Awake anesthesia for resection of gliomas located in eloquent brain

Intraoperative awake anesthesia is a safe and reliable method performed in glioma surgery in brain eloquent areas, for the purpose of a maximum resection of the lesions and protection of brain function. Plasma target⁃controlled infusion (TCI) is used in the course of opening cranium and closing cranium to maintain optimal sedation, which is supplemented by excellent scalp nerve block for analgesia, and a laryngeal mask is used to secure the patient's airway. During cerebral function monitoring and lesion excision, appropriately modifying the plasma concentration of propofol TCI can make the patient achieve optimal sedation. DOI：10.3969/j.issn.1672⁃6731.2012.06.00

Saccharin induced liver inflammation in mice by altering the gut microbiota and its metabolic functions

Maintaining the balance of the gut microbiota and its metabolic functions is vital for human health, however, this balance can be disrupted by various external factors including food additives. A range of food and beverages are sweetened by saccharin, which is generally considered to be safe despite controversial debates. However, recent studies indicated that saccharin perturbed the gut microbiota. Inflammation is frequently associated with disruptions of the gut microbiota. The aim of this study is to investigate the relationship between host inflammation and perturbed gut microbiome by saccharin. C57BL/6J male mice were treated with saccharin in drinking water for six months. Q-PCR was used to detect inflammatory markers in mouse liver, while 16S rRNA gene sequencing and metabolomics were used to reveal changes of the gut microbiota and its metabolomic profiles. Elevated expression of pro-inflammatory iNOS and TNF-α in liver indicated that saccharin induced inflammation in mice. The altered gut bacterial genera, enriched orthologs of pathogen-associated molecular patterns, such as LPS and bacterial toxins, in concert with increased pro-inflammatory metabolites suggested that the saccharin-induced liver inflammation could be associated with the perturbation of the gut microbiota and its metabolic functions

Manganese-induced sex-specific gut microbiome perturbations in C57BL/6 mice

Overexposure to manganese (Mn) leads to toxic effects, such as promoting the development of Parkinson’s-like neurological disorders. The gut microbiome is deeply involved in immune development, host metabolism, and xenobiotics biotransformation, and significantly influences central nervous system (CNS) via the gut-brain axis, i.e. the biochemical signaling between the gastrointestinal tract and the CNS. However, it remains unclear whether Mn can affect the gut microbiome and its metabolic functions, particularly those linked to neurotoxicity. In addition, sex-specific effects of Mn have been reported, with no mechanism being identified yet. Recently, we have shown that the gut microbiome is largely different between males and females, raising the possibility that differential gut microbiome responses may contribute to sex-selective toxicity of Mn. Here, we applied high-throughput sequencing and gas chromatography–mass spectrometry (GC-MS) metabolomics to explore how Mn2+ exposure affects the gut microbiome and its metabolism in C57BL/6 mice. Mn2+ exposure perturbed the gut bacterial compositions, functional genes and fecal metabolomes in a highly sex-specific manner. In particular, bacterial genes and/or key metabolites of neurotransmitter synthesis and pro-inflammatory mediators are significantly altered by Mn2+ exposure, which can potentially affect chemical signaling of gut-brain interactions. Likewise, functional genes involved in iron homeostasis, flagellar motility, quorum sensing, and Mn transportation/oxidation are also widely changed by Mn2+ exposure. Taken together, this study has demonstrated that Mn2+ exposure perturbs the gut microbiome and its metabolic functions, which highlights the potential role of the gut microbiome in Mn2+ toxicity, particularly its sex-specific toxic effects

Tetra­aqua­{1-[(1H-1,2,3-benzotriazol-1-yl)meth­yl]-1H-1,2,4-triazole}sulfato­zinc(II) dihydrate

In the title complex, [Zn(SO4)(C9H8N6)(H2O)4]·2H2O, the ZnII ion is six-coordinated by one N atom from a 1-[(1H-1,2,3-benzotriazol-1-yl)meth­yl]-1H-1,2,4-triazole ligand and five O atoms from one monodentate sulfate anion and four water mol­ecules in a distorted octa­hedral geometry. The sulfate tetra­hedron is rotationally disordered over two positions in a 0.618 (19):0.382 (19) ratio. In the crystal, adjacent mol­ecules are linked through O—H⋯O and O—H⋯N hydrogen bonds involving the cation, the anion, and the coordinated and uncoordinated water mol­ecules into a three-dimensional network

