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Biomedical subjects

Z Jin

Publications and source records attributed to Z Jin.

At least 19 recordsLinked to original sources

Spatial scaling between leaf area index maps of different resolutions.

We developed algorithms for spatial scaling of leaf area index (LAI) using sub-pixel information. The study area is located near Liping County, Guizhou Province, in China. Methods for LAI spatial scaling were investigated on LAI images with 960 m resolution derived in two ways. LAI from distributed calculation (LAID) was derived using Landsat ETM+ data (30 m), and LAI from lumped calculation (LAIL) was obtained from the coarse (960 m) resolution data derived through resampling the ETM+ data. We found that lumped calculations can be considerably biased compared to the distributed (ETM+) case, suggesting that global and regional LAI maps can be biased if surface heterogeneity within the mapping resolution is ignored. Based on these results, we developed algorithms for removing the biases in lumped LAI maps using sub-pixel land cover-type information, and applied these to correct one coarse resolution LAI product which greatly improved its accuracy.

China↗

Cloning of a cDNA encoding the Saussurea medusa chalcone isomerase and its expression in transgenic tobacco.

Chalcone isomerase (CHI; EC 5.5.1.6) is a key enzyme in the flavonoid biosynthesis pathway. We isolated a CHI gene (SmCHI) from a cDNA library derived from Saussurea medusa (Asteraceae) cell cultures. The cDNA and genomic sequences of SmCHI are the same; in other words, this gene is intronless. The coding region of the gene is 699 bp long, and its deduced protein consists of 232 amino acids with a predicted molecular mass of 24 kDa and a pI of 4.7. The deduced amino acid sequence of SmCHI shares 79.3% identity with CHI from Callistephus chinensis, a familial relative to S. medusa; this homology is higher than those with CHI's from any other plant species. A functional bioassay for SmCHI was performed by transforming Nicotiana tabacum plants in the sense or antisense orientation under the regulation of the cauliflower mosaic virus (CaMV) 35S promoter. Transgenic tobacco plants overexpressing sense SmCHI produced up to fivefold total flavonoids over wild-type tobacco plants, mainly due to an enhanced accumulation of rutin. Transgenic tobacco plants with antisense SmCHI accumulated smaller amounts of flavonoids; this is apparently brought about by suppressed expression of the endogenous CHI gene. CHI activities also positively correlated with the amounts of total flavonoids accumulated in the transgenic plants. It is concluded that overexpression of SmCHI can be used as a useful approach to increase flavonoid production in transgenic plants.

Amino Acid Sequence↗

Observation of a fast electron beam emitted along the surface of a target irradiated by intense femtosecond laser pulses.

A novel fast electron beam emitting along the surface of a target irradiated by intense laser pulses is observed. The beam is found to appear only when the plasma density scale length is small. Numerical simulations reveal that the electron beam is formed due to the confinement of the surface quasistatic electromagnetic fields. The results are of interest for potential applications of fast electron beams and deep understanding of the cone-target physics in the fast ignition related experiments.

Journal Article↗

BACH1 is a DNA repair protein supporting BRCA1 damage response.

The link between defects in BRCA1 and breast cancer development may be best understood by deciphering the role of associated proteins. BRCA1 associated C-terminal helicase (BACH1) interacts directly with the BRCA1 C-terminal BRCT repeats, which are important for BRCA1 DNA repair and are mutated in the majority of BRCA1 familial cancers. Thus, BACH1 is a likely candidate for mediating BRCA1 DNA repair and tumor suppression functions. Although previous evidence using overexpression of a dominant negative BACH1 has suggested that BACH1 is involved in BRCA1-DNA repair function, our results using BACH1 deficient cells provide direct evidence for involvement of BACH1 in DNA repair as well as for localizing BRCA1. Following DNA damage BACH1 is modified by phosphorylation, displays a BRCA1-like nuclear foci pattern and colocalizes with gamma-H2AX. Given that the BACH1/BRCA1 complex is unaltered by DNA damage and the intensity of BRCA1 foci is diminished in BACH1 deficient cells, BACH1 may serve to not only facilitate DNA repair, but also maintain BRCA1 in DNA damage foci.

BRCA1 Protein↗

Transcriptional profiling suggests that Barrett's metaplasia is an early intermediate stage in esophageal adenocarcinogenesis.

