Structure-Guided Discovery of Diverse Cytotoxic Dimeric Xanthones/Chromanones from Penicillium chrysogenum C-7-2-1 and Their Interconversion Properties.

Xanthone-chromanone homo- or heterodimers are regarded as a novel class of topoisomerase (Topo) inhibitors; however, limited information about these compounds is currently available. Here, 14 new (1-14) and 6 known tetrahydroxanthone chromanone homo- and heterodimers (15-20) are reported as isolated from Penicillium chrysogenum C-7-2-1. Their structures and absolute configurations were unambiguously demonstrated by a combination of spectroscopic data, single-crystal X-ray diffraction, modified Mosher's method, and electronic circular dichroism analyses. Plausible biosynthetic pathways are proposed. For the first time, it was discovered that tetrahydroxanthones can convert to chromanones in water, whereas chromone dimerization does not show this property. Among them, compounds 5, 7, 8, and 16 exhibited significant cytotoxicity against H23 cell line with IC50 values of 6.9, 6.4, 3.9, and 2.6 µM, respectively.

Glymphatic system dysfunction in pediatric acute lymphoblastic leukemia without clinically diagnosed central nervous system infiltration: a novel DTI-ALPS method.

BACKGROUND AND OBJECTIVE: Central nervous system (CNS) infiltration commonly occurs in children with acute lymphoblastic leukemia (ALL). Nevertheless, CNS infiltration is rarely detected at the initial diagnosis. The glymphatic system, which regulates cerebrospinal fluid (CSF) and interstitial fluid transport, is considered one of the possible routes of CNS infiltration by leukemia cells. In this study, we used diffusion tensor image analysis along the perivascular space (DTI-ALPS) method to investigate glymphatic system function and obtained CSF volume using synthetic magnetic resonance imaging (SyMRI) in pediatric ALL without clinically diagnosed CNS infiltration. MATERIALS AND METHODS: Twenty-nine ALL and 29 typically developing (TD) children were prospectively recruited (age 4-16 years) in the present study. Group differences in brain volumetric parameters, brain water diffusivities, and the ALPS index were evaluated after controlling for age, gender, and handedness. Furthermore, significant group-different parameters were correlated with clinical information using partial correlations analysis. RESULTS: Lower Dxassoc and ALPS index, and increased CSF volume were found in pediatric ALL (all pFDR-corrected < 0.05). Moreover, the ALPS index was negatively associated with the risk classification (r = - 0.59, pFDR-corrected = 0.04) in pediatric ALL. CONCLUSIONS: Dysfunction of the glymphatic system and accumulation of CSF were presented in pediatric ALL without clinically diagnosed CNS infiltration. These novel findings suggested that the glymphatic system might be essential in the early-stage process of ALL CNS infiltration, which provides a new direction for exploring underlying mechanisms and early detection of pediatric ALL CNS infiltration. KEY POINTS: • Lower Dxassoc and ALPS index, and increased CSF volume were found in pediatric ALL (all pFDR-corrected < 0.05). • The ALPS index was negatively associated with the risk classification (r = -0.59, pFDR-corrected = 0.04) in pediatric ALL. • Dysfunction of the glymphatic system and accumulation of CSF were presented in pediatric ALL without clinically diagnosed CNS infiltration, which suggested that the ALPS index and CSF volume might be promising imaging markers for early detection of pediatric ALL CNS infiltration.

Characterization of LTr1 derived from cruciferous vegetables as a novel anti-glioma agent via inhibiting TrkA/PI3K/AKT pathway.

