Genetic profile and biological implication of PIN2/TRF1-interacting telomerase inhibitor 1 (PinX1) in human cancers: an analysis using The Cancer Genome Atlas.

Pin2/TRF1-interacting telomere inhibitor 1 (PinX1) was originally identified as a telomerase inhibitor, involved in maintaining telomerase activity, telomere length, and chromosomal stability. However, research has shown that PinX1 can have opposing molecular status in its expression patterns in several other tumor types. We thus investigated the genetic profile and biological implication of PinX1 in several human cancers using the cBioportal database. Our results showed that PinX1 deletion accounted for the most alterations, with the frequency of its deletion regularly occurring in pathological types of carcinosarcoma and adenocarcinoma. We found few instances of PinX1 gene mutations and 3D structural analysis demonstrated that these mutation sites were always located within telomerase inhibitor domains. Furthermore, our analysis of several human cancers from the cBioportal database revealed more frequent PinX1 homozygous depletion and PinX1 heterozygous deficiency, but both more infrequent PinX1 gain and rare instances of PinX1 amplification. The status of PinX1 genetic alterations was correlated with prognosis and may be tumor-type specific. As such, its biological function in tumorigenesis and later prognosis is complicated and may involve co-worked with NEIL2, R3HCC1, POLR3D, GTF2E2, and INTS10. In addition, we observed that PinX1 interacts with TERT, DKC1, PTGES3, and HSP90AA1. PinX1 mRNA expression was decreased in most selected cancer tissues, which could promote tumor growth and enhance tumorigenicity. Collectively, our data reveal PinX1 expression patterns and potential mechanisms in various human cancers. Further work will be needed to comprehensively examine its role in tumor genesis and progression.

High Residual Tumor Rate for Early Breast Cancer Patients Receiving Vacuum-assisted Breast Biopsy.

Purpose: The objective of study is aiming to investigate the residual tumor rate after Vacuum-assisted Breast Biopsy (VABB) for early breast cancer excision and the efficacy of mammogram and ultrasound in detecting residual tumor. Methods: Patients who underwent VABB and were confirmed with breast cancer in Sun Yat-sen University Cancer Center from 2010 to 2015 were reviewed retrospectively. The residual tumor rate determined by histological examination was calculated, and then was compared with the results estimated by mammogram and ultrasound which were performed post VABB but before subsequent surgery. Univariate and multivariate analysis (logistic regression) were carried out to identify the independent risk factors associated with residual tumor. Results: In total, 126 eligible patients with early breast cancer were recruited for this study, of whom 79 (62.7%) had residual tumor and 47 (37.3 %) underwent complete excision. The residual tumor rates for lesions < 10mm, lesions 10 to 20 mm and lesions >20mm in size were 55.0%, 68.9% and 53.1%, respectively. The complete excision rates estimated by mammogram and ultrasound were 76.5% and 73.9%, with a negative predictive value of only 46.2% and 50.6%, respectively. In the multivariate logistic regression analysis, no specific factors were found associated with risk of residual tumor (all P > 0.05). Conclusions: There was a high residual tumor rate after VABB in early breast cancer. Both mammogram and ultrasound could not effectively detect the residual tumor after VABB.

[Role of immunologic abnormality in recurrent parotitis in children].

OBJECTIVE: To investigate the relationship between immune function and the recurrent parotitis (RP) for children. METHODS: The children diagnosed as RP were divided into two groups: aged under 6y and over 6y and the immune function were measured and compared with that of normal children. RESULTS: For RP children the ratio of CD4+ T cell in over 6y group was significantly lower than that in under 6y group (P<0.05), while IgG value in over 6y group was higher than that in under 6y group (P<0.05). Compared with normal children, RP children in under 6y group had higher CD8+ T cell ratio and IgG, IgE, IgA and C3 value (P<0.01) and lower CD4+ T cell ratio (P<0.01), while RP children over 6y group, they had higher CD8+ T cell ratio, IgE value (P<0.01) and C3 (P<0.05), lower CD4

[Histone demethylase LSD1 and its biological functions].

Discovery of histone lysine specific demethylase 1 (LSD1) indicates that even histone methylation is reversible. Structural analysis shows that LSD1 is a flavin-dependent amine oxidase, which is able to catalyze the specific removal of methyl groups from mono- and dimethylated Lys4 and Lys9 of histone H3. Functional studies demonstrate that LSD1 regulates activation and inhibition of gene transcription in the nucleus, which is known as the innermost gene switch of cells. LSD1 plays important roles in embryonic development and tumorigenesis. Here, we review recent insights into the structure and chemical mechanism of LSD1, and its regulatory roles in development and cancer.

