TCS 5861528

Rhamnolipid-enhanced aerobic biodegradation of triclosan (TCS) by indigenous microorganisms in water-sediment systems.[Pubmed:27476727]

Sci Total Environ. 2016 Nov 15;571:1304-11.

Bioremediation of triclosan (TCS) is a challenge because of its low bioavailability, persistence in the environment and recalcitrance to remediation efforts. Rhamnolipid (RL) was used to enhance TCS biodegradation by indigenous microbes in an aerobic water-sediment system. However, knowledge of the effects of TCS on the bacterial community and environmental factors in an RL-enhanced, TCS-degrading system are lacking. Therefore, in this study, the influence of environmental factors on RL-enhanced biodegradation of TCS was investigated by single factor experiments, and shifts in aerobic TCS-degrading bacterial populations, with and without RL, were analyzed by high-throughput sequencing technology. The results showed that aerobic biodegradation of TCS was significantly promoted by the addition of RL. Environmental conditions, which included RL addition (0.125-0.5g/L), medium concentrations of TCS (<90mug/g), water disturbance, elevated temperature, ionic strength (0.001-0.1mol/L NaCl) and weak alkaline environments (pH8-9), were monitored. High concentrations of TCS had a remarkable influence on the bacterial community structure, and this influence on the distribution proportion of the main microorganisms was strengthened by RL addition. Alpha-proteobacteria (e.g., Sphingomonadaceae and Caulobacteraceae) might be resistant to TCS or even capable of TCS biodegradation, while Sphingobacteria, Beta- and Delta-proteobacteria were sensitive to TCS toxicity. This research provides ecological information on the degradation efficiency and bacterial community stability in RL-enhanced bioremediation of TCS-polluted aquatic environments.

Commonality between BCS and TCS.[Pubmed:27208656]

Int J Pharm. 2016 Jul 25;509(1-2):35-40.

Both biopharmaceutics classification system (BCS) and topical drug classification system (TCS) are based on sound scientific principles with the aim of providing biowaiver and reducing regulatory burden without lowering the quality requirements and standards of approval for the drug products. BCS is based on the solubility and permeability properties of the active pharmaceutical ingredient (API, or drug substance) whereas the TCS is based on the qualitative and quantitative composition of the dosage form and the in vitro release rate of the active ingredient as key decision tools. Both BCS and TCS take drug release and dissolution as their guiding principle for providing biowaiver, increasing the availability and affordability of safe and effective medicines to the consumers and at the same time maintaining the drug product quality.

Uncertainties in calculated correction factors for true coincidence-summing (TCS).[Pubmed:28161650]

Appl Radiat Isot. 2017 Apr;122:174-179.

The aim of this work was to estimate the uncertainties in Monte Carlo calculated correction factors for true coincidence summing (TCS). In this work TCS-factors and their uncertainties were calculated for (134)Cs and then the corrected activities compared to empirical data. The study was carried out using a close-end coaxial p-type detector (O80mmx54.5mm, 80% relative efficiency) and a cylindrical glass fiber sample (O60mmx14mm). It was shown that the uncertainty in the calculated correction factor for the primary gamma ray was below 0.5%, which means it will not contribute significantly to the combined uncertainty in an activity measurement for e.g. environmental monitoring.

Different culture conditions affect the growth of human tendon stem/progenitor cells (TSPCs) within a mixed tendon cells (TCs) population.[Pubmed:28244027]

J Exp Orthop. 2017 Dec;4(1):8.

BACKGROUND: Tendon resident cells (TCs) are a mixed population made of terminally differentiated tenocytes and tendon stem/progenitor cells (TSPCs). Since the enrichment of progenitors proportion could enhance the effectiveness of treatments based on these cell populations, the interest on the effect of culture conditions on the TSPCs is growing. In this study the clonal selection and the culture in presence or absence of basic fibroblast growth factor (bFGF) were used to assess their influences on the stemness properties and phenotype specific features of tendon cells. METHODS: Cells cultured with the different methods were analyzed in terms of clonogenic and differentiation abilities, stem and tendon specific genes expression and immunophenotype at passage 2 and passage 4. RESULTS: The clonal selection allowed to isolate cells with a higher multi-differentiation potential, but at the same time a lower proliferation rate in comparison to the whole population. Moreover, the clones express a higher amounts of stemness marker OCT4 and tendon specific transcription factor Scleraxis (SCX) mRNA, but a lower level of decorin (DCN). On the other hand, the number of cells obtained by clonal selection was extremely low and most of the clones were unable to reach a high number of passages in cultures. The presence of bFGF influences TCs morphology, enhance their proliferation rate and reduce their clonogenic ability. Interestingly, the expression of CD54, a known mesenchymal stem cell marker, is reduced in presence of bFGF at early passages. Nevertheless, bFGF does not affect the chondrogenic and osteogenic potential of TCs and the expression of tendon specific markers, while it was able to downregulate the OCT4 expression. CONCLUSION: This study showed that clonal selection enhance progenitors content in TCs populations, but the extremely low number of cells produced with this method could represent an insurmountable obstacle to its application in clinical approaches. We observed that the addition of bFGF to the culture medium promotes the maintenance of a higher number of differentiated cells, reducing the proportion of progenitors within the whole population. Overall our findings demonstrated the importance of the use of specific culture protocols to obtain tendon cells for possible clinical applications.

