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X F Ma

Publications and source records attributed to X F Ma.

10 recordsLinked to original sources

Physical mapping of restriction fragment length polymorphism (RFLP) markers in homoeologous groups 1 and 3 chromosomes of wheat by in situ hybridization.

Using wheat ditelosomic lines and in situ hybridization of biotin-labelled DNA probes, 18 restriction fragment length polymorphism (RFLP) markers were physically located on homoeologous groups 1 and 3 chromosomes of wheat. Most of the markers hybridized to chromosome arms in a physical order concordant with the genetic maps. A majority of the markers studied were clustered in non-C-banded, distal euchromatic areas, indicating the presence of recombination hot spots and cold spots in those regions. However, on IBS the markers were well dispersed, which could be due to the abundance of heterochromatin throughout the arm. An inversion between Xpsr653 and Xpsr953 was observed on 1AL. One new Xpsr688 locus, approximately 20-26% from the centromere, was found on 1AS and 1BS. The physical location of Xpsr170 on group 3 chromosomes probably represents an alternative to the loci on the genetic map. Finally, Xpsr313 was mapped to two physical loci on IDL. Five markers were located to bins consistent with the deletion-based physical maps.

Chromosomes↗

[Alien chromosomal identification in VE161 wheat].

VE161 wheat which has the function of promotting homoeologous pairing is a male sterile substitution line or a fertile addition line with one pair of alien chromosomes from Agropyron elongatum. The alien chromosome in VE161 wheat was detected by means of techniques of total genomic DNA in situ hybridization, RFLP and double-ditelo chromosomal analysis. The results from in situ hybridization confirmed that the alien chromosome was derived from Agropyron elongatum. The RFLP analysis showed that it belongs to fourth homoeologous group, and the results from double-ditelo chromosomal analysis gave evidence that 4B chromosome was replaced in the substitution line, so it can be concluded that, in VE161 wheat, the alien chromosome would be 4E and the replaced wheat chromosome would be 4B in the substitution line. The reason for the replaced chromosome identified as 7B in a earlier study might be due to the rearrangement occurred in the genome of wheat.

Chromosomes↗

Selective induction of apoptosis of NB4 cells from G2+M phase by sodium arsenite at lower doses.

Apoptosis of NB4 cells induced by sodium arsenite and arsenate was studied using flow cytometry and DNA gel electrophoresis in order to investigate their effects on cell cycle and determine the relationship between apoptosis and cell cycle. In this study, we found that: 1) at low doses, sodium arsenite selectively induced apoptosis of NB4 cells in G2+M phase of cell cycle after its being arrested in G2 phase. With increment of the cells blocked in G2 phase, dUTP-specifically labeling cells in G2+M phase increased without concomitant increment of dUTP-labeling cells in other two phases of cell cycle; 2) at high doses, extensive apoptosis was induced in NB4 cells from all phases of cell cycle without cell cycle preference and cell cycle blockade; 3) sodium arsenite-induced apoptosis of NB4 cells occurred in the presence of bcl-2 expression as the unapoptotic cells; 4) sodium arsenite with As3+ induced apoptosis of NB4 cells more strongly than sodium arsenate with As5+ did although both of them affected NB4 cells in the same pattern. These results not only suggested that both arsenite and arsenate induced apoptosis of NB4 cells through 2 different mechanisms--at low doses, arsenical might directly induce apoptosis through regulation of cell cycle checkpoint, while at high doses they might directly induce it, but also indicated that bcl-2 might not play an important role in arsenite or arsenate-induced apoptosis of NB4 cells, whereas chemical valence of As in a compound might be related to efficiency in arsenical induction of apoptosis.

Apoptosis↗

[The depressor effect of intracerebroventricular injection of BQ123 and endothelin (ET)--antiserum on hypertensive rats produced by aorta stenosis and hypersaline uptake].

An experimental model of hypertensive rat was made by abdominal aorta stenosis and hypersaline uptake. The blood pressure was significantly decreased by intracerebroventricular injection (i.c.v.) of BQ123 a potent antagonist of ET-1 receptor, in a dose-dependent manner. Negative chronotropic effect on the heart was produced by high dose of BQ123, while the depressor effect was produced by i.c.v. ET-antiserum. These results indicate that endothelin in CNS may play an important role in the pathological physiology of hypertension.

Animals↗

[Effects of morphine on muscarinic receptors in limbic system in acute adjuvant-induced arthritic rats].

To induce arthritis, the adjuvant with heat-killed Mycobacterium tuberculosis was injected into the ankle joint in rats. Local redness, swelling, hotness, pain, and motor dysfunction of the inflamed joint (as well as mental dullness) were observed 48 h after inoculation. At this time, the maximal binding capacity (Bmax) of muscarinic receptors in limbic system was increased, while the dissociation constant (Kd) was unchanged. Injection of morphine (5 mg.kg-1) 3 times within 48 h after the inoculation resulted in a decrease of Bmax and an increase of Kd of M-receptors, together with diminution of pain and disappearance of dullness.

Animals↗

Mutagens in urine sampled repetitively from municipal refuse incinerator workers and water treatment workers.

Municipal refuse incinerator workers may be exposed to mutagenic compounds from combustion gases and particulates during plant operation, maintenance, and ash removal procedures. The frequency of mutagens was measured by the Ames assay in 3 urine samples collected from each of 37 workers in 4 refuse incinerators and 35 (control) workers from 8 water treatment plants during June-August 1990. When comparing the first urine samples contributed by workers in each cohort, incinerator workers had a significantly (p < .05) increased risk of both direct-acting mutagens and promutagens (8/37 or 22% for each mutagen type) compared with water treatment workers (2/35 or 6% for each mutagen type). Smoking within 24 h before urine sampling was not a confounder of these results. Interestingly, there was no significant (p > .05) difference for risk of urinary mutagens or promutagens between the two cohorts when comparing, respectively, the second and third urine samples from each cohort. The repeatability of demonstrating urinary mutagens in individual incinerator workers was poor, suggesting that their exposure was highly variable and/or that these workers modified their exposure (e.g., wore masks) as a consequence of being studied. Factors that influence production of mutagenic compounds during refuse incineration and subsequent worker exposure are discussed.

Adult↗

Benzo[e]pyrene pretreatment of immature, female C57BL/6J mice results in increased bioactivation of aflatoxin B1 in vitro.

Hepatic microsomes were prepared from immature C57BL/6J mice 24 h after receiving intraperitoneal injections of either corn oil, benzo[e]pyrene (BeP, 50 mg/kg) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 4 x 10(-3) mg/kg). The capacity of these hepatic microsomes to bioactivate aflatoxin B1 (AFB1), 2-aminoanthracene (AA), benzo[a]pyrene (BaP), 3-methylcholanthrene (MC), 7,12-dimethylbenzanthracene (DMBA), BeP and pyrene (PY) was measured using strain TA100 in the Salmonella typhimurium/microsome reversion assay. BeP pretreatment of mice resulted in a 33% increase in mutagenic potency (MP) of AFB1 over the corn oil controls and a 70% increase in MP relative to TCDD-pretreated microsomes. With AA, BaP and DMBA as promutagens, BeP pretreatment reduced MP an average of 24%, while TCDD pretreatment increased MP of these 3 promutagens 263% compared to controls. Since the general effects of BeP and TCDD on murine hepatic cytochrome P-450 (P450)-mediated activities in this study were discordant, it appears that changes in P450 activity by BeP pretreatment are not mediated through the Ah receptor.

Aflatoxin B1↗