text:
REGINA -- As the University of Regina deals with the very real possibility of less cash from the government in next month's budget, a U of R vice-president has resigned.
Barb Pollock, VP of external relations, will finish up her 11-year stint with the university at the end of April. When she leaves, her position will not be filled.
University president Vianne Timmons said Pollock's decision to leave was "completely her own" and there is no ill will.
Pollock's departure comes as the U of R faces pressures from students and faculty to redirect funds from administration into academics.
The university is currently going through a full academic program review and, earlier this month, it got rid of nine existing programs while adding four others. All faculties were also asked to develop a budget in the event of no government funding increases (the province currently provides 59 per cent of the university's funding).
"With the budgetary concerns of the university, I want to look at realigning our vice-presidents' roles," Timmons said.
"I need to be able to demonstrate to the campus and the community that I'm looking at every efficiency possible and I'm ... taking this opportunity to do so."
Not filling Pollock's $202,000-per-year position is one of the moves the U of R has made in recent years as it commits to trimming administrative costs.
Timmons said Premier Brad Wall has "made it very clear" next month's provincial budget will be a challenging one for the university, but that's something the institution has been preparing for.
"We've been working very hard to have efficiencies on our campus in preparation of ... what may be a few challenging years ahead," Timmons said.
"I would see this as a positive move by the university administration to say 'We're looking at every position quite seriously' ... and looking at how we can manage going forward with less investment in areas of administration.
"Any funds we have, we want to put into front line teaching, and that's the intent and principle we're designing our budget on."
The Saskatchewan component of the Canadian Federation of Students has applauded the decision to leave Pollock's position vacant for the time being.
"Senior administration salaries have been bloating at the University of Regina for many years, and we are pleased that the university will have one less vice-president to pay," federation spokesman Kent Peterson said in a media release.
As for how the university will deal with the loss of Pollock, Timmons said her departure would be "felt significantly" on campus.
"She's often been the spokesperson (for the university) and we'll have to look at how we manage those roles with external relations and external stakeholders," Timmons said.
"It will be a challenge for us, but it is absolutely a statement by me by not filling that position that I'm looking at administrative costs very carefully across the entire institution."


text: Owls are fascinating creatures. They have a special organ (gizzard) that stores the undigestible parts of their prey, preventing these parts (bones, teeth, fur, feathers) from proceeding through the digestive tract. The gizzard compresses these parts into a pellet which is later regurgitated. This is a pretty simplistic explanation. If you'd like to learn more, … Continue reading »

subset: commoncrawl


text:
National Cancer Institute®
Last Modified: May 1, 2002
AU - Wojnowski L; Hustert E; Klein K; Goldammer M; Haberl M; Kirchheiner J;
Koch I; Klattig J; Zanger U; Brockmoller J
Re: modification of clinical presentation of prostate tumors by a novel
genetic variant in CYP3A4.
SO - J Natl Cancer Inst 2002 Apr 17;94(8):630-1; discussion 631-2
AU - Fluiter K; ten Asbroek AL; van Groenigen M; Nooij M; Aalders MC; Baas F
Tumor genotype-specific growth inhibition in vivo by antisense
oligonucleotides against a polymorphic site of the large subunit of
human RNA polymerase II.
SO - Cancer Res 2002 Apr 1;62(7):2024-8
AD - Neurozintuigen Laboratory, Academical Medical Center, 1105 AZ,Amsterdam,
the Netherlands.
Loss of heterozygosity (LOH) reduces genes to hemizygosity in cancer
cells and presents an absolute difference between normal and cancer
cells. The regions of LOH are usually much larger than the tumor
suppressor gene, which is lost, and are expected to contain genes that
are essential for cell survival. Single nucleotide polymorphisms (SNPs)
are the most common type of genetic variation in man, often giving rise
to two or more allelic forms of most genes. SNPs of essential genes that
are frequently affected by LOH can be used as a target for a novel
therapy against cancer cells with LOH. The SNPs can be targeted by
antisense oligonucleotides (ODNs) that will discriminate between two
alleles. We have designed allele-specific phosphorothioate ODNs against
the gene of the large subunit of RNA polymerase II (POLR2A), a gene
located in close proximity to the tumor suppressor gene p53, which
frequently shows LOH in cancer cells. This report shows that
phosphorothioate antisense ODNs directed against POLR2A can inhibit
tumor growth in vivo as efficiently as a well-described antitumor
antisense ODN directed against Ha-ras. In addition, we show that a
single bp mismatch can be sufficient to obtain allele-specific
inhibition of tumor growth, demonstrating that the effects observed are
true antisense effects.
AU - Vilenchik M; Raffo AJ; Benimetskaya L; Shames D; Stein CA
Antisense RNA down-regulation of bcl-xL Expression in prostate cancer
cells leads to diminished rates of cellular proliferation and resistance
to cytotoxic chemotherapeutic agents.
SO - Cancer Res 2002 Apr 1;62(7):2175-83
AD - Department of Medicine, Columbia University, College of Physicians and
Surgeons, New York, New York 10032, USA.
bcl-xL is a M(r) 26,000 bcl-2 homologue that is highly expressed in
prostate cancer cells. In previous studies, the down-regulation of its
expression by antisense oligonucleotides led to resistance. In this
work, the 445-bp 5' terminus of the bcl-xL cDNA was cloned in the
antisense orientation and stably transfected into DU145 and LNCaP
prostate cancer cells. In the DU145 (and to a lesser extent the LNCaP)
transfectants, phenotypic changes (versus mock-transfected cells)
included an increase in doubling time (from 36 to 175 h) in the clone in
which bcl-xL protein expression was 25% of control. The transfectants
did not demonstrate characteristic apoptotic changes, as demonstrated by
4',6-diamidino-2-phenylindole staining, lack of either DNA laddering,
caspase-3 activation, or poly(ADP)ribose and lamin cleavage, and the
absence of a significant sub-G(0) population. Cell cycle analysis
demonstrated an increase in a tetraploid population (from 28% to 66%),
as well as the appearance of a hypertetraploid population. Levels of
cIAP-1 protein were almost undetectable in the mock cells but increased
at least 25-fold in the DU145 transfectants. The down-regulation of
bcl-xL in both DU145 (and to a much lesser extent in LNCaP) cells led to
their resistance to cytotoxic agents, including docetaxel, mitoxantrone,
etoposide, vinblastine, and carboplatin. Reversion of bcl-xL expression
in stable DU145 transfectants to nearly the levels found in the
mock-transfected cells was accomplished by retroviral infection of the
cells with a bcl-xL sense cDNA under control of a prolific promoter.
This led to a dramatic increase in the growth rate and in BrdUrd
incorporation, as well as a sharp decrease in the expression of cIAP-1
protein. Overall, these findings highlight the adaptability of prostate
cancer cells to loss of bcl-xL and suggest that in addition to its
prosurvival role, bcl-xL protein may also be involved in the regulation
of the rate of cellular proliferation.
AU - Asamoto M; Hokaiwado N; Cho YM; Shirai T
Effects of genetic background on prostate and taste bud carcinogenesis
due to SV40 T antigen expression under probasin gene promoter control.
SO - Carcinogenesis 2002 Mar;23(3):463-7
AD - First Department of Pathology, Nagoya City University Medical School,
Kawasumi 1, Mizuho-cho, Mizuho-ku, Nagoya City 467-8601, Japan.
The incidence of prostate carcinomas in African-American men is greater
than in white men, indicating genetic factors are involved in risk of
this neoplasia. Recently, we have developed a transgenic rat model of
prostate cancer, featuring development of malignancies within 15 weeks
of age at very high incidence. Male transgenic rats with a
Sprague-Dawley genetic background were mated with wild-type females of
F344, Wistar and ACI strains. F1 male transgenic hybrids with female
Wistar and ACI rats had significantly lowered incidences of prostate
carcinomas. However, the serum level of testosterone, and expression of
the transgene, probasin, and the androgen receptor did not correlate
with the strain variation in tumor development. Furthermore,
immunohistochemical analysis of the SV40 Tag and the androgen receptor
also did not reveal any differences between the strains. The transgenic
rats additionally developed taste bud neuroblastomas at 100% incidence
and this was suppressed in F1 male transgenic offspring with the ACI,
but not the other strains. These results clearly show that genetic
background influences prostate carcinogenesis and taste bud
tumorigenesis in rats and that the present transgenic rats could provide
a good model to identify specific factors.
AU - Fu Z; Dozmorov IM; Keller ET
Osteoblasts produce soluble factors that induce a gene expression
pattern in non-metastatic prostate cancer cells, similar to that found
in bone metastatic prostate cancer cells.
SO - Prostate 2002 Apr 1;51(1):10-20
AD - Program in Immunology, School of Medicine, University of Michigan, Ann
Arbor, Michigan 48109, USA.
BACKGROUND: Progressive prostate cancer typically metastasizes to bone
where prostate cancer cells gain an osteoblast-like phenotype and induce
osteoblastic metastases through unknown mechanisms. To investigate the
biology of prostate cancer skeletal metastases, we compared gene
expression between the non-metastatic LNCaP cell line and its derivative
cell line C4-2B that metastasizes to bone. METHODS: Total RNA from LNCaP
and C4-2B cell lines was isolated and used to probe membrane-based gene
arrays (Comparison 1). Additionally, LNCaP cells were incubated in the
absence or presence of conditioned media (CM) from a human
osteoblast-like cell line (HOBIT) and total RNA from these cells was
used to probe gene arrays (Comparison 2). Differential expression of
genes was confirmed by RT-PCR. RESULTS: Of the 1,176 genes screened, 35
were differentially expressed between LNCaP and C4-2B cells (Comparison
1). HOBIT-CM induced differential expression of 30 genes in LNCaP cells
(Comparison 2). Interestingly, 19 genes that were differentially
expressed in C4-2B vs. LNCaP also displayed a similar expression pattern
in LNCaPs grown in HOBIT-CM. These genes are primarily involved in
motility, metabolism, signal transduction, tumorigenesis, and apoptosis.
