The kidney is among the metabolic organs most susceptible to injury, particularly following exposure to xenobiotics and heavy metals. We aimed to explore the potential protective impacts of coenzyme Q10 (CoQ10) on lead acetate (PbAc)-induced nephrotoxicity in rats. Four experimental groups (n = 7) were applied as follows: control group, CoQ10 alone (10 mg/kg), PbAc alone (20 mg/kg), and PbAc with CoQ10. Exposure to PbAc led to the accumulation of Pb in the kidney and increased urea and creatinine serum levels. The deposition of Pb coupled with the elevation of malondialdehyde and nitrate/nitrite levels along with the upregulation of inducible nitric oxide synthase. Additionally, upon PbAc poisoning, glutathione content and the antioxidant enzymes were depleted along with the downregulation of Nrf2 and HO-1 expression. Moreover, PbAc injection increased the protein and mRNA levels of pro-inflammatory cytokines namely, tumor necrosis factor-alpha and interleukin-1 beta, while decreased the levels of interleukin-10, an anti-inflammatory cytokine, in the kidney. Furthermore, exposure to PbAc correlated with increased levels of pro-apoptotic markers, Bax and caspase-3, and reduced levels of the anti-apoptotic marker Bcl-2. The administration of CoQ10 alleviated the molecular, biochemical and histological changes following PbAc intoxication. Thus, CoQ10 reduces the deleterious cellular side effects of PbAc exposure due to its antioxidant, anti-inflammatory and anti-apoptotic effects.

Gamma-aminobutyric acid (GABA) and glutamate are the most abundant amino acid neurotransmitters in the brain. GABA, an inhibitory neurotransmitter, is synthesized by glutamic acid decarboxylase (GAD). Its predominant isoform GAD67, contributes up to ∼90% of base-level GABA in the CNS, and is encoded by the GAD1 gene. Disruption of GAD1 results in an imbalance of inhibitory and excitatory neurotransmitters, and as Gad1−/− mice die neonatally of severe cleft palate, it has not been possible to determine any potential neurological dysfunction. Furthermore, little is known about the consequence of GAD1 disruption in humans. Here we present six affected individuals from six unrelated families, carrying bi-allelic GAD1 variants, presenting with developmental and epileptic encephalopathy, characterized by early-infantile onset epilepsy and hypotonia with additional variable non-CNS manifestations such as skeletal abnormalities, dysmorphic features and cleft palate. Our findings highlight an important role for GAD1 in seizure induction, neuronal and extraneuronal development, and introduce GAD1 as a new gene associated with developmental and epileptic encephalopathy.

BackgroundHypophosphatemia is one of the common disorders that develop in critically ill patients. It has potential complications and is often unrecognized in those patients.ObjectiveDetermining the incidence of hypophosphatemia in critically ill children, its association with clinical outcomes and the possible risk factors.Methods50 patients were enrolled in the study. Levels of serum phosphate were measured on day 1 and day 7 of PICU (Pediatric intensive care unit) stay. The following variables were analyzed: age, gender, diagnosis on admission, malnutrition, phosphorus intake, clinical severity score on admission OFI (Organ Failure Index) and daily scores PELOD (Pediatric Logistic Organ Dysfunction), sepsis, use of dopamine, furosemide and steroids and assessment of nutrition by z scores.ResultsThe incidence of hypophosphatemia on admission was 42%. On seventh day of admission incidence of hypophosphatemia was 62%. Malnutrition was present in 24% of patients, serum phosphorus level was significantly lower in malnourished than in well-nourished children (p value = 0.018). Hypophosphatemia was associated with prolonged PICU length of stay (p < 0.001) but was not associated with increased mortality (p = 0.13). Cases on parenteral nutrition and insufficient oral intake while on mechanical ventilator significantly showed hypophosphatemia (p = 0.017). Hypophosphatemia was associated with the use of furosemide, dopamine, steroids and β2 agonist.ConclusionHypophosphatemia was common in the first 7 days of PICU hospitalization and was associated with prolonged PICU stay, Significant association between hypophosphatemia and duration of use of mechanical ventilation, use of furosemide, dopamine, steroids and β2 agonist.

The current study examined the efficacy of royal jelly (RJ) against cadmium chloride (CdCl2)-induced testicular dysfunction. A total of 28 Swiss male mice were allocated into four groups (n = 7), and are listed as follows: (1) the control group, who was intraperitoneally injected with physiological saline (0.9% NaCl) for 7 days; (2) the RJ group, who was orally supplemented with RJ (85 mg/kg daily equivalent to 250 mg crude RJ) for 7 days; (3) the CdCl2 group, who was intraperitoneally injected with 6.5 mg/kg for 7 days; and (4) the fourth group, who was supplemented with RJ 1 h before CdCl2 injection for 7 days. Cd-intoxicated mice exhibited a decrease in serum testosterone, luteinizing hormone (LH), and follicle stimulating hormone (FSH) levels. A disturbance in the redox status in the testicular tissue was recorded, as presented by the increase in lipid peroxidation and nitrate/nitrite levels and glutathione (GSH) depletion. Moreover, the activities of glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), and nuclear factor (erythroid-derived 2)-like-2 factor (Nrf2) and their gene expression were inhibited. In addition, interleukin-1ß (IL-1β) and tumor necrosis factor-α (TNF-α) levels were elevated. Furthermore, Cd triggered an apoptotic cascade via upregulation of caspase-3 and Bax and downregulation of Bcl-2. Histopathological examination showed degenerative changes in spermatogenic cells, detachment of the spermatogenic epithelium from the basement membrane, and vacuolated seminiferous tubules. Decreased cell proliferation was reflected by a decrease in proliferating cell nuclear antigen (PCNA) expression. Interestingly, RJ supplementation markedly minimized the biochemical and molecular histopathological changes in testes tissue in response to Cd exposure. The beneficial effects of RJ could be attributed to its antioxidative properties.

