Physical Therapy Management Of A Manual Laborer With Chronic Rotator Cuff Tendinopathy: A Case Report

Background: Tendinopathy is characterized by tendon thickening, localized pain and chronic degeneration reflective of failed healing. 38% of manual laborers who participate in daily moderate to heavy lifting will experience Rotator Cuff Tendinopathy(RCT). There is a lack of research investigating the PT management of manual laborers who have RCT, but must continue to participate in harmful activities to fulfill occupational responsibilities. Purpose: The purpose of this case report was to describe the PT management of a patient with rotator cuff tendinopathy who, due to work requirements continued to participate in activities detrimental to the health of the supraspinatus and function of the shoulder girdle.https://dune.une.edu/pt_studcrposter/1036/thumbnail.jp

Modulation of Fibroblast Growth Factor Signaling Is Essential for Mammary Epithelial Morphogenesis

<div><p>Fibroblast growth factor (FGF) signaling is essential for vertebrate organogenesis, including mammary gland development. The mechanism whereby FGF signaling is regulated in the mammary gland, however, has remained unknown. Using a combination of mouse genetics and 3D ex vivo models, we tested the hypothesis that <i>Spry2</i> gene, which encodes an inhibitor of signaling via receptor tyrosine kinases (RTKs) in certain contexts, regulates FGF signaling during mammary branching. We found that <i>Spry2</i> is expressed at various stages of the developing mammary gland. Targeted removal of <i>Spry2</i> function from mammary epithelium leads to accelerated epithelial invasion. <i>Spry2</i> is up-regulated by FGF signaling activities and its loss sensitizes mammary epithelium to FGF stimulation, as indicated by increased expression of FGF target genes and epithelia invasion. By contrast, <i>Spry2</i> gain-of-function in the mammary epithelium results in reduced FGF signaling, epithelial invasion, and stunted branching. Furthermore, reduction of <i>Spry2</i> expression is correlated with tumor progression in the MMTV-PyMT mouse model. Together, the data show that FGF signaling modulation by <i>Spry2</i> is essential for epithelial morphogenesis in the mammary gland and it functions to protect the epithelium against tumorigenesis.</p></div

Pups generated from self-crosses of <i>Spry2</i> heterozygous mice.

<p>Pups were genotyped on postnatal day 1 (P1; n = 42) and upon weaning on postnatal day 21 (P21; n = 359). Note the actual frequencies (Act.) of both <i>Spry2</i>^Δ/+ and <i>Spry2</i>^+/+ were more than the expected frequencies (Exp.) because a portion of the <i>Spry2</i>^Δ/Δ pups died prior to weaning.</p

Intrinsically Conductive Polymer Fibers from Thermoplastic <i>trans</i>-1,4-Polyisoprene

Herein, we report a new strategy to prepare conductive polymer fibers to overcome the insurmountable weakness of current conductive polymer fibers. First, special thermoplastic polymers are processed into polymer fibers using a conventional melt-spinning process, and then the nonconductive polymer fibers are converted into intrinsically conductive polymer fibers. Using this new strategy, intrinsically conductive polymer fibers have been prepared by melt spinning low-cost thermoplastic <i>trans</i>-1,4-polyisoprene and doping with iodine, which can be as fine as 0.01 mm, and the resistivity can be as low as 10^–2 Ω m. Moreover, it has been found that drawing can improve the orientation of <i>trans</i>-1,4-polyisoprene crystals in the fibers and, thus, the conductivity of the conductive polymer fibers. Therefore, conductive fibers with excellent conductivities can be prepared by large drawing ratios before doping. Such conductive polymer fibers with low cost could be used in textile, clothing, packing, and other fields, which would benefit both industry and daily life. The newly developed method also allows one to produce conductive polymers of any shape besides fibers for antistatic or conductive applications

<i>Spry2</i> null mice show stunted epithelial branching due to malnourishment.

