Biomedical subjects

Y Fang

Publications and source records attributed to Y Fang.

257 records · Page 15Linked to original sources

PubMed1988

[Cytogenetic studies of lung cancer].

Chromosome analysis was performed on tumor cells from 15 patients with lung cancer. The G-banding techniques were used for analysis of karyotypes. The results showed that numerical and structural abnormalities were found in each case. Chromosomal numbers varied in a range of 36-240. Aneuploids were present in 91.62% of all cells. The most common numerical alterations were subtriploidies and triploidies. Chromosomes 1, 11, 4, 5, and 3 were most frequently involved in 21 marker chromosomes. It was found that marker chromosomes M1, M3, M4 and M5 were related to chromosome 1 with the breakpoints assigned to 1p11, 1q11, 1p35 and an area of centromere. This result may suggest that breakpoint of chromosome 1 be related to the expression of oncogene of the lung cancer.

Adenocarcinoma↗

PubMedDate not supplied

Genetic analysis of wild-type 1 poliovirus isolates in China, 1985-1993.

We examined the genomic variability of 26 wild-type 1 polioviruses isolated from 12 provinces in China from 1985-1993. The poliovirus genome region that encodes the N-terminal portion of the VP1 protein was amplified by the polymerase chain reaction (PCR). The PCR product of each isolate was analysed by restriction fragment length polymorphism (PCR-RFLP) and by direct sequencing. Several groups of viruses with different PCR-RFLP patterns were found to cause outbreaks in China during this period. Viruses with identical PCR-RFLP profiles were dominantly isolated in 11 provinces from 1991 to 1993 and were considered to be the major epidemic strain in China. On the other hand, in the GuangDong province, a different group was responsible for each year's outbreak, while in the XinJiang autonomous prefecture, a single strain was consistently isolated from 1990 to 1993. Understanding of the nationwide distribution of wild poliovirus is very important for interrupting its transmission during the final stage of the eradication program in China.

Base Sequence↗

PubMedDate not supplied

Gelation of xyloglucan by addition of epigallocatechin gallate as studied by rheology and differential scanning calorimetry.

Interaction of tamarind seed xyloglucan (TSX) and epigallocatechin gallate (EGCG) was investigated. TSX alone showed the rheological behaviors of dilute and semidilute solution types in the temperature range from 10 to 50 degrees C and the concentration range from 1 to 10%. Addition of a small amount of EGCG changed the rheological properties of TSX solutions to induce a thermoreversible gelation. The sol-gel transition was detected as a crossover of the storage and loss shear moduli at a certain temperature in thermal scanning rheological measurements and an endo- and exo- thermic peaks in curves obtained by differential scanning calorimetry on heating and cooling. High storage modulus of the gels at all experimental frequencies also indicated the formation of a network structure. Increase in the gel strength and the enthalpy of the transition with increasing EGCG concentration at fixed TSX concentration suggested that EGCG was directly involved in the network formation through association with TSX. The TSX gel was obtained by addition of appropriate amount of EGCG. Addition of an excessive amount of EGCG induced precipitation.

Calorimetry, Differential Scanning↗

PubMedDate not supplied

Na+-Ca2+ exchange and Ca2+ efflux in transfected Chinese hamster ovary cells.

The objective of this study was to assess the contribution of Na+-Ca2+ exchange activity to Ca2+ efflux at various cytosolic Ca2+ concentrations ([Ca2+]i) in transfected Chinese hamster cells expressing the bovine cardiac Na+-Ca2+ exchanger. Ionomycin was added to fura-2 loaded cells and the resulting [Ca2+]i transient was monitored in Ca2+-free media with or without extracellular Na+. The presence of Na+ reduced both the amplitude and duration of the [Ca2+]i transient. Na+ had similar effects when the peak of the [Ca2+]i transient was buffered to 100 nM by cytosolic EGTA, or when Ca2+ was slowly released from internal stores with thapsigargin. Ca2+ efflux following ionomycin addition was directly measured with extracellular fura-2 and followed a biphasic time course (t(1/2) approximately = 10 s and 90s). The proportion of total efflux owing to the rapid phase was increased by Na+ and reduced by EGTA-loading. Na+ accelerated the initial rate of Ca2+ efflux by 65% in unloaded cells but only by 16% in EGTA-loaded cells. In both cases, the stimulation by Na+ was less than expected, given the pronounced effects of Na+ on the [Ca2+]i transient. We conclude that the exchanger contributes importantly to Ca2+ efflux activity at all [Ca2+]i values above 40 nM. We also suggest that Ca2+ efflux pathways may involve non-cytosolic or local routes of Ca2+ traffic.

Animals↗

PubMedDate not supplied

Evidence for the role of cell stiffness in modulation of volume-regulated anion channels.

AIM: To investigate the link between cell stiffness and volume-regulated anion current (VRAC) in aortic endothelium. METHOD: Bovine aortic endothelial cells (BAECs) were exposed to methyl-beta-cyclodextrin (MbetaCD) to deplete cellular cholesterol and the changes in cellular stiffness were measured by micropipette aspiration. VRAC density was measured electrophysiologically in the same cell populations. Furthermore, to probe the effects of cholesterol depletion on the mechanics of 'deep' cytoskeleton, we employ a novel technique to analyse correlated motion of intracellular particles. RESULTS: We show that cholesterol depletion results in cellular stiffening and an upregulation of VRAC density. Replenishing cellular sterol pool with epicholesterol, a chiral analogue of cholesterol, abrogates both of these effects. This indicates that cholesterol sensitivity of both cell mechanics and VRAC are due to changes in the physical properties of the membrane rather than due to specific sterol-protein interactions. We also show that cholesterol depletion increases the stiffness of the 'deep cytoskeleton' and that disruption of actin filaments abolishes both cell stiffening and upregulation of VRAC due to cholesterol depletion. Furthermore, comparing BAECs to human aortic endothelial cells (HAECs), we show that BAECs that are inherently stiffer also develop larger VRACs. CONCLUSIONS: Taken together, our observations suggest an increase in the cytoskeleton stiffness has a facilitatory effect on VRAC development. We suggest that stiffening of the cytoskeleton increases tension in the membrane-cytoskeleton layer and that in turn facilitates VRAC.

Animals↗