Search PubMed⌕ Search

Biomedical subjects

Y Jiang

Publications and source records attributed to Y Jiang.

At least 19 recordsLinked to original sources

Simultaneous determination of N-butyramide-tacrine and tacrine in mouse plasma and brain homogenate by high-performance liquid chromatography with a simple gradient solvent system.

A novel reversed-phase HPLC method was developed for the simultaneous determination of tacrine (THA) and the newly synthesized prodrug (N-butyramide-THA, BTHA) in mouse plasma and brain homogenate. The assay involves deproteinisation and subsequent detection at 240 nm with a gradient solvent system. Retention times were 18.5 and 9.3 min for BTHA and THA, respectively. Average recoveries for the analytes were 80.7% (BTHA) and 76.6% (THA) from plasma, and 75.0% (BTHA) and 68.4% (THA) from brain homogenate. Linear responses were observed over a wide range (0.25-20 microg/ml for BTHA in plasma and in brain homogenate, 0.025-20 microg/ml for THA in both matrices). Both BTHA and THA degraded from the prodrug can be detected even 12 h after intravenous administration of BTHA, indicating that BTHA is a promising prodrug for brain targeting.

Animals↗

An investigation into fractured surfaces of enamel of modern human teeth: a combined SEM and computer visualisation study.

It has long been recognised that the enamel microstructure may hold important information with regards to phylogeny and masticatory biomechanics. Further, the biophysical and adaptive processes involved in enamel formation and in the creation of different microstructures are poorly understood. This lack of understanding is in part due to technical difficulties when visualising the 3D structure of enamel. Using modern visualisation techniques, models of various regions of different modern human teeth were created. Underlying these models are consistent mathematical representations of the interplay between cell-to-cell adhesion, integrity of the advancing enamel front and (potentially decreasing) constraints on the prism course from the dentino-enamel junction (DEJ) to the outer surface. Seven modern human teeth (I1, 1 lower C, 1 P4, 1 M2, 2 M2 and 1 M3) were fractured longitudinally and formed the basis for the creation of the models. For validation purposes the teeth were then fractured transversely, thus allowing quantitative comparisons between the prism pathways on the newly fractured transverse plane and the transverse pathways as predicted by the model. It was found that these predictions were fairly accurate provided that (a) the light position with respect to the model corresponds with the beam position with respect to the scanned surface and (b) the path of prisms was carefully reconstructed/extrapolated from SEM in cases where prisms were broken. Given that these predictions were based on the mechanisms governing enamel formation as applied to the model, it is suggested that such theories must be reasonable. In other words, biophysical processes, rather than complicated (genetic) positional information, suffice to create different enamel microstructures. In addition, systematic differences were found in prism deviation from their c-axis in different enamel pieces. Given the nature of these differences it is suggested that enamel formation is not only the result of biophysical processes (proximal causes), but could be due to the structures having been selected for in order to counteract masticatory stress exerted during the lifetime of the species (ultimate causes). As to whether and to what extent this may be the case is not yet clear but it is apparent that computer visualisation does have potential to quantify enamel microstructure and to address such questions. Given its non-destructive nature, computer modelling could have particular relevance for studying fragmented fossilised remains.

Dental Enamel↗

Skin cancer and non-Hodgkin's lymphoma as second malignancies. markers of impaired immune function?

Successes in cancer therapy have led to increasing numbers of cancer survivors, who are at risk of developing second primary cancers. Therapy- or disease-induced suppression of the immune function may predispose cancer patients to a second malignancy. An excess of squamous cell skin cancers (SCC) and non-Hodgkin's lymphomas has been found in immunosuppressed patients. We used the nationwide Swedish Family-Cancer Database on 10.2 million individuals to calculate the risk of second primary skin cancers and non-Hodgkin's lymphomas following a previous malignancy. A total of 4301 second skin cancers and 1672 non-Hodgkin's lymphomas were identified. Standardised incidence ratios (SIR)s and 95% Confidence Intervals (CIs) were calculated and compared. Among 14 different sites for male or female first primary malignancies, 11 of these sites were followed by an increased risk of skin cancer (SIRs for males for risk of skin cancer as a second primary cancer: 14.1 for SCC; 9.7 for melanoma; 6.1 for leukaemia as the first site; SIRs for females for risk of skin cancer: 14.6 for SCC; 6.8 for larynx; 6.2 for upper aerodigestive tract (UADT) as the first site). The risk of non-Hodgkin's lymphoma was increased after 10 of 14 different male neoplasms and 12 of 17 different female neoplasms. (SIRs for males for risk of non-Hodgkin's lymphoma as a second primary cancer: 6.4 for non-Hodgkin's lymphoma; 3.2 for leukaemias; 3.1 for multiple myeloma as the first site; SIRs for females for risk of non-Hodgkin's lymphoma as a second primary cancer: 12.5 for leukaemias; 7.0 for Hodgkin's disease; 3.6 for UADT as the first site). The high, and after certain sites, very high risks of second skin cancer and non-Hodgkin's lymphoma suggest that immune suppression may be a contributory mechanism.

