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Biomedical subjects

E Zhu

Publications and source records attributed to E Zhu.

10 recordsLinked to original sources
PubMed2001

Functional magnetic stimulation for conditioning of expiratory muscles in patients with spinal cord injury.

OBJECTIVE: To evaluate the effectiveness of functional magnetic stimulation (FMS) in conditioning expiratory muscles patients with spinal cord injury (SCI). DESIGN: A prospective before-after trial. SETTING: The Functional Magnetic Stimulation Laboratory of the SCI Health Care Group, VA Long Beach Health Care System, and the Spinal Cord Injury Services, Department of Veterans Affairs, Palo Alto Health Care System. PARTICIPANTS: Eight men with tetraplegia. INTERVENTION: Expiratory muscle training was achieved by placing a magnetic stimulator with a round magnetic coil along subjects' lower thoracic spine. MAIN OUTCOME MEASURES: Measures taken were the maximal expired pressure at total lung capacity (MEP-TLC) and at functional residual capacity (MEP-FRC), expiratory reserve volume (ERV), and the forced expiratory flow rate at TLC (FEF-TLC) and at FRC (FEF-FRC) by subjects' voluntary maximal efforts. RESULTS: After 4 weeks of conditioning, the mean +/- standard error of the mean values were: MEP-TLC, 55.3 +/- 8.6cmH(2)O; MEP-FRC, 29.6 +/- 5.6cmH(2)O; ERV,.57 +/-.08L; FEF-TLC, 4.3 +/- 0.5L/s; and FEF-FRC, 1.9 +/- 0.2L/s. These values correspond to, respectively, 129%, 137%, 162%, 109%, and 127% of pre-FMS conditioning values. When FMS was discontinued for 2 weeks, the MEP-TLC returned to its pre-FMS training value. CONCLUSION: A 4-week protocol of FMS of the expiratory muscles improves voluntary expiratory muscle strength significantly, indicating that FMS can be a noninvasive therapeutic technology in respiratory muscle training for persons with tetraplegia.

Analysis of Variance↗
PubMed2000

Induction of the ATP-sensitive potassium (uK(ATP)-1) channel by endotoxemia.

The effect of sepsis on the ubiquitously expressed ATP-sensitive potassium (uK(ATP)-1) channel expression was measured in Sprague-Dawley rat diaphragms. Rats were treated with either 0.5 ml saline or 20 mg/Kg E. coli lipopolysaccharides and sacrificed at 3, 6, 12, 24, or 48 h later. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis showed that channel mRNA expression was increased at 3 h and continued to rise up to 48 h. Western blotting analysis showed a approximately 9-fold increase in channel protein expression 24 h after sepsis. Our results demonstrate that sepsis upregulates the uK(ATP)-1 channel.

Adenosine Triphosphate↗
PubMed2000

Influence of tension time on muscle fiber sarcolemmal injury in rat diaphragm.

We hypothesized that the amount of sarcolemmal injury is directly related to the total tension time (TT(tot)), calculated as mean tension x total stimulation time. Diaphragm strips from Sprague-Dawley rats were superfused at optimal muscle length with Krebs containing procion orange to identify sarcolemmal injury. TT(tot) was induced by stimulation with 100 Hz for 3 min at duty cycles of 0.02, 0.15, 0.3, and 0.6, or with continuous contractions at 0.2, 0.4, 0.6, and 1.0 of maximal tension. A significant positive correlation between TT(tot) and the percentage of fibers with injured sarcolemma (r(2) = 0.63, P < 0.05) is seen. Stimulation (at 100 Hz, duty cycle = 1) resulted in fast fatigue with low injury, likely caused by altered membrane conductivity. Stimulations inducing the largest injury are those showing progressive force loss and high TT(tot), where injury may be due to activation of membrane degradative enzymes. The maximal tension measured at 20 min poststimulation was inversely related to the number of fibers injured, suggesting loss of force is caused by cellular injury.

Animals↗
PubMed2000

Expression of myosin heavy-chain isoforms in the respiratory muscles following inspiratory resistive breathing.

We investigated the effect of inspiratory resistive breathing (IRB) on the expression of the genes encoding fast and slow isoforms of myosin heavy chain (MyHC) in respiratory muscles. Eleven mongrel dogs were studied for baseline MyHC messenger RNA (mRNA) expression, seven of which were also used to study the effects of IRB. For this latter objective, awake and spontaneously breathing animals were subjected to 2 h of IRB (80 cm H(2)O/L/s) per day for four consecutive days. mRNA expression was assessed in the diaphragm, external intercostal muscle, and a limb muscle, using both slot- blot and in situ hybridizations with isoform-specific probes. A current semiquantitative scoring method (from 0 to 4) was used to quantify the in situ mRNA expression levels, and slot-blot data were analyzed with densitometry. Prior to IRB, slow- and fast-MyHC mRNA expression was moderate, similar, and homogeneous throughout the different regions of the diaphragm, with scores of 1.50 +/- 0.54 (mean +/- SD) for slow and 2.13 +/- 0.35 for fast mRNAs in the costal region of the diaphragm, and of 1.81 +/- 0.37 for slow and 2. 13 +/- 0.64 for fast mRNAs in the crural region of the diaphragm. Although expression of fast-MyHC mRNA remained unchanged after IRB, the relative expression of the mRNA for the slow isoform increased in costal (+30%), crural (+12%), and external intercostal (+27%) muscles. MyHC mRNA expression did not change in limb muscles. We conclude that breathing with a moderate inspiratory resistance for a short period induces the expression of slow MyHC in respiratory muscles.

