197,546 research outputs found
Krill Ecology - Technical Reports and Systems Guides
No full textProgress Code: completedStatement: See the individual reports for further details.Krill Ecology - Technical Reports and Systems Guides<br/><br/>A series of documents detailing work completed and methods used at the Krill Aquarium located at the Australian Antarctic Division.<br/><br/>Technical Report # Title and Author<br/><br/>Technical Report 1. 26th January 1994. DAPI Epiflourescence Technique. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 2. 5th March 1995. Bag Culture - Cell Growth Count Protocol. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 3. 12th January 1996. Chemical 'Spiking' of Krill Aquarium Bio-filter T12. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 4. 24th June 1996. Cold Temperature Algal Bag Culture Methodology. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 5. 16th April 1997. Algal Bag Culture - Harvesting Method. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 6. 26th October 1999. Aquarium System Bulk Seawater Collection and Storage. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 7. 11th October 1999. Sodium Hypochlorite Treatment of Algal Bag Culture Filtration Unit. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 8. 18th October 1999. Feeding Krill - Algal Strains, Feeding Rate and Nutritional Values. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 9. 22nd November 1999. Krill Biology Section - Parental Algal Culture Maintenance. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 10. 10th April 2000. Krill Group Databases and Maintaining Daily Data Records. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 11. 11th May 2000. Making Up and Use of Iodine Solution as an Indicator of the Presence of Chlorine in Freshwater. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 12. 1st June 2000. Testing for Harmful Ammonia (NH3) in Aquarium Sea Water. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 13. 12th June 2000. Digitron Digilog 2088T Digital Temperature Logger/Gauge - Operating Instructions and Down-Loading Logged Data Guide. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 14. 27th June 2000. Krill Biology - Marine Science Support Shed Gear Storage. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 15. 15th October 2000. Making up of fe Growth Media Stock Solutions for Parental and Algal Bag Culture Production. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 16. 15th January 2001. Algal Bag Culture - Growth Rate Analysis. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 17. 19th July 2004. Protective Epoxy Coating of Onga Seawater Collection Fire Pump. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 18. 27th October 2004. New Krill Aquarium - Bulk Seawater Collection and Storage Logistics. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 19. 11th March 2005. New Krill Aquarium - Algal Bag Culture Filtration System. Author: P. M. Cramp. Australian Antarctic Division. <br/><br/>Technical Report 20. 6th April 2005. New Culture Cabinet Bag to Bag Inoculation Procedure. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 21. 17th June 2005. Agar Bacterial Plate Testing for Krill Algal Culture Stocks. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 22. 29th July 2004. New Algal Culture Cabinet - Bag Culture Setup Methodology. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 23. 24th May 2005. Protocol for Sterilization of Bag Culture Air Supply System. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 24. 30th May 2005. 200 litre tank Algal Batch Culture Setup. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Technical Report 25. 22nd June 2005. Making Up and Shaping Plastic Bags for Algal Culture. Author: P. M. Cramp. Australian Antarctic Division.<br/><br/>Techincal Report 26. 19th December 2005. New Krill Aquarium - Algal Strains, Feeding Rates and Nutritional Values. Author: P. M. Cramp. Australian Antarctic Division
cramp n? / cramp (knot
No full textcramp n.'knot from a tree which one would carry in the pocket in the old days, to keep off or control leg cramps'.DNE Sup [DNE cramp n attrib]G. M. Story JAN. 28 1988[check] WKUsed I and SupUsed I and SupNot Usedcramp knotChecked by Jordyn Hughes Thu 23 Jun 201
cramp ?n/ cramp knot
No full textcramp n.a gnarled lump of wood loggers used to ease foot cramps by rolling it on the ground underneath the cramped foot Is this elabotate naive etymology? Myth? cramp means twisted, gnarled.PRINTED ITEM DNE Sup [check] WKG. M. Story DEC 26 1987Used I and SupUsed I and SupUsed Supcramp knotChecked by Jordyn Hughes Thu 23 Jun 201
Pediatric writer's cramp in myoclonus-dystonia: Maternal imprinting hides positive family history
No full textMyoclonus-dystonia (M-D) is an autosomal dominantly inherited movement disorder with myoclonic jerks and dystonic contractions most frequently due to a mutation in the epsilon-sarcoglycan (SGCE, DYT11) gene. We describe two unrelated children with M-D (DYT11) who presented with writer's cramp. Due to maternal imprinting the family history appeared initially negative for M-D. In children with writer's cramp screening of the SGCE gene should be considered, even with a negative family history. (C) 2008 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved
Clinical, neurophysiological and serological clues for the diagnosis of neuromyotonia and distinction from cramp-fasciculation syndrome
