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for monitoring and management of hardware resources, virtualized environments, and applications Ops Center monitors the health of the operating system and the hardware resources for a variety of systems, including the Exadata Database Machine Some of the hardware monitoring and management features of Ops Center are monitoring of hardware health status, power management and monitoring, ability to turn systems on and off, and monitoring the hardware connectivity Ops Center also enables you to monitor the health of your Solaris, Linux, and Windows operating systems, including network connectivity, file system status, CPU usage, memory usage, and network bandwidth utilization Ops Center monitors certain parameters of the hardware and OS components that are of interest, and when these parameters cross predefined thresholds, notifications can be triggered You can edit the thresholds that control how OS monitoring takes place You can use notification profiles that trigger alerts to specific users Refer to the Oracle Enterprise Manager Ops Center documentation for further details on managing and monitoring with Ops Center Oracle Enterprise Manager Ops Center Connector If you utilize the monitoring capabilities of Ops Center within the Enterprise Manager Grid Control Console, you get the benefit of monitoring the storage, hardware, OS, and all the way up to the applications and the critical business services by using a centralized management console This integration of Ops Center with Enterprise Manager is possible through the Oracle Management Connector for Ops Center Using the connector, you can view consolidated information of the Exadata Database Machine servers, the network, and operating systems, within a single unified Grid Control Console The connector also enables the integration of alert notifications of Ops Center with Oracle Enterprise Manager The notifications in Ops Center triggered due to Exadata Database Machine hardware component failures, or due to issues with operating system performance, or failures related to software components, will now become alerts in the Oracle Enterprise Manager When combined with the System Monitoring Plug-in for Exadata, this capability provides a centralized platform for managing alerts, allowing you to better correlate alerts from Exadata Storage Servers with the alerts from Ops Center and accelerate the root-cause analysis when investigating issues.

(Isaacs and Barlow) One constellation consists of short stature, ptosis, strabismus, highly arched palate, dislocated patellae, and kyphoscoliosis, which has been noted in some families (KingDenborough syndrome) As mentioned in Chap 52 on the congenital polymyopathies, central core (multicore) myopathy (page 1247) is frequently complicated by malignant hyperthermia This is understandable insofar as both disorders have been linked to the gene encoding the ryanodine receptor; the two diseases are due to allelic variations (Quane et al) It has been pointed out that another rare muscle disease Evans myopathy (named after the affected family) may be a common predisposing condition It is inherited as an autosomal trait and may be asymptomatic until the anesthetic reaction, but some patients have wasting of the distal thigh muscles and an elevation of serum CK concentration (see Harriman et al) Diagnostic Testing Various tests for susceptibility to malignant hyperthermia have undergone phases of popularity The only currently valid test involves in vitro exposure of a muscle biopsy specimen to halothane and to caffeine and the detection of muscle contracture with both agents This is performed only in a few centers, which are listed at wwwmhausorg The review by Denborough may be consulted for further details on the testing and on the general aspects of the disease Treatment This consists of discontinuation of anesthesia at the rst hint of masseter spasm or rise of temperature The intravenous administration of dantrolene, which inhibits the release of calcium from the sarcoplasmic reticulum, may be lifesaving An infusion of 1 mg/kg is given initially and increased slowly until symptoms subside, the total dosage not to exceed 10 mg/kg Other measures should include body cooling, intravenous hydration, sodium bicarbonate infusions to correct acidosis, and mechanical hyperventilation to decrease acidosis Halothane and other volatile anesthesic agents and succinylcholine should thereafter be avoided in such individuals, and any surgical procedures, if necessary, should be done under nitrous oxide, fentanyl, thiopental (or other barbiturate), or local anesthesia Intravenous dantrolene, 25 mg/kg given slowly 1 h prior to anesthesia, prevents the syndrome.

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1 Unplug the Mouse, turn it upside-down and remove the retaining ring (usually by twisting it counter-clockwise) 2 Slowly invert the mouse so that the ball drops into your hand 3 If the ball is dirty or sticky, you can clean it with soapy water 4 Locate the rollers inside the mouse (see Figure 3-1) There are typically two long black rollers and one small metallic roller 5 Use your fingers to remove the ring of dust from each roller, taking care not to let any material fall even further into the mouse 6 If the rollers are sticky or if Step 5 is insufficient to clean the rollers, use a cotton swab dipped in isopropyl alcohol to clean them 7 When you are finished, replace the mouse ball and retaining ring, ensuring that they are secured in place

interest Only recently has it been appreciated that one form of periodic paralysis, Andersen disease, is associated with the voltagegated potassium channel

Andersen and coworkers rst drew attention to a distinct form of potassium-sensitive periodic paralysis characterized by the triad of periodic potassium-sensitive weakness, ventricular dysrhythmias with long QT syndrome, and dysmorphic features (micrognathia, short stature, scaphocephaly, hypertelorism, broad nose, low-set ears, and short index ngers) From a study of 11 additional patients with Andersen syndrome from 5 kindreds, Sansone and colleagues point out that attacks of paralysis can be associated with hypo-, normo-, or hyperkalemia and that a prolonged QT interval is an integral feature of the disease (and sometimes the only sign in a given family) Plaster and colleagues have demonstrated that most cases of Andersen disease are a consequence of dominant negative mutations in the gene KCNJ2 that encodes a particular type of K channel In vitro studies indicate that the mutation impairs the ability of preformed channels to migrate to the membrane surface and also impedes the current carrying capacity of the potassium channel system This defect would be expected to impair repolarization of the muscle membrane, thereby making both skeletal and cardiac muscle hyperexcitable

Morvan s Fibrillary Chorea (Choree Fibrillaire)

FIGURE 3-1

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