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Results for “Skeletal muscle dysfunction”

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PubMed2001

Decreased EMG inhibition following electrical stimulation over muscle tendons in myopathies.

OBJECTIVE: To assess the central EMG inhibitory action of tendon afferent input in muscle diseases. METHODS: The EMG inhibition elicited by electrical stimulation over muscle tendons was tested in 13 healthy voluntary subjects and 8 patients who had a primary muscle disease with a mild force deficit. Electrical stimuli were delivered to the tendon of the extensor carpi radialis muscle at the wrist during tonic voluntary isometric contraction at 50% of the maximum EMG level. The EMG signal was recorded by surface electrodes over the extensor carpi radialis muscle. RESULTS: The prestimulus background EMG level was reduced in 7 out 8 of the patients. Both groups had the same phases of EMG modulation following tendon stimulation (TE1, TI1, TE2) and their latency and amplitude did not differ significantly. Conversely, the area of TI1 was significantly larger (i.e. the inhibition decreased) in patients ([mean+/-SD] absolute area: controls=4.1+/-1.6 mVms, patients=6.9+/-2.9 mVms, P<0.05). CONCLUSIONS: In muscle dysfunction there are serial 'upstream' changes of central inhibitory systems, probably to maximize the residual muscle power of the affected muscle.

Adolescent↗

PubMed2005

Telomerase mediates vascular endothelial growth factor-dependent responsiveness in a rat model of hind limb ischemia.

Telomere dysfunction contributes to reduced cell viability, altered differentiation, and impaired regenerative/proliferative responses. Recent advances indicate that telomerase activity confers a pro-angiogenic phenotype to endothelial cells and their precursors. We have investigated whether telomerase contributes to tissue regeneration following hind limb ischemia and vascular endothelial growth factor 165 (VEGF(165)) treatment. VEGF delivery induced angiogenesis and increased expression of the telomerase reverse transcriptase (TERT) and telomerase activity in skeletal muscles and satellite and endothelial cells. Adenovirus-mediated transfer of wild type TERT but not of a dominant negative mutant, TERTdn, significantly induced capillary but not arteriole formation. However, when co-delivered with VEGF, TERTdn abrogated VEGF-dependent angiogenesis, arteriogenesis, and blood flow increase. This effect was paralleled by in vitro evidence that telomerase inhibition by 3'-azido-3'-deoxythymidine in VEGF-treated endothelial cells strongly reduced capillary density and promoted apoptosis in the absence of serum. Similar results were obtained with adenovirus-mediated expression of TERTdn and AKTdn, both reducing endogenous TERT activity and angiogenesis on Matrigel. Mechanistically, neo-angiogenesis in our system involved: (i) VEGF-dependent activation of telomerase through the nitric oxide pathway and (ii) telomerase-dependent activation of endothelial cell differentiation and protection from apoptosis. Furthermore, detection of TERT in activated satellite cells identified them as VEGF targets during muscle regeneration. Because TERT behaves as an angiogenic factor and a downstream effector of VEGF signaling, telomerase activity appears required for VEGF-dependent remodeling of ischemic tissue at the capillaries and arterioles level.

Adenoviridae↗

PubMed2005

Effect of foot orthoses on tibialis posterior activation in persons with pes planus.

PURPOSE: To examine the influence of footwear on tibialis posterior (TP) activation in persons with pes planus. METHODS: Six asymptomatic adults with pes planus (arch index of < or =0.16) participated. Subjects performed a resisted foot adduction with plantar flexion exercise (3 sets of 30 repetitions). The exercise was performed barefoot and shod with foot orthoses. The two testing conditions were separated by a week. Magnetic resonance image signal intensity of the tibialis posterior, tibialis anterior, soleus, medial gastrocnemius, and peroneus longus was measured immediately before and after each exercise. Multivariate analyses of variance followed by paired Student's t-test were performed for the signal intensity of each muscle assessed to determine whether TP was selectively activated during the barefoot and shod exercises. RESULTS: When barefoot, five of the six subjects activated other lower-leg muscles in addition to TP. When wearing the foot orthoses and shoes, all five participants activated only TP. Additionally, activation of TP was higher when exercises were performed in shoes with orthoses than when barefoot (P = 0.019). CONCLUSION: Wearing the foot orthoses and shoes improved selective activation of the TP in persons with flat feet. In cases where selective activation of TP is desirable, such as persons with flat feet or TP tendon dysfunction, use of shoes and an arch supporting foot orthoses may enhance selective activation of the muscle.

