Adsorption-desorption behaviors of ciprofloxacin onto aged polystyrene fragments in aquatic environments.

As two emerging pollutants of great concern, microplastics (MPs) and antibiotics inevitably cooccur in various aquatic environments and interact with each other, impacting the fate and ecological risks. Aging obviously complicates their interaction and deserves further study. Therefore, the adsorption-desorption behaviors of ciprofloxacin (CIP) onto polystyrene (PS) fragments with various aging extent were investigated, and the key physiochemical properties influencing the interaction and the interaction mechanisms were clarified by redundancy analysis, FTIR and XPS spectra. The physicochemical properties of PS MPs were significantly changed with aging time, and the morphological and chemical changes seemed to occur asynchronously. The adsorption of CIP onto the pristine PS MPs relied on physisorption, especially the ion-involving electrostatic and cation-π interaction. Due to the hydrogen bonding formed by the C-OH, CO, and O-CO groups of PS and CIP, the adsorption capacities of the aged PS MPs were greatly increased. The desorption efficiency of CIP from MPs in the gastric fluid was closely related to the solution ionic strengths, C-OH and CO groups of MPs, while that in the intestinal fluid was associated with O-CO groups of MPs. The different impact factors could be well described by the differences in the chemical components and pHs of the simulated gastric and intestinal fluids. This study gives a comprehensive understanding of the adsorption-desorption behaviors of antibiotics onto MPs at a molecular level and indicates that MPs could act as Trojan horses to transport antibiotics into aquatic organisms.

[Mutation analysis of LITAF, RAB7, LMNA and MTMR2 genes in Chinese Charcot-Marie-Tooth disease.].

The purpose of this study was to understand the mutation features of lipopolysaccharide-induced tumor necrosis factor-alpha factor (LITAF), ras-associated protein RAB7 (RAB7), lamin A/C (LMNA) and myotubularin-related protein 2 (MTMR2) genes in Chinese Charcot-Marie-Tooth disease (CMT) patients. Mutation analysis of LITAF gene was carried out using PCR combined with DNA sequencing, and mutation analysis of RAB7 gene by PCR-single strand conformation polymorphism (PCR-SSCP) combined with DNA sequencing in 33 CMT patients including 6 probands of autosomal domi-nated CMT families and 27 sporadic patients; mutation analysis of LMNA and MTMR2 genes was observed using PCR-SSCP combined with DNA sequencing in 41 CMT patients, including 14 probands of autosomal recessive CMT fami-lies and 27 sporadic patients. Two sequence variations c.269G-->A and c.274A-->G were detected in LITAF gene and two sequence variations c.1243G-->A and c.1910C-->T were detected in LMNA gene. No sequence variation was found in RAB7 and MTMR2 gene. Variations of c.269G-->A in LITAF gene and c.1243G-->A, c.1910C-->T in LMNA gene are newly found SNPs in this study. Variation of c.274A-->G in LITAF gene is known SNP reported in SNP database. Mutations in LITAF, RAB7, LMNA, and MTMR2 genes are rare in Chinese CMT patients.

[The clinical characteristics of a pedigree with incompletely penetrated autosomal dominant hereditary spastic paraplegia and its exclusion analysis of genetic loci].

OBJECTIVE: To describe the clinical features of a big family with incompletely penetrated autosomal dominant hereditary spastic paraplegia (SPG) and perform the exclusion analysis of genetic loci. METHODS: The clinical information of this SPG family was analyzed retrospectively. Exclusion analysis of the known autosomal dominant SPG loci was performed by using multiplex fluorescence PCR, capillary electrophoresis and Linkage package. RESULTS: There were eleven affected members available in this SPG family and the age at onset ranged from 2 to 10 years. The first symptoms were a bilateral, symmetrical, progressive lower limb weakness and spasticity. Patients presented with spasticity and hyperreflexia, positive Babinski sign and scissors gait, and the upper limbs were involved more severely than the lower limbs. No urinary inconsistence, sensory impairment, nystagmus and dementia were found. Genetic analysis showed that this family was consistent with autosomal dominant inheritance. The linkage analysis and mutation analysis revealed this family was not linked to the known autosomal dominant loci. CONCLUSION: This SPG family had typical "pure" clinical symptoms. The age at onset was early and the signs in the upper limbs were more obvious than those in the lower limbs. The result of linkage analysis shows that this family represents a new SPG subtype.

A novel candidate locus on chromosome 11p14.1-p11.2 for autosomal dominant hereditary spastic paraplegia.

BACKGROUND: Hereditary spastic paraplegia (HSP) is a group of inherited neurodegenerative disorders with the shared characteristics of slowly progressive spasticity and weakness of the lower limbs. Thirteen loci for autosomal dominant HSP have been mapped. METHODS: A Chinese family with HSP was found in the Shandong province and Inner Mongolia Autonomous Region of China and genomic DNA of all 19 family members was isolated. After exclusion of known autosomal dominant loci, a genome wide scan and linkage analysis were performed. RESULTS: The known autosomal dominant loci of SPG3A, SPG4, SPG6, SPG8, SPG9, SPG10, SPG12, SPG13, SPG17, SPG19, SPG29, SPG31 and SPG33 were excluded by linkage analysis. The results of a genome wide scan demonstrated candidate linkage to a locus on chromosome 11p14.1-p11.2, over an 18.88 cM interval between markers D11S1324 and D11S1933. A maximal, two point LOD score of 2.36 for marker D11S935 at a recombination fraction (theta) of 0 and a multipoint LOD score of 2.36 for markers D11S1776, D11S1751, D11S1392, D11S4203, D11S935, D11S4083, and D11S4148 at theta=0, suggest linkage to this locus. CONCLUSION: The HSP neuropathy in this family may represent a novel genetic entity, which will facilitate discovery of this causative gene.

[Gene screening in five Chinese families with hereditary spastic paraplegia with thin corpus callosum].

OBJECTIVE: To screen all ten genes between D15S971 and D15S1012 in five Chinese families with hereditary spastic paraplegia with thin corpus callosum (HSP-TCC). METHODS: DNA samples from 5 HSP-TCC families were screened for mutations in AK128197, MGC14798, HH114, MEIS2, MGC35118, SPRED1, AK128458, FLJ38426, RASGRP1 and AK093014 on chromosome 15q13-15 between microsatellites D15S971 and D15S1012 by polymerase chain reaction, direct sequencing and cosegreagation analysis. RESULTS: No disease-causing mutations were found in the 10 genes, but 13 polymorphisms were identified in which two were novel. CONCLUSION: This study did not support the ten genes between D15S971 and D15S1012 were the disease-causing genes of the 5 HSP-TCC families.

[Effect of PPC preoxidation on BAC process for removing organic matters].

The effect of PPC preoxidation on BAC process for organic pollutants removal was conducted by measuring the distribution of relative molecular mass, the concentrations of organic and inorganic matters on BAC. The results show that organic matters of relative molecular mass less than 3 x 10(3) is the main part of BDOC. Organic matters of relative molecular mass more than 10 x 10(3) is effectively removed in the process of coagulation with PPC preoxidation. On the other hand, organic matters of relative molecular mass less than 3 x 10(3) is increased with PPC preoxidation, which improves the biological activity of BAC process. The concentrations of organic and inorganic matters on BAC with PPC preoxidation are reduced 5.0 mg x g(-1) and 4.16 mg x g(-1) respectively than that on BAC alone, which reduces the block of hole on GAC and increases the life time of BAC process.