<p>(<b>A–C</b>) <i>Spry2</i> mRNA expression as detected by quantitative RT-PCR (qPCR). (<b>A</b>) <i>Spry2</i> mRNA expression was measured by qPCR using RNA harvested from mammary glands from female mice at 3-weeks, 5-weeks, and 10-weeks of age as virgins, during pregnancy (P) on day 5 and 17, on day 1 of lactation (Lac), and on day 1, 3, and 10 of involution (Inv). <i>Spry2</i> expression at 3-weeks was set as base value against which other stages were compared. Abbreviations: wks, weeks; P, pregnancy; L, lactation; Inv, involution. (<b>B</b>, <b>C</b>) MECs were sorted based on their expression of CD24 and Integrin-α6 (CD49f). CD24^medCD49f^hi cells were basal (ba), whereas CD24^hiCD49f^l°^w cells and CD24^l°^wCD49f^l°^w were luminal (lu) and stromal (st), respectively. RNA was harvested from the three cell partitions to generate DNA templates for qPCR reactions (<b>C</b>). (<b>D</b>, <b>E</b>) The mammary branching tree at 6-weeks of age, as revealed by Carmine Red staining of glands in wholemount. Proximal (close to the nipple) is to the left and distal is to the right. Arrowheads indicate TEBs at the tips of invading mammary epithelium, which persist until branching morphogenesis ceases in adult glands. Arrows indicate the extent of ductal penetration in the fat pad. Note epithelial branching was severely stunted in (<b>E</b>) mutant (<i>Spry2</i>^Δ/Δ; n = 8) mice when compared with (<b>D</b>) control (<i>Spry2</i>^Δ/+; n = 12) mice. Scale bars: 2 mm. Abbreviation: epi, epithelium; st, stroma; LN, lymph node. (<b>F–M</b>) <i>Spry2</i> null mice showed growth retardation (<b>F</b>, <b>G</b>) and an insufficiency in energy storage (<b>H–M</b>). (<b>F</b>) Growth curve of pups born from <i>Spry2</i>^Δ/+ crosses. Weights between <i>Spry2</i>^Δ/+ (n = 15) and <i>Spry2</i>^+/+ (n = 4) mice were indistinguishable and combined. Values shown are the mean ± SD for each data point. (<b>G</b>) Dorsal view of typical appearances of <i>Spry2</i>^Δ/+ and <i>Spry2</i>^Δ/Δ mice at 12-weeks of age. Note <i>Spry2</i>^Δ/Δ mice were shorter than normal and had enlarged midsection (flanked by dotted black lines) due to distended intestines (not shown). Scale bars: 2 cm. (<b>H–M</b>) Glycogen and lipid storage, as revealed by Periodic Acid-Schiff and Oil-Red-O staining, respectively, and histology of white adipose tissue from <i>Spry2</i>^Δ/+ (<b>H</b>–<b>J</b>) and <i>Spry2</i>^Δ/Δ mice (<b>K</b>–<b>M</b>). Note that <i>Spry2</i>^Δ/Δ mutant liver lacked glycogen (<b>K</b>) and lipid storage (<b>L</b>) as was evident in control liver (purple-magenta color in <b>H</b> and red droplets in <b>I</b>); moreover, adipocytes from white adipose tissue in <i>Spry2</i>^Δ/Δ mutant (<b>M</b>) mice were smaller than normal (<b>J</b>). Scale bars: 100 μm.</p

<i>Spry2</i> null epithelium shows enhanced FGF signaling activities and increased epithelial branching activities.