Adult↗

PubMed2000

Effect of knee and hip position on hip extension range of motion in individuals with and without low back pain.

STUDY DESIGN: A 2-group, nonrandomized, mixed design with 1 between-subjects factor (group) and 2 within-subjects factors (knee and hip position). OBJECTIVES: To determine the amount of passive hip extension during changes in the knee angle in the sagittal plane, and the hip angle in the frontal plane in back-healthy (BH) subjects and subjects with low back pain (LBP). BACKGROUND: Information regarding the specific contributions of hip flexor muscles to limitations in hip extension range of motion (ROM) is necessary for the prescription of appropriate treatment. METHODS AND MEASURES: Thirty-five BH subjects (24 women and 11 men, mean age = 31.37 +/- 11.36) and 10 subjects with LBP (6 women and 4 men, mean age = 33.70 +/- 9.31) participated in the study. The passive length of the one- and two-joint hip flexor muscles was tested in 4 different conditions in which the positions of the knee and the hip were varied. The knee was positioned passively in full extension or 80 degrees of flexion while the hip was positioned passively in zero abduction or full abduction. RESULTS: Subjects with LBP displayed less passive hip extension than BH subjects (LBP, -5.61 degrees +/- 4.30; BH, -2.57 degrees +/- 4.18). Both groups had less hip extension when the knee was in flexion of 80 degrees than when the knee was fully extended (flexed, -5.51 +/- 4.50; extended, -0.98 degrees +/- 4.65), and when the hip was in zero hip abduction than when the hip was fully abducted (zero, -7.55 degrees +/- 5.03; full, 1.06 degrees +/- 4.31). The contribution of the different hip flexors to a hip extension limitation differed between BH and subjects with LBP. BH subjects demonstrated an effect of knee angle on hip extension when the hip was in zero abduction (flexed, -11.43 degrees +/- 5.81; extended, -2.49 degrees +/- 5.39), but not when the hip was in full abduction (flexed, 1.74 degrees +/- 3.91; extended, 1.89 degrees +/- 3.94). Subjects with LBP demonstrated an effect of knee angle on hip extension when the hip was in zero abduction (flexed, -12.60 degrees +/- 4.91; extended, -6.65 degrees +/- 5.03) and when the hip was in full abduction (flexed, -3.10 degrees +/- 5.53; extended, -0.10 degrees +/- 5.18). CONCLUSIONS: The results of this study provide evidence that changing the knee joint angle in the sagittal plane and the hip joint angle in the frontal plane, during the hip flexor length test, can affect the amount of passive hip extension ROM. The contribution of specific hip flexor muscles to a hip extension limitation may differ depending on the individual's movement dysfunction. Modifying the hip flexor length test, as described, should provide information about the specific muscles contributing to a hip joint extension limitation.

Adult↗

PubMed2003

Practice and principles of pharmacodynamic determination of HISS-dependent and HISS-independent insulin action: methods to quantitate mechanisms of insulin resistance.

