Ionisk selvsamling med farvestoffet hydroxynaphtol blue og tensidet benzyldimethyldodecylammonium- chlorid

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The Relative Contributions of the Medial Sural and Peroneal Communicating Nerves to the Sural Nerve

The medial sural cutaneous nerve (MSCN) and peroneal communicating nerve (PCN) conjoin in the calf area to form the sural nerve (SN). In previous anatomic studies, there was unresolved debate as to the main contributor to the sural nerve, and the relative contributions of MSCN and PCN had not been studied. The purpose of this study is to determine their relative neurophysiologic contributions to the SN by nerve conduction study (NCS). A total of 47 healthy subjects (25 males and 22 females, mean age 29.6 ± 10.4 yrs, range 20-59 yrs) participated in the study. This study employed the orthodromic nerve conduction technique: stimulation at the ankle and recording at the mid calf (SN); specifically, we preformed stimulation at the mid calf (MSCN, PCN) and recording at 14 cm proximal to the middle of the popliteal fossa (MSCN) and fibular head (PCN). The onset and peak latencies (ms) were SN 2.3 ± 0.2 and 3.0 ± 0.2; MSCN 2.1 ± 0.2 and 2.8 ± 0.2; and PCN 2.1 ± 0.2 and 2.8 ± 0.2. The peak-to-peak amplitudes (µV) and areas (nVsec) of the SN, MSCN, and PCN were 9.7 ± 3.9, 7.0 ± 4.7, and 5.0 ± 3.2; and 7.2 ± 2.9, 5.7 ± 3.4, and 4.0 ± 2.4, respectively. The side-to-side difference was not statistically significant. The main contributor to the SN was found to be the MSCN. The relative contribution ratio of the MSCN to the PCN was 1.37:1 by amplitude and 1.42:1 by area. However, in 32.9% of the subjects, the contribution of the PCN was greater than that of the MSCN

Conduction in ulnar nerve bundles that innervate the proximal and distal muscles: a clinical trial

<p>Abstract</p> <p>Background</p> <p>This study aims to investigate and compare the conduction parameters of nerve bundles in the ulnar nerve that innervates the forearm muscles and hand muscles; routine electromyography study merely evaluates the nerve segment of distal (hand) muscles.</p> <p>Methods</p> <p>An electrophysiological evaluation, consisting of velocities, amplitudes, and durations of ulnar nerve bundles to 2 forearm muscles and the hypothenar muscles was performed on the same humeral segment.</p> <p>Results</p> <p>The velocities and durations of the compound muscle action potential (CMAP) of the ulnar nerve bundle to the proximal muscles were greater than to distal muscles, but the amplitudes were smaller.</p> <p>Conclusions</p> <p>Bundles in the ulnar nerve of proximal muscles have larger neuronal bodies and thicker nerve fibers than those in the same nerve in distal muscles, and their conduction velocities are higher. The CMAPs of proximal muscles also have smaller amplitudes and greater durations. These findings can be attributed to the desynchronization that is caused by a wider range of distribution in nerve fiber diameters.</p> <p>Conduction parameters of nerve fibers with different diameters in the same peripheral nerve can be estimated.</p

Polyphenols enhance the activity of alkylating agents in leukaemia cell lines

Polyphenols have been shown to sensitize solid tumours to alkylating agents such as cisplatin, and induce apoptosis and/or cell-cycle arrest. Here, we assess the effects of five polyphenols alone and in combination with three alkylating agents: cisplatin, cyclophosphamide and chlorambucil in lymphoid and myeloid leukaemia cells lines, and non-tumour control cells. In lymphoid leukaemia cell lines there was a synergistic reduction in ATP and glutathione levels, an induction of cell cycle arrest, DNA damage and apoptosis when quercetin, apigenin, emodin and rhein were combined with cisplatin and cyclophosphamide; and when apigenin and rhein were combined with chlorambucil. In myeloid leukaemia cells quercetin, apigenin and emodin showed a similar synergistic effect with all alkylating agents; however antagonistic effects were observed with some or all alkylating agents when combined with emodin, rhein and cis-stilbene. All synergistic effects were associated with reduced glutathione levels, DNA damage and apoptosis; whilst during antagonism the reverse effects were observed. The combination of alkylating agents, particularly cisplatin with polyphenols could be promising for the treatment of lymphoid leukaemias, with apigenin showing the greatest effects. Likewise in myeloid cells apigenin also synergised the action of all alkylating agents, suggesting that apigenin may also be beneficial in myeloid leukaemias

Tissue Plasminogen Activator–Mediated Fibrinolysis Protects against Axonal Degeneration and Demyelination after Sciatic Nerve Injury

Tissue plasminogen activator (tPA) is a serine protease that converts plasminogen to plasmin and can trigger the degradation of extracellular matrix proteins. In the nervous system, under noninflammatory conditions, tPA contributes to excitotoxic neuronal death, probably through degradation of laminin. To evaluate the contribution of extracellular proteolysis in inflammatory neuronal degeneration, we performed sciatic nerve injury in mice. Proteolytic activity was increased in the nerve after injury, and this activity was primarily because of Schwann cell–produced tPA. To identify whether tPA release after nerve damage played a beneficial or deleterious role, we crushed the sciatic nerve of mice deficient for tPA. Axonal demyelination was exacerbated in the absence of tPA or plasminogen, indicating that tPA has a protective role in nerve injury, and that this protective effect is due to its proteolytic action on plasminogen. Axonal damage was correlated with increased fibrin(ogen) deposition, suggesting that this protein might play a role in neuronal injury. Consistent with this idea, the increased axonal degeneration phenotype in tPA- or plasminogen-deficient mice was ameliorated by genetic or pharmacological depletion of fibrinogen, identifying fibrin as the plasmin substrate in the nervous system under inflammatory axonal damage. This study shows that fibrin deposition exacerbates axonal injury, and that induction of an extracellular proteolytic cascade is a beneficial response of the tissue to remove fibrin. tPA/plasmin-mediated fibrinolysis may be a widespread protective mechanism in neuroinflammatory pathologies

Electrodiagnostic evaluation of carpal tunnel syndrome

Carpal tunnel syndrome (CTS) is the most common nerve entrapment. Electrodiagnostic (EDX) studies are a valid and reliable means of confirming the diagnosis. This monograph addresses the various EDX techniques used to evaluate the median nerve at the wrist. It also demonstrates the limitations of EDX studies with a focus on the sensitivity and specificity of EDX testing for CTS. The need to use reference values for populations such as diabetics and active workers, where normative values differ from conventional cutoffs used to confirm suspected CTS, is presented. The value of needle electromyography (EMG) is examined. Muscle Nerve, 2011Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/87013/1/22208_ftp.pd