Articulatory Kinematic Characteristics during Speech Production for Individuals with Dysarthria: A Study Based on Electromagnetic Articulography / 中国康复理论与实践

@#Objective:To explore the kinematics characteristics of articulators (including lips, tongue and jaw) during articulation in dysarthric individuals post brain injury by using electromagnetic articulography (electromagnetic articulography, EMA). Methods:From October, 2017 to October, 2018, six eligible individuals with dysarthria were recruited as dysarthria group, and ten age-gender matched healthy adults were recruited as healthy control group. Both groups received EMA assessment, and the dysarthria group was assessed with Chinese modified version of Frenchay Dysarthria Assessment before EMA assessment. To track and record kinematic parameters data (including duration, velocity, acceleration, distance) and displacement movement trajectories, a series of sensors were attached on the participant's lips, tongue (tip, blade and back of tongue) and jaw, the reference sensor was attached on the bridge of nose, all of the sensors were along midsagittal plane. During EMA assessment, each participant was received syllable repetition task, which containing consonants (/d/, /t/, /j/, /q/, /g/, /k/, /b/, /p/) at word initial position and vowels (/a/, /ia/, /iu/), to produce the single word with the Chinese linguistic meaning, every syllable produced was repeated three times. Then Praat software and Matlab software were used to process acoustic and kinematic data, so as to compare the differences of articulatory kinematic performance between two groups. Results:The outcome of the Frenchay Dysarthria Assessment indicated that the severity of dysarthria was from moderate to extreme severe. EMA assessment demonstrated that, compared with the healthy control group, the dysarthria group showed a reduction of velocity, acceleration and distance of tongue and lip movement (<italic>t</italic> > 2.422, <italic>P</italic> < 0.05), and longer duration of tongue tip, tongue back and jaw movement (<italic>t</italic> > 3.369, <italic>P</italic> < 0.05). There was no statistical difference in duration of tongue blade and lip movement (<italic>t</italic> < 2.146, <italic>P</italic> > 0.05), the same as the velocity, acceleration and distance of jaw movement between two groups (<italic>t</italic> < 1.016, <italic>P</italic> > 0.05). Image analysis of kinematics parameters and synchronous audio data showed that, compared with the healthy control group, the dysarthria group varied unstably in velocity and acceleration, and the audio data showed that, when repeated /da/ three times, the duration of each syllable was not equal. The coordination of articulation movement displacement in the anterior-posterior dimension and inferior-superior dimension was poor, there were significant differences in visual inspection of movement trajectories between two groups, and a smaller displacement was found in the anterior-posterior dimension in the dysarthric group. Conclusion:EMA assessment has significant advantages in evaluating kinematics parameters quantitatively, which could reveal the kinematics characteristics of articulators.

Overexpression of ALK5 Induces Human Tenon's Capsule Fibroblasts Transdifferentiation and Fibrosis In Vitro.

PURPOSE: To investigate the involvement of activin receptor-like kinase 5 (ALK5) in human Tenon's capsule fibroblasts (HTFs) transdifferentiation and fibrosis. METHODS: (1) Cultured HTFs were treated with transforming growth factor beta 1 (TGF-ß1) at different concentrations for different durations, mRNA expression of ALK5 and plasminogen activator inhibitor-1 (PAI-1) was measured by quantitative polymerase chain reaction (PCR) while protein expression of ALK5, α-smooth muscle actin (α-SMA), and extracellular matrix deposition including fibronectin (FN) and collagen I (Col1) was assessed by western blot. HTFs with or without TGF-ß1 were also treated with an ALK5 activity inhibitor, SB-431542, and fibrosis-related genes were assessed. (2) HTFs were transduced with ALK5 lentivirus (ALK5-OE group) or empty lentivirus (NC-OE) with or without the treatment of SB-431542. Protein expression of ALK5, α-SMA, FN, and Col1 was evaluated. (3) HTFs in the ALK5-OE group and NC-OE group were subjected to a scratch-wound assay and their migratory activities assessed. RESULTS: (1) TGF-ß1, in a concentration-dependent manner, upregulated ALK5 and PAI-1 expressions in the HTFs, which peaked between 24 and 36 h. These changes were associated with increases in protein levels of FN, Col1, and α-SMA. These TGF-ß1 effects were blocked by the ALK5 inhibitor SB-431542. (2) Similarly, overexpression of ALK5 by lentiviral vector significantly increased protein expression of α-SMA, FN, and Col1. Addition of TGF-ß1 to the ALK5-OE cells did not produce additional expression of any of the marker proteins. The upregulation of extracellular matrix and α-SMA can be reduced by SB-431542. (3) In ALK5-OE group, HTFs migration was significantly increased compared with normal control and TGF-ß1 could still promote ALK5-OE cells migration. CONCLUSIONS: Our findings suggest that ALK5 is an important mediator of HTFs fibrosis. ALK5 is a potential therapeutic target to suppress scar formation after filtration surgery.

