An Affordable NIR Spectroscopic System for Fraud Detection in Olive Oil.

Adulterations of olive oil are performed by adding seed oils to this high-quality product, which are cheaper than olive oils. Food safety controls have been established by the European Union to avoid these episodes. Most of these methodologies require expensive equipment, time-consuming procedures, and expert personnel to execute. Near-infrared spectroscopy (NIRS) technology has many applications in the food processing industry. It analyzes food safety and quality parameters along the food chain. Using principal component analysis (PCA), the differences and similarities between olive oil and seed oils (sesame, sunflower, and flax oil) have been evaluated. To quantify the percentage of adulterated seed oil in olive oils, partial least squares (PLS) have been employed. A total of 96 samples of olive oil adulterated with seed oils were prepared. These samples were used to build a spectra library covering various mixtures containing seed oils and olive oil contents. Eighteen chemometric models were developed by combining the first and second derivatives with Standard Normal Variable (SNV) for scatter correction to classify and quantify seed oil adulteration and percentage. The results obtained for all seed oils show excellent coefficients of determination for calibration higher than 0.80. Because the instrumental aspects are not generally sufficiently addressed in the articles, we include a specific section on some key aspects of developing a high-performance and cost-effective NIR spectroscopy solution for fraud detection in olive oil. First, spectroscopy architectures are introduced, especially the Texas Instruments Digital Light Processing (DLP) technology for spectroscopy that has been used in this work. These results demonstrate that the portable prototype can be used as an effective tool to detect food fraud in liquid samples.

Reduced bone mineral density in adolescents with Duchenne Muscular Dystrophy (DMD) and scoliosis.

Duchenne muscular dystrophy is a progressive disease usually associated with loss of ambulation and progressive scoliosis. Immobilisation and glucocorticoid treatment are predisposing factors for reduced bone mineral density (BMD). Analysis of quantitative computed tomography revealed low BMD in thoracic and lumbar vertebrae in comparison to age- and sex-matched healthy controls. INTRODUCTION: Evaluation of vertebral bone mineral density (BMD) in Duchenne Muscular Dystrophy (DMD) adolescents with untreated advanced scoliosis and comparison with the BMD values of healthy age-matched controls, based on quantitative computer tomography. METHODS: Thirty-seven DMD adolescents (age 15.6 ± 2.5 years) with spinal deformity were evaluated clinically and radiologically prior to definite spinal fusion and compared to 31 male and age-matched healthy individuals (age 15.7 ± 2.3 years). Data related to previous medical treatment, physiotherapy and ambulatory status was also analysed. Scoliotic curves were measured on plain sitting radiographs of the spine. The BMD Z-scores of the thoracic and lumbar vertebrae were calculated with QCTpro® (Mindways Software Inc., USA), based on data sets of preoperative, phantom pre-calibrated spinal computed tomography scans. RESULTS: A statistically significant lower BMD could be found in DMD adolescents, when compared to healthy controls, showing an average value for the lumbar spine of 80.5 ± 30.5 mg/cm3. Z-scores deteriorated from the upper thoracic towards the lower lumbar vertebrae. All but the uppermost thoracic vertebrae had reduced BMD values, with the thoracolumbar and lumbar region demonstrating the lowest BMD. No significant correlation was observed between BMD and the severity of the scoliotic curve, previous glucocorticoid treatment, cardiovascular impairment, vitamin D supplementation, non-invasive ventilation or physiotherapy. CONCLUSION: DMD adolescents with scoliosis have strongly reduced BMD Z-scores, especially in the lumbar spine in comparison to healthy controls. These findings support the implementation of a standardised screening and treatment protocol. Level of evidence/clinical relevance: therapeutic level III.

TRPC3, but not TRPC1, as a good therapeutic target for standalone or complementary treatment of DMD.

