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Biomedical subjects

W Wang

Publications and source records attributed to W Wang.

At least 55 records · Page 3Linked to original sources

Microencapsulated nerve growth factor-expressing NIH3T3 cells-incorporated tissue engineering skin: a preliminary study.

INTRODUCTION: In order to find a suitable carrier to deliver the product of gene transfection to improve the performance of bioengineered dermis, we used microencapsulation and gene transfection technology together for the first time and found that it was feasible. METHODS: We used a recombinant nerve growth factor (pcDNA3.1+/NGF) to modify NIH3T3 cells genetically. Control of NIH3T3-NGF cells were encapsulated within microspheres composed of alginate-poly-L-lysine-alginate and cultivated in-vitro. The concentration of NGF released from the microencapsulated NIH3T3-NGF cells was confirmed using ELISA assay. We co-cultivated microencapsulated NIH3T3-NGF cells, NIH3T3 cells (control) with human keratinocytes and fibroblasts, and tested the percentage of cycle of these cells. The alkaline hydrolysis method was used to analyse the content of hydroxyproline (Hyp). Immunohistochemistry method was used to calculate the transformation efficiency from fibroblasts to myofibroblasts. RESULTS: The concentration of NGF released from the microencapsulated NIH3T3-NGF cells lasted about six weeks in the supernatant of bioengineered dermis in-vitro. The proliferation of keratinocytes, as well as the concentration of Hyp in supernatant of fibroblasts, were promoted about three times. Transformation efficiency from fibroblasts to myofibroblasts was increased approximately two-fold because of the bio-effects of NGF. Two kinds of microencapsulations were seeded into collagen which contained human fibroblasts to form bioengineered skin. Microencapsulated NIH3T3-NGF cells formed a thicker dermis. The concentration of Hyp in the bioengineered skin which indicated the level of collagen synthesis was increased due to existing NGF. CONCLUSION: Microencapsulated NIH3T3-NGF cells can be used to enhance performance of bioengineered dermis and it also can be deduced that other cytokines can be used to treat local wound areas.

Alginates↗

Direct transmission of the 18q- syndrome from mother to daughter.

A 34-year-old mother presented moderate mental retardation, short stature, microcephaly, and characteristic facial dysmorphism. Her 12-year-old daughter manifested moderate mental retardation, short stature, microcephaly, dysplastic external ear canals, hearing impairment, and characteristic facial dysmorphism. Cytogenetic analysis of the family revealed a normal karyotype, 46,XY, in the father, and a 46,XX,del(18)(q22.2) karyotype in both mother and daughter. Molecular marker analysis determined direct transmission of the distal 18q deletion from mother to daughter. The present case provides evidence of fertility of the affected females and a mother-to-daughter direct transmission in the familial 18q- syndrome. Identification of affected females with the 18q- syndrome should include genetic counseling of possible direct transmission and consideration of birth control or prenatal genetic testing at reproductive age.

Abnormalities, Multiple↗

Partial trisomy 1p (1p36.22-->pter) and partial monosomy 9p (9p22.2-->pter) associated with achalasia, flexion deformity of the fingers and epilepsy in a girl.

We report on a 12-year-old girl presenting with mental retardation, trigonocephaly, midface hypoplasia, upward-slanting palpebral fissures, arched eyebrows, bilateral epicanthal folds, hypertelorism, a flattened nasal bridge, a short nose, anteverted nares, a long philtrum, a small mouth, micrognathia, low-set ears, a short neck, long digits, flexion deformity of the fingers of the hands, hypoplasia of the labia majora, hyperplasia of the labia minora, flat feet, dysphagia, frequent regurgitation, prominent esophageal dilation, and achalasia. Seizures were noted since 5 years of age. Cytogenetic analysis of her peripheral blood revealed a karyotype of 46,XX, der(9)t(1;9)(p36.22;p22.2)pat. Achalasia, an uncommon esophageal motor disorder, has not been previously described in association with either a deletion of 9p or a duplication of 1p.

Child↗

NMDA receptors mediate calcium accumulation in myelin during chemical ischaemia.

