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Biomedical subjects

B Xie

Publications and source records attributed to B Xie.

At least 55 records · Page 3Linked to original sources
PubMed1999

Principles of enzyme thermistor systems: applications to biomedical and other measurements.

This chapter presents an overview of thermistor-based calorimetric measurements. Bioanalytical applications are emphasized from both the chemical and biomedical points of view. The introductory section elucidates the principles involved in the thermometric measurements. The following section describes in detail the evolution of the various versions of enzyme-thermistor devices. Special emphasis is laid on the description of modern "mini" and "miniaturized" versions of enzyme thermistors. Hybrid devices are also introduced in this section. In the sections on applications, the clinical/biomedical areas are dealt with separately, followed by other applications. Mention is also made of miscellaneous applications. A special section is devoted to future developments, wherein novel concepts of telemedicine and home diagnostics are highlighted. The role of communication and information technology in telemedicine is also mentioned. In the concluding sections, an attempt is made to incorporate the most recent references on specific topics based on enzyme-thermistor systems.

Biosensing Techniques↗
PubMed1999

Sex hormone-induced mammary carcinogenesis in female Noble rats: expression of TGF-beta1 and its receptors, TGF-alpha, and EGF-R in mammary carcinogenesis.

We have established a Noble rat model to explore the mechanisms of hormonal mammary carcinogenesis, in which the role of androgen in promoting mammary carcinogenesis was highlighted. We have also established that stromal-epithelial interactions may be responsible for the promotional effects of testosterone in mammary carcinogenesis. Based on these understandings, in the present study we examined the expression of transforming growth factor beta-1 (TGF-beta1) and its receptors (TGF-beta RI, TGF-beta RII), transforming growth factor alpha (TGF-alpha), and epidermal growth factor receptor (EGF-R) in 'pre-malignant' mammary glands treated with different protocols of sex hormones, as well as in mammary cancers. We observed that TGF-beta1 was strongly expressed in most mammary tumors, whereas TGF-beta RI and TGF-beta RII were negative in most mammary tumor cells. The results from comparative study of 'pre-malignant' glands further showed that when the animals were treated with testosterone, either alone or in combination with 17beta-estradiol, the mammary gland epithelial cells expressed high levels of TGF-beta1. This over-expression of TGF-beta1 can be blocked by flutamide, indicating that testosterone may be responsible for the expression of TGF-beta1 in mammary glands. TGF-beta RI and TGF-beta RII were also expressed strongly in testosterone-treated mammary epithelial cells and only weakly detectable in 17beta-estradiol treated and control mammary epithelial cells. Furthermore, TGF-beta RI and TGF-beta RII were also expressed in stromal cells, both in mammary tumors and in hormone-treated mammary glands. These observations indicate that the mechanism of testosterone in mammary carcinogenesis may be through its regulation of expression of TGF-beta1 and its receptors. On the other hand, TGF-alpha was also expressed in all 39 mammary cancers, while only 81% of the cancers were EGF-R positive. TGF-alpha was also strongly expressed in stromal cells in all three experimental groups, but only moderately expressed in epithelial cells when treated with a combination of testosterone and 17beta-estradiol. By contrast, EGF-R was strongly expressed in epithelial cells in the three experimental groups but negative in stromal cells. Flutamide or tamoxifen was unable to block the expression of TGF-alpha induced by the combined sex hormone treatment. However, they were effective in blocking the expression of TGF-alpha when the animals were treated with testosterone or 17beta-estradiol alone, respectively. These results suggest that both testosterone and 17beta-estradiol may be required for the over-expression of TGF-alpha in the mammary carcinogenesis induced by sex hormones. To our knowledge, this is the first experimental study to explore the regulation of TGF-beta1, TGF-alpha, and their receptors by testosterone and 17beta-estradiol in mammary carcinogenesis.

Animals↗
PubMed1999

Co-expression of vascular endothelial growth factor (VEGF) and its receptors (flk-1 and flt-1) in hormone-induced mammary cancer in the Noble rat.