BACKGROUND: Duchenne muscular dystrophy (DMD) is an X-linked inherited disease caused by mutations in the gene encoding dystrophin that leads to a severe and ultimately life limiting muscle-wasting condition. Recombinant adeno-associated vector (rAAV)-based gene therapy is promising, but the size of the full-length dystrophin cDNA exceeds the packaging capacity of a rAAV. Alternative or complementary strategies that could treat DMD patients are thus needed. Intracellular calcium overload due to a sarcolemma permeability to calcium (SPCa) increase is an early and critical step of the DMD pathogenesis. We assessed herein whether TRPC1 and TRPC3 calcium channels may be involved in skeletal muscle SPCa alterations and could represent therapeutic targets to treat DMD. METHODS: All experiments were conducted in the DMDmdx rat, an animal model that closely reproduces the human DMD disease. We measured the cytosolic calcium concentration ([Ca2+]c) and SPCa in EDL (Extensor Digitorum Longus) muscle fibers from age-matched WT and DMDmdx rats of 1.5 to 7 months old. TRPC1 and TRPC3 expressions were measured in the EDL muscles at both the mRNA and protein levels, by RT-qPCR, western blot and immunocytofluorescence analysis. RESULTS: As expected from the malignant hyperthermia like episodes observed in several DMDmdx rats, calcium homeostasis alterations were confirmed by measurements of early increases in [Ca2+]c and SPCa in muscle fibers. TRPC3 and TRPC1 protein levels were increased in DMDmdx rats. This was observed as soon as 1.5 months of age for TRPC3 but only at 7 months of age for TRPC1. A slight but reliable shift of the TRPC3 apparent molecular weight was observed in DMDmdx rat muscles. Intracellular localization of both channels was not altered. We thus focused our attention on TRPC3. Application of Pyr10, a specific inhibitor of TRPC3, abolished the differences between SPCa values measured in WT and DMDmdx. Finally, we showed that a rAAV-microdystrophin based treatment induced a high microdystrophin expression but only partial prevention of calcium homeostasis alterations, skeletal muscle force and TRPC3 protein increase. CONCLUSIONS: All together our results show that correcting TRPC3 channel expression and/or activity appear to be a promising approach as a single or as a rAAV-based complementary therapy to treat DMD.

ß-Glucans as Dietary Supplement to Improve Locomotion and Mitochondrial Respiration in a Model of Duchenne Muscular Dystrophy.

Duchenne muscular dystrophy (DMD) is a severe X-linked neuromuscular childhood disorder that causes progressive muscle weakness and degeneration. A lack of dystrophin in DMD leads to inflammatory response, autophagic dysregulation, and oxidative stress in skeletal muscle fibers that play a key role in the progression of the pathology. ß-glucans can modulate immune function by modifying the phagocytic activity of immunocompetent cells, notably macrophages. Mitochondrial function is also involved in an important mechanism of the innate and adaptive immune responses, owing to high need for energy of immune cells. In the present study, the effects of 1,3-1,6 ß-glucans on five-day-old non-dystrophic and dystrophic (sapje) zebrafish larvae were investigated. The effects of the sonication of ß-glucans and the dechorionation of embryos were also evaluated. The results showed that the incidence of dystrophic phenotypes was reduced when dystrophic embryos were exposed to 2 and 4 mg L-1 of 1,3-1,6 ß-glucans. Moreover, when the dystrophic larvae underwent 8 mg L-1 treatment, an improvement of the locomotor performances and mitochondrial respiration were observed. In conclusion, the observed results demonstrated that 1,3-1,6 ß-glucans improve locomotor performances and mitochondrial function in dystrophic zebrafish. Therefore, for ameliorating their life quality, 1,3-1,6 ß-glucans look like a promising diet supplement for DMD patients, even though further investigations are required.

Targeting of CAT and VCAM1 as Novel Therapeutic Targets for DMD Cardiomyopathy.