Baicalin attenuates oxygen-glucose deprivation-induced injury by inhibiting oxidative stress-mediated 5-lipoxygenase activation in PC12 cells.

AIM: To determine whether the flavonoid baicalin attenuates oxygen-glucose deprivation (OGD)-induced injury by inhibiting oxidative stress-mediated 5-lipoxygenase (5-LOX) activation in PC12 cells. METHODS: The effects of baicalin and the 5-LOX inhibitor zileuton on the changes induced by OGD/recovery or H(2)O(2) (an exogenous reactive oxygen species [ROS]) in green fluorescent protein-5-LOX-transfected PC12 cells were compared. RESULTS: Both baicalin and zileuton attenuated OGD/recovery- and H(2)O(2)-induced injury and inhibited OGD/recovery-induced production of 5-LOX metabolites (cysteinyl leukotrienes) in a concentration-dependent manner. However, baicalin did not reduce baseline cysteinyl leukotriene levels. Baicalin also reduced OGD/recovery-induced ROS production and inhibited 5-LOX translocation to the nuclear envelope and p38 phosphorylation induced by OGD/recovery and H(2)O(2). In contrast, zileuton did not show these effects. CONCLUSION: Baicalin can inhibit 5-LOX activation after ischemic injury, which may partly result from inhibition of the ROS/p38 mitogen-activated protein kinase pathway.

Effect of nitric oxide on the proliferation of AGS gastric cancer cells.

BACKGROUND AND OBJECTIVE: Nitric oxide (NO) is involved in many physiologic and pathologic processes. As an important biologic mediator, NO has been the focus of cancer study for its function in tumorigenesis, tumor progression, and death. This study investigated the effect of NO donor sodium nitroprusside (SNP) on the growth and proliferation of gastric cancer cell line AGS. METHODS: The growth inhibition of AGS cells was analyzed using MTT assay. The cell cycle was measured using flow cytometry. The changes of mRNA expression of proliferating cell nuclear antigen (PCNA) and caspase-3 were examined using reverse transcriptase polymerase chain reaction (RT-PCR), and the protein expressions of PCNA and caspase-3 were analyzed using Western blot. RESULTS: Dose-dependent SNP inhibited cell growth and proliferation. When the AGS cells were treated with SNP at 100, 500, 1000, 1500, and 2000 mumol/L for 24 h, the growth inhibition rates were (2.02 +/- 2.96)%, (10.82 +/- 2.21)%, (18.95 +/- 3.35)%, (26.88 +/- 2.54)%, and (42.57 +/- 1.27)%, respectively (P < 0.05). SNP altered the cell cycle in AGS cells. Compared with the control group, treatment with SNP at 100, 500, 1000, 1500, and 2000 mumol/L for 24 h reduced the number of cells in the S phase by 2.29%, 7.8%, 11.34%, 20.49%, and 23.6%, respectively, and enhanced the number of cells in the G1/G0 phases by 3.33%, 9.3%, 13.46%, 21.37%, and 24.73%, respectively (P < 0.05). With the increasing concentration and action time of SNP, the expressions of PCNA mRNA and protein decreased. The expression of caspase-3 mRNA remained unchanged, but procaspase-3 was activated. CONCLUSION: NO not only inhibits cell growth and proliferation, but also induces apoptosis in gastric cancer cells, and such effects of NO showed significant dose-dependent activity.

[Urethral guidance probe applied to surgical urethral realignment].

OBJECTIVE: To search for a safe and convenient surgical method for management of urethral disruption. METHODS: We performed urethral realignment for 18 cases of posterior urethral disruption and 4 cases of ruptured bulbous urethra using the urethral guidance probe following bladder puncture stoma. RESULTS: Urethral realignment was accomplished in 21 of the cases, 18 under epidural and 3 under local anesthesia, with the mean blood loss of 20 ml and the average operation time of 18 minutes. Open surgery was necessitated in 1 case due to the complication of bladder rupture. Routine postoperative urethral dilation extended for 3 months, and all the cases were followed up for 3 to 24 months. The maximum urine flow rate was 15-22 ml/s in 13 cases and 10-14 ml/s in 7. One case received urethral anastomosis 3 months later because of urethrostenosis. CONCLUSIONS: Urethral realignment with the urethral guidance probe is a safe, convenient and effective surgical strategy for the management of urethral disruption.

