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Biomedical subjects

R L Ruff

Publications and source records attributed to R L Ruff.

At least 73 records · Page 4Linked to original sources
PubMed1989

Neurologic complications of endocrine diseases.

The endocrine system maintains a constant internal milieu for proper nervous system functioning. It is not surprising that abnormalities develop anywhere along the neuroaxis when disease of the endocrine organs occurs. Appreciating the neurologic signs and symptoms of endocrine disease is of utmost importance, given the relative ease in confirming the diagnosis, their excellent response to treatment, and the devastating consequences if not appreciated. This article reviews the findings seen in disorders of calcium metabolism, thyroid and adrenal disease, diabetes mellitus, and acromegaly.

Cushing Syndrome↗
PubMed1988

Slow sodium channel inactivation in mammalian muscle: a possible role in regulating excitability.

Sodium currents were recorded in rat fast and slow twitch muscle fibers. Changes in the membrane potential around the resting potential produced slow changes in the sodium current amplitude due to alterations of the slow inactivation process that was increased by steady depolarization and removed by prolonged hyperpolarization. In contrast, classical fast inactivation was not operative around the resting potential, and depolarizations of greater than 20 mV were required to close half of the channels by fast inactivation. Because slow inactivation is operative around the resting potential of mammalian muscle fibers, it may partially explain why small depolarizations, such as those that occur in some patients with periodic paralysis, can reduce excitability.

Animals↗
PubMed1988

Dissociated weakness of sternocleidomastoid and trapezius muscles with lesions in the CNS.

We describe three patients with lesions in the CNS that produced dissociated weakness of trapezius (TM) and sternocleidomastoid muscles (SCM). One patient with a right cerebral hemisphere lesion had left TM weakness and right SCM weakness. A second, with a brainstem lesion, and a third, with a high cervical cord lesion, had TM weakness with preserved SCM strength. We discuss the findings according to the known neuroanatomy.

Adult↗
PubMed1988

A case of persistent cortical deafness: clinical, neurophysiologic, and neuropathologic observations.

A 61-year-old man became deaf after the second of two cerebral infarctions which successively involved the temporal and adjacent cortices. He remained completely deaf until death 27 months later. Click stimulation demonstrated normal short-latency potentials, middle-latency responses better developed to stimulation of the right than of the left ear, and absent long-latency potentials. Neuropathologic examination showed cystic infarctions involving both transverse temporal gyri and adjacent cortical areas with preservation of the brainstem auditory nuclei. Persistent deafness can result from bilateral lesions involving the auditory and adjoining cortices.

Cerebral Infarction↗
PubMed1988

Endocrine myopathies.

The atrophy produced by endocrine disorders is primarily due to alterations in protein and carbohydrate metabolism. Type II muscle fibers are more severely affected than are Type I fibers. Steroid myopathy and the myopathy associated with excess ACTH have a typical pattern of proximal weakness affecting the legs more than the arms. Steroid myopathy is usually not apparent until other signs of glucocorticoid excess are present. Treatments of steroid myopathy are as follows: Lower the dose of steroid, use a nonfluorinated glucocorticoid, and exercise or physical therapy. Adrenal insufficiency produces generalized weakness, muscle cramping, and fatigue in 50 per cent of patients. Some patients also develop hyperkalemic paralysis. The treatment is hormone replacement. Thyrotoxicosis produces myopathy caused by net protein catabolism, accelerated basal metabolic rate and impaired carbohydrate metabolism. Shortening of contraction time may result from accelerated myosin ATPase activity and enhanced calcium uptake by the sarcoplasmic reticulum. Depolarization of the muscle fiber and impaired Na-K activity in muscle may predispose to thyrotoxic periodic paralysis. Neuromuscular presynaptic impairment may account for the worsening of myasthenia gravis by thyrotoxicosis. In hypothyroidism, impaired energy metabolism may limit force generation. Slow contraction and relaxation reflect reduction in myosin ATPase activity and impaired calcium uptake by the sarcoplasmic reticulum. Treatment for thyroid-associated muscle disorders is restoration of a euthyroid state. Muscle weakness associated with hypopituitarism is due to loss of thyroid and adrenal cortical hormones. Children require growth hormone for muscle development. T3 and growth hormone synergize to maintain normal protein synthesis. Primary and secondary hyperparathyroidism and osteomalacia are often associated with proximal weakness and fatigability. The myopathy improves with restoration of normal PTH levels and vitamin D replacement. Hypoparathyroidism and pseudohypothyroidism are associated with tetany. Tetany is worsened by alkalosis and is treated by calcium and magnesium replacement.