Duchenne muscular dystrophy (DMD) related cardiomyopathy is the leading cause of early mortality in DMD patients. There is an urgent need to gain a better understanding of the disease molecular pathogenesis and develop effective therapies to prevent the onset of heart failure. In the present study, we used DMD human induced pluripotent stem cells (DMD-hiPSCs) derived cardiomyocytes (CMs) as a platform to explore the active compounds in commonly used Chinese herbal medicine (CHM) herbs. Single CHM herb (DaH, ZK, and CQZ) reduced cell beating rate, decreased cellular ROS accumulation, and improved structure of DMD hiPSC-CMs. Cross-comparison of transcriptomic profiling data and active compound library identified nine active chemicals targeting ROS neutralizing Catalase (CAT) and structural protein vascular cell adhesion molecule 1 (VCAM1). Treatment with Quecetin, Kaempferol, and Vitamin C, targeting CAT, conferred ROS protection and improved contraction; treatment with Hesperidin and Allicin, targeting VCAM1, induced structure enhancement via induction of focal adhesion. Lastly, overexpression of CAT or VCAM1 in DMD hiPSC-CMs reconstituted efficacious effects and conferred increase in cardiomyocyte function. Together, our results provide a new insight in treating DMD cardiomyopathy via targeting of CAT and VCAM1, and serves as an example of translating Bed to Bench back to Bed using a muti-omics approach.

Evaluation of the effect of Dahuang-Mudan decoction on TNBS-induced colitis using UPLC-QTOF/MS-based metabolomic analysis.

Dahuang-Mudan decoction (DMD) is a formula that has been widely used as a complementary treatment for inflammatory bowel disease (IBD). However, the mechanism of action of DMD in IBD has not been clearly elucidated. Therefore, we developed a metabolomics-based method to evaluate the effects and potential mechanisms of DMD in a 2,4,6-trinitobenzene sulfonic acid (TNBS)-induced colitis model. The ultra-high-performance liquid chromatography/quadrupole time-of-flight mass spectrometry (UPLC/QTOF-MS) method combined with multiple analysis approaches including principal component analysis, partial least square discriminant analysis and orthogonal partial least square discriminant analysis were used to investigate the different urinary metabolites. We identified 29 potential biomarkers of TNBS-induced colitis that returned to normal conditions after DMD administration. Pathway analysis indicated that changes in these metabolites were associated with cysteine and methionine metabolism, citric acid cycle, glycolysis and glycolic regeneration, pyruvate metabolism, biosynthesis of valine, leucine and isoleucine, biosynthesis of primary bile acids, glycine, serine and threonine metabolism, caffeine metabolism, arginine and proline metabolism and phenylalanine metabolism. It is worth noting that DMD has potential therapeutic effects on TNBS-induced colitis, which functions by restoring the balance of multiple disturbed pathways to a normal condition. This study suggests the reliability of metabolomics-based approaches to identifying biomarkers and pathways, which facilitate further investigation of the potential mechanisms of DMD.

Clinical effect of Rougan Tongdu combined with point-pressing massage therapy on children at high risk of delayed motor development.

BACKGROUND: Delayed motor development (DMD) is an extremely common development disorder in children. Multiple factors, including mother's influence, diseases, physical or chemical factors and trauma, are strongly associated with DMD. Infancy is a key period in the development of neuromotor function. For children who are at high risk of DMD, early clinical intervention can, to a certain extent, reverse and repair the damaged function of the brain, improving the child's prognosis and their quality of life. This study aimed to evaluate the effect of Rougan Tongdu combined with point-pressing massage therapy (RT-PMT) in children at high risk of DMD. METHODS: Between March 2017 and March 2019, a total of 63 children at high risk of DMD were admitted and treated with RT-PMT in our hospital. These children were divided into three intervention groups (IGs) based on their age in months: IG I (22, 0-3 months), IG II (25, 4-6 months), and IG III (16, 7-12 months). An additional 63 healthy age-matched children were enrolled as a control group (CG) and split into the CG I (0-3 months), CG II (4-6 months), and CG III (7-12 months). All of the children underwent Gesell Infant Development Scale (GESELL) examination both before and three months after intervention and the motor function was scored. RESULTS: After 3 months of RT-PMT, the gross motor function scores in the three IGs were 88.55±8.56, 81.83±7.95, and 78.89±7.52, respectively. Fine motor function scores in the three IGs were 89.12±6.45, 82.32±6.78, and 78.18±6.69, respectively. Total motor function scores in the three IGs were 89.85±7.20, 82.65±7.05, and 79.52±7.16, respectively. The differences between the scores before and after intervention were statistically significant (all P<0.05). The improvements in the gross, fine, and total motor function scores in IG I were better than those in the other two IGs (P<0.05), and the clinical curative effect in IG I, II, and III was 95.5%, 80.0% and 62.6%, respectively. The clinical curative effect in IG I was better than those in the other groups (P<0.05). CONCLUSIONS: RT-PMT is beneficial for children at high risk of DMD.

