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This study investigates the hydrochemical formation mechanism of shallow groundwater in the Upper Kebir upstream sub-basin (Northeastern Algeria). The objective is to evaluate water quality suitability for domestic purposes through the application of water quality index (WQI). A total of 24 water points (wells and borewells) evenly distributed in the basin were collected and analyzed in the laboratory for determining the major ions and other geochemical parameters in the groundwater. The groundwater hydrochemical types were identified as Cl–Na and Cl–HCO3 –Na, with the dominant major ions were found in the order of Na+ > Ca2+ > Mg2+ for cations, and Cl− > SO42− > HCO3– > NO3− for anions. Results suggest that weathering, dissolution of carbonate, sulfate, salt rocks, and anthropogenic activities were the major contributors to ion content in the groundwater. The Water Quality Index (WQI) was calculated to assess the water quality of potable water. Approximately 50% of the sampled sites exhibited good water quality. However, the study highlights significant NO3 contamination in the study area, with 50% of samples exceeding permissible limits. Therefore, effective treatment measures are crucial for the safe consumption of groundwater.

Background: The present study compared two methods used successfully in a large-scale program for the collection of scorpion venoms, namely the milking of adult scorpions via manual and electrical stimulation., Results: Our immunobiochemical characterizations clearly demonstrate that regularly applied electrical stimulation obtains scorpion venom more easily and, most importantly, in greater quantity. Qualitatively, the electrically collected venom showed lack of hemolymph contaminants such as hemocyanin. In contrast, manual obtainment of venom subjects scorpions to maximal trauma, leading to hemocyanin secretion. Our study highlighted the importance of reducing scorpion trauma during venom milking., Conclusions: In conclusion, to produce high quality antivenom with specific antibodies, it is necessary to collect venom by the gentler electrical stimulation method.

In many species, delayed sexual maturation occurs when metabolic conditions are not satisfactory. Recently, leptin was shown to be involved in the regulation of food intake and body mass. Furthermore, leptin administration was shown to advance sexual maturation in mice and to rescue sexual function in adverse metabolic conditions. We examined plasma leptin levels in female rats during development and evaluated the role of leptin on sexual maturation in rats subjected to food restriction. In normal rats, plasma leptin levels were low at day 24 of life, then steadily increased during the juvenile period, reaching 740+/-56 pg/ml at 40 days at time of vaginal opening (VO) and further increasing by day 60 (957+/-73 pg/ml). Food restriction initiated at day 25 strongly impaired this increase, in proportion to the severity of the restriction. With a daily food intake reduced to 7-8 g/day, that permanently prevented VO, plasma leptin levels were very low at day 53 (169+/-67 pg/ml). Following switch to ad libitum feeding, plasma leptin reached high levels within 2 days (1577+/-123 pg/ml), and VO occurred 4 days later. If the severe food restriction was maintained and a central infusion of leptin (10 microg/day) was initiated, a significant decrease in body weight compared with vehicle-infused controls was observed. In these conditions, VO occurred in eight out of the nine leptin-treated rats, representing induction of the process of sexual maturation confirmed by increases in ovarian and uterine weights. This induction of sexual maturation exclusively results from a central effect of leptin because no leak of the i.c.v. administered leptin to the general circulation was observed. These data suggest that the rising plasma levels of leptin in the prepubertal period represent a signal to the brain indicating that the young animal is metabolically ready to go through the process of sexual maturation.

The obese gene (OB) product, leptin, has been shown to exert control on metabolic processes such as food intake and body weight homeostasis, possibly through a neuropeptide Y (NPY) neurotransmission. More recently, leptin has been shown to control several neuroendocrine axes, modulating pituitary hormone secretions in function of metabolic conditions. Since in the rat growth hormone (GH) secretion is dependent upon prevailing metabolic conditions, and NPY has been shown to be implicated in the feedback mechanisms of this hormone, we reasoned that leptin could also exert control over GH secretion and we examined this hypothesis in male rats submitted to a 3-day fast. Circulating leptin concentrations measured by RIA abruptly fell to low values after 24 h of fasting and remained low thereafter. Upon refeeding, leptin secretion regularly increased. As shown by others, pulsatile GH secretion had disappeared after 3 days of fasting. Centrally administered leptin (10 microg/day, i.c.v. infusion initiated at the beginning of the fasting period) totally prevented the disappearance of pulsatile GH secretion. No leak of centrally administered leptin to the general circulation was observed. Infusing the same amount of leptin intracerebroventricularly to rats receiving ad libitum feeding produced a severe reduction in food intake but maintained a normal GH secretory pattern. In contrast, pair-fed rats, submitted to the same food restriction, exhibited a marked reduction in GH secretion. Hypothalamic NPY gene expression, estimated by Northern blot analysis, was significantly increased in fasting rats, and decreased in leptin-treated, fasting rats. In rats receiving ad libitum feeding, leptin treatment reduced NPY gene expression, consistent with the observed reduction in food intake, whereas pair-fed animals logically exhibited increased NPY gene expression. In both situations with reduced feeding, normal GH secretion was seen in leptin-treated animals exhibiting low NPY gene expression, whereas decreased or abolished GH secretion was seen in animals not receiving leptin and exhibiting increased NPY mRNA levels. Interestingly, despite maintenance of normal GH secretion in leptin-treated, fasting rats, plasma IGF-I levels were low, as in vehicle-treated rats. Indeed, hepatic gene expression for both GH receptor and IGF-I was markedly reduced by fasting, and no correction was seen with leptin treatment. In summary, the regulation of GH secretion, at least the changes linked with malnutrition, appears to be dependent upon a leptin signal, perceived centrally, possibly related to circulating levels of this new hormone. The present data suggest that leptin can rescue normal pulsatile GH secretion by preventing the documented inhibitory action of NPY on GH secretion.