Central nervous system myelin is a specialized structure produced by oligodendrocytes that ensheaths axons, allowing rapid and efficient saltatory conduction of action potentials. Many disorders promote damage to and eventual loss of the myelin sheath, which often results in significant neurological morbidity. However, little is known about the fundamental mechanisms that initiate myelin damage, with the assumption being that its fate follows that of the parent oligodendrocyte. Here we show that NMDA (N-methyl-d-aspartate) glutamate receptors mediate Ca2+ accumulation in central myelin in response to chemical ischaemia in vitro. Using two-photon microscopy, we imaged fluorescence of the Ca2+ indicator X-rhod-1 loaded into oligodendrocytes and the cytoplasmic compartment of the myelin sheath in adult rat optic nerves. The AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid)/kainate receptor antagonist NBQX completely blocked the ischaemic Ca2+ increase in oligodendroglial cell bodies, but only modestly reduced the Ca2+ increase in myelin. In contrast, the Ca2+ increase in myelin was abolished by broad-spectrum NMDA receptor antagonists (MK-801, 7-chlorokynurenic acid, d-AP5), but not by more selective blockers of NR2A and NR2B subunit-containing receptors (NVP-AAM077 and ifenprodil). In vitro ischaemia causes ultrastructural damage to both axon cylinders and myelin. NMDA receptor antagonism greatly reduced the damage to myelin. NR1, NR2 and NR3 subunits were detected in myelin by immunohistochemistry and immunoprecipitation, indicating that all necessary subunits are present for the formation of functional NMDA receptors. Our data show that the mature myelin sheath can respond independently to injurious stimuli. Given that axons are known to release glutamate, our finding that the Ca2+ increase was mediated in large part by activation of myelinic NMDA receptors suggests a new mechanism of axo-myelinic signalling. Such a mechanism may represent a potentially important therapeutic target in disorders in which demyelination is a prominent feature, such as multiple sclerosis, neurotrauma, infections (for example, HIV encephalomyelopathy) and aspects of ischaemic brain injury.

Animals↗

Antibacterial and mechanical properties of bone cement impregnated with chitosan nanoparticles.

Although total joint replacement has become commonplace in recent years, bacterial infection remains a significant complication following this procedure. One approach to reduce the incidence of joint replacement infection is to add antimicrobial agents to the bone cement used to fix the implant. In this in vitro study, we investigated the use of chitosan nanoparticles (CS NP) and quaternary ammonium chitosan derivative nanoparticles (QCS NP) as bactericidal agents in poly(methyl methacrylate) (PMMA) bone cement with and without gentamicin. The antibacterial activity was tested against Staphylococcus aureus (S. aureus) and Staphylococcus epidermidis (S. epidermidis). A 10(3)-fold reduction in the number of viable bacterial cells upon contact with the surface was achievable using QCS NP at a nanoparticle/bone cement weight ratio of 15%. The inhibition of S. aureus and S. epidermidis growth on the surface of the CS NP and QCS NP-loaded bone cements was clearly shown using the LIVE/DEAD Baclight bacterial viability kits and fluorescence microscopy. The CS NP and QCS NP also provided a significant additional bactericidal effect to gentamicin-loaded bone cement. The antibacterial effectiveness remained high even after the modified bone cements had been immersed for 3 weeks in an aqueous medium. No cytotoxic effect of the CS NP- and QCS NP-loaded cements was shown in a mouse fibroblast MTT cytotoxicity assay. Mechanical tests indicated that the addition of the CS and QCS in nanoparticulate form allowed the retention of a significant degree of the bone cement's strength. These results indicate a new promising strategy for combating joint implant infection.

3T3 Cells↗

Initial evaluation of the early aberration reporting system--Florida.