Ratcheting strain and theoretical prediction of articular cartilage under cyclic loading / 医用生物力学

Objective To obtain the ratcheting strain of articular cartilage under different loading conditions,and construct the theoretical model so as to predict the ratcheting strain of cartilage.Methods The fresh articular cartilage obtained from the trochlear of distal femur was used as experimental subject.The ratcheting strain of articular cartilage was tested under cyclic compressive loads by applying the non-contact digital image correlation technique.The theoretical model was constructed to predict the ratcheting strain of articular cartilage with different stress amplitudes and stress rates.The results from predictions were compared with the experimental results.Results The ratcheting strain of cartilage increased rapidly at initial stage and then showed the slower increase with cycles increasing.The ratcheting strain increased with stress amplitude increasing when the stress rate was constant.However,the ratcheting strain decreased with stress rate increasing when the stress amplitude was constant.When the stress rate increased,the ratcheting stain decreased.The prediction results of the established theoretical model were in good agreement with experimental results.Conclusions The ratcheting strain of articular cartilage is proportional to the stress amplitude,and inversely proportional to the stress rate.The established theoretical model can predict the ratcheting strain of articular cartilage and provide guidance for the construction of tissue engineered artificial cartilage.

Ratcheting strain and theoretical prediction of articular cartilage under cyclic loading / 医用生物力学

Objective To obtain the ratcheting strain of articular cartilage under different loading conditions,and construct the theoretical model so as to predict the ratcheting strain of cartilage.Methods The fresh articular cartilage obtained from the trochlear of distal femur was used as experimental subject.The ratcheting strain of articular cartilage was tested under cyclic compressive loads by applying the non-contact digital image correlation technique.The theoretical model was constructed to predict the ratcheting strain of articular cartilage with different stress amplitudes and stress rates.The results from predictions were compared with the experimental results.Results The ratcheting strain of cartilage increased rapidly at initial stage and then showed the slower increase with cycles increasing.The ratcheting strain increased with stress amplitude increasing when the stress rate was constant.However,the ratcheting strain decreased with stress rate increasing when the stress amplitude was constant.When the stress rate increased,the ratcheting stain decreased.The prediction results of the established theoretical model were in good agreement with experimental results.Conclusions The ratcheting strain of articular cartilage is proportional to the stress amplitude,and inversely proportional to the stress rate.The established theoretical model can predict the ratcheting strain of articular cartilage and provide guidance for the construction of tissue engineered artificial cartilage.

Ratcheting strain and theoretical prediction of articular cartilage under cyclic loading / 医用生物力学

Objective To obtain the ratcheting strain of articular cartilage under different loading conditions, and construct the theoretical model so as to predict the ratcheting strain of cartilage. Methods The fresh articular cartilage obtained from the trochlear of distal femur was used as experimental subject. The ratcheting strain of articular cartilage was tested under cyclic compressive loads by applying the non-contact digital image correlation technique. The theoretical model was constructed to predict the ratcheting strain of articular cartilage with different stress amplitudes and stress rates. The results from predictions were compared with the experimental results. Results The ratcheting strain of cartilage increased rapidly at initial stage and then showed the slower increase with cycles increasing. The ratcheting strain increased with stress amplitude increasing when the stress rate was constant. However, the ratcheting strain decreased with stress rate increasing when the stress amplitude was constant. When the stress rate increased, the ratcheting stain decreased. The prediction results of the established theoretical model were in good agreement with experimental results. Conclusions The ratcheting strain of articular cartilage is proportional to the stress amplitude, and inversely proportional to the stress rate. The established theoretical model can predict the ratcheting strain of articular cartilage and provide guidance for the construction of tissue engineered artificial cartilage.

Functional characteristics of connective tissue growth factor on human tenon's capsule fibroblast.

PURPOSE OF THE STUDY: To explore the characteristic of connective tissue growth factor (CTGF) on the phenotype transition, extracellular matrix (ECM) synthesis and proliferation of human Tenon's capsule fibroblasts (HTFs). MATERIALS AND METHODS: HTFs were obtained from patients during cataract surgery and induced by CTGF (1 to 100 µg/L). Western blot and immunofluorescence were performed to observe the expression of alpha smooth muscle actin (α-SM-actin) protein. The levels of mRNAs were quantified by real-time PCR. Col I and FN expression at both protein and RNA levels were tested after induction by CTGF and transforming growth factor ß (TGF-ß), respectively. Statistical significance was assumed if p < 0.05. RESULTS: CTGF upregulated the expression of α-SM-actin in cultured HTFs. Its maximum effect at protein level attained under the optimal concentration of 50 µg/L at the peak time of 48 hours, though still weaker than the effect of TGF-ß1 (10 µg/L, p < 0.05). The expression of Col I and FN at both protein and mRNA levels was elevated by the induction of CTGF (50 µg/L) (p < 0.01) and TGF-ß1 (10 µg/L) (p < 0.05), while CTGF (50 µg/L) showed a greater effect than the latter (p < 0.05). CTGF (1 to100 µg/L) increased the proliferation of HTFs significantly (p < 0.05). CONCLUSIONS: CTGF induced the phenotype transition of HTFs individually and significantly promoted their proliferation. Moreover, it promoted ECM synthesis, thus demonstrating its role as a crucial factor in fibrosis. Thus, CTGF could potentially be a safer and more efficient target than TGF-ß at suppressing scar formation after filtering surgery.

