood pressure and sleep-wakefulness patterns were monitored in the sleep laboratory over four consecutive nights in six patients with mild hypertension and six age- and sex-matched controls. In both hypertensives and normals, blood pressure levels decreased during sleep compared with presleep levels by 16.6 and 8.4%, respectively; levels for hypertensives, however, remained significantly above those for the normals. The nocturnal drop in blood pressure for both groups appeared to be related primarily to the general state of sleep rather than to any specific sleep stage. Nocturnal patterns of sleep stages and sleep cycling were almost identical for the two groups. Nocturnal blood pressure fluctuation was correlated positively with the distribution of nocturnal wakefulness in hypertensives but not in normotensives. This suggests that with hypertension there is some diminution of the dampening effect of sleep itself upon blood pressure which normally carries over into periods of nocturnal wakefulness. This alteration in patients with mild hypertension may reflect a decrease in the sensitivity of the baroreceptor reflex or some other pathophysiological process.     

Nocturnal sleep and wakefulness: effects of age and sex in normal sleepers

Sleep patterns were evaluated in 100 normal men and women who did not have any complaints of a sleep disorder and who were divided into three broad age groups: 19-29, 30-49, and 50-80 years. Total laboratory recording time was held constant across all four study nights. The amount of nightly wakefulness was positively correlated with age; total wake time for the oldest age group was about two times that of the youngest group, due primarily to an increase in wake time after sleep onset, because sleep latency did not change with age. Within each of the three age groups, especially the two oldest groups, the greatest amount of wakefulness following sleep onset occurred in the final hours of the recording period. Sleep in men was characterized by a higher number of nocturnal awakenings, and in elderly men by a longer final awakening; however, other parameters of sleep efficiency did not differ considerably between the sexes.     

Acute weight gain induced by amisulpride monotherapy in a first-episode schizophrenic patient

The introduction of atypical antipsychotics into clinical practice has lead to an increase of adverse metabolic effects in psychotic patients. Amisulpride is a substituted benzamide derivative, and its use is associated with a lower risk of weight gain compared to other atypical antipsychotics. The case of an acute and excessive weight increase in a female first-episode schizophrenic patient who was treated with amisulpride monotherapy is reported. The improvement in psychopathology was remarkable. However, the patient gained 12.9 kg of body weight in the first 2 months of amisulpride administration and a total of 17.3 kg, 6 months after initiation of the treatment. Glucose and insulin levels, as well as a glucose tolerance test, remained normal throughout the observation period.     

NO-donating aspirin isomers downregulate peroxisome proliferator-activated receptor (PPAR)delta expression in APC(min/+) mice proportionally to their tumor inhibitory effect: Implications for the role of PPARdelta in carcinogenesis

Nitric oxide donating aspirin (NO-ASA), consisting of a traditional ASA to which a NO-releasing moiety is covalently attached, is a promising chemopreventive agent against colon cancer. Its mechanism of action is not fully delineated. Here we examined its effect on the expression of the nuclear receptor PPARdelta, whose role in colon carcinogenesis remains highly controversial. We studied histochemically the effect of the meta and para positional isomers of NO-ASA on PPARdelta expression in Min (multiple intestinal neoplasia) and wild-type mice, and on cell proliferation and apoptosis. PPARdelta, minimally expressed in wild-type mice, was significantly expressed in Min mice. para NO-ASA inhibited intestinal tumor incidence (59%) and PPARdelta expression (55.3%) more than meta NO-ASA (38 and 41.5%, respectively). Neither isomer affected cell proliferation, but both induced apoptosis in Min mice (para 52.5% for normal mucosa and 70.3% for tumors; meta 31.4 and 21.9%, respectively). The changes in PPARdelta expression correlated significantly with changes in apoptosis. Furthermore, NO-ASA induced areas of necrosis in intestinal tumors are probably resulting from the induction of atypical apoptosis. Our data suggest that NO-ASA suppresses intestinal tumorigenesis possibly in part through its inhibitory effect on PPARdelta, the expression of which may contribute to intestinal carcinogenesis.     