To investigate the relationship between Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), we determined gene expression profiles of discrete pathological stages of esophageal neoplasia using a sequence-verified human cDNA microarray. Fifty one RNAs, comprising 24 normal esophagi (NE), 18 BEs, and nine EACs were hybridized to cDNA microarrays. Five statistical analyses were used for the data analysis. Genes showing significantly different expression levels among the three sample groups were identified. Genes were grouped into functional categories based on the Gene Ontology Consortium. Surprisingly, the expression pattern of BE was significantly more similar to EAC than to NE, notwithstanding the known histopathologic differences between BE and EAC. The pattern of NE was clearly distinct from that of EAC. Thirty-six genes were the most differentially modulated, according to these microarray data, in BE-associated neoplastic progression. Twelve genes were significantly differentially expressed in cancer-associated BE's plus EAC (as a single combined tissue group) vs noncancer-associated BE's. These genes represent potential biomarkers to diagnose EAC at its early stages. Our results demonstrate that molecular events at the transcriptional level in BE are remarkably similar to BE's-associated adenocarcinoma of the esophagus. This finding alarmingly implies that BE is biologically closer to cancer than to normal esophagus, and that the cancer risk of BE is perhaps higher than we had imagined. These findings suggest that changes modulated at the molecular biologic level supervene earlier than histologic changes, and that BE is an early intermediate stage in the process of EAC.

Adenocarcinoma↗

Hip resurfacing arthroplasty: the evolution of contemporary designs.

Metal-on-metal hip resurfacing is considered by many as the most significant recent development in hip arthroplasty. It preserves proximal femoral bone stock, optimizes stress transfer to the proximal femur, and offers inherent stability and optimal range of movement. The early results of hip resurfacing in the 1970s and 1980s were poor and the procedure was largely abandoned by the mid-1980s. The expectation that these prostheses would be easy to revise was not often fulfilled. The large diameter of the articulation combined with thin polyethylene cups or liners resulted in accelerated wear and the production of large volumes of biologically active particulate debris, leading to bone loss and implant loosening. Failure has been attributed to other factors, mainly avascular necrosis of the femoral head. However, this concern has not been confirmed by retrieval studies. The failure of early hip resurfacings was essentially a consequence of the use of inappropriate materials, poor implant design, inadequate instrumentation, and crude surgical technique. It was not an inherent problem with the procedure itself. The renaissance of metal-on-metal articulations for total hip arthroplasty enabled the introduction of new hip resurfacings and most of the major implant manufacturers have already introduced such systems. Early results are encouraging and complications commonly seen in the 1970s and 1980s, such as early implant loosening and femoral neck fracture, now appear to be rare. Whilst early results should be regarded with caution, modern metal-on-metal hip resurfacing potentially offers the ultimate bone preservation and restoration of function in appropriately selected young patients.

Arthroplasty, Replacement, Hip↗

The role of the surface amorphous layer of articular cartilage in joint lubrication.

Articular cartilage is a complex soft tissue that performs multiple functions in the joint. In particular, the amorphous layer that covers the surface of articular cartilage is thought to play some role in lubrication. This study aimed to characterize the surface amorphous layer (SAL) using a variety of techniques, including environmental scanning electron microscopy, transmission electron microscopy, white light interferometry, and biochemical analysis of its composition. Friction tests were conducted to investigate the role of the SAL in lubrication. A protocol to remove successfully the SAL without damaging the underlying cartilage was developed and the material removed from healthy cartilage was found to contain approximately equal quantities of glycosaminoglycan (GAG), protein, and lipid. Cartilage-on-cartilage friction tests were conducted on fresh, healthy cartilage with and without the SAL, under both dynamic and static operating conditions. Removal of the SAL was not found to change the friction coefficient. However, subsequent staining of specimens indicated that the SAL had replenished during the test following loading. The replenished SAL was characterized and found to contain lipids and sulphated GAGs with undetectable protein. This study revealed experimental evidence of surface layer replenishment in articular cartilage. It was postulated that the surface layer regeneration mechanism was purely mechanical and associated with movement of GAGs and lipids through the cartilage matrix during deformation, since the experimental set-up did not contain any means of biochemical activation.

Animals↗

Demonstration of bulk acceleration of ions in ultraintense laser interactions with low-density foams.

Ion acceleration inside low-density foams irradiated by ultraintense laser pulses has been studied experimentally and theoretically. It is found that the ion generation is closely correlated with the suppressed hot electron transport inside the foams. Particle-in-cell simulations suggest that localized electrostatic fields with multi peaks around the surfaces of lamellar layers inside the foams are induced. These fields inhibit hot electron transport and meanwhile accelerate ions inside the foams, forming a bulk acceleration in contrast to the surface acceleration at the front and rear sides of a thin solid target.

Journal Article↗

Spontaneous lymphocyt ic thyroiditis in interferon regulatory factor-1 deficient non-obese diabetic mice.