CONCLUSIONS: These results suggest that osteoblasts produce soluble
factors that contribute to the progression of prostate cancer skeletal
metastases, including their transition to an osteoblast-like phenotype.
Additionally, these data provide targets to explore for further
investigations towards defining the biology of skeletal metastases.
Copyright 2002 Wiley-Liss, Inc.
AU - Wubah JA; Fischer CM; Rolfzen LN; Khalili M; Kang J; Green JE; Bieberich
Ventral prostate predominant l, a novel mouse gene expressed exclusively
in the prostate.
SO - Prostate 2002 Apr 1;51(1):21-9
AD - Department of Biological Sciences, University of Maryland, Baltimore
County, Baltimore, Maryland 21250, USA.
BACKGROUND: Despite the region-specific nature of human prostate
disease, there is a paucity of information regarding the molecular basis
of prostate regionalization and patterning. To elucidate genetic
mechanisms that underlie prostate growth and development, we
investigated differential gene expression in mouse prostate lobes.
METHODS: mRNA differential display analysis was used to identify
differentially expressed genes during development of ventral, anterior,
and dorsolateral prostate lobes. Differential gene expression was
confirmed by Northern blot analysis and RT-PCR. RESULTS: A novel gene,
Ventral prostate predominant1 (Vpp1) was identified. Vpp1 mRNA was
evident in all lobes but accumulated predominantly in the ventral
prostate, and was detected on postnatal day 7 through adulthood
exclusively in the prostate gland. The steady-state level of Vpp1 mRNA
decreased markedly in response to castration, suggesting androgen
regulation of Vpp1 expression. Analysis of TRAMP tumors demonstrated a
dramatic decrease in the level of Vpp1 mRNA. CONCLUSIONS: The spatial
distribution and early postnatal onset of Vpp1 expression is consistent
with a role for this gene in prostate regionalization. The absolute
prostate specificity of Vpp1 expression may allow this gene to serve as
a paradigm to study the molecular basis of gene expression that is
restricted exclusively to the prostate gland. Copyright 2002 Wiley-Liss,
AU - Gsur A; Madersbacher S; Haidinger G; Schatzl G; Marberger M; Vutuc C;
Micksche M
Vitamin D receptor gene polymorphism and prostate cancer risk.
SO - Prostate 2002 Apr 1;51(1):30-4
AD - Division of Applied and Experimental Oncology, Institute of Cancer
Research, University of Vienna, Austria. firstname.lastname@example.com
BACKGROUND: 1,25-dihydroxyvitamin D, the active form of vitamin D,
exerts antiproliferative effect on prostatic cells, mediated through the
vitamin D receptor. In a case-control study, we examined whether the
vitamin D receptor (VDR) gene polymorphism in exon 9 could affect
prostate cancer susceptibility. METHODS: One hundred ninety newly
diagnosed prostate cancer patients and 190 age-matched men with benign
prostatic hyperplasia (BPH), in whom the presence of prostate cancer was
excluded clinically or histologically, were recruited for this study.
The VDR TaqI polymorphism was investigated by polymerase chain reaction
(PCR) following restriction fragment length polymorphism using DNA from
lymphocytes. Depending on the presence or absence of the TaqI
restriction site at the third position of codon 352, patients were
classified as TT, Tt, or tt. RESULTS: The frequency of the tt genotype
was not significantly different between prostate cancer patients (18%)
and controls (12%; P = 0.07). The odds ratio (OR), calculated relative
to individuals with the TT genotype was 1.76 (95% confidence limit (CL)
= 0.90-3.45). After stratification for Gleason score and prostate
specific antigen levels in a case-case comparison (n = 190), no
significant associations with the VDR genotypes were detectable either.
CONCLUSIONS: In this case-control study of Austrian Caucasians, no
statistically significant association of the VDR TaqI polymorphism and
prostate cancer risk was found. Copyright 2002 Wiley-Liss, Inc.
AU - Bharaj BB; Luo LY; Jung K; Stephan C; Diamandis EP
Identification of single nucleotide polymorphisms in the human
kallikrein 10 (KLK10) gene and their association with prostate, breast,
testicular, and ovarian cancers.
SO - Prostate 2002 Apr 1;51(1):35-41
AD - Department of Pathology and Laboratory Medicine, Mount Sinai Hospital,
Toronto, Ontario, Canada.
BACKGROUND: The KLK10 gene (also known as the normal epithelial
cell-specific 1 gene) is a member of the expanded human kallikrein gene
family. Recently, it has been reported that KLK10 is a tumor suppressor
gene and that its expression is downregulated in various forms of cancer
and cancer cell lines. KLK10 is also upregulated in ovarian cancer. We
thus hypothesized that the KLK10 gene may be a target for mutations in
various cancers. METHODS: We sequenced the five coding exons of the
KLK10 gene using genomic DNA from various tumors, normal tissues, and
blood, by PCR amplification and automated sequencing. RESULTS: In none
of the tumor-derived DNAs, we identified somatic mutations that could
inactivate this gene. However, we identified a prevalent germline single
nucleotide variation at codon 50 (exon 3) of this gene [GCC (alanine) to
TCC (serine)]. The GCC genotype was less prevalent in prostatic cancer
patients in comparison to control subjects (P = 0.027) but no
differences were seen with testicular, ovarian, and breast cancer. We
also identified four genetic variations in exon 4, at codons106 [GGC
(glycine) to GGA (glycine)], codon 112 [ACG (threonine) to ACC
(threonine)], codon 141 [CTA (leucine) to CTG (leucine)], and at codon
149 [CCG (proline) to CTG (leucine)]. None of these variations was
significantly different between normal subjects and cancer groups.
CONCLUSIONS: We found no evidence for somatic mutations of the KLK10
gene in cancers of the prostate, breast, ovary, and testis. The single
nucleotide variation at codon 50 appears to be associated with prostate
cancer risk. Copyright 2002 Wiley-Liss, Inc.
AU - Bondar VM; McConkey DJ
Anoikis is regulated by BCL-2-independent pathways in human prostate
carcinoma cells.
SO - Prostate 2002 Apr 1;51(1):42-9
AD - Department of Cancer Biology, University of Texas, M.D. Anderson Cancer
Center, Houston, Texas 77030, USA.
BACKGROUND: Loss of contact with the extracellular matrix (ECM) triggers
a specialized form of apoptosis known as "anoikis" in normal epithelial
cells. Dependence on adhesion to ECM is often lost in transformed cells,
and the degree of anchorage independence may vary in non-metastatic and
metastatic cancer cells. BCL-2 oncoprotein overexpression correlates
with the progression and metastases of prostate cancer. Materials and
Methods We studied anoikis in suspension cultures of PC-3 and LNCaP
prostate carcinoma cells selected for enhanced metastatic potential in
vivo and in PC-3 and LNCaP cells stably transfected with BCL-2.
Apoptosis-associated DNA fragmentation was measured by agarose gel
electrophoresis and propidium iodide staining and flow cytometry.
Expression of BCL-2 family polypeptides was determined by
immunoblotting. RESULTS: Non-metastatic PC-3P cells were significantly
more sensitive to anoikis than the metastatic PC-3 variants (PC-3M,
PC-3M-PRO-4, and PC-3M-LN-4), but anoikis resistance did not correlate
with metastatic potential in LNCaP-derived cell lines. Expression of
BCL-2 was higher in metastatic PC-3 and LNCaP subclones compared to
isogenic non-metastatic cells, but these levels were not affected by
anoikis. Enforced overexpression of BCL-2 did not protect either PC-3P
or LNCaP-PRO-5 cells from anoikis, even though it rendered them
resistant to thapsigargin and inhibited cytochrome c release.
Strikingly, cells that died of anoikis maintained their pretreatment
levels of BCL-2, whereas the cells that survived anoikis expressed much
lower levels of the protein. CONCLUSIONS: Sensitivity to anoikis is
regulated by BCL-2 independent mechanisms in LNCaP and PC-3 prostate
cancer cells. Copyright 2002 Wiley-Liss, Inc.
AU - Shi XB; Nesslinger NJ; Deitch AD; Gumerlock PH; deVere White RW
Complex functions of mutant p53 alleles from human prostate cancer.
SO - Prostate 2002 Apr 1;51(1):59-72
AD - Department of Urology, University of California, Davis, School of
Medicine, Sacramento, California 95817, USA.
BACKGROUND: Few studies have used multiple assays to examine the
functionality of mutant p53 in prostate cancer (CaP). We employed seven
functional assays to study 16 representative mutant p53 alleles, six
from localized and ten from metastatic CaP. METHODS: Yeast assays were
employed to determine loss of function (LOF), partial function (PF), and
dominant-negative status. Assays using p53-null Saos2 cells were used to
determine whether mammalian cells transfected with mutant p53 could
up-regulate the MDR-1 or PCNA promoters, alter IL-6 expression or confer
the ability to grow in soft agar. As a further test of gain of function
(GOF), p53-null PC3 cells stably transfected with these mutant p53
alleles were examined for cell cycle distributions. RESULTS: All 16
mutant p53 alleles demonstrated either total or partial LOF. All but one
allele also had at least one gain of function; however, the pattern of
GOF was different for each mutant allele. Alleles derived from both
localized and metastatic CaP had similar GOF characteristics; however,
only alleles from metastatic disease had significantly increased S-phase
fractions. CONCLUSIONS: Different mutant p53 alleles from CaP had
different, complex functional profiles. The lack of predictable patterns
for these alleles suggest that each mutation may uniquely affect p53
function. Copyright 2002 Wiley-Liss, Inc.
AU - Kay PA; Riehle DL; Cheville JC; Lohse CM; Pankratz VS; Hill EM; Sebo TJ
Comparison of quantitative histomorphometry and DNA ploidy in tissue
sections of prostate carcinoma.
SO - Anal Quant Cytol Histol 2002 Feb;24(1):7-14
AD - Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester,
Minnesota 55905, USA.
