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Biomedical subjects

Y Hu

Publications and source records attributed to Y Hu.

At least 73 records · Page 4Linked to original sources

The colonic response to genotoxic carcinogens in the rat: regulation by dietary fibre.

The apoptotic response to DNA damage appears to be an innate biological mechanism for protection against tumourigenesis. It is possible that agents that protect against colorectal cancer act by enhancing the apoptotic deletion of cells suffering DNA damage, with consequent removal of those with tumourigenic mutations. We examined the acute apoptotic response to genotoxic carcinogens ("AARGC") in colonic epithelium and the possibility that dietary fibres of different fermentability might regulate AARGC. To fully define the time-course and nature of AARGC in response to the carcinogen azoxymethane (AOM), a single injection of AOM (10 mg/kg) was given to rats and apoptosis monitored in the colon by light microscopy and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling staining over a 72 h period. Having defined the site and time of maximum response, two groups of eight rats were fed diets containing 10% wheat bran fibre (WB; fermentable) or 10% methylcellulose (MC; poorly fermentable) for 4 weeks. Colonic AARGC was compared by light microscopy; lumenal short chain fatty acids (SCFAs) and pH were measured as indicators of the fermentative environment. AOM-induced AARGC was maximal at 8 h and greater in distal compared with proximal colon. Apoptotic cells were situated predominantly in the lower half of the crypt, with the median at position 9 indicating involvement of daughter as well as stem cells. There was no "second wave" of apoptosis within 72 h as follows irradiation in small intestine. Distal colonic AARGC in rats fed WB was twice that in rats fed MC (P < 0.01). Compared with MC, WB significantly lowered lumenal pH and increased all SCFAs including butyrate, while proliferation did not differ between the fibres. Certainly, dietary fibres can regulate AARGC and further studies are warranted to determine if this biological effect is the way in which dietary factors regulate tumourigenesis. Lumenal generation of butyrate may enhance AARGC as butyrate is proapoptotic in vitro.

Animals↗

Complete genomes of two Human hepatitis A virus isolates from China: analysis and comparison with other isolates.

Complete sequences of the genomes of two wild type (wt) Human hepatitis A virus (HHAV) isolates, LU38 and LY6 from China were determined and compared with those of wt HHAV isolates AH1, AH2, AH3, FH1, FH2, FH3, GBM, HM175, LA and MBB. The genomes of both LU38 and LY6 consisting of 7477 nucleotides (nts) contained a 5'-non-translated region (5'-NTR, 733 nts), an open reading frame (ORF, 6681 nts), and a 3'-NTR (63 nts) followed by a poly(A)-tail. It encoded a polyprotein of 2227 amino acids (aa) Sequence comparison showed that LU38 shared the highest identities of 98.1% for nt (140 differences) and 99.2% for as (17 differences) with AH1, and the lowest identities of 91.4% for nt (741 differences) with HM175 and 98.1% for aa (43 differences) with GBM. LY6 shared the highest identities of 97.4% for nt (196 differences) and 98.7% for aa (28 differences) with H1 and the lowest identities of 91.2% for nt (642 differences) with HM175 and 97.7% for as (51 differences) with GBM. The subgenotyping revealed that the LU38 and LY6 isolates are of IA subgenotype. The phylogenetic analysis showed that LU38 is closest to AH1 and the LY6 to FH3, suggesting that the epidemiological link of hepatitis A (HA) had developed in China and Japan.

Amino Acid Sequence↗

Computational characterization of substrate binding and catalysis in S-adenosylhomocysteine hydrolase.