INTRODUCTION: In recent years, many syndromic surveillance systems have been deployed around the United States for the early detection of biologic terrorism-related and naturally occurring outbreaks. These systems and the associated aberration detection methods need to be evaluated. OBJECTIVE: This study evaluated several detection methods of the Early Aberration Reporting System (EARS) under serially correlated syndromic data and to demonstrated the need for calibrating these methods. METHODS: In an initial evaluation of the Syndromic Tracking and Reporting System in Hillsborough County, Florida, serially correlated syndromic data were simulated using statistical models in conjunction with real syndromic data. The detection methods were tested against two patterns of simulated outbreaks. They were compared using a conditional average run length and a receiver operating characteristic curve under defined patterns of detection. RESULTS: Increasing serial correlation inflates the false alarm rate and elevates sensitivity. Among the detection methods in EARS, C2 and P-chart have the best overall receiver operating characteristic curve within the context of the simulations. C2 is least affected by the serial correlation, the outbreak type, and the defined patterns of detection signal. CONCLUSION: Evaluation of the detection methods needs to be adaptable to the constantly changing nature of syndromic surveillance. Deployment of EARS and other methods requires adjusting the false alarm rate and sensitivity in accordance with the syndromic data, the operating resources, and the objectives of the local system. For timely detection, C2 is superior to other methods, including C3, under the simulation conditions. P-chart is the most sensitive when the serial correlation is negligible.

Algorithms↗

A simulation model of the surface EMG signal for analysis of muscle activity during the gait cycle.

This work describes a model able to synthetize the surface EMG (electromyography) signal acquired from tibialis anterior and gastrocnemious medialis muscles during walking of asymptomatic adult subjects. The model assumes a muscle structure where the volume conductor is represented by multiple layers of anisotropic media. This model originates from analysis of the single fiber action potential characterized by the conduction velocity. The surface EMG of voluntary contraction is calculated by gathering motor unit action potentials estimated by the summation of all activities of muscle fibers assumed to have a uniformly parallel distribution. The parameters related to the gait cycle, such as onset and cessation timings of muscle activation, amplitude of muscle contraction, periods and sequences of motor units' recruitment, are included in the model presented. In addition, the relative positions of the electrodes during gait can also be specified in order to adapt the simulation to the different acquisition settings.

Computer Simulation↗

Why are many mRNAs translated to the vicinity of mitochondria: a role in protein complex assembly?

The longstanding question of the presence of mitochondria-bound polysomes has been recently revisited using new approaches. Genome-wide analyses provided evidence that many genes are actually translated on mitochondria-bound polysomes and GFP-labeling techniques have shown that, in vivo, the 3'UTR sequence of these genes contains signals which can target hybrid RNA molecules to the proximity of mitochondria. Evolutionary conservation of some of these signals will be presented. Interestingly, class I mRNA which are translated on free polysomes and class II mRNA which are translated on mitochondria-bound polysomes have, mostly, eukaryotic and prokaryotic origins respectively. Using ATP2, a typical prokaryotic-derived gene, as a model for class II mRNA, we showed that its 3'UTR sequence is essential both for a correct addressing of mRNA to mitochondria proximity and to a proper production of functional ATP synthases. These different observations suggest that prokaryotic-derived genes are, like the contemporary mitochondrial genes, translated near mitochondrial membranes. In both cases this locus specific translation process might be connected to a correct complex assembly program and the cases of ATP synthase and cytochrome c oxidase complexes will be considered in this respect.

3' Untranslated Regions↗

Homing in on the specific phenotype(s) of central respiratory chemoreceptors.

To some it may seem that we now know less about respiratory chemoreception than we did 20 years ago. Back then, it was widely accepted that the central respiratory chemoreceptors (CRCs) were located exclusively on or near the surface of the ventrolateral medulla (VLMS). Now, instead, it is generally believed that there are widespread sites of chemoreception, and there is little agreement on when and how each of these sites is involved in respiratory control. However, those in the field know that this actually is progress, primarily because we have gone from simply identifying candidate regions, to identifying specific neuronal subtypes that may be the sensors. In this invited review, we have been asked to discuss some of the current controversies in the field. First, we define the minimal requirements for a cell to be a CRC, and what assumptions can not be made without more data. Then we review the evidence that two neuronal subtypes, serotonergic neurones of the midline raphe and glutamatergic neurones of the retrotrapezoid nucleus, are chemoreceptors. There is evidence supporting a role in respiratory chemoreception for both types of neurone, as well as the other candidates, but there is also information that is missing. Future work will need to focus on which of the candidates are indeed chemoreceptors, what percentage of the overall response each one contributes, and how this percentage varies under different conditions.

