Adverse health and environmental outcomes of sewage treatment plant on surrounding groundwater with emphasis on some mitigation recommendations.

Water quality deterioration hinders economic and social development in developing countries that are facing freshwater security and shortages. Based on the collection of 29 water samples, this study focused on the relationship between sewage treatment plant and groundwater system surrounding it using multidisciplinary approach that combines the characterization of groundwater system and its connection with surrounding canal and drains, using chemical and isotopic characterization revealing that there is a direct relation between the surface water system and surrounding groundwater system. About 58% of the groundwater samples and all surface water samples in the investigated area are threatened by high concentrations of trace elements. The multivariate statistical analysis elucidates that anthropogenic effect and fertilizers sewage contamination are the main causes of groundwater pollution. Nearly, 31% and 11.5% of groundwater samples were posing oral chronic non-carcinogenic health risk and dermal chronic risk for adult, respectively, while all surface water samples were posing oral chronic non-carcinogenic health risk, with no dermal hazard. The uncharged species of Fe and Al are expected to be more mobile in groundwater because they would not be attracted to the surface charge of minerals. Inorganic ligands (HCO3-, SO42-, Cl-, and NO3-) act as nucleation centers that were linked with those trace elements creating new species with higher solubility degree in water that are transported away randomly for long distances in the water path.

Two new records of flies causing myiasis from Saudi Arabia with a survey of flies parasitizing goats and sheep in Jazan Region.

Despite the medical, veterinary and forensic relevance of myiasis-causing flies, knowledge of their diversity in Saudi Arabia is limited especially in the southern region. Therefore, a survey of myiasis-causing flies in the Jazan region was carried out using Red Top Fly Catcher traps baited with either decomposing beef liver or a lure composed primarily from fishmeal during the period April 2013-March 2014. Twelve known species were identified and recorded in this study, seven species of them belonging to Calliphoridae (Chrysomya, Lucilia, and Hemipyrella) and five species belonging to Sarcophagidae (Sarcophaga). Two of these species were recorded for the first time for Saudi Arabia, namely Hemipyrella pulchra (Wiedemann, 1830) and Sarcophaga (Liosarcophaga) exuberans Pandellé, 1896. Images of the species recorded are also provided for the first time. The results expand the knowledge of geographical distribution, fauna, and habitat of the myiasis-causing flies in Saudi Arabia. Biological information and world-wide geographical distribution of these species are included together with some taxonomic remarks.

Two new records of flies causing myiasis from Saudi Arabia with a survey of flies parasitizing goats and sheep in Jazan Region

@#Despite the medical, veterinary and forensic relevance of myiasis-causing flies, knowledge of their diversity in Saudi Arabia is limited especially in the southern region. Therefore, a survey of myiasis-causing flies in the Jazan region was carried out using Red Top Fly Catcher traps baited with either decomposing beef liver or a lure composed primarily from fishmeal during the period April 2013-March 2014. Twelve known species were identified and recorded in this study, seven species of them belonging to Calliphoridae (Chrysomya, Lucilia, and Hemipyrella) and five species belonging to Sarcophagidae (Sarcophaga). Two of these species were recorded for the first time for Saudi Arabia, namely Hemipyrella pulchra (Wiedemann, 1830) and Sarcophaga (Liosarcophaga) exuberans Pandellé, 1896. Images of the species recorded are also provided for the first time. The results expand the knowledge of geographical distribution, fauna, and habitat of the myiasis-causing flies in Saudi Arabia. Biological information and world-wide geographical distribution of these species are included together with some taxonomic remarks.

Reversal of impaired calcium homeostasis in the rat diaphragm subjected to Monocrotaline-induced pulmonary hypertension.

Monocrotaline (MCT) pneumotoxicity is known to alter the structure of pulmonary vascular wall and impairs endothelial cell function resulting in pulmonary hypertension. Its effect on the diaphragm muscle has not yet been elucidated. This study examines the effect of MCT pneumotoxicity on calcium transport in the rat diaphragm. Pulmonary hypertension induced by MCT pneumotoxicity caused a significant increase (P < 0.001) in calcium accumulation in strips isolated from rat diaphragms. Treatment of rats having received MCT with Indapamide reduced calcium uptake by diaphragmatic strips to levels that are not significantly different from the control (P > 0.05). Treatment with Indapamide alone did not elicit any change in calcium accumulation in the diaphragmatic strips. Treatment of the animals with MCT, Indapamide or both did not produce any significant change (P > 0.05) in the cell volume of the diaphragmatic strips. Pulmonary hypertension increased calcium uptake by the muscle cells in the rat diaphragm which may alter diaphragmatic contractility; an effect that was prevented by Indapamide.

Prostacyclin-enhanced calcium sequestration by microsomes isolated from rat left ventricle.

The objective of these experiments was to investigate the direct effect of prostacyclin on calcium binding and uptake by microsomal vesicles isolated from rat left ventricle. The protein content of the preparation was found to be 2.73 +/- 0.18 mg microsomal protein/g of left ventricular wet weight. Steady-state calcium binding and uptake by microsomal vesicles was reached at 6 minutes in control animals and 20 sec in prostacyclin-treated experiments. Prostacyclin increased steady-state calcium binding and uptake from a control of 52.48 +/- 4.16 up to 109.31 +/- 3.06 nmol/mg protein (p less than 0.05) and from 238.07 +/- 12.37 up to 314.85 +/- 1.23 nmol/mg protein (p less than 0.05) respectively. Doubling the concentration of prostacyclin from initial dose of 1.2 x 10(-8) M did not alter calcium binding and uptake further.