Oxygen-glucose deprivation activates 5-lipoxygenase mediated by oxidative stress through the p38 mitogen-activated protein kinase pathway in PC12 cells.

5-Lipoxygenase (5-LOX) is a key enzyme catalyzing arachidonic acid to form leukotrienes. We have reported that ischemic-like injury activates 5-LOX in PC12 cells; however, the mechanisms are unknown. To determine whether ischemic-like injury activates 5-LOX mediated by oxidative stress through the p38 MAPK pathway, we transfected GFP-5-LOX into PC12 cells and induced ischemic-like injury by oxygen-glucose deprivation (OGD). We found that the transfected GFP-5-LOX was localized primarily in the nuclei and translocated to the nuclear envelope after OGD/recovery reaching a maximum 2 hr after a 2-hr exposure to OGD. The nonselective 5-LOX inhibitor caffeic acid, 5-LOX-activating protein inhibitor MK886, and selective 5-LOX inhibitor zileuton attenuated the cell injury and reduced the production of 5-LOX products, cysteinyl leukotrienes, after OGD/recovery. However, only caffeic acid inhibited OGD/recovery-induced 5-LOX translocation. OGD/recovery also increased reactive oxygen species (ROS), which was inhibited by caffeic acid only. Hydrogen peroxide, an exogenous ROS, evoked similar cell injury and 5-LOX translocation, and the inhibitors had effects on the changes after H(2)O(2) similar to those after OGD/recovery. Both OGD/recovery and H(2)O(2) increased the phosphorylated p38 MAPK level, which was inhibited by caffeic acid and the ROS scavenger edaravone, but not by MK886 or zileuton. Moreover, SB203580 (a p38 MAPK inhibitor) and edaravone inhibited the cell injury and 5-LOX translocation induced by OGD/recovery and H(2)O(2). Thus, we conclude that OGD/recovery-induced ischemic-like injury induces 5-LOX activation, which is mediated by oxidative stress through activating the p38 MAPK pathway.

[5-Lipoxygenase/cysteinyl leukotriene pathway is not involved in injury of rat C6 glioma cells induced by oxygen-glucose deprivation].

OBJECTIVE: To determine whether oxygen-glucose deprivation (OGD) induces C6 cell injury, and whether 5-lipoxygenase (5-LOX)/cysteinyl leukotriene (CysLT) pathway is involved in OGD-induced injury. METHODS: After OGD treatment and recovery for various durations, the viability of C6 cells was determined, and the effects of 5-LOX inhibitors and CysLT receptor antagonists were investigated. Intracellular distribution of 5-LOX protein was detected by immunocytochemistry, and the mRNA expressions of CysLT1 and CysLT2 receptors were detected by RT-PCR. The effect of leukotriene D(4) (LTD(4)) on C6 cells was also investigated. RESULT: OGD for 4-8 h followed by recovery for 24-72 h significantly induced C6 cell injury. Neither 5-LOX inhibitors nor CysLT receptor antagonists inhibited OGD-induced injury. OGD did not induce 5-LOX translocation into the nuclear membrane. C6 cells highly expressed CysLT(2) receptor, but the expression of CysLT1receptor was much weaker; the expression was not affected by OGD. In addition, LTD(4) did not affect C6 cells significantly. CONCLUSION: OGD can induce C6 cell injury, but 5-LOX/CysLT pathway might be not involved in OGD-induced injury.

Dihydroartemisinin potentiates the cytotoxic effect of temozolomide in rat C6 glioma cells.

Gliomas are the most common primary brain tumor in adults, but the efficacy of chemotherapy is limited. Artemisinin and its analogs, such as dihydroartemisinin (DHA), can kill cancer cells via generating free radicals. In the present study, we determined whether DHA at low concentrations potentiates the cytotoxic effect of temozolomide in rat glioma C6 cells. We found that the IC50 values of DHA and temozolomide for cell viability were 23.4 and 560 micromol/l, respectively. The cytotoxic effect of temozolomide was enhanced by 177% at a nontoxic DHA concentration (1 micromol/l), and by 321% at a low-toxic DHA concentration (5 micromol/l). DHA substantially increased temozolomide-induced apoptosis and necrosis. The generation of intracellular reactive oxygen species (ROS) was increased by temozolomide combined with DHA at noneffective concentrations of both agents. Edaravone (20 micromol/l), a ROS scavenger, reversed the effects of temozolomide/DHA on both ROS generation and cell viability reduction. These results indicate that DHA at low concentrations potentiates the cytotoxic effects of temozolomide in C6 cells partly via generating ROS, suggesting a beneficial combination for the chemotherapy of gliomas.

