Biomedical subjects
Publications and source records attributed to Z Tao.
Tissue engineering is a new field in biomedical engineering. In this review, progress in the field of tissue engineering is presented in detail, including a general introduction, design and fabrication principles, key technologies, various applications, new directions, as well as related market and R&D issues.
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Ischemic insults to the brain result in a time-dependent increase in neuronal death that is responsible for some of the functional deficits associated with stroke. Our working hypothesis is that ischemia results in a prompt depletion of high energy phosphate species resulting in decreased pH and glutathione levels in brain in a temporal and spatial pattern that disrupts nerve growth factor homeostasis and increases neuronal apoptosis. Here we show hemispheric depletion of active phosphate species after ischemia. Also, we observed that the striatum is an early target for oxidative stress that is followed by energy metabolic impairment and altered neurotrophin levels that were detected by noninvasive magnetic resonance imaging (MRI) measurements of cytotoxicity and conventional biochemical determinations of apoptosis, glutathione, and nerve growth factor (NGF) protein levels in a pattern distinct from that observed in the hippocampus. Furthermore, early assessment of intracellular pH by 31P-magnetic resonance spectroscopy (31P-MRS) was a predictor of later infarct development as determined by MRI. We also show that pretreatment with pharmacological doses of NGF did not have overall significant beneficial consequences on irreversible ischemia in an intraluminal unilateral irreversible model of stroke in rat brain.
Hypoxia and hypoxia/reoxygenation are known to affect vascular smooth muscle cell physiology. In this study, we first investigated proteoglycan synthesis by human aortic smooth muscle cells exposed to normoxia, hypoxia, or hypoxia/reoxygenation. We then compared the newly synthesized proteoglycans from normoxic and hypoxic-reoxygenation cultures for their ability to bind low density lipoprotein (LDL). Confluent smooth muscle cells under normoxia, hypoxia, or hypoxia/reoxygenation were pulsed with [35S]sulfate, and secreted and cell-associated proteoglycans were analyzed. Secreted proteoglycans in cultures exposed to hypoxia (4 h)/reoxygenation (19 h) increased 28% over those of cells continuously exposed to normoxia. Cell-associated proteoglycans did not differ significantly between the two groups. In contrast, hypoxia (4 h) followed by a 30-min reoxygenation produced a 37% decrease in newly synthesized proteoglycans. Hypoxia alone also resulted in a 24% decrease in secreted proteoglycans and a 20% decrease in cell-associated proteoglycans. Proteoglycans newly synthesized by smooth muscle cells exposed to normoxia and hypoxia/reoxygenation did not differ in their charge densities and molecular size but did differ in glycosaminoglycan composition. Exposure of smooth muscle cells to hypoxia/reoxygenation produced a 60% increase in a proteoglycan subfraction that bound LDL with very high affinity. The incorporation of [3H]leucine into total cellular protein decreased significantly following exposure of smooth muscle cells to hypoxia as well as hypoxia/reoxygenation. These results indicate that hypoxia and hypoxia/reoxygenation cause major alterations in proteoglycan metabolism by vascular smooth muscle cells.
OBJECTIVE: To estimate cancer risk associated with the low level radiation exposure of average annual effective dose of 6.4 mSv in HBRA the high background radiation area (HBRA) of Yangjiang, China. METHODS: The cancer mortality data of 1979-1986 were collected from a dynamic cohort by prospective survey. The data of 1987-1995 were obtained from a fixed cohort by retrospective and/or prospective survey. The mortality investigation on the spot consisted of two steps, i.e. the follow-up of the members in the cohort and the ascertainment of the death causes. The estimate of cumulative individual dose of the cohort members included that of the exposure from natural external and internal sources. Both direct (TLD measurement) and indirect (environmental measurement and occupancy pattern) approaches were used for individual external dose estimate. On the basis of the hamlet-specific average annual external dose, the cohort members were classified into four groups for internal comparison: high, medial and low dose groups from HBRA and control group from control area (CA). Relative risk (RR) and excess relative risk coefficient (ERR per sievert) and its 95% confidence interval (CI) was estimated using AMFIT program in Epicure. RESULTS: During the period 1979-1995, there were 10,415 total deaths and 1003 cancer deaths among 1,698,350 person-years at risk in the cohort of 125,079 subjects. The adjusted RR (95% CI) with sex and age group for all cancers of whole HBRA was 0.99 (0.87-1.14). As for the site-specific cancer of whole HBRA, the RRs of cancers of stomach, colon, liver, lungs, bone, female breast, and thyroid were less than one, while the RRs of cancers of nasopharynx, esophagus, rectum, pancreas, skin, cervix uterus, brain and central nervous system, leukemia and lymphoma were larger than one. However, all of them except for esophagus cancer were not different statistically from one (P > 0.05). The homogeneity tests of RRs for all cancers and for site-specific cancer among the three dose groups in HBRA revealed that the RRs in these dose groups were not different statistically (P > 0.05) for all. The ERR (95% CI)/Sv of all cancers for both sexes and all ages was -0.10 (-0.67, 0.69). CONCLUSION: An increased cancer risk associated with the high levels of natural radiation in HBRA was not found. On the contrary, the mortality of all cancers in HBRA was generally lower than that in CA, but not significant statistically.
