Aim: Oxidative stress has been implicated as a potential responsible mechanism in the pathogenesis of vancomycin (VCM)-induced renal toxicity. Therefore, we aimed to investigate the protective effect of thymoquinone (TQ) against VCM-induced nephrotoxicity by tissue oxidant/antioxidant parameters and histological changes in rats. Materials and methods: Wistar albino rats were randomly separated into four groups consisting of seven rats per group. The groups had normal saline (control group), VCM, VCM and TQ and TQ, respectively. VCM was injected intraperitoneally at a dose of 200 mg/kg and continued at 12-h intervals for 7 days. TQ was injected intraperitoneally at a dose of 10 mg/kg and continued at 24 h intervals for 8 days. Animals were killed and blood samples were analyzed for the levels of serum blood urea nitrogen (BUN) and creatinine (Cr). Kidney specimens were analyzed for levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well as for histopathological changes. Results: We found that the levels of serum BUN, Cr and kidney tissue MDA were increased in the VCM group. Activities of SOD and GSH-Px in kidney tissue were decreased. TQ administration ameliorated significantly these changes. Conclusion: These results indicate that the TQ produces a protective mechanism against VCM-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

Two randomized controlled clinical trials have shown that Lactobacillus (L) reuteri DSM 17938 reduces the duration of diarrhea in children hospitalized due to acute infectious diarrhea. This was the first trial evaluating the efficacy of L. reuteri DSM 17938 in outpatient children with acute infectious diarrhea. This was a multicenter, randomized, single-blinded, case control clinical trial in children with acute watery diarrhea. A total of 64 children who presented at outpatient clinics were enrolled. The probiotic group received 1×10(8)CFU L. reuteri DSM 17938 for five days in addition to oral rehydration solution (ORS) and the second group was treated with ORS only. The primary endpoint was the duration of diarrhea (in hours). The secondary endpoint was the number of children with diarrhea at each day of the five days of intervention. Adverse events were also recorded. The mean duration of diarrhea was significantly reduced in the L. reuteri group compared to the control group (approximately 15h, 60.4±24.5h [95% CI: 51.0-69.7h] vs. 74.3±15.3h [95% CI: 68.7-79.9h], p<0.05). The percentage of children with diarrhea was lower in the L. reuteri group (13/29; 44.8%) after 48h than the control group (27/31; 87%; RR: 0.51; 95% CI: 0.34-0.79, p<0.01). From the 72nd hour of intervention onwards, there was no difference between the two groups in the percentage of children with diarrhea. No adverse effects related to L. reuteri were noted. L. reuteri DSM 17938 is effective, safe, and well-tolerated in outpatient children with acute infectious diarrhea.

Evidence from the literature has shown thatSaccharomyces boulardiiprovides a clinically significant benefit in the treatment of acute infectious diarrhoea in children. In this multicentre, randomised, prospective, controlled, single blind clinical trial performed in children with acute watery diarrhoea, we aimed to evaluate the impact ofS. boulardiiCNCM I-745 in hospitalised children, in children requiring emergency care unit (ECU) stay and in outpatient settings. The primary endpoint was the duration of diarrhoea (in hours). Secondary outcome measures were duration of hospitalisation and diarrhoea at the 3^rdday of intervention. In the whole study group (363 children), the duration of diarrhoea was approximately 24 h shorter in theS. boulardiigroup (75.4±33.1 vs 99.8±32.5 h,P<0.001). The effect ofS. boulardii(diarrhoea-free children) was observed starting at 48 h. After 72 h, only 27.3% of the children receiving probiotic still had watery diarrhoea, in contrast to 48.5% in the control group (P<0.001). The duration of diarrhoea was significantly reduced in the probiotic group in hospital, ECU and outpatient settings (P<0.001,P<0.01 andP<0.001, respectively). The percentage of diarrhoea-free children was significantly larger after 48 and 72 h in all settings. The mean length of hospital stay was shorter with more than 36 h difference in theS. boulardiigroup (4.60±1.72 vs 6.12±1.71 days,P<0.001). The mean length of ECU stay was shorter with more than 19 h difference in the probiotic group (1.20±0.4 vs 2.0±0.3 days,P<0.001). No adverse effects related to the probiotic were noted. Because treatment can shorten the duration of diarrhoea and reduce the length of ECU and hospital stay, there is likely a social and economic benefit ofS. boulardiiCNCM I-745 in adjunction to oral rehydration solution in acute infectious gastroenteritis in children.

Carbon monoxide (CO) poisoning is one of the most common types of poisoning causing death worldwide. In our country, it occurs particularly during winter as a result of leak from stove or water heater, or as result of inhalation during a fire. Although most poisonings occur accidentally, some cases are suicide attempt. As CO is a substance that is not visible and has no taste or smell and is therefore difficult to detect, the gas can be a "silent killer" that is not noticed until effects develop. CO reacts with oxygen, creating carboxy hemoglobin (COHb), which leads to tissue hypoxia. In addition, it has direct effect of causing cellular damage. Although symptoms of acute poisoning are most commonly observed in patients admitted to emergency rooms, effects of chronic exposure to CO can also seen. Clinically, although it affects all organ systems, involvement of central nervous system (CNS) and cardiovascular system is predominant. Most common poisoning symptoms are weakness, dizziness, headache, nausea, and nonspecific flu-like symptoms, like vomiting. Depending on severity of exposure, seizures, syncope, and arrhythmia may also be observed. In pregnant women, fetus can be harmed with relatively low level of COHb. Poisoning in infants has a more severe course than seen in other age groups. Symptoms must be associated with cause of poisoning, and careful anamnesis and treatment must be conducted quickly. Oxygen is the antidote for CO. It is administered through a mask in the form of normobaric oxygen therapy or through specific devices in the form of hyperbaric oxygen therapy. In this review, clinical data and current diagnostic and therapeutic approaches concerning CO poisoning are discussed.