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We review the ultrasound (US) findings in patients who present with meralgia paresthetica (MP). The anatomy of the lateral femoral cutaneous nerve at the level where the nerve exits the pelvis and potential entrapment sites that can lead to MP are discussed. A wide range of pathological cases are presented to help in recognizing the US patterns of MP. Finally, our experience with US-guided treatment is discussed.
Microvascular network architecture defines coupling of fluid and protein exchange. Network arrangements markedly reduce capillary hydrostatic pressures and resting fluid movement while increasing the capacity for change The presence of vascular remodelling or angiogenesis puts constraints of network behaviour The sites of fluid and protein exchange can be segregated to different portions of the network Although there is a net filtration of fluid from a network of exchange vessels, there are specific areas where fluid moves into the circulation (reabsorption) and while protein is moving into tissue the amount is insufficient under basal conditions to result in changes in oncotic pressure.
Integration of functional results obtained across scales, from chemical signalling to the whole organism is a daunting task requiring the marriage of experimental data with mathematical modelling. In this paper a novel coupled computational fluid dynamics model is developed incorporating fluid and protein transport using ncorporating measures of individual vessel surface area, demonstrates additional lowering of p
from inlet values favoring a > 70% reduction of J
in the face of a ≈ 120% increase in protein movement into the tissues relative to the Homogeneous Scenario. Beyond the impacts of network architecture, an unanticipated finding was the influence of a blind-end microvessel on model convergence, indicating a profound influence of the largely unexplored dynamics of vascular remodelling on tissue perfusion. This article is protected by copyright. All rights reserved.
70% reduction of Jf,T in the face of a ≈ 120% increase in protein movement into the tissues relative to the Homogeneous Scenario. Beyond the impacts of network architecture, an unanticipated finding was the influence of a blind-end microvessel on model convergence, indicating a profound influence of the largely unexplored dynamics of vascular remodelling on tissue perfusion. This article is protected by copyright. All rights reserved.
What is the central question of this study? While muscle fibre atrophy in response to immobilisation has been extensively examined, intramuscular connective tissue, particularly endomysium, has been largely neglected does endomysium content of the soleus muscle increase during bed rest? What is the main finding and its importance? Absolute endomysium content did not change, and previous studies reporting an increase are explicable by muscle fibre atrophy. It must be expected that even a relative connective tissue accumulation will lead to an increase in muscle stiffness.
Muscle fibres atrophy during conditions of disuse. Whilst animal data suggest an increase in endomysium content with disuse, that information is not available for humans. We hypothesised that endomysium content increases during immobilisation. To test this hypothesis, biopsy samples of the soleus muscle obtained from 21 volunteers who underwent 60days of bed rest were analysed using immunofluorescence-labelled laminin γ-1 to delineate indese results demonstrate that an increase in EFAr is likely to be a direct effect of muscle fibre atrophy. Based on the assumption that the total number of muscle fibres remains unchanged during 55 days of bed rest, this implies that the absolute amount of connective tissue in the soleus muscle remained unchanged. The increased relative endomysium content, however, could be functionally related to an increase in muscle stiffness.
Focal segmental glomerulosclerosis (FSGS, OMIM®#603 965) is an overriding cause that leads to end-stage renal disease (ESRD). As a member of TRP superfamily, mutations of TRPC6 gene are closely linked to FSGS. By now, 20 missense mutations have been reported, among them, nine gain-of-function (GOF), and five loss-of-function (LOF) mutations have been recognized according to the effect on TRPC6 channel activity. Systematic investigations of functional mutations will provide valuable evidences for understanding the pathophysiology of TRPC6 involved in FSGS. The aim of this study is to investigate the pathogenicity of a novel TRPC6 mutation p.Q134P in FSGS.
High-throughput sequencing was performed to analyse 436 genes which are associated with hereditary kidney diseases in a Chinese pedigree. Then we constructed TRPC6 expression plasmids of wide type and variant. Immunofluorescence, cell-surface biotinylation assays and electrophysiology were used to analyse the localization, cell surface expression, and calcium transport activity of TRPC6.
A novel variant c.401A>C (p.Q134P) in exon 2 of TRPC6 gene was found. There was no significant difference between the expression levels of p.Q134P mutant and WT TRPC6 protein in the whole cell lysate and cell-surface fraction. Q134P mutant-bearing TRPC6 elicited much higher Ca
current amplitude than WT.
We identified a novel GOF mutation p.Q134P of TRPC6 which contributed to late-onset FSGS. Our study expands the mutational spectrum of TRPC6 associated with FSGS and furtherly supports the hypothesis of calcium dose-response dependency that a moderate increased calcium influx elicited a mild FSGS phenotype.
We identified a novel GOF mutation p.Q134P of TRPC6 which contributed to late-onset FSGS. Our study expands the mutational spectrum of TRPC6 associated with FSGS and furtherly supports the hypothesis of calcium dose-response dependency that a moderate increased calcium influx elicited a mild FSGS phenotype.Aerobic exercise is an important non-pharmacological means of antitumor intervention, but related mechanisms are poorly understood. In this review, previous studies are summarized from the aspects of tumor oxygenation, autophagy versus apoptosis, and organismal immunity. Current findings on the antitumor effects of aerobic exercise involve AMPK signaling, PI3K/Akt signaling, Th1/Th2 cytokine balance related to immunity, PD-1/PD-L1 immunosuppressive signaling, and related cytokine pathways. Several directions for further research are proposed, including whether newly discovered subgroups of cytokines influence the effects of aerobic exercise on tumors, tailoring corresponding exercise prescriptions based on the bidirectional effects of certain cytokines at different stages, identifying the potential effects of exercise time and intensity, and elucidating details of the unclear mechanisms. Through the discussion of the existing data, we hope to provide new ideas for the future research of exercise therapy.