OBJECTIVE: To analyse the causes of unsuccessful septoplasty. METHOD: 28 cases were investigated by high-resolution CT scan and nasal endoscopy. Another operation was completed in endoscopic sinus surgery. RESULT: 16 upper or posterior nasal septal deviation and 12 paraseptal structural deformities and chronic sinus diseases were observed, which were neglected in the first operation. CONCLUSION: Before septoplasty, CT and endoscopic evaluation of the paranasal sinuses and paraseptal structures should be performed and accompanied nasal diseases should be considered.
AIM: To determine whether immunization with recombinant filarial chitinase or a fragment containing the epitope recognized by McAbMF1 and SXP-1 could protect jirds against microfilaremia resulting from infection with B. malayi. METHODS: Test jirds were immunized with the following recombinant parasite antigens: filarial chitinase, the c-terminal fragments F7R2 or F8R2 of r-chitinase, filarial SXP-1, myosin or maltose binding protein (MBP). Employing immunochemical techniqe (SDS-PAGE, Western Blotting) and serology (ELISA) measured antifilarial antibodies level. RESULTS: Immunization of jirds with recombinant chitinase induced partial protection against microfilaremia resulting from subsequent infection with B. malayi, but did not reduce adult worm burdens. Vaccination was much less effective when administered during the prepatent stage of infection and was ineffective when given to microfilaremic jirds. Immunization of jirds with SXP-1, an antigen present in multiple worm stages also reduced microfilaremia and, in some experiments, adult worm burdens. CONCLUSION: The recombinant chitinase, fragments F7R2 and F8R2 and SXP-1 could provide partial protection against microfilaremia in jirds.
The change in fluorescence of human serum albumin (HSA) and salicylic acid due to their interaction has been studied in 0.05 mol/L, pH 9.50 borate buffer (contains 0.01 mol/L KCl). The dissociation constant of salicylic acid from HSA was obtained by using two different methods.
Modifications of (D-Trp32) neuropeptide Y (NPY) led to the development of potential peptide-based lower molecular weight (500-800 Da) NPY feeding antagonists. One compound, WRYamide (N-Ac-Trp-Arg-Tyr-NH2), blocked NPY-induced feeding for 1 to 4 h when injected intrahypothalamically (i.h.t.) at 1 to 40 microgram. Schedule-induced feeding was also antagonized for up to 24 h by 20 microgram of WRYamide, i.h.t. Injection of 2.5 mg/kg (1 mg/rat) of WRYamide, i.v., also reduced significantly schedule-induced feeding for 4 h. A conditioned taste aversion could not be classically conditioned to saccharin using WRYamide as the unconditioned stimulus. These results may lead to the development of systemically active anti-obesity drugs.
GR231118, BW1911U90, Bis(31/31')[[Cys31, Trp32, Nva34] neuropeptide Y(31-36)] (T-190) and [Trp-Arg-Nva-Arg-Tyr]2-NH2 (T-241) are peptide analogs of the C-terminus of neuropeptide Y that have recently been shown to be antagonists of the neuropeptide Y Y1 receptor. In this study, the activity of these peptides at each of the cloned neuropeptide Y receptor subtypes is determined in radioligand binding assays and in functional assays (inhibition of forskolin-stimulated cAMP formation). GR231118 is a potent antagonist at the human and rat neuropeptide Y Y1 receptors (pA2 = 10.5 and 10.0, respectively; pKi = 10.2 and 10.4, respectively), a potent agonist at the human neuropeptide Y Y4 receptor (pEC50 = 8.6; pKi = 9.6) and a weak agonist at the human and rat neuropeptide Y Y2 and Y5 receptors. GR231118 also has high affinity for the mouse neuropeptide Y Y6 receptor (pKi = 8.8). Therefore, GR231118 is a relatively selective neuropeptide Y Y1 receptor antagonist, but has appreciable activity at the neuropeptide Y Y4 and Y6 receptors as well. BW1911U90, T-190 and T-241 are moderately potent neuropeptide Y Y1 receptor antagonists (pA2 = 7.1, 5.8 and 6.5, respectively; pKi = 8.3, 6.5 and 6.8, respectively) and neuropeptide Y Y4 receptor agonists (pEC50 = 6.8, 6.3 and 6.6, respectively; pKi; 8.3, 7.7 and 8.3, respectively). These data suggest that the C-terminus of neuropeptide Y and related peptides is sufficient for activation of the neuropeptide Y Y4 receptor, but is not sufficient for activation of the neuropeptide Y Y1 receptor. Because BW1911U90, T-190 and T-241 are significantly less potent at the cloned human neuropeptide Y Y1 receptor than at the neuropeptide Y receptor in human erythroleukemia cells, these cells may express a novel neuropeptide Y receptor with high affinity for these peptides.
