Search PubMed⌕ Search

Biomedical subjects

Y Jiang

Publications and source records attributed to Y Jiang.

At least 307 records · Page 17Linked to original sources

Mathematical model of gas bubble evolution in a straight tube.

Deep sea divers suffer from decompression sickness (DCS) when their rate of ascent to the surface is too rapid. When the ambient pressure drops, inert gas bubbles may form in blood vessels and tissues. The evolution of a gas bubble in a rigid tube filled with slowly moving fluid, intended to simulate a bubble in a blood vessel, is studied by solving a coupled system of fluid-flow and gas transport equations. The governing equations for the fluid motion are solved using two techniques: an analytical method appropriate for small nondeformable spherical bubbles, and the boundary element method for deformable bubbles of arbitrary size, given an applied steady flow rate. A steady convection-diffusion equation is then solved numerically to determine the concentration of gas. The bubble volume, or equivalently the gas mass inside the bubble for a constant bubble pressure, is adjusted over time according to the mass flux at the bubble surface. Using a quasi-steady approximation, the evolution of a gas bubble in a tube is obtained. Results show that convection increases the gas pressure gradient at the bubble surface, hence increasing the rate of bubble evolution. Comparing with the result for a single gas bubble in an infinite tissue, the rate of evolution in a tube is approximately twice as fast. Surface tension is also shown to have a significant effect. These findings may have important implications for our understanding of the mechanisms of inert gas bubbles in the circulation underlying decompression sickness.

Atmospheric Pressure↗

Bacterium-dependent induction of cytokines in mononuclear cells and their pathologic consequences in vivo.

Viridans streptococci are a heterogeneous group of gram-positive bacteria that are normal inhabitants of the mouth. These organisms are thought to contribute significantly to the etiology of infective endocarditis, although recently they have been implicated in serious infections in other settings. Another group of oral bacteria, gram-negative anaerobes, is associated with chronic dental infections, such as periodontal diseases or endodontic lesion formation. We evaluated the ability of the oral pathogens Streptococcus mutans and Porphyromonas endodontalis to induce a pathogenic response in vivo, with the goal of quantifying the inflammatory response in soft tissue by measuring leukocyte recruitment and hard tissues by measuring osteoclastogenesis. S. mutans induced a strong inflammatory response and was a potent inducer of osteoclast formation, while P. endodontalis was not. To further study the mechanisms by which P. endodontalis and S. mutans elicit significantly different levels of inflammatory responses in vivo, we tested the capacity of each to induce production of cytokines by mononuclear cells in vitro. S. mutans stimulated high levels of interleukin-12 (IL-12), gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha), all of which are associated with inflammation, enhanced monocyte function, and generation of a Th1 response. In contrast, P. endodontalis stimulated production of IL-10 but not of TNF-alpha, IL-12, or IFN-gamma. These results demonstrate that oral pathogens differ dramatically in their abilities to induce inflammatory and immunoregulatory cytokines. Moreover, there is a high degree of correlation between the cytokine profile induced by these bacteria in vitro and their pathogenic capacity in vivo.

Animals↗

DNA microarrays of the complex human cytomegalovirus genome: profiling kinetic class with drug sensitivity of viral gene expression.

We describe, for the first time, the generation of a viral DNA chip for simultaneous expression measurements of nearly all known open reading frames (ORFs) in the largest member of the herpesvirus family, human cytomegalovirus (HCMV). In this study, an HCMV chip was fabricated and used to characterize the temporal class of viral gene expression. The viral chip is composed of microarrays of viral DNA prepared by robotic deposition of oligonucleotides on glass for ORFs in the HCMV genome. Viral gene expression was monitored by hybridization to the oligonucleotide microarrays with fluorescently labelled cDNAs prepared from mock-infected or infected human foreskin fibroblast cells. By using cycloheximide and ganciclovir to block de novo viral protein synthesis and viral DNA replication, respectively, the kinetic classes of array elements were classified. The expression profiles of known ORFs and many previously uncharacterized ORFs provided a temporal map of immediate-early (alpha), early (beta), early-late (gamma1), and late (gamma2) genes in the entire genome of HCMV. Sequence compositional analysis of the 5' noncoding DNA sequences of the temporal classes, performed by using algorithms that automatically search for defined and recurring motifs in unaligned sequences, indicated the presence of potential regulatory motifs for beta, gamma1, and gamma2 genes. In summary, these fabricated microarrays of viral DNA allow rapid and parallel analysis of gene expression at the whole viral genome level. The viral chip approach coupled with global biochemical and genetic strategies should greatly speed the functional analysis of established as well as newly discovered large viral genomes.