S-Adenosylhomocysteine (AdoHcy) hydrolase catalyzes the reversible hydrolysis of AdoHcy to adenosine (Ado) and homocysteine (Hcy), playing an essential role in modulating the cellular Hcy levels and regulating activities of a host of methyltransferases in eukaryotic cells. This enzyme exists in an open conformation (active site unoccupied) and a closed conformation (active site occupied with substrate or inhibitor) [Turner, M. A., Yang, X., Yin, D., Kuczera, K., Borchardt, R. T., and Howell, P. L. (2000) Cell Biochem. Biophys. 33, 101-125]. To investigate the binding of natural substrates during catalysis, the computational docking program AutoDock (with confirming calculations using CHARMM) was used to predict the binding modes of various substrates or inhibitors with the closed and open forms of AdoHcy hydrolase. The results have revealed that the interaction between a substrate and the open form of the enzyme is nonspecific, whereas the binding of the substrate in the closed form is highly specific with the adenine moiety of a substrate as the main recognition factor. Residues Thr57, Glu59, Glu156, Gln181, Lys186, Asp190, Met351, and His35 are involved in substrate binding, which is consistent with the crystal structure. His55 in the docked model appears to participate in the elimination of water from Ado through the interaction with the 5'-OH group of Ado. In the same reaction, Asp131 removes a proton from the 4' position of the substrate after the oxidation-reduction reaction in the enzyme. To identify the residues that bind the Hcy moiety, AdoHcy was docked to the closed form of AdoHcy hydrolase. The Hcy tail is predicted to interact with His55, Cys79, Asn80, Asp131, Asp134, and Leu344 in a strained conformation, which may lower the reaction barrier and enhance the catalysis rate.

Adenosine↗

Systemic cancer therapy with a tumor-selective vaccinia virus mutant lacking thymidine kinase and vaccinia growth factor genes.

We have demonstrated previously the oncolytic effects of a systemically delivered, replicating vaccinia virus. To enhance the tumor specificity of this vector, we have developed a combined thymidine kinase-deleted (TK-) and vaccinia growth factor-deleted (VGF-) vaccinia virus and investigated its properties in vitro and in vivo. The gene for enhanced green fluorescent protein (EGFP) was inserted into the TK locus of a VGF- vaccinia virus by homologous recombination creating a double-deleted mutant vaccinia virus (vvDD-GFP). Infection of resting and dividing NIH3T3 cells with vvDD-GFP yielded reduced viral recovery compared with wild-type (WT), TK-, or VGF- viruses from resting cultures but equivalent virus recovery from dividing cultures. Eight days after nude mice were injected i.p. with 10(7) plaque-forming units (pfu) of WT, TK-, VGF-, or vvDD-GFP vaccinia virus, tissues and tumor were harvested for viral titer determination. No virus was recovered from the brains of mice injected with vvDD-GFP compared with the other viruses, which ranged from 130 to 28,000 pfu/mg protein; however, equivalent amounts were recovered from tumor. There was no toxicity from vvDD-GFP because nude mice receiving 10(8) pfu of IP vvDD-GFP lived >100 days, whereas mice receiving WT, VGF-, or TK- virus had median survivals of only 6, 17, and 29 days, respectively. Similar results were seen when 10(9) pfu of vvDD-GFP were given. Nude mice bearing s.c. murine colon adenocarcinoma (MC38) had significant tumor regression after treatment with 10(9) pfu of systemic (i.p.) vvDD-GFP compared with control (mean tumor size, 180.71 +/- 35.26 mm(3) versus 2796.79 +/- 573.20 mm(3) 12 days after injection of virus). Our data demonstrate that a TK- and VGF- mutant vaccinia virus is significantly attenuated in resting cells in vitro and demonstrates tumor-specific replication in vivo. It is a promising vector for use in tumor-directed gene therapy, given its enhanced safety profile, tumor selectivity, and the oncolytic effects after systemic delivery.

3T3 Cells↗

Timing of cognitive deficits following neonatal seizures: relationship to histological changes in the hippocampus.

Neonatal seizures are frequently associated with cognitive impairment and reduced seizure threshold. Previous studies in our laboratory have demonstrated that rats with recurrent neonatal seizures have impaired learning, lower seizure thresholds, and sprouting of mossy fibers in CA3 and the supragranular region of the dentate gyrus in the hippocampus when studied as adults. The goal of this study was to determine the age of onset of cognitive dysfunction and alterations in seizure susceptibility in rats subjected to recurrent neonatal seizures and the relation of this cognitive impairment to mossy fiber sprouting and expression of glutamate receptors. Starting at postnatal day (P) 0, rats were exposed to 45 flurothyl-induced seizures over a 9-day period of time. Visual-spatial learning in the water maze and seizure susceptibility were assessed in subsets of the rats at P20 or P35. Brains were evaluated for cell loss, mossy fiber distribution, and AMPA (GluR1) and NMDA (NMDAR1) subreceptor expression at these same time points. Rats with neonatal seizures showed significant impairment in the performance of the water maze and increased seizure susceptibility at both P20 and P35. Sprouting of mossy fibers into the CA3 and supragranular region of the dentate gyrus was seen at both P20 and P35. GluR1 expression was increased in CA3 at P20 and NMDAR1 was increased in expression in CA3 and the supragranular region of the dentate gyrus at P35. Our findings indicate that altered seizure susceptibility and cognitive impairment occurs prior to weaning following a series of neonatal seizures. Furthermore, these alterations in cognition and seizure susceptibility are paralleled by sprouting of mossy fibers and increased expression of glutamate receptors. To be effective, our results suggest that strategies to alter the adverse outcome following neonatal seizures will have to be initiated during, or shortly following, the seizures.

