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Abstract  

The Laboratory of the Government Chemist (LGC) is a focal point for the production, analysis and certification of reference materials. Within the field of thermal analysis the LGC is concerned with the development of purity standards and materials certified for enthalpy of fusion and melting point. For some time the LGC has been concerned with the significant differences in purity data which can be produced by the different manufactures' differential scanning calorimeters. This paper will highlight the initiatives the LGC is undertaking in overcoming this uncertainty in purity measurements through the use of certified thermal standards.

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Abstract  

A melting point measurement facility for the UK has been developed and accredited to ISO/IEC 17025 Calibration status for the determination of the liquefaction temperature of pure substances from 35 to 250°C. The facility is based upon a commercial instrument, i.e. an oil bath fitted with an aluminium block (Isotech, model 798 EHT), a precision multimeter (Isotech TTI-7), a thermocouple directly inserted in the sample under investigation and a platinum resistance thermometer (PRT) tracking the block temperature. The homogeneity of temperature bath/block was investigated and the PRT used for the traceability of the measurements was calibrated by NPL and traceable to ITS-90. The process was validated using four current LGC Certified Reference Materials (CRMs): •  Phenyl salicylate; material number: LGC2411, batch number: 001; liquefaction point: 41.85±0.05°C •  4-Nitrotoluene; material number: LGC2401, batch number: 007; liquefaction point: 51.71±0.21°C •  Benzoic acid; material number: LGC2405, batch number: 005; liquefaction point: 122.37±0.21°C •  Carbazole; material number: LGC2409, batch number: 007; liquefaction point: 245.58±0.07°C •  Different approaches were used to identify reproducible features of the melting point (time-temperature) curves of these four CRMs. Excellent correlation was observed between the certified values for the liquefaction point of the four CRMs and the temperature at the end of their respective melting point curve plateau, determined using a temperature differential approach. An uncertainty budget was derived and the expanded uncertainty at the 95% confidence interval (k=2) was found to be •  Phenyl salicylate: ±0.20°C; 4-Nitrotoluene: ±0.17°C; Benzoic acid: ±0.24°C; Carbazole: ±0.27°C

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Abstract

Though several treatments effectively address the pervasive impact of trauma, they do not achieve complete symptom resolution for all clients, inspiring the search for alternatives. Internal Family Systems (IFS) therapy has grown popular, especially in informal psychedelic-assisted treatments (PAT). Compared to stereotypes of empirically validated, exposure-based treatments, IFS has novel facets with widespread appeal. The model encourages improved quality of interactions among multiple, naturally arising “parts” or subpersonalities potentially generated by traumatic experience. The body of IFS literature is extensive, enthusiastic, and thought-provoking. Outcome data for applying the model to Post-Traumatic Stress Disorder are limited. Attempts to operationalize and falsify the theory's assumptions and proposed mechanisms will likely prove challenging. Nevertheless, the model's popularity underscores a problem with perceptions of the empirically-supported treatments. Contemplating ethical ways to present the IFS approach given the state of relevant research, we note strategies that would apply to recommendations for PAT of any type. These strategies include detailed psychoeducation about empirically-supported treatments, candid description of the experimental nature of alternatives, frequent assessments of improvement, and detailed monitoring of potential iatrogenic effects. Drawing on facets of IFS to improve perceptions of the empirically validated treatments might provide an efficient way to appeal to more clients, decrease drop out, and increase gains as we await results of empirical investigations of IFS-influenced PAT. These steps can allow clients to choose an approach consistent with their own impressions of a credible intervention, potentially leading to better outcomes.

Open access
Interventional Medicine and Applied Science
Authors:
Peethambaran Arun
,
Manojkumar Valiyaveettil
,
Lionel Biggemann
,
Yonas Alamneh
,
Yanling Wei
,
Samuel Oguntayo
,
Ying Wang
,
Joseph B. Long
, and
Madhusoodana P. Nambiar

Abstract

Emerging studies show that blast exposure causes traumatic brain injury (TBI) and auditory dysfunction without rupture of tympanic membrane, suggesting central auditory processing impairment after blast exposure. There is limited information on the mechanisms of blast-induced TBI and associated peripheral and central auditory processing impairments. We utilized a repetitive blast exposure mouse model to unravel the mechanisms of blast TBI and auditory impairment. C57BL/6J mice were exposed to three repeated blasts (20.6 psi) using a shock tube, and the cerebellum was subjected to proteomic analysis. The data showed that calretinin and parvalbumin, two major calcium buffering proteins, were significantly up-regulated after repeated blast exposures, and this was confirmed by Western blotting. Since these proteins are reportedly involved in auditory dysfunction, we examined the inner ear and found both calretinin and parvalbumin were up-regulated, suggesting that modulation of these proteins plays a role in blast-induced peripheral and central auditory processing impairments. Expression of cleaved caspase-3 was also up-regulated in both regions indicating ongoing cellular apoptosis, possibly due to altered calcium homeostasis. These results provide a molecular basis for changes in central and peripheral auditory processing involving abnormal calcium homeostasis resulting in hearing impairment after blast exposure.

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Pasteurella multocida B:2 is responsible for haemorrhagic septicaemia in cattle and buffaloes, causing severe economic losses in the developing countries. In the present study, the ahpA gene of P. multocida B:2 (P52) was cloned, sequenced and compared with the previously reported ahpA gene sequence in P. multocida A:1, which is responsible for its haemolytic phenotype. E. coli DH5α cells were further transformed with recombinant plasmid carrying the ahpA gene from P. multocida B:2 (P52) but SDS-PAGE analysis failed to show the expression of haemolysin protein. Slight haemolysis was albeit observed in horse blood agar plates streaked with recombinant E. coli carrying the ahpA gene. Our study indicates that there is 99.6% similarity and 0.4% divergence between ahpA gene of P. multocida B:2 (P52) and P. multocida A:1, while membrane topology analysis has predicted that ahpA is an inner membrane protein with two strong hydrophobic regions at the N and C terminals. The presence of significant homology in ahpA sequence in A:1 and B:2 perhaps suggests a common mechanism of pathogenesis in different species of animals.

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