Malignant glioma is the most fatal, invasive brain cancer with limited treatment options. Our previous studies show that 2-(indol-3-ylmethyl)-3,3'-diindolylmethane (LTr1), a major metabolite of indole-3-carbinol (I3C) derived from cruciferous vegetables, produces anti-tumour effect against various tumour cell lines. In this study we characterized LTr1 as a novel anti-glioma agent. Based on screening 134 natural compounds and comparing the candidates' efficacy and toxicity, LTr1 was selected as the lead compound. We showed that LTr1 potently inhibited the viability of human glioma cell lines (SHG-44, U87, and U251) with IC50 values of 1.97, 1.84, and 2.03 µM, respectively. Furthermore, administration of LTr1 (100,300 mg· kg-1 ·d-1, i.g. for 18 days) dose-dependently suppressed the tumour growth in a U87 xenograft nude mouse model. We demonstrated that LTr1 directly bound with TrkA to inhibit its kinase activity and the downstream PI3K/AKT pathway thus inducing significant S-phase cell cycle arrest and apoptosis in SHG-44 and U87 cells by activating the mitochondrial pathway and inducing the production of reactive oxygen species (ROS). Importantly, LTr1 could cross the blood-brain barrier to achieve the therapeutic concentration in the brain. Taken together, LTr1 is a safe and promising therapeutic agent against glioma through inhibiting TrkA/PI3K/AKT pathway.

Complications after radiofrequency ablation of hyperparathyroidism secondary to chronic kidney disease.

OBJECTIVE: To study the complications of ultrasound-guided radiofrequency ablation (RFA) in chronic kidney disease (CKD) patients undergoing renal replacement therapy with secondary hyperparathyroidism (SHPT). METHODS: This retrospective study reviewed the clinical data, including general information, examination results, treatment times, time interval, and postoperative complications, of 103 SHPT patients who received ultrasound-guided RFA treatment from July 2017 to January 2021. RESULTS: Of 103 patients, 52 required two sessions of RFA within a month. The incidence of recurrent laryngeal nerve injury at the second treatment was significantly higher than that at the first treatment (first session vs. second session, 5.77% vs. 21.15%; p = .021). Of all the enrolled 103 patients, 27 suffered complications after the first session of RFA. When we separated patients into complications group and non-complication group, we detected more ablated nodules in the complications group (Z = -2.222; p = .0026). Subgroup analysis further showed that the patients in the severe hypocalcemia group were younger (p = .005), had more ablated nodules (p = .003) and higher blood phosphorus (p = .012) and alkaline phosphatase (ALP) levels (p = .002). Univariate analysis showed that age, serum phosphorus, ALP, and number of ablated nodules were associated with a higher risk of severe hypocalcemia after the first session of RFA. CONCLUSIONS: An interval of more than 1 month between two treatments may help to avoid recurrent laryngeal nerve injury. Age, serum phosphorus, ALP, and number of ablated nodules were associated with a higher risk of severe hypocalcemia after the first session of RFA.

Simvastatin Downregulates Cofilin and Stathmin to Inhibit Skeletal Muscle Cells Migration.

Statins are the most effective therapeutic agents for reducing cholesterol synthesis. Given their widespread use, many adverse effects from statins have been reported; of these, musculoskeletal complications occurred in 15% of patients after receiving statins for 6 months, and simvastatin was the most commonly administered statin among these cases. This study investigated the negative effects of simvastatin on skeletal muscle cells. We performed RNA sequencing analysis to determine gene expression in simvastatin-treated cells. Cell proliferation and migration were examined through cell cycle analysis and the transwell filter migration assay, respectively. Cytoskeleton rearrangement was examined through F-actin and tubulin staining. Western blot analysis was performed to determine the expression of cell cycle-regulated and cytoskeleton-related proteins. Transfection of small interfering RNAs (siRNAs) was performed to validate the role of cofilin and stathmin in the simvastatin-mediated inhibition of cell migration. The results revealed that simvastatin inhibited the proliferation and migration of skeletal muscle cells and affected the rearrangement of F-actin and tubulin. Simvastatin reduced the expression of cofilin and stathmin. The knockdown of both cofilin and stathmin by specific siRNA synergistically impaired cell migration. In conclusion, our results indicated that simvastatin inhibited skeletal muscle cell migration by reducing the expressions of cofilin and stathmin.

Lidocaine Inhibited Tendon Cell Proliferation and Extracellular Matrix Production by Down Regulation of Cyclin A, CDK2, Type I and Type III Collagen Expression.

