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At least 487 records · Page 27Linked to original sources
PubMed2004

Three Arabidopsis MBF1 homologs with distinct expression profiles play roles as transcriptional co-activators.

Multiprotein bridging factor 1 (MBF1) is known to be a transcriptional co-activator that mediates transcriptional activation by bridging between an activator and a TATA-box binding protein (TBP). We demonstrated that expression of every three MBF1 from Arabidopsis partially rescues the yeast mbf1 mutant phenotype, indicating that all of them function as co-activators for GCN4-dependent transcriptional activation. We also report that each of their subtypes shows distinct tissue-specific expression patterns and responses to phytohormones. These observations suggest that even though they share a similar biochemical function, each MBF1 has distinct roles in various tissues and conditions.

Arabidopsis↗
PubMed2005

Risk factors for Helicobacter pylori infection in children: an examination of the role played by intrafamilial bed sharing.

BACKGROUND: The exact mode of transmission of Helicobacter pylori is yet to be established. Close personal contact among family members appears to be a key factor. The aim of this study was to establish whether sharing a bed or bedroom with an infected family member is an important risk factor for primary childhood H. pylori infection. METHODS: Fifty-two families with at least 1 child (the index case) with H. pylori infection were recruited. The resultant study population comprised 126 siblings of the index cases. H. pylori infection was established by culture or by histology and urease testing on antral biopsies in index cases and by C-urea breath testing in family members. Data regarding sleeping arrangements within the family were collected. RESULTS: Sharing a bed or bedroom with an infected sibling at the age of 3 years significantly increased the risk of childhood H. pylori infection [odds ratio, 4.84; 95% confidence intervals, 1.54-15.20; P < 0.01 and 3.68 (1.26-10.75), P = 0.017, respectively]. In addition, a child was at significantly increased risk of being infected if his/her mother or father was H. pylori-positive [odds ratio, 2.52; 95% confidence intervals, 1.03-6.13], P = 0.042 and 2.99 (1.04-8.61), P = 0.042, respectively). CONCLUSIONS: Sharing a bed or bedroom with an infected sibling in early childhood increases significantly the risk of childhood H. pylori infection. This provides evidence to support horizontal transmission of H. pylori among siblings.

Adult↗
PubMed2025

Meiosis-specific genes play roles in ploidy reduction in Cryptococcus neoformans titan cells.

Cryptococcus neoformans is a fungal pathogen of humans that causes life-threatening meningoencephalitis. During infection, enlarged, polyploid titan cells are produced that promote survival, evade immune cells, and generate diverse progeny. These titan cells divide to produce haploid, aneuploid or diploid daughter cells with enhanced stress tolerance; however, how ploidy reduction occurs is poorly understood. Here, we show that titan cells developed from diploid strains predominantly produce diploid daughter cells with haploid daughters observed infrequently. We further demonstrate that meiosis-specific genes, including DMC1 and SPO11, are critical for stable inheritance of a diploid genome in the daughter cells. Specifically, deletion of these genes in a heterozygous diploid background results in: 1) titan cells with a significantly reduced capacity to produce daughter cells; 2) increased phenotypic variation among daughter cells produced by the titan cells, including traits that could be relevant to cell growth and viability; and 3) daughter cells produced by the titan cells exhibiting high levels of loss of heterozygosity (LOH) and aneuploidy, suggested elevated genome instability. Taken together, these findings demonstrate the importance of meiosis-specific genes in the ploidy reduction process of titan cells derived from a heterozygous diploid background in an important human fungal pathogen.

Dmc1↗
PubMed2003

Human cytomegalovirus (HCMV) IE1 plays role in resistance to apoptosis with etoposide in cancer cell line by Cdk2 accumulation.

