Pathology and laboratory medicine

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Archive for October, 2010

Specimen Collection and Laboratory Diagnosis Presentation Lectures

Clinically Relevant Microbiology Starts at the Source
http://med-videos.blogspot.com/2009/12/clinically-relevant-microbiolo…

Specimen Collection and Laboratory Diagnosis of Lower Respiratory
Infections
http://med-videos.blogspot.com/2009/12/specimen-collection-and-labora…

Obtaining Specimens for Microbiological Evaluation
http://med-videos.blogspot.com/2009/12/obtaining-specimens-for-microb…

Specimen collection Role of the Nurse
http://med-videos.blogspot.com/2009/12/specimen-collection-role-of-nu…

Successful laboratory investigations
http://med-videos.blogspot.com/2009/12/laboratory-specimen-collection…

Pre-analytical Laboratory Errors
http://med-videos.blogspot.com/2009/12/pre-analytical-laboratory-erro…

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MIXET GIVE AWAY HJÄLPINSAMLING

Hjälpinsamling via Internet

Mixet.se® Give Away!  - Katastrof migration / Emerging migration 2010

UNICEF är helt beroende av frivilliga bidrag. Genom att skänka en gåva
hjälper du och ditt företag UNICEF att ge fler barn ett bättre liv.
Vill ni ge en gåva direkt med kreditkort eller via bankkonto gör ni
det här, ge en gåva online. Ni kan också köpa gåvor i vår gåvoshop för
att ge till kunder eller personal.  http://www.unicef.se/stod-oss/gavoshop?fr=mixetgiveaway

Stöd Mixet.se® Give Away! Insamling via Mobil SMS

Ge 50 kr med SMS genom att skicka SMS:  KÄMPA MIXETGIVEAWAY  till 72
900
Ge pengar eller bli Världsförälder direkt på webben. Du kan även
handla i gåvoshopen eller i butiken. Besök insamlingen och kolla hur
det går samt vilka andra som hjälpt till. Pengarna går till UNICEFs
kamp för varenda unge.

Keyword search: Humanitär organisation, Humanitär Fond, Insamling till
Haiti, Insamlingen för Barn i Haiti, UN, FN, UNHCR, Världssamfundet,
Stiftelser, Hjälporganisationer, Hjälporganisation, Katastrofstöd,
Katastrofbidrag, Nödhjälp, Barnfond, Barnfonden, Barnkonventionen, EU,
Europa, Hjälpinsamlingen, Biståndsorgan, Donation, Donationer,
Internationella fonder, Globala fonder, fond för barn, Amnesty,
Sverige, UN Sweden, Mixet insamlingar,

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Molecular Therapy of Breast Cancer: Classicism Meets Modernity (by Marc Lacroix).

Molecular Therapy of Breast Cancer: Classicism Meets Modernity
(A book by Marc Lacroix)

Nova Sciences Publishers, New York, ISBN 978-1-60741-593-0

(hardcover): https://www.novapublishers.com/catalog/product_info.php?products_id=1…
(online book): https://www.novapublishers.com/catalog/product_info.php?products_id=1…

Breast cancer is the most frequently diagnosed type of cancer and a
second leading cause of cancer death in women after lung cancer.
Despite their proven efficacy, classical therapies are, however,
unable to cure metastatic breast cancer and are often associated with
significant toxicity and side-effects, due to a wide spectrum of
action. During the last years, our increasing knowledge of the
molecular pathways underlying cancer development has led to the
introduction of new drugs, of which most are directed towards very
specific targets. Rather than to be used as single agents, these
“modern” compounds could ultimately be combined with “classical”
molecules.

Here are described nearly 150 drugs that are currently (2009) used in
routine therapy or are in clinical trials in breast cancer patients.
From the classical tamoxifen, fluorouracil, cyclophosphamide,
doxorubicin, epirubin, docetaxel, paclitaxel…, to the more recently
introduced ixabepilone, lapatinib, vorinostat, everolimus,
bevacizumab…, they also include capecitabine, gemcitabine,
trastuzumab, fulvestrant, aromatase inhibitors, cancer vaccines,
inhibitors of tumor-induced osteolysis, insulin-like growth factor-I
receptor inhibitors, poly(ADP-ribose) polymerase (PARP)-1 inhibitors,
and many others.

