Patterns and determinants of small‐quantity LNS utilization in rural Malawi and Mozambique: considerations for interventions with specialized nutritious foods

Small‐quantity, lipid‐based nutrient supplements (SQ‐LNS) show promise to improve the quality of maternal and child diets, particularly during the first 1000 days of life. The potential of SQ‐LNS to impact positively upon nutritional status relies on numerous factors, including complementary dietary intake, disease prevalence and dynamics of household utilization, including sharing practices. Therefore, this study sought to elucidate the patterns and determinants of SQ‐LNS utilization among children 6–23 months and potential sharing practices of other household members prior to intervention development. In Ntchisi, Malawi and Cabo Delgado, Mozambique, both rural, agricultural settings, we conducted two home‐feeding trials of 8 and 6 weeks, respectively, nested within a larger multi‐phase, emergent formative research design. Multiple methods, including in‐depth interviews (n = 38), direct meal observations (n = 80), full‐day child observations (n = 38) and spot checks of SQ‐LNS supply (n = 23), were conducted with households (n = 35 in Malawi; n = 24 in Mozambique). Overall, the SQ‐LNS was utilized contrary to its recommended use, with 50% of households in Malawi reporting running out of stock too early and 87% of households in Mozambique either overusing or underusing the product. Utilization of SQ‐LNS was manifested in four patterns of overuse and two of underuse and was determined by factors at multiple levels of influence. Maternal and child health efforts need to consider the reasons behind choices by households to overuse or underuse SQ‐LNS and design intervention strategies to increase the likelihood of its appropriate utilization.     

A comparison between enamel matrix derivative and a bioabsorbable membrane to enhance healing around transmucosal immediate post-extraction implants

BACKGROUND: This clinical report compares the use of an enamel matrix derivative (EMD) and bioabsorbable barrier membrane to enhance healing following the immediate placement of transmucosal implants into extraction sockets. METHODS: Thirty-two adult patients scheduled for tooth replacement with dental implants agreed to participate. Following the insertion of a transmucosal implant into the extraction site, the subjects were assigned to one of two treatment alternatives of the remaining bone defects around the implants: 1) the residual bone defects were filled with EMD (EMD group) or 2) the residual bone defects were covered with a bioabsorbable membrane (membrane group). Flaps were then coronally positioned around implant cover screws. Patients followed weekly maintenance recalls for the first 6 weeks and then monthly recalls until the final prosthetic restoration was completed (after 6 months). The treatment outcome was evaluated after 12 months by the use of clinical variables. The null hypothesis of no treatment group differences was tested by the use of analysis of variance (ANOVA). RESULTS: At a 12-month follow-up, all of the implants were completely osseointegrated and successfully functioning, showing a success rate of 100%. The membrane group showed a significantly lower mean probing attachment level than the EMD group at proximal (0.60 mm, standard deviation (SD) 0.37 versus 1.19 mm, SD 1.10), buccal (0.80 mm, SD 0.79 versus 1.77 mm, SD 1.16), and lingual sites (0.44 mm, SD 0.52 versus 1.48 mm, SD 1.46). The difference was statistically significant at all sites (P < 0.05). With respect to the position of the soft tissue margin around the implant shoulder, the membrane group showed a consistently higher value than the EMD group at, respectively, proximal (1.30 mm, SD 2.37 versus 1.16 mm, SD 1.0), buccal (0.90 mm, SD 1.29 versus 0.22 mm, SD 1.47), and lingual sites (1.12 mm, SD 1.10 versus 0.55 mm, SD 1.42). CONCLUSIONS: The membrane group obtained more favorable results in terms of both the probing attachment level and peri-implant position of soft tissues compared to the EMD group. The use of a bioabsorbable membrane around immediately placed transmucosal implants enhanced soft and hard tissue healing and might be an advisable treatment choice particularly in areas with high esthetic demands.     