Animals↗

The role of preoperative pulmonary function tests in the surgical treatment of scoliosis.

STUDY DESIGN: A retrospective study on the correlation between preoperative pulmonary function tests, preoperative pulmonary symptoms, and postoperative pulmonary complications. OBJECTIVE: To evaluate the incidence of immediate postoperative pulmonary complications and their correlation to pulmonary function tests, preoperative pulmonary symptoms, and surgical approaches. SUMMARY OF BACKGROUND DATA: The pulmonary function of patients with scoliosis is likely to be abnormal, whereas surgical procedures may lead to further deterioration and postoperative pulmonary complications. Evaluation of the pulmonary symptoms and pulmonary function before surgery is helpful to predict and avoid postoperative pulmonary complications by selecting the appropriate surgical approach. METHODS: This study reviewed 298 scoliosis patients (107 male, 191 female) who underwent anterior and/or posterior operation. The mean age of the patients was 16.4 years (range 6-62 years). The average coronal Cobb angle was 73.26 degrees (range 45-141 degrees). Preoperative pulmonary function tests of 115 cases were normal, whereas the other 183 cases were abnormal. Seventeen cases had preoperative pulmonary symptoms and 3 of them had normal preoperative pulmonary function tests. Seventy-nine cases received transthoracic surgery, and 19 cases had postoperative pulmonary complications, including postoperative ventilation support in 6 cases, atelectasis in 4 cases, hydrothorax in 2 cases, pneumothorax in 3 cases, pneumonia in 3 cases, and hypoxemia in 1 case. Of these 19 patients, 12 patients received anterior transthoracic procedure. When the patients with abnormal pulmonary function tests were divided into 3 groups: 1) 60% < or = forced vital capacity ratio < 80%; 2) 40% < or = forced vital capacity ratio < 60%; and 3) forced vital capacity ratio < 40%, the incidence of postoperative pulmonary complications were 2.72% (3 out of 110), 7.40% (4 out of 54) and 31.60% (6 out of 19), respectively. RESULTS: There was significant correlation between abnormal preoperative pulmonary function tests and preoperative pulmonary symptoms (P = 0.0086). No significant correlation was found between preoperative pulmonary symptoms and postoperative pulmonary complications (P = 0.5164). There was a trend that the postoperative complications increased with the deterioration of pulmonary function. The correlation between postoperative pulmonary complications and the surgical approach was statistically significant (P = 0.0000); the incidence of postoperative pulmonary complication of transthoracic procedure was 18 times as that of posterior approach. No significant difference was noted regarding ages, preoperative coronal Cobb angles, and preoperative pulmonary function between these 2 groups. There was no significant correlation between preoperative pulmonary symptoms and postoperative complications. CONCLUSIONS: The incidence of postoperative pulmonary complications increased with the deterioration of pulmonary function tests. The posterior procedure had a very low incidence of postoperative pulmonary complications, but a transthoracic procedure increased the complications significantly. Preoperative pulmonary symptoms usually predicted abnormal results of pulmonary function tests but had no correlation with postoperative pulmonary complication.

Adolescent↗

Removal of eye blinking artifact from the electro-encephalogram, incorporating a new constrained blind source separation algorithm.

A robust constrained blind source separation (CBSS) algorithm has been developed as an effective means to remove ocular artifacts (OAs) from electro-encephalograms (EEGs). Currently, clinicians reject a data segment if the patient blinked or spoke during the observation interval. The rejected data segment could contain important information masked by the artifact. In the CBSS technique, a reference signal was exploited as a constraint. The constrained problem was then converted to an unconstrained problem by means of non-linear penalty functions weighted by the penalty terms. This led to the modification of the overall cost function, which was then minimised with the natural gradient algorithm. The effectiveness of the algorithm was also examined for the removal of other interfering signals such as electrocardiograms. The CBSS algorithm was tested with ten sets of data containing OAs. The proposed algorithm yielded, on average, a 19% performance improvement over Parra's BSS algorithm for removing OAs.