Lidocaine injection is a common treatment for tendon injuries. However, the evidence suggests that lidocaine is toxic to tendon cells. This study investigated the effects of lidocaine on cultured tendon cells, focusing on the molecular mechanisms underlying cell proliferation and extracellular matrix (ECM) production. Tendon cells cultured from rat Achilles tendons were treated with 0.5, 1.0, or 1.5 mg/mL lidocaine for 24 h. Cell proliferation was evaluated by Cell Counting Kit 8 (CCK-8) assay and bromodeoxyuridine (BrdU) assay. Cell apoptosis was assessed by Annexin V and propidium iodide (PI) stain. Cell cycle progression and cell mitosis were assessed through flow cytometry and immunofluorescence staining, respectively. The expression of cyclin E, cyclin A, cyclin-dependent kinase 2 (CDK2), p21, p27, p53, matrix metalloproteinases-2 (MMP-2), matrix metalloproteinases-9 (MMP-9), type I collagen, and type III collagen were examined through Western blotting, and the enzymatic activity of MMP-9 was determined through gelatin zymography. Lidocaine reduced cell proliferation and reduced G1/S transition and cell mitosis. Lidocaine did not have a significant negative effect on cell apoptosis. Lidocaine significantly inhibited cyclin A and CDK2 expression but promoted p21, p27, and p53 expression. Furthermore, the expression of MMP-2 and MMP-9 increased, whereas that of type I and type III collagen decreased. Lidocaine also increased the enzymatic activity of MMP-9. Our findings support the premise that lidocaine inhibits tendon cell proliferation by changing the expression of cell-cycle-related proteins and reduces ECM production by altering levels of MMPs and collagens.

Efficient Capture and Effective Sensing of Cr2O72- from Water Using a Zirconium Metal-Organic Framework.

Highly efficient decontamination of heavily toxic Cr2O72- from water remains a serious task for public health and ecosystem protection. An easily regenerative and reused sorbent with suitable porosity may address this task. Herein, a series of water-stable and ecofriendly metal-organic frameworks (MOFs) with large surface areas were assessed for their ability to adsorb and separate Cr2O72- from aqueous solutions. Among these tested MOFs, NU-1000 shows an extraordinary capability to efficiently capture (within 3 min) Cr2O72- with a sorption capacity of up to 76.8 mg/g, which is the largest one for the neutral MOF-based Cr2O72- sorbents. NU-1000 also shows remarkable selectivity for Cr2O72- capture and can effectively reduce the Cr(VI) concentration from 24 ppm to 60 ppb, which is below the acceptable limit for the drinking water standard (100 ppb by the U.S. Environmental Protection Agency). Moreover, this adsorbent can be easily regenerated by Soxhlet extraction with an acidic methanol solution (2.5 M HCl) and can be reused at least three times without a significant loss of it adsorption ability. More intriguingly, NU-1000 can also serve as an efficient photoluminescent probe for the selective detection of Cr2O72- in aqueous media. The Cr2O72- detection limit is as low as 1.8 µM, and the linear range is from 1.8 to 340 µM. Our work shows that NU-1000 is a unique material combining both efficient sorption and exceptional fluorescent sensing of Cr2O72- in aqueous media.

Platelet rich plasma releasate promotes proliferation of skeletal muscle cells in association with upregulation of PCNA, cyclins and cyclin dependent kinases.

Platelet rich plasma (PRP) contains various cytokines and growth factors which may be beneficial to the healing process of injured muscle. The purpose of this study is to investigate the effect and molecular mechanism of PRP releasate on proliferation of skeletal muscle cells. Skeletal muscle cells intrinsic to Sprague-Dawley rats were treated with PRP releasate. Cell proliferation was evaluated by 3-[4,5-Dimethylthiazol- 2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay and immunocytochemistry with Ki-67 stain. Flow cytometric analysis was used to evaluate the cell cycle progression. Western blot analysis was used to evaluate the protein expressions of PCNA, cyclin E1, cyclin A2, cyclin B1, cyclin dependent kinase (cdk)1 and cdk2. The results revealed that PRP releasate enhanced proliferation of skeletal muscle cells by shifting cells from G1 phase to S phase and G2/M phases. Ki-67 stain revealed the increase of proliferative capability after PRP releasate treatment. Protein expressions including cyclin A2, cyclin B1, cdk1, cdk2 and PCNA were up-regulated by PRP releasate in a dose-dependent manner. It was concluded that PRP releasate promoted proliferation of skeletal muscle cells in association with the up-regulated protein expressions of PCNA, cyclin A2, cyclin B1, cdk1 and cdk2.