Animals↗

[Diagnostic value of tau in cerebrospinal fluid in alzheimer disease].

OBJECTIVE: To search for reliable and quantitative biochemical marker for diagnosis of Alzheimer disease. METHODS: ELISA-double enzyme amplification assay was used to detect the total tau and abnormally hyperphosphorylated (p-tau) in cerebrospinal fluid specimens of patients with Alzheimer disease (AD, N = 52, 30 from the Netherlands and 22 from Wuhan and Haikou, China), vascular dementia (VD, N = 46, 18 from the Netherlands and 28 from Haikou), and non-neurological disease (N = 37, 13 from the Netherlands and 24 from Haikou) and of normal elderly controls (N = 56, 26 from the Netherlands, and 30 from Wuan and Haikou). RESULTS: The measurement of CSF specimens from Netherlands Brain Bank showed that the levels of total tau and p-tau in CSF specimens of AD patients were significantly higher than those in CSF of patients with VD and non-dementia neurological disorders, and of age-matched non-neurological normal controls. With CSF tau > or = 370 pg/ml as the marker for diagnosis of AD, the sensitivity, specificity, reliability as well as differentiation rate of AD from VD were 90.0%, 79.0%, 82.8% and 66.7%, respectively. With CSF p-tau > or = 120 pg/ml as the marker for diagnosis of AD, the sensitivity, specificity, reliability as well as differentiation rate of AD from VD were 93.3%, 89.5%, 90.8%, and 83.3% respectively. The measurement of total and phosphorylated taus in CSF specimens of AD and non-AD patients and normal controls collected in China showed the similar results; and the sensitivity, specificity, reliability as well as differentiation rate of AD from VD were 77.3%, 85.4%, 83.7% and 71.4% with CSF tau > or = 120 pg/ml as the marker for diagnosis of AD. There was no correlation between CSF tau and p-tau and age, sex, and seriousness of disease. CONCLUSION: Increased phosphorylated tau in human cerebrospinal fluid is a reliable biomarker for diagnosis of Alzheimer disease.

Aged↗

Improved efficacy of chemotherapy for glioblastoma by radiation-induced opening of blood-brain barrier: clinical results.

PURPOSE: To improve the efficacy of chemotherapy for glioblastoma through the radiation-induced opening of the blood-brain barrier (BBB). METHODS AND MATERIALS: In two previous articles, we have described the results of brain scanning using technetium 99m-labeled somatostatin and the measurement of methotrexate (MTX) concentrations in blood and cerebrospinal fluid (CSF) after i.v. injection. We discovered that the BBB and blood-cerebrospinal fluid barrier opened to a certain extent after 20- to 40-Gy irradiation, thus increasing the degree to which MTX permeated the brain tissue. On the basis of these findings, we retrospectively analyzed the outcome in 56 patients with glioblastoma given either chemotherapy (CCNU) after 20- to 40-Gy irradiation (28 patients) or radiation therapy alone (28 patients). RESULTS: The 1-, 3-, and 5-year survival rates were 57.14%, 22.50%, and 15.00% in the combined-therapy group and 17.86%, 7.14%, and 3.57% in the radiotherapy alone group, respectively. The respective median survival times were 29.11 +/- 6.99 and 9.86 +/- 3.45 months (p < 0.001), which represented a statistically significant difference. CONCLUSION: Our study further confirms that opening of the BBB induced by irradiation with 20-40 Gy may optimize the effects of intracranial chemotherapy.

Adolescent↗

Molecular events in transmembrane signaling via E-selectin. SHP2 association, adaptor protein complex formation and ERK1/2 activation.

