Evolution of in vitro digestibility techniques: a systematic review

The inability to reproduce certain digestive processes in vivo, high research costs and ethical aspects have led to the development of a large number of in vitro digestion models. These models allow us to take into account various factors of modeling complex multistage physiological processes occurring in the gastrointestinal tract, which makes them promising and widely used. A significant part of in vitro methods includes assessment by enzymatic digestion and are based on the calculation of nitrogen remaining after digestion in relation to the initial total nitrogen (according to the Dumas, Kjeldahl method, spectrophotometric or chromatographic method). There are also a number of titrometric methods (pH‑stat), which are mainly used to assess the digestibility of feed, most successfully for aquatic animals due to the simplicity of their digestive tract. Methods for assessing the digestibility of food products by enzymatic digestion have undergone various stages of evolution (since 1947) and have been widely modified by including various enzymes (pepsin, trypsin, pancreatin, erepsin, etc.) in model systems, indices for various products have been determined on their basis (pepsin-digest-residue (PDR) index, 1956; pepsin pancreatin digest (PPD) index, 1964; pepsin digest dialysate (PDD), 1989). As a result, a single protocol was formed to study the digestibility of food — INFOGEST (2014–2019), which includes three stages of digestion (oral, gastric and intestinal). It allows researchers to accurately reproduce the conditions of the human gastrointestinal tract and is widely used by scientists around the world

Spectrum of Genetic Changes in Patients with Non-Syndromic Hearing Impairment and Extremely High Carrier Frequency of 35delG GJB2 Mutation in Belarus

The genetic nature of sensorineural hearing loss (SNHL) has so far been studied for many ethnic groups in various parts of the world. The single-nucleotide guanine deletion (35delG) of the GJB2 gene coding for connexin 26 was shown to be the main genetic cause of autosomal recessive deafness among Europeans. Here we present the results of the first study of GJB2 and three mitochondrial mutations among two groups of Belarusian inhabitants: native people with normal hearing (757 persons) and 391 young patients with non-syndromic SNHL. We have found an extremely high carrier frequency of 35delG GJB2 mutation in Belarus −5.7%. This point deletion has also been detected in 53% of the patients with SNHL. The 312del14 GJB2 was the second most common mutation in the Belarus patient cohort. Mitochondrial A1555G mt-RNR1 substitution was found in two SNHL patients (0.55%) but none were found in the population cohort. No individuals carried the A7445G mutation of mitochondrial mt-TS1. G7444A as well as T961G substitutions were detected in mitochondrial mt-RNR1 at a rate of about 1% both in the patient and population cohorts. A possible reason for Belarusians having the highest mutation carrier frequency in Europe 35delG is discussed