This book offers an insight into current developments of breast cancer
therapy, when classicism meets modernity.

Table of Contents:

Chapter 1. Introduction
Chapter 2. Selective estrogen receptor modulators (SERMs) and down-
regulators (SERDs)
Chapter 3. Aromatase inhibitors
Chapter 4. Agents inducing ovarian suppression
Chapter 5. Antimetabolites
Chapter 6. Alkylating agents
Chapter 7. Anthracyclines
Chapter 8. Microtubule-binding agents
Chapter 9. Topoisomerase inhibitors
Chapter 10. HER family inhibitors
Chapter 11. Angiogenesis inhibitors
Chapter 12. Insulin-like growth factor-I receptor inhibitors
Chapter 13. RAS-RAF-MEK-ERK pathway inhibitors
Chapter 14. Ubiquitin-proteasome system inhibitors
Chapter 15. Histone deacetylases inhibitors
Chapter 16. Mitotic inhibitors
Chapter 17. Inhibitors of heat-shock proteins 90 and 27
Chapter 18. PI3K/AKT/mTOR pathway inhibitors
Chapter 19. Cyclooxygenase-2 inhibitors
Chapter 20. Poly(ADP-ribose) polymerase (PARP)-1 inhibitors
Chapter 21. Tumor-induced osteolysis inhibitors
Chapter 22. Vaccines and immunomodulators
Chapter 23. Varia
Index

List of drugs/compounds discussed in the book:

ABT-888, ABT-869, Ad-sig-hMUC-1/ecdCD40L vaccine, AE37 peptide/GM-CSF
vaccine, Aflibercept, AFP464, AG014699, Alendronate, Aldesleukin,
Allogeneic GM-CSF-secreting breast cancer vaccine, ALT-801, AMG 386,
AMG 479, Anastrozole, Apricoxib, ARRY-334543, AS1402, ATN-224,
Autologous dendritic cell-adenovirus p53 vaccine, AV-951, AVE1642,
AVX701, AZD0530, AZD6244, Bavituximab, Belinostat, Bevacizumab,
BGT226, BIBW 2992, BMS-754807, Bortezomib, Bosutinib, BSI-201,
Busulfan, BZL101, Capecitabine, Carboplatin, CDX-1307, Celecoxib,
Cetuximab, CHP-HER2, CHP-NY-ESO-1, Cisplatin, Cixitumumab, Clodronate,
CNF2024, CR011-vcMMAE, Cyclophosphamide, Dasatinib, Deforolimus,
Denileukin diftitox, Denosumab, Docetaxel, Doxorubicin, Entinostat,
Enzastaurin, Epirubicin, Eribulin , Erlotinib, Ertumaxomab, Etoposide,
Everolimus, Exemestane, Falimarev, Figitumumab, Fluorouracil,
Fulvestrant, Gefitinib, Gemcitabine, Goserelin, GP2 peptide/GM-CSF
vaccine, GRN163L, GSK1059615, HER2/neu (extracellular domain) peptide
vaccine, hTERT/Survivin Multi-Peptide Vaccine, Ibandronate,
Ifosfamide, Imatinib, IMP321, Inalimarev, Interleukin-12, Irinotecan,
Ispinesib, Ixabepilone, Lapatinib, Larotaxel, Letrozole, Leuprolide,
Lonafarnib, Lonaprisan, Mammaglobin-A DNA vaccine, Melphalan,
Methotrexate, MK0646, MK-0752, MLN8237, Modified vaccinia Ankara
(Bavarian Nordic)-HER2 vaccine, Neratinib, NVP-AUY922, NVP-BEZ235,
Odanacatib, OGX-427, Olaparib, OSI-906, Ovarian Cancer Peptide Mix
Immunotherapeutic Vaccine, Oxaliplatin, Paclitaxel, Panobinostat,
Patupilone, Pazopanib, PD-0332991, Pemetrexed, Pertuzumab,Picoplatin,
pNGVL3-hICD vaccine, PTC299, Ramucirumab, Recombinant fowlpox-CEA(6D)/
TRICOM vaccine, Recombinant vaccinia-CEA(6D)-TRICOM vaccine,
Retaspimycin, Rexin-G, Risedronate, Sagopilone, SCH 727965, Sialyl
Lewisª-keyhole limpet hemocyanin (KLH) conjugate vaccine, Sirolimus,
Sorafenib, Sunitinib, Tamoxifen, Telomerase: 540-548 peptide vaccine,
Temozolomide, Temsirolimus, Tesmilifene, Thiotepa, Tipifarnib,
Toremifene, Trabectedin, Trastuzumab, Trastuzumab-MCC-DM1,
Triptorelin, TTK peptide (mixed with adjuvant Montanide ISA-51),
Valproic Acid, Vandetanib, Vinflunine, Vinorelbine, Vorinostat,
WX-671, Zoledronic Acid