Activation of CysLT receptors induces astrocyte proliferation and death after oxygen-glucose deprivation.

We recently found that 5-lipoxygenase (5-LOX) is activated to produce cysteinyl leukotrienes (CysLTs), and CysLTs may cause neuronal injury and astrocytosis through activation of CysLT(1) and CysLT(2) receptors in the brain after focal cerebral ischemia. However, the property of astrocyte responses to in vitro ischemic injury is not clear; whether 5-LOX, CysLTs, and their receptors are also involved in the responses of ischemic astrocytes remains unknown. In the present study, we performed oxygen-glucose deprivation (OGD) followed by recovery to induce ischemic-like injury in the cultured rat astrocytes. We found that 1-h OGD did not injure astrocytes (sub-lethal OGD) but induced astrocyte proliferation 48 and 72 h after recovery; whereas 4-h OGD moderately injured the cells (moderate OGD) and led to death 24-72 h after recovery. Inhibition of phospholipase A(2) and 5-LOX attenuated both the proliferation and death. Sub-lethal and moderate OGD enhanced the production of CysLTs that was inhibited by 5-LOX inhibitors. Sub-lethal OGD increased the expressions of CysLT(1) receptor mRNA and protein, while moderate OGD induced the expression of CysLT(2) receptor mRNA. Exogenously applied leukotriene D(4) (LTD(4)) induced astrocyte proliferation at 1-10 nM and astrocyte death at 100-1,000 nM. The CysLT(1) receptor antagonist montelukast attenuated astrocyte proliferation, the CysLT(2) receptor antagonist BAY cysLT2 reversed astrocyte death, and the dual CysLT receptor antagonist BAY u9773 exhibited both effects. In addition, LTD(4) (100 nM) increased the expression of CysLT(2) receptor mRNA. Thus, in vitro ischemia activates astrocyte 5-LOX to produce CysLTs, and CysLTs result in CysLT(1) receptor-mediated proliferation and CysLT(2) receptor-mediated death.

[Children's temperament characteristics and dental fear].

OBJECTIVE: To evaluate the relationship between children's temperament and dental fear. METHODS: 254 children(aged 4-6 years) during first dental treatment took part in the investigation. Their parents answered the Chinese preschool children's temperament scales (CPTS). The Frankl method was used to classify the degree of the children's dental fear. The K independent samples test and One-way ANOVA test were performed to find the differences of the type of temperament and the scores of temperament dimension among three groups. RESULTS: Among the 254 children(aged 4-6 years), 104 had no fear, 80 had fear and 70 had extreme fear. The incidence of dental fear in children was 59.06%. There were no statistical differences (P > 0.05) of dental fear between boys and girls. There were statistically significant differences for the type of temperament among no fear group, fear group and extreme fear group. The scores of adaptability and quality of mood were higher in the extreme fear group and fear group than that in the no fear group. The differences in scores of adaptability and quality of mood was statistically significant between the extreme fear group and no fear group. But the scores of other seven temperament dimensions had no statistical significant differences among three groups. CONCLUSION: Children's dental fear is correlated to their temperaments. The tendencies of negative mood and slow adaptability should be considered that the patients were at risk of developing dental fear problem.

Dihydroartemisinin exerts cytotoxic effects and inhibits hypoxia inducible factor-1alpha activation in C6 glioma cells.

Artemisinin and its analogue dihydroartemisinin exert cytotoxic effects in some kinds of cancer cell lines. Here we determined whether dihydroartemisinin inhibits the growth and induces apoptosis of rat C6 glioma cells. We found dihydroartemisinin (5-25 microM) inhibited the growth and induced apoptosis of C6 cells in a concentration- and time-dependent manner; however, it was much less toxic to rat primary astrocytes. Dihydroartemisinin (5-25 microM) also increased the generation of reactive oxygen species in C6 cells. These effects of dihydroartemisinin were enhanced by ferrous ions (12.5-100 microM) and reduced by the iron chelator deferoxamine (25-200 microM). Immunoblotting analysis revealed that dihydroartemisinin (5-25 microM) significantly reduced hypoxia- and deferoxamine-induced expression of hypoxia inducible factor-1alpha and its target gene protein, vascular endothelial growth factor, in C6 cells. The results showed that dihydroartemisinin exerts a selective cytotoxic effect on C6 cells by increasing the reactive oxygen species and inhibiting hypoxia inducible factor-1alpha activation.