Education in mental health promotion and its impact on the participants' attitudes and perceived mental health

Awareness of the importance of maintaining physical health for patients with severe mental illnesses has recently been on the increase. Although there are several elements contributing to poor physical health among these patients as compared with the general population, risk factors for cardiovascular disease such as smoking, diabetes mellitus, hypertension, dyslipidemia, metabolic syndrome, and obesity are of particular significance due to their relationship with mortality and morbidity. These patients present higher vulnerability to cardiovascular risk factors based on several issues, such as genetic predisposition to certain pathologies, poor eating habits and sedentary lifestyles, high proportions of smokers and drug abusers, less access to regular health care services, and potential adverse events during pharmacological treatment. Nevertheless, there is ample scientific evidence supporting the benefits of lifestyle interventions based on diet and exercise designed to minimize and reduce the negative impact of these risk factors on the physical health of patients with severe mental illnesses.     

Carboxylesterases 1 and 2 hydrolyze phospho-nonsteroidal anti-inflammatory drugs: relevance to their pharmacological activity

Phospho-nonsteroidal anti-inflammatory drugs (phospho-NSAIDs) are novel NSAID derivatives with improved anticancer activity and reduced side effects in preclinical models. Here, we studied the metabolism of phospho-NSAIDs by carboxylesterases and assessed the impact of carboxylesterases on the anticancer activity of phospho-NSAIDs in vitro and in vivo. The expression of human liver carboxylesterase (CES1) and intestinal carboxylesterase (CES2) in human embryonic kidney 293 cells resulted in the rapid intracellular hydrolysis of phospho-NSAIDs. Kinetic analysis revealed that CES1 is more active in the hydrolysis of phospho-sulindac, phospho-ibuprofen, phospho-naproxen, phospho-indomethacin, and phospho-tyrosol-indomethacin that possessed a bulky acyl moiety, whereas the phospho-aspirins are preferentially hydrolyzed by CES2. Carboxylesterase expression leads to a significant attenuation of the in vitro cytotoxicity of phospho-NSAIDs, suggesting that the integrity of the drug is critical for anticancer activity. Benzil and bis-p-nitrophenyl phosphate (BNPP), two carboxylesterase inhibitors, abrogated the effect of carboxylesterases and resensitized carboxylesterase-expressing cells to the potent cytotoxic effects of phospho-NSAIDs. In mice, coadministration of phospho-sulindac and BNPP partially protected the former from esterase-mediated hydrolysis, and this combination more effectively inhibited the growth of AGS human gastric xenografts in nude mice (57%) compared with phospho-sulindac alone (28%) (p = 0.037). Our results show that carboxylesterase mediates that metabolic inactivation of phospho-NSAIDs, and the inhibition of carboxylesterases improves the efficacy of phospho-NSAIDs in vitro and in vivo.     

Phosphosulindac (OXT-328) Selectively Targets Breast Cancer Stem Cells In Vitro and in Human Breast Cancer Xenografts

Pharmacological targeting of breast cancer stem cells (CSCs) is highly promising for the treatment of breast cancer, as the small population of CSCs appears responsible for tumor initiation and progression and also for resistance to conventional treatment. Here we report that the novel phosphosulindac (OXT-328, PS) selectively and effectively eliminates breast CSCs both in vitro and in vivo. PS reduced cell proliferation and induced apoptosis in various breast CSCs. Breast CSCs are resistant to conventional cancer drugs but are sensitive to PS. Long-term treatment of mixtures of cultured breast CSCs and breast cancer cells with PS preferentially eliminated the CSCs. PS impaired the ability of CSCs to form mammospheres and markedly suppressed the expression of CSC-related genes. More importantly, PS prevented by half (p =.06) the formation of tumors initiated by CSCs in immunodeficient mice, and inhibited by 83% (p <.05) the growth of already formed breast cancer xenografts, reducing the proportion of CSCs in them. PS suppressed the Wnt/β-catenin pathway by stimulating the degradation of β-catenin and its relocalization to the cell membrane and also blocked the epithelial-mesenchymal transition and the generation of breast CSCs. These results indicate that PS has a strong inhibitory effect against breast cancer, acting, at least in part, by targeting CSCs through a signaling mechanism involving Wnt signaling. STEM Cells2012;30:2065-2075.