Isolation of undescribed cladosporols and spirobisnaphthalenes from a plant pathogen Cladosporium cladosporioides F-10-2-A.

Two undescribed cladosporol derivatives, cladosporols J-K (1-2), and three previously unreported spirobisnaphthalenes, urnucratins D-F (3-5), as well as eleven known cladosporols (6-16), were characterized from Cladosporium cladosporioides (Cladosporiaceae), a common plant pathogen isolated from the skin of Chinese toad. Cladosporols J-K (1-2) with a single double bond have been rarely reported, while urnucratins D-F (3-5) featured an unusual benzoquinone bisnaphthospiroether skeleton, contributing to an expanding category of undiscovered natural products. Their structures and absolute configurations were determined using extensive spectroscopic methods, including NMR, HRESIMS analyses, X-ray single crystal diffraction, as well as through experimental ECD analyses. Biological assays revealed that compounds 1 and 2 exhibited inhibitory activity against A549 cells, with IC50 values of 30.11 ± 3.29 and 34.32 ± 2.66 µM, respectively.

Leukocyte-poor platelet-rich plasma and leukocyte-rich platelet-rich plasma promote myoblast proliferation through the upregulation of cyclin A, cdk1, and cdk2.

Muscle injuries are common among athletes and often treated with platelet-rich plasma (PRP). However, whether the leukocyte concentration affects the efficacy of PRP in treating muscle injuries remains unclear. This study investigated the effects of leukocyte-poor platelet-rich plasma (LP-PRP) and leukocyte-rich platelet-rich plasma (LR-PRP) on myoblast proliferation and the molecular mechanisms underlying these effects. Myoblasts were treated with 0.5% LP-PRP, 0.5% LR-PRP, 1% LP-PRP, or 1% LR-PRP for 24 h. The gene expression of the LP-PRP- and LR-PRP-treated myoblasts was determined using RNA sequencing analysis. Cell proliferation was evaluated using an bromodeoxyuridine (BrdU) assay, and cell cycle progression was assessed through flow cytometry. The expression of cyclin A, cyclin-dependent kinase 1 (cdk1), and cdk2 was examined using Western blotting. The expression of myoblast determination protein 1 (MyoD1) was examined through Western blotting and immunofluorescence staining. The LP-PRP and LR-PRP both promoted the proliferation of myoblasts and increased differential gene expression of myoblasts. Moreover, the LP-PRP and LR-PRP substantially upregulated the expression of cyclin A, cdk1, and cdk2. MyoD1 expression was induced in the LP-PRP and LR-PRP-treated myoblasts. Our results corroborate the finding that LP-PRP and LR-PRP have similar positive effects on myoblast proliferation and MyoD1 expression.

Lidocaine inhibits migration of tenocytes by downregulating focal adhesion kinase and paxillin phosphorylation.

Lidocaine is the most frequently applied local infiltration anesthetic agent for treating tendinopathies. However, studies have discovered lidocaine to negatively affect tendon healing. In the current study, the molecular mechanisms and effects of lidocaine on tenocyte migration were evaluated. We treated tenocytes intrinsic to the Achilles tendons of Sprague-Dawley rats with lidocaine. The migration ability of cells was analyzed using electric cell-substrate impedance sensing (ECIS) and scratch wound assay. We then used a microscope to evaluate the cell spread. We assessed filamentous actin (F-actin) cytoskeleton formation through immunofluorescence staining. In addition, we used Western blot analysis to analyze the expression of phospho-focal adhesion kinase (FAK), FAK, phospho-paxillin, paxillin, and F-actin. We discovered that lidocaine had an inhibitory effect on the migration of tenocytes in the scratch wound assay and on the ECIS chip. Lidocaine treatment suppressed cell spreading and changed the cell morphology and F-actin distribution. Lidocaine reduced F-actin formation in the tenocyte during cell spreading; furthermore, it inhibited phospho-FAK, F-actin, and phospho-paxillin expression in the tenocytes. Our study revealed that lidocaine inhibits the spread and migration of tenocytes. The molecular mechanism potentially underlying this effect is downregulation of F-actin, phospho-FAK, and phospho-paxillin expression when cells are treated with lidocaine.