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The role of microRNAs in breast cancer

MicroRNAs in Breast Cancer
by Marc Lacroix
InTextoResearch, Baelen, Wallonia, Belgium.
in Breast Cancer: Causes, Diagnosis and Treatment, Nova Sciences
Publishers, ISBN 978-1-60876-463-1 (2010).

https://www.novapublishers.com/catalog/product_info.php?products_id=1…

MicroRNAs (miRNAs) are a recently discovered class of small
regulatory
RNAs that influence the stability and translational efficiency of
target mRNAs. Alterations in miRNA expression are associated with an
increasing number of biological processes, including breast cancer.
Some miRNAs are down-regulated in breast tumors, such as miR-21,
miR-155, miR-373, and miR-520c, and appears as putative tumor
suppressors. Other miRNAs are up-regulated, such as miR-126, and
miR-145, and members of the let-7 family; functional studies support
their oncogenic nature. miRNAs associated with estrogen receptor
expression and function, such as miR-181, miR-206, miR-221 and
miR-222, have also been identified. Of peculiar interest are miRNAs
(miR-200 family members, miR-205) involved in epithelial-mesenchymal
transition (EMT), a process that is likely to play an important role
in cancer cell metastasis. Functional assays and the developpement of
highly sensitive methods to detect miRNAs will undoubtedly lead to
rapid advances in a field that could considerably change our vision
of
breast cancer biology.

MicroRNAs examined:

let-7a, let-7b, let-7c, let-7d, let-7e, let-7g, let-7i, let-7f,
miR-7,
miR-9, miR-10, miR-15  & miR-16, miR-17 and the miR~17~92 cluster,
miR-20, miR-21, miR~23a~27a~24-2 & miR~23b~27b~24-1 clusters, miR-26,
miR-29, miR-30, miR-31, miR-34, mir-98, mir-103, mir-107,
mir~106a~363
& mir~106b~25 clusters, miR-122, mir-124, mir-125, miR-126, mir-127,
miR-128, miR-130, miR-140, miR-141, miR-145, miR-146, miR-148,
miR-152, miR-155, miR-181, mir-196, miR-200 family, miR-205, miR-206,
miR-210, miR-213, miR~222~221 cluster,  miR-224, miR-320, miR-335,
miR-342 , miR-365, miR-373, miR-429, miR-489, miR-497, miR-499,
miR-516, miR-520, miR-663

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(New Book) Molecular Therapy of Breast Cancer: Classicism Meets Modernity

NEW BOOK ! (September 2009)

Molecular Therapy of Breast Cancer: Classicism Meets Modernity
(by Marc Lacroix)

Nova Sciences Publishers, New York, ISBN 978-1-60741-593-0

(hardcover): https://www.novapublishers.com/catalog/product_info.php?products_id=1…
(online book): https://www.novapublishers.com/catalog/product_info.php?products_id=1…

Breast cancer is the most frequently diagnosed type of cancer and a
second leading cause of cancer death in women after lung cancer.
Despite their proven efficacy, classical therapies are, however,
unable to cure metastatic breast cancer and are often associated with
significant toxicity and side-effects, due to a wide spectrum of
action. During the last years, our increasing knowledge of the
molecular pathways underlying cancer development has led to the
introduction of new drugs, of which most are directed towards very
specific targets. Rather than to be used as single agents, these
“modern” compounds could ultimately be combined with “classical”
molecules.