Human cytomegalovirus (HCMV) has many strategies to survive the attack of the host. HCMV infection of host cells induces cellular activation and disturbance of the cell cycle. It is possible that HCMV modulates the behavior of certain cancer cells that are susceptible to HCMV infection. This study was performed to identify the possible mechanism of resistance to apoptotic stimuli in some cancer cell lines by HCMV infection. HCMV-infected cancer cells showed resistance to apoptosis induced by the topoisomerase II inhibitor etoposide. UMG1-2, which constitutively expresses HCMV immediate-early protein-1 (IE1), had resistance to apoptosis induced by etoposide as compared with the parental cell line U373MG. Measurement of caspases activity with fluorogenic substrates in etoposide-treated U373MG and UMG1-2 cells and the direct activation of caspase-3 with peptides containing arginine-glycine-aspartate in U373MG and UMG1-2 cells revealed that the inhibition level of apoptosis by HCMV IE1 would be upstream of caspase-3 in the caspase cascade pathway. Cellular expression of Cdk2 was increased in UMG1- 2 after etoposide treatment while the expression of E2F-1 in UMG1-2 was decreased as compared with that in U373MG. The Cdk2 inhibitor, roscovitine, decreased the resistance to apoptosis on etoposide-treated UMG1-2. These results suggest that aberrant HCMV infection confers resistance to anticancer drugs on some cancer cells and protects cells from apoptosis, possibly due to the deregulation of cyclin-dependent kinase by HCMV immediate-early protein.

Antineoplastic Agents, Phytogenic↗
PubMed2005

Tobacco abstinence symptom suppression: the role played by the smoking-related stimuli that are delivered by denicotinized cigarettes.

AIMS: Cigarette smoking causes cancer and disease, yet people find quitting difficult due to aversive symptoms that accompany tobacco abstinence. Understanding how to suppress these symptoms is critical in developing effective smoking cessation treatments. Pharmacologically, pure nicotine suppresses tobacco abstinence symptoms partially, and non-nicotine, smoking-related stimuli suppress these abstinence symptoms fully, at least for 24 hours. The current study was designed to clarify the impact of smoking-related stimuli on tobacco withdrawal, and to explore the duration of their ability to suppress withdrawal in smokers. DESIGN: Three double-blind, within-subjects, Latin square-ordered, 5-day conditions in which participants smoked nicotinized, denicotinized or no cigarettes. SETTING: Out-patient laboratory at Virginia Commonwealth University. PARTICIPANTS: Thirteen women and 19 men. MEASUREMENTS: Subjective, physiological and performance measures were collected daily and compliance with study conditions was verified objectively. FINDINGS: Smoking-related stimuli are sufficient for suppressing some symptoms of tobacco abstinence over a 5-day period [i.e. Questionnaire of Smoking Urges (QSU) factor 1, 'Desire for sweets', 'Hunger' and 'Urges to smoke'], while in this study a combination of nicotine and smoking-related stimuli suppressed other symptoms (i.e. 'Difficulty concentrating', 'Increased eating', 'Restlessness' and 'Impatient'). CONCLUSIONS: These results indicate that, while some tobacco abstinence symptoms may be suppressed with nicotine, suppressing others may also require strategies that address the absence of smoking-related stimuli.

Adolescent↗
PubMed1987

Circadian synchronization of hepatocyte proliferation in young rats: the role played by adrenal hormones.

The circadian rhythm of hepatic cell proliferation in rats appears on the 20th day of life, when the hypothalamo-adrenal axis is mature enough for circadian activity to occur. From the 20th day to the 30th day of life, the mitotic rhythm is progressively induced by a reduction in nocturnal values, while diurnal rhythms remain unchanged. Mitotic peaks emerge at 10.00 hours. A labelling index wave occurs 8 hr before the corresponding mitotic wave, with a peak at 02.00 hours and a minimum in the evening, coincidental with the acrophase of plasma corticosterone level (activity phase). Labelled mitoses curves and metaphase accumulation after colchicine injection show that the duration of the S, G2 and M phases remain approximately constant and that the circadian variation is due to a variation in the rate of cells that enter these successive phases. During the synchronization period (from day 20 to 30), the growth fraction decreases progressively. Adrenalectomy at this time is followed by a higher cell proliferation and all rhythms disappear after 2 days. Corticosterone injected before the triggering of the rhythmic activity in 17-day-old rats immediately reduces the labelling index, while the mitotic index is decreased 10 hr later; this delay is equal to the S + G2 duration. The results are discussed. They favour the hypothesis that the circadian variation of corticosterone is responsible for the induction of a circadian variation in developmental cell proliferation by inhibition of the G1-S transition when it is higher in the evening.

Adrenal Glands↗