Interferon regulatory factor-1 (IRF-1) is a transcription factor involved in interferon-mediated immune reaction, CD8+ T cell differentiation and development of T helper 1 immune reaction. We have recently demonstrated that IRF-1 is pivotal in iodine-induced lymphocytic thyroiditis (LT) in non-obese diabetic (NOD) mice. However, it remains unclear whether the mechanism involved in spontaneous LT is identical with iodine-induced LT in NOD mice. To determine the role of IRF-1 in spontaneous LT, we used IRF-1 deficient NOD mice as well as IRF-1 +/+ and +/- mice which were free from treatments for LT induction, and LT was evaluated at 24 weeks of age. IRF-1 +/+, +/- and -/- mice developed LT spontaneously, and there were no differences among the 3 IRF-1 genotypes in the incidence and severity of LT. Whereas both CD4+ and CD8+ T cells were present in the diseased thyroid of IRF-1 +/+ mice, CD8+ T cells were absent in the thyroid of IRF-1 -/- mice. MHC class II antigen expression was induced in the inflamed thyroid of IRF-1 -/- mice comparable to IRF-1 +/+ mice. There was a selective reduction in the number of CD8+ T cells in the spleen of IRF-1 -/- mice. IFNgamma production, but not IL-10, by concanavalin A-stimulated splenocytes was significantly reduced in IRF-1 deficient mice. These results suggest that IRF-1 plays only a minor role in spontaneous LT in NOD mice and, furthermore, the mechanism involved in spontaneous LT is different from that of iodine-induced LT in NOD mice.

Animals↗

Emission direction of fast electrons in laser-solid interactions at intensities from the nonrelativistic to the relativistic.

The emission direction of outward-ejecting fast electrons generated in laser-solid interactions by 30 fs laser pulses is measured for laser intensities varying from the nonrelativistic to the relativistic. For an s-polarized incident laser beam at nonrelativistic intensities, the ejected electrons are close to the polarization direction of the laser beam. With the increase of the laser intensity, the ejected electrons are still mainly within the polarization plane, but turn away from the laser polarization direction towards the opposite direction of the incident laser beam. At relativistic intensities, electrons eject towards the direction of the reflected laser beam. The increasing ponderomotive force acceleration with the laser intensities might be responsible for the observed changes.

Journal Article↗

Energetic electrons emitted from ethanol droplets irradiated by femtosecond laser pulses.

We investigate the angular distribution and the energy spectrum of hot electrons emitted from ethanol droplets irradiated by linearly polarized 150-fs laser pulses at an intensity of 10(16) W/cm(2). Two hot electron jets symmetrically with respect to the laser propagation direction are observed within the polarization plane. This is due to the spherical geometry of droplets in the intense laser field. The maximum energy of the hot electrons is found to be more than 600 keV. Particle-in-cell simulations suggest that the resonance absorption is the main mechanism for hot electron generation.

Journal Article↗

Blast waves produced by interactions of femtosecond laser pulses with water.

The behaviors of the blast waves produced by femtosecond laser-water interactions, and the blast waves induced by laser self-focusing in air, have been investigated using optical shadowgraphy at a maximum intensity of 1 x 10(16) W/cm(2). The temporal evolution of the blast wave launched by the water plasma can be described by a planar blast wave model including source mass. An aneurismlike structure, due to the quick propagation inside a hollow channel formed by laser self-focusing, is observed. The expansion of the channel in air is found to agree with a cylindrical self-similar blast wave solution.

Journal Article↗

Effect of aggregate size in cell cultures of Saussurea medusa on cell growth and jaceosidin production.

Cell suspension cultures of Saussurea medusa were grown in shake flasks and a 5-l stirred tank bioreactor. Biomass and jaceosidin distribution in cell aggregates of different sizes were investigated during the cultivation period. The results showed that on day 10, jaceosidin accumulation showed an increase with increasing size of the cell aggregate to 4 mm in diameter, with the highest jaceosidin accumulation being 12.2 mg/g. An inverse tendency was observed with cell aggregates larger than 4 mm in diameter, with the lowest accumulation being 3.1 mg/g. However, all of the cell aggregates, despite their size, synthesized almost the same amount of jaceosidin at day 12. Oxygen diffusion limitation and cell-cell contact may explain this behavior. In comparison with cells cultivated in shake flasks, decreased biomass and decreased jaceosidin concentration were observed when the cells were cultivated in a stirred tank bioreactor. The sublytic effects caused by the hydrodynamic stress in combination with insufficient nutrients in the bioreactor may cause cell damage.

Biomass↗

Critical roles of CD30/CD30L interactions in murine autoimmune diabetes.