Endocrine System Diseases↗
PubMed1987

Specific tension measurements in single soleus and medial gastrocnemius muscle fibers of the cat.

Direct measurements of the sizes of and forces produced by single fibers of the cat soleus and medial gastrocnemius muscles were made to determine whether or not different fiber types have characteristically distinct specific tensions. Single fibers (5-mm lengths), whose sarcolemmas had been chemically removed using a 5-mM EGTA "skinning" solution, were attached to a photodiode force transducer. Each single fiber was first placed in "relaxing" solution (22 +/- 1 degrees C, pH 7.0, pCa 8), its sarcomere length set at 2.7 micron using its laser diffraction pattern, and its diameter measured using the calibrated graticule of a microscope eyepiece (+/- 2 micron). Subsequently, each fiber was transferred to an activating bathing solution (pCa 3.6) in which the fiber produced its maximum tension. The specific tension values for single soleus muscle fibers displayed a threefold range (1.19 to 3.53 kg/cm2) with a mean value of 2.30 +/- 0.61 (SD) kg/cm2 (N = 42). The medial gastrocnemius fibers studied had a fourfold range in specific tensions (1.05 to 4.47 kg/cm2) and a mean value of 2.42 +/- 0.61 (SD) kg/cm2 (N = 104). Many medial gastrocnemius fibers (N = 64) were type-identified using a standard actomyosin ATPase histochemical assay. Type I medial gastrocnemius fibers had mean specific tension values of 2.45 +/- 0.47 kg/cm2 (N = 18), whereas, type II single fibers had mean specific tension values of 2.43 +/- 0.67 kg/cm2 (N = 46). Our results suggest that there is no significant difference between the specific tensions of the different muscle fiber types within the cat medial gastrocnemius muscle.

Adenosine Triphosphatases↗
PubMed1987

Comparison between slow sodium channel inactivation in rat slow- and fast-twitch muscle.

1. Voltage-clamp Na+ currents (INa) were studied in rat soleus slow-twitch muscle fibres at about 18 degrees C using the loose-patch-clamp technique. The maximum inward current density was produced by depolarizations to about -19 mV. 2. Fast inactivation was studied utilizing 20 ms conditioning potentials. INa was reduced by 50% with conditioning potentials to about -70 mV. 3. Changes in the conditioning membrane potential produced slow changes in the peak INa due to a slow inactivation process. INa was reduced by 50% at about -86 mV due to slow inactivation. 4. The mean maximum inward INa when slow inactivation was fully removed was 6.83 mA cm-2. 5. Due to the slow inactivation process, slow-twitch fibres were less susceptible to reduction in INa than fast-twitch fibres.

Animals↗
PubMed1987

Radiculomeningeal vascular malformations of the spine: MR imaging.

Three patients (two men, one woman; 63-81 years old) with radiculomeningeal vascular malformations of the spine were examined using high-resolution surface coil magnetic resonance (MR) imaging at 1.5 T. The findings included previously described high-velocity signal loss within the vessels of the malformation as well as previously unreported signal-intensity changes within the cord (long T1/long T2) distal to the malformation. The MR images correlate well with previous reports of location and pathophysiology of these dural lesions.

Aged↗
PubMed1987

See-saw nystagmus and brainstem infarction: MRI findings.

A patient with see-saw nystagmus had a lesion localized by Magnetic Resonance Imaging (MRI) to the paramedian ventral midbrain with involvement of the right interstitial nucleus of Cajal. This the first MRI study of see-saw nystagmus associated with a presumed brainstem vascular event. Our findings support animal and human studies suggesting that dysfunction of the interstitial nucleus of Cajal or its connections is central in this disorder.

Brain Stem↗
PubMed1986

Ionic channels: I. The biophysical basis for ion passage and channel gating.