Here are described nearly 150 drugs that are currently (2009) used in
routine therapy or are in clinical trials in breast cancer patients.
From the classical tamoxifen, fluorouracil, cyclophosphamide,
doxorubicin, epirubin, docetaxel, paclitaxel…, to the more recently
introduced ixabepilone, lapatinib, vorinostat, everolimus,
bevacizumab…, they also include capecitabine, gemcitabine,
trastuzumab, fulvestrant, aromatase inhibitors, cancer vaccines,
inhibitors of tumor-induced osteolysis, insulin-like growth factor-I
receptor inhibitors, poly(ADP-ribose) polymerase (PARP)-1 inhibitors,
and many others.

This book offers an insight into current developments of breast cancer
therapy, when classicism meets modernity.

Table of Contents:

Chapter 1. Introduction
Chapter 2. Selective estrogen receptor modulators (SERMs) and down-
regulators (SERDs)
Chapter 3. Aromatase inhibitors
Chapter 4. Agents inducing ovarian suppression
Chapter 5. Antimetabolites
Chapter 6. Alkylating agents
Chapter 7. Anthracyclines
Chapter 8. Microtubule-binding agents
Chapter 9. Topoisomerase inhibitors
Chapter 10. HER family inhibitors
Chapter 11. Angiogenesis inhibitors
Chapter 12. Insulin-like growth factor-I receptor inhibitors
Chapter 13. RAS-RAF-MEK-ERK pathway inhibitors
Chapter 14. Ubiquitin-proteasome system inhibitors
Chapter 15. Histone deacetylases inhibitors
Chapter 16. Mitotic inhibitors
Chapter 17. Inhibitors of heat-shock proteins 90 and 27
Chapter 18. PI3K/AKT/mTOR pathway inhibitors
Chapter 19. Cyclooxygenase-2 inhibitors
Chapter 20. Poly(ADP-ribose) polymerase (PARP)-1 inhibitors
Chapter 21. Tumor-induced osteolysis inhibitors
Chapter 22. Vaccines and immunomodulators
Chapter 23. Varia
Index

List of drugs/compounds discussed in the book:

