Selective Conversion of Scenedesmus into Lactic Acid over Amine-Modified Sn-ß.

Amine-modified Sn-ß was synthesized to improve the yield of lactic acid produced from Scenedesmus. After studying the growth of Scenedesmus, we selected Scenedesmus with the highest sugar content of 46.7% after 8 days of culture as the reaction substrate. The results showed that the yield of lactic acid from Scenedesmus was greatly increased after being catalyzed by 3-aminopropyltrimethoxysilane (APTMS)-modified Sn-ß. After the pretreatment of Scenedesmus in an ice bath ultrasound, under the optimal reaction conditions (190 °C and 5 h), the yield of lactic acid reached the highest (37%). The acid-base characterization results of the catalyst confirmed that there are both Lewis acidic sites and medium-strength basic sites in the catalyst. Both of these sites can promote the hydrolysis of Scenedesmus, while the Lewis acidic sites can promote the production of lactic acid and the basic sites can effectively inhibit the production of the byproduct 5-hydroxymethylfurfural (HMF). This study proved that this amination catalyst is a useful strategy to increase the yield of lactic acid.

Microbiota from alginate oligosaccharide-dosed mice successfully mitigated small intestinal mucositis.

BACKGROUND: The increasing incidence of cancer and intestinal mucositis induced by chemotherapeutics are causing worldwide concern. Many approaches such as fecal microbiota transplantation (FMT) have been used to minimize mucositis. However, it is still unknown whether FMT from a donor with beneficial gut microbiota results in more effective intestinal function in the recipient. Recently, we found that alginate oligosaccharides (AOS) benefit murine gut microbiota through increasing "beneficial" microbes to rescue busulfan induced mucositis. RESULTS: In the current investigation, FMT from AOS-dosed mice improved small intestine function over FMT from control mice through the recovery of gene expression and an increase in the levels of cell junction proteins. FMT from AOS-dosed mice showed superior benefits over FMT from control mice on recipient gut microbiotas through an increase in "beneficial" microbes such as Leuconostocaceae and recovery in blood metabolome. Furthermore, the correlation of gut microbiota and blood metabolites suggested that the "beneficial" microbe Lactobacillales helped with the recovery of blood metabolites, while the "harmful" microbe Mycoplasmatales did not. CONCLUSION: The data confirm our hypothesis that FMT from a donor with superior microbes leads to a more profound recovery of small intestinal function. We propose that gut microbiota from naturally produced AOS-treated donor may be used to prevent small intestinal mucositis induced by chemotherapeutics or other factors in recipients. Video Abstract.

Pubertal exposure to low doses of zearalenone disrupting spermatogenesis through ERα related genetic and epigenetic pathways.

Endocrine disruptor zearalenone (ZEA) has been found to damage the reproductive system especially spermatogenesis. In our previous report, we have found that low dose (lower than No-Observed Effect Level, NOEL) ZEA exposure disturbed mouse spermatogenesis and diminished mouse semen quality. The purpose of current investigation was to explore the underlying mechanisms of pubertal low dose ZEA exposure upsetting spermatogenesis. And it was demonstrated that pubertal low dose ZEA exposure disrupted the meiosis process and the important genetic pathways to inhibit the spermatogenesis and even to diminish the semen quality with the decrease in spermatozoa motility and concentration. The DNA methylation markers 5mC and 5hmC were decreased, the histone methylation marker H3K27 was increased, at the same time estrogen receptor alpha was diminished in mouse testis after pubertal low dose ZEA exposure. The data indicate that the disruption in spermatogenesis by pubertal low dose ZEA exposure may be through the alterations in genetic and epigenetic pathways, and the interactions with estrogen receptor signaling pathway. Therefore, we should pay great attention on ZEA exposure to reduce its adverse impacts on male reproductive health.

Gestational exposure to low-dose zearalenone disrupting offspring spermatogenesis might be through epigenetic modifications.