Base Sequence↗

Effects of ramp shortening during linear phase of relaxation on [Ca2+]i in intact skeletal muscle fibers.

The effects of shortening distance at Vu, the unloaded shortening speed, and filament overlap on the amount of extra Ca2+ released during relaxation in muscle, as indicated by the bump area, were studied. Single, intact frog skeletal muscle fibers at 3 degreesC were used. The myoplasmic free Ca2+ concentration ([Ca2+]i) was estimated by using fura 2 salt injected into the myoplasm. Ramps were applied, either at full overlap with different sizes or at varying overlaps with a fixed size, in the linear phase of relaxation. At full overlap, a plot of bump area vs. ramp size was fit by using a sigmoidal curve with one-half of the bump area equal to 25.9 nm. With a fixed ramp size of 100 nm/half-sarcomere, the plot of bump area vs. mean sarcomere length (SLm) was fit by a straight line intersecting the SLm axis at approximately 3.5 micrometers, close to just no overlap. The results suggest that the transition in the distribution of attached cross bridges from the isometric case to one appropriate for unloaded shortening at Vu is completed within 50 nm/half-sarcomere and support the view that attached cross bridges in the overlap zone influence the affinity of Ca2+ for troponin C in the thin filament.

Animals↗

Postprandial hypotension is associated with asymptomatic cerebrovascular damage in essential hypertensive patients.

offelucidate the relationship between postprandial hypotension (PPH) and asymptomatic cerebrovascular damage, we evaluated changes in blood pressure after a meal by 24-hour blood pressure monitoring in 70 hospitalized essential hypertensive patients aged >/=50 years. They received a diet containing standard nutritional ingredients with 120 mmol (7 g) NaCl and were free from medication for at least 1 week. PPH was defined as the mean reduction of systolic blood pressure during 2 hours after a meal. Patients were divided into three groups according to mean values of PPH after 3 meals: PPH-1 (n=16, 5 mm Hg</=PPH<10 mm Hg), PPH-2 (n=18, PPH>/=10 mm Hg), and normal (n=36, PPH<5 mm Hg). As asymptomatic cerebrovascular damage, lacunae and leukoaraiosis were evaluated by magnetic resonance imaging. PPH did not correlate with daytime or nighttime blood pressure or the nondipper phenomenon; however, PPH was significantly related to asymptomatic cerebrovascular damage. The prevalence of lacunae in the normal, PPH-1, and PPH-2 groups was 44%, 69%, and 83%, respectively (chi2=8.22, P<0.05). The number of lacunae in the normal, PPH-1, and PPH-2 groups was 1.0+/-1.3, 1.3+/-1.2, and 1. 9+/-1.4, respectively (F[2,67]=3.2, P<0.05). The prevalence of advanced leukoaraiosis in the normal, PPH-1, and PPH-2 groups was 44%, 50%, and 83%, respectively (chi2=7.63, P<0.05). Severity score of leukoaraiosis in the normal, PPH-1, and PPH-2 groups was 1.5+/-0. 7, 1.7+/-0.8, and 2.1+/-0.7, respectively (F[2,67]=4.3, P<0.05). These findings indicate that elderly hypertensive patients with marked PPH should be considered to have advanced cerebrovascular damage even in the absence of abnormal neurological findings.

Aged↗

Low wall shear stress contributes to atherosclerosis of the carotid artery in hypertensive patients.

Numerous in vitro studies have indicated that low shear stress may contribute to intimal thickening and development of atherosclerosis. In the present study, we investigated wall shear stress in hypertensive patients and its relevance to atherosclerosis in the carotid arteries by means of a non-invasive technique. Fifty-five hypertensive patients and 23 normotensive controls were investigated. Intima-media thickness, number of plaques, internal dimension and blood flow velocity of the carotid artery were evaluated. Wall shear stress was calculated using the Poiseuillean parabolic model of velocity distribution as follows: shear stress = 4 X blood viscosity X central line flow velocity/internal dimension. Hypertensive patients showed increased intima-media thickness and dilated common carotid arterial dimension relative to normotensive controls. There was no difference in blood viscosity between the two groups. Both the mean shear stress and systolic peak shear stress were significantly lower in hypertensive patients than normotensive controls. Further, wall shear stress at both mean and peak velocity was significantly and negatively related to intima-media thickness and number of plaques in hypertensive patients, as well as in the total study population. These findings indicate that structural and functional alterations in the common carotid artery of hypertensive patients further precipitates atherosclerosis through low shear stress.