OBJECTIVE: To examine the ability of quantitative histomorphometry to
predict DNA ploidy of prostate carcinoma in biopsy tissue sections
assigned after quantitation by nuclear digital image analysis. STUDY
DESIGN: Thirty-five diploid, 35 tetraploid and 35 aneuploid prostatic
carcinomas in biopsies, assessed by the CAS 200 image analyzer (Bacus
Laboratories, Lombard, Illinois, U.S.A.), were reevaluated by the Bacus
Laboratories Incorporated Slide Scanner, a microscope that quantifies
histologic images. Thirty-one histomorphometric features from cancer
cells were captured at 40 x magnification, averaged across tilesfor each
case and incorporated into a multivariate discriminant model to
determine which features predicted ploidy interpretation by nuclear
image analysis using the CAS 200. RESULTS: On average, 60 and 15 minutes
were required to perform nuclear image analysis and histomorphometry,
respectively. The multivariate discriminant model identified
configurable run length, difference variance, contrast, inverse
difference moment, sum entropy and diagonal variance as histomorphometry
features capable of distinguishing diploid from nondiploid tumors (P <
.05). Cross-validation studies showed the model correctly classified
74.3% of the diploid and 57.1% of the nondiploid cases. CONCLUSION:
Quantitative histomorphometry can predict the ploidy of prostate
carcinoma in biopsy tissue sections. Quantitative histomorphometry has
potential as a method of rapidly assessing DNA ploidy otherwise
earmarked for nuclear image analysis, resulting in savings of time and
AU - Tsubaki J; Hwa V; Twigg SM; Rosenfeld RG
Differential activation of the IGF binding protein-3 promoter by
butyrate in prostate cancer cells.
SO - Endocrinology 2002 May;143(5):1778-88
AD - Department of Pediatrics, School of Medicine, Oregon Health Sciences
University, 3181 Southwest Sam Jackson Park Road, Portland, OR
Sodium butyrate (NaB), a dietary micronutrient, is a potent growth
inhibitor that initiates cell differentiation in many cell types,
including prostate cancer cells. The molecular mechanisms by which these
effects occur remain largely unknown. In this study, we investigated the
effects of NaB on the expression of IGF binding protein (IGFBP)-3, a
known growth regulator, in two human prostate cancer cell lines (PC-3
and LNCaP). Treatment with NaB (0-10 mM) caused a dose-dependent
stimulation of IGFBP-3 mRNA expression and parallel increases in protein
levels. A specific histone deacetylase inhibitor, trichostatin A (TSA)
similarly induced IGFBP-3 expression, indicating that histone
hyperacetylation may be critical in the regulation of IGFBP-3
expression. To investigate the molecular mechanism of NaB-regulated
IGFBP-3 expression, 1.87 kb of the human IGFBP-3 gene promoter was
cloned into the pGL2-basic luciferase reporter vector. In both PC-3 and
LNCaP cells, NaB (10 mM) significantly increased luciferase activity 20-
to 30-fold, compared with the untreated control. However, using 5'
sequential deletion constructs of the IGFBP-3 promoter, the NaB response
sequences in the IGFBP-3 promoter were different in PC-3 and LNCaP
cells. Our studies identified a region, -75 to +69 from the start of
transcription (+1), that is fully inducible by NaB treatment in LNCaP
cells, but not in PC-3 cells. Unlike other well characterized
NaB-regulated genes, Sp1 DNA sequences are not involved in NaB
up-regulation of IGFBP-3 gene in LNCaP cells. Further deletion studies
identified two independent regions critical for NaB-induced
transactivation in LNCaP cells. These regions contain consensus binding
sites for p53 and GATA, respectively, but mutational analyses and gel
shift assays suggested that, while the p53 response element is required
for NaB responsiveness, neither p53 nor GATA are involved. In summary,
we have demonstrated that 1) NaB significantly up-regulates IGFBP-3 mRNA
and protein levels in PC-3 and LNCaP prostate cancer cells; and 2) novel
butyrate- responsive elements lacking consensus Sp1 sites are used in
LNCaP cells.
AU - Hsu L; Prentice RL; Stanford JL
Some further results on incorporating risk factor information in
assessing the dependence between paired failure times arising from
case-control family studies: an application to prostate cancer.
SO - Stat Med 2002 Mar 30;21(6):863-76
AD - Public Health Sciences Division, Fred Hutchinson Cancer Research Center,
1100 Fairview Avenue North, MP-665, P.O. Box 19024, Seattle, Washington
98109-1024, U.S.A. email@example.com
In a typical case-control family study, detailed risk factor information
is often collected on cases and controls, but not on their relatives for
reasons of cost and logistical difficulty in locating the relatives. The
impact of missing risk factor information for relatives on estimation of
the strength of dependence between the disease risk of pairs of
relatives is largely unknown. In this paper, we extend our earlier work
on estimating the dependence of ages at onset between paired relatives
from case-control family data to include covariates on cases and
controls, and possibly relatives. Using population-based case-control
families as our basic data structure, we study the effect of missing
covariates for relatives and/or cases and controls on the bias of
certain dependence parameter estimators via a simulation study. Finally
we illustrate various analyses using a case-control family study of
early onset prostate cancer. Copyright 2002 John Wiley & Sons, Ltd.
AU - Arnold JT; Isaacs JJ
Mechanisms involved in the progression of androgen-independent prostate
cancers: it is not only the cancer cell's fault.
SO - Endocr Relat Cancer 2002 Mar;9(1):61-73
AD - National Center for Complementary and Alternative Medicine (NCCAM),
National Institutes of Health, 8 West Drive MSC 2669, Qtrs. 15B1,
Bethesda, MD 20892-2669, USA. email@example.com
The acquisition of an androgen-independent phenotype by prostate cancer
cells is presently a death sentence for patients. In order to have a
realistic chance of changing this outcome, an understanding of what
drives the progression to androgen independence is critical. We review
here a working hypothesis based on the position that the development of
androgen-independent epithelial cells is the result of a series of
cellular and molecular events within the whole tissue that culminates in
the loss of normal tissue-maintained growth control. This tissue
includes the epithelial and stromal cells, the supporting extracellular
matrix and circulating hormones. This review discusses the
characteristics of these malignant cells, the role of stromal cells
involved in growth and the differentiation of epithelial cells, and the
role of the extracellular matrix as a mediator of the phenotypes of
stromal and epithelial cells. In addition, environmental, neuroendocrine
and immune factors that may contribute to disturbance of the fine
balance of the epithelial-stromal-extracellular matrix connection are
considered. While the goal of many therapeutic approaches to prostate
cancer has been androgen ablation or targeting the androgen receptor
(AR) of epithelial cells, these therapies become ineffective as the
cells progress beyond dependence on androgen for growth control. Twenty
years ago Sir David Smithers debated that cancer is the result of loss
of tolerance within tissues and the organizational failure of normal
growth-control mechanisms. This is precipitated by prolonged or abnormal
demands for regeneration or repair, rather than of any inherent disorder
peculiar to each of the individual components involved. He wrote "It is
not the cell itself that is disorderly, but its relationship with the
rest of the tissue". We have gained significantly large amounts of
precise data on the effects of androgenic ablation on cancerous prostate
cells and on the role of the AR in prostate cancer. The need has come to
compile this information towards a perspective of dysregulation of
tissue as a whole, and to develop experimental systems to address this
broader perspective to find and develop therapies for treatment and
AU - Chang BL; Zheng SL; Hawkins GA; Isaacs SD; Wiley KE; Turner A; Carpten
JD; Bleecker ER; Walsh PC; Trent JM; Meyers DA; Isaacs WB; Xu J
Polymorphic GGC repeats in the androgen receptor gene are associated
with hereditary and sporadic prostate cancer risk.
SO - Hum Genet 2002 Feb;110(2):122-9
AD - Center for Human Genomics, Wake Forest University School of Medicine,
Winton-Salem, NC 27157, USA.
Androgen receptor (AR) has long been hypothesized to play an important
role in prostate cancer etiology. Two trinucleotide repeat polymorphisms
(CAG and GGC repeats in exon 1 of the AR gene) have been investigated as
risk factors for prostate cancer in several studies. However, the
results are inconclusive, probably because of the variations of study
designs, characteristics of study samples, and choices of analytical
methods. In this study, we evaluated evidence for linkage and
association between the two AR repeats and prostate cancer by using the
following comprehensive approaches: (1) a combination of linkage and
association studies, (2) a test for linkage by parametric analysis and
the male-limited X-linked transmission/disequilibrium test (XLRC-TDT),
(3) a test for association by using both population-based and
family-based tests, and (4) a study of both hereditary and sporadic
cases. A positive but weak linkage score (HLOD=0.49, P=0.12) was
identified in the AR region by parametric analysis; however, stronger
evidence for linkage in the region, especially at the GGC locus, was
observed in the subset of families whose proband had < or = 16 GGC
repeats (HLOD=0.70, P=0.07) or by using XLRC-TDT ( z'=2.65, P=0.008).
Significantly increased frequencies of the < or = 16 GGC repeat alleles
in 159 independent hereditary cases (71%) and 245 sporadic cases (68%)
cases compared with 211 controls (59%) suggested that GGC repeats were
associated with prostate cancer ( P=0.02). Evidence for the association
between the < or = 16 GGC repeats and prostate cancer risk was stronger
with XLRC-TDT ( z'=2.66, P=0.007). No evidence for association between
the CAG repeats and prostate cancer risk was observed. The consistent
results from both linkage and association studies strongly implicate the
GGC repeats in the AR as a prostate cancer susceptibility gene. Further
studies on this polymorphism in other independent data sets and
functional analysis of the GGC repeat length on AR activity are
AU - Stephan DA; Howell GR; Teslovich TM; Coffey AJ; Smith L; Bailey-Wilson
JE; Malechek L; Gildea D; Smith JR; Gillanders EM; Schleutker J; Hu P;
Steingruber HE; Dhami P; Robbins CM; Makalowska I; Carpten JD; Sood R;
Mumm S; Reinbold R; Bonner TI; Baffoe-Bonnie A; Bubendorf L; Heiskanen
M; Kallioneimi OP; Baxevanis AD; Joseph SS; Zucchi I; Burk RD; Isaacs W;
Ross MT; Trent JM
Physical and transcript map of the hereditary prostate cancer region at
SO - Genomics 2002 Jan;79(1):41-50
AD - Cancer Genetics Branch, National Human Genome Research Institute,
National Institutes of Health, Bethesda, MD 20892, USA.