Epstein-Barr virus (EBV) is detected in a variety of B-cell lymphomas (BCLs) and B-cell lymphoproliferative disorders (B-LPDs). Immunodeficiency has been considered to play a key role in the pathogenesis of these diseases. In addition, immune escape of tumor cells may also contribute to the development of EBV
BCLs and B-LPDs. The PD-1/PD-L1 pathway is particularly important for immune escape of tumor cells that contribute to development of lymphoma through suppression of cytotoxic T-cell function. selleck compound We now consider PD-L1 immunohistochemistry (IHC) a very useful method for predicting whether tumor cells of lymphoid malignancies are characterized by the immune escape mechanism.
We reviewed articles of EBV
BCLs and B-LPDs from the perspective of immune escape and immunodeficiency, particularly focusing on PD-L1 IHC.
Based on PD-L1 IHC, we consider that EBV
BCL and B-LPD can be classified into three types "immunodeficiency", "immune escape", and "immunodeficiency + immune escape" type. The immunodeficiehological perspective, we suggest that lymphoma diagnosis should be made considering immune escape and immunodeficiency.
Hereditary sensory and autonomic neuropathies (HSANs) are a group of genetic disorders affecting the peripheral nervous system. Two different associated variants have been identified in dogs 1 in Border Collies and 1 in Spaniels and Pointers.
Clinically and genetically characterize HSAN in a family of mixed breed dogs.
Five 7-month-old mixed breed dogs from 2 related litters were presented for evaluation of a 2-month history of acral mutilation and progressive pelvic limb gait abnormalities.
Complete physical, neurological, electrodiagnostic, and histopathological evaluations were performed. Whole genome sequencing of 2 affected dogs (1 from each litter) was used to identify variants that were homozygous or heterozygous in both cases, but wild type in 217 control genomes of 100 breeds. Immunohistochemistry was used to assess protein expression.
Complete physical, neurological, electrodiagnostic, and histopathological evaluations confirmed a disorder affecting sensory and autonomic nerves. Whole genome sequencing identified a missense variant in the RETREG1 (reticulophagy regulator 1) gene (c.656C > T, p.P219L). All affected dogs were homozygous for the variant, which was not detected in 1193 dogs from different breeds. Immunohistochemistry showed no expression of RETREG1 in the cerebellum of affected dogs. One of the affected dogs lived for 5 years and showed gradual progression of the clinical signs.
We confirmed the diagnosis of HSAN in a family of mixed breed dogs and identified a novel and possibly pathogenic RETREG1 variant. Affected dogs experienced gradual deterioration over several years.
We confirmed the diagnosis of HSAN in a family of mixed breed dogs and identified a novel and possibly pathogenic RETREG1 variant. Affected dogs experienced gradual deterioration over several years.Porous carbon materials demonstrate extensive applications for their attractive characteristics. Mechanical flexibility is an essential property guaranteeing their durability. After decades of research efforts, compressive brittleness of porous carbon materials is well resolved. However, reversible stretchability remains challenging to achieve due to the intrinsically weak connections and fragile joints of the porous carbon networks. Herein, it is presented that a porous all-carbon material achieving both elastic compressibility and stretchability at large strain from -80% to 80% can be obtained when a unique long-range lamellar multi-arch microstructure is introduced. Impressively, the porous all-carbon material can maintain reliable structural robustness and durability under loading condition of cyclic compressing-stretching process, similar to a real metallic spring. The unique performance renders it as a promising platform for making smart vibration and magnetism sensors, even capable of operating at extreme temperatures. Furthermore, this study provides valuable insights for creating highly stretchable and compressible porous materials from other neat inorganic components for diverse applications in future.At the molecular level, cellular ageing involves changes in multiple gene pathways. Cellular senescence is both an important initiator and a consequence of natural ageing. Senescence results in changes in multiple cellular mechanisms that result in a natural decrease in cell cycle activity. Liver senescence changes impair hepatic function. Given the well-established sexual dimorphism in ageing, we hypothesized that the natural hepatic ageing process is driven by sex-dependent gene mechanisms. We studied our well-characterized normal, chow-fed rat ageing model, lifespan ∼850 days, in which we have reported ageing of metabolism, reproduction and endocrine function. We performed liver RNA-seq on males and females at 110 and 650 days to determine changes in the cell cycle and cellular senescence signalling pathways. We found that natural liver ageing shows sexual dimorphism in these pathways. RNA-seq revealed more male (3967) than female (283) differentially expressed genes between 110 and 650 days. Cell cycle pathway signalling changes in males showed decreased protein and expression of key genes (Cdk2, Cdk4, Cycd and PCNA) and increased expression ofp57 at 650 vs 110 days.