Aged↗

Regulated expression of MCP-1 by osteoblastic cells in vitro and in vivo.

Inflammation is characterized by the recruitment of leukocytes from the vasculature. Recent studies have implicated chemokines as an important class of mediators that function principally to stimulate leukocyte recruitment, and in some cases, leukocyte activity. There are four defined chemokine subfamilies based on their primary structure, CXC, CC, C and CX3C. Members of the CC chemokine subfamily, such as monocyte chemoattractant protein 1 (MCP-1), are chemotactic for monocytes and other leukocyte subsets. The studies described below focus on the expression of MCP-1 in vitro and in vivo in an osseous environment. These studies indicate that MCP-1 is typically not expressed in normal bone or by normal osteoblasts in vitro. Upon stimulation by inflammatory mediators, MCP-1 is up-regulated. This expression is temporally and spatially associated with the recruitment of monocytes in both osseous inflammation and during developmentally regulated bone remodelling. Furthermore, exogenous MCP-1 applied to inflamed bone enhances the recruitment of monocytes. Because monocytes produce factors that influence osseous metabolism, including but not limited to prostglandins, platelet-derived growth factor, interleukin-1 or tumor necrosis factor, chemokines that initiate their recruitment are likely to be highly important.

Animals↗

Periodontal pathogens stimulate CC-chemokine production by mononuclear and bone-derived cells.

BACKGROUND: Chemokines are chemotactic cytokines that stimulate recruitment of leukocytes. Monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha, and RANTES (regulated on activation, normal T cell expressed, and secreted) are 3 well-characterized CC-chemokines that regulate mononuclear cell recruitment. The recruitment of inflammatory cells is of particular importance in the oral cavity because of the likelihood that cells will be challenged with bacteria either during acute infection or following surgical procedures. Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans are putative periodontal pathogens that may be harbored in subgingival and supragingival plaque. The capacity of the host to respond to these bacteria by the elaboration of chemoattractants may represent an important defense mechanism. METHODS: In the present study, we examined CC-chemokine production by human mononuclear cells and bone-derived cells in response to P. gingivalis, A. actinomycetemcomitans and lipopolysaccharides (LPS) stimulation in vitro. The chemokines produced were measured by ELISA. RESULTS: The results demonstrate that P. gingivalis and A. actinomycetemcomitans induce high levels of MIP-1alpha in mononuclear cells. P. gingivalis and A. actinomycetemcomitans stimulated high levels of MCP-1 in bone-derived cells and induced moderate levels of RANTES production in both mononuclear and osteoblastic cells. In mononuclear cells, LPS induced high levels of MIP-1alpha and RANTES and moderate levels of MCP-1; in osteoblasts LPS only induced MCP-1. CONCLUSIONS: The capacity of bacteria to induce a given chemokine depends upon the cell type stimulated. That different cell types would exhibit differences in the CC-chemokines produced under the same stimulus provides a mechanism to explain tissue-specific recruitment of leukocytes.

Adult↗

[Isolating candidate inserted fragment from positive fused phage clones using quantitative PCR].

OBJECTIVE: To isolate quickly and exactly the specific inserted fragment from fused phage clones which were obtained from cDNA library by hybridization. METHODS: According to the amplification principle of quantitative polymerase chain reaction (PCR) and based on the difference of original template quantity,target cDNA fragment was isolated and identified by two PCRs. RESULTS: A positive clone with specific cDNA fragment of HumGT-H1 gene was obtained from a two-phage fused clone by using this method,and the inserted fragment was verified to be the 5' cDNA sequence of HumGT-H1,1.9kb in length. So another hybridization screening is not necessary. CONCLUSION: The method presented is effective and rapid in gene cloning and can greatly save time and materials.

Bacteriophages↗

Evaluation of the components of the chylomicron remnant removal mechanism by use of the isolated perfused mouse liver.