Vascular endothelial growth factor (VEGF) is recognized to play a predominant role in breast cancer prognosis. The action of VEGF is mediated by two high-affinity receptors with ligand-stimulated tyrosine kinase activity: VEGFR-1/flt-1 and VEGFR-2/flk-1, which are expressed mainly in vascular endothelial cells. To the best of our knowledge, no previous studies on the expression of these receptors in breast cancer cells has been made. We have established a new animal model for breast cancer, using a combination of 17beta-oestradiol and testosterone as 'carcinogens'. Taking advantage of the animal model, we have demonstrated that mammary cancer cells expressed not only high levels of VEGF but also, surprisingly, its receptors (fit-1 and flk-1) in mammary cancer cells. Intense reactivities to VEGF, flt-1 and flk-1 were observed in mammary cancer cells, especially in invasive mammary carcinoma. Western blot analysis confirmed the increase in flk-1 and flt-1 proteins in induced mammary cancers. Based on these observations, we hypothesize that in mammary cancer, VEGF regulates, in addition to endothelial proliferation and angiogenesis, also growth of cancer cells by an autocrine mechanism mediated through its receptors. To further verify this hypothesis, we investigated the correlation between cellular proliferation and the expression of VEGF, flt-1 and flk-1. Using double-labelling immunocytochemistry, we have shown a correlation between high VEGF activity and Ki-67 expression. The Ki-67 indices in the areas of strong and weak VEGF reactivities were 58.3% and 3.7% respectively. Similarly, there was also a correlation of strong flk-1 and Ki-67 reactivity. The Ki-67 indices for areas of strong and weak flk-1 reactivities were 53.9% and 3.1% respectively. On the other hand, there was a reverse correlation between fit-1 and Ki-67 activities. These results indicate that overexpression of VEGF and flk-1 is correlated with high Ki-67 index. The data, therefore, suggest that VEGF may act as an autocrine growth factor for mammary cancer cells in vivo and this autocrine regulatory role may be mediated through flk-1. The present study is the first report showing that VEGF may act as a growth stimulator for mammary cancer cells.

Animals↗
PubMed1999

Induction of high incidence of mammary tumour in female Noble rats with a combination of 17beta-oestradiol and testosterone.

Breast cancer is the most common cancer and the second most frequent cause of cancer death in women. Despite extensive research, the precise mechanisms of breast carcinogenesis remain unclear. One of the reasons for this is due, at least in part, to a lack of a suitable animal model which can closely mimic the breast carcinogenesis in normal situations without using chemical carcinogens. We have developed an animal model of mammary gland carcinogenesis using a combination of oestradiol and testosterone, and succeeded in inducing a high percentage of female Noble rats to develop mammary cancer in a relatively short time (approximately 6 months). The results showed that androgens might work as a promoter to shorten the latency time of mammary gland carcinogenesis. Histopathological examination revealed that hyperplasia and dysplasia were first observed 2 months after treatment, in situ carcinoma after 3 months, and fully developed carcinoma of various forms including cribriform, papillary and camedo types were observed from 5 to 6 months after hormone implantation. Animals implanted with oestrogen or testosterone alone also developed mammary cancers, though with a lower overall incidence than the two hormones combined. They ranged from well differentiated to poorly differentiated forms with predominantly infiltrating ductal carcinoma. We have also observed a case of secondary cancer in the uterus. In addition to the high incidence of carcinoma, there was also a peculiar unexplained ipsilateral correlation between the site of hormonal implantation and the location of tumours, and the highest incidence of carcinogenesis was found to be in thoracic mammary gland. The study showed that both oestrogens and androgens are important in mammary cancer development. The animal model would prove to be a useful model for analysis of the mechanism(s) of hormonal carcinogenesis.

Animals↗
PubMed1999

Sex hormone-induced mammary carcinogenesis in female noble rats: the role of androgens.

