Gentiopicroside (GPS) is a highly water-soluble small-molecule drug and the main bioactive secoiridoid glycoside of Gentiana scabra that has been shown to have hepatoprotective effects against non-alcoholic steatohepatitis (NASH), a form of non-alcoholic fatty liver disease (NAFLD) that can progress to cirrhosis and hepatocellular carcinoma. However, the effects of GPS on NASH and the underlying mechanisms remain obscure. Firstly, a high-fat, high-cholesterol (HFHC) diet and a high-sugar solution containing d-fructose and d-glucose were used to establish a non-alcoholic steatohepatitis (NASH) mice model. Secondly, we confirmed GPS supplementation improve metabolic abnormalities and reduce inflammation in NASH mice induced by HFHC and high-sugar solution. Then we used metabolomics to investigate the mechanisms of GPS in NASH mice. Metabolomics analysis showed GPS may work through the Peroxisome Proliferator-Activated Receptor (PPAR) signaling pathway and glycine, serine, and threonine metabolism. Functional metabolites restored by GPS included serine, glycine, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Western blot and qRT-PCR analysis confirmed GPS improve NASH by regulating PPARα and Hypoxia-Inducible Factor-1α (HIF-1α) signaling pathways. In vitro, studies further demonstrated EPA and DHA enhance fatty acid oxidation through the PPARα pathway, while serine and glycine inhibit oxidative stress through the HIF-1α pathway in palmitic acid-stimulated HepG2 cells. Our results suggest GPS’s anti-inflammatory and anti-steatosis effects in NASH progression are related to the suppression of HIF-1α through the restoration of L-serine and glycine and the activation of PPARα through increased EPA and DHA.

AbstractThe metabolic implications in Alzheimer’s disease (AD) remain poorly understood. Here, we conducted a metabolomics study on a moderately aging Chinese Han cohort (n = 1397; mean age 66 years). Conjugated bile acids, branch-chain amino acids (BCAAs), and glutamate-related features exhibited strong correlations with cognitive impairment, clinical stage, and brain amyloid-β deposition (n = 421). These features demonstrated synergistic performances across clinical stages and subpopulations and enhanced the differentiation of AD stages beyond demographics and Apolipoprotein E ε4 allele (APOE-ε4). We validated their performances in eight data sets (total n = 7685) obtained from Alzheimer’s Disease Neuroimaging Initiative (ADNI) and Religious Orders Study and Memory and Aging Project (ROSMAP). Importantly, identified features are linked to blood ammonia homeostasis. We further confirmed the elevated ammonia level through AD development (n = 1060). Our findings highlight AD as a metabolic disease and emphasize the metabolite-mediated ammonia disturbance in AD and its potential as a signature and therapeutic target for AD.

Mycotoxins and pesticides are the most concerning chemical contaminants that can affect the quality of Pu-erh tea during its production and storage. This study presents a method that can simultaneously determine 31 pesticide residues and six mycotoxins in Pu-erh tea within 11 min using ultra-high-performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS) after QuEChERS extraction. The lower limit of quantification (LOQ) for all analytes ranged between 0.06 and 50 ppb. Recoveries for each pesticide and mycotoxin ranged between 62.0 and 130.3%, with intra- and inter-day precisions lower than 15%. Good linear relationships were obtained, with correlation coefficients of r2 > 0.991 for all analytes. The established method was applied to 31 Pu-erh tea samples, including raw and ripened Pu-erh tea with different storage times. As a result, pesticide residues were not detected in any of the collected samples, and the mycotoxins detected in the samples were well below the official maximum residue limits (MRLs). Notably, the levels of aflatoxin B1 (AFB1), aflatoxin G1 (AFG1) and aflatoxin G2 (AFG2) were lower than 1 ppb in the samples stored for more than 30 years.