Algorithms↗

Neuroimaging studies of brain corpus striatum changes among heroin-dependent patients treated with herbal medicine, U'finer capsule.

Chronic exposure to heroin is associated with structural changes in dopaminergic (DA) neurones. The present study examined the effects of a new herbal medicine, U'finer capsule, on the brain corpus striatum and DA systems, comparing pre- and post- treatment in 36 heroin-dependent patients. Neuroimaging studies were performed by using single photon emission computed tomography (SPECT) with 99mTc-TRODAT-1 as radiotracer. The results show that U'finer significantly repaired the damaged bilateral corpus striatum, restoring it to a 'panda eye' shape, analogous in size and shape to that of the healthy volunteers. DA transporter (DAT) function in the bilateral corpus striatum was restored to a normal state after recovery from neurotoxic insult. These findings suggest that U'finer is a reliable herbal medicine in the treatment of heroin dependency.

Adult↗

Pulmonary hypertensive responses of broilers to bacterial lipopolysaccharide (LPS): evaluation of LPS source and dose, and impact of pre-existing pulmonary hypertension and cellulose micro-particle selection.

Previous studies demonstrated that bacterial lipopolysaccharide (LPS, endotoxin) triggers pulmonary vasoconstriction leading to pulmonary hypertension (PHS, ascites) in broilers. The lungs of broilers are constantly challenged with LPS that can trigger pulmonary vasoconstriction. Among broilers from a single genetic line, some individuals respond to LPS with large increases in pulmonary arterial pressure (PAP), whereas others fail to exhibit any response to the same supramaximal dose of LPS. In the present study we evaluated the impact of a variety of factors on the magnitude of the PAP response of male broilers to LPS, including: (1) the role of the initial PAP (low vs. high initial PAP); (2) the source of the LPS (Salmonella typhimurium vs. Escherichia coli); (3) the dose of LPS (0.02, 0.1, and 0.5 mg/kg of BW); and (4) the role of micro-particle selection for improved pulmonary vascular capacity (cellulose survivors vs. saline-injected controls). Broilers in the low initial PAP group (21 +/- 0.34 mmHg, mean +/- SEM) did not differ in their pulmonary hypertensive response to LPS compared with broilers in the high initial PAP group (29 +/- 0.55 mmHg, mean +/- SEM). Lipopolysaccharide from S. typhimurium elicited pulmonary hypertensive responses qualitatively similar to those elicited by E. coli LPS. A detailed evaluation revealed that an LPS dose of 0.1 mg/kg of BW elicits a maximal pulmonary hypertensive response in male broilers, and broilers selected by micro-particle injection for a robust pulmonary vascular capacity did not differ in their pulmonary hypertensive response to LPS compared with unselected broilers. This research confirms that the variable pulmonary hypertensive responses among broilers cannot be attributed to the source or dosage of LPS, or to differences in the baseline pulmonary arterial pressure or micro-particle selection before injecting LPS. These findings are consistent with the hypothesis that innate rather than acquired variability may influence the profile of chemical mediators released during the inflammatory cascade.

Animals↗

Mannan-binding lectin recognizes structures on ischaemic reperfused mouse kidneys and is implicated in tissue injury.

Organ damage as a consequence of ischaemia and reperfusion (I/R) is a major clinical problem in an acute renal failure and transplantation. Ligands on surfaces of endothelial cells that are exposed due to the ischaemia may be recognized by pattern recognition molecules such as mannan-binding lectin (MBL), inducing complement activation. We examined the contribution of the MBL complement pathway in a bilateral renal I/R model (45 min of ischaemia followed by 24 h of reperfusion), using transgenic mice deficient in MBL-A and MBL-C [MBL double knockout (MBL DKO)] and in wildtype (WT) mice. Kidney damages, which were evaluated by levels of blood urea nitrogen (BUN) and creatinine, showed that MBL DKO mice were significantly protected compared with WT mice. MBL DKO mice, reconstituted with recombinant human MBL, showed a dose-dependent severity of kidney injury increasing to a comparable level to WT mice. Acute tubular necrosis was evident in WT mice but not in MBL DKO mice after I/R, confirming renal damages in WT mice. MBL ligands in kidneys were observed to be present after I/R but not in sham-operated mice. C3a (desArg) levels in MBL DKO mice were decreased after I/R compared with that in WT mice, indicating less complement activation that was correlated with less C3 deposition in the kidneys of MBL DKO mice. Our data implicate a role of MBL in I/R-induced kidney injury.

