World at work: manufacturing "tatami" mats in China.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to X Zhang.
Explore the source record for details and available documents.
OBJECTIVE: To develop estimates of the direct and indirect costs of smoking for California in 1999. METHODS: A prevalence based approach was used to estimate the annual costs of smoking. Econometric models were used to estimate the smoking attributable fraction (SAF) for direct costs (hospitalisations, ambulatory care, prescription drugs, home health care, and nursing home services) and indirect costs due to lost productivity from smoking related illness. The models controlled for socioeconomic factors and other risk behaviours. Epidemiological methods were used to estimate the SAF for indirect costs due to lost productivity from premature deaths. The SAFs were applied to total health care expenditures, days lost, and deaths to obtain smoking attributable total costs. RESULTS: In 1999, the total costs of smoking in California were 15.9 billion dollars, 475 dollars per resident, and 3331 dollars per smoker. Direct costs were 8.6 billion dollars (54% of the total), indirect costs due to lost productivity from illness were 1.5 billion dollars (10%), and indirect costs due to premature deaths were 5.7 billion dollars (36%). The cost of smoking was 9.4 billion dollars for men and 6.3 billion dollars for women. There were 43,137 deaths attributed to smoking, representing a total of 535,000 years of life lost. The value of life lost per death averaged 132,000 dollars, or 12.4 years. CONCLUSIONS: California smoking related costs are high. The cost methodology presented is useful for other states and nations interested in estimating their costs of smoking. Cost estimates can be used to evaluate the level of cigarette taxes and other policies related to smoking.
BACKGROUND/AIMS: Advanced glycated end products (AGE) are endogenous proteins that have formed covalent complexes with sugars by a nonenzymatic process. Being proinflammatory molecules, AGE are thought to contribute to chronic systemic and local inflammatory processes associated with pathological changes in various diseases. In patients with end-stage renal disease, AGE are believed to play a role in the progression of atherosclerosis and worsening of renal failure. In patients receiving hemodialysis, AGE are thought to contribute to the inflammatory components of the therapy, particularly in diabetic patients. METHODS: In the present study, AGE were produced using 5% human serum albumin (HSA) and 50% glucose, both used for intravenous infusion into humans and both released after strict control for endotoxin content. The presence of AGE formed by HSA and glucose was confirmed using 2 independent assays. The inflammatory properties of these AGE were assessed using synthesis and release of the proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor (TNF) and IL-8, a chemokine. RESULTS: Alone, AGE did not induce these cytokines from peripheral blood mononuclear cells (PBMC) obtained from 14 healthy human donors. However, in the presence of 1 or 10 ng/ml of endotoxin, AGE augmented the production of IL-1 and TNF above that induced by endotoxin alone. Although the amount of augmentation of LPS-induced cytokines by AGE varied between the blood donors, the response was consistently observed and reached statistical significance. The augmentation of cytokine production was confirmed using AGE prepared with different lots of HSA and glucose. CONCLUSION: These results demonstrate that in the strict absence ofendotoxins, AGE are formed that do not stimulate cytokine production from PBMC of healthy donors, however, AGE significantly augment the synthesis and release of proinflammatory cytokine in the presence of low concentrations of endotoxins. The data suggest that renal replacement therapies should consider the role of microbial products in potentiating the biological consequences of naturally formed AGE and their potential to contribute to systemic and local inflammation in renal replacement therapies. Therefore, although the formation of AGE is unavoidable, excluding microbial products during renal replacement therapy should reduce the pathological consequences of AGE.
Explore the source record for details and available documents.