Breast cancer is the most common cancer and the second most frequent cause of cancer death in women. Despite extensive research, the precise mechanisms of breast carcinogenesis remain unclear. We have shown that in female rats, treatment with a combination of oestrogen and testosterone can induce a high incidence of mammary cancer. The dosage of testosterone affects only the latency period of mammary cancer, not the final incidence. Based on these observations, we hypothesize that oestrogen and androgens may act in concert on the mammary gland to induce mammary carcinogenesis, with oestrogen serving as the predominant initiator whereas the androgen acts as a major promoter. In the present study, we report the changes in morphology of the mammary gland with special emphasis on the perialveolar or interlobular stroma after treatment with various sex hormone protocols. Our data showed that after treatment with testosterone, either alone or in combination with 17beta-oestradiol, there was overexpression of the androgen receptor in alveolar or ductal epithelial cells. Concurrent with strong expression of the androgen receptor in epithelium, there was also an increase in the amount of perialveolar and interlobular connective tissue, a decrease in surrounding adipose tissue and an increase in proliferation rate of fibroblast-like cells in the stroma. All these changes were blocked by simultaneous implantation of flutamide, indicating that androgens play a crucial role in the process despite the absence of androgen receptors in stromal cells. We further measured the mammary gland density (MGD), in order to determine the ratio of fatty to non-fatty tissue. The data showed that MGD values were significantly higher in animals treated with testosterone alone or in combination with 17beta-oestradiol than in those treated with 17beta-oestradiol alone or in controls. Furthermore, treatment with different doses of testosterone resulted in an increase in MGD in a dose-dependent manner. These findings highlight the effect of androgens on the stroma, probably through a paracrine action of epithelial cells. The stroma may, in turn, promote mammary carcinogenesis in a reciprocal fashion.

Animals↗
PubMed1999

Dual chamber pacing for neurally mediated syncope with a prominent cardioinhibitory component.

The role of cardiac pacing for treatment of recurrent neurally mediated syncope (NMS) remains controversial. We hypothesized that dual chamber pacing in NMS patients with a prominent cardioinhibitory component may be beneficial. Twelve patients (mean age = 37.8+/-17 years, range 15-78 years, 7 men and 5 women) with a mean of 4+/-2.2 episodes of syncope underwent tilt table evaluation. Patients were passively tilted to 70 degrees head-up position for 20 minutes and then returned to the supine position. Isoproterenol was then infused at 1-2 microg/min to increase heart rate by > or = 25% and tilt was repeated. Patients lost consciousness after 16+/-6 minutes of tilt; nine patients had syncope in the baseline state and three during isoproterenol infusion. All patients had at least 5 seconds of asystole with a mean of 9.5+/-4 seconds (range 5-20 s). A dual chamber permanent pacemaker with a special feature allowing heart rate acceleration in response to bradycardia was implanted in all patients. During a mean follow-up of 18.6+/-4.2 months, 11 (92%) of these patients were free of syncope and had negative tilt table test. One (8%) patient had two episodes of syncope. We conclude that dual chamber pacing may be beneficial in patients with NMS with a prominent cardioinhibitory component.

Adolescent↗
PubMed1999

[Gas chromatography-infrared spectroscopy(GC-IR) analysis of the oxidation products of cyclohexene].

Gas chromatography-infrared spectroscopy technique integrates the excellent resolution ability of GC with the structural information of IR. Based on the GC and IR spectra, the complicated products of a reaction can be analyzed quantitatively and qualitatively. From the analysis of the products, the reaction process and its mechanism can be elucidated. In this work, analysis by GC-IR of the oxidation products of cyclohexene catalyzed by zeolite TS-1 in H2O2 was performed. The products are 2-cyclohexenone, 2-cyclohexen-1-ol and 2,3-epoxy-1-cyclohexanone. 2,3-Epoxy-1-cyclohexanone is an unexpected product. It must be a further oxidation product of 2-cyclohexenone. From the analysis, the reaction mechanisms were presumed.

Alkanes↗
PubMed1998

Fibronectin-mediated cell adhesion is required for induction of 92-kDa type IV collagenase/gelatinase (MMP-9) gene expression during macrophage differentiation. The signaling role of protein kinase C-beta.