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This study was conducted in the neonatal intensive care unit of Benha University Hospital, Egypt from 1 August 2012 to the 31 January 2013 to identify medical errors and to determine the risk factors and consequences of these errors. Errors were detected by follow-up of neonates and review of reports including nursing followup sheets, resident progression notes and investigation reports. We detected 3819 errors that affected 97% of neonates. Types of errors included 403 medication errors (10.55% of total errors), 652 errors in daily routine procedures (17.07%), 1042 errors in invasive procedures (27.28%), 68 errors in nutrition (1.78%), 63 equipment errors (1.64%), 260 administration errors (6.8%), 656 staffing errors (17.18%), 107 environmental errors (2.8%), 448 infection control errors (11.73%) and 120 nosocomial infection errors (3.14%). Medical errors were high in low birth weight, low gestational age neonates and increased with duration of admission. RÉSUMÉ La présente étude a été conduite dans l'unité néonatale de soins intensifs du centre hospitalier universitaire de Banha, en Égypte, du 1 er août 2012 au 31 janvier 2013, dans le but d'identifier les erreurs médicales et de déterminer les facteurs de risque et les conséquences associés. Des erreurs ont été détectées dans le suivi des nouveau-nés et l'analyse de rapports incluant des fiches de suivi des soins infirmiers, des notes sur la progression des internes, et des rapports d'enquête. Nous avons détecté 3 819 erreurs ayant affecté 97 % des nouveau-nés. Les types d'erreurs incluaient 403 erreurs de médication (10,55 % du nombre total d'erreurs), 652 erreurs dans les actes de routine journaliers (17,07 %), 1 042 erreurs dans les procédures invasives (27,28 %), 68 erreurs de nutrition (1,78 %), 63 erreurs d'équipement (1,64 %), 260 erreurs administratives (6,8 %), 656 erreurs au niveau du personnel (17,18 %), 107 erreurs en matière de pratiques environnementales (2,8 %), 448 erreurs liées à la lutte contre les infections (11,73 %) et 120 erreurs entraînant des infections nosocomiales (3,14 %). Les erreurs médicales étaient nombreuses dans les cas de nouveau-nés souffrant d'une insuffisance pondérale à la naissance ou étant nés prématurément, et elles augmentaient en fonction de la durée de l'hospitalisation. ‫مرص‬

BackgroundIn critically ill patients, there are reduced stores of antioxidants, which are associated with increased organ failure and even higher mortality. Trace elements, especially zinc and selenium, are the cornerstone of the antioxidant defense in acute systemic inflammatory response syndrome. Prolactin (PRL) is the counterregulatory stress hormone that prevents cortisol/stress-induced lymphocyte apoptosis. The aim of our study is to detect the serum levels of zinc, selenium, and PRL hormone as important immunomodulators in critically ill children and to investigate the relationship between these immunomodulators and the severity of illness.Subjects and methodsThis was a prospective study that included two groups; group 1: 50 critically ill children within 72 hours of intensive care unit admission, and group 2: 30 healthy children as controls. Blood samples were collected from the two groups for zinc, selenium, and PRL level measurement.ResultsZinc and PRL levels were found to be decreased in critically ill children compared to control group, and these levels were inversely correlated with organ failure index and pediatric logistic organ dysfunction scores. Selenium levels were decreased in patients with sepsis and in patients with multiple organ failure.ConclusionSerum concentrations of zinc and PRL are generally low in critically ill children, with a greater decrease in patients with sepsis and in the presence of multiple organ failure. The levels of zinc and PRL are inversely correlated with severity of illness. Selenium levels were decreased in patients with sepsis and in patients with multiple organ failure.

Background: In preterm newborns, acute kidney damage (AKI) often develops. Administration of caffeine may prevent acute renal damage in extremely low neonates of birth weight. The objective of this research was to determine if administering caffeine citrate to premature infants will alter the occurrences of AKI. Methods: This case-control research was conducted on preterm neonates hospitalised to Benha University and Algalaa Teaching Hospital in neonatal critical care centres. All neonates were divided into two groups: Group I: included (50) premature newborns receiving citrate of caffeine. Group II: comprised (50) non-caffeine citrate preterm newborns. The definition of the modified newborn kidney disease (KDIGO) has been utilised for the evaluation of acute kidney injury stage. Result: 45 percent of all preliminary newborns admitted to our neonatal intensive care unit (NICU) had AKI in this research. The AKI rate among exposed groups of caffeine was 38 percent, statistically significantly lower than AKI among exposed groups of non-caffeine (52 percent). Wert P = 0.015. Statistically significantly shorter gestational age and birth weight were in Group I than Group II There was no statistically significant difference in delivery method, sex, apgar scores for 1 and 5 minutes between group I and group II. Conclusions: Caffeine is linked with decreased risk of acute renal damage in preterm babies.