Assessment of the supraspinatus muscle fiber architecture with diffusion tensor imaging in healthy volunteers.

OBJECTIVES: This study presents a framework for the calculation of supraspinatus (SSP) muscle pennation angles (PAs) from diffusion tensor imaging (DTI). MATERIALS AND METHODS: Ten healthy individuals (five females and five males; age 32.0 ± 4.7 years) underwent three sessions of 3-T MRI, including a stimulated echo acquisition mode DTI sequence. The imaging plane of the DTI sequence was angled along the intramuscular part of the SSP tendon. A custom-built software was developed and implemented to compute DTI-based PAs of the anterior and posterior SSP in relation to the orientation of the tendon. Subsequently, three readers measured PAs from the post-processed images. Test-retest reliability, inter-reader agreement, and intra-reader agreement of PA measurements were evaluated with intraclass correlation coefficients (ICCs). RESULTS: The mean PA in the anterior SSP was 15.6 ± 2.1° and 10.7 ± 0.9° in the posterior SSP. MRI-derived PAs showed good to excellent test-retest reliability (ICC: 0.856-0.945), inter-reader agreement (ICC: 0.863-0.955), and intra-reader agreement (ICC: 0.804-0.955). CONCLUSION: PAs derived from DTI demonstrated good to excellent test-retest reliability, inter-reader agreement, and intra-reader agreement. We successfully implemented a highly standardized technique for evaluating PAs of the SSP muscle. CRITICAL RELEVANCE STATEMENT: This proposed low-complex method might facilitate the increased use of the PA as a biomarker for pathological conditions of the rotator cuff. KEY POINTS: A low-complex method for measuring PAs of the SSP might help identify pathology early. The mean PA was 15.6 ± 2.1° and 10.7 ± 0.9° in the anterior and posterior SSP, respectively. ICCs were ≥ 0.856 for test-retest reliability, ≥ 0.863 for inter-reader agreement, and ≥ 0.804 for intra-reader agreement.

Enhancing the membrane bioreactor efficiency: The impact of rotating membrane modules and aeration strategies on the transmembrane pressure.

The study analyses the performance of a pilot plant using a rotating hollow fibre (HF) membrane bioreactor system. The experiments evaluated the effect of operational parameters such as rotational speed, aeration strategies, and maintenance cleaning (MC) procedures on the efficiency of the system, in particular transmembrane pressure (TMP) and filtrate quality. The results indicate that the rotating membrane module reduces TMP increase and can operate for 48 days with satisfactory performance, even without aeration. This has the potential to significantly improve efficiency, resulting in significant energy savings. In addition, two MC methods, clean in air and clean in place, were tested and found to be efficient for weekly MC. It was observed that operating without aeration during colder seasons may not be effective. Therefore, adaptive strategies are needed to address seasonal temperature variations.

The impact of solid/floc holdup on oxygen transfer in a rotating hollow fiber membrane bioreactor under endogenous conditions.

A set of oxygen transfer experiments in clean water and three different activated sludge concentrations were conducted with fine and coarse bubble aeration in a rotating hollow fiber membrane bioreactor to observe the impact of different rotational speeds on the oxygen transfer rate. The results showed that with increasing membrane rotational speed, the oxygen transfer coefficient enhanced while the α-factor showed similar values at comparable sludge concentrations and solid/floc holdups. The highest improvement rates occurred during the experiments with coarse bubble aeration at 50 rpm and the lowest specific airflow rate. The solid/floc holdup appears to universally impact oxygen transfer depletion regardless of what reactor type, diffuser setup and membrane rotational speed were used in the wastewater experiments.

Moderate hypermutability of a transgenic lacZ reporter gene in Myc-dependent inflammation-induced plasma cell tumors in mice.