We have recently mapped a locus for hereditary prostate cancer (termed
HPCX) to the long arm of the X chromosome (Xq25-q27) through a
genome-wide linkage study. Here we report the construction of an
approximately 9-Mb sequence-ready bacterial clone contig map of
Xq26.3-q27.3. The contig was constructed by screening BAC/PAC libraries
with markers spaced at approximately 85-kb intervals. We identified
overlapping clones by end-sequencing framework clones to generate 407
new sequence-tagged sites, followed by PCR verification of overlaps.
Contig assembly was based on clone restriction fingerprinting and the
landmark information. We identified a minimal overlap contig for genomic
sequencing, which has yielded 7.7 Mb of finished sequence and 1.5 Mb of
draft sequence. The transcriptional mapping effort localized 57 known
and predicted genes by database searching, STS content mapping, and
sequencing, followed by sequence annotation. These transcriptional units
represent candidate genes for HPCX and multiple other hereditary
diseases at Xq26.3-q27.3.
AU - Ribeiro ML; Santos A; Carvalho-Salles AB; Hackel C
Allelic frequencies of six polymorphic markers for risk of prostate
SO - Braz J Med Biol Res 2002 Feb;35(2):205-13
AD - Centro de Biologia Molecular e Engenharia Genetica, Universidade
Estadual de Campinas, Campinas, SP, Brasil.
The aim of the present study was to evaluate the distribution of
polymorphisms for the androgen receptor (AR) (CAG, StuI, GGN), SRD5A2
(Ala49Thr, Val89Leu) and CYP17 (MspA1) genes that are considered to be
relevant for risk of prostate cancer. We studied 200 individuals from
two cities in the State of Sao Paulo, by PCR, PCR-RFLP and ASOH
techniques. The allelic frequencies of the autosomal markers and the
StuI polymorphism of the AR gene were very similar to those described in
most North American and European populations. In relation to the CAG and
GGN number of repeats, the study subjects had smaller repeat lengths
(mean of 20.65 and 22.38, respectively) than those described in North
American, European and Chinese populations. In the present study, 30.5%
of the individuals had less than 22 CAG repeats and 45.5% had less than
23 GGN repeats. When both repeat lengths are considered jointly, this
Brazilian population is remarkably different from the others. Further
studies on prostate cancer patients need to be conducted to assess the
significance of these markers in the Brazilian population.
AU - Zhang L; Adams JY; Billick E; Ilagan R; Iyer M; Le K; Smallwood A;
Gambhir SS; Carey M; Wu L
Molecular engineering of a two-step transcription amplification (TSTA)
system for transgene delivery in prostate cancer.
SO - Mol Ther 2002 Mar;5(3):223-32
AD - Department of Biological Chemistry, University of California, Los
Angeles School of Medicine, Los Angeles, California 90095-1737, USA.
Gene therapy is founded on the concept that tissue-specific promoters
can express heterologous genes for molecular imaging or therapeutic
applications. The engineering of cell-specific enhancers to improve
potency and the development of two-step transcriptional activation
(TSTA) approaches have significantly improved the efficacy of transgene
expression. Here we combine these technologies to create a robust,
titratable, androgen-responsive system targeted to prostate cancer
cells. Our "chimeric" TSTA system uses a duplicated variant of the
prostate-specific antigen (PSA) gene enhancer to express GAL4
derivatives fused to one, two, or four VP16 activation domains. We
targeted the resulting activators to cells with reporter templates
bearing one, two, or five GAL4 binding sites upstream of firefly
luciferase. We monitored activity via firefly luciferase assays in
transfected cell extracts and in live nude mice using a cooled
charge-coupled device (CCD) imaging system. In this system, we found
that firefly luciferase expression in prostate cancer cells can be
varied over an 800-fold range. We also found that a single plasmid
bearing the optimized enhancer, GAL4-VP16 derivative, and reporter
expressed firefly luciferase at 20-fold higher levels than the
cytomegalovirus enhancer. We discuss the implications of this strategy
and its application to molecular imaging and therapy.
AU - Rokman A; Ikonen T; Seppala EH; Nupponen N; Autio V; Mononen N;
Bailey-Wilson J; Trent J; Carpten J; Matikainen MP; Koivisto PA; Tammela
TL; Kallioniemi OP; Schleutker J
Germline alterations of the RNASEL gene, a candidate HPC1 gene at 1q25,
in patients and families with prostate cancer.
SO - Am J Hum Genet 2002 May;70(5):1299-304
AD - Laboratory of Cancer Genetics, Institute of Medical Technology, Temepere
University, and Tempere University Hospital, Tempere, Finland.
The RNASEL gene (2',5'-oligoisoadenylate-synthetase dependent) encodes a
ribonuclease that mediates the antiviral and apoptotic activities of
interferons. The RNASEL gene maps to the hereditary-prostate-cancer
(HPC)-predisposition locus at 1q24-q25 (HPC1) and was recently shown to
harbor truncating mutations in two families with linkage to HPC1. Here,
we screened for RNASEL germline mutations in 66 Finnish patients with
HPC, and we determined the frequency of the changes in the index
patients from 116 families with HPC, in 492 patients with unselected
prostate cancer (PRCA), in 223 patients with benign prostatic
hyperplasia (BPH), and in 566 controls. A truncating mutation, E265X,
was found in 5 (4.3%) of the 116 patients from families with HPC. This
was significantly higher (odds ratio [OR] =4.56; P=.04) than the
frequency of E265X in controls (1.8%). The highest mutation frequency
(9.5%) was found in patients from families with four or more affected
members. Possible segregation was detected only in a single family.
However, the median age at disease onset for E265X carriers was 11 years
less than that for noncarriers in the same families. In addition, of the
four missense variants found, R462Q showed an association with HPC
(OR=1.96; P=.07). None of the variants showed any differences between
controls and either patients with BPH or patients with PRCA. We conclude
that, although RNASEL mutations do not explain disease segregation in
Finnish families with HPC, the variants are enriched in families with
HPC that include more than two affected members and may also be
associated with the age at disease onset. This suggests a possible
modifying role in cancer predisposition. The impact that the RNASEL
sequence variants have on PRCA burden at the population level seems
small but deserves further study.
AU - Narayanan BA; Narayanan NK; Stoner GD; Bullock BP
Interactive gene expression pattern in prostate cancer cells exposed to
phenolic antioxidants.
SO - Life Sci 2002 Mar 1;70(15):1821-39
AD - Microarray Systems Laboratory, American Health Foundation, Valhalla, NY
10595, USA. firstname.lastname@example.com
Dietary phenolic compounds are known to elicite vital cellular responses
such as cell cycle arrest, apoptosis and differentiation by activating a
cascade of molecular events. As there is an increasing interest to
improve the efficacy of these compounds for use as potential
chemopreventive agents, we wanted to understand the impact of phenolic
compounds on target genes in prostate cancer. In this study we used
human cDNA microarrays with 2400 clones consisting of 17 prosite motifs
to characterize alterations in gene expression pattern in response to
the phenolic antioxidants ellagic acid (EA) and resveratrol (RE). Over a
48-hr exposure of androgen - sensitive LNCaP cells to EA and RE, a total
of 593 and 555 genes respectively, showed more than a two fold
difference in expression. A distinct set of genes in both EA-and
RE-treated cells may represent the signature profile of phenolic
antioxidant-induced gene expression in LNCaP cells. Although extensive
similarity was found between effects of EA - and RE - responsive genes
in prostate cancer cells, out of 246 genes with overlapping responses,
25 genes showed an opposite effect. Quantitative RT-PCR was used to
verify and validate the differential expression of selected genes
identified from cDNA microarrays. In-depth analysis of the data from
this study provided insight into the alterations in the p53 - responsive
genes, p300, Apaf-1, NF-kBp50 and p65 and PPAR families of genes,
suggesting the activation of multiple signaling pathways that leads to
growth inhibition of LNCaP cells. This is a first study to look for
changes in a large number of human genes in response to dietary
AU - Maruyama R; Toyooka S; Toyooka KO; Virmani AK; Zochbauer-Muller S;
Farinas AJ; Minna JD; McConnell J; Frenkel EP; Gazdar AF
Aberrant promoter methylation profile of prostate cancers and its
relationship to clinicopathological features.
SO - Clin Cancer Res 2002 Feb;8(2):514-9
AD - Hamon Center for Therapeutic Oncology Research, Department of Pathology,
University of Texas Southwestern Medical Center, 6000 Harry Hines
Boulevard, Dallas, TX 75390, USA.
PURPOSE: We investigated the aberrant methylation profile of prostate
cancers and correlated the data with clinical findings. EXPERIMENTAL
DESIGN: Gene promoter methylation was analyzed in 101 prostate cancer
samples. In addition, we analyzed 32 nonmalignant prostate tissue
samples, which included 25 with benign disease, benign prostatic
hypertrophy, or prostatitis, and 7 normal tissues adjacent to cancer.