Injection of insulin causes release of HISS (hepatic insulin sensitizing substance) from the liver in the fed state. HISS action accounts for 50-60% of the glucose disposal produced by a wide range of insulin doses (5-100 mU/kg). Although the chemical nature of HISS is unknown, precluding pharmacokinetic studies, the pharmacodynamics of HISS has advanced because of the use of the rapid insulin sensitivity test (RIST) which is a transient euglycemic clamp used following a bolus of insulin. HISS action can be blocked by hepatic denervation and restored by intraportal but not intravenous infusion of acetylcholine or a nitric oxide donor. HISS release is prevented by blockade of hepatic muscarinic receptors, nitric oxide synthase blockers, indomethacin, and animal models of insulin resistance, including chronic liver disease, sucrose feeding, hypertension, aging, obesity, and fetal alcohol exposure. HISS acts on skeletal muscle but not liver, gut, or adipose tissue. HISS is released by insulin in the fed state but decreases to insignificance after 24-hr fasting in rats. Cats and dogs appear to require a longer period of fasting to prevent HISS action. Lack of HISS action is suggested to be the cause of post-meal hyperglycemia and hyperlipidemia in type 2 diabetes and other disease states with similar metabolic dysfunction. The RIST can be carried out up to six times in the same animal, is not affected by pentobarbital anesthesia, and can readily differentiate HISS-dependent and HISS-independent insulin action.

Animals↗

PubMed2004

Optimising the detection of upper motor neuron function dysfunction in amyotrophic lateral sclerosis--a transcranial magnetic stimulation study.

Evidence of upper motor neuron (UMN) dysfunction is essential in making the diagnosis of amyotrophic lateral sclerosis (ALS). Central motor conduction (CMC) abnormalities detected using transcranial magnetic stimulation (TMS) are presumed to reflect UMN dysfunction. CMC is, however, often normal in patients with classical sporadic ALS. The aim of the study was to determine whether the utility of the CMC measure in ALS could be enhanced. We measured CMC to four pairs of muscles (abductor digiti minimi (ADM), biceps, vastus medialis (VM) and abductor hallucis (AH) in 20 controls and 25 ALS patients. The commonest abnormality detected in the ALS patients was an absent MEP, found in 11 patients (44 %) and in 25 of 200 muscles examined. Studying a minimum of three muscles increased the probability of detecting UMN dysfunction. Weakness in the muscle as well as selecting a distal rather than a proximal muscle was significantly associated with an abnormal CMC. Interside differences in CMC were significantly more pronounced in the patient group. In 30% of patients a significant interside difference in AH CMC time was the sole abnormality, suggesting mild UMN dysfunction on the side with the longer CMC.

Adult↗

PubMed2000

Secondary respiratory chain defect in a boy with long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency: possible diagnostic pitfalls.

UNLABELLED: We report on a boy who suffered from microcephaly, growth retardation, cardiomyopathy and hepatic dysfunction. When he had his first febrile infection at the age of 3 months he showed metabolic decompensation. Laboratory parameters and clinical features were compatible with a beta-oxidation defect or a respiratory chain disorder. Measurement of beta-oxidation enzymes showed long-chain 3-hydroxyacyl CoA dehydrogenase (LCHAD) deficiency; determination of respiratory chain complex activities revealed complete absence of complex I, II, III and IV activities in skeletal muscle and reduced activities of complexes II and IV in cultured fibroblasts, with secondary dysregulation of ATP synthase. The patient was found to be homozygous for the MTP:G1528 C mutation (LCHAD-deficiency). CONCLUSION: This patient had LCHAD deficiency as his primary metabolic disorder, leading to secondary inhibition of respiratory chain enzymes by 'toxic' metabolites.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed2006

Cytotoxicity of Lachesis muta muta snake (bushmaster) venom and its purified basic phospholipase A2 (LmTX-I) in cultured cells.