ABT-888, ABT-869, Ad-sig-hMUC-1/ecdCD40L vaccine, AE37 peptide/GM-CSF
vaccine, Aflibercept, AFP464, AG014699, Alendronate, Aldesleukin,
Allogeneic GM-CSF-secreting breast cancer vaccine, ALT-801, AMG 386,
AMG 479, Anastrozole, Apricoxib, ARRY-334543, AS1402, ATN-224,
Autologous dendritic cell-adenovirus p53 vaccine, AV-951, AVE1642,
AVX701, AZD0530, AZD6244, Bavituximab, Belinostat, Bevacizumab,
BGT226, BIBW 2992, BMS-754807, Bortezomib, Bosutinib, BSI-201,
Busulfan, BZL101, Capecitabine, Carboplatin, CDX-1307, Celecoxib,
Cetuximab, CHP-HER2, CHP-NY-ESO-1, Cisplatin, Cixitumumab, Clodronate,
CNF2024, CR011-vcMMAE, Cyclophosphamide, Dasatinib, Deforolimus,
Denileukin diftitox, Denosumab, Docetaxel, Doxorubicin, Entinostat,
Enzastaurin, Epirubicin, Eribulin , Erlotinib, Ertumaxomab, Etoposide,
Everolimus, Exemestane, Falimarev, Figitumumab, Fluorouracil,
Fulvestrant, Gefitinib, Gemcitabine, Goserelin, GP2 peptide/GM-CSF
vaccine, GRN163L, GSK1059615, HER2/neu (extracellular domain) peptide
vaccine, hTERT/Survivin Multi-Peptide Vaccine, Ibandronate,
Ifosfamide, Imatinib, IMP321, Inalimarev, Interleukin-12, Irinotecan,
Ispinesib, Ixabepilone, Lapatinib, Larotaxel, Letrozole, Leuprolide,
Lonafarnib, Lonaprisan, Mammaglobin-A DNA vaccine, Melphalan,
Methotrexate, MK0646, MK-0752, MLN8237, Modified vaccinia Ankara
(Bavarian Nordic)-HER2 vaccine, Neratinib, NVP-AUY922, NVP-BEZ235,
Odanacatib, OGX-427, Olaparib, OSI-906, Ovarian Cancer Peptide Mix
Immunotherapeutic Vaccine, Oxaliplatin, Paclitaxel, Panobinostat,
Patupilone, Pazopanib, PD-0332991, Pemetrexed, Pertuzumab,Picoplatin,
pNGVL3-hICD vaccine, PTC299, Ramucirumab, Recombinant fowlpox-CEA(6D)/
TRICOM vaccine, Recombinant vaccinia-CEA(6D)-TRICOM vaccine,
Retaspimycin, Rexin-G, Risedronate, Sagopilone, SCH 727965, Sialyl
Lewisª-keyhole limpet hemocyanin (KLH) conjugate vaccine, Sirolimus,
Sorafenib, Sunitinib, Tamoxifen, Telomerase: 540-548 peptide vaccine,
Temozolomide, Temsirolimus, Tesmilifene, Thiotepa, Tipifarnib,
Toremifene, Trabectedin, Trastuzumab, Trastuzumab-MCC-DM1,
Triptorelin, TTK peptide (mixed with adjuvant Montanide ISA-51),
Valproic Acid, Vandetanib, Vinflunine, Vinorelbine, Vorinostat,
WX-671, Zoledronic Acid

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Mutants

It seems these guys find that rust / oxidation to BE .. the BE ALL END
ALL ..

Whoda thunk ..

Study of huge numbers of genetic mutations point to oxidative stress
as underlying cause
Science Centric | 8 September 2009 10:32 GMT

A study that tracked genetic mutations through the human equivalent of
about 5,000 years has demonstrated for the first time that oxidative
DNA damage is a primary cause of the process of mutation – the fuel
for evolution but also a leading cause of ageing, cancer and other
diseases.

The research, just published in Proceedings of the National Academy of
Sciences, also indicated that natural selection is affecting the parts
of the genome that don’t contain genes – supposedly ‘junk’ DNA that
increasingly appears to have important roles in life processes that
are very poorly understood.

The analysis was done by scientists at Oregon State University,
Indiana University, the University of Florida and University of New
Hampshire, in studies supported by the National Institutes of Health.

This research was unusual, scientists say, because the model animal
used for the study, a type of roundworm called C. elegans, was tracked
through 250 generations and in that period of time accumulated 391
genetic mutations through normal life processes. That’s more than 10
times as many mutations as have ever before been tracked in a study
such as this.

Several Nobel Prizes have been awarded based on studies done with this
roundworm, which was the first animal to have its entire genome
sequenced. And despite their vast evolutionary separation as life
forms, this tiny roundworm and humans still share comparable forms of
DNA maintenance.

‘Genetic mutations in animals are actually pretty rare, they don’t
happen very often unless they are induced by something,’ said Dee
Denver, an assistant professor of zoology at OSU and principal
investigator on the study. ‘The value of using this roundworm is that
it reaches reproductive age in about four days, so we can study
changes that happen through hundreds of generations, using advanced
genome sequencing technology.’