E-selectin is a cytokine-inducible adhesion molecule that is expressed by activated endothelial cells at sites of inflammation. In addition to supporting rolling and stable arrest of leukocytes, there is increasing evidence that E-selectin functions in transmembrane signaling into endothelial cells during these adhesive interactions. We have previously shown that adhesion of HL-60 cells (which express ligands for E-selectin), or antibody-mediated cross-linking of E-selectin, results in formation of a Ras/Raf-1/phospho-MEK macrocomplex, extracellular signal-regulated protein kinase (ERK1/2) activation, and c-fos up-regulation. All of these downstream signaling events appear to require an intact cytoplasmic domain of E-selectin. Here we demonstrate that tyrosine 603 in the cytoplasmic domain of E-selectin is required for the E-selectin-dependent ERK1/2 activation. Tyrosine 603 plays an important role in mediating the association of E-selectin with SHP2, and the catalytic domain of SHP2 is, in turn, critical for E-selectin-dependent ERK1/2 activation. An adapter protein complex consisting of Shc.Grb2.Sos bridges between SHP2 and the Ras.Raf.phospho-MEK macrocomplex. These molecular events thus outline a mechanism by which cross-linking of E-selectin by engagement of ligands on adherent leukocytes can initiate a multifunctional signaling pathway in the activated endothelial cell at sites of inflammation.

Adaptor Proteins, Signal Transducing↗

An ossified Meckel's cartilage in two Cretaceous mammals and origin of the mammalian middle ear.

An ossified Meckel's cartilage has been recovered from two early Cretaceous mammals from China. This element is similar to Meckel's cartilage in prenatal and some postnatal extant mammals and indicates the relationship of Meckel's cartilage with the middle ear in early mammals. The evidence shows that brain expansion may not be the initial factor that caused the separation of postdentary bones from the dentary as middle ear ossicles during mammalian evolution. The failure of the dentary to seize reduced postdentary elements during ontogeny of early mammals is postulated as an alternative mechanism for the separation. Modifications of both feeding and hearing apparatuses in early mammals may have led to the development of the definitive mammalian middle ear.

Animals↗

[Experimental study of in osteogenesis in duced by NIH-3T3 cells transfected with bone morphogenetic protein 3 gene].

OBJECTIVE: To investigate the gene expression, protein synthesis and inducing osteogenetic capacity of NIH-3T3 cells transfected with recombinant human bone morphogenetic protein 3 (rhBMP3) gene. METHODS: Gene recombination technique was used to clone the BMP3 cDNA into PcDNA3 vector directly, and to form a recombined BMP3-PcDNA3 cDNA, which was introduced into NIH-3T3 cells by means of lipofectamine transfer. The total RNA of transfected NIH-3T3 cells was then extracted to verify the mRNA expression of BMP3 using Northern blot method. BMP3 protein synthesis and AKP activity in the transfected cells was checked. Then, the NIH-3T3 cells transfected with BMP3 gene were injected into nude mouse muscle to evaluate the inducing osteogenesis in the muscle. RESULTS: BMP3 gene had been inserted into PcDNA3 vector successfully. There was BMP3 mRNA expression in the total RNA of NIH-3T3 cells with the peak level appearing in the 6th week after transfection, and BMP3 protein was found in NIH-3T3 cells, and the AKP level is much higher in the transfected NIH-3T3 cells than in non-transfected NIH-3T3 cells. Histologic examination revealed that there were a large number of chondrocytes and trabeculae seen in the nude mouse muscle 4 weeks after injection of the transfected NIH-3T3 cells. CONCLUSION: BMP3 is a protein that possesses osteogenetic effect. After transfection with BMP3-PCDNA3, BMP3 mRNA expression and protein formation can be found in NIH-3T3 cells, and the transfected NIH-3T3 cells have the effect of inducing osteogenesis in vivo.

3T3 Cells↗

Site-directed sulfhydryl labeling of the lactose permease of Escherichia coli: helices IV and V that contain the major determinants for substrate binding.

