Treatment of spasmodic dysphonia (laryngeal dystonia) with local injections of Botulinum toxin

In 1984 the authors performed the first laryngeal injection of Botulinum toxin for laryngeal dystonia via percutaneous, electromyographically guided technique. Since that time we have treated 450 patients with adductor spasmodic dysphonia, abductor spasmodic dysphonia, and adductor breathing dystonia. In general, the adductor patients received bilateral injections of 1.25 U to 3.75 U, obtaining greater than 90% of normal voice. The abductor patients received unilateral or staged bilateral injections of the posterior cricoarytenoid muscles with 0.6 to 3.75 U, obtaining 70% of normal function. We have found laryngeal injections of Botulinum toxin to be safe and effective therapy for the symptoms of laryngeal dystonia (spasmodic dysphonia).     

LOCATION OF 43 kD MOSQUITO-LARVICIDAL TOXIN GENE OF HIGHLY TOXIC Bacillus sphaericus 10

The direct evidence of the location of the mosquito-larvicidal gene of Bacillus sphaericus10 (isolated from Jiangsu Province of China) on megaplasmid pFW1 was given by molecularcloning. The clone (pFL109) containing the 1.4 kb HindⅢ DNA fragment from pFW1expressed the mosquito-larvicidal toxin protein (43 kD). The location of the gene codingfor the 43 kD toxin protein within the Xhol B fragment on the restriction map of pFW1 wasconfirmed by Southern blotting using the 1.4 kb HindⅢ DNA fragment as a probe. The non-toxic strains of Bacillus sphaericus were revealed to be 43 kD toxin gene dele-tion mutants by Southern and Western analyses. The 1.4 kb HindⅢ fragment of pFL109 can be used as a probe for differentiating thenon-toxic strains of Bacillus sphaericus from the toxic ones.     

Botulinum toxin treatment of spasmodic dysphonia: Techniques, indications, efficacy

A group of 58 patients with spasmodic dysphonia (SD) was treated perorally or transcutaneously with botulinum toxin (BT), and followed for at least 6 months. Most were treated by peroral injection using indirect laryngoscopy to facilitate precise placement. An effort was made to disperse the toxin over the entire thyroarytenoid muscle in order to affect the greatest number of motor end-plates using the smallest possible effective dose. Severely symptomatic patients with primarily adductor SD had the best results. A potentiation effect is suggested by analysis of a subpopulation of patients, mostly injected unilaterally, for whom the outcome was more favorable for those who had had prior injections. One-month postinjection studies reflect significant improvement in measured readings of a standard passage, and this is consistent with the subjective and perceptual improvements noted. There were no severe complications. Peroral injection seems inadvisable for patients with mixed or abductor SD as well as for those with an uncontrollable gag reflex.     

Botulinum toxin in the treatment of recalcitrant mutational dysphonia

Mutational falsetto is the failure of the normal drop in vocal pitch at puberty. Voice therapy almost always achieves an appropriate pitch; however, in cases of failure, surgical treatment has also been recommended. We report a case of a 47-year-old man with an above-average fundamental frequency and a thin voice quality in the absence of any signs of androgen insufficiency. Laryngeal examination revealed atrophy of the vocalis muscle. Voice therapy was unsuccessful in achieving a stable voice. Injection of 15 units of botulinum toxin into each cricothyroid muscle initially resulted in aphonia, but the voice returned by 1 week. Average fundamental frequency was 84 Hz at 1 week, 104 Hz at 1 month, and 100 Hz at 1 year. We hypothesize that mutational dysphonia is an habitual dysfunction of the voice with inappropriate activation of the cricothyroid muscle and disuse of laryngeal adductor muscles. Temporary deactivation of the cricothyroid muscle enforces adoption of a more appropriate vocal mechanism. Botulinum toxin as an adjunct to voice therapy should be considered before surgical alteration of the glottis in patients with recalcitrant mutational falsetto.     