Genetic mutations can take various forms, such as a disruption in the
sequence of DNA bases, larger deletions of whole sections of DNA, or
other events. They are a fundamental part of the biological process of
life and the basis of evolution, allowing organisms to change –
sometimes in ways that are good and lead to greater survival value,
sometimes bad and leading to decline or death. But the process is
difficult to study and a real understanding of the driving forces
behind mutation, its frequency, and the types of mutation that happen
most often has been elusive, researchers say.

A primary finding of the new study is that a predominant number of
genetic mutations – most, but not all of them – are linked to guanine,
one of the four basic nucleotides that make up DNA and form the
genetic code of life. Guanine is known to be particularly sensitive to
oxidative damage.

‘Most life on Earth depends in some form on oxygen, which is great at
the production of energy,’ Denver said. ‘But we pay a high price for
our dependence on oxygen, because the process of using it is not 100
percent efficient, and it can result in free oxygen radicals that can
damage proteins, fats and DNA. And this process gets worse with age,
as free radicals accumulate and begin to cause disease.’

This is one of the first studies, Denver said, that is clearly
demonstrating the effects of oxidative damage at a genome-wide scale.

‘The research showed that the majority of all DNA mutations bear the
signature of oxidative stress,’ Denver said. ‘That’s exactly what you
would expect if you believe that oxidative stress is an underlying
cause of ageing and disease.’

Beyond that, however, the study also found that mutation and natural
selection is also operating in the ‘junk DNA’ parts of the roundworm,
which actually comprises about 75 percent of its genome but
traditionally was not thought to play any major role in life and
genetic processes. This suggests that these poorly-understood and
little appreciated parts of the genome may have important biological
roles that are not yet known, Denver said.

Oxidative stress for decades has been suspected as a mechanism for
some of the processes that lead to ageing and disease, and it has been
studied extensively for that reason. This research provides a better
fundamental understanding of the genetic impacts of oxidative stress
and its role in both genetic disease and evolution, researchers say.

Source: Oregon State University

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh

Man Is A Herbivore!
http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

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SAUNDERS-Laboratory Tests and Diagnostic Procedures

Laboratory Tests and Diagnostic Procedures
By Cynthia C. Chernecky, Barbara J. Berger

Publisher: Saunders
Number Of Pages: 1232
Publication Date: 2007-06-14
Sales Rank: 275605
ISBN / ASIN: 1416037047
EAN: 9781416037040
Binding: Paperback

CHM Format, 5th Edition
TOC in TriPane, Removal of links in HTML
RAR 8.9 MB

Book Description:

Look no further for quick, complete answers to questions such as which
laboratory tests to order or what the results might mean. Laboratory
Tests And Diagnostic Procedures, 5th Edition covers more tests than
any other reference of its kind, with over 900 lab tests and
diagnostic procedures in all. In Part I, you’ll find a unique,
alphabetical list of hundreds of diseases, conditions, and symptoms,
including the tests and procedures most commonly used to confirm or
rule out a suspected diagnosis. Part II presents key information on
virtually every laboratory and diagnostic test available. All test
entries are up-to-date, concise, complete, and consistently presented,
making this resource the perfect choice for students or practitioners
who need fast, accurate information on diagnostic tests.

http://www.drfouly.com/showthread.php?p=52190

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Chronic Concussion Pigment

I wonder what this dark brown pigment could be ..

http://www.cbsnews.com/video/watch/?id=5372209n&tag=mg;60minutes

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh

Man Is A Herbivore!
http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

posted by admin in Uncategorized and have No Comments

Pathological Iron Perturbs Pregnancy

Depressed Antioxidant Status in Pregnant Women on
Iron Supplements: Pathologic and Clinical Correlates.
Biol Trace Elem Res. 2009 Oct 8.
Anetor JI, Ajose OA, Adeleke FN, Olaniyan-Taylor GO, Fasola FA.
Department of Chemical Pathology, College of Medicine,
University of Ibadan, Ibadan, Nigeria, aneto…@yahoo.com.