Nutraceutical and pharmaceutical cocktails did not improve muscle function or reduce histological damage in D2-mdx mice.

Progressive muscle injury and weakness are hallmarks of Duchenne muscular dystrophy. We showed previously that quercetin (Q) partially protected dystrophic limb muscles from disease-related injury. As quercetin activates PGC-1α through Sirtuin-1, an NAD+-dependent deacetylase, the depleted NAD+ in dystrophic skeletal muscle may limit quercetin efficacy; hence, supplementation with the NAD+ donor, nicotinamide riboside (NR), may facilitate quercetin efficacy. Lisinopril (Lis) protects skeletal muscle and improves cardiac function in dystrophin-deficient mice; therefore, it was included in this study to evaluate the effects of lisinopril used with quercetin and NR. Our purpose was to determine the extent to which Q, NR, and Lis decreased dystrophic injury. We hypothesized that Q, NR, or Lis alone would improve muscle function and decrease histological injury and when used in combination would have additive effects. Muscle function of 11-mo-old DBA (healthy), D2-mdx (dystrophin-deficient), and D2-mdx mice was assessed after treatment with Q, NR, and/or Lis for 7 mo. To mimic typical pharmacology of patients with Duchenne muscular dystrophy, a group was treated with prednisolone (Pred) in combination with Q, NR, and Lis. At 11 mo of age, dystrophin deficiency decreased specific tension and tetanic force in the soleus and extensor digitorum longus muscles and was not corrected by any treatment. Dystrophic muscle was more sensitive to contraction-induced injury, which was partially offset in the QNRLisPred group, whereas fatigue was similar between all groups. Treatments did not decrease histological damage. These data suggest that treatment with Q, NR, Lis, and Pred failed to adequately maintain dystrophic limb muscle function or decrease histological damage.NEW & NOTEWORTHY Despite a compelling rationale and previous evidence to the contrary in short-term investigations, quercetin, nicotinamide riboside, or Lisinopril, alone or in combination, failed to restore muscle function or decrease histological injury in dystrophic limb muscle from D2-mdx mice after long-term administration. Importantly, we also found that in the D2-mdx model, an emerging and relatively understudied model of Duchenne muscular dystrophy dystrophin deficiency caused profound muscle dysfunction and histopathology in skeletal muscle.

The Effect of Vitamin D Supplementation on Skeletal Muscle in the mdx Mouse Model of Duchenne Muscular Dystrophy.

Vitamin D (VitD) has shown to be beneficial in reversing muscle weakness and atrophy associated with VitD deficiency. Duchenne muscular dystrophy is characterized by worsening muscle weakness and muscle atrophy, with VitD deficiency commonly observed. This study aimed to investigate the effect of VitD supplementation on dystrophic skeletal muscle. Eight-week old female control (C57BL/10; n = 29) and dystrophic (C57BL/mdx; n = 23) mice were randomly supplemented with one of three VitD enriched diets (1000, 8000 & 20,000 IU/kg chow). Following a four-week feeding period, the extensor digitorum longus (EDL) and soleus muscles contractile and fatigue properties were tested ex vivo, followed by histological analysis. As expected, mdx muscles displayed higher mass yet lower specific forces and a rightward shift in their force frequency relationship consistent with dystrophic pathology. There was a trend for mdx muscle mass to be larger following the 20,000 IU/kg diet, but this did not result in improved force production. Fiber area in the EDL was larger in mdx compared to controls, and there were higher amounts of damage in both muscles, with VitD supplementation having no effect. Four weeks of VitD supplementation did not appear to have any impact upon dystrophic skeletal muscle pathology at this age.

iPSCs as a Platform for Disease Modeling, Drug Screening, and Personalized Therapy in Muscular Dystrophies.