Sex disparities in serum bile acid (BA) levels and Alzheimer's disease (AD) prevalence have been established. However, the precise link between changes in serum BAs and AD development remains elusive. Here, authors quantitatively determined 33 serum BAs and 58 BA features in 4 219 samples collected from 1 180 participants from the Alzheimer's Disease Neuroimaging Initiative. The findings revealed that these BA features exhibited significant correlations with clinical stages, encompassing cognitively normal (CN), early and late mild cognitive impairment, and AD, as well as cognitive performance. Importantly, these associations are more pronounced in men than women. Among participants with progressive disease stages (n = 660), BAs underwent early changes in men, occurring before AD. By incorporating BA features into diagnostic and predictive models, positive enhancements are achieved for all models. The area under the receiver operating characteristic curve improved from 0.78 to 0.91 for men and from 0.76 to 0.83 for women for the differentiation of CN and AD. Additionally, the key findings are validated in a subset of participants (n = 578) with cerebrospinal fluid amyloid-beta and tau levels. These findings underscore the role of BAs in AD progression, offering potential improvements in the accuracy of AD prediction.

An essential function of the epidermis is to provide a physical barrier that prevents the loss of water. Essential mediators of this barrier function include ceramides, cholesterol, and very long chain fatty acids, and their alteration causes human pathologies, including psoriasis and atopic dermatitis. A frameshift mutation in the human ZNF750 gene, which encodes a zinc finger transcription factor, has been shown to cause a seborrhea-like dermatitis. Here, we show that genetic deletion of the mouse homolog ZFP750 results in loss of epidermal barrier function, which is associated with a substantial reduction of ceramides, nonpolar lipids. The alteration of epidermal lipid homeostasis is directly linked to the transcriptional activity of ZFP750. ZFP750 directly and/or indirectly regulates the expression of crucial enzymes primarily involved in the biosynthesis of ceramides. Overall, our study identifies the transcription factor ZFP750 as a master regulator epidermal homeostasis through lipid biosynthesis and thus contributing to our understanding of the pathogenesis of several human skin diseases.

Chiral drugs are very complex substances since individual enantiomers may differ in pharmacological and toxic effects, making it necessary to analyze enantiomers separately. In this study, we investigated the chiral differentiation of two ezetimibe enantiomers (i.e., SRS-EZM and RSR-EZM) and their mechanisms in complex with β-cyclodextrins (CDs) and metal ions as the auxiliary ligands. For this purpose, two complementary approaches have been employed: electrospray-tandem mass spectrometry (ESI-MS/MS) with collision induced dissociation (CID) and molecular modeling methods, including density functional theory (DFT) calculations and molecular dynamics (MD) simulations. The results showed a good agreement between experimental and theoretical data. It was demonstrated that SRS-EZM can be easily distinguished from RSR-EZM by applying CID in ESI-MS/MS. SRS-EZM is likely to form a more stable complex with β-CD and metal ions, and thus the [SRS-EZM]-Cu-[β-CD] cluster is more energetically difficult to separate from the SRS-EZM molecule compared with RSR-EZM. Such a difference may be attributed to the interactions between the drug molecule and the metal ion, as well as the cavity shape changes of the β-CDs upon complexation with molecular guests. Therefore, enantiomers in chiral drug can be recognized as ternary complexes of metal-analyte-β-CD by ESI-MS/MS with CID.