Tetraphenylethylene‐based Glycoconjugate as a Fluorescence “Turn‐On” Sensor for Cholera Toxin

Tetraphenylethylene (TPE)‐based glycoconjugates were easily synthesized by copper(I)‐catalyzed “click reactions” between propargyl‐attached TPE and azido‐functionalized sugars. The TPE compound bearing lactosyl moieties ( Lac‐TPE ) was found to be a fluorescence “turn‐on” sensor for cholera toxin by virtue of aggregation‐induced emission characteristics of the TPE motif owing to the specific interaction of lactose with the cholera toxin B subunit, whilst a cellobiose‐functionalized TPE derivative did not show any response to the toxin. Therefore, Lac‐TPE shows promising applications in the detection of cholera toxin, as well as in the investigation of carbohydrate–protein interaction.     

A European perspective on progress in moving away from the mouse bioassay for marine-toxin analysis

This review considers the ethical and technical problems currently associated with employing mouse bioassays for marine-toxin analysis and the challenges and the difficulties that alternative methods must overcome before being deemed applicable for implementation into a regulatory monitoring regime. We discuss proposed alternative methods, classified as functional, immunological and analytical, for well-established European toxins as well as emerging toxins in European waters, highlighting their advantages and disadvantages. We also consider emerging tools and technologies for future toxin analysis.Even though regulatory bodies have recently recommended analytical methods for a number of toxins, there is still scope for functional and immunological methods in rapid screening and detecting emerging toxins. Future developments foreseen in the analysis of marine biotoxins are multiplex-based analysis, miniaturization and portability for on-site testing. However, the longstanding lack of reference materials and standards continues to pose a severe limitation on progress in development, validation and therefore implementation of any alternative method based on the criteria stipulated by European Union legislation.     

Dynamic adsorption of diarrhetic shellfish poisoning (DSP) toxins in passive sampling relates to pore size distribution of aromatic adsorbent

Solid-phase adsorption toxin tracking (SPATT) technology was developed as an effective passive sampling method for dissolved diarrhetic shellfish poisoning (DSP) toxins in seawater. HP20 and SP700 resins have been reported as preferred adsorption substrates for lipophilic algal toxins and are recommended for use in SPATT testing. However, information on the mechanism of passive adsorption by these polymeric resins is still limited. Described herein is a study on the adsorption of OA and DTX1 toxins extracted from Prorocentrum lima algae by HP20 and SP700 resins. The pore size distribution of the adsorbents was characterized by a nitrogen adsorption method to determine the relationship between adsorption and resin porosity. The Freundlich equation constant showed that the difference in adsorption capacity for OA and DTX1 toxins was not determined by specific surface area, but by the pore size distribution in particular, with micropores playing an especially important role. Additionally, it was found that differences in affinity between OA and DTX1 for aromatic resins were as a result of polarity discrepancies due to DTX1 having an additional methyl moiety.     

T-2 Toxin—The Most Toxic Trichothecene Mycotoxin: Metabolism,Toxicity, and Decontamination Strategies

Among trichothecenes, T-2 toxin is the most toxic fungal secondary metabolite produced by different Fusarium species. Moreover, T-2 is the most common cause of poisoning that results from the consumption of contaminated cereal-based food and feed reported among humans and animals. The food and feed most contaminated with T-2 toxin is made from wheat, barley, rye, oats, and maize. After exposition or ingestion, T-2 is immediately absorbed from the alimentary tract or through the respiratory mucosal membranes and transported to the liver as a primary organ responsible for toxin''s metabolism. Depending on the age, way of exposure, and dosage, intoxication manifests by vomiting, feed refusal, stomach necrosis, and skin irritation, which is rarely observed in case of mycotoxins intoxication. In order to eliminate T-2 toxin, various decontamination techniques have been found to mitigate the concentration of T-2 toxin in agricultural commodities. However, it is believed that 100% degradation of this toxin could be not possible. In this review, T-2 toxin toxicity, metabolism, and decontamination strategies are presented and discussed.