Disease relevance of NLN

• Reliable prediction of the course of multiple sclerosis for individual patients is not possible from VEP and MEP data [1].
• However, we conclude that, for groups of patients with secondary progressive or relapsing-remitting multiple sclerosis the combined testing of VEP and MEP yields numerical data that allow objective estimation of the course and prognosis of the disease [1].
• A short interruption of tetanus (<1 min) during MEPP-hump quickly reduced MEPP frequency to a level attained under the effect of TMB-8 or thapsigargin, while resuming tetanus swiftly raised MEPP frequency to the previous or higher level [2].
• RESULTS: A total of 16 patients (28.6%) showed MEP evidence of spinal cord ischemia, only 4 of whom had delayed congruent SSEP changes [3].
• In a sample of 28 subacute anterior circulation ischemic stroke patients with severe arm paresis, reduced motor cortex excitability (increased motor thresholds, reduced MEP amplitudes, reduced number of active points) and a reduced conduction velocity in the corticospinal system were found in the affected hemisphere [4].

High impact information on NLN

• The methylerythritol phosphate (MEP or nonmevalonate) pathway, localized in the plastids, is thought to provide IPP and dimethylallyl diphosphate for hemiterpene, monoterpene, and diterpene biosynthesis, whereas the cytosol-localized mevalonate pathway provides C5 units for sesquiterpene biosynthesis [5].
• We suggested earlier that compounds synthesized by the 2-C:-methyl-D-erythritol 4-phosphate (MEP) pathway of isopentenyl pyrophosphate synthesis are responsible for the V gamma 9/V delta 2 T cell reactivity of many pathogens [6].
• To validate the visual and motor evoked potentials (VEP and MEP) as measures for the course of multiple sclerosis, we examined prospectively 30 patients with relapsing-remitting or secondary progressive multiple sclerosis [1].
• The N-terminal amino acid sequence of rat mitochondrial oligopeptidase M contains 19 out of 20 residues identical with a segment of rabbit microsomal endopeptidase and 17 matching the corresponding segment of pig-soluble angiotensin II-binding protein [7].
• Measurements of primary motor cortical excitability (motor evoked potential; MEP), the resting motor threshold (RMT), and cortical inhibition (CI) were taken before and after the rTMS [8].

Chemical compound and disease context of NLN

• Between May 1990 and February 1995, 16 patients with adenocarcinoma or adenosquamous carcinoma of the uterine cervix were prescribed neoadjuvant chemotherapy consisting of cisplatin (50 mg/m2) on day 1, mitomycin C (10 mg/m2) on day 1, and etoposide (100 mg/m2) on days 1, 3, and 5 (MEP) [9].
• Most Streptomyces strains are equipped with only the 2-C-methyl-D-erythritol 4-phosphate (MEP) pathway for the formation of isopentenyl diphosphate, a common precursor of isoprenoids [10].

Biological context of NLN

• In our previous reports, IP3, but not other second messengers releasing Ca2+ from internal Ca2+ stores, is able to enhance the MEPP amplitude [11].
• METHODS: Fifty-six patients (descending thoracic, 25; thoracoabdominal, 31) were monitored intraoperatively with both motor- (MEP) and somatosensory- (SSEP) evoked potentials [3].
• During a sustained MVC, while the motor responses to peripheral and to cortical stimulation grow concurrently, growth of the MEP cannot be entirely accounted for by changes in the muscle action potential [12].
• METHODS: Maximal inspiratory and expiratory pressures (MIP and MEP), sniff nasal inspiratory pressure (SNIP), FVC, peak expiratory flow rate (PEF), and forced expiratory volume in 1 s (FEV1) were measured in 15 healthy subjects before and after 1, 6, and 12 h of exposure to an equivalent altitude of 4267 m in a hypobaric chamber [13].
• There were no apparent changes in the resting membrane potential or the frequency of the miniature endplate potential (MEPP) [14].

Anatomical context of NLN

• Continuous nerve stimulation (20-50 Hz) caused slow transient increases in miniature end-plate potential (MEPP) frequency (MEPP-hump) and intracellular free Ca2+ ([Ca2+]i) in presynaptic terminals (Ca2+-hump) in frog skeletal muscles over a period of minutes in a low Ca2+, high Mg2+ solution [2].
• Miniature endplate potential (MEPP) amplitude distributions, MEPP frequencies and percentages of small MEPPs were determined as well as synaptic vesicle diameters and numbers in the frog neuromuscular junction during La3+ treatment [15].
• There were considerable variations in MEPP frequencies in adjacent junctions so single junctions on edge muscle fibers were recorded for the duration of many experiments and later identified in the electron microscope [15].
• In this study, we examined the effects of IP4 and IP6 on spontaneous transmitter release in the form of miniature endplate potentials (MEPP) and on enhanced vesicular recycling by high K+ at frog motor nerve endings [11].
• In both types of RNAi cell lines, expression of a subset of genes involved in the early stage of monoterpenoid biosynthetic pathway (ESMB genes), including the MEP pathway, is strongly decreased [16].

Associations of NLN with chemical compounds

• Both the Ca2+- and MEPP-humps were blocked by 8-(N, N-diethylamino)octyl3,4,5-trimethoxybenzoate hydrochloride (TMB-8), ryanodine, and thapsigargin, but enhanced by CN-. Thus, Ca2+-hump is generated by the activation of CICR via ryanodine receptors by Ca2+ entry, producing MEPP-hump [2].
• Miniature end-plate potential (MEPP) amplitude decreased in neostigmine-treated preparations [17].
• Furthermore, amantadine had no significant effects on motor thresholds, MEP recruitment curves, CSP, or peripheral excitability [18].
• The mevalonate-independent 2-C-methyl-D-erythritol 4-phosphate (MEP) pathway for isoprenoid biosynthesis is essential in many eubacteria, plants, and the malaria parasite [19].
• Likewise, adenosine (200 microm) reduced miniature EPP (MEPP) frequency, but not amplitude, in a high-K(+) (6 mm) solution [20].

Analytical, diagnostic and therapeutic context of NLN

• After rTMS, MEP size was suppressed in the control group and increased in the patient group, whereas RMT increased in the normal control group and decreased in the patient group [8].
• The short-latency electromyographic response evoked by transcranial magnetic stimulation (MEP) increases in size during fatigue, but the mechanisms are unclear [12].
• Side effects of chemotherapy with MEP were within acceptable limits [9].
• One stage IIB patient, 1 stage IIIB patient and 1 stage IVB patient underwent standard radiotherapy and 1 stage IIIB patient underwent chemotherapy with another regimen because MEP therapy was without effect [9].
• CONCLUSIONS: The results demonstrate that compared with SSEP, MEP, especially myogenic MEP, is more sensitive and specific in detection of spinal cord ischemia, and that intraoperative monitoring can indeed help prevent paraplegia [3].

References