Quantitative evaluation of CTP derived time-density alterations versus CTP for collateral status prediction with stroke.

BACKGROUND AND OBJECTIVES: Collateral status is a pivotal determinant of clinical outcomes in acute ischemic stroke (AIS); however, its evaluation can be challenging. We investigated the predictive value of CT perfusion (CTP) derived time and density alterations versus CTP for collateral status prediction in AIS. METHODS: Consecutive patients with anterior circulation occlusion within 24 h were retrospectively included. Time-density curves of the CTP specified ischemic core, penumbra, and the corresponding contralateral unaffected brain were obtained. The collateral status was dichotomised into robust (4-5 scores) and poor (0-3 scores) using multiphase collateral scoring, as described by Menon et al.. Receiver operating characteristic curves and multivariable regression analysis were performed to assess the predictive ability of CTP-designated tissue time and density alterations, CTP for robust collaterals, and favourable outcomes (mRS score of 0-2 at 90 days). RESULTS: One-hundred patients (median age, 68 years; interquartile range, 57-80 years; 61 men) were included. A smaller ischemic core, shorter peak time delay, lower peak density decrease, lower cerebral blood volume ratio, and cerebral blood flow ratio in the CTP specified ischemic core were significantly associated with robust collaterals (PFDR ≤ 0.004). The peak time delay demonstrated the highest diagnostic value (AUC, 0.74; P < 0.001) with 66.7 % sensitivity and 73.7 % specificity. Furthermore, the peak time delay of less than 8.5 s was an independent predictor of robust collaterals and favourable clinical outcomes. CONCLUSIONS: Robust collateral status was significantly associated with the peak time delay in the ischemic core. It is a promising image marker for predicting collateral status and functional outcomes in AIS.

Silver-gold alloy nanoclusters as a fluorescence-enhanced probe for aluminum ion sensing.

In this paper, the development of a simple method is described for preparing highly red fluorescent mercaptosuccinic acid stabilized AgAu alloy nanoclusters (MSA-AgAu NCs) through the core etching of Ag nanoparticles (NPs) and a galvanic exchange reaction using nonorganic solvent and no multistep centrifuge washing. The as-prepared MSA-AgAu NCs were characterized using spectroscopic and microscopic techniques. After covalently attaching methoxy-poly(ethylene glycol)-NH2 (m-PEG-NH2), PEGylated MSA-AgAu NCs were still stable even in 1 M NaCl. Probably based on the deposition of Al(3+)-enhanced fluorescence, the PEGylated MSA-AgAu NCs offered highly selective and sensitive sensing of Al(3+) in aqueous solution with a detection limit of 0.8 µM.

Zr(H2O)2EDTA modulated luminescent carbon dots as fluorescent probes for fluoride detection.

A novel fluorescent probe (Zr(CDs-COO)(2)EDTA) has been designed for fluoride ion (F(-)) content detection based on the competitive ligand reactions carried out between the carboxylate groups (-COOH) on the surface of the luminescent carbon dots (CDs) and F(-) coordinated to Zr(H(2)O)(2)EDTA. The strong and stable fluorescence signal of this probe was quenched upon the addition of F(-) as a result of the formation of the non-fluorescent complex Zr(F)(2)EDTA, due to the stronger affinity of F(-) than the -COOH in the CDs to Zr(IV). The fluorescence change (ΔF) in this process was linear with respect to the content of F(-), ranging from 0.10 µM to 10 µM. The probe has been applied to F(-) detection in toothpaste and water samples with satisfactory results. Moreover, the mechanism of this Zr(H(2)O)(2)EDTA modulated fluorescent probe for the detection of F(-) was also discussed.

