Digestive enzyme replacement relieves growth failure in preterm infants with poor exocrine pancreatic function: a retrospective case series

In orally fed preterm infants, poor weight gain may be linked to low fecal pancreatic elastase-1 (FPE-1) activity, indicative of exocrine pancreatic insufficiency. The objective of this study was the retrospective assessment of the effect of exogenous digestive enzyme replacement by gavage in preterm infants with growth failure and low FPE-1 (<200 mu g/g). We analyzed weight gain relative to baseline and caloric intake during 14-day periods before and after institution of digestive enzyme replacement containing 6000 U lipase and 240 U protease kg(-1) d(-1). Among 46 of 132 preterm infants < 1250g birth weight surviving to at least 14 days in whom FPE-1 was determined, 38 infants had low FPE-1 (< 200 mu g/g), and 33 infants received exogenous digestive enzyme replacement. Average daily weight gain significantly increased from 14.4 [range 2.6-22.4] g kg(-1) d(-1) to 17.4 [8.4-29.0] g kg(-1) d(-1) (P = 0.001), as did weight gain per kcal, from 0.08 [0.02-0.13] g kcal(-1) d(-1) to 0.11 [0.05-0.18] g kcal(-1) d(-1). Conclusion: In preterm infants with signs and symptoms of exocrine pancreatic insufficiency, exogenous digestive enzyme replacement is associated with improved growth. What is Known: center dot Very preterm infants on full enteral nutrition may display growth failure linked to transient poor exocrine pancreatic function. center dot Porcine pancreatic enzymes covered with an acid-resistant coating are too large to pass the internal diameter of most gavage tubes used in very preterm infants. What is New: center dot Administration of a liquid formulation of acid-resistant microbial digestive enzymes in preterm infants with growth failure and low fecal pancreatic elastase-1 values was associated with improved weight gain. center dot Response to exogenous digestive enzyme replacement was associated with the prior extent of growth failure

Searching for the hidden Iodine in beverages

Jod ist ein essentielles Spurenelement, welches der Mensch zur Aufrechterhaltung des ungestörten Schilddrüsenmetabolismus und davon beeinflussten verschiedenen Körperfunktionen benötigt. Weltweit gab und gibt es einen Jodmangel, der schwerwiegende gesundheitliche Folgen für das Individuum und wirtschaftliche Folgen für die Gesundheitssysteme des jeweiligen Landes hat. Auch Deutschland galt mit weiteren europäischen Ländern bis vor wenigen Jahren als Jodmangelgebiet. Durch intensive Aufklärungsarbeit und Programme zur Beseitigung des Jodmangels gelang es, diesen in vielen Ländern zu vermindern. Außer einer generellen Verwendung von Jodsalz in der Lebensmittelproduktion und den Privathaushalten, konnten noch weitere wichtige Jodquellen für die Bevölkerung in verschiedenen Studien belegt werden. Diese Studie beschäftigt sich mit der Ermittlung von Jodgehalt in Alltagsgetränken. Die Ergebnisse sind vergleichbar zu bereits veröffentlichen Studien und zeigen einen hohen Jodgehalt von Milch und Milchgetränken, sowie von Bier und Wein. Kein Jod in größeren Mengen hingegen enthält das regionale Leitungswasser, sowie Mineralwässer und diverse Fruchtsäfte. Somit kann der Verzehr von Milch und Milchgetränken und in Maßen auch Bier und Wein für eine jodreiche Ernährung empfohlen werden. Hingegen sollten Patienten in Vorbereitung zum Beispiel auf eine Radiojodtherapie Milch, Biere und Wein eher meiden und jodarme Getränke bevorzugen.Iodine is an essential trace element, which is required to maintain the undisturbed thyroid metabolism. It influences various body functions. Worldwide there is a lack of iodine which has serious health consequences for the individual. There are also economic consequences for the health systems of each country. A few years ago Germany was, with other European countries,a iodine deficiency area. With intensive educational work and programs for the elimination of iodine deficiency, it was possible to reduce the iodine deficiency in many countries. A general use of iodized salt in the food production and households, other important sources of iodine could be found in various studies. This study deals with the determination of iodine content in everyday drinks. The results are comparable to previously published studies and show a high iodine content of milk and milk-based drinks, as well as beer and wine. No iodine in larger amounts, however, contains the local tap water, mineral water and various fruit juices. The consumption of milk, milk-based drinks, beer and wine in moderation can be recommended for an iodine-rich diet. In contrast, patients in preparation for a radioiodine therapie shoud avoid milk, beer and wine

Inflammation and the redox-sensitive AGE-RAGE pathway as a therapeutic target in Alzheimer's disease

Alzheimer's disease (AD) is the most common cause of dementia. Neuritic amyloid plaques and concomitant chronic inflammation are prominent pathological features of AD. β-amyloid peptide (Aβ), the major component of plaques, and advanced glycation end products (AGEs), post-translational protein modifications, are key activators of plaque-associated inflammation. Aβ, AGEs, S100b, and amphoterin bind to the receptor for AGEs (RAGE), which transmits the signal from RAGE via redox-sensitive pathways to nuclear factor kappa-B (NF-κB)-regulated cytokines. RAGE-mediated inflammation caused by glial cells and subsequent changes in neuronal glucose metabolism are likely to be important contributors to neurodegeneration in AD. As long as the neuronal damage is reversible, drugs interfering with the Aβ and AGE–RAGE pathways might be interesting novel therapeutics for the treatment of AD

Digestive enzyme replacement relieves growth failure in preterm infants with poor exocrine pancreatic function: a retrospective case series