Human envenoming by Lachesis muta muta venom, although infrequent, is rather severe, being characterized by pronounced local tissue damage and systemic dysfunctions. Studies on the pharmacological actions of L. m. muta venom are relatively scant and the direct actions of the crude venom and its purified phospholipase A(2) (PLA(2)) have not been addressed using in vitro models. In this work, we investigated the cytotoxicity of L. m. muta venom and its purified PLA(2) isoform LmTX-I in cultured Madin-Darby canine kidney (MDCK) and in a skeletal muscle (C2C12) cell lines. As revealed by neutral red dye uptake assay, the crude venom (10 or 100 microg/ml) induced a significant decrease in cell viability of MDCK cells. LmTX-I at the concentrations tested (70-270 microg/ml or 5-20 microM) displayed no cytotoxicity in both MDCK and C2C12 cell lines. Morphometric analysis of Feulgen nuclear reaction revealed a significant increase in chromatin condensation (pyknosis), apparent reduction in the number of mitotic nuclei and nuclear fragmentation of some MDCK cells after incubation with L. m. muta venom. Monolayer exposure to crude venom resulted in morphological changes as assessed by scanning electron microscopy. The staining with TRITC-labelled phalloidin showed a marked disarray of the actin stress fiber following L. m. muta venom exposure. In contrast, LmTX-I had no effect on nucleus and cell morphologies as well as on stress fiber organization. These results indicate that L. m. muta venom exerts toxic effects on cultured MDCK cells. The LmTX-I probably does not contribute per se to the direct venom cytotoxicity, these effects are mediated by metalloproteinases/disintegrins and other components of the venom.

Animals↗

PubMed2003

Inclusion body myositis--sensory dysfunction revealed with quantitative determination of somatosensory thresholds.

In order to evaluate sensory function in inclusion body myositis (IBM), nine patients were subjected to sensibility screening and quantitative determination of somatosensory thresholds. Data were compared with results from electrophysiological examination and muscle biopsy. On sensibility screening all but one of the IBM patients had abnormal findings in hands and/or feet mostly affecting thermal sensibility. Vibratory thresholds were abnormal in five and thermal thresholds in four of the patients. Mean vibratory thresholds were significantly (P < 0.05) higher in the IBM patients when compared with the controls. Significantly increased heat pain thresholds were found in hands and feet when compared with the controls while thermal thresholds were normal. Nerve conduction velocities were decreased in three patients, EMG showed both myopathic and neuropathic abnormalities in six patients. Eight patients had neuropathic abnormalities on muscle biopsy. The sensory dysfunction found suggests an affection of peripheral nerves in IBM mainly affecting large diameter myelinated nerve fibres corroborating earlier findings of a peripheral neuropathy in IBM.

Aged↗

PubMed2002

Flumazenil recovers diaphragm muscle dysfunction caused by midazolam in dogs.

UNLABELLED: We studied the effects of flumazenil on diaphragm muscle dysfunction caused by midazolam in dogs. Animals were divided into three groups of eight each. In each group, anesthetic doses (0.1 mg/kg initial dose plus 0.5 mg. kg(-1). h(-1) maintenance dose) of midazolam were administered for 60 min. Immediately after the end of midazolam administration, Group 1 received no study drug; Group 2 was infused small-dose (0.004 mg. kg(-1). h(-1)) flumazenil; Group 3 was infused with large-dose (0.02 mg. kg(-1). h(-1)) flumazenil. We assessed diaphragm muscle function (contractility and electrical activity) by transdiaphragmatic pressure (Pdi) and integrated electrical activity of the diaphragm (Edi). After midazolam was administered in each group, Pdi at low-frequency (20-Hz) and high-frequency (100-Hz) stimulation decreased from baseline values (P < 0.05), and values of Edi at 100-Hz stimulation were less than those obtained during baseline (P < 0.05). In Group 1, Pdi and Edi to each stimulus did not change from midazolam-induced values. In Groups 2 and 3, with an infusion of flumazenil, Pdi at both stimuli and Edi at 100-Hz stimulation increased from midazolam-induced values (P < 0.05). The increase in Pdi and Edi was more in Group 3 than in Group 2 (P < 0.05). We conclude that flumazenil recovers the diaphragm muscle dysfunction (reduced contractility and inhibited electrical activity) caused by anesthetic doses of midazolam in dogs. IMPLICATIONS: In dogs, flumazenil recovers diaphragm muscle dysfunction (reduced contractility and inhibited electrical activity) caused by midazolam in a dose-related manner.

Anesthetics, Intravenous↗

PubMed2004

No correlation between number of MRI-evident lesions in cerebrum and the soleus stretch reflex in multiple sclerosis patients.