Induction of the 92-kDa gelatinase (MMP-9) gene expression is associated with macrophage differentiation. In this study, we explored the regulatory mechanisms underlying this differentiation-associated MMP-9 gene expression in human HL-60 myeloid leukemia cells and human peripheral blood monocytes. Phorbol 12-myristate 13-acetate (PMA) markedly induced MMP-9 gene expression in HL-60 cells; the induction closely paralleled the timing and extent of PMA-induced cell adhesion and spreading, a hallmark of macrophage differentiation. Similarly, treatment with PMA or macrophage-colony stimulating factor stimulated adherence and spreading of blood monocytes with a concurrent 7- or 5-fold increase in MMP-9 production, respectively. In protein kinase C (PKC)-beta-deficient HL-60 variant cells (HL-525), PMA failed to induce cell adhesion and MMP-9 gene expression. Transfecting HL-525 cells with a PKC-beta expression plasmid restored PKC-beta levels and PMA inducibility of cell adhesion and spreading as well as MMP-9 gene expression. Induction of cell adhesion and MMP-9 gene expression in HL-60 cells and blood monocytes was strongly inhibited by neutralizing monoclonal antibodies to fibronectin (FN) and its receptor alpha5 beta1 integrin. HL-525 cells, which constitutively display high levels of surface alpha5 beta1 integrin, adhered and spread on immobilized FN with concomitant induction of MMP-9 gene expression. Cytochalasins B and D were each a potent inhibitor of MMP-9 production. Our results suggest that alpha5 beta1 integrin-mediated interaction of immature hematopoietic cells with FN plays a critical role in modulating matrix-degrading activities during macrophage differentiation.

Cell Adhesion↗
PubMed1998

Autocrine regulation of macrophage differentiation and 92-kDa gelatinase production by tumor necrosis factor-alpha via alpha5 beta1 integrin in HL-60 cells.

Tumor necrosis factor-alpha (TNF-alpha) gene is one of the early response genes induced by phorbol 12-myristate 13-acetate (PMA) in human HL-60 myeloid leukemia cells. In the present study, we examined the role of the TNF-alpha autocrine loop in PMA-induced macrophage differentiation and gene expression of 92- and 72-kDa gelatinases (MMP-9 and MMP-2). In HL-60 cells, PMA inhibited cell proliferation and induced cell adhesion and spreading, expression of surface maturation marker OKM1 and phagocytic activity, as well as the expression of both gelatinases, which all characterize the macrophage phenotype. In contrast, TNF-alpha alone was only effective in inhibiting cell proliferation. Blocking the endogenous TNF-alpha activity with neutralizing anti-TNF-alpha antibodies abolished all these PMA-induced events with the exception of MMP-2 gene expression. Since fibronectin (FN)-mediated cell adhesion and spreading are prerequisite for both macrophage differentiation and MMP-9 gene expression in HL-60 cells, we hypothesized that TNF-alpha might be involved in modulating the expression of either the FN or its integrin receptor genes. Whereas PMA substantially enhanced the steady state mRNA and protein levels of both FN and alpha5 beta1 integrins, TNF-alpha alone had little effect on the expression of these genes. However, anti-TNF-alpha antibodies blocked PMA-induced augmentation of both alpha5 and beta1 integrin gene expression without affecting the expression of the FN gene. Our results suggest that TNF-alpha may regulate macrophage differentiation and critical matrix-degrading activities of myeloid progenitor cells in an autocrine manner by augmenting surface levels of the alpha5 beta1 integrin, thus promoting interactions with the extracellular matrix, a key event for maturation and migration of these cells during inflammation.

Autocrine Communication↗
PubMed1998

Biochemical characterization of the Cys138Arg substitution associated with the AB variant form of GM2 gangliosidosis: evidence that Cys138 is required for the recognition of the GM2 activator/GM2 ganglioside complex by beta-hexosaminidase A.

