Salbutamol Residue Rapid Test Strip (Meat)

Microencapsulation of stearyl alcohol (SAL) with silica shell using sol-gel method has been attempted to obtain microencapsulated phase change materials (MPCM). Tetraethoxysilane (TEOS) was used as silica precursor to form silica shell. In order to investigate thermal properties of the MPCM, some tests were carried out. The results of Fourier transformation infrared spectroscope (FT-IR) indicated that the combination of the SAL with silica by sol-gel method is a physical action. X-ray diffractometer (XRD) was used to confirm PCM maintains stable crystal structure. Scanning electronic microscope (SEM) was employed to determine the MPCM has relatively stable physical structure. Thermal properties of MPCM were measured by Differential scanning calorimeter (DSC), where melting temperature and latent heat of MPCM1 (made from 10 g SAL, 10 g TEOS) is 55.89 degrees C and 229.73 J/g, respectively. Liquid-solid phase change has latent heat of 112.05 J/g at 56.74 degrees C while solid-solid phase change has latent heat of 72.01 J/g at 49.75 degrees C. Thermogravimetric analyzer (TGA) analysis confirms that MPCM has good thermal stability. After 100 thermal cycles of the MPCM1, there was no change in phase transition temperature and latent heat, which confirms that the MPCM has good reliability. The thermal conductivity of MPCM1 was measured to be 0.1508 W/m.K over melting point of MPCM1 and 0.1412 W/m.K at room temperature. Therefore, MPCM1 is found to be a promising candidate for thermal energy storage applications.

Despite advances in medical therapy, pulmonary arterial hypertension (PAH) remains an inexorably progressive and highly lethal disease. Signal transducer and activator of transcription (STAT)-3 is one of the main intracellular transcription factors implicated in PAH vascular remodeling. We hypothesized that niclosamide, a STAT3 inhibitor, would reduce vascular remodeling in an established pulmonary arterial hypertension model, thus enhancing cardiac function. Male Wistar rats were treated either with monocrotaline (60 mg/kg), to induce PAH, or saline (C group) by intraperitoneal injection. On day 14, PAH animals were randomly assigned to receive oral (1) saline (PAH-SAL); (2) niclosamide (75 mg/kg/day) (PAH-NICLO); (3) sildenafil (20 mg/kg/day) (PAH-SIL); or (4) niclosamide + sildenafil (PAH-NICLO + SIL), once daily for 14 days. On day 28, right ventricular systolic pressure was lower in all treated groups compared to PAH-SAL. Pulmonary vascular collagen content was lower in PAH-NICLO (37 +/- 3%) and PAH-NICLO + SIL (37 +/- 6%) compared to PAH-SAL (68 +/- 4%), but not in PAH-SIL (52 +/- 1%). CD-34, an endothelial cell marker, was higher, while vimentin, a mesenchymal cell marker, was lower in PAH-NICLO and PAH-NICLO + SIL compared to PAH-SAL, suggesting attenuation of endothelialmesenchymal transition. Expression of STAT3 downstream targets such as transforming growth factor (TGF)beta, hypoxia-inducible factor (HIF)-1, and provirus integration site for Moloney murine leukemia virus (PIM-1) in lung tissue was reduced in PAH-NICLO and PAH-NICLO + SIL compared to PAH-SAL. In conclusion, niclosamide, with or without sildenafil, mitigated vascular remodeling and improved right ventricle systolic pressure. This new role for a well-established drug may represent a promising therapy for PAH.