INTRODUCTION There is evidence that there are differences in the serum levels of bile acids (BAs) in males and females and their risk of developing Alzheimer’s disease (AD). We previously reported that serum BAs are associated with AD. It remains unclear, however, how changes in serum BAs may relate to the development of AD in a sex-dependent manner. METHODS We analyzed 33 BAs in the sera of 4219 samples from 1180 subjects in the ADNI cohort. Using linear models, we examined the associations between BAs and mild cognitive impairment (MCI) progression and clinical markers. RESULTS Significant alterations in BA profiles occurred at an early stage of MCI and were associated with the onset and progression of MCI. These changes were more dramatic in men than in women. BA markers improved the ability of current clinical markers to diagnose MCI and predict its progression. DISCUSSION Our results highlight the role of BAs in the development of AD and may help improve AD prediction and personalized therapies. Research in context 1. Systematic review: We examined the relationship between bile acid (BA), mild cognitive impairment (MCI), and Alzheimer’s disease (AD). We previously reported this association. Our findings were consistent with those of other studies, although previous research did not consider sex differences or comprehensively evaluate the potential of BAs as diagnostic markers for AD. 2. Interpretation : Our results suggest that changes in BA profiles may play a role in the development of AD and that sex-specific differences may be important for personalized prediction and management of the disease. 3. Future directions : In the future, it will be important to confirm our findings with other independent samples and further investigate the ways in which BA metabolism, including cholesterol catabolism in the liver and brain, may contribute to AD. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This work was supported by National Key R&D Program of China (2021YFA1301300) and National Natural Science Foundation of China (82270917, 81974073, and 31972935). Funding for ADMC (Alzheimer's Disease Metabolomics Consortium, led by Dr R.K.D. at Duke University) was provided by the National Institute on Aging grant R01AG046171, a component of the Accelerating Medicines Partnership for AD (AMP AD) Target Discovery and Preclinical Validation Project () and the National Institute on Aging grant RF1 AG0151550, a component of the M2OVE-AD Consortium (Molecular Mechanisms of the Vascular Etiology of AD Consortium ). ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: Metabolomics datasets used in the current analyses for the ADNI 1 and ADNI GO 2 cohorts are available via the Accelerating Medicines Partnership Alzheimer's Disease (AMP AD) Knowledge Portal and can be accessed at (ADNI 1) and (ADNI GO 2). The full complement of clinical and demographic data for the ADNI cohorts are hosted on the LONI data sharing platform and can be requested at . I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines and uploaded the relevant EQUATOR Network research reporting checklist(s) and other pertinent material as supplementary files, if applicable. Yes Metabolomics datasets used in the current analyses for the ADNI 1 and ADNI GO 2 cohorts are available via the Accelerating Medicines Partnership Alzheimer's Disease (AMP AD) Knowledge Portal and can be accessed at (ADNI 1) and (ADNI GO 2). The full complement of clinical and demographic data for the ADNI cohorts are hosted on the LONI data sharing platform and can be requested at . * Abbreviations: NC : Normal cognition MCI : Mild cognitive impairment EMCI : Early mild cognitive impairment LMCI : Late mild cognitive impairment AD : Alzheimer’s disease sMCI : sustained MCI cMCI : converted MCI ADNI : Alzheimer’s Disease Neuroimaging Initiative ROSMAP : Religious Orders Study and Rush Memory and Aging BA : Bile acid TBA : Concentration of total bile acids CA : Cholic acid CA% : Concentration percentage of cholic acid to total bile acids DCA/CA : Ratio of deoxycholic acid and cholic acid GDCA/CA : Ratio of deoxycholic acid glycine conjugate and cholic acid CDCA : Chenodeoxycholic acid A/T/N : Amyloid-beta, tau, and neurodegenerative APOE-4 : apolipoprotein E ε4 genotype UK CPRD : Clinical Practice Research Datalink database of United Kingdom AUC : Area under Receiver Operating Characteristic Curve UPLC-MS/MS : ultra-performance liquid chromatography coupled to tandem mass spectrometry PCA : Principle component analysis LOESS : locally weighted regression

The contribution of nutrient availability to control epidermal cell proliferation, inflammation, and hyperproliferative diseases remains unknown. Here, we studied extracellular serine and serine/glycine metabolism using human keratinocytes, human skin biopsies, and a mouse model of psoriasis-like disease. We focused on a metabolic enzyme, serine hydroxymethyltransferase (SHMT), that converts serine into glycine and tetrahydrofolate-bound one‑carbon units to support cell growth. We found that keratinocytes are both serine and glycine auxotrophs. Metabolomic profiling and hypoxanthine supplementation indicated that SHMT silencing/inhibition reduced cell growth through purine depletion, leading to nucleotide loss. In addition, topical application of an SHMT inhibitor suppressed both keratinocyte proliferation and inflammation in the imiquimod model and resulted in a decrease in psoriasis-associated gene expression. In conclusion, our study highlights SHMT2 activity and serine/glycine availability as an important metabolic hub controlling both keratinocyte proliferation and inflammatory cell expansion in psoriasis and holds promise for additional approaches to treat skin diseases.