Carcinoma, Squamous Cell↗

Identification of a high-risk haplotype for the dystrobrevin binding protein 1 (DTNBP1) gene in the Irish study of high-density schizophrenia families.

A recent report showed significant associations between several SNPs in a previously unknown EST cluster with schizophrenia. (1). The cluster was identified as the human dystrobrevin binding protein 1 gene (DTNBP1) by sequence database comparisons and homology with mouse DTNBP1. (2). However, the linkage disequilibrium (LD) among the SNPs in DTNBP1 as well as the pattern of significant SNP-schizophrenia association was complex. This raised several questions such as the number of susceptibility alleles that may be involved and the size of the region where the actual disease mutation(s) could be located. To address these questions, we performed different single-marker tests on the 12 previously studied and 2 new SNPs in DTNBP1 that were re-scored using an improved procedure, and performed a variety of haplotype analyses. The sample consisted of 268 Irish multiplex families selected for high density of schizophrenia. Results suggested a simple structure where the LD in the target region could be explained by 6 haplotypes that together accounted for 96% of haplotype diversity in the whole sample. From these six, a single high-risk haplotype was identified that showed a significant association with schizophrenia and explained the pattern of significant findings in the analyses with individual markers. This haplotype was 30 kb long, had a large effect, could be measured with two tag SNPs only, had a frequency of 6% in our sample, seemed to be of relatively recent origin in evolutionary terms, and was equally distributed over Ireland. Implications of these findings for follow-up and replication studies are discussed.

Carrier Proteins↗

FP-TDI SNP scoring by manual and statistical procedures: a study of error rates and types.

For technologies that are commonly used in ordinary laboratories such as fluorescence-polarization detection with template-directed, dye-terminator incorporation (FP-TDI), SNP genotype scoring is usually done manually. Here we study rates of errors and missing genotypes obtained with this procedure. We also introduce three statistical genotype scoring methods to examine whether they form a viable alternative. Data consisted of eight SNPs typed in about 1400 individuals from 268 pedigrees. The statistical procedures performed better on several internal criteria, such as the number of Mendelian errors, and showed much higher agreement with discrepant genotypes re-scored by two raters. The best results were obtained with the statistical procedure that incorporated information about regularities in the error structure of the FP-TDI data. We estimated that there were about 1.6% more errors if genotypes were scored manually. About 0.6% of these errors could be explained by data manipulation errors, leaving 1% as the result of possible incorrect scoring. There were 3.3% more missing genotypes in the manual scoring due to errors in data manipulation (1.7%) and conservative scoring (1.6%).

Algorithms↗

Degradation of trace contaminants using coupled sonochemistry and Fenton's reagent.

The degradations of phenol in air-equilibrated aqueous media were investigated using coupled sonochemistry and Fenton's reagent for a variety of operating conditions. The decomposition yields of phenol (100-500 microM) were substantially enhanced due to the addition of Fenton's reagent (FeSO4 into the solutions irradiated at 608 kHz with 30 W and with reaction temperature 25 +/- 1 degree C. The decomposition process follows a pseudo-first-order reaction kinetics with respect to phenol concentration, and the rate constant of phenol disappearance observed increases by approximately 2-3 fold when FeSO4 was between 400 and 1000 M at pH = 3.5 +/- 0.2 (controlled by phosphate buffer) as a result of Fe(II) reaction with H2O2 enabling further production of additional OH* radicals. The results obtained here also indicate that the decomposition rate of aqueous phenol using coupled ultrasound and Fenton's reagent was strongly dependant on the initial concentration of reactant, the amount of Fe(II) added as well as the pH of solution. The optimal operating conditions for 100-500 microM phenol decomposition in the air-equilibrated aqueous media were obtained when FeSO4 concentration was between 400 and 1,000 microM with pH in the range 3.5-4.2 under ultrasonic irradiation at 608 kHz, 30 W and reaction temperature 25 +/- 1 degree C.