Multi-Omics Reveals that Lead Exposure Disturbs Gut Microbiome Development, Key Metabolites, and Metabolic Pathways

Lead exposure remains a global public health issue, and the recent Flint water crisis has renewed public concern about lead toxicity. The toxicity of lead has been well established in a variety of systems and organs. The gut microbiome has been shown to be highly involved in many critical physiological processes, including food digestion, immune system development, and metabolic homeostasis. However, despite the key role of the gut microbiome in human health, the functional impact of lead exposure on the gut microbiome has not been studied. The aim of this study is to define gut microbiome toxicity induced by lead exposure in C57BL/6 mice using multiomics approaches, including 16S rRNA sequencing, whole genome metagenomics sequencing, and gas chromatography-mass spectrometry (GC-MS) metabolomics. 16S rRNA sequencing revealed that lead exposure altered the gut microbiome trajectory and phylogenetic diversity. Metagenomics sequencing and metabolomics profiling showed that numerous metabolic pathways, including vitamin E, bile acids, nitrogen metabolism, energy metabolism, oxidative stress, and the defense/detoxification mechanism, were significantly disturbed by lead exposure. These perturbed molecules and pathways may have important implications for lead toxicity in the host. Taken together, these results demonstrated that lead exposure not only altered the gut microbiome community structures/diversity but also greatly affected metabolic functions, leading to gut microbiome toxicity

Insights into high temperature pretreatment on cellulase processing of bamboo

Bamboo processing was performed with commercial cellulase. The properties of cellulase and the effect of high temperature pretreatment on cellulase hydrolysis of bamboo were investigated. Results indicated that cellulase hydrolysis performed fast and dramatically within 30 minutes, and then gradually reached its balance. It was found that pretreatment played an active role in cellulase processing, which enhanced the saccharification of bamboo and benefited high-molecular-weight lignin degradation and removal. Additionally, a better performance of bamboo processing was achieved under the cellulase concentration of 15IU in total reaction system of 100 ml at 50°C, pH 4.8, together with the high temperature pretreatment of 120°C for 15 minutes

Swimming exercise ameliorates hypertension-induced kidney dysfunction via alleviating renal interstitial fibrosis and apoptosis

Background: Hypertensive nephropathy is one of the major causes of ESRD. Exercise has been considered a nonpathological therapy for hypertension and its complications, yet mechanisms remain unclear. We sought to investigate whether periodic swimming could ameliorate hypertension-induced kidney dysfunction and its underlying mechanisms. Methods: Four-week male spontaneously hypertensive rats (SHRs) were randomly divided into the hypertension group (SHR, n = 8) and exercise group (SE, n = 8, 60 min swimming/day, 6 days per week, for 8 weeks). Wistar-Kyoto rats (WKY, n = 8) were served as a sedentary normotensive group. Bodyweight and blood pressure (BP) were recorded weekly. After 8-week sedentary or swimming exercise, lipids profile, BUN, and Cr were measured. The renal interstitial fibrosis was examined by the histopathological analysis using Masson\u27s trichrome staining and hematoxylin and eosin staining. The kidney cell apoptosis was tested by TUNEL staining. The expressions of critical proteins responsible for the TGF-β1/Smad signaling of fibrosis, that is, TGF-β1, Smad2/3, and Smad7, as well as apoptosis related proteins, Bax and Bcl-2 in kidney cortex tissues were measured. Results: The 8-week swimming exercise reduced BP and bodyweight, lowered concentrations of BUN, and serum Cr, compared with SHR. Exercise remarkably inhibited hypertension-induced tubular degeneration, cellular cluster, and tubular cell swelling as well as glomerular degeneration in the kidney cortical tissues, attenuated renal interstitial fibrosis, and renal cell apoptosis. Moreover, expressions of TGF-β1, Smad2/3, and Bax were higher in the SHR than the WKY, which were significantly suppressed by the exercise. In contrast, hypertension-reduced expressions of Smad7 and Bcl-2 were enhanced by the swimming exercise. Strong correlations were found between kidney function indices, blood lipids, and key protein expressions. Conclusion: Our results demonstrate beneficial effects of the periodic swimming on ameliorating hypertension-induced kidney dysfunction highlighting the potential of swimming exercise as a nonpathological therapy for early prevention of hypertension-caused kidney diseases