The aim of the study was to investigate if the stretch reflex of the soleus muscle was useful in quantifying upper motor neuron lesions. The soleus stretch reflex was recorded in 10 healthy subjects and 20 patients with active relapsing-remitting multiple sclerosis and correlated to the number of MRI lesions in cerebrum and clinical scores (expanded disability status scale and regional functional scoring system). The short latency stretch reflex was elicited by rotating the left ankle joint 4 degrees with a rise time in the interval of 40-640 ms. The amplitude of the stretch was larger in multiple sclerosis patients being 88.5 microV in patients and 12.8 microV in controls, P = 0.007. The sensitivity of the stretch reflex expressed as the slope of the best linear fit was increased in MS patients to 2.6 microVs/degree compared with 0.6 microVs/degree (0.1-2.2) in controls, P = 0.009. There was no correlation between amplitude of the stretch reflex and number of MRI lesions (r = -0.03). In conclusion, the soleus stretch reflex might be useful to quantify spasticity but is not useful in detecting dysfunction of upper motor neurons in MS.

Adult↗

PubMed2006

Effects of high-sucrose feeding on insulin resistance and hemodynamic responses to insulin in spontaneously hypertensive rats.

This study was designed to investigate the effects of a sucrose diet on vascular and metabolic actions of insulin in spontaneously hypertensive rats (SHR). Male SHR were randomized to receive a sucrose or regular chow diet for 4 wk. Age-matched, chow-fed Wistar-Kyoto (WKY) rats were used as normotensive control. In a first series of experiments, the three groups of rats had pulsed Doppler flow probes and intravascular catheters implanted to determine blood pressure, heart rate, and blood flows. Insulin sensitivity was assessed during a euglycemic hyperinsulinemic clamp performed in conscious rats. In a second series of experiments, new groups of rats were used to examine glucose transport activity in isolated muscles and to determine endothelial nitric oxide synthase (eNOS) protein expression in muscles and endothelin content in vascular tissues. Sucrose feeding was shown to markedly enhance the pressor response to insulin and its hindquarter vasoconstrictor effect when compared with chow-fed SHR. A reduction in eNOS protein content in muscle, but no change in vascular endothelin-1 protein, was noted in sucrose-fed SHR when compared with WKY rats, but these changes were not different from those noted in chow-fed SHR. Similar reductions in insulin-stimulated glucose transport were observed in soleus muscles from both groups of SHR when compared with WKY rats. In extensor digitorum longus muscles, a significant reduction in insulin-stimulated glucose transport was only seen in sucrose-fed rats when compared with the other two groups. Environmental factors, that is, high intake of simple sugars, could possibly potentiate the genetic predisposition in SHR to endothelial dysfunction and insulin resistance.

Animals↗

PubMed2002

Reduced endplate currents underlie motor unit dysfunction in canine motor neuron disease.

Hereditary canine spinal muscular atrophy (HCSMA) is an autosomal dominant degenerative disorder of motor neurons. In homozygous animals, motor units produce decreased force output and fail during repetitive activity. Previous studies suggest that decreased efficacy of neuromuscular transmission underlies these abnormalities. To examine this, we recorded muscle fiber endplate currents (EPCs) and found reduced amplitudes and increased failures during nerve stimulation in homozygotes compared with wild-type controls. Comparison of EPC amplitudes with muscle fiber current thresholds indicate that many EPCs from homozygotes fall below threshold for activating muscle fibers but can be raised above threshold following potentiation. To determine whether axonal abnormalities might play a role in causing motor unit dysfunction, we examined the postnatal maturation of axonal conduction velocity in relation to the appearance of tetanic failure. We also examined intracellularly labeled motor neurons for evidence of axonal neurofilament accumulations, which are found in many instances of motor neuron disease including HCSMA. Despite the appearance of tetanic failure between 90 and 120 days, average motor axon conduction velocity increased with age in homozygotes and achieved adult levels. Normal correlations between motor neuron properties (including conduction velocity) and motor unit properties were also observed. Labeled proximal motor axons of several motor neurons that supplied failing motor units exhibited little or no evidence of axonal swellings. We conclude that decreased release of transmitter from motor terminals underlies motor unit dysfunction in HCSMA and that the mechanisms determining the maturation of axonal conduction velocity and the pattern of correlation between motor neuron and motor unit properties do not contribute to the appearance or evolution of motor unit dysfunction.