<p>(<b>A</b>) Expression, as measured by qPCR, of <i>Spry2</i> and target genes of FGF signaling, including <i>Etv4</i>, <i>Etv5</i>, and <i>Mkp3</i>, in response to a 24-hour treatment of FGF2 (10 nM) or FGF10 (10 nM). Expression is relative to that of the untreated samples. Values shown are the mean ± standard deviation (SD) of three independent experiments. Statistically significant differences of p<0.05 (t test) were observed between expression of untreated and treated samples for all genes except for <i>Etv5</i> in response to FGF2 and FGF10 treatment. (<b>B</b>) Schematic diagram depicting the experimental procedure in sample preparation, treatment, and analysis. Mammary organoids were prepared from <i>Spry2</i>^+/+ and <i>Spry2</i>^fl/fl mice and were infected with adenovirus-Cre-GFP, which generated control (<i>Spry2</i>^+/+) and mutant (<i>Spry2</i>^Δ/Δ) organoids, respectively. Transduced cells were then purified by FACS based on their expression of GFP before they were subjected to analyses on gene expression and epithelial morphogenesis in the presence or absence of FGF2 or FGF10. (<b>C–D</b>) Expression, as measured by qPCR, of <i>Etv4</i>, <i>Etv5</i>, and <i>Mkp3</i> in control and mutant MECs in response to 24-hour treatment of FGF2 (200 ng/ml, <b>C</b>) or FGF10 (200 ng/ml, <b>D</b>). Expression is relative to that of the control samples. Statistically significant differences of p<0.05 (t test) were observed between expression of control and mutant samples for all genes except for <i>Etv5</i> in response to FGF2 treatment and <i>Etv4</i> in response to FGF10 treatment. (<b>E–I</b>) in vitro branching assay in which control (<b>E</b>, <b>F</b>) and mutant organoids (<b>G</b>, <b>H</b>) were subjected to cultures in basal medium with (<b>F</b>, <b>H</b>) or without FGF2 (<b>E</b>, <b>G</b>). When stimulated by FGF2 at progressively higher concentrations from 0.025 nM to 0.5 nM, a progressively higher percentage of organoids underwent branching. At 1.0 nM and 2.5 nM, FGF2 did not stimulate a higher percentage of branched organoids to form. In addition to their differences in branching kinetics, <i>Spry2</i>^Δ/Δ organoids overall formed larger branched structures than control organoids. Scale bars: 100 μm. (<b>I</b>) Quantitative comparisons of control and mutant MECs in their ability to undergo epithelial branching in vitro. Data were from experiments repeated three times or more. At least 100–150 organoids were examined for each treatment conditions. Values shown are the mean ± SD for each data point: *P<0.0005, unpaired, two-tailed Student’s <i>t</i> tests.</p

Gain of <i>Spry2</i> function in the mammary epithelium causes retarded epithelial branching.

<p>(<b>A</b>) Schematic diagram depicting the <i>Spry2</i>-GOF transgene. The β<i>-Geo</i> gene was driven by the CAGG promoter and followed by a triple poly-adenylation sequence (3x pA). Upon Cre-mediated recombination, the β<i>-Geo</i> gene was deleted and the mouse <i>Spry2</i> and human placental alkaline phosphatase (PLAP), constructed as a bi-cistronic mRNA containing an internal ribosome entry site (IRES) directing PLAP translation, were expressed. (<b>B–C</b>) Assay for PLAP activities in control (M-Cre or <i>Spry2</i>-GOF) and mutant (M-Cre;<i>Spry2</i>-GOF) #3 glands from adult female mice at 15-weeks of age. Note PLAP activities were detected in mutant (<b>C</b>) but not in control glands (<b>B</b>). The area in the dashed red box is highlighted in a close-up picture in the inset, illustrating the branching network that was positive for PLAP activities. (<b>D–I</b>) The mammary branching tree from #4 glands at the postnatal stages indicated. Samples were assayed for PLAP activities and were then stained with Carmine Red. (<b>D–F</b>) glands from control mice; (<b>G–I</b>) glands from mutant mice. Arrows indicate the extent of ductal penetration in the fat pad. Dotted white line illustrates the epithelial invasion front. Insets in (<b>G</b>), (<b>H</b>), and (<b>I</b>) show high-magnification views of the rudimentary ductal tree (area in dashed box), illustrating only some of the mammary epithelial cells showed PLAP activities due to the mosaic activity of the M-Cre transgene. Solid arrowheads indicate TEBs from 4-week (<b>G</b>) and 7-week (<b>H</b>) mammary glands that were more heavily stained for PLAP activities than other TEBs indicated by open arrowheads (<b>H</b>). These data suggest that the mammary glands from the bi-transgenic mice (M-Cre;<i>Spry2</i>-GOF) are mosaic, containing both Cre-expressing and non-Cre-expressing cells. (<b>J</b>, <b>K</b>) Quantitative comparisons of ductal penetration and branch point formation between control and mutant glands. At 7 weeks, ductal penetration measurements were 7.0±1.9 (control, n = 6) and 1.8±1.0 (mutant, n = 6); at 8 weeks, the measurements were 9.9±1.2 (control, n = 4) and 7.7±2.3 (mutant, n = 10); at 10 weeks, they were 12.4±0.3 (control, n = 8) and 12.7±0.04 (mutant, n = 4). Measurements of branching points were 2.1±0.3 (control) and 1.2±0.2 (mutant) at 7 weeks, 1.7±0.1 (control) and 2.3±0.4 (mutant) at 8 weeks, and 2.3±0.2 (control) and 2.4±0.2 (mutant) at 10 weeks. Values shown are the mean ± SD for each data point: *, P<0.05, unpaired, two-tailed Student’s <i>t</i> test. Scale bars: 2.5 mm. N is the number of mammary glands examined.</p