The isolated perfused mouse liver was utilized to evaluate the relative contribution of various molecules believed to participate in the removal of chylomicron remnants by the liver. Sixty percent of asialofetuin was removed from the perfusate per pass; bovine serum albumin was not removed. Normal mouse livers removed chylomicron remnants more efficiently (40-50%/pass) than nascent chylomicrons (10-20%/pass). The fractional removal rate of remnants decreased as their concentration in the perfusate increased demonstrating saturability. Remnant removal by livers of low density lipoprotein receptor-deficient (LDLRD) mice paralleled that of normal mice at low remnant concentrations (0.05, 0.2 microg protein/ml); as concentration increased (4-16 microg protein/ml), removal by LDLRD livers was reduced. About 50% of the capacity to remove remnants was due to the LDL receptor. The role of the LDLR-related protein (LRP) was estimated using the receptor-associated protein (RAP). Four microg/ml of RAP inhibited only LRP; it reduced the removal of remnants by 30-40% in normal livers. When RAP was included in the perfusate of LDLRD livers, remnant removal persisted but was diminished, particularly late in the perfusion; the capacity was approximately 30% of controls. The present study has established that there is more than one mechanism operating for the removal of chylomicron remnants by the liver, provides estimates of the concentration of each to the removal of remnants, and indicates a method for further studies. It is concluded that in normal livers, the LDL receptor has the greatest capacity for removing chylomicron remnants. The LRP contributes to the process as well and a third component, perhaps "sequestration," accounts for up to 30% of the capacity for the initial removal of chylomicron remnants.

Animals↗

Repair of stricture of cervical esophagus with platysma myocutaneous flaps.

OBJECTIVE: To observe the effect of repairing stricture of the cervical esophagus with platysma myocutaneous flaps. METHODS: Fifteen patients with stricture of the cervical esophagus were treated by repair with platysma myocutaneous flaps. The causes of stricture included anastomotic stenosis of the cervical esophagus after colon graft transplantation due to esophageal caustic injury (12 patients), anastomotic stenosis after stomach transposition due to resection of the upper esophageal cancer (2), and stricture caused by limited erosive injury of the cervical esophagus (1). The lengths of stricture were about 3.5-4.5 cm. The stricture was incised longitudinally. The platysma myocutaneous flaps about 4 cm-5 cm x 6 cm-7 cm were resected and were transposed to repair the stricture. RESULTS: All flaps survived and no death or serious complications occurred after operation. All patients gained normal functions in swallowing food. CONCLUSION: Repairing stricture of the cervical esophagus with platysma myocutaneous flaps is simple, safe and effective.

Adolescent↗

[Repairing the defects of volar surface of distal finger with a reverse insular fascial flap of dorsum of juxta positioned digit].

OBJECTIVE: To introduce a method for one-stage repair of skin defects of the volar surface of distal finger or fingers. METHODS: The reverse fascial flap was designed and created on the dorsum of the juxta positioned digit, and it was then rotated 180 degrees to cover the defects of the volar surface of the distal finger. Since May 1992, a total of 20 reverse fascial flaps were used to treat 14 patients. RESULTS: All flaps survived except one with partial necrosis. Follow-up of one half to one year showed satisfactory results functionally and cosmetically. The finger is plump but not swollen. CONCLUSION: The method is easy and effective. The surgical treatment requires short time and causes little pain. The flap has good blood supply, suitable thickness, softness and resistance to wear and tear.

Adolescent↗

[Detection of three common G6PD gene point mutations in Guangdong province by using ARMS].

OBJECTIVE: To detect three common G6PD gene point mutations, G1388A, G1376T and A95G, in Guangdong province and to estimate the approximate frequencies. METHODS: Using the amplification refractory mutation system(ARMS) method to detect G1388A and G1376T and the newly developed ARMS to identify A95G mutation. RESULTS: Ninety cases of G6PD deficient male were examined, and 42 of them were identified to be G1388A(46.7%), 14 G1376T(15.6%), and 12 A95G(13.3%). Totally 68 out of the 90 cases(75.6%) were of the three common mutations. The rest belong to rare or undefined mutations. CONCLUSION: ARMS method can be used in detecting common mutations of G6PD gene with the benefits of simple, fast, economic, and accurate.

Alleles↗

Effects of the configuration of a multi-epitope chimeric malaria DNA vaccine on its antigenicity to mice.

OBJECTIVE: Four B and Th cell epitopes were selected from conservative domain of Plasmodium falciparum antigens to construct two groups of chimeric malaria DNA vaccines with different configurations and their antigenicities were studied. METHODS: The partially synthesized oligonucleotide was annealed, PCR amplified and cloned into a mammalian cell expression vector. By using a pair of isocaudamers on the vector, different single copies of B epitopes were multiplied and were tenderly stringed into two groups of chimeric DNA vaccine with different configurations. BALB/c mice were immunized with these DNA plasmids by either intramuscular or intradermal injections. RESULTS: The antisera from the immunized mice tested by ELISA showed that only the configuration which had a single copy of universal T helper cell epitope, CS. T3, located at the C terminal of the multi-copy B cell epitopes induced a high antibody response. The T helper cell epitope at any other position of the peptide, or the double T helper cell epitopes configured with the B cell epitopes did not enhance antibody response, and some configurations even decreased the humoral response to a B cell epitope. CONCLUSION: This study demonstrated that both combination and configuration of the epitope may affect the antigenicity of a chimeric multiple antigen.

