The process mechanism and current application status of boron removal in reverse osmosis(RO)desalination were introduced.The characteristic and proper application range of eachboron removal process was summarized.Also,the running conditions of two practical desalination cases were analyzed and compared.Eventually,the future of application and the research direction of boron removal process in RO desalination were prospected.

AIM:To explore the expression level of tristetraprolin(TTP)in rats after subarachnoid hemor-rhage(SAH)as well as the potential role of TTP in the early brain injury(EBI)after SAH in rats.METHODS:In the first experiment setting,total 56 adult male SD rats were randomly divided into sham group and SAH group.The SAH mod-el was performed by endovascular perforation.The brain tissues were taken out after SAH at 5 different time points(0,12, 24,48,72 h and 1 week).The expression of TTP in the brain tissues was detected by Western blot.In the second experi-ment,a total of 60 SD rats were divided into 4 groups: sham group, SAH group, SAH +vector group and SAH +TPP group.Neurological score,brain water content and blood-brain barrier were evaluated at 48 h after SAH.TUNEL staining was performed to detect cell apoptosis in the rat brain tissue.ELISA method was used for quantitative detection of interleu-kin-6(IL-6)and tumor necrosis factor-α(TNF-α).The protein levels of TTP,Bax,Bcl-2 and cleaved caspase-3 in the rat brain tissue were detected by Western blot.RESULTS:The protein expression of TTP in the brain was downregulated markedly from 12 h after SAH,reached the lowest level at 48 h,and then had an upward trend.After modeling for 48 h, Garcia neurological score was significantly reduced,and brain water content and Evans blue(EB)content of the brain tis-sue of the rats in SAH group were significantly higher than those in sham group(P<0.05).SAH induced significant in-creases in IL-6 and TNF-αlevels in the brain tissue(P<0.05).The number of TUNEL-stained cells was increased in the subcortical brain region after SAH compared with sham group.In addition,a lower level of Bcl-2 and higher levels of Bax and cleaved caspase-3 in the rat brains were observed at 48 h after SAH.However,the neurological deficit score was signif-icantly increased,and the brain water content and EB content in the rat brains were significantly reduced in SAH +TTP group in comparison with SAH +vector group(P<0.05).Over-expression of TTP dramatically suppressed the levels of IL-6 and TNF-αin the rat brains,and reduced the number of TUNEL positive cells.Furthermore,upregulation of TTP signifi-cantly decreased the levels of cleaved caspase-3 and Bax, and evidently enhanced the expression of Bcl-2(P<0.01). CONCLUSION:The expression of TTP is significantly decreased in early period after SAH, and enhancing the level of TTP effectively inhibits EBI following SAH in rats.

OBJECTIVETo investigate mutations of ABCD1 gene in X- linked adrenoleukodystrophy (ALD) patients in China.

METHODSPolymerase chain reaction and DNA direct sequencing were employed to analyze the 10 exons of ABCD1 gene in 25 ALD patients.

RESULTSSeventeen mutations in different exons (except exons 4, 9 and 10) were identified in 18 of 25 patients. Most of the mutations were missense mutations, including R182P, G266R, H283D, S404P, N509I, R518G, L520Q, Q556R, S606L and R617C, four (H283D, S40 4P, N509I, R518G) of 10 missense mutations were novel. Also identified were 3 nonsense mutations (W132X, W242X, W595X), 1 dinucleotides deletion mutation (1414 del AG) resulting in frameshift, and 1 base pair deletion at splice acceptor site (IVS5-6 del C). Two synonymous mutations (L516L and V349V) appeared simultaneously in 2 unrelated patients, and no other mutations could be found with them in all 10 exons screened.

CONCLUSIONThere were no hot spot mutations in ABCD1 gene in China. Mutations in gene were found over 70% of patients with ALD in China. The ABCD1 gene mutations identified revealed no obvious correlation between the type of mutation and phenotype.

ATP Binding Cassette Transporter, Sub-Family D, Member 1 ; ATP-Binding Cassette Transporters ; genetics ; Adrenoleukodystrophy ; genetics ; pathology ; Age of Onset ; Base Sequence ; China ; Codon, Nonsense ; DNA ; chemistry ; genetics ; DNA Mutational Analysis ; Humans ; Male ; Mutation ; Mutation, Missense

OBJECTIVETo detect the mutations in exon 6 of ABCD1 gene encoding adrenoleukodystrophy protein(ALDP) in Chinese X-linked adrenoleukodystrophy (ALD MIM 300100) patients.

METHODSGenomic DNA from 14 unrelated patients and two patients' parents with X-linked ALD was extracted using standard procedures from the peripheral blood leukocytes. Polymerase chain reaction (PCR) and DNA direct sequencing were employed to analyze exon 6 of ABCD1 gene.