Induced pluripotent stem cells (iPSCs) are the foundation of modern stem cell-based regenerative medicine, especially in the case of degenerative disorders, such as muscular dystrophies (MDs). Since their introduction in 2006, many studies have used iPSCs for disease modeling and identification of involved mechanisms, drug screening, as well as gene correction studies. In the case of muscular dystrophies, these studies commenced in 2008 and continue to address important issues, such as defining the main pathologic mechanisms in different types of MDs, drug screening to improve skeletal/cardiac muscle cell survival and to slow down disease progression, and evaluation of the efficiency of different gene correction approaches, such as exon skipping, Transcription activator-like effector nucleases (TALENs), Zinc finger nucleases (ZFNs) and RNA-guided endonuclease Cas9 (CRISPR/Cas9). In the current short review, we have summarized chronological progress of these studies and their key findings along with a perspective on the future road to successful iPSC-based cell therapy for MDs and the potential hurdles in this field.

Evaluation of the influence of mirabilite on the absorption and pharmacokinetics of the ingredients in Dahuang-mudan decoction by a validated UPLC/QTOF-MS/MS method.

Dahuang-mudan decoction (DMD) has been widely used for disease treatment in China for 1700 years. The formula consists of Rhubarb, moutan bark, Prunus persica, wax gourd kernel and mirabilite, which have been well studied by multidisciplinary approaches. However, the role of the mineral mirabilite in DMD is unclear. The objective of this study was to investigate the effects of mirabilite on the absorption and pharmacokinetics of the ingredients in DMD. The constituents were identified in DMD extract and the plasma of mirabilite-DMD (MDMD, 50 g kg-1 ) treated rats and nonmirabilite-DMD (NMDMD, 50 g kg-1 ) treated rats. The plasma was also used to investigate the effects of mirabilite on the pharmacokinetics of active ingredients in DMD using a new validated UPLC-MS/MS method. The results showed that 63 compounds were identified in the extract of DMD, 27 and 22 of which were found in the plasmas of MDMD- and NMDMD-treated rats, respectively. Furthermore, the results of a pharmacokinetic study suggested that mirabilite influenced the absorption of the five constituents by decreasing the absorption of emodin and rhein while increasing the absorption of aloe-emodin, paeoniflorin and amygdalin; the pharmacokinetic parameters, including the Tmax , Cmax , AUC0-t , MRT0-t , CLz and t1/2 of five constituents, significantly changed in MDMD-treated rats compared with the NMDMD. The method validation for selectivity, precision, accuracy, matrix effect, recovery and stability met the acceptance criteria. These findings uncover the roles of mirabilite in DMD and demonstrate the application of scientific principles to the study of DMD in human health care.

Taurine and Methylprednisolone Administration at Close Proximity to the Onset of Muscle Degeneration Is Ineffective at Attenuating Force Loss in the Hind-Limb of 28 Days Mdx Mice.

An increasing number of studies have shown supplementation with the amino acid taurine to have promise in ameliorating dystrophic symptoms in the mdx mouse model of Duchenne Muscular Dystrophy (DMD). Here we build on this limited body of work by investigating the efficacy of supplementing mdx mice with taurine postnatally at a time suggestive of when dystrophic symptoms would begin to manifest in humans, and when treatments would likely begin. Mdx mice were given either taurine (mdx tau), the steroid alpha methylprednisolone (PDN), or tau + PDN (mdx tau + PDN). Taurine (2.5% wt/vol) enriched drinking water was given from 14 days and PDN (1 mg/kg daily) from 18 days. Wild-type (WT, C57BL10/ScSn) mice were used as a control to mdx mice to represent healthy tissue. In the mdx mouse, peak damage occurs at 28 days, and in situ assessment of contractile characteristics showed that taurine, PDN, and the combined taurine + PDN treatment was ineffective at attenuating the force loss experienced by mdx mice. Given the benefits of taurine as well as methylprednisolone reported previously, when supplemented at close proximity to the onset of severity muscle degeneration these benefits are no longer apparent.

