Hyperkalemic periodic paralysis (HyperKPP) is an autosomal dominant human skeletal muscle channelopathy that causes periods of myotonic discharge and periodic paralysis due to defective Nav1.4 sodium channels. Patients are asymptomatic at birth, attacks become short and frequent during childhood, and more severe during adolescence. Since the Nav1.4 content in the cell membrane is relatively constant during childhood, it was hypothesized that some symptoms start with the defective Nav1.4 channels, while other symptoms start after some changes occur in gene expression affecting other membrane channel content and/or activity. To test the hypothesis, the contractile characteristics of EDL and soleus muscles from HyperKPP mice from the age of 0.5 to 12 months were tested in vitro. For both EDL and soleus, contractile defects, including low force generation, instability and large unstimulated force were observed by two weeks of age. With aging, the defects did not worsen, but muscles actually showed some improvement. Considering that Nav1.4 protein content reaches maximum at three weeks of age, the data suggests that HyperKPP symptoms are solely due to the defective Nav1.4 channels.

Hyperkalemic periodic paralysis (HyperKPP) is an autosomal dominant human skeletal muscle channelopathy that causes periods of myotonic discharge and periodic paralysis due to defective Nav1.4 sodium channels. Patients are asymptomatic at birth, attacks become short and frequent during childhood, and more severe during adolescence. Since the Nav1.4 content in the cell membrane is relatively constant during childhood, it was hypothesized that some symptoms start with the defective Nav1.4 channels, while other symptoms start after some changes occur in gene expression affecting other membrane channel content and/or activity. To test the hypothesis, the contractile characteristics of EDL and soleus muscles from HyperKPP mice from the age of 0.5 to 12 months were tested in vitro. For both EDL and soleus, contractile defects, including low force generation, instability and large unstimulated force were observed by two weeks of age. With aging, the defects did not worsen, but muscles actually showed some improvement. Considering that Nav1.4 protein content reaches maximum at three weeks of age, the data suggests that HyperKPP symptoms are solely due to the defective Nav1.4 channels.

Objective: To compare the effects of thiopental, propofol and alfaxalone on arytenoid cartilage motion and establish dose rates to achieve a consistent oral laryngoscopy examination. Study design: Prospective, randomised, blinded crossover study. Animals: Six healthy adult beagle dogs. Methods: Each dog was administered three induction agents in a random order with a one week washout period between treatments. No premedication was used prior to induction of anaesthesia. Thiopental, propofol or alfaxalone were administered at 7.5 mg/kg, 3 mg/kg and 1.5 mg/kg, over 1 minute to effect, for induction of anaesthesia, respectively. If the dog was deemed inadequately anaesthetised then top-up boluses of 1.8 mg/kg, 0.75 mg/kg and 0.4 mg/kg, respectively, were administered over 10 seconds, repeated every 20 seconds, until an adequate anaesthetic plane had been reached. Continual examination of the larynx, using a laryngoscope, commenced once an adequate anaesthetic depth had been reached until recovery from anaesthesia. The number of arytenoid motions and deep inspiratory efforts (vital breaths) were counted within three time periods and compared over time among treatments. Data were analysed using Friedman test, Mann-Whitney U test, Spearman's rho, linear mixed model with post-hoc pairwise comparison with Tukey correction. Results interpreted at a 5% level of significance. Results: The median (range) induction time was 2.8 (2.0, 3.0), 2.7 (2.0, 3.3) and 2.5 (1.7, 3.3) minutes for thiopental, propofol and alfaxalone, respectively (p = 0.727). The median (range) dose rate required to achieve an adequate depth of anaesthesia was 6.3 (6.0, 6.6), 2.4 (2.4, 2.4) and 1.2 (1.2, 1.2) mg/kg/minute for thiopental, propofol and alfaxalone, respectively. Therefore, the median (range) total dose administered over the induction time was 17.8 (13.2, 18.8), 6.8 (5.3, 8.3) and 3.2 (2.3, 4.1) mg/kg for thiopental, propofol and alfaxalone, respectively. There was no significant difference for the total number of arytenoid motions (p =0.662) or vital breaths (p = 0.789) among induction agents. The median (range) examination times were 14.1 (8.0, 41.8), 5.4 (3.3, 14.8) and 8.5 (3.8, 31.6) minutes for thiopental, propofol and alfaxalone, respectively (p=0.016). Conclusion and clinical relevance: There was no significant difference in the total number of arytenoid motions among the induction agents. However, at the dose rates used in this study, propofol provided adequate conditions for evaluation of the larynx within a shorter examination time which may be advantageous during laryngoscopy in dogs. / Mini Dissertation (MMedVet)--University of Pretoria, 2016. / Companion Animal Clinical Studies / MMedVet / Unrestricted