High glucose concentration up-regulates the expression of matrix metalloproteinase-9 and -13 in tendon cells.

BACKGROUND: Diabetes mellitus is associated with tendinopathy or tendon injuries. However, the mechanism underlying diabetic tendinopathy is unclear. The purpose of this study was to examine the effects of high glucose concentrations on the activity and expression of matrix metalloproteinases, type I collagen, and type III collagen in tendon cells. METHODS: Tendon cells from rat Achilles tendons were treated with 6 mM, 12 mM, and 25 mM glucose, and then cell proliferation was evaluated by the 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. Messenger RNA (mRNA) expression of MMP-2, MMP-8, MMP-9, and MMP-13 and type I and type III collagen was assessed by quantitative real-time polymerase chain reaction (PCR). The enzymatic activity of MMP-2 and MMP-9 was measured by gelatin zymography. RESULTS: The MTT assay results showed that the glucose concentration did not affect tendon cell proliferation. The results of the real-time PCR assay revealed that the mRNA expression of MMP-9 and MMP-13 was up-regulated by treatment with 25 mM glucose, whereas the mRNA expression of type I and III collagen was not affected. Gelatin zymography showed that 25 mM glucose increased the enzymatic activity of MMP-9. CONCLUSIONS: High glucose concentration up-regulates the expression of MMP-9 and MMP-13 in tendon cells, which may account for the molecular mechanisms underlying diabetic tendinopathy.

Determination of trace human chorionic gonadotropin by using multiwall carbon nanotubes as phosphorescence labeling reagent.

Taking advantage of the cutting effect of the strong oxidation of benzoyl peroxide [(C(6)H(5)CO)(2)O(2)] on the end of multiwall carbon nanotubes (MWNTs) to obtain water-soluble multiwall nanotubes (MWNTs') and the spiking effect of polyacrylamide (PA) on the room temperature phosphorescence (RTP) of MWNTs', a new phosphorescent labeling reagent, MWNTs'-PA, has been developed in this study. The product ß-Ab(HCG)-MWNTs'-PA obtained by MWNTs'-PA labeling human chorionic gonadotropin-ß-subunit three-dimensional core monoclonal antibody (ß-Ab(HCG)) not only could maintain good RTP characteristics of MWNTs' but also could take specific immunoreaction with ß-HCG to form ß-HCG- ß-Ab(HCG)-MWNTs'-PA, resulting in the increase of MWNTs' RTP signal. Thus, a new solid substrate room temperature phosphorescence immunoassay (SSRTPIA) for the determination of ß-HCG has been established. The limits of detection (LODs) of the new method were 0.021pgspot(-1) for the direct way at 447/615nm (λ(ex)(max)/λ(em)(max)) and 0.016pgspot(-1) for the sandwich way at 447/614nm (λ(ex)(max)/λ(em)(max)). This sensitive, accurate, and precise method was used to determine ß-HCG and diagnose human diseases by the direct way or the sandwich way, with the results coinciding with those obtained by chemiluminescence immunoassay. Meanwhile, the mechanisms of MWNTs' labeling ß-Ab(HCG) and determining ß-HCG are also discussed.

Highly selective and sensitive detection of Cu2+ with lysine enhancing bovine serum albumin modified-carbon dots fluorescent probe.

Based on the ability of lysine (Lys) to enhance the fluorescence intensity of bovine serum albumin modified-carbon dots (CDs-BSA) to decrease surface defects and quench fluorescence of the CDs-BSA-Lys system in the presence of Cu(2+) under conditions of phosphate buffer (PBS, pH = 5.0) at 45 °C for 10 min, a sensitive Lys enhancing CDs-BSA fluorescent probe was designed. The environment-friendly, simple, rapid, selective and sensitive fluorescent probe has been utilized to detect Cu(2+) in hair and tap water samples and it achieved consistent results with those obtained by inductively coupled plasma mass spectroscopy (ICP-MS). The mechanism of the proposed assay for the detection of Cu(2+) is discussed.

