Successful weight loss after bariatric surgery in Appalachian state regardless of food access ranking score.

BACKGROUND: Following bariatric surgery, an explicit dietary regimen is required to facilitate and maintain successful weight loss. Without adequate access to healthy foods, weight maintenance can be hindered. OBJECTIVE: Examine influence degree of food access has on Appalachian bariatric surgery patient weight loss outcomes. SETTING: Appalachian University hospital, United States. METHODS: A retrospective chart review was used to examine the influence of food accessibility on weight loss outcomes in an Appalachian bariatric surgery patient population at a large tertiary hospital in West Virginia between 2013 and 2017. Demographic characteristics, health and family history, and 1-year surgery outcomes were collected. A state-specific food accessibility score was calculated for each patient address using the geographic information system. Patients were assigned a food access ranking score (FARS) between 0 (low food access) and 4 (high food access) based on criteria of quantity, quality, income, and vehicle access. RESULTS: Patients (n = 369) were predominately married (60.5%), white (92.4%), female (77.8%), and underwent laparoscopic Roux-en-Y gastric bypass surgery (75.9%), with a mean age of 45 years. Most patients had low FARS (M = 1.67 ± .73; 72.6%). Nonwhite patients (P = .03) with a preoperative diagnosis of depression (P = .02) or without a family history of obesity (P = .01) were found to be in the lower FARS categories. FARS was not indicative of weight loss post surgery (P > .05). CONCLUSIONS: Food accessibility in West Virginia was not associated with bariatric surgery weight outcomes at 1-year post operation. Lower food access was associated with nonwhite race/ethnicity, diagnosed depression at baseline, and no family history of obesity. Future studies should include more extended follow-up data collection and mixed-method approaches to capture perceptions of food access and its impact on the patients' postoperative journey.

[Chronic interstitial lung disease in children: Diagnostic approach and management]. / Pneumopathies infiltrantes diffuses chroniques de l'enfant : démarche diagnostique et approche thérapeutique.

Chronic interstitial lung disease (ILD) in children is a heterogeneous group of rare lung disorders characterized by an inflammatory process of the alveolar wall and the pulmonary interstitium that induces gas exchange disorders. The diagnostic approach to an ILD involves three essential steps: recognizing the ILD, appreciating the impact, and identifying the cause. The spectrum of clinical findings depends to a large extent on age. In the newborn, the beginning is often abrupt (neonatal respiratory distress), whereas there is a more gradual onset in infants (failure to thrive, tachypnea, indrawing of the respiratory muscles). In older children, the onset is insidious and the diagnosis can only be made at an advanced stage of the disease. The diagnosis is based on noninvasive methods (clinical history, respiratory function tests, chest X-ray, and high-resolution CT scan) and invasive techniques (bronchoalveolar lavage, transbronchial biopsy, video-assisted thoracoscopic biopsy, and open lung biopsy). The treatment of interstitial lung disease in children depends on the nature of the underlying pathology. The most common therapeutic approach involves the use of corticosteroids and immunosuppressive agents for their anti-inflammatory and antifibrotic effects. Children with ILD also need support therapy (oxygen therapy, nutritional support, treatment of pulmonary arterial hypertension, vaccination). Lung transplantation is discussed in patients with severe respiratory failure.

MPTP intoxication in mice: a useful model of Leigh syndrome to study mitochondrial diseases in childhood.

The basal ganglia, which are interconnected in the striato-nigral dopaminergic network, are affected in several childhood diseases including Leigh syndrome (LS). LS is the most common mitochondrial disorder affecting children and usually arise from inhibition of the respiratory chain. This vulnerability is attributed to a particular susceptibility to energetic stress, with mitochondrial inhibition as a common pathogenic pathway. In this study we developed a LS model for neuroprotection trials in mice by using the complex I inhibitor MPTP. We first verified that MPTP significantly inhibits the mitochondrial complex I in the brain (p = 0.018). This model also reproduced the biochemical and pathological features of LS: MPTP increased plasmatic lactate levels (p = 0.023) and triggered basal ganglia degeneration, as evaluated through dopamine transporter (DAT) autoradiography, tyrosine hydroxylase (TH) immunohistochemistry, and dopamine dosage. Striatal DAT levels were markedly decreased after MPTP treatment (p = 0.003). TH immunoreactivity was reduced in the striatum and substantia nigra (p = 0.005), and striatal dopamine was significantly reduced (p < 0.01). Taken together, these results confirm that acute MPTP intoxication in young mice provides a reproducible pharmacological paradigm of LS, thus opening new avenues for neuroprotection research.