Animals↗

[The effect of EBNA-1 ribozyme on the ability of tumor genesis of lymphoblastoid cell lines in SCID mice].

OBJECTIVE: To explore the effect of EBNA-1 specific ribozyme on the tumor genesis ability of lymphoblastoid cell lines (LCLs) in severe combined immunodeficiency (SCID) mice. METHODS: Using molecular cloning technique, recombinant adenovirus vectors expressing EBNA-1 ribozyme (RZ1) or its inactive mutant (RZ1mut) were constructed as Ad.RZ1 or Ad.RZ1mut. Recombinant adenoviruses were generated by homologous recombination and isolated by plaque formation. LCLs were established and infected with recombinant adenovirus and then injected in SCID mice (1 x 10(7) cells/animal). The SCID mice were sacrificed six weeks after injection, then the tumors were excised from these mice and their size and weight were measured. The expression of EBNA-1 ribozyme and EBNA-1 mRNA in the tumor was analyzed by RT-PCR, and the expression of EBNA-1 protein in the tumor was detected by Western blot. RESULTS: The tumors (0.27 +/- 0.18) g formed from the Ad.RZ1-treated LCLs were much smaller than those of the untreated LCLs (1.04 +/- 0.27) g or LCLs treated with control vector of adenovirus (1.12 +/- 0.32) g (P < 0.01), and also smaller than those of Ad.RZ1mut-treated LCLs (0.76 +/- 0.28) g (P < 0.05). The expression of EBNA-1 mRNA and protein in the tumors of Ad.RZ1-treated LCLs decreased significantly than that of other groups. CONCLUSIONS: Adenovirus delivery of EBNA-1 ribozyme was able to suppress LCL tumors significantly and depress the tumor genesis ability of B lymphocyte induced by EBV.

Adenoviruses, Human↗

[The role of activation of p38 MAPK induced by LPS in TNF-alpha gene expression].

OBJECTIVE: To study the molecular mechanisms of TNF-alpha expression induced by LPS for the exploring of novel methods to prevent and treat clinical patients of endotoxic shock. METHODS: Protein kinase assay was used to detect the kinase activity stimulated by LPS; Confocal laser scan technique was used to show the translocation of p38 on the activation; RT-PCR and reporter gene system were used to study the molecular mechanism of TNF-alpha gene transcription. RESULTS: In RAW cells, p38 was activated on the stimulation of LPS, and activated p38 moved into nucleus from cytosol. TNF-alpha mRNA increased on the stimulation of LPS and the increased promoter transactivity induced by LPS could be inhibited significantly by specific inhibitor for p38. CONCLUSION: p38 MAPK was activated on the stimulation of LPS, which brought about its translocation to the nucleus to act on transcription factors to regulate cellular processes. p38 MAPK is an important regulator of TNF-alpha gene expression induced by LPS.

Cells, Cultured↗

[The inhibiting effect of antisense thrombin receptor gene on the proliferation of pig vascular smooth muscle cell].

OBJECTIVE: To search for an effective approach to prevent the formation of restenosis after angioplasty. METHODS: A recombinant eukaryotic expression plasmid vector containing partial antisense thrombin receptor (ATR) gene named pcDNA3/ATR was constructed using recombinant DNA technique. Mini-pig aorta injury model was established by over-sized balloon catheter combined with high cholesterol diet feeding and its aortic smooth muscle cells(ASMC) were cultured. The effect of ATR gene expression in mini pig ASMC proliferation and growth factor gene expression were studied by 3H-TdR incorporation and Northern blot. RESULTS: The DNA synthesis in pig ASMC could be inhibited by ATR gene expression (The DNA synthesis in normal ASMC was lowered by 41.8%, and that in ASMC from injured artery was lowered by (50.3%). The mRNA and protein synthesis of TR could be down regulated by ATR gene expression. The mRNA expression of PDGF-A chain and bFGF stimulated by fetal calf serum (FCS) with thrombin were both downregulated in pig ASMC with expressed ATR gene. CONCLUSION: ATR gene expression can inhibit the proliferation of pig ASMC, and this is induced by its inhibiting effect on TR and finaly the signal transduction in ASMC.

Animals↗