The function of the GM2 activator protein is to act as a substrate-specific cofactor in the hydrolysis of GM2 ganglioside by beta-hexosaminidase A. Mutations in the gene encoding it result in the AB variant form of GM2 gangliosidosis. One such mutation, Cys138 Arg, results in the mutant protein being retained and degraded in the endoplasmic reticulum of mammalian cells. In order to characterize the biochemical effects of this substitution, we expressed the mutant protein in transformed bacteria. We first compared the wild-type protein produced by two bacterial expression methods, one requiring protein refolding, with activator purified from the medium of transfected CHO cells. The "activity" and circular dichroism spectrum (alpha-helical content) of all three proteins were similar, justifying the use of refolded activator from transformed bacteria in structure/function studies. Second, the mutant protein was expressed in both bacterial systems and in each retained approximately 2% of the wild type's specific activity. The presence of even this small amount of activity in the mutant protein coupled with a calculated alpha-helical content nearly identical to the wild type, strongly suggest that no major tertiary or secondary structural changes, respectively, had occurred due to the mutation. However, we demonstrate that its heat stability at 60 degrees C is reduced 14-fold, suggesting some localized change in tertiary structure. The loss of a disulfide loop was confirmed by reacting the mutant protein with Ellman's reagent. A kinetic analysis detected a large increase in the apparent K(m) of beta-hexosaminidase A for the mutant; however, there was no apparent change in Vmax. A fluorescence dequenching assay was used to evaluate the ability of the mutant protein to transport lipids and bind GM2 ganglioside. These assays detected no difference between the wild-type and mutant proteins, indicating that the Cys138 Arg substitution has no effect on these functions. We conclude that the mutation specifically affects a domain in the activator protein that is responsible for the recognition of the activator-GM2 ganglioside complex by beta-hexosaminidase A.

Amino Acid Sequence↗
PubMed1998

Clinical differentiation of narrow QRS complex tachycardias.

Supraventricular tachycardias generally present with narrow QRS complexes and are quite commonly seen in the emergency department. Regular narrow QRS complex tachycardias occur in all age groups and may be associated with minimal symptoms, such as palpitations, or, present with hemodynamic compromise resulting in syncope. While history and physical examination are indispensable, they usually do not lead to a definitive diagnosis. The diagnosis is made by careful analysis of the 12-lead ECG. Therapy is based on hemodynamic assessment and understanding of the tachycardia mechanism.

Diagnosis, Differential↗
PubMed1998

Clinical approach to wide QRS complex tachycardias.

Wide QRS complex tachycardia is a frequently encountered arrhythmia in the emergency department and presents a diagnostic challenge to the emergency physician. The history, physical examination, chest radiograph, and electrocardiogram analysis are important in making the correct diagnosis. The diagnosis of ventricular tachycardia is supported by, 1) a history of prior myocardial infarction or congestive heart failure; 2) a physical examination showing cannon A-waves in the jugular venous pulsation or variable heart sounds; 3) a chest radiograph showing cardiomegaly or evidence of prior cardiac surgery; and 4) characteristic ECG features that include AV dissociation, fusion-capture beats, QRS concordance, or, typical morphologic features in leads V1 and V6. This article presents the diagnostic and therapeutic approaches to wide QRS tachycardias.

Diagnosis, Differential↗
PubMed1998

Permanent cardiac pacing.

Implantation of a permanent pacemaker is the most commonly performed surgical operation involving the heart. The modern cardiac pacemaker is a complex device that can sense and pace in both the atrium and ventricle. It also modulates the pacing rate based on sensed physiologic parameters. This article reviews the fundamental principles of pacemaker technology and provides the emergency physician with approaches to common pacemaker problems.

Electrocardiography↗
PubMed1998

Implantable cardioverter defibrillators.

Implantable cardioverter defibrillators have proven to be an effective therapy for life-threatening ventricular arrhythmias. Given the ever-increasing number of patients who have these devices, increasing numbers of patients are likely to present to emergency departments with defibrillator-related problems. This article discusses normal device function, indications for implantation, and technique of implantation. It also focuses on the evaluation and management of patients with these devices presenting to the emergency department.

Arrhythmias, Cardiac↗
PubMed1998

[Survey on breakfast-eating behavior among residents in Beijing, Guangzhou and Shanghai].

A survey of breakfast-eating behavior among residents in Beijing, Guangzhou and Shanghai was carried out in 1994-1995. The results showed that the breakfast-eating rates in three cities were 74.8%-90.5%. Subjects aged below 35 years skipped breakfast more often. "Time limiting" in the morning became the main cause of breakfast-skipping. Nearly half of subjects in three cities got their breakfast out of home. Moreover, compared with two years ago, the present rates of eating outside increased at various levels in three cities. Steamed bun, bread and congee were main foods consumed at breakfast. In addition, 39% to 56% of subjects often drank milk. Through this survey, the authors got an all-round understanding on breakfast-eating rates, eating outside rates and variety of food consumed of residents in 3 cities. This survey will also provide a background for nutrition intervention and education in the future.

Adult↗