The methylation status of 10 genes was determined. The methylation index
(MI) was calculated as a reflection of the methylated fraction of the
genes examined. RESULTS: Methylation percentages of the genes tested in
prostate cancers were: RARbeta, 53%; RASSF1A, 53%; GSTP1, 36%; CDH13,
31%; APC, 27%; CDH1, 27%; FHIT, 15%; p16(INK4A), 3%; DAPK, 1%; and MGMT,
0%. Methylation percentages in nonmalignant tissues were much lower. For
clinicopathological correlations, we divided the cancer cases into low
(6 or less) or high (7 or more) Gleason score (GS) groups, and into low
(8 ng/ml or less) or high (greater than 8 ng/ml) preoperative serum
prostate-specific antigen (PSA) groups. Methylation of RASSF1A, GSTP1,
RARbeta, and CDH13 genes was significantly more frequent in the high GS
group than in the low GS group. Methylation of RASSF1A, CDH1, and GSTP1
genes was significantly more frequent in the high PSA group than in the
low PSA group. The median MIs were significantly higher in the high GS
and the high PSA groups. According to the Spearman rank-correlation
test, there was significant correlation between MI and GS (coefficient =
0.43, P < 0.0001) and the preoperative serum PSA (coefficient = 0.37, P
= 0.0003). CONCLUSIONS: Our results indicate that the methylation
profile of prostate cancers correlates with clinicopathological features
of poor prognosis.
AU - Lee YJ; Lee H; Borrelli MJ
Gene transfer into human prostate adenocarcinoma cells with an
adenoviral vector: Hyperthermia enhances a double suicide gene
expression, cytotoxicity and radiotoxicity.
SO - Cancer Gene Ther 2002 Mar;9(3):267-74
AD - Department of Pharmacology and Cancer Institute, University of
Pittsburgh, Pittsburgh, Pennsylvania 15213, USA. email@example.com
We have previously developed a recombinant adenovirus containing a
fusion gene of Escherichia coli cytosine deaminase (CD) and herpes
simplex virus type 1 thymidine kinase (HSV-1 TK) controlled by a
cytomegalovirus (CMV) enhancer-promoter. This replication-incompetent
adenovirus effectively transduced the CD-TK gene into human prostate
adenocarcinoma DU-145 or PC-3 cells. Interestingly, heat shock at 41
degrees C for 4 hours elevated the level of CD-TK by approximately 5- to
20-fold at a multiplicity of infection (MOI) of 1. Heat-enhanced
expression of CD-TK promoted cytotoxicity by 23-, 9-, or 47-fold in the
presence of 50 microg/mL ganciclovir (GCV), 500 microg/mL
5-fluorocytosine (5-FC), or 50 microg/mL GCV+500 microg/mL 5-FC,
respectively, at an MOI of 1. Moreover, there was an increase in
radiosensitivity when adenovirus-infected cells were heated at 41
degrees C for 4 hours followed by irradiation in the presence of the
prodrugs. Virus+heat+1 microg/mL GCV treatment increased
radiosensitivity by a dose-modifying factor (DMF) of 2.2, whereas
virus+heat+10 microg/mL 5-FC exposure resulted in a DMF of 2.3.
Radiosensitization was clearly enhanced as a result of combined prodrug
exposure (DMF=4.4). Our results suggest that the efficiency in
expression of suicide genes from an adenoviral vector used for cytotoxic
anticancer therapy could be improved by combining heat treatment with
radiation therapy.
AU - Chu DC; Chuang CK; Fu JB; Huang HS; Tseng CP; Sun CF
The use of real-time quantitative polymerase chain reaction to detect
hypermethylation of the CpG islands in the promoter region flanking the
GSTP1 gene to diagnose prostate carcinoma.
SO - J Urol 2002 Apr;167(4):1854-8
AD - Department of Clinical Pathology and Division of Urology, Chang Gung
Memorial Hospital and School of Medical Technology, Chang Gung
University, Tao-Yuan, Taiwan, Republic of China.
PURPOSE: We developed a real-time, quantitative, methylation sensitive
polymerase chain reaction (PCR) protocol to analyze hypermethylation of
the CpG islands in the promoter region of the pi class
glutathione-S-transferase gene GSTP1 in prostate cancer tissue.
MATERIALS AND METHODS: A total of 21 prostate cancer and 72 benign
prostate hyperplasia (BPH) tissue samples were analyzed. Genomic DNA was
digested with restriction enzyme, followed by real-time quantitative PCR
amplification. Cycle threshold values were used to determine whether
cancer genome was present in these tissues. A cutoff cycle threshold
value of 35 was arbitrarily assigned. Samples with a cycle threshold of
35 or less were considered positive for prostate cancer. Conventional
nested PCR was also performed for comparison. RESULTS: The mean cycle
threshold values plus or minus standard deviation in prostate cancer and
BPH cases were 30.12 +/- 2.88 and 37.77 +/- 2.72, respectively. All
prostate cancer samples analyzed showed positive results, while 5 of the
72 BPH samples tested positive. Conventional nested PCR data indicated
that 19 of 21 prostate cancer cases were positive for the methylation
change, while 71 of 72 BPH cases tested negative. The test limitations
of real-time PCR and the nested PCR protocols were determined to be
0.048 and 0.64 ng. DNA, respectively. CONCLUSIONS: We established a
novel protocol for detecting the methylation change in the 5' regulatory
sequence flanking the GSTP1 gene. The sensitivity of this protocol was
superior to that of conventional nested PCR. The data also suggest that
this novel protocol may accurately discriminate prostate carcinoma from
AU - Ni Z; Lou W; Lee SO; Dhir R; DeMiguel F; Grandis JR; Gao AC
Selective activation of members of the signal transducers and activators
of transcription family in prostate carcinoma.
SO - J Urol 2002 Apr;167(4):1859-62
AD - Department of Urology, University of Pittsburgh Medical Center,
Pittsburgh, Pennsylvania, USA.
PURPOSE: Cytokines, hormones and growth factors use signal transducers
and activators of transcription (STAT) signaling pathways to control
various biological responses, including development, differentiation,
cell proliferation and survival. Constitutive activation of STATs has
been found in a wide variety of human tumors. In this study we examined
the activity of STATs in primary human prostate tissues. MATERIALS AND
METHODS: STAT activity was determined in 104 human primary prostate
tissues, including 42 tumors, 42 matched normal prostates adjacent to
tumors and 20 normal prostates from donors without cancer by
electromobility shift assay. RESULTS: Significant levels of activated
Stat4 and Stat6 were detected in primary prostate tissues. However,
little or no expression of active Stat1, Stat2 or Stat5 was detected in
primary prostate tissues. Significantly higher levels of constitutive
Stat6 activity were found in prostate carcinomas compared with levels in
normal tissue adjacent to tumors and normal prostates from donors
without prostate cancer. There was no significant difference in Stat6
activity in normal prostate tissues adjacent to tumors and normal
prostates from donors without prostate cancer. The levels of Stat4
activity varied but failed to yield statistically significant
differences among tumors, matched normal prostates adjacent to tumors
and normal prostates from donors without cancer. CONCLUSIONS: We have
previously shown that Stat3 is activated in prostate cancer. The results
of the current study demonstrate that in addition to Stat3, Stat6 is
selectively activated in prostate cancer.
AU - Luo J; Zha S; Gage WR; Dunn TA; Hicks JL; Bennett CJ; Ewing CM; Platz
EA; Ferdinandusse S; Wanders RJ; Trent JM; Isaacs WB; De Marzo AM
Alpha-methylacyl-CoA racemase: a new molecular marker for prostate
SO - Cancer Res 2002 Apr 15;62(8):2220-6
AD - Department of Pathology, Brady Urological Institute, Johns Hopkins
University, School of Medicine, Baltimore, MD 21287, USA.
Identification of genes that are dysregulated in association with
prostate carcinogenesis can provide disease markers and clues relevant
to disease etiology. Of particular interest as candidate markers of
disease are those genes that are frequently overexpressed. In this
study, we describe a gene, alpha-methylacyl-CoA racemase (AMACR), whose
expression is consistently up-regulated in prostate cancer. Analysis of
mRNA levels of AMACR revealed an average up-regulation of approximately
9 fold in clinical prostate cancer specimens compared with normal.
Western blot and immunohistochemical analysis confirms the up-regulation
at the protein level and localizes the enzyme predominantly to the
peroxisomal compartment of prostate cancer cells. A detailed
immunohistochemical analysis of samples from 168 primary prostate cancer
cases using both standard slides and tissue microarrays demonstrates
that both prostate carcinomas and the presumed precursor lesion
(high-grade prostatic intraepithelial neoplasia) consistently scored
significantly higher than matched normal prostate epithelium; 88% of the
carcinomas had a staining score higher than the highest score observed
for any sample of normal prostate epithelium. Both untreated metastas


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WWW.ipetitions.com/petition/Movetheimam Regarding Rap Brown-Imam Jamil El-Amin
Cuba Trip: 804-549-7492 or 202-714-9435-African Awareness Association
Chimernga ! Freedom Nows agenda for this June 16,2012 will commence with the African drum beat Historical calendar . We follow with the raising the political prisoner segment with Kari El Amin the son of Iman El Amin or more popular known as H.Rap Brown. Kari will provide a overview of his fathers contribution to African peoples liberation during the 60ties,70ties and 80ties as well as an update on the Imans strange judicial status within the US prison system. Bro Lee from the African Awareness Association which is the link organization between the African in American movement and the revolutionary government of Cuba will update us on a upcoming campaign to break the US travel boycott of Cuba as well as Cuba's relation to Pan Africanism. Brotha Billion will facilitate the Free your mind your butt will follow ideological weapons giveaway. Our central theme is Syria another Libya?. Once again we find the progressive media, the anti-war movement joining hands with US Imperialism, Zionist Israel, Feudal Saudi Arabia, Qatar's Al Jazerri in the demonization of the government and ruling political party of Syria . This demonization sets in motion US public opinion rallying for US covert and overt regime change. Another war. Whereas the fundamental principle of Self-determination demands that internal contradictions within any nation be resolved through the political process without massive foreign governments arming, financing and conducting covert activates to overthrow one of the most progressive governments in the middle East. Our guest wills Include Dr.Gerald Horne a regular commentator here at FN, Joyce Chediac a middle east journalist and scholar and Jonnie Achi an organizer with the Arab Americans for Syria.