Background: Previously, we demonstrated that the chlamydial protein pGP3 forms a stable complex with LL-37 to neutralize its proinflammatory activity during the pathogenesis of psoriasis. The middle domain of pGP3 (pGP3M) is critical for the binding and neutralization of LL-37. Here, we further examined the mechanism underlying pGP3-mediated inhibition of psoriasis progression and evaluated the inhibitory effect of pGP3M on the development of psoriasis-like skin lesions in mice. Material/Methods: Stock solutions of pGP3M and pGP3 (100 mu g/mL) were prepared using sterile ultrapure water and intramus-cularly injected into the left leg of the imiquimod (IMQ)-induced psoriasis mouse model. The severity of skin lesions was evaluated based on the psoriasis area and severity index score and ear skin thickness. The skin biopsy and blood samples were collected on the 8th day for histological analysis and inflammatory cytokines detection. Results: Erythema, scaling, and thickening were observed on the dorsal skin and the right ear skin of IMQ-treated mice. Treatment with pGP3 and pGP3M alleviated the IMQ-induced erythema, inflammatory cell infiltration, and scaly plaques. Compared with IMQ-treated and PBS-treated mice, pGP3- and PGP3M-treated mice had less inflammatory cell infiltration in skin tissues and had significantly reduced IL-17A, IFN-gamma, and IL-22 levels in serum. Conclusions: The anti-psoriatic efficacy of exogenous pGP3M was similar to that of pGP3. This indicated that pGP3M attenuated the IMQ-induced inflammatory and psoriatic symptoms in mice by binding and inhibiting LL-37. Further research is needed to examine the toxicity of pGP3 and pGP3M before clinical trial evaluation.

The application of metabolomics in translational research suffers from several technological bottlenecks, such as data reproducibility issues and the lack of standardization of sample profiling procedures. Here, we report an automated high-throughput metabolite array technology that can rapidly and quantitatively determine 324 metabolites including fatty acids, amino acids, organic acids, carbohydrates, and bile acids. Metabolite identification and quantification is achieved using the Targeted Metabolome Batch Quantification (TMBQ) software, the first cross-vendor data processing pipeline. A test of this metabolite array was performed by analyzing serum samples from patients with chronic liver disease (N = 1234). With high detection efficiency and sensitivity in serum, urine, feces, cell lysates, and liver tissue samples and suitable for different mass spectrometry systems, this metabolite array technology holds great potential for biomarker discovery and high throughput clinical testing. Additionally, data generated from such standardized procedures can be used to generate a clinical metabolomics database suitable for precision medicine in next-generation healthcare.

SUMMARYFructose metabolism is increasingly recognized as a preferred energy source for cancer cell proliferation. However, it remains unclear why cancer cells favor fructose metabolism and how they acquire a sufficient amount of fructose. Here we report that cancer cells convert glucose into fructose through intra- and extracellular polyol pathways. The fructose metabolism bypasses normal aerobic respiration’s self-control to supply excessive metabolites to glycolysis and promotes the Warburg effect. Inhibition of fructose production drastically suppressed glycolysis and ATP production in cancer. Furthermore, we determined that a glucose transporter, SLC2A8/GLUT8, exports intracellular fructose to other cells in the tumor microenvironment. Taken together, our study suggests that the Warburg effect is achieved by means of fructose metabolism, instead of glucose metabolism alone.

Fructose metabolism is increasingly recognized as a preferred energy source for cancer cell proliferation. However, dietary fructose rarely enters the bloodstream. Therefore, it remains unclear how cancer cells acquire a sufficient amount of fructose to supplement their energy needs. Here we report that the cancer cells can convert glucose into fructose through intraand extracellular polyol pathways. The fructose metabolism bypasses normal aerobic respiration’s self-control to supply excessive metabolites to glycolysis and causes the Warburg effect. Inhibition of fructose production drastically suppressed glycolysis and ATP production in cancers. Furthermore, we determined that a glucose transporter, SLC2A8/GLUT8, exports intracellular fructose to other cells in the tumor microenvironment. Taken together, our study identified overlooked fructose resources for cancer cells as an essential part of their metabolic reprogramming and caused the Warburg effect. Declaration of Interests The authors declare no competing interests. 1 Cancer Biology Program, University of Hawaii Cancer Center, Honolulu, HI, 96813, USA. 2 Human Metabolomics Institute, Inc., Shenzhen, Guangdong, 518109, China. 3 Shanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China. 4 School of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong. *Equal contributions. Correspondence: WJia@cc.hawaii.edu.