Roles of cutaneous versus spinal TRPA1 channels in mechanical hypersensitivity in the diabetic or mustard oil-treated non-diabetic rat.[Pubmed:20004676]

Neuropharmacology. 2010 Mar;58(3):578-84.

Previous results indicate that intaperitoneal administration of a TRPA1 channel antagonist attenuates diabetic hypersensitivity. We studied whether the antihypersensitivity effect induced by a TRPA1 channel antagonist in diabetic animals is explained by action on the TRPA1 channel in the skin, the spinal cord, or both. For comparison, we determined the contribution of cutaneous and spinal TRPA1 channels to development of hypersensitivity induced by topical administration of mustard oil in healthy controls. Diabetes mellitus was induced by streptozotocin in the rat. Hypersensitivity was assessed by the monofilament- and paw pressure-induced limb withdrawal response. Intrathecal (i.t.) administration of Chembridge-5861528 (CHEM, a TRPA1 channel antagonist) at doses 2.5-5.0 microg/rat markedly attenuated diabetic hypersensitivity, whereas 20 microg of CHEM was needed to produce a weak attenuation of diabetic hypersensitivity with intraplantar (i.pl.) administrations. In controls, i.pl. administration of CHEM (20 microg) produced a weak antihypersensitivity effect at the mustard oil-treated site. I.t. administration of CHEM (10 microg) in controls produced a strong antihypersensitivity effect adjacent to the mustard oil-treated area (site of secondary hyperalgesia), while it failed to influence hypersensitivity at the mustard oil-treated area (site of primary hyperalgesia). A reversible antagonism of the rat TRPA1 channel by CHEM was verified using in vitro patch clamp recordings. The results suggest that while cutaneous TRPA1 channels contribute to mechanical hypersensitivity induced by diabetes or topical mustard oil, spinal TRPA1 channels, probably on central terminals of primary afferent nerve fibers, play an important role in maintenance of mechanical hypersensitivity in these conditions.

Attenuation of mechanical hypersensitivity by an antagonist of the TRPA1 ion channel in diabetic animals.[Pubmed:19512877]

Anesthesiology. 2009 Jul;111(1):147-54.

BACKGROUND: The TRPA1 ion channel modulates excitability of nociceptors, and it may be activated by compounds resulting from oxidative insults. Diabetes mellitus produces oxidative stress and sensory neuropathy. The authors tested the hypothesis that diabetes-induced endogenous compounds acting on the TRPA1 ion channel contribute to development and maintenance of mechanical hypersensitivity. METHODS: Diabetes mellitus was induced by streptozotocin. Mechanical hypersensitivity was assessed by the monofilament and paw pressure tests. Chembridge-5861528 (CHEM; a TRPA1 channel antagonist, a derivative of HC-030031) or vehicle was administered acutely or twice daily for 10 days in diabetic animals. For comparison, effects of CHEM were assessed in a group of healthy control animals. RESULTS: Acute administration of CHEM attenuated mechanically induced withdrawal responses in diabetic and control groups. The maximal effect (over 50% elevation of the paw pressure threshold) by acute administration of CHEM was obtained in 30 min. The lowest dose producing a significant attenuation was 10 mg/kg in the diabetic group and 30 mg/kg in the healthy controls. Chronic administration of CHEM (30 mg/kg twice daily) for a week in the diabetic group attenuated development of mechanical hypersensitivity. CONCLUSIONS: Reduction of pain-related behavior by a lower dose of the TRPA1 channel antagonist in the diabetic than in the control group suggests that endogenous compounds resulting from diabetes mellitus and acting on the TRPA1 channel contribute to diabetic hypersensitivity. Prolonged antihypersensitivity effect after chronic treatment suggests that daily administration of a TRPA1 channel antagonist may prevent development of diabetic hypersensitivity.

Chembridge-5861528 is a TRPA1 channel blocker that antagonizes AITC- and 4-HNE-evoked calcium influx (IC50 values are 14.3 and 18.7μM respectively).

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