Restrictive pulmonary dysfunction at spirometry and mortality in the elderly

OBJECTIVES: To evaluate the association between pulmonary restriction and mortality in the elderly, taking into account potential confounders not considered in the past (disability, cognitive dysfunction, diabetes, and visceral obesity). DESIGN: Longitudinal study. SETTING: Community-based. PARTICIPANTS: Twelve hundred sixty-five patients (51.9% men) aged 65-97 years old from the Salute Respiratoria nell'Anziano (SaRA) Italian multicentric study. MEASUREMENTS: Participants were divided in 4 groups: normal spirometry (NS): FEV1/FVC>/=70%, FVC>/=80% of predicted; restrictive ventilatory pattern (RVP): FEV1/FVC>/=70%, FVC<80%; obstructive ventilatory pattern (OVP): FEV1/FVC<70%, FVC>/=80%, and mixed ventilatory pattern (MVP): FEV1/FVC<70%, FVC<80%. We calculated the association between restriction and mortality corrected for potential confounders using a multivariable Cox regression model. RESULTS: We found a prevalence of RVP, OVP and MVP of 10.9%, 25.4%, and 17.3%, respectively. Compared to people with normal spirometric pattern, disability (19.6% vs. 10.1%), poor physical performance (35.4% vs. 22.3%), cognitive impairment (21.0% vs. 11.5%), increased waist circumference (62.1% and 26.8%), and kyphoscoliosis (56.8 and 13.5%) were more prevalent in the RVP group. After correction for potential confounders, RVP was associated with increased mortality (HR: 1.89; 95% CI: 1.15-3.11), as well as OVP (HR: 2.33; 95% CI: 1.58-3.11) and MVP (HR: 2.60; 95% CI: 1.74-3.93). Other factors associated with mortality were disability (HR: 1.92; 95% CI: 1.35-2.72), poor physical performance (HR: 1.37; 95% CI: 1.01-1.85), cognitive impairment (HR: 1.55; 95% CI: 1.06-2.27), depression (HR: 1.57; 95% CI: 1.16-2.13) and diagnosis of stroke (HR: 1.90; 95% CI: 1.18-3.05). CONCLUSIONS: RVP is associated with higher mortality in the elderly and, thus, deserves the same attention paid to an obstructive pattern. However, mechanisms mediating this association need to be clarified.     

Proteasome activity as a target of hormone replacement therapy-dependent plaque stabilization in postmenopausal women

The molecular mechanisms of the atheroprotective effect evoked by hormone replacement therapy in postmenopausal women is not well known. Recently, we have demonstrated enhanced activity of the ubiquitin-proteasome system in human atherosclerotic plaques and evidenced that it is associated with inflammatory-induced plaque rupture. Therefore, we hypothesized that hormone replacement therapy may exert the cardioprotective effects modulating the ubiquitin-proteasome activity. To investigate this possibility, this study examined the differences in inflammatory infiltration, as well as ubiquitin-proteasome activity, between asymptomatic carotid plaques of postmenopausal women with and without concomitant hormone replacement therapy. Plaques were obtained from 20 postmenopausal women treated with hormone replacement therapy (current users) and 32 nontreated women (never-users) enlisted to undergo carotid endarterectomy for extracranial high-grade (>70%) internal carotid artery stenosis. Plaques were analyzed for macrophages, T lymphocytes, human leukocyte antigen-DR+ cells, ubiquitin-proteasome system, nuclear factor kappaB, inhibitor of nuclear factor kappaBbeta, tumor necrosis factor-alpha, nitrotyrosine, matrix metalloproteinase-9, and collagen content (immunohistochemistry and ELISA). Compared with plaques from current users, plaques from never-users had more macrophages, T lymphocytes, and human leukocyte antigen-DR+ cells (P<0.001); more ubiquitin-proteasome activity, tumor necrosis factor-alpha, and nuclear factor kappaB (P<0.001); and more nitrotyrosine and matrix metalloproteinase-9 (P<0.001), along with a lesser collagen content and inhibitor of nuclear factor kappaBbeta levels (P<0.001). This study supports the hypothesis that hormone replacement therapy inhibits plaque ubiquitin-proteasome activity by decreasing oxidative stress generation in postmenopausal women. This effect, in turn, might contribute to plaque stabilization by inhibiting the activation of nuclear factor kappaB-dependent inflammation, responsible for plaque rupture.     

Acetyl-L-Carnitine selectively prevents post-ischemic LTP via a possible action on mitochondrial energy metabolism

It has been hypothesized that Acetyl-L-Carnitine (ALC) contributes to mitochondrial ATP production through maintenance of key mitochondrial proteins and protects mitochondria against oxidative stress. We have investigated the role of ALC on the expression of two forms of synaptic plasticity in the striatum: (i) the physiological long-term potentiation (LTP) and (ii) the ischemic long-term potentiation (i-LTP), an aberrant form of synaptic plasticity occurring after in vitro ischemia. The application in vitro of ALC did not alter the induction or the maintenance of physiological activity-dependent LTP, while it prevented i-LTP in a dose-dependent manner. The ability of ALC to prevent i-LTP was not affected by previous application of scopolamine, a non-selective muscarinic receptors antagonist. Given the susceptibility of mitochondrial complex IV to ischemic oxidative insult, we investigated the role of this complex as possible target of ALC action. Thus, the application of a low dose of the mitochondrial toxin sodium azide, conventionally used as a model of hypoxia due to its capability to inhibit mitochondrial complex IV, induced a pathological synaptic potentiation that was fully prevented by ALC application. In the presence of a very low dose of the mitochondrial uncoupler FCCP, ALC no longer prevented i-LTP suggesting that neuroprotective effects of ALC require a compensatory activity of mitochondrial energy metabolism. Our data demonstrate that ALC exerts neuroprotective effects by preventing the expression of pathological synaptic plasticity induced by ischemia. These effects crucially depend on the ability on ALC to affect mitochondrial processes.