Sentence examples for putative defects from inspiring English sources

In the current study we have screened for functional deficiencies consistent with putative defects of CatSper function in men with normal semen parameters attending for IVF treatment.

Nevertheless, because of the simultaneous accumulation of fat in the liver, visceral depot, and skeletal muscle, we were unable to differentiate the individual effect of each one of these on putative defects in glucose and lipid metabolism.

To assess the putative defects in growth cone anatomy, we first analyzed potential differences in the intracellular localization or quantity of actin and tubulin, two generally utilized markers for initial characterization of the integrity of neuronal projections.

The present data also provides an indication of a putative defect in GAG sulfation, which may lead to dramatic biological effects, as exemplified by mutations in PAPSS2, SLC26A2, gPAPP or SUMF1, all causing skeletal dysplasias [41] [44].

To determine which of these mutations were able to compensate for the putative defect in the chimeric GBV-B/HCV genome, we introduced either one or a combination of these nucleotide substitutions into the chimeric GB/IIIHC genome and assessed the infectivity of each corresponding synthetic RNA by intrahepatic inoculation into a GBV-B-naïve tamarin (Fig. 4).

The following text has been added: "A putative defect in regulatory T cells cannot explain the increased CD44 expression on naïve Rasgrp1 Anaef CD4+ cells, because in mixed chimeras bearing many wild-type Foxp3+ cellsells, CD44 expression was still increased on Rasgrp1 Anaef but not on co-resident wild-type CD62L+ FOXP3– CD4+ splenocytes".

A putative defect in regulatory T cells cannot explain the increased CD44 expression on naïve Rasgrp1 Anaef CD4+ cells, because in mixed chimeras bearing many wild-type Foxp3+ cellsells, CD44 expression was still increased on Rasgrp1 Anaef but not on co-resident wild-type CD62L+ FOXP3− CD4+ splenocytes.

As a result, the putative structural defects in condensin-depleted chromosomes persist through anaphase, where SMC2-depleted cells fail to segregate a substantial proportion of chromosomes.

Understanding the underlying putative metabolic defects leading to the development of type 2 diabetes requires studies that focus on the earliest stages of the disease before the onset of any alterations in glucose tolerance.

Because the mature T cells are resting, it would be possible to test whether restoring BAF57 expression in these cells can rescue the pre-existing phenotype, and we are therefore systematically searching for the putative functional defects in the mature T cells.

Because ClC-7 is not dependent on Ostm1 to reach the lysosomes in general [10], the function of Ostm1 in our experiments might be to compensate a putative folding defect caused by the G213R mutation.