Aging↗

PubMed2002

Radiation myelitis in a 5-year-old girl.

Myelopathy is an uncommon complication of radiotherapy, particularly in the pediatric age group. A 5-year-old girl with acute lymphoblastic leukemia developed a severe but transient radiculopathy after intrathecal administration of methotrexate and cytarabine for an isolated central nervous system relapse. Chemotherapy was then given through an intraventricular catheter. Owing to a second central nervous system recurrence, she was treated with craniospinal radiation. The whole brain down to the level of C2 received a dose of 2400 cGy. Two months after completion of radiation, the child developed a progressive tetraparesis, and magnetic resonance imaging revealed an enhancing lesion involving the medulla and upper cervical cord. A biopsy was consistent with a treatment-related necrotizing leukoencephalopathy. This case suggests that patients who develop neurologic dysfunction when treated with methotrexate can also be particularly susceptible to radiation-related injury.

Child, Preschool↗

PubMed2000

Experimental models to investigate inflammatory processes in chronic venous insufficiency.

Chronic venous insufficiency (CVI) is characterized by leukocyte adhesion and infiltration, venous hypertension and dilatation, and valvular dysfunction. The fact that activated white cells can direct a powerful cytotoxic arsenal at parenchymal cells following their extravasation into the tissues led to the original proposal that leukocytes may play a causative role in the pathogenesis of venous disease. A large body of subsequent work indicates that white blood cells are indeed activated in CVI. However, identification of the factors responsible for initiating leukosequestration and activation in such disorders and determination of whether these activated cells then contribute to the progression of venous disease have been hampered by the lack of appropriate animal models that accurately mimic the human condition. Tantalizing evidence suggesting that cyclical periods of ischemia and reperfusion (I/R) may occur in diseased regions of the skin is beginning to accumulate. As is the case with CVI, leukocyte infiltration is a prominent feature in I/R and activated neutrophils play a causative role in the reperfusion component of tissue injury via the targeted release of reactivate oxygen metabolites and hydrolytic enzymes. In light of these considerations, many investigators have suggested that examining the mechanisms of I/R injury in skin and skeletal muscle, where ischemia is produced by arterial occlusion, may provide a relevant model for studying the pathogenesis of CVI. Others have suggested that venous occlusion may represent a more appropriate model, as this approach also produces the venous hypertension that is characteristic of the disease. The purpose of this review is to summarize the evidence pointing to the involvement of I/R and venous hypertension as causative factors in CVI-induced leukocyte recruitment. In addition, we will describe the evidence in favor of the view that white blood cells contribute to the pathogenesis of CVI. Finally we will describe several different experimental models that have been used to examine the role of I/R-induced microvascular dysfunction as it may pertain to the development of CVI, together with a discussion of the relative advantages and limitations of the various models.

Animals↗

PubMed2001

Contraction and intracellular Ca(2+) handling in isolated skeletal muscle of rats with congestive heart failure.