Micellization of Lactosylammonium Surfactants with Different Counter Ions and Their Interaction with DNA

So far, the studies about the physical chemical properties of sugar-based surfactants have been still unsystematic; most of the studies have been focused on nonionic sugar-based surfactants. In the present work, we studied the micellization of four lactose-based surfactants, with the same headgroup (lactosylammonium) and the same hydrophobic alkyl chain (dodecyl) but different counterions (malonate, adipate, propionate, and hexanoate), at 25.0 and/or 50.0 °C. We found that these four surfactants could decrease the surface tension of water to ca. 30 mN/m. When the number of carboxylate groups in the counterion was the same, the counterion having a shorter alkyl chain could lead to a smaller minimum area per surfactant molecule. Moreover, the surfactants with monocarboxylates as counterions had much lower critical micelle concentrations than those with dicarboxylates as counterions, and the micelles from the former surfactants had a lower counterion binding degree. The lactosylammonium surfactants could bind with DNA, and low content of the surfactant could decrease the CD signal of DNA, while high content of the surfactant could make DNA unfold somewhat

Image2_Case report: A novel c.1842_1845dup mutation of ETFDH in two Chinese siblings with multiple acyl-CoA dehydrogenase deficiency.jpeg

This article reports the characterization of two siblings diagnosed with late-onset multiple Acyl-CoA dehydrogenase deficiency (MADD) caused by mutations in electron transfer flavoprotein(ETF)-ubiquinone oxidoreductase (ETF-QO) (ETFDH) gene. Whole exome sequencing (WES) was performed in the proband's pedigree. Clinical phenotypes of Proband 1 (acidosis, hypoglycemia, hypotonia, muscle weakness, vomiting, hypoglycemia, hepatomegaly, glutaric acidemia, and glutaric aciduria) were consistent with symptoms of MADD caused by the ETFDH mutation. However, Proband 2 presented with only a short stature. The patients (exhibiting Probands 1 and 2) showed identical elevations of C6, C8, C10, C12, and C14:1. c.1842_1845 (exon13)dup, and c.250 (exon3) G > A of the ETFDH gene were compound heterozygous variants in both patients. The novel variant c.1842_1845dup was rated as likely pathogenic according to the American College of Medical Genetics and Genomics guidelines (ACMG). This is the first report on the c.1842_1845dup mutation of the ETFDH gene in patients with late-onset MADD, and the data described herein may help expand the mutation spectrum of ETFDH.</p

Image1_Case report: A novel c.1842_1845dup mutation of ETFDH in two Chinese siblings with multiple acyl-CoA dehydrogenase deficiency.jpeg

This article reports the characterization of two siblings diagnosed with late-onset multiple Acyl-CoA dehydrogenase deficiency (MADD) caused by mutations in electron transfer flavoprotein(ETF)-ubiquinone oxidoreductase (ETF-QO) (ETFDH) gene. Whole exome sequencing (WES) was performed in the proband's pedigree. Clinical phenotypes of Proband 1 (acidosis, hypoglycemia, hypotonia, muscle weakness, vomiting, hypoglycemia, hepatomegaly, glutaric acidemia, and glutaric aciduria) were consistent with symptoms of MADD caused by the ETFDH mutation. However, Proband 2 presented with only a short stature. The patients (exhibiting Probands 1 and 2) showed identical elevations of C6, C8, C10, C12, and C14:1. c.1842_1845 (exon13)dup, and c.250 (exon3) G > A of the ETFDH gene were compound heterozygous variants in both patients. The novel variant c.1842_1845dup was rated as likely pathogenic according to the American College of Medical Genetics and Genomics guidelines (ACMG). This is the first report on the c.1842_1845dup mutation of the ETFDH gene in patients with late-onset MADD, and the data described herein may help expand the mutation spectrum of ETFDH.</p