Animals↗
PubMed1999

Dystonin-deficient mice exhibit an intrinsic muscle weakness and an instability of skeletal muscle cytoarchitecture.

Dystonia musculorum (dt) was originally described as a hereditary sensory neurodegeneration syndrome of the mouse. The gene defective in dt encodes a cytoskeletal linker protein, dystonin, that is essential for maintaining neuronal cytoskeletal integrity. In addition to the nervous system, dystonin is expressed in a variety of other tissues, including muscle. We now show that dystonin cross-links actin and desmin filaments and that its levels are increased during myogenesis, coinciding with the progressive reorganization of the intermediate filament network. A disorganization of cytoarchitecture in skeletal muscle from dt/dt mice was observed in ultrastructural studies. Myoblasts from dt/dt mice fused to form myotubes in culture; however, terminally differentiated myotubes contained incompletely assembled myofibrils. Another feature observed in dt/dt myotubes in culture and in skeletal muscle in situ was an accumulation and abnormal distribution of mitochondria. The diaphragm muscle from dt/dt mice was weak in isometric contractility measurements in vitro and was susceptible to contraction-induced sarcolemmal damage. Altogether, our data indicate that dystonin is a cross-linker of actin and desmin filaments in muscle and that it is essential for establishing and maintaining proper cytoarchitecture in mature muscle.

Actins↗
PubMed1998

Ontogenesis of nitric oxide synthases in the ventilatory muscles.

Nitric oxide (NO) acts as an endogenous mediator in mature skeletal muscle. In this study, we investigated the regulation of the endothelial (eNOS) and neuronal (nNOS) isoforms of nitric oxide synthase (NOS) in skeletal-muscle development (rat diaphragm). Muscle NOS activity, nNOS and eNOS protein, and mRNA expressions were markedly increased during the late gestational and early postnatal periods. Expression of both isoforms, however, declined progressively thereafter. Similarly, argininosuccinate lyase and argininosuccinate synthetase, both involved in the recycling of L-citrulline to L-arginine, were expressed at high levels in rat embryonic and neonatal diaphragms, with gradual reduction in their expression during late postnatal development. Immunostaining revealed extensive nNOS expression at the sarcolemma in neonatal and mature diaphragms, whereas eNOS expression was limited to the endothelium. Both neonatal and adult diaphragms expressed an alternatively spliced nNOS isoform with an insert of 34 amino acids between exons 16 and 17. In vitro-generated muscle force rose significantly after NOS inhibition in both neonatal and adult diaphragms, but the magnitude of force augmentation was larger in adult than in neonatal diaphragm. These results indicate that constitutive NOS isoforms are developmentally regulated in skeletal muscles, suggesting multiple roles for NO in developing and mature skeletal-muscle fibers.

Aging↗
PubMed1997

Diaphragm muscle fiber injury after inspiratory resistive breathing.

Five awake previously tracheotomized mongrel dogs were challenged with inspiratory resistive breathing (IRB). The mean peak tracheal pressure = -35.4 +/- 1.1 cmH2O, ETCO2 = 39.8 +/- 1.5 mmHg was sustained for 2 h/d over 4 consecutive d. On the fourth day, following IRB, the dogs were placed under general anaesthesia, and the diaphragm was perfused via the internal mammary artery with a low molecular weight fluorescent tracer (Procion orange, FW = 631), to which normal muscle fibers are impermeable. Muscle fiber membrane damage was identified on tissue sections by using fluorescent microscopy showing the presence of the tracer in the cytoplasm. Four dogs undergoing the same protocol (except IRB) served as control. The dye was seen in 7.6 +/- 2.6% and in 0.3 +/- 0.1% of fibers in the IRB and control groups, respectively (p < 0.05). Via ATPase staining, it was found that fibers of type I were predominantly affected as compared to type II (p < 0.05). In addition, an increased area fraction of fibers demonstrating sarcomere disruption was found after IRB (2.4 +/- 0.5%) compared to pre-IRB (0.4 +/- 0.1%; p < 0.05). We conclude that resistive breathing of a magnitude similar to that seen in some respiratory diseases, or used in respiratory muscle training programs induces muscle membrane and sarcomere injury.

Animals↗
PubMed1990

[Dental lamina as presumptive source of odontogenic cyst].

The possibility of the dental lamina as a source of odontogenic cyst was investigated. The mandibular first molar tooth germs with the dental lamina and surface oral epithelium were cut from 17.5-day-old C3H mouse embryos. The following 5 kinds of grafts were prepared: (I) recombinant of the dental lamina and dental papilla, (II) dental lamina, (III) dental papilla, (IV) recombinant of the oral epithelium and dental papilla and (V) oral epithelium. After the renal subcapsular transplantation to the 3-month-old syngenic male mice, each graft was harvested at timed sequences from 2 to 24 weeks and was examined histopathologically. The recombinant of the dental lamina and dental papilla (1) grew into a cyst lined by para-keratinized stratified squamous epithelium. The cyst enlarged gradually and might be compared to the odontogenic keratocyst of the human being. The recombinant of the oral epithelium and dental papilla (IV) and the oral epithelium (V) developed into a cyst lined by orthokeratinized stratified squamous epithelium which differed from the epithelium seen in Experiment (I). The dental papilla (III) grew to be a bone tissue while nothing developed from the dental lamina (II). These results suggest that the dental lamina is one of the sources of the odontogenic keratocyst and the dental papilla plays an important role in its histogenesis.

Animals↗