16 research outputs found

    Occult nitric oxide inhalation improves oxygenation in mechanically ventilated children

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    Objectives: Auto-inhalation of nitric oxide (NO) produced in the upper airways may have physiologic effects on lung function. For intubated patients, the upper airway source of NO is eliminated, but the hospital compressed air source from the environment is contaminated with varying levels of NO, creating an 'occult' form of NO therapy. We examined the physiologic significance of occult inhaled NO in ventilator-dependent pediatric patients. We hypothesized that very low levels of NO contamination in inspired gas improve PaO2 in ventilator-dependent children. Study design: Inspired NO levels at the mouth were measured by chemiluminescence in 4 pediatric subjects with normal lungs and 3 with parenchymal lung disease. Subjects were sequentially ventilated with first standard hospital gas (H1), switched to pure nitrogen-oxygen at a similar FIO2 but with no NO contamination (A2), hospital gas again (H2), the nitrogen-oxygen (A2) to control for time and sequence, and finally the nitrogen-oxygen mixture with supplemental NO in an amount equal to the NO previously measured in hospital gas (A2 + NO). Inhaled NO levels and PaO2 were recorded 15 minutes into each of the 5 steps. Two patients were studied a second time, remote from their first examination. Results: NO levels in inhaled hospital gas mixtures ranged from 13 to 79 ppb (mean H1 = 53.3 ± 23.7 ppb, mean H2 = 53.2 ± 20.7 ppb, mean A2 + NO = 45 ± 15.3 ppb; P < .0001). Removing NO from ventilator gas decreased PaO2 in all subjects, whereas replacing NO in artificial gas restored PaO2 to baseline values (P < .0001). Conclusion: Concentrations of NO in hospital compressed air are variable and have physiologic effects. The long-term implications of these findings remain to be defined

    Associations of hippocampal subfields in the progression of cognitive decline related to Parkinson's disease

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    Objective Hippocampal atrophy has been associated with mild cognitive impairment (MCI) in Parkinson's disease (PD). However, literature on how hippocampal atrophy affects the pathophysiology of cognitive impairment in PD has been limited. Previous studies assessed the hippocampus as an entire entity instead of their individual subregions. We studied the progression of cognitive status in PD subjects over 18 in relation to hippocampal subfields atrophy. Methods 65 PD subjects were included. Using the MDS task force criteria, PD subjects were classified as either having no cognitive impairment (PD-NCI) or PD-MCI. We extended the study by investigating the hippocampal subfields atrophy patterns in those who converted from PD-NCI to PD-MCI (PD-converters) compared to those who remained cognitively stable (PD-stable) over 18 months. Freesurfer 6.0 was used to perform the automated segmentation of the hippocampus into thirteen subregions. Results PD-MCI showed lower baseline volumes in the left fimbria, right CA1, and right HATA; and lower global cognition scores compared to PD-NCI. Baseline right CA1 was also correlated with baseline attention. Over 18 months, decline in volumes of CA2–3 and episodic memory were also seen in PD-converters compared to PD-stable. Baseline volumes of GC-DG, right CA4, left parasubiculum, and left HATA were predictive of the conversion from PD-NCI to PD-MCI. Conclusion The findings from this study add to the anatomical knowledge of hippocampal subregions in PD, allowing us to understand the unique functional contribution of each subfield. Structural changes in the hippocampus subfields could be early biomarkers to detect cognitive impairment in PD

    Associations of hippocampal subfields in the progression of cognitive decline related to Parkinson's disease

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    Objective Hippocampal atrophy has been associated with mild cognitive impairment (MCI) in Parkinson's disease (PD). However, literature on how hippocampal atrophy affects the pathophysiology of cognitive impairment in PD has been limited. Previous studies assessed the hippocampus as an entire entity instead of their individual subregions. We studied the progression of cognitive status in PD subjects over 18 in relation to hippocampal subfields atrophy. Methods 65 PD subjects were included. Using the MDS task force criteria, PD subjects were classified as either having no cognitive impairment (PD-NCI) or PD-MCI. We extended the study by investigating the hippocampal subfields atrophy patterns in those who converted from PD-NCI to PD-MCI (PD-converters) compared to those who remained cognitively stable (PD-stable) over 18 months. Freesurfer 6.0 was used to perform the automated segmentation of the hippocampus into thirteen subregions. Results PD-MCI showed lower baseline volumes in the left fimbria, right CA1, and right HATA; and lower global cognition scores compared to PD-NCI. Baseline right CA1 was also correlated with baseline attention. Over 18 months, decline in volumes of CA2–3 and episodic memory were also seen in PD-converters compared to PD-stable. Baseline volumes of GC-DG, right CA4, left parasubiculum, and left HATA were predictive of the conversion from PD-NCI to PD-MCI. Conclusion The findings from this study add to the anatomical knowledge of hippocampal subregions in PD, allowing us to understand the unique functional contribution of each subfield. Structural changes in the hippocampus subfields could be early biomarkers to detect cognitive impairment in PD
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