Disinfectants↗

Quantum hydrodynamic equations and quantum-hierarchy decoupling scheme.

There is a need to extract the relevant device physics from exact quantum transport formulations, and hence to reduce the complexity of quantum transport simulations for practical applications. We use a Hermite polynomial expansion to drastically reduce the number of degrees of freedom associated with the momentum variables. The result is a quantum hierarchy in real space. We also give a general procedure for the quantum-hierarchy decoupling scheme to derive the quantum hydrodynamic (QHD) and quantum drift-diffusion transport equations. We present some numerical results for the quantum hierarchy. A rigorous foundation of a decoupling procedure is given whereby the lower-order equations are renormalized in terms of a self-consistent effective potential, quantum diffusion coefficient, and moments, endowed with all the quantum corrections to order variant Planck's over h(2). Our decoupling scheme is based on the general expression of Tr H(n) to order variant Planck's over h(2), valid at all temperatures without the need for expansion in terms of the small parameter and high temperature assumption. This is very important conceptually since existing QHD formulations, using expansion to order h(2), are based on a Boltzmann distribution with the restrictive assumption of a small parameter, which is not valid in abrupt heterojunction semiconductor devices. They also fail to account for important quantum nonlinearity in the form of nonequilibrium quantum corrections. These nonequilibrium quantum corrections are expected to play a major role in approximating the coherence manifested by the highly nonlinear current-voltage characteristics of resonant tunneling structures.

Journal Article↗

Cancer risks among long-standing spouses.

We estimated risks for concordant and discordant cancers in spouses in order to quantify cancer risks from the shared environment. The study was restricted to spouses who had one or more children in common and who lived together for at least 15 years after the first child's birth. The nation-wide Family-Cancer Database was used as the source of family and cancer data. Standardised incidence ratios were calculated for concordant and discordant cancers in spouses after 50 years of age. Among the 18 cancer sites considered, only three sites, stomach, lung and bladder, showed concordant increases of cancer among spouses, standardised incidence ratios ranging only from 1.19 to 1.38. Additionally, gastric and pancreatic cancer were associated among spouses, as did many cancers which were related to tobacco smoking or human papilloma virus infection. By contrast, standardised incidence ratios of colon, rectal, renal and skin cancers showed no increases among spouses. Shared lifestyle among family members seems to explain only a small proportion of familial cancer susceptibility. Because lifestyles are likely to differ more between parents and offspring than between spouses, familial cancer risks between parents and offspring are even more likely to be due to heritable than environmental effects.

Databases, Factual↗

Induction of apoptosis by norcantharidin in human colorectal carcinoma cell lines: involvement of the CD95 receptor/ligand.

PURPOSE: Cantharidin, a natural toxin, is the active substance of mylabris and has antitumor effects in man. Norcantharidin, the demethylated analogue of cantharidin, has been used in the treatment of patients with primary hepatoma and those with leukopenia in China. The present study was designed to investigate whether norcantharidin exerts cytotoxic activity against colorectal cancer cells by inducing apoptosis and to examine the possible mechanism in the phenomenon. METHODS: Inhibition of proliferation of norcantharidin on Colo205, HT-29, and SW480 colorectal cancer cells was determined by the trypan blue dye exclusion test. Apoptosis of norcantharidin-treated cells was determined by morphological analysis, agarose gel DNA electrophoresis, and quantitated by flow cytometry after staining with propidium iodide. Cell cycle and the cell surface expression of the CD95/CD95 ligand were evaluated by flow cytometry. Caspase 8-like protease and protein phosphatase 1 and 2A activities were also analyzed. RESULTS: Treatment with norcantharidin of colorectal cancer cells not only inhibited cell proliferation, but also induced apoptosis. Norcantharidin induced apoptosis mainly in two phases: rapid apoptosis in S-phase cells and delayed apoptosis in G2/M arrested cells. Treatment with norcantharidin resulted in an upregulation of the CD95 receptor and CD95 ligand on the cell surface. Furthermore, stimulation with anti-CD95 monoclonal antibody (mAb) resulted in further induction of apoptosis after treatment with norcantharidin. In addition, the apoptosis-inducing effect of norcantharidin was almost completely inhibited by anti-CD95 ligand mAb. Norcantharidin-treated cells showed the activation of caspase 8. Both zVAD-FMK (a broad range caspase inhibitor) and IETD-FMK (a caspase-8 inhibitor) showed apparent inhibition of the apoptosis-inducing effect. Norcantharidin did not show an inhibitory effect on protein phosphatase. CONCLUSIONS: These results suggest that norcantharidin triggers apoptosis in colorectal cancer cell lines via the activation of the CD95 receptor/ligand system, and that this agent may be useful for developing new therapeutic regimens for the treatment of colorectal carcinoma.