Helices IV and V in the lactose permease of Escherichia coli contain the major determinants for substrate binding [Glu126 (helix IV), Arg144 (helix V), and Cys148 (helix V)]. Structural and dynamic features of this region were studied by using site-directed sulfhydryl modification of 48 single-Cys replacement mutants with N-[(14)C]ethylmaleimide (NEM) in the absence or presence of ligand. In right-side-out membrane vesicles, Cys residues in the cytoplasmic halves of both helices react with NEM in the absence of ligand, while Cys residues in the periplasmic halves do not. Five Cys replacement mutants at the periplasmic end of helix V and one at the cytoplasmic end of helix V label only in the presence of ligand. Interestingly, in addition to native Cys148, a known binding-site residue, labeling of mutant Ala122 --> Cys, which is located in helix IV across from Cys148, is markedly attenuated by ligand. Furthermore, alkylation of the Ala122 --> Cys mutant blocks transport, and protection is afforded by substrate, indicating that Ala122 is also a component of the sugar binding site. Methanethiosulfonate ethylsulfonate, an impermeant thiol reagent shown clearly in this paper to be impermeant in E. coli spheroplasts, was used to identify substituted Cys side chains exposed to water and accessible from the periplasmic side. Most of the Cys mutants in the cytoplasmic halves of helices IV and V, as well as two residues in the intervening loop, are accessible to the aqueous phase from the periplasmic face of the membrane. The findings indicate that the cytoplasmic halves of helices IV and V are more reactive/accessible to thiol reagents and more exposed to solvent than the periplasmic half. Furthermore, positions that exhibit ligand-induced changes are located for the most part in the vicinity of the residues directly involved in substrate binding, as well as the cytoplasmic loop between helices IV and V.

Affinity Labels↗

Activation by IKKalpha of a second, evolutionary conserved, NF-kappa B signaling pathway.

In mammals, the canonical nuclear factor kappaB (NF-kappaB) signaling pathway activated in response to infections is based on degradation of IkappaB inhibitors. This pathway depends on the IkappaB kinase (IKK), which contains two catalytic subunits, IKKalpha and IKKbeta. IKKbeta is essential for inducible IkappaB phosphorylation and degradation, whereas IKKalpha is not. Here we show that IKKalpha is required for B cell maturation, formation of secondary lymphoid organs, increased expression of certain NF-kappaB target genes, and processing of the NF-kappaB2 (p100) precursor. IKKalpha preferentially phosphorylates NF-kappaB2, and this activity requires its phosphorylation by upstream kinases, one of which may be NF-kappaB-inducing kinase (NIK). IKKalpha is therefore a pivotal component of a second NF-kappaB activation pathway based on regulated NF-kappaB2 processing rather than IkappaB degradation.

Animals↗

Interference with immunoglobulin (Ig)alpha immunoreceptor tyrosine-based activation motif (ITAM) phosphorylation modulates or blocks B cell development, depending on the availability of an Igbeta cytoplasmic tail.

To determine the function of immunoglobulin (Ig)alpha immunoreceptor tyrosine-based activation motif (ITAM) phosphorylation, we generated mice in which Igalpha ITAM tyrosines were replaced by phenylalanines (Igalpha(FF/FF)). Igalpha(FF/FF) mice had a specific reduction of B1 and marginal zone B cells, whereas B2 cell development appeared to be normal, except that lambda1 light chain usage was increased. The mutants responded less efficiently to T cell-dependent antigens, whereas T cell-independent responses were unaffected. Upon B cell receptor ligation, the cells exhibited heightened calcium flux, weaker Lyn and Syk tyrosine phosphorylation, and phosphorylation of Igalpha non-ITAM tyrosines. Strikingly, when the Igalpha ITAM mutation was combined with a truncation of Igbeta, B cell development was completely blocked at the pro-B cell stage, indicating a crucial role of ITAM phosphorylation in B cell development.

Amino Acid Motifs↗

Evaluation of various evoked potential techniques for spinal cord monitoring during scoliosis surgery.

STUDY DESIGN: This prospective study compared the outcomes of different evoked potential (EP) techniques for intraoperative spinal cord monitoring. OBJECTIVES: To evaluate the reliability of different EP techniques administered during scoliosis surgery. SUMMARY OF BACKGROUND DATA: A number of different methods of intraoperative spinal cord monitoring are available. Because each has its own advantages and limitations, multimodal spinal cord monitoring has been proposed to improve monitoring reliability. MATERIALS AND METHODS: Cortical somatosensory-evoked potential (CSEP), cortical motor-evoked potential (CMEP), spinal somatosensory-evoked potential (SSEP), and spinal cord-evoked potential (SCEP) were applied simultaneously to 30 patients undergoing surgical correction for spinal deformity. The presence of the EP waveforms and their reproducibilities over separate tests were compared. In addition, the monitoring outcomes were evaluated with the clinical results. RESULTS: Of the 30 patients, CSEP waveforms were successfully recorded in 28 cases (93%), SCEP in 25 cases (83%), CMEP in 24 cases (80%), and SSEP in 21 cases (70%). Latencies of each EP technique showed no significant variability. However, amplitudes showed significant differences between different techniques. SCEP and CMEP showed clearer waveforms of greater amplitude that could be detected faster than CSEP and SSEP waveforms. SCEP and SSEP waveforms were more easily influenced by the surgical procedure. CONCLUSION: CSEP and CMEP are recommended for routine monitoring, so that both ascending and descending tracts are monitored. If adequate signals for either of these proposed monitoring methods cannot be easily obtained, SSEP can substitute for CSEP, whereas SCEP can substitute for CMEP.