In orally fed preterm infants, poor weight gain may be linked to low fecal pancreatic elastase-1 (FPE-1) activity, indicative of exocrine pancreatic insufficiency. The objective of this study was the retrospective assessment of the effect of exogenous digestive enzyme replacement by gavage in preterm infants with growth failure and low FPE-1 (&amp;lt;200 μg/g). We analyzed weight gain relative to baseline and caloric intake during 14-day periods before and after institution of digestive enzyme replacement containing 6000 U lipase and 240 U protease k

α-lipoic acid in the treatment of diabetic polyneuropathy and Alzheimer’s disease

α-lipoic acid (LA) is a naturally occurring cofactor for mitochondrial enzymes, including pyruvate dehydrogenase (PDH) and α-ketoglutarate dehydrogenase (KGDH). LA acts as a powerful micronutrient with diverse pharmacological properties. LA improves glucose uptake and insulin sensitivity, and thus decreases blood glucose levels and increases mitochondrial energy levels. LA chelates redox-active transition metals, thus inhibiting the formation of hydroxyl radicals from hydrogen peroxide and also scavenges reactive oxygen species, thereby increasing the levels of reduced glutathione. Via the same mechanisms, down-regulation of redox-sensitive inflammatory processes is achieved. Furthermore, LA can scavenge lipid peroxidation products such as hydroxynonenal and acrolein. LA is currently studied for the treatment of some neurodegenerative diseases with diverse pathophysiology, including diabetic polyneuropathy and Alzheimer’s disease. For diabetic polyneuropathy, LA has been used for decades in Germany with a number of clinical trials showing benefits in insulin-stimulated glucose uptake and attenuating symptoms of neuropathy. In Alzheimer’s disease, an open-label trial in patients with mild and moderate Alzheimer’s disease is currently conducted at a at the memory clinic of the Henriettenstiftung hospital in Hannover, Germany. Interim analysis of the data after 4 years show that the progression rate of the patient treated with 600 mg LA daily is significantly slower than to the non-treated control group - particularly in early stages of dementia - and other control groups in published studies

Advanced glycation endproducts and their receptor RAGE in Alzheimer's disease

Alzheimer's disease (AD) is the most common dementing disorder of late life. Although there might be various different triggering events in the early stages of the disease, they seem to converge on a few characteristic final pathways in the late stages, characterized by inflammation and neurodegeneration. In this review, we revisit the hypothesis that advanced glycation endproducts (AGEs) and their receptor RAGE may play an important role in disease pathogenesis. Accumulation of AGEs in cells and tissues is a normal feature of aging, but is accelerated in AD. In AD, AGEs can be detected in pathological deposits such as amyloid plaques and neurofibrillary tangles. AGEs explain many of the neuropathological and biochemical features of AD such as extensive protein crosslinking, glial induction of oxidative stress and neuronal cell death. Oxidative stress and AGEs initiate a positive feedback loop, where normal age-related changes develop into a pathophysiological cascade. RAGE and its decoy receptor soluble RAGE, may contribute to or protect against AD pathogenesis by influencing transport of β-amyloid into the brain or by manipulating inflammatory mechanisms. Targeted pharmacological interventions using AGE-inhibitors, RAGE-antagonists, RAGE-antibodies, soluble RAGE or RAGE signalling inhibitors such as membrane-permeable antioxidants may be promising therapeutic strategies to slow down the progression of AD

Effets de l'ilomédine sur les marqueurs endothéliaux solubles (sICAM, sVCAM, E Selectine) et de l'endothéline 1 au cours de la sclérodermie systémique

PARIS-BIUM (751062103) / SudocCentre Technique Livre Ens. Sup. (774682301) / SudocSudocFranceF

Climate change, negative emissions and solar radiation management: It is time for an open societal conversation

This white paper resulted from a risk dialogue project with climate scientists and experts on the subject of climate engineering – conducted by the neutral and independent Risk-Dialogue Foundation St. Gallen between April 2016 and March 2017. The aim was to identify the current state of research on the topic as well as related risk and to evaluate a potential need for wider public deliberation. The project was carried out on behalf of the Swiss Federal Office for the Environment (FOEN), Climate Division. In line with views expressed during the dialogue, the sole objective of this paper is to argue for an open and public deliberation process and not to favour or promote any technologies or deployment thereof. The views expressed in this report are solely those of its authors, and do not reflect any official position

A versatile high throughput screening system for the simultaneous identification of anti-inflammatory and neuroprotective compounds

In many chronic neurodegenerative diseases including Frontotemporal Dementia and Alzheimer's disease (AD), microglial activation is suggested to be involved in pathogenesis or disease progression. Activated microglia secrete a variety of cytokines, including interleukin-1β, interleukin-6, and tumor necrosis factor as well as reactive oxygen and nitrogen species (ROS/RNS). ROS and RNS contribute to alterations in neuronal glucose uptake, inhibition of mitochondrial enzymes, a decrease in mitochondrial membrane potential, impaired axonal transport, and synaptic signaling. In addition, ROS act as signaling molecules in pro-inflammatory redox-active signal transduction pathways. To establish a high throughput screening system for anti-inflammatory and neuroprotective compounds, we have constructed an "Enhanced Green Fluorescent protein" (EGFP) expressing neuronal cell line and set up a murine microglia/neuron co-culture system with these EGFP expressing neuronal cells. We show that microglia activation leads to neuronal cell death, which can be conveniently measured by loss of neuronal EGFP fluorescence. Moreover, we used this system to test selected polyphenolic compounds for their ability to downregulate inflammatory markers and to protect neurons against microglial insult. We suggest that this system might allow accelerated drug discovery for the treatment of inflammation-mediated neurodegenerative diseases