In 1986-1996, four childish patients with parapharyngeal space tumour were treated in our hospital. In the beginning, we ought to define the size and range by CT scanning. The second, we excized it from neck-flank. The patients had a satisfying effect after surgical operation. Meantimes, it's necessary to protect the important vessel and nerve in surgical operation.
This study investigated the rabbits facial nerve regeneration over a 8 mm transectional gap of the bucal branches through autologous degenerated skeletal muscle and autologous vein respectively. At 20 weeks following the implantation of the mentioned non-neural materials, all the nerve defects of the experimented animals were repaired. In the electrophysiologic indices and morphometeric analysis, the differences between the respective experimental group and the nerve autografts group had no statistical significance. The results indicated that the non-neural tissues could guide facial nerve regenerating effectively, which suggested that they can be clinically practicable.
OBJECTIVE: To further investigate the mechanism of nasal secretion closely related to the innervation patterns in nasal mucosa with emphasis on the acetylcholinesterase (AChE)-positive fibers and peptidergic terminals in nasal mucosa as well as trigeminal ganglion (TG) cells. METHODS: Histochemical demonstration of AChE-positive fibers, immunohistochemical study of the distribution patterns of multiple peptidergic terminals, double labelling of AChE and substance P (SP) and somatostatin (SOM) mRNA in situ hybridization were carried out in nasal mucosa and trigeminal ganglion (TG) in rats. RESULTS: AChE-positive terminals were mainly distributed in the mid to posterior one third of septal nasal mucosa, with greater staining density on the walls of small vessels and glands. There were fewer such terminals in turbinate mucosa. Tachykinins-ergic terminals, including substance P (SP)-, neurokinin A (NKA)-, neurokinin B (NKB)- and calcitonin gene-related peptide (CGRP)-ergic terminals, had an extensive localizations in nasal mucosa, involving the following areas: between epithelial cells, submucosa, the walls of small vessels, glands and venous sinusoids in both septal and turbinate nasal mucosa. Septal mucosa had the greater density. There were overlaps in the distribution of these peptidergic terminals. There were also vasoactive intestinal peptide (VIP)-, neuropeptide Y (NPY)- and galanin (GAL)-ergic terminals in nasal mucosa. But no neurotensin (NT)- and somatostatin (SOM)-ergic terminals were found. In situ hybridization revealed SOMmRNA expression in TG cells. AChE and nine neuropeptides existed in the cytoplasms of TG cells. Besides, AChE and SP could exist simultaneously in cytoplasms of TG cells. CONCLUSIONS: AChE-positive (corresponding to parasympathetic nerves) and peptidergic terminals have different distribution patterns in the nasal mucosa of rats, although an overlap does exist, indicative of their different physiological effects on the regulation of nasal secretion and other functions; AChE and multiple neuropeptides in the cytoplasm of TG cells might play a role in modulating the nasal secretion in response to stimuli in the nasal mucosa.
AIM: To evaluate the usefulness of immunochromatographic test (ICT) for rapid diagnosis and surveillance of Wuchereria bancrofti infection. METHODS: The monoclonal antibody based-ICT assay was used to detect filarial antigens in the sera from bancroftian filariasis patients. RESULTS: 111 out of 116 bancroftian microfilaria cases showed positive ICT reaction, giving a positive rate of 95.7%. Serum samples from 12 malayian microfilaremia cases, 33 ascariasis cases, 20 schistosomiasis japonica cases and 6 trichinellosis cases were all found negative in ICT, demonstrating a specificity of 100%. In 73 chronic filariasis cases with elephantiasis, hydrocoele, and chyluria cases, 18 showed ICT positive, among whom 16 revealed microfilaremia, suggesting that the ICT positive cases were with active infections. Of the 30 microfilaremia cases before single dose ivermectin treatment, 29 were ICT positive (96.7%). A negative conversion of microfilaremia was observed in all cases 8-14 days post-treatment. Upon following up to 6 and 12 months, microfilaremia reappeared in 5 and 7 cases, respectively. 5 out of 13 ICT positive cases were found microfilaremic at 6 month post-treatment, while among the rest of 8, 5 were found microfilaremic at 12 month post-treatment. Parallel use of ICT with routine blood film examination in Houda village, Zhecheng County, Henan Province for a post-control surveillance survey in 132 local individuals revealed 9 microfilaremia cases were also ICT positive. Of the 123 persons with negative blood examination, only 1 was ICT positive. CONCLUSION: ICT is a rapid and simple method with high sensitivity and specificity, and might be used for the diagnosis, efficacy evaluation as well as a tool for post-control surveillance of bancroftian filarasis.