Selective determination of cysteine using BSA-stabilized gold nanoclusters with red emission.

Gold nanoclusters (AuNCs) were synthesized by a macromolecules template using bovine serum albumin (BSA) as stabilizer which can emit red photoluminescence under illumination of ultraviolet light. The fluorescence intensity of AuNCs enhanced through decreasing the surface defects of AuNCs modified with cysteine, herein we present a novel fluorometry for determination of trace cysteine. This method with a wider linear range from 2.0 to 800 nmol mL(-1), higher sensitivity (detection limit was 1.2 nmol mL(-1)) and better selectivity has been utilized to determine cysteine content in real samples, and the results were in a good agreement with those determined by electrochemical biosensor. At the same time, the structures of AuNCs and AuNCs-cysteine were characterized by Fourier-transform infrared spectroscopy (FTIR) and high resolution transmission electron microscopy (HRTEM) and the mechanism of the proposed assay for the detection of cysteine has been discussed.

A promising CdSe@CdS-quantum dots-cysteine for the determination of trace IgE by solid substrate room temperature phosphorescence immunoassay.

The labelling reagent CdSe@CdS-QDs-Cys (QDs-Cys) with the grain diameter of 4.5 nm was synthesized by modifying CdSe@CdS quantum dots (QDs) with cysteine (Cys). At the same time, QDs-Cys-Ab(IgE), a phosphorescent quantum dot probe, was developed based on the labelling reaction between -COOH of QDs-Cys and -NH(2) of goat anti human IgE antibody (Ab(IgE)). This probe with excellent biocompatibility and high specificity could not only emit strong and stable room temperature phosphorescence (RTP), but also could carry out specific immunoassay (IA) with immunoglobulin E (IgE), causing the RTP of the system to sharply enhance. Thus, a new solid substrate room temperature phosphorescence immunoassay (SSRTPIA) for the determination of IgE was established. The limit of quantification (LOQ) of the method was 0.12 fg spot(-1), corresponding concentration was 3.0 × 10(-13) g mL(-1) and sampling quantity was 0.40 µL spot(-1). This highly selective, sensitive and accurate SSRTPIA has been applied to determine IgE in biological samples and diagnose diseases, and the results agreed well with those obtained by enzyme-link immunoassay (ELISA). Meanwhile, the mechanisms of QDs-Cys labelling Ab(IgE) and the determination of IgE by SSRTPIA were also discussed.

Highly sensitive detection of residual chlorpromazine hydrochloride with solid substrate room temperature phosphorimetry.

Under the condition of 60 °C and 20 min at pH 6.12, chlorpromazine hydrochloride (CPZ) could react with fluorescein isothiocyanate (FITC) to produce FITC-CPZ, which increased the π-electron density (δ) of carbon atom in FITC conjugated system and the room temperature phosphorescence (RTP) intensity of FITC. Thus, a new solid substrate room temperature phosphorimetry (SSRTP) for the determination of residual CPZ was established. The regression equation of working curve was ΔI (p) = 4.254 + 7.906 m(CPZ) (ag spot(-1)) with the correlation coefficient (r) of 0.9990 in the range of 0.036-9.6 ag spot(-1) (corresponding concentration: 0.090-24 fg ml(-1), sample volume: 0.40 µl spot(-1)), and the detection limit (LD) was 0.018 ag spot(-1) (corresponding concentration: 4.5 × 10(-17) g ml(-1)). This method with wide linear range and high sensitivity was not only used to diagnose human disease based on the correlation between the residual quantity and lethal dose of CPZ in human serum, but also used to determine residual CPZ in biological samples with the results consisting with those obtained by gas chromatography (GC), showing good accuracy. The constituent of FITC-CPZ was analyzed by GC-MS (mass spectrometry) and the reaction mechanism of SSRTP for the determination of trace CPZ was also discussed.