Three-dimensional evaluation of the effect of low-level laser therapy on facial swelling after lower third molar surgery: A randomized, placebo-controlled study.

PURPOSE: This study aimed to evaluate the effect of a low-level laser therapy (LLLT) on pain, trismus, and swelling of patients whose impacted 3rd molar tooth was extracted compared to placebo or "sham" treatment and measure volumetrically the edema with a three-dimensional (3D) surface imaging device (3dMD face system). MATERIALS AND METHODS: Forty-five patients over 17 years of age were included in the study. Patients were randomized to three groups; Group 1, the control group, received only routine management (ice application) (n = 15); Group 2, received single-dose LLLT immediately after surgery (n = 15); and Group 3, placebo group, received sham therapy immediately after surgery (n = 15). In this study, a gallium-aluminum-arsenide diode laser device was used. The laser was applied extraorally (0.3 W, 40 s, 4 J/cm2). The trismus, pain, and facial swelling were evaluated. A 3D surface imaging device (3dMD Photogrammetric System) was used to evaluate the volumetric changes of the swelling. The 3D morphology of the facial swelling was recorded using this imaging device immediately before surgery, the second day after surgery, and the 7th day after surgery. IBM SPSS statistics 22.0 program was used in the statistical assessment and P < 0.05 was considered statistically significant. RESULTS: There was no statistically significant difference in the edema and trismus between the groups. The pain level in Group 2 was significantly lower than that in Group 3 at all-time points. Furthermore, the pain level in Group 2 was significantly lower than that in Group 1 on day 7. CONCLUSIONS: LLLT reduced the intensity of pain following third molar surgery by single dose. The results of this study revealed that LLLT reduced facial swelling, but no significant differences were found among the three groups. In addition, a 3D craniomaxillofacial imaging method provided insight into volume changes after 3rd molar surgery and the evaluation of facial swelling in an objective way.

Mitochondrial content is preserved throughout disease progression in the mdx mouse model of Duchenne muscular dystrophy, regardless of taurine supplementation.

Mitochondrial dysfunction is a pathological feature of Duchenne muscular dystrophy (DMD), a debilitating and fatal neuromuscular disorder characterized by progressive muscle wasting and weakness. Mitochondria are a source of cellular ATP involved in Ca2+ regulation and apoptotic signaling. Ameliorating aberrant mitochondrial function has therapeutic potential for reducing DMD disease severity. The dystrophic mdx mouse exhibits peak muscle damage at 21-28 days, which stabilizes after 8 wk. The amino acid taurine is implicated in mitochondrial health and function, with endogenous concentrations low when measured during the cycle of peak muscle damage in mdx mice. Using whole soleus and extensor digitorum longus (EDL) muscle homogenates from 28- and 70-day mdx mice, we found that there was no change in native state mitochondrial complexes using blue native-PAGE. NADH:ubiquinone oxidotreductase subunit-A9 (NDUFA9) protein abundance was lower in soleus muscle of 28- and 70-day mdx mice and EDL muscle of 70-day mdx mice compared with same muscles in WT (C57/BL10ScSn) animals. There were age-dependent increases in both NDUFA9 protein abundance and citrate synthase activity in soleus muscles of mdx and wild-type mice. There was no change in abundances of mitochondrial dynamics proteins mitofusin 2 (Mfn2) and mitochondrial dynamics protein 49 (MiD49). Taurine administration essentially did not affect any measurements of mitochondria. Collectively, these findings suggest mitochondrial content and dynamics are not reduced in the mdx mouse regardless of disease severity. We also elucidate that taurine affords no significant benefit to mitochondrial content or dynamics in the mdx mouse at either 28 or 70 days.

Supplementation action with ascorbic acid in the morphology of the muscular layer and reactive acetylcholinesterase neurons of ileum of mdx mice.