Taro (Colocasia esculenta) is a high fiber tuber that holds cultural and agricultural importance in the Pacific. The high fiber content offers potential as a dietary prebiotic through the presence of resistant starch (RS). RS aids gut bacteria in the production of short-chain fatty acids (SCFA), which have health benefits to the host. As such, this study aimed to investigate the effect of taro on gut bacteria composition and SCFA production through in vitro human digestion and fecal fermentation methodology. Five taro varieties (Bun Long, Mana Ulu, Moi, Kauai Lehua, Tahitian) were processed. RS concentration of taro was determined using Megazyme Resistant Starch kit. Taro samples were subjected to in vitro human digestion, replicating oral, gastric, small intestinal, and large intestinal phases. Digested taro samples were mixed with fresh human fecal slurries and fermented at 37°C for 24 hours. During fermentation, samples were collected at specific time points for analyzation of SCFA contents using gas chromatography and bacterial composition using 16S rRNA gene targeted amplicon sequencing. Tahitian variety had the highest RS concentration of 25.1%, with no significantly difference between Tahitian, Bun Long, and Moi varieties. All taro varieties exhibited statistically similar SCFA concentrations for 3-hydroxybutyric acid, acetic acid and propionic acid. Bun-Long, Tahitian, and Moi varieties exhibited significantly higher butyric acid levels than two other taro varieties. Butyric acid production had the highest correlation coefficient with RS concentration of 0.80. The bacterial community present in all taro varieties after 24 hours of fermentation was markedly different from that of the control communities, including shifts in both the Bacteriodes and Firmicutes phyla. Different taro varieties have varying RS concentrations that affect the production of SCFA in an in vitro human digestion and fecal fermentation. The production of health-promoting butyric acid shows a strong positive correlation with the resistant starch concentration of taro. Taro distinctly causes shifts after 24 hours of fecal fermentation in Bacteriodes and Firmicutes phyla. These results provide new insights into the modulation of gut microbiota through dietary interventions. USDA-NIFA Hatch C-Maīki, University of Hawaii.

目前磷酸化肽段鉴定主要依赖于质谱技术,但磷酸化肽段的低丰度性以及来自非磷酸化肽段的干扰等因素,影响质谱的分析与鉴定.因此质谱分析前磷酸化肽段的富集,是深入研究磷酸化蛋白质组学的先决条件.该文介绍了磷酸化蛋白质组学中传统的以及新建立的一些磷酸化肽段分离富集方法的原理及优缺点,这些方法包括固相金属离子亲和色谱法(IMAC)、金属氧化亲和色谱法(MOAC)、强阳/阴离子交换色谱法(SCX/SAX)、亲水相互作用色谱法(HILIC)、静电排斥亲水相互作用色谱法(ERLIC)、化学衍生法、MALDI靶盘富集法以及多种富集方法相结合.

Background: Hepatocellular carcinoma (HCC) pathogenesis involves the alteration of multiple liver-specific metabolic pathways. We systematically profiled cancer- and liver-related classes of metabolites in HCC and adjacent liver tissues and applied supervised machine learning to compare their potential yield for HCC biomarkers. Methods: Tumor and corresponding liver tissue samples were profiled as follows: Bile acids by ultra-performance liquid chromatography (LC) coupled to tandem mass spectrometry (MS), phospholipids by LC-MS/MS, and other small molecules including free fatty acids by gas chromatography—time of flight MS. The overall classification performance of metabolomic signatures derived by support vector machine (SVM) and random forests machine learning algorithms was then compared across classes of metabolite. Results: For each metabolite class, there was a plateau in classification performance with signatures of 10 metabolites. Phospholipid signatures consistently showed the highest discrimination for HCC followed by signatures derived from small molecules, free fatty acids, and bile acids with area under the receiver operating characteristic curve (AUC) values of 0.963, 0.934, 0.895, 0.695, respectively, for SVM-generated signatures comprised of 10 metabolites. Similar classification performance patterns were observed with signatures derived by random forests. Conclusion: Membrane phospholipids are a promising source of tissue biomarkers for discriminating between HCC tumor and liver tissue.