Antibodies, Monoclonal↗

Kashin-Beck disease in children: radiographic findings in the wrist.

OBJECTIVE: To characterize the features and prevalence of radiographic abnormalities of the wrist in children with Kashin-Beck disease (KBD) and to determine whether the presence of radiographic abnormalities in the wrist correlates with the severity of KBD. DESIGN AND PATIENTS: Two hundred and eight posteroanterior radiographs of the right hand (including wrist) in children with KBD, ranging in age from 4 to 11 years (mean age 7.7 years), from endemic areas of China were reviewed. Carpal bony margins were evaluated for blurring, thinning, irregularity with and without sclerosis, interruption, depression or destruction. The radiocarpal, intercarpal and carpometacarpal joints were assessed for widening or narrowing. The severity of the disease was graded using the hand criteria from the Chinese Radiographic Criteria of KBD Diagnosis, which classifies the following five types according to the location of the hand involved: I, metaphysis; II, diaphysis; III, I+II; IV, metaphysis and epiphysis; V, II+IV. RESULTS: Of the 208 children, 95 had abnormalities in the hand but not in the wrist; 108 had both hand and wrist abnormalities; only five had abnormal wrist findings without any hand abnormalities. Of the 108 cases with wrist abnormalities, all the carpal bones were involved in 33 cases, of which the hand types were either IV or V. However, any individual carpal bone, or combination of bones, may become involved. The carpal bones most likely to show abnormalities were the capitate and the hamate (93%), followed by the triquetrum (31%), the lunate (9%), the scaphoid (6%), and the trapezoid and the trapezium (5%). The pisiform bones were not evaluated because they cannot be seen on the overlapping posteroanterior radiographs. The most commonly involved carpal joint was the midcarpal joint (42%). CONCLUSIONS: Recognizing carpal abnormalities on radiographs is helpful for the diagnosis of KBD and the evaluation of the severity of the disease. The more severe the KBD, the more likely that the carpal bones will be involved. The capitate and hamate are frequently affected if the disease involves the carpal bones.

Bone Diseases, Developmental↗

Rho and rho kinase modulation of barrier properties: cultured endothelial cells and intact microvessels of rats and mice.

Previous experiments using cultured endothelial monolayers indicate that Rho-family small GTPases are involved in modulation of endothelial monolayer permeability by regulating assembly of the cellular actin filament scaffold, activity of myosin-based contractility and junctional distribution of the Ca2+-dependent endothelial cell adhesion molecule, VE-cadherin. We investigated these mechanisms using both cultured endothelial cells (from porcine pulmonary artery and mouse heart) and vascular endothelium in situ (mouse aorta, and individually perfused venular microvessels of mouse and rat mesentery). Exposure to Clostridium difficile toxin B (100 ng x ml(-1)) inactivated 50-90% of all endothelial Rho proteins within 60-90 min. This was accompanied by considerable reduction of actin filament stress fibres and junctional F-actin in cultured endothelial monolayers and in mouse aortic endothelium in situ. Also, VE-cadherin became discontinuous along endothelial junctions. Inhibition of Rho kinase with Y-27632 (30 microM) for 90-120 min induced F-actin reduction both in vitro and in situ but did not cause redistribution or reduction of VE-cadherin staining. Perfusion of microvessels with toxin B increased basal hydraulic permeability (L(p)) but did not attenuate the transient increase in L(p) of microvessels exposed to bradykinin. Perfusion of microvessels with Y-27632 (30 microM) for up to 100 min reduced basal L(p) but did not attenuate the permeability increase induced by platelet activating factor (PAF) or bradykinin. These results show that toxin B-mediated reduction of endothelial barrier properties is due to inactivation of small GTPases other than RhoA. Rho proteins as well as RhoA-mediated contractile mechanisms are not involved in bradykinin- or PAF-induced hyperpermeability of intact microvessels.