Our music mix will include: Zap Mama, Burning spears, Chilites,Bob Marley,Tauubu and others.So stay tune tell a friend and take note tonight's program can be reheard for the next 60 days at KPFK.org Audio archives freedom Now and as always we stand ready for the revolution.


text:
The Anti-Fitness Gift Guide – 5 Gifts Not Intended for a Fit New Year
By Anthony Heredia | December 6th, 2011 | Category: Fitness Couture, Gift Guides & Gift Suites | No Comments »So maybe you know someone who just can't keep from flaunting his/her perfect body, which takes no effort whatsoever to obtain according to that person. This anti-fitness gift guide is for you yourself to avoid, but you might want to use it to gift a small pebble in the path of that pesky perfect body person you might know. We really shouldn't have even made this gift guide, but what the heck! What's life without a little fun? Avoid these and enjoy the New Year!
The 26-lb Party Gummy Bear – 32,000 Calories!!!
Who really needs this monster of a gummy bear, I mean really! If we catch you eating this alone, you will be chased down. In case you were wondering, 32,000 calories is 10 lbs of fat gain. You have been warned!
Video for you to embed:
Price: $149.99
Buy at: www.vat19.com
Distributor's Description:
Need an epic centerpiece for your next party? Look no further than the Party Gummy Bear. This 26-pound candy beast ensures that your shindigs have no equal. Imagine the shock of your partygoers when they realize that your 32,000-calorie gummy bear also features an integrated one-liter serving bowl! Serve punches, candies, or even more gummy bears from within this seventeen-inch-long confection. The Party Gummy Bear is handmade in the USA, features a 1-year shelf life, and is available in a variety of delicious flavors.
Alcohol in a Book
What better way to hide your spirits than to disguise them in your favorite piece of literature. This gift is just asking to increase the alcoholic based incidences at work and puzzle loved ones at home as to the constant aroma of whisky in a sober household.
Price: $99.95
Buy at: www.benderbound.com
Distributor's Description:
Vintage federal supplement handcrafted to include a hidden 250 ml swing-top glass flask imported from Italy. Behind the flask we've inlaid handmade decorative paper imported from Nepal. Alcohol, Advil, and gavel sold separately. Our handmade book bars will ship in six to eight weeks (sooner if possible).
Gummy Shot Glasses
If copious amounts of alcohol as part of your new year's plans weren't a bad enough idea, why not go for broke by adding edible candy shot glasses!
Price: $14.95 (mix and match six)
Buy at: www.giantgummybears.com
Distributor's Description:
These little edible glasses are each 2.7 ounces of gummy goodness that will add a splash of flavor to your drinks! 6 Glasses per Pack! Pick any flavor combination you want. Great party conversation pieces! Each Gummy Shot Glass is 29 times the nutritional value of the average gummy bear! We handcraft these gummy shot glasses out of the same recipes we use for all our gummy bears so each one is unique. Candy-infused vodka is all the rage on the Internet, but how do you serve it properly? Gummy shot glasses, of course! Jello shots in gummy glasses, the way it was intended. Get your green gummy shot glasses before Saint Patrick's Day. It's a religious thing. Rum and cola without the cola! Just drink your rum and then nibble the glass. It's like Willy Wonka grew up and took his "you can even eat the dishes" to a new level. Next time your trekker friends come over to play Star Trek drinking games, serve them their Romulan Ale shots out of these multi-color gummy shot glasses that look like they came right out of Ten-Forward. How can you drink an appletini and still look like a man? Drink it out of a sour apple shot glass . . . and then after a few drinks, you just pop the "glass" in your mouth and eat it. Let's see your girlfriend do that with her martini glass! It's not just for alcohol anymore! The perfect mini-candy dish holders for your party guests. Was the last shot glass you ate fat-free? These are! Trying to decide between serving drinks and serving snacks? Why not serve your drink in your snack?
Gumball Baseball or Soccer Machine
If you must give candy as a gift, you can at least make the recipients work for their candy. This sure does look like fun, but remember each win is a deposit in time working out, so if you must play, gift your winnings away!
Price: $1,000
Buy at: www.hammacher.com
Distributor's Description:
This is the gumball machine that requires the deft skill of a pinball maven to extract up to three 1″ diameter chewy confections. Available only at Hammacher Schlemmer, it has a baseball-themed playing field that includes four "Win" holes and three "Lose" holes. Relying purely on precise mechanical movement without electricity, a turn of the coin slot crank (no coins required) drops three gumballs into play. A player uses two spring-loaded flippers to knock each gumball into one of the winning holes; gumballs that bypass the flippers are returned to play using the game's plunger. Successful scores deposit winnings via the flip-up candy door while losing gumballs are held in a container for later re-filling of the hopper. This unit comes with 850 1″ multi-colored gumballs (it holds up to 1,700) that are held in its "backglass" as an enticing display to encourage continued play. Made in the U.S. from durable powder-coated steel, tempered safety glass, and Plexiglas. 52″ H x 18″ W x 32″ D. (97 lbs.)
Yes you are reading this correctly. The team over at thinkgeek.com decided that bacon and mayonnaise needed to be married before hitting your palate. At the very least don't spread this on your giant gummy bear or you will be chased down. Be ready for 27 other bacon flavored items once you check their website. Why thinkgeek.com, why?
Price: $5.99
Buy at: www.thinkgeek.com
Distributor's Description:
Throughout history there have been many legendary couplings – peanut butter & chocolate, oatmeal & raisins, Anthony & Cleopatra. Each of these combinations is magnificent in their own right. None of them can stand up to the truly glorious union between bacon and mayonnaise.
Baconnaise, as this manna from the heavens is called, goes well on everything from sandwiches to French fries. Ever been too busy to cook bacon for a BLT? Just take some bread and spread on the Baconnaise (At castle ThinkGeek we typically skip the L and the T). You could even combine it with one of the other legendary pairings! Well, maybe not Tony and Cleo. BUT! Baconnaise mixed with chocolate and peanut butter has to be good! Right? Vegetarian and Kosher friendly.
Canned Unicorn Meat
Wow! If I have to explain why you shouldn't eat a canned unicorn, then we have a larger discussion that we need to have than that of your eating habits. Before you salivate too much at the thought of rare unicorn meat, I should confess this item isn't actually edible, but it was worth rounding out our anti-fitness list. Found inside that can is a poor dismembered, plush unicorn. I hope it goes without saying that you should NOT eat that plush unicorn.
Price: $12.99
Buy at: www.thinkgeek.com
Distributor's Description:
No foolin' – Unicorn meat is real! Excellent source of sparkles!
Unicorns, as we all know, frolic all over the world, pooping rainbows and marshmallows wherever they go. What you don't know is that when unicorns reach the end of their lifespan, they are drawn to County Meath, Ireland. The Sisters at Radiant Farms have dedicated their lives to nursing these elegant creatures through their final days. Taking a cue from the Kobe beef industry, they massage each unicorn's coat with Guinness daily and fatten them on a diet comprised entirely of candy corn. As the unicorn ages, its meat becomes fatty and marbled, and the living bone in the horn loses density in a process much like osteoporosis. The horn's outer layer of keratin begins to develop a flavor very similar to candied almonds. Blending the crushed unicorn horn into the meat adds delightful, crispy flavor notes in each bite. We are confident you will find a world of bewilderment in every mouthful of scrumptious unicorn meat.
Unfortunately, due to restrictions on the importation of mythical processed meatstuff, we are unable to bring you Canned Unicorn Meat in the way the Sisters of Radiant Farms intended. When you open your can, you will find one tiny unicorn which has been appropriately sliced into its main cuts of meat. Simply use your Growth Ray to re-"embiggen" the unicorn before skinning it and processing its flesh. Or if you're lazy, just bring it to your local Mad Scientist-Butcher. He'll know what to do.
Radiant Farms Canned Unicorn Meat Specifications
14 ounces of delicious unicorn meat, canned for your convenience
Imported from a small independent cannery in County Meath, Ireland
Crunchy horn bits in every bite – an excellent source of Calcium
Tastes like rotisserie chicken but with a hint of marshmallow sweetness
Sparkly meat lends the unmistakable air of class and sophistication to your parties
Okay, for real: you can't eat this. It's a dismembered stuffed unicorn in a can.
The bottom of the tin is easily removable to gain access to the mini dead unicorn inside. No can opener needed!


text:
Item #1659855 (OEM Part)
Thread cutting screw used to secure the mandrel/spindle assembly to the deck.
Genuine OEM Part - Manufacturer #173984
Click for shipping speed calculator.
Order now and this item will ship out tomorrow - or it's FREE!
Lubricate this screw prior to installing into a new spindle to make thread cutting easier.


text:
EAST GREENBUSH - Police arrested a town man Wednesday for alleged sexual abuse charges, police said.
Arun Patel, 49, 110 Columbia Turnpike, was charged with third-degree forcible touching and sexual abuse after he allegedly subjected a 21-year-old-woman to sexual contact by forcibly grabbing her breasts without permission.
According to police, the incident occurred on Oct. 2, when the victim was staying at the Econolodge, located at 110 Columbia Turnpike in East Greenbush.
Patel is the owner of the motel and reportedly went to the victim's room to advise her and her friends that they had rented a non-smoking room. It was during this time that Patel, who was described as being loud, threatening and drunk, allegedly committed the acts for which he was charged.
Patel was arraigned and is scheduled to appear in East Greenbush Town Court on Oct. 18 at 5:30 p.m.
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Definition of Scan, radionuclideScan, radionuclide: See: Radionuclide scan. Source: MedTerms™ Medical Dictionaryhttp://www.medterms.com/script/main/art.asp?articlekey=10357 Last Editorial Review: 9/20/2012 Medical Dictionary Definitions A - ZSearch Medical Dictionary
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RCBS 2-Die Set 375 H&H Magnum
Product #: 682696
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RCBS has been making some of the best reloading equipment for over 60 years. Their 2-Die sets are known in many reloading circles for their high-quality. Each 2-Die Set includes a full length sizer die has an expander-decapping unit to remove the spent primer while expanding the case mouth. Vent holes prevent case damage caused by trapped air or excessive lubricant. The seater die includes a bullet seater plug and built-in roll or taper crimp as appropriate for the particular cartridge. Shellholders sold separately.