Acute Kidney Injury↗

Transmural gradients in Na/K pump activity and [Na+]I in canine ventricle.

There are well-documented differences in ion channel activity and action potential shape between epicardial (EPI), midmyocardial (MID), and endocardial (ENDO) ventricular myocytes. The purpose of this study was to determine if differences exist in Na/K pump activity. The whole cell patch-clamp was used to measure Na/K pump current (I(P)) and inward background Na(+)-current (I(inb)) in cells isolated from canine left ventricle. All currents were normalized to membrane capacitance. I(P) was measured as the current blocked by a saturating concentration of dihydro-ouabain. [Na(+)](i) was measured using SBFI-AM. I(P)(ENDO) (0.34 +/- 0.04 pA/pF, n = 17) was smaller than I(P)(EPI) (0.68 +/- 0.09 pA/pF, n = 38); the ratio was 0.50 with I(P)(MID) being intermediate (0.53 +/- 0.13 pA/pF, n = 19). The dependence of I(P) on [Na(+)](i) or voltage was essentially identical in EPI and ENDO (half-maximal activation at 9-10 mM [Na(+)](i) or approximately -90 mV). Increasing [K(+)](o) from 5.4 to 15 mM caused both I(P)(ENDO) and I(P)(EPI) to increase, but the ratio remained approximately 0.5. I(inb) in EPI and ENDO were nearly identical ( approximately 0.6 pA/pF). Physiological [Na(+)](i) was lower in EPI (7 +/- 2 mM, n = 31) than ENDO (12 +/- 3 mM, n = 29), with MID being intermediate (9 +/- 3 mM, n = 22). When cells were paced at 2 Hz, [Na(+)](i) increased but the differences persisted (ENDO 14 +/- 3 mM, n = 10; EPI 9 +/- 2 mM, n = 10; and MID intermediate, 11 +/- 2 mM, n = 9). Based on these results, the larger I(P) in EPI appears to reflect a higher maximum turnover rate, which implies either a larger number of active pumps or a higher turnover rate per pump protein. The transmural gradient in [Na(+)](i) means physiological I(P) is approximately uniform across the ventricular wall, whereas transporters that utilize the transmembrane electrochemical gradient for Na(+), such as Na/Ca exchange, have a larger driving force in EPI than ENDO.

Action Potentials↗

The cooperative transforming effects of PAX3-FKHR and IGF-II on mouse myoblasts.

Alveolar rhabdomyosarcoma (ARMS) cells express high levels of PAX3-FKHR and IGF-II. In this study, we have investigated the effects of PAX3-FKHR and IGF-II on the expression of muscle regulatory factors (myf5, MyoD and myogenin), and platelet derived growth factor-B (PDGF-B) and vascular endothelial growth factor (VEGF) in mouse C2C12 myoblasts in vitro. PAX3-FKHR induced cell cycling of C2C12 cells and promoted proliferation whilst blocking myogenesis. IGF-II inhibited their differentiation without influencing proliferation. Western blotting showed that PAX3-FKHR and IGF-II blocked the expression of myogenin and MyoD respectively. Since MyoD affects early myogenesis and myogenin controls terminal differentiation, a combination of PAX3-FKHR and IGF-II synergistically blocks myogenesis at several different stages in differentiation. We have also shown that the major survival and angiogenic cytokines, PDGF-B and VEGF, were induced by IGF-II and PAX3-FKHR respectively. A combination of PAX3-FKHR and IGF-II could synergistically up regulate the expression of PDGF-B and VEGF and stabilize their high expression levels. Our results suggest that high expression of PAX3-FKHR and IGF-II in ARMS synergistically play a key role in oncogenesis and tumour progression of ARMS.

Animals↗