Acute-Phase Proteins↗

Novel ultrasonic fusion imaging method based on cyclic variation in myocardial backscatter.

Quantitative ultrasonic tissue characterisation of the myocardium based on integrated backscatter (IB) has the potential of becoming an effective method for detecting and evaluating myocardial ischaemia. To facilitate IB-based clinical applications, a new imaging method has been developed that combines the anatomical information of a B-mode image with the contractile performance of a selected myocardial region. To produce such a fusion image, a region of interest (ROI) in a B-mode cardiac image was first selected by the user. Algorithms for detection of the endocardium and epicardium were developed, and the resulting mean distance between the computer-detected curve and the manually traced curve was 0.83mm for the endocardium and 0.58mm for the epicardium. The cyclic variation of IB (CVIB) of each myocardial tissue element within the ROI was then calculated over one cardiac cycle. Finally, a grey-scale B-mode image at the end of diastole was displayed as a still image, and the pixels representing the myocardial tissue in the ROI colour-coded according to the corresponding CVIB over the past heart cycle. Both the B-mode image and the colour-coded region were refreshed (up-dated) at the next end-of-diastole. Preliminary results from normal (CVIB= 10-12dB) and ischaemic (CVIB = 5-7 dB) canine hearts are presented that demonstrate the utility of this new imaging method.

Diagnosis, Computer-Assisted↗

A case-control study of occupation and breast-cancer risk in Connecticut.

BACKGROUND: Several occupations have recently been related to breast-cancer. The results, however, are inconsistent. We analyse data from a case-control study of breast cancer in Connecticut conducted in 1994-97 to further examine the potential relationship between occupation and breast-cancer risk. METHODS: A total of 608 breast-cancer cases and 609 controls, 31-85 years old, were included in the study. Information regarding occupation and other breast-cancer risk-factors was obtained through in-person interviews by trained interviewers, using a standardised, structured questionnaire. RESULTS: after adjustment for major breast-cancer risk-factors, a significantly increased risk of breast cancer was observed for teachers and librarians [odds ratio (OR), = 1.9, 95% confidence interval (CI) 1.3-2.7]. A significantly reduced risk, on the other hand, was observed for technicians and related supports (OR = 0.5, 95% CI 0.3-0.9). No other occupational groups showed a significant association with breast-cancer risk. CONCLUSIONS: The observed increase in breast-cancer risk among teachers and librarians is consistent with most earlier studies. It is currently unknown, however, what factors may explain the observed increase. Considering that teachers and librarians represent one of the largest single occupational groups among employed US women, further investigation of this association is warranted.

Adult↗

Mice lacking monocyte chemoattractant protein 1 have enhanced susceptibility to an interstitial polymicrobial infection due to impaired monocyte recruitment.

Monocyte chemoattractant protein 1 (MCP-1) is an important chemokine that induces monocyte recruitment in a number of different pathologies, including infection. To investigate the role of MCP-1 in protecting a host from a chronic interstitial polymicrobial infection, dental pulps of MCP-1(-/-) mice and controls were inoculated with six different oral pathogens. In this model the recruitment of leukocytes and the impact of a genetic deletion on the susceptibility to infection can be accurately assessed by measuring the progression of soft tissue necrosis and osteolytic lesion formation. The absence of MCP-1 significantly impaired the recruitment of monocytes, which at later time points was threefold higher in the wild-type mice than in MCP-1(-/-) mice (P < 0.05). The consequence was significantly enhanced rates of soft tissue necrosis and bone resorption (P < 0.05). We also determined that the MCP-1(-/-) mice were able to recruit polymorphonuclear leukocytes (PMNs) to a similar or greater extent as controls and to produce equivalent levels of Porphyromonas gingivalis-specific total immunoglobulin G (IgG) and IgG1. These results point to the importance of MCP-1 expression and monocyte recruitment in antibacterial defense and demonstrate that antibacterial defense is not due to an indirect effect on PMN recruitment or modulation of the adaptive immune response.

Animals↗