A decreased exercise tolerance is a common symptom in patients with congestive heart failure (CHF). This decrease has been suggested to be partly due to altered skeletal muscle function. Therefore, we have studied contractile function and cytoplasmic free Ca(2+) concentration ([Ca(2+)](i), measured with the fluorescent dye indo 1) in isolated muscles from rats in which CHF was induced by ligation of the left coronary artery. The results show no major changes of the contractile function and [Ca(2+)](i) handling in unfatigued intact fast-twitch fibers isolated from flexor digitorum brevis muscles of CHF rats, but these fibers were markedly more susceptible to damage during microdissection. Furthermore, CHF fibers displayed a marked increase of baseline [Ca(2+)](i) during fatigue. Isolated slow-twitch soleus muscles of CHF rats displayed slower twitch contraction and tetanic relaxation than did muscles from sham-operated rats; the slowing of relaxation became more pronounced during fatigue in CHF muscles. Immunoblot analyses of sarcoplasmic reticulum proteins and sarcolemma Na(+),K(+)-ATPase showed no difference in flexor digitorum brevis muscles of sham-operated versus CHF rats. In conclusion, functional impairments can be observed in limb muscle isolated from rats with CHF. These impairments seem to mainly involve structures surrounding the muscle cells and sarcoplasmic reticulum Ca(2+) pumps, the dysfunction of which becomes obvious during fatigue.

Animals↗

PubMed2005

Chloroquine-induced lipidosis mimicking Fabry disease.

Intracellular accumulation of phospholipids may be a consequence of inherited or acquired metabolic disorders. In Fabry disease, deficiency of alpha-galactosidase A results in storage of globotriasylceramide in numerous cells including endothelium, striated muscle (skeletal, cardiac), smooth muscle, and renal epithelium among others; the ultrastructural appearance of the inclusions is of whorled layers of alternating dense and pale material ('zebra bodies' or myeline figures). Chloroquine therapy may result in storage of biochemically and ultrastructurally similar inclusions in many of the same cells as Fabry disease and often results in similar clinical manifestations. We report a 56-year-old woman with rheumatoid arthritis treated with chloroquine, who developed muscle weakness and renal insufficiency; information regarding therapy was not emphasized at the time of renal biopsy, leading to initial erroneous interpretation of Fabry disease. Following muscle biopsy, genetic and enzyme evaluation, and additional studies on the kidney biopsy, a diagnosis of chloroquine toxicity was established. One year following cessation of chloroquine, renal and muscle dysfunction greatly improved. In chloroquine toxicity, inclusions in glomeruli are not only in visceral epithelial, endothelial and mesangial cells but are in infiltrating monocytes/macrophages, which are most commonly present in the mesangium. Curvilinear bodies, the ultrastructural features of chloroquine toxicity in striated muscle, are not present in renal cells. This report documents differences in appearance, cells affected and morphological differential diagnostic features to distinguish these two entities.

Antirheumatic Agents↗

PubMed2001

The MAS (mandibular advancement series) difference.

So now it may be seen what is meant by the term "The MAS Difference". The American orthodontic specialty has for the most part been slow, or even in isolated pockets, willfully resistant to expansion of orthodontic technique up out of the "Procrustean bed" of fixed appliance limitations to the panorama of attacking the teeth-bone-muscle triangle of malocclusion with separate techniques and appliance systems designed specifically for each. What makes this anathema to those of a broader view is that it is only with those expanded, combined fixed AND functional techniques, that one has any chance at all of rendering anything close to significantly successful treatment of major TMJ-pain-headache-dysfunction chronic pain problems. And that is serious stuff. So, if you want to do "ortho" you had better know "TMJ". And, if you want to do "TMJ", at least TMJ to any meaningful degree, you had better know "ortho", and that means the discipline of functional orthodontics (or "maxillofacial orthopedics" if you will). The "why" of it is easily understandable once one truly understands the orthopedic (condylar displacement), myofunctional (Class II neuromuscular sling), and neurological (chronic repetitive compression nerve damage) aspects of the common functionally induced TMJ problem. The "how" of it all is another matter. That is why knowledge of a broad variety of various specific orthodontic techniques is required for the clinician because there are a vast variety of malocclusive situations with their own unique demands. But in the broadest sense, since a major portion of the orthodontic patient population suffers from somewhat of a skeletal Class II relationship, or "Class II effect" with respect to the joint, somewhere in the proposed treatment plan for these patients the clinician will have to consider some form of mandibular advancement series, whatever that series may be. But it is that MAS difference that sets that clinician and his or her specific treatment plan apart from the older, more restricted ways. It is a difference we must pay attention to, for Nature surely will.

Activator Appliances↗