CD30/CD30L is a member of tumour necrosis factor (TNF) receptor/TNF superfamily and has been implicated in immune-regulation. A genetic study has also suggested a possible implication of CD30 in spontaneous autoimmune diabetes in NOD mice. In this study, we investigated the involvement of CD30/CD30L in the development of diabetes in NOD mice. Flow cytometric analysis showed that CD30 and CD30L were highly expressed on CD4+ or CD8+ T cells in the spleen and pancreatic lymph node of younger NOD mice. In addition, islet-specific CD4+ or CD8+ T cell lines expressed CD30 and CD30L. Administration of a neutralizing anti-CD30L monoclonal antibody (mAb) from 2 to 10 week of age completely suppressed the development of spontaneous diabetes in NOD mice. In addition, the treatment with anti-CD30L mAb also inhibited the development of diabetes induced by adoptive transfer of spleen cells from diabetic NOD mice or islet-specific CD4+ or CD8+ T cell lines into NOD-SCID mice. Furthermore, anti-CD30L mAb inhibited T cell proliferation in response to islet antigens. These results suggested that CD30/CD30L interaction plays important roles in both induction and effector phases of autoimmune diabetes in NOD mice.

Adoptive Transfer↗

Striatal neuronal loss or dysfunction and choline rise in children with attention-deficit hyperactivity disorder: a 1H-magnetic resonance spectroscopy study.

Twelve previously untreated boys suffering from attention-deficit hyperactivity disorder (ADHD) were investigated by using proton magnetic resonance spectroscopy (1H MRS) before and after one dose (10 mg) of methylphenidate. Pre- and post-methylphenidate spectra were acquired bilaterally in the globus pallidus. Peaks of N-acetylaspartate (NAA), choline (Cho), myo-inositol, glutamate and creatine (Cr) were measured and the ratios of the peaks were calculated and compared with data from ten matched controls. In children having ADHD, NAA/Cr ratio decreased significantly in the bilateral striatum while Cho/Cr ratio showed a mild unilateral increase. One oral dose of methylphenidate did not affect the ratios significantly. These findings suggest that the striatum was bilaterally involved in pediatric ADHD patients. Approximately 20-25% of neurons may have died or may be severely dysfunctional. There seems to be a mild hyperactivity of the cholinergic system.

Adolescent↗

[Mannose-binding lectin gene site mutations and the susceptibility of rheumatic heart disease].

OBJECTIVE: To investigate the relationship between mannose-binding lectin (MBL) gene exon 1 site mutations and chronic rheumatic heart disease (CRHD). METHODS: Polymerase chain reaction (PCR) and restrictive fragment length Polymorphism (RFLP) were used to investigate the MBL exon 1 alleles in 36 patients with CRHD and 39 normal people. RESULTS: No C and D alleles of MBL gene were found in both groups. Eleven patients had A/B alleles, 1 patient had B/B alleles, 15 normal people had A/B alleles but none of the 39 normal people had B/B alleles. Statistic analyses showed no significant difference between CRHD group and normal group. But when the age of heart-disease-symptom-onset (HDSO) of the CRHD group were considered, we found that the mean HDSO age of patients with B allele was 30 +/- 14 years and the mean HDSO age of patients with AA homozygous was 37 +/- 11 years. P < 0.05. CONCLUSION: MBL gene mutations may not be a main factor of the pathogenesis of CRHD, but MBL deficiency may facilitate the development of CRHD in younger people and accelerate the progress of CRHD. This is consistent with the phenomenon that the most susceptible people of rheumatic heart disease are teenagers.

Adolescent↗

Adenomatous polyposis coli (APC) gene promoter hypermethylation in primary breast cancers.

Similar to findings in colorectal cancers, it has been suggested that disruption of the adenomatous polyposis coli (APC)/beta-catenin pathway may be involved in breast carcinogenesis. However, somatic mutations of APC and beta- catenin are infrequently reported in breast cancers, in contrast to findings in colorectal cancers. To further explore the role of the APC/beta-catenin pathway in breast carcinogenesis, we investigated the status of APC gene promoter methylation in primary breast cancers and in their non-cancerous breast tissue counterparts, as well as mutations of the APC and beta- catenin genes. Hypermethylation of the APC promoter CpG island was detected in 18 of 50 (36%) primary breast cancers and in none of 21 non-cancerous breast tissue samples, although no mutations of the APC and beta- catenin were found. No significant associations between APC promoter hypermethylation and patient age, lymph node metastasis, oestrogen and progesterone receptor status, size, stage or histological type of tumour were observed. These results indicate that APC promoter CpG island hypermethylation is a cancer-specific change and may be a more common mechanism of inactivation of this tumour suppressor gene in primary breast cancers than previously suspected.

Adult↗