[Dihydroartemisinin inhibits proliferation and induces apoptosis of rat glioma C6 cells].

OBJECTIVE: To determine the effects of dihydroartemisinin (DHA) on the proliferation and apoptosis of rat glioma C6 cells. METHODS: DHA (1~ 125 micromol/L) was added into the cultured C6 cells and incubated for 24, 48 and 72 h. The cell proliferation and viability were determined by trypan blue exclusion assay and 3-(4, 5-dimethylthiazol-2yl)-2, 5 diphenyl tetrazolium bromide (MTT) reduction assay. The apoptosis was detected by Hoechst 33342 staining. The intracellular reactive oxygen species (ROS) was measured by H(2)DCFDA oxidative reaction. RESULTS: DHA 5 ~ 125 micromol/L inhibited the proliferation of C6 cells in concentration- and time-dependent manners, the IC50 at 48 h was 23.4 micromol/L. DHA 5 ~ 25 micromol/L induced C6 cell apoptosis (P<0.05), and 5 ~ 125 micromol/L increased the intracellular ROS (P<0.01). CONCLUSION: DHA inhibits the proliferation and induces the apoptosis of C6 cells; its cytotoxic effect may result from the increase of intercellular ROS.

Leukotriene D4 induces brain edema and enhances CysLT2 receptor-mediated aquaporin 4 expression.

Cysteinyl leukotrienes (including LTC(4), LTD(4), and LTE(4)), potent inflammatory mediators, can induce brain-blood barrier (BBB) disruption and brain edema. These reactions are mediated by their receptors, CysLT(1) and CysLT(2) receptors. On the other hand, aquaporin 4 (AQP4) primarily modulates brain water homeostasis and edema after various injuries. Here, we aimed to determine whether AQP4 is involved in LTD(4)-induced brain edema. LTD(4) (1ng in 0.5mul PBS) microinjection into the cortex increased endogenous IgG exudation (BBB disruption) and water content (brain edema), and enhanced AQP4 expression in mouse brain. The selective CysLT(1) receptor antagonist pranlukast inhibited the IgG exudation, but not the increased water content and AQP4 expression induced by LTD(4). In the cultured rat astrocytes, LTD(4) (10(-9)-10(-7)M, for 24h) similarly enhanced AQP4 expression. The enhanced AQP4 expression was inhibited by Bay u9773, a non-selective CysLT(1)/CysLT(2) receptor antagonist, but not by pranlukast. LTD(4) (10(-9)-10(-7)M) also induced the mRNA expression of CysLT(2) (not CysLT(1)) receptor in astrocytes. These results indicate that LTD(4) modulates brain edema; CysLT(1) receptor mediates vasogenic edema while CysLT(2) receptor may mediate cytotoxic edema via up-regulating AQP4 expression.

[The characteristics of uncooperative children's temperament during dental treatment].

PURPOSE: To compare the temperament of uncooperative and cooperative children during dental treatment, and find out the characteristics of the uncooperative children's temperament. METHODS: Fifty-two cooperative children (aged from 3 to 7 years) and thirty-five uncooperative children (aged from 3 to 7 years) during dental treatment were included in the investigation. Their parents were asked to answer the Chinese Preschool Children's Temperament Scale (CPTS). The two independent sample's Mann-whitney test and Student's t test were performed to find the difference of the type of temperament and the temperamental dimension between the two groups. RESULTS: (1) There was a statistically significant difference (P<0.05) in the type of temperament between the uncooperative group and the cooperative group. In the uncooperative group, the number of difficult temperament children was significantly larger than that in the uncooperative group. (2) The scores of adaptability and quality of mood were significantly higher in the uncooperative group than that in the cooperative group. CONCLUSIONS: Children's cooperation in pediatric dentistry was correlated to their temperament. The tendencies of negative mood and slow adaptation and difficult temperament should be considered patients at risk of uncooperation in pediatric dentistry.

Activation of 5-lipoxygenase after oxygen-glucose deprivation is partly mediated via NMDA receptor in rat cortical neurons.