Mutator phenotypes, a common and largely unexplained attribute of human cancer, might be better understood in mouse tumors containing reporter genes for accurate mutation enumeration and analysis. Previous work on peritoneal plasmacytomas (PCTs) in mice suggested that PCTs have a mutator phenotype caused by Myc-deregulating chromosomal translocations and/or phagocyte-induced mutagenesis due to chronic inflammation. To investigate this hypothesis, we generated PCTs that harbored the transgenic shuttle vector, pUR288, with a lacZ reporter gene for the assessment of mutations in vivo. PCTs exhibited a 5.5 times higher mutant frequency in lacZ (40.3 +/- 5.1 x 10(-5)) than in normal B cells (7.36 +/- 0.77 x 10(-5)), demonstrating that the tumors exhibit the phenotype of increased mutability. Studies on lacZ mutant frequency in serially transplanted PCTs and phagocyte-induced lacZ mutations in B cells in vitro indicated that mutant levels in tumors are not determined by exogenous damage inflicted by inflammatory cells. In vitro studies with a newly developed transgenic model of inducible Myc expression (Tet-off/MYC) showed that deregulated Myc sensitizes B cells to chemically induced mutations, but does not cause, on its own, mutations in lacZ. These findings suggested that the hypermutability of PCT is governed mainly by intrinsic features of tumor cells, not by deregulated Myc or chronic inflammation.

Redox imbalance and mutagenesis in spleens of mice harboring a hypomorphic allele of Gpdx(a) encoding glucose 6-phosphate dehydrogenase.

Mice harboring the activity-attenuated Gpdx(a-m2Neu) allele and also harboring a chromosomally integrated lacZ reporter gene to study mutagenesis (pUR288) were used to demonstrate that moderate glucose 6-phosphate dehydrogenase (G6PD) deficiency causes elevated mutagenesis and endogenous oxidative stress in the spleen. G6PD-deficient spleens with a residual enzyme activity of 22% exhibited a dramatic shift in the mutational pattern of lacZ (4.6-fold increase in the prevalence of recombination mutations of lacZ) together with a 1.8-fold increase in mutant frequencies in lacZ. A concomitant 3-fold reduction in catalase activity (dependent upon NADPH) indicated that the in vivo supply of G6PD-generated NADPH was insufficient. An additional 3-fold increase in oxidized glutathione suggested that redox control was disturbed in G6PD-deficient spleens. These findings indicate that G6PD is required for limiting oxidative mutagenesis in the mouse spleen. Gpdx(a-m2Neu) is the first hypomorphic allele of a mouse housekeeping gene associated with elevated somatic mutagenesis in vivo.

Moderate G6PD deficiency increases mutation rates in the brain of mice.

Mice that harbored the x-ray-induced low efficiency allele of the major X-linked isozyme of glucose-6-phospate dehydrogenase (G6PD), Gpdx(a-m2Neu), and, in addition, harbored the transgenic shuttle vector for the determination of mutagenesis in vivo, pUR288, were employed to further our understanding of the interdependence of general metabolism, oxidative stress control, and somatic mutagenesis. The Gpdx(a-m2Neu) mutation conferred moderate G6PD deficiency in hemizygous males (Gpdx(a-m2Neu/y)) displaying residual enzyme activities of 27% in red blood cells and 13% in brain (compared to wild-type controls, Gpdx(a/y) males). In spite of this mild phenotype, the brains of G6PD-deficient males exhibited a significant distortion of redox control ( approximately 3-fold decrease in the ratio of reduced glutathione to oxidized glutathione), a considerable accumulation of promutagenic etheno DNA adducts ( approximately 13-fold increase in ethenodeoxyadenosine and approximately 5-fold increase in ethenodeoxycytidine), and a substantial elevation of somatic mutation rates ( approximately 3-fold increase in mutant frequencies in lacZ, the target and reporter gene of mutagenesis in the shuttle vector, pUR288). The mutation pattern in the brain was dominated by illegitimate genetic recombinations, a presumed hallmark of oxidative mutagenesis. These findings suggested a critical function for G6PD in limiting oxidative mutagenesis in the mouse brain.