The fluorescence properties of humic acid derived from DaYaWan soil were analyzed using the conventional fluorescence and synchronous scan fluorescence spectroscopy. The results show that synchronous technique applied to the study of humic acid can reduce the fluorescence spectrum of a compound to a single sharp peak, and decrease the signal overlapping. In addition, the effects of various deltalambda, concentration and pH values on synchronous fluorescence spectroscopy were investigated in detail.
Smooth muscle cell (SMC) proliferation and increased production of arterial wall proteoglycans (PG) are implicated in atherogenesis. We investigated the effect of SMC proliferation on the biosynthesis of PG and the ability of the newly synthesized PG to bind low density lipoprotein (LDL). Proliferating and quiescent human aortic SMC were pulsed with [35S]sulfate for 24 h. Secreted and cell-associated PG were then analyzed. When SMC plated at a low density were induced to proliferate, PG synthesis increased significantly in comparison with quiescent cells. This was the net result of a 2.7-fold increase in secreted PG and a 1.3-fold increase in cell-associated PG. The increased PG synthesis in proliferating SMC correlated with a significant increase in the steady-state level of mRNA for perlecan and biglycan, and a modest increase in the versican-specific mRNA. The mRNA for decorin showed a 40% decrease. The increased PG secretion in proliferating cultures was due to increases in heparan sulfate PG, dermatan sulfate PG, and chondroitin sulfate PG secretion. Quiescent SMC at confluency produced 50% less PG than the corresponding SMC plated at a low density. Although confluent SMC stimulated to proliferate also had increased PG synthesis, this was 50% less than the PG synthesis by proliferating SMC that were initially plated at a low density. The PG synthesized by proliferating and quiescent SMC did not differ in charge density and molecular size. Secreted PG from both quiescent and proliferating cultures contained subfractions that bound LDL with high affinity. However, compared with quiescent cultures, the proliferating cultures produced more of a PG subfraction that exhibited very high affinity to LDL (31.6% in quiescent cultures versus 40.8% in proliferating cultures). These results indicate that PG metabolism is altered significantly in proliferating human SMC which might have implications in the pathophysiology of atherosclerosis.
We investigated the biosynthesis of proteoglycans (PG) in endothelial cells following their treatment with phorbol 12-myristate 13-acetate (PMA). Confluent cultures of bovine aortic endothelial cells were incubated in the presence and absence of PMA (100 ng/ml) and then pulsed with [35S]sulfate, [3H]glucosamine, or [35S]sulfate plus [3H]leucine for varying times in the absence of PMA. Alternatively, confluent endothelial cells were simultaneously incubated with PMA and [35S]sulfate for varying times. The metabolically labeled PG in the cell layer and medium were analyzed. Both short-term and prolonged exposure of endothelial cells to PMA significantly stimulated PG synthesis, regardless of the experimental conditions. [35S]sulfate incorporation into newly synthesized PG in PMA-treated cells also increased by 1.7-fold and 3.6-fold over control cells, following a 15-min and 30-min pulse, respectively. Cycloheximide markedly inhibited the increased synthesis of PG in PMA-treated cells, while actinomycin D produced a moderate inhibition. PG secretion was increased in PMA-treated cells compared with control cells, while there was no significant difference in PG degradation between the two cultures. PG from control and PMA-treated endothelial cell cultures did not differ in composition or hydrodynamic sizes. The incorporation of [3H]leucine into total cellular proteins decreased significantly following exposure of endothelial cells to PMA. Endothelial cells exposed to PMA for 3 h had significantly more protein kinase C (PKC) activity than did control cells. Inhibition of PKC by calphostin C abolished the PMA-mediated stimulation of PG synthesis in endothelial cells. The results indicate that PMA stimulates PG synthesis in endothelial cells either directly or indirectly through a PKC dependent mechanism.
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