A systematic comparison of sugar content in low-fat vs regular versions of food

Obesity remains a significant public health concern. One of the primary messages from providers and health-care organizations is to eat healthier foods with lower fat. Many in the lay press, however, have suggested that lower fat versions of foods contain more sugar. To our knowledge, a systematic comparison of the sugar content in food with lower fat alternatives has not been performed. In this study, we compared fat free, low fat and regular versions of the same foods using data collected from the USDA National Nutrient Database. We found that the amount of sugar is higher in the low fat (that is, reduced calorie, light, low fat) and non-fat than ‘regular'' versions of tested items (Friedman P=0.00001, Wilcoxon P=0.0002 for low fat vs regular food and P=0.0003 for non-fat vs regular food). Our data support the general belief that food that is lower in fat may contain more sugar.     

Lokale Medikamententherapie bei Innenohrschwerhörigkeit

HNO - Zu den Indikationen für eine lokale Medikamententherapie bei Innenohrschwerhörigkeit gehören z. B. Hörsturz, M. Menière, autoimmunassoziierter...     

Identification and Characterization of Hydrolytic Degradation Products of Cefditoren Pivoxil using LC and LC-MS/TOF

The present research work was carried out to determine stability of cefditoren pivoxil, an orally absorbed prodrug that is rapidly hydrolysed by intestinal esterases to the active cephalosporin cefditoren. Cefditoren was subjected to stress conditions recommended by the International Conference on Harmonization of Technical Requirements for Registration of Pharmaceuticals for Human Use guideline Q1A (R2). Cefditoren pivoxil was susceptible for degradation under acidic, alkaline and neutral hydrolytic conditions while it was stable under photolytic and thermal stress conditions. Separation of cefditoren and degradation products were carried out by using HPLC. The unknown degradation products were characterized by liquid chromatography-mass spectrometry/time of flight studies. Structures were proposed for each fragment based on best possible molecular formula and complete degradation pathways were reported for cefditoren and its degradants.     

Metalloproteinase Inhibition Protects against Reductions in Circulating Adrenomedullin during Lead‐induced Acute Hypertension

Intoxication with lead (Pb) results in increased blood pressure by mechanisms involving matrix metalloproteinases (MMPs). Recent findings have revealed that MMP type two (MMP‐2) seems to cleave vasoactive peptides. This study examined whether MMP‐2 and MMP‐9 levels/activities increase after acute intoxication with low lead concentrations and whether these changes were associated with increases in blood pressure and circulating endothelin‐1 or with reductions in circulating adrenomedullin and calcitonin gene‐related peptide (CGRP). Here, we expand previous findings and examine whether doxycycline (a MMPs inhibitor) affects these alterations. Wistar rats received intraperitoneally (i.p.) 1st dose 8 μg/100 g of lead (or sodium) acetate, a subsequent dose of 0.1 μg/100 g to cover daily loss and treatment with doxycycline (30 mg/kg/day) or water by gavage for 7 days. Similar whole‐blood lead levels (9 μg/dL) were found in lead‐exposed rats treated with either doxycycline or water. Lead‐induced increases in systolic blood pressure (from 143 ± 2 to 167 ± 3 mmHg) and gelatin zymography of plasma samples showed that lead increased MMP‐9 (but not MMP‐2) levels. Both lead‐induced increased MMP‐9 activity and hypertension were blunted by doxycycline. Doxycycline also prevented lead‐induced reductions in circulating adrenomedullin. No significant changes in plasma levels of endothelin‐1 or CGRP were found. Lead‐induced decreases in nitric oxide markers and antioxidant status were not prevented by doxycycline. In conclusion, acute lead exposure increases blood pressure and MMP‐9 activity, which were blunted by doxycycline. These findings suggest that MMP‐9 may contribute with lead‐induced hypertension by cleaving the vasodilatory peptide adrenomedullin, thereby inhibiting adrenomedullin‐dependent lowering of blood pressure.