The Duchenne Muscular Dystrophy (DMD) is a genetic disorder characterized by the absence of dystrophin protein, causing severe myopathy from increases of oxidative stress. Injuries of intestinal muscle can compromise the myenteric plexus. This study aimed to evaluate the disorders occurred in the muscular layer and in the acetylcholinesterase myenteric neurons (ACHE-r) of ileum of mdx mice, and the effects of supplementation with ascorbic acid (AA) in both components. 30 male mice C57BL/10, and 30 male mice C57BL/10Mdx were separated according to the age and treatment (n=10/group): 30-days-old control group (C30); 30-days-old dystrophic group (D30); 60-days-old control group (C60); 60-days-old dystrophic group (D60); 60-days-old control group supplemented with AA (CS60); and 60-days-old dystrophic group supplemented with AA (DS60). The animals were euthanized and the ileum was collected and processed. Semi-serial sections were stained by Masson's trichrome, and acetylcholinesterase histochemical technique in whole-mounts preparations to identify the myenteric neurons. The muscular layer thickness and the area of smooth muscle of ileum were lower in dystrophic groups, especially in D30 group. The DS60 group showed the muscular layer thickness similar to C60. The density of ACHE-r neurons of myenteric plexus of ileum was lower in D30 animals; however, it was similar in animals of 60-days-old without treatment (C60 and D60) and, higher in DS60. The cell body profile area of ACHE-r neurons was similar in C30-D30 and C60-D60; however, it was higher in DS60. DMD caused damage to the ileum's musculature and myenteric plexus, and the AA prevented the ACHE-r neuronal loss.

Evaluation of the effects of the low-level laser therapy on swelling, pain, and trismus after removal of impacted lower third molar.

BACKGROUND: In current study we aimed to examine the effect of a low-level laser therapy on the pain, mouth opening and swelling of patients whose impacted 3rd molar tooth was extracted in addition measurement volumetrically to the edema with 3dMD face system. METHODS: It was surveyed 15 patients who had bilateral symmetric lower 3rd molars. Surgical sides of patients were randomly separated into two groups: the study group and the control group. It was applied extra oral low-level laser therapy (LLLT, 0.3 W, 40 s, 4 J/cm(2)) to the study group (n = 15) after the surgical operation and on the 2nd day. Only routine postoperative recommendation (ice application) was made in the control (n = 15) group. The maximum mouth opening, pain level and facial swelling evaluated. 3dMD Face® (3dMD, Atlanta, GA) Photogrammetric System was used to evaluate volumetric changes of the swelling. RESULTS: There was no statistically significant difference in the edema and interincisal opening between the groups and the pain level in the laser group was significantly lower than in the control group on the 7(th) postoperative day. CONCLUSIONS: Although there were decreasing trismus, swelling, and pain level, with this LLLT, there was significant difference only in the 7th day pain level in the laser group compared with the control group.

Comparative study of inorganic elements determined in whole blood from Dmd(mdx)/J mice strain by EDXRF and NAA analytical techniques.

Several diseases can be diagnosed observing the variation of specific elements concentration in body fluids. In this study the concentration of inorganic elements in blood samples of dystrophic (Dmd(mdx)/J) and C57BL/6J (control group) mice strain were determined. The results obtained from Energy Dispersive X-ray Fluorescence (EDXRF) were compared with Neutron Activation Analysis (NAA) technique. Both analytical techniques showed to be appropriate and complementary offering a new contribution for veterinary medicine as well as detailed knowledge of this pathology.

Near fatal 5-FU gut toxicity post surgery--remarkable effect of high-dose sucralfate.

