Biosorption of Strontium from Aqueous Solutions by Micrococcus luteus Sr02

Although strontium (Sr²⁺) is found in soils, sediments and surface waters, there is limited evidence about its biosorption. In this study, a surface water strain being highly tolerant to Sr²⁺ was isolated and identified as Micrococcus luteus Sr02 by using 16S rRNA sequencing. Biosorption behavior and mechanisms of Sr²⁺ by M. luteus Sr02 were investigated through batch experiments, zeta potential measurements, Fourier transform infrared spectroscopy and scanning electron microscopy. The results showed that M. luteus Sr02 have potential to sorb Sr²⁺ and can be used efficiently for the removal of Sr²⁺ from aqueous solutions.     

High Levels of Cadmium and Lead in Seminal Fluid and Blood of Smoking Men are Associated with High Oxidative Stress and Damage in Infertile Subjects

We measured the levels of malondialdehyde (MDA), protein carbonyls, glutathione S-transferase (GST) and reducte glutathione (GSH) in seminal plasma and spermatozoa from 95 subjects including 50 infertile patients to evaluate the association between oxidative stress and damage and the components of the anti-oxidant defenses in seminal plasma and spermatozoa of infertile subjects and concentrations of cadmium (Cd) and lead (Pb) in the blood and seminal plasma because of tobacco smoke exposure. The reactive oxygen species (ROS) in spermatozoa were also evaluated by luminol (5-amino-2,3-dihydro-1,4-phthalazinedione)-enhanced chemiluminescence assay. The sperm count, motility, and morphology in the smokers infertile group were found to be lower than those in the fertile male group and nonsmokers infertile group (p < 0.001). Concentrations of Cd, Pb, MDA, protein carbonyls, and ROS levels in the smokers infertile group were significantly higher than those in the fertile male and nonsmokers infertile male groups (p < 0.001). However, GSH levels and GST activities were decreased in the smokers infertile male group than those in the fertile male and nonsmokers infertile male groups (p < 0.001). The results indicate that smoking could affect semen quality and oxidative lipid and protein damage in human spermatozoa. From Pearson correlation analysis, positive correlations were demonstrated between the seminal plasma Cd and seminal plasma protein carbonyls and between seminal plasma Pb and spermatozoa ROS levels in smokers of the subfertile group, while there was a significant positive correlation between blood Cd and ROS levels in smokers of the fertile group. There was also a significant negative correlation of the Cd level of the blood and GSH levels of the sperm and seminal plasma. These findings suggest that cigarette smoking enhances the levels of Cd and Pb in seminal plasma and blood and the extent of oxidative damage associated with a decrease in components of the anti-oxidant defenses in the sperm of infertile males.     

Peroxynitrite and NO donors form colored nitrite adducts with sinapinic acid: potential applications

Sinapinic acid (3,5-dimethoxy-4-hydroxycinnamic acid, SA) reacted with peroxynitrous acid at neutral pH with a second-order rate constant of 812 M(-1)s(-1), to yield a red product (lambda(max), 532 nm). The identical colored product could be formed with acidified decomposed peroxynitrous acid solutions or nitrite at slower rates (0.1M HCl, 8.32 M(-1)s(-1); 10% acetic acid, 0.0004 M(-1)s(-1)). The red compound is thought to be O-nitrososinapinic acid (3,5-dimethoxy-4-nitrosooxycinnamic acid) which can be formed by reaction with either peroxynitrous acid or nitrous acid. The extinction coefficient of O-nitrososinapinic acid (ONSA) was estimated to be 8419 M(-1)cm(-1) at 510 nm in 10% acetic acid and 90% acetonitrile. ONSA was also formed via NO(+) transfer from S-nitrosoglutathione (GSNO). ONSA in turn can S-nitrosate low molecular weight thiols and protein thiols. SA was also shown to act as a peroxynitrite sink as it effectively prevented the oxidation of dihydrorhodamine under physiological conditions. The fact that O-nitrososinapinic acid is stable and can be used to S-nitrosate thiol containing amino acids, peptides, and proteins makes it a potentially useful reagent in the study of S-nitrosothiol biochemistry and physiology. In addition, the relatively high extinction coefficient of O-nitrososinapinic acid means that it could be utilized as an analyte for the spectroscopic detection of peroxynitrite or NO(+)-donors in the submicromolar range.     