RESULTSThree mutations in exon 6 were identified in 3 of 14 patients. One mutation was deleted 1 base pair at splice acceptor-site (1489-6 del C). It was not clear what the effect of this mutation is on the ALD protein, maybe induce splicing error. One missense mutation: T1559A(L520Q). These two patients' mothers were heterozygous. The third patient had a mutation: G1548A (L516 L), which is a known polymorphism. It was not a disease causing mutation, so there should be another mutation in this patient.

CONCLUSIONFor the first time, mutations in ABCD1 are identified in Chinese ALD patients in the mainland of China. No major gene deletion or rearrangement is detected in exon 6. Despite many mutations having been identified in patients with these clinical phenotypes, the genotype-phenotype correlations have not been clarified, suggesting that other genetic or environmental factors may also be involved in determining phenotypic expression in ALD. Two carriers are also confirmed.

ATP Binding Cassette Transporter, Sub-Family D, Member 1 ; ATP-Binding Cassette Transporters ; genetics ; Adolescent ; Adrenoleukodystrophy ; genetics ; pathology ; Base Sequence ; Child ; Child, Preschool ; China ; DNA ; chemistry ; genetics ; DNA Mutational Analysis ; Humans ; Mutation

OBJECTIVETo estimate the number of drug users in Hongjiang, Hunan and to develop strategy for drug reduction in the future.

METHODSTwo capture-recapture methods were used to estimate the numbers of drug addicts. Random stratified sampling survey was used to verify the optimum allocation. The first capture-recapture method (CR1) referred to the number from optimum allocation random stratified sampling survey conducted in the communities and the number from local Public Security Bureau list being the second capture. The second capture-recapture method (CR2) referred to the collection of records in the detoxification unit with an interval of 4 months. The estimated number was calculated under Seber's adjustment formula. Face to face interview was carried out during the optimum allocation random stratified sampling survey process.

RESULTSOf 1388 interviewed in the communities, 24 (1.73%) were identified as drug addicts under the optimum allocation random stratified sampling survey. When the figure 1.73% was applied to the total population (72,709) in Hongjiang, the result yielded an estimation of 1258 drug addicts. The estimated numbers of CR1 and CR2 were 904 and 1069 respectively. However, the number was 1.3 to 1.6 fold higher than the reported number (687) by local Public Security Bureau.

CONCLUSIONThe capture-recapture method seemed a better method in estimating the number of drug addicts.

China ; epidemiology ; Female ; Humans ; Incidence ; Male ; Needle Sharing ; Population Surveillance ; methods ; Substance Abuse, Intravenous ; epidemiology

This study was aimed to investigate the expression of osteopontin (OPN) in central nervous system leukemia (CNSL) and to understand its clinical significance. The expression level of OPN in serum of 62 pediatric patients (22 cases of CNSL, 20 cases of acute leukemia without extramedullary infiltration and 20 cases of nontumor patients) and 19 cases of CNSL with complete remission (CR)were assayed by ELISA; the expression changes of OPN mRNA in bone marrow of the CNSL patients were detected by RT-PCR. The results indicated that the serum OPN level was significantly higher in CNSL group (25.21 ± 6.87 ng/ml) than that in acute leukemia group (13.24 ± 2.73 ng/ml) (P < 0.001) and nontumorous group (3.14 ± 1.60 ng/ml) (P < 0.001); the serum OPN level (4.35 ± 1.50 ng/ml) in CNSL group with CR decreased obviously (P < 0.001) after therapy; RT-PCR analysis showed that the expression of OPN mRNA was higher in CNSL group as compared with other two groups (P < 0.01). It is concluded that the OPN expression may play a role in central nervous system infiltration of leukemia, the mechanism of which remains to need further clinical exploration.
Bone Marrow Examination ; Case-Control Studies ; Central Nervous System Neoplasms ; blood ; pathology ; Child, Preschool ; Female ; Humans ; Leukemia ; blood ; pathology ; Male ; Osteopontin ; blood ; metabolism

Female ; Humans ; Manipulation, Orthopedic ; Middle Aged ; Radius Fractures ; surgery ; Ulna Fractures ; surgery ; Ulnar Nerve Compression Syndromes ; surgery

OBJECTIVETo evaluate the relationship between peroxisome proliferator-activated receptor-γ2 (PPARγ2) Pro12Ala polymorphism and type 2 diabetes mellitus (T2DM) in Chinese Han population.

METHODSPubMed, Chinese Biomedicine Database (CBM), China National Knowledge Infrastructure (CNKI) and Wanfang database were searched for all relevant articles investigating the association between PPARγ2 Pro12Ala polymorphism and T2DM that were available from January, 1990 to June, 2011. A total of 29 relevant articles were selected. A Meta-analysis was performed to estimate heterogeneity and the pooled odds ratio (OR) to evaluate the relationship between PPARγ2 Pro12Ala polymorphism and T2DM. The sensitivity analysis was also assessed.