No full textNeuromyotonia and cramp-fasciculation syndrome diagnosis currently relies on neurophysiological examination. In this study we investigated the clinical features and neural antibody profile of patients with neuromyotonia and cramp-fasciculation syndrome to assess the diagnostic value of serological testing. Available sera from adult patients with electromyography-defined neuromyotonia and cramp-fasciculation syndrome were tested for neural antibodies by indirect immunofluorescence on mouse brain sections and live cell-based assays. Forty patients were included, 14 with neuromyotonia and 26 with cramp-fasciculation syndrome. Neural antibodies were detected in 10/10 neuromyotonia sera, most commonly against contactin-associated protein 2 (7/10, 70%), and in 1/20 (5%) cramp-fasciculation syndrome sera. Clinical myokymia, hyperhidrosis, and paresthesia or neuropathic pain were more common in neuromyotonia and mostly associated with contactin-associated protein 2 antibodies. Central nervous system involvement was present in 4/14 (29%) neuromyotonia patients. A tumor was detected in 13/14 (93%) neuromyotonia patients (thymoma, 13), and in 4/26 (15%) with cramp-fasciculation syndrome (thymoma, 1; other neoplasms, 3). Twenty-one/27 (78%) patients achieved a significant improvement or complete remission. Our findings highlight clinical, neurophysiological and serological clues that can be useful in the diagnosis of neuromyotonia and cramp-fasciculation syndrome. Antibody testing is valuable for neuromyotonia diagnosis, while its usefulness in cramp-fasciculation syndrome confirmation is limited
In affectionale remembrance of Frances Cramp, beloved wife of George B. Muir, and daughter of the late J. M. Cramp
No full textCognitive response control in writer's cramp
No full textDisturbances of the motor and sensory system as well as an alteration of the preparation of movements have been reported to play a role in the pathogenesis of dystonias. However, it is unclear whether higher aspects of cortical – like cognitive – functions are also involved. Recently, the NoGo-anteriorization (NGA) elicited with a visual continuous performance test (CPT) during recording of a 21-channel electroencephalogram has been proposed as an electrophysiological standard-index for cognitive response control. The NGA consists of a more anterior location of the positive area of the brain electrical field associated with the inhibition (NoGo-condition) compared with that of the execution (Go-condition) of a prepared motor response in the CPT. This response control paradigm was applied in 16 patients with writer’s cramp (WC) and 14 age matched healthy controls. Topographical analysis of the associated event-related potentials revealed a significant (P < 0.05) NGA effect for both patients and controls. Moreover, patients with WC showed a significantly higher global field power value (P < 0.05) in the Go-condition and a significantly higher difference-amplitude (P < 0.05) in the NoGo-condition. A source location analysis with the low resolution electromagnetic tomography (LORETA) method demonstrated a hypoactivity for the Go-condition in the parietal cortex of the right hemisphere and a hyperactivity in the NoGo-condition in the left parietal cortex in patients with WC compared with healthy controls. These results indicate an altered response control in patients with WC in widespread cortical brain areas and therefore support the hypothesis that the pathogenesis of WC is not restricted to a pure sensory-motor dysfunction
Possible mechanisms of muscle cramp from temporal and spatial surface EMG characteristics
No full text In this study, the initiation and development of muscle cramp are investigated. For this, we used a 64-channel surface electromyogram (EMG) to study the triceps surae muscle during both cramp and maximal voluntary contraction (MVC) in four cramp-prone subjects and during cramp only in another four cramp-prone subjects. The results show that cramp presents itself as a contraction of a slowly moving fraction of muscle fibers, indicating that either the spatial arrangement of the motoneurons and muscle fibers is highly related or that cramp spreads at a level close to the muscle. Spectral analyses of the EMG and peak-triggered average potentials show the presence of extremely short potentials during cramp compared with during MVC. These results can also be interpreted in two ways. Either the motoneurons fire with enlarged synchronization during MVC compared with cramp, or smaller units than motor units are active, indicating that cramp is initiated close to or even at the muscle fiber level. Further research is needed to draw final conclusions. </jats:p
Cramp-fasciculation syndrome associated with monofocal motor neuropathy
No full textINTRODUCTION: Cramp-fasciculation syndrome is a peripheral nerve hyperexcitability disorder, which could be caused by inflammatory neuropathy.
CASE REPORT: We describe a 51-year-old woman who presented with a 4- to 5-year history of fasciculations and painful cramping of the right thenar eminence.
RESULTS: Electrophysiological studies showed motor conduction block in the right median nerve between the axilla and the elbow with fasciculation potentials and cramp discharges on electromyography in the right abductor pollicis brevis muscle. High titers of serum anti-GM1 immunoglobulin M antibodies were detected.