Inhibition of serine palmitoyltransferase delays the onset of radiation-induced pulmonary fibrosis through the negative regulation of sphingosine kinase-1 expression

The enforcement of sphingosine-1-phosphate (S1P) signaling network protects from radiation-induced pneumonitis. We now demonstrate that, in contrast to early postirradiation period, late postirradiation sphingosine kinase-1 (SphK1) and sphingoid base-1-phosphates are associated with radiation-induced pulmonary fibrosis (RIF). Using the mouse model, we demonstrate that RIF is characterized by a marked upregulation of S1P and dihydrosphingosine-1-phosphate (DHS1P) levels in the lung tissue and in circulation accompanied by increased lung SphK1 expression and activity. Inhibition of sphingolipid de novo biosynthesis by targeting serine palmitoyltransferase (SPT) with myriocin reduced radiation-induced pulmonary inflammation and delayed the onset of RIF as evidenced by increased animal lifespan and decreased expression of markers of fibrogenesis, such as collagen and α-smooth muscle actin (α-SMA), in the lung. Long-term inhibition of SPT also decreased radiation-induced SphK activity in the lung and the levels of S1P-DHS1P in the lung tissue and in circulation. In vitro, inhibition or silencing of serine palmitoyltransferase attenuated transforming growth factor-β1 (TGF-β)-induced upregulation of α-SMA through the negative regulation of SphK1 expression in normal human lung fibroblasts. These data demonstrate a novel role for SPT in regulating TGF-β signaling and fibrogenesis that is linked to the regulation of SphK1 expression and S1P-DHS1P formation.     

Intermedin/adrenomedullin-2 dilates the rat pulmonary vascular bed: dependence on CGRP receptors and nitric oxide release

Intermedin/adrenomedullin-2 (IMD/AM2) is a 47 amino acid peptide formed by enzymatic degradation of preprointermedin. The present study was undertaken to investigate the effects of rat IMD (rIMD) in the isolated buffer perfused rat lung (IBPR) under resting conditions and under conditions of elevated pulmonary vasoconstrictor tone (PVT). Under resting conditions in the IBPR, rIMD had little or no activity. When PVT was actively increased by infusion of U46619, bolus injection of IMD decreased pulmonary arterial pressure (PAP) in a dose-dependent manner. Since the pulmonary perfusion rate and left atrial pressure were constant, these reductions in PAP directly reflect reductions in pulmonary vascular resistance (PVR). The pulmonary vasodilator response to rIMD, when compared to calcitonin gene-related peptide (CGRP) on a molar basis, was greater at the lowest and midrange doses. The degree of inhibition by CGRP8-37 on pulmonary vasodilator response to rIMD was significantly less when compared to CGRP. Pretreatment with L-nitro-arginine-methyl ester (L-NAME), unlike meclofenamate and glybenclamide, significantly reduced the pulmonary vasodilator responses to rIMD. rIMD administration induced cross-tachyphylaxis to the pulmonary vasodilator response to CGRP whereas CGRP administration did not alter the ability of rIMD to dilate the IBPR. Pulmonary vasodilator responses to repeated injections of rIMD did not undergo tachyphylaxis. The present data demonstrate rIMD possesses direct vasodilator activity in the rat pulmonary vascular bed. The present data suggest activation of CGRP1 receptors and release of nitric oxide (NO*) mediate the pulmonary vasodilator response to rIMD whereas cyclooxygenase products and KATP channels do not contribute to the pulmonary vasodilator response to rIMD. The ability of rIMD to induce heterologous desensitization of CGRP1 receptor activation, to retain much of its pulmonary vasodilator activity after inhibition of CGRP1 receptors, and to lack homologous desensitization together suggests the pulmonary, unlike the systemic, vasodilator response to rIMD may depend on other vasodilator mechanisms including receptors in the calcitonin-receptor-like-receptor (CRLR) family.     

Surgical outcomes of the brachial plexus lesions caused by gunshot wounds in adults

Background

The management of brachial plexus injuries due to gunshot wounds is a surgical challenge. Better surgical strategies based on clinical and electrophysiological patterns are needed. The aim of this study is to clarify the factors which may influence the surgical technique and outcome of the brachial plexus lesions caused by gunshot injuries.

Methods

Two hundred and sixty five patients who had brachial plexus lesions caused by gunshot injuries were included in this study. All of them were male with a mean age of 22 years. Twenty-three patients were improved with conservative treatment while the others underwent surgical treatment. The patients were classified and managed according to the locations, clinical and electrophysiological findings, and coexisting lesions.

Results

The wounding agent was shrapnel in 106 patients and bullet in 159 patients. Surgical procedures were performed from 6 weeks to 10 months after the injury. The majority of the lesions were repaired within 4 months were improved successfully. Good results were obtained in upper trunk and lateral cord lesions. The outcome was satisfactory if the nerve was intact and only compressed by fibrosis or the nerve was in-contunuity with neuroma or fibrosis.

Conclusion

Appropriate surgical techniques help the recovery from the lesions, especially in patients with complete functional loss. Intraoperative nerve status and the type of surgery significantly affect the final clinical outcome of the patients.