BACKGROUND: The objective of this review article and case report was to investigate the effectiveness of high-dose sucralfate on severe life-threatening 5-fluorouracil (5-FU) gut toxicity, with reference to, but not limited to dihydropyrimidine dehydrogenase (DPD) deficiency. METHODS: A search was conducted on PubMed from 1950 to July 2013 for original studies on 5-FU gut toxicity and sucralfate. Studies were limited to human trials and English language and all articles included in this study were assessed with the application of predetermined selection criteria. Each article was then reviewed independently by two reviewers. A case report from our own centre was included in this review. RESULTS: From 33 results, 6 manuscripts were identified including 4 randomized controlled trial. One trial evaluated the use of sucralfate to alleviate stomatitis in patients with 5-FU-based chemotherapy. The other three trials evaluated the role of sucralfate in radiation toxicity. There was one case report which showed gastroscopy confirmed normalization of severe dysplastic erosive gastroduodenitis attributed to hepatic arterial infusion of 5-FU following a 2-month course of sucralfate and cimetidine and one case series showing clinical and sigmoidoscopically demonstrated improvement in ulcerative colitis in majority of patients receiving sucralfate enemas. There was no current literature specifically focussed on the role of sucralfate in 5-FU gut toxicity. Our case report describes the clinical course and successful treatment with sucralfate of a patient with Pseudomyxoma peritonei (PMP) who experienced 5-FU gut toxicity resulting in life-threatening bleeding due to presumed DPD deficiency post intraperitoneal 5-FU administration. CONCLUSION: This review article showed a lack of literature concerning the use of sucralfate in 5-FU gut toxicity. In our patient's case, sucralfate had a crucial role in the management of near fatal 5-FU gut toxicity, and further evaluation is required.

Quantitative assessment of the T2 relaxation time of the gluteus muscles in children with Duchenne muscular dystrophy: a comparative study before and after steroid treatment.

OBJECTIVE: To determine the feasibility of using T2 mapping as a quantitative method to longitudinally follow the disease activity in children with Duchenne muscular dystrophy (DMD) who are treated with steroids. MATERIALS AND METHODS: ELEVEN BOYS WITH DMD (AGE RANGE: 5-14 years) underwent evaluation with the clinical functional score (CFS), and conventional pelvic MRI and T2 mapping before and during steroid therapy. The gluteus muscle inflammation and fatty infiltration were evaluated on conventional MRI. The histograms and mean T2 relaxation times were obtained from the T2 maps. The CFS, the conventional MRI findings and the T2 values were compared before and during steroid therapy. RESULTS: None of the patients showed interval change of their CFSs. On conventional MRI, none of the images showed muscle inflammation. During steroid treatment, two boys showed increased fatty infiltration on conventional MRI, and both had an increase of the mean T2 relaxation time (p < 0.05). The remaining nine boys had no increase in fatty infiltration. Of these, three showed an increased mean T2 relaxation time (p < 0.05), two showed no change and four showed a decreased mean T2 relaxation time (p < 0.05). CONCLUSION: T2 mapping is a feasible technique to evaluate the longitudinal muscle changes in those children who receive steroid therapy for DMD. The differences of the mean T2 relaxation time may reflect alterations in disease activity, and even when the conventional MRI and CFS remain stable.

Quantitative Assessment of the T2 Relaxation Time of the Gluteus Muscles in Children with Duchenne Muscular Dystrophy: a Comparative Study Before and After Steroid Treatment

OBJECTIVE: To determine the feasibility of using T2 mapping as a quantitative method to longitudinally follow the disease activity in children with Duchenne muscular dystrophy (DMD) who are treated with steroids. MATERIALS AND METHODS: Eleven boys with DMD (age range: 5-14 years) underwent evaluation with the clinical functional score (CFS), and conventional pelvic MRI and T2 mapping before and during steroid therapy. The gluteus muscle inflammation and fatty infiltration were evaluated on conventional MRI. The histograms and mean T2 relaxation times were obtained from the T2 maps. The CFS, the conventional MRI findings and the T2 values were compared before and during steroid therapy. RESULTS: None of the patients showed interval change of their CFSs. On conventional MRI, none of the images showed muscle inflammation. During steroid treatment, two boys showed increased fatty infiltration on conventional MRI, and both had an increase of the mean T2 relaxation time (p < 0.05). The remaining nine boys had no increase in fatty infiltration. Of these, three showed an increased mean T2 relaxation time (p < 0.05), two showed no change and four showed a decreased mean T2 relaxation time (p < 0.05). CONCLUSION: T2 mapping is a feasible technique to evaluate the longitudinal muscle changes in those children who receive steroid therapy for DMD. The differences of the mean T2 relaxation time may reflect alterations in disease activity, and even when the conventional MRI and CFS remain stable.