CONCLUSIONS: Monofocal motor neuropathy of the right median nerve was diagnosed. Intravenous immunoglobulin treatment led to significant improvement of symptoms and signs. Although fasciculations and cramps have been reported in multifocal motor neuropathy and are considered supporting criteria for the diagnosis, the occurrence of cramp-fasciculation syndrome as the presenting feature and predominant manifestation in monofocal motor neuropathy, a variant of multifocal motor neuropathy, is uniqu
Neutrophil antimicrobial defense against Staphylococcus aureus. contribution of cathelicidin and the NADPH oxidase
No full textNeutrophils are among the most important components of the innate immune
response, which provides the first line of host defense. The antimicrobial potential of
neutrophils has been traditionally divided into either non-oxidative or oxidative
mechanisms. Two of the most important antimicrobial systems of these mechansims
are granule-associated antimicrobial proteases and peptides and the nicotinamid
adenine dinucleotide phosphate (NADPH) oxidase generating reactive oxygen species
(ROS). In the past, studies often focused on the effects of either non-oxidative or
oxidative mechanisms and decades of research have provided a detailed
understanding of the regulation, generation and actions of these processes alone.
Recent evidence challenged the established view of two independent mechanisms and
proposed the cooperation of the NADPH oxidase with granule proteases in the killing
of microorganisms. Furthermore, a novel phagocytosis-independent antimicrobial
mechanism was found by the discovery of neutrophil extracellular traps (NETs). The
formation of NETs was found dependent on NADPH oxidase activation and the
production of ROS but NETs are believed to kill entrapped pathogens by NETsassociated
granule proteases and peptides. Consequently, NETs present additional
evidence for the interaction of non-oxidative and oxidative killing mechanisms.
Together, these findings opened a new field of investigation with many controversies
to be elucidated and underscored that we need further insight into the mechanisms by
which neutrophils specifically recognize and overcome pathogens.
In this thesis, we followed the question whether the murine antimicrobial peptide
cathelin-related antimicrobial peptide (CRAMP) is an important component of the non-oxidative arm of neutrophil defense against S. aureus. This was motivated
because little is known about cathelicidin function and activity in neutrophils and
seems of crucial interest since mice lack the major constituent of human neutrophils -
the -defensins. We further aimed to specify the relationship between the NADPH
oxidase and CRAMP with focus on the antimicrobial activity of CRAMP in
association with NETs and in NADPH oxidase-deficient mice (gp91phox-/-). As a
result, we could demonstrate a previously unknown intracellular antimicrobial activity
of CRAMP against S. aureus. Specifically, CRAMP colocalized with S. aureus in
phagolysosomes and we showed first evidence for the presence of intracellular active
CRAMP. Most interestingly, phagolysosomal localization and intracellular activity of
CRAMP was found independent of a functional NADPH oxidase controversially to
our expectations. Investigation of NET-dependent killing of S. aureus revealed a
negligible role for CRAMP due to inactivation of the peptide in association with
NETs. This point is of particular relevance and should be considered in the current
opinion of NETs-mediated antimicrobial activity. In summary, our data provided
deeper knowledge about one specific member of the non-oxidative killing mechanism
and gives reason to reconsider the controversial results about interaction of NADPH
oxidase in activating non-oxidative mechanisms.
In addition, we followed the question whether recognition of S. aureus by TLR2
regulates the induction of non-oxidative and oxidative killing responses as well as the
induction of NETs. The background of this study is based on several previous reports.
First, results of our group evidenced a relationship between TLR2-mediated
staphylococcal killing by neutrophils and the susceptibility of S. aureus to cationic
antimicrobial peptides. Additionally, TLR2 activation has been shown to up-regulate 7
cathelicidin expression. Second, TLR2 was demonstrated to induce phosphorylation
of p47phox and up-regulation of p47phox mRNA in macrophages. However, little
attention has been paid to similar studies in neutrophils. Third, recognition of
pathogens by TLRs was hypothesized to induce formation of NETs but there is as yet
no evidence. First results unraveled a role for TLR2 in rapid induction of the NADPH
oxidase, whereas TLR2 signaling had no influence on CRAMP activity. Interestingly,
pathogen sensing for the induction of NETs formation did not depend on TLR2-
MyD88 signaling. Taken together, the results demonstrate a role for TLR2 in
mediating rapid killing of S. aureus by accelerating the activation of the NADPH
oxidase complex possibly by influencing assembly.
Further studies of the mechanisms underlying the relationship between pathogen
sensing and non-oxidative and oxidative killing mechanisms would contribute greatly
to our understanding of how the innate immune system resolves bacterial infections
and will help in the development of therapeutic strategies to assist in clearance of
pathogenic bacteria
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