Protective effect of pioglitazone on retinal ischemia/reperfusion injury in rats.

PURPOSE: To investigate the protective effect of pioglitazone on the rat retina after ischemia/reperfusion (I/R) injury and to explore its possible mechanisms. METHODS: Retinal ischemia was induced by increasing the intraocular pressure to 110 mm Hg for 60 minutes, and pioglitazone was delivered 3 hours before the I/R. Retinal damage was quantified by measuring the thickness of the retina, the functional changes of visual evoked potential (VEP) and electroretinography (ERG), and the number of retinal ganglion cells (RGCs) at 7 days after I/R injury. Real-time PCR and Western blot analysis were performed to measure the glial fibrillary acidic protein (GFAP) expression. Retinal cell apoptosis was detected by TUNEL assay at 24 hours after reperfusion. Nuclear factor-κB (NF-κB), Bax, and Bcl-2 in the retina were determined by Western blot analysis. RESULTS: The I/R produced a degenerative effect primarily in the ganglion cell layer, inner plexiform layer, and inner nuclear layer. Pioglitazone maintained the retinal thickness, promoted the survival of RGCs, and attenuated the destruction of ERG and VEP caused by I/R. Pioglitazone pretreatment also suppressed NF-κB activation and altered GFAP overexpression. The number of TUNEL-labeled cells significantly decreased in the retinas pretreated with pioglitazone, and the Bax-Bcl-2 ratio was much lower in the retinas pretreated with pioglitazone than in the I/R group. CONCLUSIONS: Pioglitazone could inhibit activation of the glia cells, prevent cell apoptosis, and protect the retina from subsequent cellular damage caused by the retinal I/R. The possible mechanism might involve the NF-κB pathway.

SB-431542 inhibition of scar formation after filtration surgery and its potential mechanism.

PURPOSE: To explore the inhibitive effect of SB-431542 (an ALK5 inhibitor) on scar formation after glaucoma surgery and to identify the potential pharmacologic target(s). METHODS: Twenty-four New Zealand rabbits underwent filtration surgery on the right eye and were divided into a control group and three experimental groups (n=6). Human Tenon's fibroblast monolayer was scraped to generate a single gap, and then the control medium with SB-431542 only or containing 10 microg/L TGF-beta1 and SB-431542 (1-20 microM) was added. The cells were pretreated with SB-431542 or in control medium for 30 minutes before induction with 10 microg/L TGF-beta1 or 1 microg/L TGF-beta2. The expression of alpha-SM-actin, CTGF, and Col I, as well as changes in the Smad, ERK, P38, and AKT signaling pathways were detected. RESULTS: In comparison with the control rabbits, the IOPs in the experimental groups remained at lower levels until day 25 (P<0.05) after the surgery. Histologic profiles showed that there was only a mild deposition of collagen in the subconjunctival space in the experimental groups. The cell growth and migration were inhibited effectively by SB-431542, regardless of whether TGF-beta was present in the culture system. SB-431542 abrogated TGF-beta-induced upregulation of alpha-SM-actin, CTGF, and Col I. It effectively inhibited the phosphorylation of Smad2 stimulated by TGF-beta but not that of the components of the MAPK pathways. CONCLUSIONS: SB-431542 inhibits scar formation after glaucoma filtration surgery. The mechanism may be that SB-431542 interferes in the phosphorylation of Smad2, thus abrogating TGF-beta-induced fibroblast transdifferentiation and then decreasing Col I synthesis.

[Clinical and pathological analysis of 2734 cases of eyelid neoplasms].

OBJECTIVE: To study the histopathological classification and changes of eyelid neoplasms. METHOD: In this retrospective case series, the pathological specimens of 2734 cases with eyelid neoplasms examined between 1993-2005 were claimed and analyzed. RESULTS: There were 1248 eyelid tumors (45.65%) in 2734 cases with eyelid neoplasms, including 875 benign neoplasms (71.11%) and 960 malignant cases (29.89%). The three leading malignant eyelid tumors were basal cell carcinoma, meibomian gland carcinoma and squamous cell carcinoma The mean ages of the occurrence of these three tumors were 64.16, 63.30 and 60.38 years old, respectively. CONCLUSION: Pathologic classification of eyelid neoplasms is helpful for the pathological diagnosis and provides information for the diagnosis and treatment of these diseases.