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Humphries Plans to Submit Official Resignation Soon
First District State Senator-elect Stan Humphries plans to submit his letter of resignation as Trigg County Judge Executive in the coming days. Gov. Steve Beshear will have 30 days to select a replacement for the remaining two years of Humphries' term.
Humphries, a Republican, says it's likely the Democratic Governor will choose someone from his own party. He says Beshear has not yet consulted with him on a successor.
Trigg County Democratic Executive Committee Chairman Thornton Bryan says the group sent three recommendations to the Governor. They are Cadiz police chief Hollis Alexander, Kentucky Transportation Department official Doug Taylor, and Trigg County magistrate Michael Wright. Governor's office spokesperson Ann Gibson says she can't comment on the matter until the resignation is official. Humphries takes the oath of office as a senator on Jan. 8.


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Angels' Night-Music Cultural Exchange
Little Angel Symphony Orchestra is the largest, most complete, world-renowned and abroad of young amateur symphony orchestra in 20 years in China. It was the only Chinese Youth Symphony Orchestra which was invited by the Austrian group to attend the U.S. Winter Olympic Games, International Olympic Arts Festival on February 2, 2002. This year will be the third time visiting the United States for music culture exchange. It is also the first Youth Orchestra invited by the Council of the United States having a special performance in United Nations. The age of the musicians in this performance are aged 8-14, many have access to domestic and international music awards and professional performance certificate. Some musicians from the orchestra group have grown up to become a world renowned professional music performing artists, active in different areas around the world in the music corner. The Little Angle Symphony Orchestra will perform both Chinese and Western music using Chinese and Western instruments. Guangzhou Little Angels Symphony Orchestra is specially invited for this performance by Friends of United Nations.


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- January 14, 2013
- 10:39 a.m.
- Suggest removal
- Reply to this post
rowhoe#214492 writes:
in response to autoguy57#233546:
Remember how Candidate Romney stated Chrysler was going to move Jeep proeduction to China? Then Chrysler, the United Auto WOrkers, and the President of FIAT all denied it? Well read on:
Fiat, Chrysler deal to build Jeeps in China nears:
"Fiat, Chrysler and Guangzhou Automobile Group Co. are getting closer to reaching an agreement to produce Jeeps in China for the Chinese market, an Italian newspaper reported Sunday," (Detroit Free Presee, 2013).I remember Oblaimer laughing about Romney's claim. Now who's laughing Oblaimer? Colin Powell better stick to War Gaming now, and quit backing a President who is a failure. If this President was any other color than what he is, Colin Powell wouldn't even be commenting. Oblaimer and Blowden are ruining this country, and all the Libs and Dumbocrats can see is color.
Mitt made the claim about Jeep as though they were going to shut down the American plant and move the jobs to China. What Chrysler and all others concerned said was that they were not closing the plant in the US.
This is what was said.
"I saw a story today that one of the great manufacturers in this state, Jeep, now owned by the Italians, is thinking of moving all production to China," Romney said during a rally in Defiance, Ohio, before 12,000 cheering supporters, according to several reports. "I will fight for every good job in America, I'm going to fight to make sure trade is fair, and if it's fair, America will win."
Romney apparently was referencing conservative bloggers who misrepresented a Bloomberg story from Monday that discussed Chrysler's decision to consider starting Jeep production in China, the world's largest new-vehicle market.
That story, while accurate, sparked a raft of other stories and blogs that incorrectly concluded that Chrysler might close plants or move Jeep production from the U.S. to China.
Gualberto Ranieri, Chrysler's vice president of communications, criticized those stories Thursday even before Romney made his comments.
"Let's set the record straight: Jeep has no intention of shifting production of its Jeep models out of North America to China," Ranieri said. "It's simply reviewing the opportunities to return Jeep output to China, for the world's largest auto market. U.S. Jeep assembly lines will continue to stay in operation."
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So, I'm looking to change it up from clean to 'perpetual days stubble'... now what? by Aorianin wicked_edge
Scribblenauts Unmasked announced, featuring ever DC Comics hero & villain ever! by tb89in comicbooks
My room mate went to the hospital last week for liver failure. This is what we found in his room while we were cleaning it. by branch455in WTF
they are probably gonna [SPOILER] Gwen Stacy in the next Amazing Spiderman film.... by alsobrantein Spiderman
Sterling Archer, Agent of ISIS in...DANGER ZONE (by Bruce McCorkindale) by DJToastyBunsin comicbooks
I wanted a dark and quite place to sleep, so I moved my bed into my walk in closet. Now I have so much room for activities! by robrs5in pics
I am Rick Remender, writer of Marvel's UNCANNY AVENGERS, CAPTAIN AMERICA, Dark Horse's FEAR AGENT, Image's XXXOMBIES. AMA" by Remenderin comicbooks
Guy says, "I have no cell phone or social media, I need a website. I'm a semi-retired artist, spending the last two years on my dream... a comic series..." by JeremyBDahlin comicbooks
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From 2 April 2013, under changes to the consumer landscape, introduced by Government, the OFT will no longer be responsible for approving consumer facing codes of practice. The Government has invited the Trading Standards Institute (TSI) to operate a successor scheme to CCAS. You can find further details of the TSI scheme here.
In addition to the OFT Approved code, other codes of practice exist. Codes of practice are important because they help to ensure that you, the consumer, get a fair deal from a trustworthy business. Below you will find more information about additional schemes in place throughout the UK.
TrustMark is a scheme supported by the Department for Business, Innovation and Skills, trade bodies, local trading standards and consumer groups to help people find reliable and reputable trades people to carry out repair, maintenance and improvement work inside and outside their homes.
All the Local Authority Assured Trader Scheme Network member schemes have to meet minimum standard. The schemes have the common aims of:
Your local council can tell you if they are a member of this scheme or visit the OFT's page for a list of network members.
Register for email alerts or amend your existing account details here.


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The Greek prime minister, George Papandreou, has called for a referendum on "changes to the political system", including to the country's constitution, as he embarked on a three-day parliamentary marathon that will culminate in a confidence vote in his beleaguered government on Tuesday.
Papandreou blames Greece's bloated state sector for bringing the country to its knees and has vowed to effect deep changes. He said the constitutional revision would make it easier to prosecute delinquent government officials.
Papandreou also made a last-ditch plea to his country to pull together behind his latest package of austerity measures, which he says are essential to save Greece from bankruptcy. He said Greece was negotiating a new international bailout package that was "roughly equal" to last year's €110bn lifeline.
European eurozone ministers are meeting in Luxembourg on Sunday night to thrash out a new deal for Greece that officials hope will spare it from default and buy it breathing space to get its public finances in order. Greece's debt is currently more than €300bn – 150% of its annual economic output.
Papandreou appealed to parliament to approve a new five-year package of tax hikes and spending cuts agreed with international lenders, saying that the alternative was a debt default that would prove catastrophic. Last week, he failed to muster enough support from MPs for the package, and was forced to sack his finance minister and reshuffle his government.
His new finance minister, Evangelos Venizelos, headed to Luxembourg to meet eurozone ministers. But the real opposition to Greece's austerity plans comes from closer to home, where protesters have vowed to step up demonstrations and unions are planning new strikes to pressure MPs into rejecting the budgetary package. Workers at that Greek state utility PPC said they would launch a 48-hour strike at midnight that may result in rolling power outages, to oppose government plans to sell the company.


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It's no secret that Donald Trump tends to get embroiled in drama. Last night on "The Situation Room with Wolf Blitzer," Trump was at it again, sparring with Blitzer over President Obama's Hawaiian birth certificate. This morning, Wolf talks to Ashleigh on "Early Start" about why the Donald cannot let go of the birther movement.
"I've known Donald Trump for a long time and interviewed him on many many occasions," Blitzer says. "He's an intelligent guy, not a stupid guy or anything like that. I assume maybe it's an obvious reason, he believes it."
Last night, Trump called in from Las Vegas where he was holding a fundraiser for the Republican presidential nominee. When Blitzer told him he was being ridiculous for continuing the birther movement after the state of Hawaii affirmed Obama's birth certificate, Trump went on a rant attacking CNN's ratings and the confirmation itself.
"Let me tell you something," Trump starts. "I think you sound ridiculous. And if you would ask me a question and let me answer it, instead of making [...] And many people put those announcements in because they wanted to get the benefit of being so-called born in this country. Many people did it. It was something that was done by many people, even if they weren't born in the country. You know it, and so do I. And so do a lot of your viewers."
Blitzer tried to get an explanation out of Trump as to why he is fighting this fight even though so many other Republicans have dropped the issue. He tells Ashleigh that "Mitt Romney disagrees with him, Newt Gingrich disagrees with him, all the other Republican presidential candidates basically disagree with him. They accept the fact that Barack Obama was born in Hawaii back in 1961. Even Karl Rove, the head of the largest pro-Republican superpac out there disagrees. So, it's not controversial."
Romney's association with and refusal to refute Trump's claims are a legitimate campaign issue. President Obama was criticized (and still is) for his association with Jeremiah Wright who made fiery, controversial statements from the pulpit. While Pres. Obama did not disassociate himself from Pastor Wright, he roundly denounced the pastor's statements publicly. If Romney doesn't beleive what Trump is saying, he will do the same and denounce the comments. Otherwise, to me, he seems of weak character.
Donald Trump must remove a side of his brain that is rotten. Even to suggest that the President of the United States is an illegal immigrant is absurd. Why doesn't he ask Hillary Clinton and/or any high official of the USA government agencies such as the Homeland Security, Immigration Office, the FBI, if they made a "real search" about Obama's birth ceritificate?
Is Trump doubting the efficiency of the US government about something so serious as the possibility of the president being an illegal immigrant? Trump should be arrested for defamatory accusation against the Pre of the USA.