RESULTSA total of 21 qualified articles including 3870 patients with T2DM and 3333 healthy controls were analyzed in the study. The frequencies of the allele Ala12 in T2DM and control groups were 4.13% (320/7740) and 4.56% (304/6666), respectively. There were not heterogeneity (χ(2) = 25.96, P = 0.17) among the 21 qualified articles. The pooled OR (95%CI) value of the frequencies of the PPARγ2 genotype (PA + AA)/PP calculated by fixed effects model was 0.96 (0.81 - 1.14) (P = 0.64). There was not heterogeneity among the remaining articles after excluding the article with the largest weight and the article with larger frequencies of the allele Ala12 respectively (χ(2) values were 24.23, 16.87 respectively, both P values > 0.05). The pooled OR (95%CI) value of the frequencies of the PPARγ2 genotype (PA + AA)/PP of the remaining articles were 1.01 (0.84 - 1.21) and 1.07 (0.89 - 1.28) after excluding the article with the largest weight and the article with larger frequencies of the allele Ala12 (both P values > 0.05).

CONCLUSIONPPARγ2 Pro12Ala polymorphism was not associated with type 2 diabetes mellitus in Chinese Han population.

Alleles ; Asian Continental Ancestry Group ; genetics ; China ; Diabetes Mellitus, Type 2 ; genetics ; Gene Frequency ; Genotype ; Humans ; PPAR gamma ; genetics ; Polymorphism, Single Nucleotide

OBJECTIVETo explore the effects of brain-derived neurotrophic factor (BDNF) pretreatment on beta amyloid protein (Abeta) induced impairment of in vivo hippocampal long-term potentiation (LTP) in the CA1 region of rats.

METHODSThirty-six adult male SD rats were randomly divided into six groups (n = 6): control, Abeta25-35, BDNF, (0.02 microg, 0.1 microg, 0.5 microg) BDNF + Abeta25-35. A self-made hippocampal local drug delivery catheter and a parallel bound stimulating/recording electrode were used to deliver drugs/stimulation and record field excitatory post-synaptic potentials (fEPSPs) in the hippocampal CA1 region of rats. High-frequency stimulation (HFS) was used to induce in vivo LTP.

RESULTS(1) Abeta25-35 (2 nmol) injection into CA1 region of rats did not affect the baseline fEPSPs, but inhibited the HFS-induced LTP significantly (P < 0.01). (2) Hippocampal CA1 injection of BDNF (0.1 microg) alone did not affect the baseline fEPSPs and HFS-induced LTP. (3) Compared with Abeta25-35 alone group, the averaged amplitude of LTP in BDNF (0.1 microg and 0.5 microg) plus Abeta25-35 groups significantly increased at 0 min, 30 min, and 60 min after HFS (P < 0.01), indicating that pretreatment with BDNF effectively protected against the Abeta,25-35 induced depression of LTP in a dose-dependent manner.

CONCLUSIONIntrahippocampal injection of BDNF can protect against the Abeta25-35-induced LTP impairment, suggesting that the up-regulation of BDNF in the brain could maintain the normal hippocampal synaptic plasticity and may contribute to the improvement of learning and memory in Alzheimer's (AD) disease patients.

Amyloid beta-Peptides ; antagonists & inhibitors ; Animals ; Brain-Derived Neurotrophic Factor ; pharmacology ; CA1 Region, Hippocampal ; drug effects ; physiology ; Excitatory Postsynaptic Potentials ; physiology ; Long-Term Potentiation ; physiology ; Male ; Peptide Fragments ; antagonists & inhibitors ; Rats ; Rats, Sprague-Dawley

Objective A resistin binding peptide (RBP) was selected by phage display in our previous work. Studies had shown that RBP could antagonize the role of resistin on the lipid metabolism and endocrine function of adipose tissue, but whether RBP affects the insulin secretion of pancreatic cells is still unknown. The aim of this study is to assess the effect of RBP on basal insulin secretion in RINm5F insulinoma cells. Methods The cell viability was measured by 3-[4,5-dimethyhhiazol-2-yl]-2,5-diphenyltetra-zolium bromide (MTT) cytotoxicity assay. The supernatants were assayed for insulin content by enzyme linked immunosorbent assay (ELISA). Reverse transcriptase-PCR assay and Western blotting were used to determine the expression of glucose transporter 2 (GLUT2) involved in insulin secretion. Cytosolic Ca2+, the trigger of insulin exocytosis, was analyzed with the fluorescent probe FURA-3/AM. Results RBP did no effect on the cell viability with a concentration of 10-8-10-12mol/L of 2 hours intervention. But it stimulated basal insulin secretion of RINm5F cells, accompanied by up-regulated increased expression of GLUT2 and elevated concentration of cytosolic Ca2+. Conclusion RBP could stimulate basal insulin secretion without affecting the cell viability.