This article reviews the biophysics of ion passage through membrane pores, as well as the physical factors that control the ion selectivity, gating, and conductance of an ionic channel. Different voltage clamp techniques are discussed in detail. The biophysical properties of sodium channels are reviewed.

Action Potentials↗
PubMed1986

Magnetic resonance imaging in patients with diplopia. A review.

Magnetic resonance imaging may be the procedure of choice for evaluating patients with diplopia; the absence of signals from cortical bone enables the brain stem and individual cranial nerves to be visualized and the imaging planes selected easily, and there is excellent contrast resolution of pathologic lesions. A clinical assessment of diplopia including the identification of associated neurologic disturbances is necessary prior to MR imaging, however, to assure that appropriate anatomic areas are studied and imaging sessions kept within acceptable time limits. The relevant physiology and anatomy critical to normal ocular motility are reviewed and the value of MR imaging for diplopia demonstrated by selected patient examples.

Adult↗
PubMed1985

Effects of glucocorticoid treatment on excitation-contraction coupling.

We studied the myofibrillar calcium affinity and mechanical threshold of single muscle fibers from the extensor digitorum longus (EDL) and soleus muscles of male Sprague-Dawley rats treated with daily intramuscular injections of dexamethasone, 1.5 mg/kg, for 14 days. The strength-duration and pCa-tension relationships of EDL fibers were not altered by glucocorticoid treatment. However, in soleus fibers the mechanical threshold was increased and the myofibrillar calcium sensitivity was reduced by dexamethasone treatment. Glucocorticoid treatment did not change the maximum tension per cross-sectional area of single-skinned EDL or soleus fibers. The glucocorticoid-induced atrophy and impaired force-generating capacity of fast-twitch muscle are probably not caused by impaired excitation-contraction coupling.

Animals↗
PubMed1984

Voltage clamp of rat and human skeletal muscle: measurements with an improved loose-patch technique.

Intact fibres of human intercostal and rat omohyoid muscles were studied at 23 degree C with a loose-patch voltage-clamp technique that employed two concentric micropipettes to electrically isolate small-diameter (10-15 microns) patches of sarcolemma. This method allows investigation of membrane excitability under highly physiological conditions. Step depolarizations to 0 mV elicited sodium inward currents that reached peak values of up to 20 mA/cm2 within 250 microseconds, and then declined. In human muscle, the reversal potential (ENa) was approximately 40 mV, and maximal conductances (GNa) ranged from 44 to 360 mS/cm2. In rat muscle, ENa was 42 mV and GNa ranged from 100 to 250 mS/cm2. Sodium channels in rat and human muscle were indistinguishable in most aspects of their kinetic behaviour and voltage dependence. Outward potassium currents were small by comparison (usually less than 2 mA/cm2) and saturated at positive potentials. The maximum potassium conductance (GK) ranged from 0 to 19 mS/cm2 (human) and from 4 to 12 mS/cm2 (rat muscle).

Action Potentials↗
PubMed1984

Choline acts as agonist and blocker for Aplysia cholinergic synapses.

Several identified neurons of the Aplysia buccal ganglia respond to choline. Iontophoretic applications of either choline or acetylcholine (ACh) to voltage-clamped inhibitory follower neurons produce similar currents. Peak amplitudes of choline responses were 10-100% of ACh responses on the same cell. Choline currents were curare blockable and reversed at -69 +/- 2 mV, within 1 mV of postsynaptic current (IPSC) reversal. Application of 1 mM choline to the bath produces more prolonged effects than an initial conductance change. Choline depressed IPSC amplitude by 42 +/- 5% and prolonged IPSC decay time constant by 25 +/- 7%. The slowing was reversible but the depression was not. Use of choline as a Na substitute may therefore involve unexpected partial agonist action; even where conductance changes are transient or inapparent, choline may alter synaptic responses. Bath choline had variable effects on cholinergic self-inhibitory synapses, blocking in six trials but not in three others. Voltage clamping cells BL and BR7, in which monosynaptic cholinergic PSPs are diphasic, reveals underlying early inward and late outward currents. Choline activates only the late outward current component. Correspondingly, bath choline blocks only the late outward component, as does eserine and ACh. This block is not seen with neostigmine, and so is unlikely to be related to cholinesterase inhibition. The early inward current component, revealed by block of the late component by choline or ACh, decays exponentially. Decay time constant is exponentially dependent on membrane potential over the range -20 to -100 mV, with 63-mV depolarization speeding decay e-fold. Eserine prolongs decay and steepens voltage dependence. The late outward component decays with voltage-independent time constant of 48 +/- 5 ms. Both the time integral of synaptic conductance and the ratio of synaptic charge transfer to peak synaptic current of the early inward component of the cell 7 response are reduced by depolarization. Voltage-dependent duration thus combines with reduced driving force in diminishing the excitatory effect of this component at depolarized levels, allowing the inhibitory component to predominate. In this diphasic synapse, voltage dependence of the time course of one component thus serves an easily identified function.