Chitosan, a naturally abundant biopolymer, has widely been studied for metal adsorption from various aqueous solutions, but the extension of chitosan as an adsorbent to remove humic substances from water has seldom been explored. In this study, chitosan was coated on the surface of polyethyleneterephthalate (PET) granules through a dip and phase inversion process and was examined for humic acid removal in a series of batch adsorption experiments. Scanning electron microscopic (SEM) images showed that the PET granules were uniformly covered with a layer of chitosan and the chitosan layer possessed numerous open pores on the surface. Zeta potential study indicated that the chitosan-coated granules had positive zeta potentials at pH < 6.6 and negative zeta potentials at pH > 6.6. Adsorption of humic acid onto the chitosan-coated granules was found to be strongly pH-dependent. Significant amounts of humic acid were adsorbed under acidic and neutral pH conditions, but the adsorption capacity was reduced remarkably with increasing solution pH values. The adsorption isothermal data under various initial humic acid concentrations (at the same solution pH value) can be adequately modeled by the Langmuir and Freundlich models. X-ray photoelectron spectroscopy (XPS) revealed that the amino groups of the chitosan layer were protonated due to humic acid adsorption, suggesting the formation of organic complex between the protonated amino groups and humic acid. Kinetic study indicated that the adsorption process was transport-limited at low solution pH values, but became both transport- and attachment-limited at high solution pH values.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Using the cultured chicken embryonic chondrocytes as a model, the effects of simulated microgravity on the microtubular system of the cellular skeleton, extracellular matrix, alkaline phosphatase activity, intracellular free calcium concentration and mitochondrial ATP synthase activity with its oligomycin inhibition rate were studied with a clinostat. The microtubular content was measured by a flow cytometer. The decrease of microtubular content showed the impairment of the cellular skeleton system. Observation on the extracellular matrix by the scanning electron microscopy showed that it decreased significantly after rotating, and the fibers in the extracellular matrix were more tiny and disorderly than that of the control group. It can be concluded that the simulated microgravity can affect the secreting and assembly of the extracellular matrix. In contrast to the control, there was a time course decrease in alkaline phosphatase activity of chondrocytes, a marker of matrix mineralization. Meanwhile a significant drop in the intracellular calcium concentration happened at the beginning of rotation. These results indicate that simulated microgravity can suppress matrix calcification of cultured chondrocytes, and intracellular free calcium may be involved in the regulation of matrix calcification as the second signal transmitter. No significant changes happened in the mitochondrial ATP synthase activity and its oligomycin inhibition rate. Perhaps the energy metabolism wasn't affected by the simulated microgravity. The possible mechanisms about them were discussed.
Ionotropic glutamate receptors are ligand-gated ion channels that help mediate rapid excitatory neurotransmission in the CNS. alpha-Amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors are critical for synaptic plasticity in central nociceptive transmission. The current study was designed to investigate the role of the AMPA receptor subunit, GluR1, and its phosphorylated forms (at Ser-831 and Ser-845) in central sensitization in rat spinal cord. Western blots and immunohistochemistry were performed to examine the expression and localization of GluR1 and the phosphorylated forms of GluR1 (phospho-GluR1) at Ser-831 and Ser-845 with specific antibodies. Results showed that immunolabeling of GluR1 protein in rat spinal cord can be detected at 110 kD, and two phospho-GluR1 proteins were found at 106 kD. A significant upregulation of phospho-GluR1 both at Ser-831 and Ser-845 was found by 5 min after capsaicin treatment, and this increase lasted at least 60 min. Immunostaining showed that GluR1 and its phosphorylated forms were localized in the superficial laminae of dorsal horn and quantitative image analysis supported the immunoblotting results. Our findings are consistent with the suggestions that AMPA receptors show increased responsiveness because of their phosphorylation and that this may contribute to central sensitization following intradermal injection of capsaicin.
Prostate adenocarcinoma is associated with the formation of osteoblastic metastases in bone. It is hypothesized that osteoclastogenesis is a critical component in the development of skeletal metastases. These findings, however, were generally noted in predominantly osteolytic lesions. The pathophysiology of osteoblastic lesions remains unknown but the type of bone lesion formed may be influenced by the cytokines produced by prostate tumors. To test this theory, we implanted PC-3 and LAPC-9 cells into the tibias of SCID mice. These mice were sacrificed at 1, 2, 4, 6, and 8 weeks after implantation and histologic analysis was performed on these tibias. PCR analysis was also performed on bulk tumors. The results showed that the PC-3 implanted tibias developed pure osteolytic lesions while the LAPC-9 implanted tibias developed pure osteoblastic lesions on radiographs. Analysis of tibias after injection with PC-3 cells revealed progressive osteolytic lesions with abundant osteoclast activity at 2 weeks and destruction of the proximal tibia at 6 weeks after cell implantation. In contrast, the LAPC-9 cells formed osteoblastic lesions six weeks after cell injection. There were rare osteoclasts prior to the establishment of the osteoblastic lesions but greater osteoclast activity was noted with remodeling of the osteoblastic lesion 8 weeks after implantation of the tumor cells. PCR analysis revealed that PC-3 cells produced RANKL, IL-1, and TNF-alpha, which are associated with osteoclastogenesis. In contrast, LAPC-9 cells produced osteoprotegerin, which blocks osteoclast production and no detectable levels of RANKL or IL-1 and only minimal amounts of TNF-alpha were noted. These cells secreted BMP-2, -4, -6, and IL-6, which are associated with bone formation. These results suggest that the role of the osteoclast in the development of a metastatic lesion is variable depending on the phenotype of the prostate cancer cells, and that tumor-induced osteolysis may not be required for osteoblastic metastases.