Prostacyclin-inhibition of lysine accumulation by the rat left ventricle.

1. Left ventricular slices of male Sprague-Dawley rats were incubated with a fixed concentration of 0.5 microCi/ml 3H-lysine and several concentrations of unlabelled lysine ranging from 0.2 to 5.0 mM in control and prostacyclin-treated experiments. The time of incubation ranged from 0.5 to 90 min. 2. Left ventricular slices were cut to have an optimal thickness of 0.47 +/- 0.09 mm. 3. Lysine was taken up against a concentration gradient. Saturation was reached at 0.5 mM and steady state accumulation of lysine was attained within 60 min. 4. Prostacyclin in concentrations ranging from 1.2 x 10(-8) to 4.8 x 10(-8) M inhibited lysine transport in left ventricular slices significantly (P less than 0.01).

Enzymatic inhibition of lysine transport across the small intestine in vivo.

1. Trypsin, at different concentrations, significantly inhibited lysine absorption (P less than 0.05) in a dose-dependent pattern. 2. Maximum inhibition equivalent to 35% below control value was reached with 10 micrograms/ml (100 BAEE units) trypsin with a non-reversible inhibitory effect. 3. Chymotrypsin at 10 micrograms/ml produced a significant decrease (P less than 0.05) of lysine absorption although it did not exceed 5%. Perfusion of both enzymes did not show an additive inhibitory effect. 4. Lysine absorption showed a 39% decrease with 10 micrograms/ml trypsin and 1 X 10(-4) M ouabain, whereas ouabain alone produced 34% inhibition. 5. Lysine absorption showed a 71% decrease with 10 micrograms/ml trypsin in a sodium-free medium, and 70% inhibition with Na-free medium alone. 6. The inhibition of lysine absorption after trypsin treatment could be due to inhibition of the active component of lysine transport.

Cytoskeletal control of calcium absorption across the rat small intestine.

1. The effect of colchicine, cytochalasin-B and procaine on calcium transport across the rat small intestine was investigated. The results obtained show the following: 2. Colchicine and cytochalasin-B at different concentrations inhibited significantly (P less than 0.001) calcium accumulation in rat intestinal cells, whereas procaine at different concentrations increased significantly (P less than 0.001) calcium accumulation in the rat small intestine. 3. Unidirectional influx of calcium across the rat small intestine was significantly inhibited (P less than 0.01) in the presence of colchicine and cytochalasin-B in the preincubation medium. Procaine, on the other hand, caused a significant increase (P less than 0.01) in the unidirectional influx of calcium across the rat intestinal cells. 4. The cell water content was not altered in the presence of the different drugs indicating that the changes in calcium transport across the rat intestinal cells are not due to alterations in the structure of the cell membrane.

Dopamine receptors in normal and diabetic liver plasma membrane.

Dopamine binding to liver plasma membrane isolated from diabetic livers was significantly reduced (P less than 0.01) as compared to dopamine binding to the normal membrane. Diabetic membranes exhibited a significant decrease (P less than 0.01) in specific dopamine binding as compared to the normal membranes; whereas no significant change (P less than 0.5) was noticed in the nonspecific binding patterns. The dopamine binding capacity of both membranes is temperature dependent. Procaine at different concentrations inhibited significantly (P less than 0.01) dopamine binding to normal and diabetic membranes. Treatment of the normal and diabetic membranes with insulin showed a 33% decrease in the binding capacity of the normal and 42% decrease in the binding capacity of the diabetic membrane.

Effect of enzymatic digestion on phenylalanine transport across the small intestine.

Phenylalanine accumulation in mucosal strips isolated from rat small intestine was significantly inhibited (P less than 0.01) after preincubation with trypsin, chymotrypsin, phospholipase D and neuraminidase. Unidirectional phenylalanine influx across the small intestine was significantly reduced (P less than 0.01) when the mucosal strips were preincubated with the above mentioned enzymes. Intestinal cell water and volume were not significantly changed (P greater than 0.6) when the intestinal tissues were preincubated with these enzymes.

Receptors of prostaglandin E1 in the plasma membrane of normal liver. Effect of membrane fluidity on PGE1 binding.

Prostaglandin E1 binding to isolated liver plasma membrane as a function of PGE1 concentration showed saturability of the binding sites at PGE1 concentration of 2.5 X 10(-4) M. Scatchard analysis revealed heterogeneous population of binding sites with a binding capacity of 470 and 990 nmol/mg protein for the higher and lower affinity binding sites respectively. PGE1 binding to liver plasma membrane was progressively and significantly decreased (P less than 0.01) as the incubation temperature was reduced to 22 degrees and 4 degrees C. Procaine at 1 X 10(-3) M concentration showed a significant decrease (P less than 0.01) in the binding capacity of the liver plasma membrane. Colchicine plus cytochalasin-B inhibited PGE1 binding significantly (P less than 0.01) but their inhibition is not equivalent to that of procaine.

Calcium binding to normal, regenerating and diabetic liver plasma membrane.

Calcium binding to liver plasma membrane isolated from diabetic and regenerating livers was significantly reduced (P less than 0.01) when compared to Ca binding to the normal membrane. Procaine at different concentrations inhibited significantly (P less than 0.01) calcium binding to the normal, diabetic and regenerating liver plasma membrane, with the most pronounced inhibition noticed in the normal. Colchicine at a concentration exceeding 5 X 10(-4)M showed a significant decrease (P less than 0.01) in calcium binding to the normal, diabetic and regenerating liver plasma membrane with the maximum inhibition noticed in the regenerating liver membrane.