Acetylcholine↗
PubMed1984

Inhibitors of prostaglandin synthesis or cathepsin B prevent muscle wasting due to sepsis in the rat.

Systemic infection with Streptococcus pneumoniae produced atrophy, decreased twitch and tetanic tension, and altered intracellular electrolyte composition in rat skeletal muscle. Cathepsin B activity was selectively elevated early in the course of illness. Luepeptin, a cathepsin B inhibitor, and indomethacin, a prostaglandin synthesis inhibitor, prevented muscle atrophy and impaired contractility. Indomethacin, but not leupeptin, prevented the intracellular electrolyte changes. Acetaminophen reduced fever but did not prevent muscle atrophy, impaired contractility, or altered intracellular electrolytes. Muscle wasting and impaired contractility associated with sepsis may involve selective prostaglandin stimulation of cathepsin B activity. Intracellular electrolyte changes may involve prostaglandin synthesis but do not require cathepsin B activation.

Animals↗
PubMed1983

Incidence and treatment of peripheral venous thrombosis in patients with glioma.

The incidence, prevention, and treatment of peripheral venous thrombosis were studied retrospectively in 381 patients with malignant glioma. Of 264 patients who did not receive antithrombotic prophylaxis, 97 (36.7%) developed clinical phlebitis confirmed by venography. Sixty-six cases occurred within 6 weeks of craniotomy. By contrast, only 12 (10%) of 117 patients who received intermittent pneumatic pressure to the calves during craniotomy developed phlebitis (4 patients with 6 weeks of the surgery). Of the 109 patients with venous thrombosis, 103 were treated with anticoagulants. Of the 6 patients treated conservatively, 3 died of pulmonary emboli. Intracranial hemorrhage occurred in 1.9% of the patients taking anticoagulants and in 2.2% of those who did not develop phlebitis. We conclude that patients with malignant gliomas have a high risk of developing peripheral venous thrombosis; that antithrombotic therapy reduces the incidence of thrombosis following craniotomy; and that, in patients who develop phlebitis, anticoagulation reduces the risk of pulmonary emboli without increasing the risk of intracranial hemorrhage.

Astrocytoma↗
PubMed1982

Effect of glucocorticoid treatment on the excitability of rat skeletal muscle.

Dexamethasone treatment in the rat produced depolarization of extensor digitorum longus (EDL) muscle fibers but not soleus (SOL) fibers studied in vitro at 23 degrees C. The depolarization of EDL fibers was most prominent after 1 day of treatment (treated -77.5 +/- 1.1 mV, control -87.2 +/- 0.8 mV; mean +/- S.E.), and was associated with elevation of the action potential threshold and reduction of the action potential overshoot. In vivo, or in vitro in chloride-free solution, the resting potential and action potential threshold and overshoot of EDL fibers from glucocorticoid-treated and control rats were similar. Sodium currents were studied with a patch voltage clamp. Glucocorticoid treatment did not alter the voltage dependence of sodium channel activation or inactivation in fast twitch muscle fibers. Maximal inward currents occurred at about -29 mV and half-maximal inward currents at about -50 mV. Sodium channels were half inactivated at about -71 mV. Glucocorticoid treatment did not alter the sarcolemmal resistance or capacitance. We conclude that glucocorticoid treatment does not produce muscle weakness or atrophy by altering the excitability of muscle fibers.

Action Potentials↗