5-Lipoxygenase (5-LOX) is the enzyme metabolizing arachidonic acid to produce pro-inflammatory leukotrienes. We have reported that 5-LOX is translocated to the nuclear envelope after ischemic-like injury in PC12 cells. In the present study, we determined whether 5-LOX is activated (translocation and production of leukotrienes) after oxygen-glucose deprivation (OGD) in primary rat cortical neurons; if so, whether this activation is mediated by NMDA receptor. After OGD, 5-LOX was translocated to the nuclear envelope as detected by immunoblotting, immunostaining and green fluorescent protein-5-LOX transfection. 5-LOX metabolites, cysteinyl-leukotrienes (CysLTs) but not leukotriene B4, in the culture media were increased 0.5-1.5 h after recovery. Similarly, NMDA (100 microm) also induced 5-LOX translocation, and increased the production of CysLTs during 0.5-1 h NMDA exposure. Both OGD and NMDA reduced neuron viability. NMDA receptor antagonist MK-801 inhibited almost all the responses to OGD and NMDA; whereas 5-LOX activating protein inhibitor MK-886 and 5-LOX inhibitor caffeic acid inhibited the reduction of neuron viability and the production of CysLTs, but did not affect 5-LOX translocation. From these results, we conclude that OGD can activate 5-LOX in primary rat cortical neurons, and that this activation may be partly mediated via activating NMDA receptor.

Minocycline protects PC12 cells against NMDA-induced injury via inhibiting 5-lipoxygenase activation.

Recently, we have reported that minocycline, a semi-synthetic tetracycline with neuroprotective effects, inhibits the in vitro ischemic-like injury and 5-lipoxygenase (5-LOX) activation in PC12 cells. In the present study, we further determined whether minocycline protects PC12 cells from excitotoxicity via inhibiting 5-LOX activation. We used N-methyl-d-aspartate (NMDA, 200 microM) to induce early (exposure for 6 h) and delayed (exposure for 6 h followed by 24 h recovery) injuries. We found that NMDA receptor antagonist ketamine, 5-LOX inhibitor caffeic acid and minocycline concentration dependently attenuated NMDA-induced early and delayed cell injuries (viability reduction and cell death). However, only ketamine (1 microM) inhibited NMDA-evoked elevation of intracellular calcium. In addition, immunohistochemical analysis showed that NMDA induced 5-LOX translocation to the nuclear membrane after 1- to 6-h exposure which was confirmed by Western blotting, indicating that 5-LOX was activated. Ketamine, caffeic acid and minocycline (each at 1 microM) inhibited 5-LOX translocation after early injury. After delayed injury, PC12 cells were shrunk, and 5-LOX was translocated to the nuclei and nuclear membrane; ketamine, caffeic acid and minocycline inhibited both cell shrinking and 5-LOX translocation. As a control, 12-LOX inhibitor baicalein showed a weak effect on cell viability and death, but no effect on 5-LOX translocation. Therefore, we conclude that the protective effect of minocycline on NMDA-induced injury is partly mediated by inhibiting 5-LOX activation.

[Study of the separation factors of basic compounds in HPLC using a reversed-phase amino-type column].

The chromatographic behaviors of some basic probes and a neutral reference compound were investigated as functions of temperature, buffer cation strength and flow-rate using a novel reversed-phase amino-type column at both pH 3.0 and pH 7.0. The results showed that the retention of basic compounds declined steeply at first, but then slowly when temperature increased continually at pH 3.0 while decreased slowly in the whole range of temperature at pH 7.0. The column efficiency increased and the peak shape improved with increased temperature. The buffer cation strength has a strong effect on the retention of bases. The optimum flow-rate for the highest efficiency is generally lower for basic compounds than neutral compounds, and due to the steepness of the van Deemter curves obtained, high flow-rates appear to be particularly detrimental in the chromatography of basic compounds. All the results indicated that the retention mechanism, was more complex for the analysis of bases on amino-type columns than on traditional reversed-phase columns because of the existence of amino group in the alkyl group of amino-type columns.

[New species of selectors of chiral stationary phase in high performance liquid chromatography--macrocyclic antibiotics].

The recent development and applications of chiral stationary phase (CSP) of macrocyclic antibiotics are reviewed. The characteristics of its chiral separation are discussed according to the structures and the comparisons are made between macrocyclic antibiotics-CSPs and the other CSPs.