Sleep paralysis is a condition in which the REM sleep in an individual fails to disengage after they awaken. This leads to full body paralysis, during which vivid and often terrifying hallucinations occur. I myself suffer from sleep paralysis. That being said, I have always been intrigued by the concept of exploring serious topics through the use of comedy. In essence, that is what my project is about. I wanted to make light of sleep paralysis. By doing so, I hoped to deescalate the terror in the mind of the sufferer. Comedy is possibly the most effective method I have in my arsenal, as I have found that it has helped me to overcome my own issues with the condition. I have attempted to create a source of information for my fellow sufferers that is both informative and non-threateningly simple in its delivery of the information. To summarize, this project was to give people like me something that I never had access to when I first developed the condition and was severely unprepared for dealing with it. I aim to be an artist that is both humorous and helpful in everything that I do, and it is my hope that I was able to succeed in this task.

Neuromuscular paralysis caused by salivary proteins of ticks is a well-known complication after tick bites in Australia, North America, and South Africa. Symptoms may include general weakness, difficulty walking, ascending paralysis, and bulbar paralysis with diplopia, culminating in respiratory failure. In Europe, toxin-mediated paralysis has rarely been noted. We report a case of cranial nerve paralysis with delayed onset after a tick bite in northern Germany.

No description available.

Diss. (sammanfattning) Linköping : Univ., 2002. / Härtill 4 uppsatser.

No description available.

Hyperkalemic periodic paralysis, HyperKPP, is an inherited progressive disorder of the muscles caused by mutations in the voltage gated sodium channel (NaV1.4). The objectives of this thesis were to develop a technique for measurement symptoms in vivo using electromyography (EMG) and to determine the mechanism by which Ca2+ alleviates HyperKPP symptoms, since this is unknown. Increasing extracellular [Ca2+] ([Ca2+]e) from 1.3 to 4 mM did not result in any increases in45Ca2+ influx suggesting no increase in intracellular [Ca2+] ([Ca2+]i) acting on an intracellular signaling pathway or on an ion channel such as the Ca2+sensitive K+ channels. HyperKPP muscles have larger TTX-sensitive22Na+ influx than wild type muscles because of the defective NaV1.4 channels. When [Ca2+] was increased from 1.3 to 4 mM, the abnormal 22Na+ influx was completely abolished. Thus, one mechanism by which Ca2+alleviates HyperKPP symptoms is by reducing the abnormal Na+ influx caused by the mutation in the NaV1.4 channel.

In James Joyce criticism, and by implication Irish and modernist studies, the word paralysis has a very insular meaning. The word famously appears in the opening page of Dubliners, in “The Sisters,” which predated the collection’s 1914 publication by ten years, and in a letter to his publisher Grant Richards. The commonplace conception of the word is that it is a metaphor that emanates from the literal fact of the Reverend James Flynn’s physical condition the narrator recalls at the beginning of “The Sisters.” As a metaphor, paralysis has signified two immaterial, or spiritual, states: one individual or psychological and the other collective or social. The assumption is that as a collective and individual signifier, paralysis is the thing from which Ireland needs to be freed. Rather than relying on this received tradition of interpretation and assumptions about the term, I consider that paralysis is a two-sided term. I argue that paralysis is a problem and a solution and that sometimes what appears to be an escape from paralysis merely reinforces its negative manifestation. Paralysis cannot be avoided. Rather, it is something that should be engaged and used to redefine individual and social states.