Zearalenone (ZEA), a F-2 mycotoxin produced by Fusarium, has been found to be an endocrine disruptor through oestrogen receptor signalling pathway to impair spermatogenesis. The disruption on reproductive systems by ZEA exposure might be transgenerational. In our previous report, we have found that low dose (lower than no-observed effect level, NOEL) of ZEA impaired mouse spermatogenesis and decreased mouse semen quality. The purpose of the current investigation was to explore the impacts of low-dose ZEA on spermatogenesis in the offspring after prenatal exposure and the underlying mechanisms. And it demonstrated that prenatal low-dose ZEA exposure disrupted the meiosis process to inhibit the spermatogenesis in offspring and even to diminish the semen quality by the decrease in spermatozoa motility and concentration. The DNA methylation marker 5hmC was decreased, the histone methylation markers H3K9 and H3K27 were elevated, and oestrogen receptor alpha was reduced in the offspring testis after prenatal low-dose ZEA exposure. The data suggest that the disruption in spermatogenesis by prenatal low-dose ZEA exposure may be through the modifications on epigenetic pathways (DNA methylation and histone methylation) and the interactions with oestrogen receptor signalling pathway. Moreover, in the current study, the male offspring were indirectly exposed to low-dose ZEA through placenta and the spermatogenesis in offspring was disrupted which suggested that the toxicity of ZEA on reproductive systems was very severe. Therefore, we strongly recommend that greater attention should be paid to this mycotoxin to minimize its adverse impact on human spermatogenesis.

Genome sequence of Shigella flexneri 2a: insights into pathogenicity through comparison with genomes of Escherichia coli K12 and O157.

We have sequenced the genome of Shigella flexneri serotype 2a, the most prevalent species and serotype that causes bacillary dysentery or shigellosis in man. The whole genome is composed of a 4 607 203 bp chromosome and a 221 618 bp virulence plasmid, designated pCP301. While the plasmid shows minor divergence from that sequenced in serotype 5a, striking characteristics of the chromosome have been revealed. The S.flexneri chromosome has, astonishingly, 314 IS elements, more than 7-fold over those possessed by its close relatives, the non-pathogenic K12 strain and enterohemorrhagic O157:H7 strain of Escherichia coli. There are 13 translocations and inversions compared with the E.coli sequences, all involve a segment larger than 5 kb, and most are associated with deletions or acquired DNA sequences, of which several are likely to be bacteriophage-transmitted pathogenicity islands. Furthermore, S.flexneri, resembling another human-restricted enteric pathogen, Salmonella typhi, also has hundreds of pseudogenes compared with the E.coli strains. All of these could be subjected to investigations towards novel preventative and treatment strategies against shigellosis.

A functional promoter region of the CKLFSF2 gene is located in the last intron/exon region of the upstream CKLFSF1 gene.

The genes for CKLFSF1 (chemokine-like factor super family member 1) and CKLFSF2 (chemokine-like factor super family member 2) are very closely linked, within 312 bp of each other. Here, we present evidence that the last intron/exon region of the CKLFSF1 gene contains a novel eukaryotic promoter capable of directing the expression of the downstream gene, CKLFSF2. We identified two segments of the upstream region of the CKLFSF2 gene, 2146 bp (-2134/+12, relative to ATG +1) and 1483 bp (-2134/-652), that were capable of efficiently driving expression of a linked reporter gene upon transient transfection into several kinds of cell lines. The 1483 bp segment exhibited more than a two-fold increase in luciferase activity relative to the 2146 bp segment. By analyzing 5'-deletion mutants of the 1483 bp segment, we identified a 195 bp segment (-846/-625) located in the last intron/exon region of the CKLFSF1 gene that was critical for promoter activity. DNA decoy experiments revealed that a 122 bp (-846/-725) fragment markedly inhibited CKLFSF2 mRNA transcription. Furthermore, we found that the putative promoter region of the CKLFSF2 gene is separated from the transcription start site by about 500 bp. Accumulating reports suggest that introns have many functions, including the modulation of regulation and structure. This work provides evidence that a eukaryotic gene promoter sequence from one gene located in an intron/exon of another.