Cavitation induced by ultrasonic vibrations can cause nucleation of ice in supercooled water. In this study, the time required for ultrasonic-induced nucleation of ice was measured for water containing two different size distributions of air bubbles. When the water was supersaturated with air bubbles, there was a time lag of about 0.5 s between the onset of ultrasonic irradiation and the onset of ice nucleation, and the probability of ice nucleation was unusually high within 0.5-1.1 s after the onset of ultrasonic irradiation. These results cannot be explained by conventional models alone, in which the collapse of a cavitation bubble triggers the nucleation of ice. Secondary effects appear to also influence ice nucleation.
BACKGROUND: It is of clinical importance to localize pathologic brain tissue in epilepsy. Noninvasive localization of cortical areas associated with interictal epileptiform spikes may provide important information to facilitate presurgical planning for intractable epilepsy patients. METHODS: A cortical potential imaging (CPI) technique was used to deconvolve the smeared scalp potentials into the cortical potentials. A 3-spheres inhomogeneous head model was used to approximately represent the head volume conductor. Five pediatric epilepsy patients were studied. The estimated cortical potential distributions of interictal spikes were compared with the subsequent surgical resections of these same patients. RESULTS: The areas of negativity in the reconstructed cortical potentials of interictal spikes in 5 patients were consistent with the areas of surgical resections for these patients. CONCLUSIONS: The CPI technique may become a useful alternative for noninvasive mapping of cortical regions displaying epileptiform activity from scalp electroencephalogram recordings.
Confinement of transgene expression to target cells is highly desirable in gene therapy. Current strategies of transcriptional targeting to tumors usually rely on tissue-specific promoters to control gene expression. However, such promoters generally have much lower activity than the constitutive viral promoters. We have explored an alternative approach, using a strict-late viral promoter (UL38p) in the context of an oncolytic herpes simplex virus (HSV) for tumor-selective gene expression. As with many DNA viruses, the genomic transcription of HSV is a tightly regulated molecular cascade in which early and late phases of gene expression are separated by viral DNA replication. In particular, some of the late transcripts are categorized as strict-late, whose expression depends rigorously on the initiation of viral DNA replication. Our in vitro and in vivo characterization showed that in normal nondividing cells, where the oncolytic HSV has limited ability to replicate, the UL38p has minimal activity. However, in tumor or cycling cells where the virus can fully replicate, transgene expression from UL38p was almost as high as from the cytomegalovirus immediate-early promoter. These results suggest that delivery of therapeutic genes driven by UL38p through an oncolytic HSV may be an effective approach to gene therapy for malignant diseases.
The acute inflammatory response elicited by adenovirus vectors results in loss of gene expression and tissue injury in the target organ. This acute inflammation is now believed to be the major limiting factor for the use of adenovirus vectors in gene therapy. While exploring the level of acute inflammation caused by the adenovirus encoding the gene for the anti-inflammatory enzyme heme oxygenase-1, we discovered that this adenovirus not only did not elicit acute inflammation, but could prevent the inflammation caused by a second adenovirus. Here we describe a new approach to gene therapy, which uses the encoding of the potent anti-inflammatory enzyme heme oxygenase-1 to prevent early host inflammatory responses normally associated with adenovirus vectors.
Cervical lymphadenitis caused by Candida albicans developed in an 8-year-old Chinese child. There was no evidence of disseminated infection. The infection apparently confined to a lymph node was interpreted as a stage of fungal invasion. The child showed lymphopenia with a proportionate decrease in T-helper and T-suppressor cells. The child was successfully treated intravenously with fluconazole.
With 1.3 billion people, China has the largest population in the world, and therefore has the largest population of persons with haemophilia (PWH). As there is no national registry for haemophilia, it is difficult to ascertain how many PWH have actually been diagnosed. Between January 1983 and June 2002, 1312 patients with coagulation disorders were referred to our hospital, and 1190 patients were evaluable. Among them, 1069 (89.8%) patients had haemophilia, 68 had vWD, 20 had factor XI deficiency, 10 had acquired factor VIII inhibitor and 23 had other coagulation disorders. Of the 1069 PWH, 14.7% were unclassified, 38.4% severe, 35.7% moderate and 11.1% mild. If the unclassified cases were excluded, 45.1% were severe, 41.9% moderate and 13.0% mild. Twenty-nine of the 68 vWD patients had vWF:Ag <5%, and subcategorized as type 3 vWD. Because vWF multimer analysis was not performed in our centre, the remaining vWD patients were not subdivided.