Objective To determine whether reduction In central pressure augmentation and central systolic blood pressure by nitroglycerine (NTG) results from effects on pre-lead or is due to arterial dilation. Methods We compared effects of NTG with these of lower body negative pressure (LBNP). Hemodyunmic measurements were made at rest, during LBNP (10, 20 and 30 mmHg, each for 15 min) and after NTG (10, 30 and 100μg/min, each dose for 15 min) in ten healthy volunteers. Cardiac pre-lead, stroke volume and cardiac output were assessed by echacardiography. Central pressure an mnentation and central systolic pressure were obtained by radial tonometry using a transfer function. Results LBNP (20 mmHg) and NTG (30μg/min) reduced pre-lead (as measured by the peak velocity of the S wave in the superior vena eava) to a similar degree [by (26. 8 ± 3.8) % and (23.9 ± 3. 4) %, respectively]. Compared to LBNP, NTG reduced systemic vascular resistance [by (32. 9 ± 7.5) %, p< 0. 01], decreased peripheral and central pressure augmentation [by (20. 8 ± 3. 4)% units and (12. 9±2. 9)% units, respectively, each P< 0. 01]. Conclusion These results suggest that a reduction in pre-load does not explain reduction in pressure augmentation and central systolic blood pressure by NTG and that these effects are mediated through arterial dilation.

OBJECTIVE: To explore the relationship between serum IL-4, IFN-gamma, IL-10 levels and the aetiology of juvenile-onset recurrent respiratory papillomatosis. METHOD: Serum IL-4, IFN-gamma, IL-32 levels of 15 JORRP children were detected by use of enzyme-linked immunosorbent assay (ELISA) and compared with those of healthy control group. RESULT: Serum IL-4 levels were significantly higher in the JORRP children (P<0.01): (524.65 +/- 147.77)pg/ml in the JORRP children and (213.27 +/- 87.48) pg/ml in the healthy control group. Serum IFN-gamma levels were significantly lower in the JORRP children (P<0.01): (2.87 +/- 0.84) pg/ml in the JORRP children and (10.63 +/- 5.09) pg/ml in the healthy control group. Serum IL-32 levels were significantly lower in the JORRP children (P< 0.01): (2.47 +/- 1.60) pg/ml in the JORRP children and (9.08 +/- 2.66) pg/ml in the healthy control group. CONCLUSION 1) While the concentration of Th2 like cytokine IL-4 in children with JORRP was higher than that in control group, the concentration of Th1 like cytokine IFN-gamma in children with JORRP was lower than that in controls, indicating that the polarization of Th1 /Th2 T cell in children with JORRP; 2) The polarization of Th1/Th2 T cell may cause the reduction of the serum IL-32 as a proinflammatory role in host immunity system that could not eradicate HPVs because of lacking enough inflammatory stimulation.
Case-Control Studies ; Child ; Female ; Humans ; Infant ; Interferon-gamma ; blood ; Interleukin-4 ; blood ; Interleukins ; blood ; Male ; Papillomavirus Infections ; blood ; Respiratory Tract Infections ; blood

Astaxanthine (AST) has important biological activities including antioxidant and anti-inflammatory effects that could alleviate neurological and heart diseases, but its role in the prevention of cisplatin-induced hearing loss (CIHL) is not yet well understood. In our study, a steady interaction between AST and the E3 ligase adapter Kelch-like ECH-associated protein 1, a predominant repressor of nuclear factor erythroid 2-related factor 2 (NRF2), was performed and tested via computer molecular docking and dynamics. AST protected against cisplatin-induced ototoxicity via NRF2 mediated pathway using quantitative PCR and Western blotting. The levels of reactive oxygen species (ROS) and mitochondrial membrane potential revealed that AST reduced ROS overexpression and mitochondrial dysfunction. Moreover, AST exerted anti-apoptosis effects in mouse cochlear explants using immunofluorescence staining and HEI-OC1 cell lines using quantitative PCR and Western blotting. Finally, AST combined with poloxamer was injected into the middle ear through the tympanum, and the protection against CIHL was evaluated using the acoustic brain stem test and immunofluorescent staining in adult mice. Our results suggest that AST reduced ROS overexpression, mitochondrial dysfunction, and apoptosis via NRF2-mediated pathway in cisplatin-exposed HEI-OC1 cell lines and mouse cochlear explants, finally promoting cell survival. Our study demonstrates that AST is a candidate therapeutic agent for CIHL.