Adolescent↗

Increased levels of sigJ mRNA in late stationary phase cultures of Mycobacterium tuberculosis detected by DNA array hybridisation.

In order to determine which genes are involved in maintaining viability of 100-day stationary-phase bacteria and persistent bacteria after antibiotic treatment, we used a mini-DNA array to examine the transcription of 82 genes of M. tuberculosis in the 100-day stationary-phase cultures before and after rifampicin treatment. We found that the mRNA level of a sigma factor gene, sigJ, was strongly up-regulated in the late stationary-phase cultures. Other genes were also up-regulated, although to a lesser extent than sigJ. Surprisingly, after rifampicin treatment there was no significant change in sigJ expression, and most of the other 82 genes in the mini-DNA array also maintained expression, some at relatively high levels. These results suggest that SigJ may control gene expression in the quiescent state and may be an important component in the mechanisms by which M. tuberculosis survives prolonged stationary phase even in the presence of sterilising antibiotics.

Anti-Bacterial Agents↗

Hepatitis B virus X protein differentially activates RAS-RAF-MAPK and JNK pathways in X-transforming versus non-transforming AML12 hepatocytes.

The hepatitis B virus (HBV) X protein (pX) is implicated in hepatocarcinogenesis of chronic HBV patients by an unknown mechanism. Activities of pX likely relevant to hepatocyte transformation include activation of the mitogenic RAS-RAF-MAPK and JNK pathways. To assess the importance of mitogenic pathway activation by pX in transformation, we employed a cellular model system composed of two tetracycline-regulated, pX-expressing cell lines, constructed in AML12-immortalized hepatocytes. This system includes the differentiated 3pX-1 and the de-differentiated 4pX-1 hepatocytes. Our studies have demonstrated that conditional pX expression transforms only 3pX-1 cells. Here, comparative in vitro kinase assays and various in vivo analyses demonstrate that pX affects an inverse activation of RAS-RAF-MAPK and JNK pathways in 3pX-1 versus 4pX-1 cells. Sustained pX-dependent RAS-RAF-MAPK pathway activation is observed in pX-transforming 3pX-1 cells, whereas sustained pX-dependent JNK pathway activation is observed in pX non-transforming 4pX-1 cells. This differential, pX-dependent mitogenic pathway activation affects differential activation of cAMP-response element-binding protein and c-Jun and determines the proliferative response of 3pX-1 and 4pX-1 cells. Furthermore, tetracycline-regulated, pX-NLS-expressing cell lines demonstrate that expression of the nuclear pX-NLS variant minimally activates the RAS-RAF-MAPK pathway and results in markedly reduced transformation. These results link sustained, pX-mediated activation of RAS-RAF-MAPK pathway to hepatocyte transformation.

Cell Division↗

Purification of lactonic sophorolipids by crystallization.

Various experimental methods for purifying lactonic sophorolipids (SLs) via crystallization were studied. The commonly used solvent, ethanol, was found to have much higher solubility of the lactonic SLs than the acid SLs. Consequently, for purification of lactonic SLs, ethanol not only lacked the selectivity in removing acidic SLs but also resulted in significant loss of desired products. Aqueous buffers were subsequently studied as the solvent, based on the rationale that acidic SLs, having the free carboxylic acid group(s), are more hydrophilic than the lactonic SLs, especially at higher pH. Both phthalate and phosphate buffers were found more suitable for purifying lactonic SLs than ethanol. A practical and effective method for purifying lactonic SLs to about 99% purity using phosphate buffers was developed. The FTIR spectra also showed significantly less SL components with free acid groups in the purified SLs than in the crude SLs, confirming the removal of acidic SLs in the purification.

Buffers↗