Cockcroft-Gault formula showed the worst agreement with GFR, regardless of using published or recalculated constants. The cystatin C-based approach resulted in the least error, and should be used for estimation of GFR.
Long-term memory for fear of an environment (contextual fear conditioning) emerges later in development (postnatal day; PD 23) than long-term memory for fear of discrete stimuli (PD 17). As contextual, but not explicit cue, fear conditioning relies on the hippocampus; this has been interpreted as evidence that the hippocampus is not fully developed until PD 23. Alternatively, the hippocampus may be functional prior to PD 23, but unable to cooperate with the amygdala for fearful learning. The current experiments investigate this by separating the phases of conditioning across developmental stages. Rats were allowed to learn about the context on one day and to form the fearful association on another. Rats exposed to the context on PD 17 exhibited significant fear only when trained and tested a week later (PD 23, 24), but not on consecutive days (PD 18, 19), demonstrating that rats can learn about a context as early as PD 17. Further experiments clarify that it is associative mechanisms that are developing between PD 18 and 23. Finally, the hippocampus was lesioned prior to training to ensure the task is being solved in a hippocampus-dependent manner. These data provide compelling evidence that the hippocampus is functional for contextual learning as early as PD 17, however, its connection to the amygdala or other relevant brain structures may not yet be fully developed.Research in recent decades has yielded a great deal of information regarding the neural substrates of cognitive processes, such as emotional expression and learning and memory in adult organisms, but relatively little regarding the neural substrates underlying these processes in developing organisms. Pavlovian fear conditioning has proven a useful tool for studying cognition in adult organisms (Malenka and Nicoll 1997;Anagnostaras et al. 2001;Maren 2001) and ought to be an especially powerful tool to help uncover the neural substrates of various cognitive processes in adolescent organisms due to its reliance on relatively basic sensory, motor, and affective systems (Campbell and Spear 1972). Indeed, several behavioral and toxicological studies have already adapted methods pioneered in the adult for use in developing animals with great success (Rudy
To examine the role of commercially available kefir, a fermented milk similar to yogurt but containing different fermentation microbes, in preventing antibiotic-associated diarrhea (AAD). Probiotics have shown some promise in preventing AAD.Design: A double-blinded randomized placebocontrolled allocation concealment clinical trial.Setting: Primary care patients in the Washington, DC, metropolitan area.Participants: A total of 125 children aged 1 to 5 years presenting to primary care physicians.Intervention: Kefir drink or heat-killed matching placebo.Main Outcome Measure: The primary outcome was the incidence of diarrhea during the 14-day follow-up period in children receiving antibiotics.Results: There were no differences in the rates of diarrhea per group, with 18% in the active group and 21.9% in the placebo group (relative risk, 0.82; 95% confidence interval, 0.54-1.43). Additionally, there were no differences in any secondary outcomes among the groups. However, there were some interesting interactions among initial health at enrollment, age of participants, and sex that require further study.
Conclusions:In our trial, kefir did not prevent AAD. Further independent research on the potential of kefir needs to be conducted.
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