建立了QuEChERS/高效液相色谱-串联质谱(HPLC-MS/MS)测定土壤中61种激素类药物残留的分析方法.样品经乙腈提取,QuEChERS方法净化后进行HPLC-MS/MS测定.采用电喷雾离子源(ESI),正、负模式扫描,多反应监测(MRM)模式采集,基质匹配工作曲线法定量.结果 表明:61种目标化合物在各自浓度范围内线性良好,相关系数(r2)为0.991 8 ～0.999 8,检出限(LOD,S/N≥3)为0.01 ～2.3 μg/kg,定量下限(LOQ,S/N≥10)为0.03 ～7.5 μg/kg;在10、50、200 μg/kg 3个加标水平下,平均回收率为62.6％ ～ 102％,相对标准偏差(n=6)为1.0％～11％.该方法简单、快速、重现性好、稳定性高,可满足土壤中61种激素类药物残留的检测要求.

Introduction: Pyruvate kinase is a key enzyme in glucose metabolism, converting phosphoenolpyruvate to pyruvate. The muscle-specific isoform (Pkm1) is highly expressed in the heart and directs pyru...

PHT2, a member of the proton-coupled oligopeptide transporter family, participates in the transportation of small peptides and histidine from lysosomes to the cytosol. It facilitates maintenance of intracellular peptide homeostasis. However, it remains a challenge to elucidate the functional properties of PHT2 due to its localization in the lysosomal membrane. The aim of this study was to explore the transport function and substrate properties of human PHT2 (hPHT2) by transfecting Madin-Darby canine kidney cells with hPHT2 mutants to obtain stably expressed protein in the cell membrane. Using this cell model, we found that the transport activity of hPHT2 reached a maximum capacity when the extracellular pH was 5.5. hPHT2 showed relatively low affinity for Gly-Sar and relatively high affinity for d3-L-histidine, with Km values of 428 ± 88 μM and 66.9 ± 5.7 μM, respectively. Several typical substrates or inhibitors of PEPT1 and PEPT2, including valacyclovir, Gly-Gly-Gly, and cefadroxil but not 5-aminolevulinic acid or captopril, were proven to be substrates of hPHT2. However, hPHT2 showed low affinity for valacyclovir with a Km value of 5350 ± 1234 μM. In conclusion, this study established a suitable and efficient cell model to explore the function of hPHT2 in vitro and provided important information on the transport activity and substrate properties of hPHT2.

A mass spectrometric method is introduced for rapid and accurate chiral quantification by examining a trimeric metal complex into which a chiral reference is incorporated with the analyte. Several metal ions (CuII , NiII , MgII , MnII , CoII , and ZnII ) were selected as the central metal ion, and chiral drugs ezetimibe (EZM) and ambrisentan (AMB) were used as the reference to each other for isomeric differentiation by using electrospray ionization quadrupole time-of-flight mass spectrometry. Doubly charged trimeric cluster ions instead of the singly charged clusters were applied in this study. Kinetic method (KM) and chiral recognition (CR) method were used for construction of a calibration curve for chiral quantitation. The results from the two methods were found to be complementary to each other, which improved quantitative analysis of stereoisomers for EZM. Furthermore, we have successfully used S-AMB as reference for the chiral differentiation of enantiomeric atorvastatin (ATO), which is frequently combined with EZM as a codrug. Experimental results showed that the binary mixture of EZM and ATO enantiomers can be determined simultaneously without prior separation steps. The direct measurement of chiral purity within 5% was demonstrated. This mass spectrometric method represents an effective alternative to commonly used chromatographic techniques as means of chiral purity determination and is of potential use in rapid screening experiments.