Is the administration of the State of Hawaii ready to sue Trump for slander?
Just to shut up the nut-job Birthers?
I think it's time because by filing this action against Trump (et al)
and Romney the state of Hawaii stands to spend more time and money by
defending other folks born in Hawaii in birth certificate issues in
the future, I guess that's their call.
The state has an obligation to 1) defend it's process from
slander and rumors 2) Only state ( and the NAACP maybe in assist) has
the sole obligation to fortify it's citizens from future slander and
suspicions for such things as job interviews and discrimination
against native Hawaiians.
JJ O' Denver
Blah, blah, blah.
"He's a very charitable guy....he takes care of his own." Does the fact he 'takes care of his own' make him charitable? I'd invite him to open up his tax forms and show us just how charitable he is. But then, isn't that why we always knew he'd never run for President? Because he'd have to show his returns?
Trump is the personification of a world class jerk.
Donald Trump is a loser! He has no evidence of Obama being ET from another planet or being born in Kenya. Get over yourself Drumpy, and get a decent haircut. Meaning get rid of the damn comb over! Do you know how silly you hair looks? What a redneck tool! Go Obama!
Trump is a rich idiot, he says things that are not true and the rest of the rightwing idiots believe what he says. Trump Obama is the president, many milion voters voted for him. As I see it more will vote for him during the next November's election. If you do not like who we the people vote to be our president than you perhaps can move to some other parts of the wold, and please take the ser of the jerks with you.
I'd like to see Mitt prove that he's not the offspring of an illegitimate polygamist marriage!!
Wolf misses the obvious answer. Trump isn't stupid, he's just insane..
Donald trump is that guy that most people have to deal with because of who he is, what he brings to the table, or the power his family has. In Donald's case, it is all 3. Trump is a celebrity, and therefore a percentage of people will always listen. Donald has money, and can use it to influence others. and Donald has a presence in business, which is supposed to make hime crediable.
That is why Mitt won't tell him to go away, that is why no major republican will. Because they need his money, voice, and support. Mitt knows that Donald is not converting anyone on the fence, but he is energizing a part of the far right. Notice I said part of the far right. He's energizing the birthers. me personally I don't care if you are left, right, far left or right, in the middle, up north or sideways, to each ther own. Mitt knows he can't reach out to the birthers with out hurting his chances with independants, so if donald wants to do it for him... Mitt is going to look the other way and let donald talk.
The problem is not Romney, or Obama. ( choose who ever you want). the problem is the media giving Trump airtime.
Trump is rich, and infamous, and NOT an expert on politics. He is not an expert on much of anything. Yes He made billions in real estate, and he has a TV show.... good on him for BOTH. So in the real estate world he is one of the best, however it would be a stretch to call him a good actor. Real estate developers, are 1 part of business, and they interface with dozens of other parts of business.... that does not make one an expert in the other businesses.
Can you imagine if Trump ran a grocery chain, .... mable floors, fountains in the entrance, and $80 dollar packs of gum. How about a Car company, Leather on the ceiling, marble on the dash, and 2 million dollars to lease it for a year.
Now I just gave some harsh critizisms on donald based on his track record and reputation.... however he could do each sucessfully..... On a small scale. If he is making 1500 cars a year like mazerati, or opening a total of 5 grocery store in north America. He could do it cattering to the less than 1% that can afford it.... and that is ok.
The question is how does someone like donald know ANYTHING about what affect someone like me. I'm not pitting the 1% against the 99%. I am saying that SOME of the those in the 1% like donald has no idea what matters to the MARORITY of the population. Certainly some people in the 1% do, some are domecrats, some independants, and some republicans. Some know because they where in the 99% not to long ago, some because even though they have always had money... they were taught to be truely grateful.\
I won't call out any one with money and say you could do this, and you should do that... its your money, not mine, so enjoy. However in a democracy, it is the most votes, the majority vote that wins, not the money. So even though both candidates in virtually ANY election will has far more money and power that I ever will. I will look for the one who has, walked in my shoes. And If neither one has, Who has walked, a similar path, who knows what my shoes look like.
When Romney told college students to go borrow money from good old mom and dad to start a business... I can see the path is different, and the shoes are not recognizable. When you see the look on the face of the graduates he told that to, you know they felt it to.
I don't dislike or hate the 1%, and I am not envious either. I am just going to use my vote on the person who realizes what actually affects my life. I am a father of 3, a homeowner, a vet, a college student, and work full time. I consider my self about middle class.
How does Trump or Romney relate to Me?
ROFLOL....GIVE IT UP for CRISSAKE....
now who would EVER do business with this whacko...I'd try to get as far away from any association to him as possible. He's leprosy to the GOP.....
I wish Wolf Blitzer had done a little more homework and had been able to refute Trump point by point.
The only example quoted in the article is Trump's claim that "many people put those announcements in," and that's simply a lie. As the newspapers have confirmed, their birth announcements came from the Hawaiian Department of Health, not from individuals. I wish Wolf had called him on that.
And on all the other birther lies too. The facts are not hard to find.
Wolf says Donald Trump has to have evidence. Wolf is flat out WRONG!
Da Trump don't need no evidence to rouse the rabble.


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breaking news
PSU Mens' and Womens' Lacrosse Make NCAA Tourney
Monday, May 6, 2013 @ 6:48 PMThe Penn State men's lacrosse team earns the 8 seed and will take on Yale; while the women earn the 7 seed, and will play...
Penn State Adds Another Night Game to Schedule
Monday, May 6, 2013 @ 5:33 PMNittany Lions will host UCF at 6 PM on September 14th.
Both PSU Lax Squads Get NCAA Bids
Sunday, May 5, 2013 @11:50 PMWomen will host Canisius Friday, Men will host Yale Saturday.
NCAA Softball: PSU Altoona Wins 1st Ever AMCC Title
Sunday, May 5, 2013 @ 5:07 PMLady Lions defeat Pitt-Bradford on Sunday, 8-1.
Curve Swept in Erie on Sunday
Sunday, May 5, 2013 @ 5:04 PMLambo hits 5th homer of the year in the loss.
Page 8 of 570
WTAJ Sports covers the Nittany Nation and all Penn State Athletics.
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HighSchool Sports
- Little Lions Prepare for PIAA State Playoffs
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- H.S. Hoops: More District Titles Handed Out
- Lady Tigers Claim District 6 Title
- Championship Match-ups are Decided on High School Hardwood
- Fields get Smaller in District Basketball Tournaments
- Bishop Guilfoyle and Northern Bedford Winners on Playoff Hardwood
- Central Mountain and DuBois Advance
- Bishop Guilfoyle and Southern Fulton Win on the Girls Hardwood
- Bellwood and State College Winners on the Hardwood
Page 11 of 75


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About: 1215 1st Ave, 65th & 66th, New York, NY 10021 212-439-0660
Description: UPPER EAST SIDE. This Irish-style pub tends to get lively at times especially if there is a big boxing match or game on the tube. Indeed, the pub is a safe harbor for sports junkies, who clamor here in the early evening and tend to stay late. Also popular with the neighborhood folk, area business types, and the occasional bartender, O'Flanagan's is the type of place where everybody is welcome and treated the same. TRAIN: 4, 5, 6 to 86th St
Hours:Daily 11am-4pm
Payment Methods:Visa,Master Card,Discover,American Express,Diner's Club
Website:Visit O'Flanagan's Online
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This means that by October 2013, the vast majority of employers will be expected to file pay and tax details for their employees online when wages are paid rather than at the end of the tax year.
Now the Mail on Sunday says that even enterprises with just one or two employees will have to buy expensive software and computer equipment so that they can feed pay details into a vast real time earnings database being assembled by HMRC and should they fail to do so, the Revenue plans to levy escalating fines that could total more than £2,000 a year for the smallest firms, and even more for larger companies.
Phil McCabe, of the Forum of Private Business, said: "Given the Revenues long history of computer problems and website glitches, it beggars belief that businesses could be fined for not complying with the new online-only filing requirements, even if honest mistakes are made, in what can be a frustrating, time-consuming process. Fining firms is a backwards step, particularly at this difficult economic time."
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The phone rang this morning, just as I was walking out the door with the girls. "Hey Bridgett!" was the voice. I didn't recognize him, but once he said, "This is Ian," I felt bad. I hadn't talked to my brother since December--we communicate mostly through gmail chat and forwarded youtube videos (like the lovely Amet).
He had a job for me. Go up to the computer and google this phone number for me, was the request. 770-783-1965. He explained that it Ashley had answered it, on the phone at home, and was totally freaked out. Kind of like a collection agency, but not quite--references to a lawsuit against him in his local municipality, for instance. Even had a court case number. Kinda threatening on the phone. Her name was Lynn Deatrix, she told her, but when Ashley tried to call her back, it was disconnected. Seemed fishy to Ian--he even looked up the area code, which is Fulton County, Georgia. Called their sheriff department, who told Ian that there weren't enough numbers in the court case reference to be one of theirs. But Ian, who is a small business owner with previous horrendous credit (college plus credit cards, you know...) thought he'd better just be sure.
Sure enough, you google the number and it goes to several message boards. Total scam. Trying to play on folks' fears--after the phone calls get more and more threatening, letters get sent demanding money for this court case (or sometimes they take the position of debt collectors). Seems they buy information, because they knew Ian's name and phone number (their land line is listened in Ashley's maiden name), but it's all out of date and just a little off-kilter.
I told Ian to maybe pull his credit reports, forgetting that he's not a car salesman anymore and this is more complicated for a layman. He figured he would, just to be sure. I let him go and quickly took girls to school and went to coffee. When I got home, Ian had left a message: the sheriff's department was apologetic. Please disregard all that nonsense. They get at least 10 calls a day from around the country asking about Ms. Deatrix and her friends.
Ian and I considered the current economy, how people even with good credit can't get loans. He figured times must be tough for identity thieves, too. So, are they switching tactics to "collection agencies"? I just can't quite feel bad.
Wednesday, February 25, 2009
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