Iron (Fe) remains a commonly prescribed supplement in pregnancy.
Its possible pathologic potential is either uncommonly considered or
ignored.
We determined the antioxidant status in pregnant women with and
without Fe supplements.
Fifty-eight apparently healthy pregnant women on Fe supplements
were selected for the study from the antenatal clinic of the
University
College Hospital, Ibadan, Nigeria.
Fifty-five aged matched pregnant women who were not on Fe from
various parishes of the Christ Apostolic Church, Ibadan (non-drug
using Christian sect) were randomly selected as controls.
Both groups were classified according to the trimesters of pregnancy.
The gestational age in both pregnant women on Fe supplements and
non-supplement pregnant women was similar.
Fruit and vegetables consumption was higher in the supplement than
in the non-supplement group (57.2% vs. 37.3%).
Anthropometric indices, weight, height, and BMI, were also similar.
But while the weight of the Fe supplement group decreased by nearly
3% in the third trimester, it increased by over 10% (p < 0.00) in the
non-supplement group in the same period.
Serum Fe level was significantly higher in the supplement than the
non-supplement group (p < 0.001). In contrast, the levels of the
antioxidants, ascorbic acid, copper (Cu), zinc (Zn), and bilirubin
were
all significantly decreased (p < 0.05, p < 0.001, p < 0.05, and p <
0.05,
respectively).
Uric acid level though also lower in the supplement group did not
reach
statistical significance (p > 0.05), while vitamin E was similar in
both
groups.
There was relative stability of all antioxidants except uric acid,
which
declined from the first to the last trimester in the non-supplement
group.
The significantly higher Fe level in the second trimester was
sustained
in the third trimester though to a lesser degree (p < 0.05) and
associated
with significant decreases in the following antioxidant levels in the
supplement group, ascorbic acid, bilirubin, Cu, and Zn (p < 0.02, p <
0.02,
p < 0.02, and p < 0.001, respectively).
Uric acid and vitamin E though lower in the supplement group were not
significantly different.
Remarkably, percentage changes between the first and third trimesters
revealed that serum Fe increased by over 116% in the Fe supplement
group, while it only increased by over 50% in the non-supplement
group.
This was associated with 23.50% decrease in ascorbate level (p <
0.003)
in the supplement group, while it decreased by only 3.70% in the
non-supplement group (p > 0.05).
Again vitamin E decreased by 17.22% in the supplement group, while
it decreased by only 7.30% in the non-supplement group during the
period.
Uric acid and bilirubin levels decreased by similar proportions during
the
period, while Zn decreased by 18.55% in the supplement group and by
14.86% in the non-supplement group.
In contrast Cu increased by 7.20% in the supplement group, while it
increased by only 2.96 in the non-supplement group.
Additionally, all the antioxidants in the supplement group except
vitamin E,
viz, ascorbic acid, bilirubin, Cu, uric acid, and Zn, were
significantly inversely
correlated with serum Fe level (r – 0.299, p < 0.05, r – 0.278, p <
0.05, r – 0.383,
p < 0.05, and r – 0.0369, p < 0.05).
These data imply markedly depressed antioxidant status in the Fe
supplement
pregnant group with attendant oxidative stress (most probably pro-
oxidant
Fe-induced).
This is associated with molecular and cellular damage as well as a
number
of pathologic and clinical correlates that underlie the exacerbation
of
morbidity and mortality in maternal and child populations,
particularly in the
developing countries.
This appears to call for serious caution and prior evaluation of
antioxidant
and Fe status and during the use of Fe supplements in pregnancy for
monitoring and prognostic purposes and to avert or ameliorate
oxidative
stress-induced pathologies in maternal and fetal systems.

PMID: 19812902

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh

Man Is A Herbivore!
http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

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Migraine Hails Death

Migraine With Aura Frequency Plays a Role in Risk of Stroke, MI

ST. PAUL, Minn — June 25, 2009 — Women who have migraines with aura
may be more likely to have a stroke or myocardial infarction (MI) than
women who don’t have the condition, and the association varies by
migraine frequency, according to a study published in the June 24
online issue of the journal Neurology.

The study found that women with migraine with aura whose migraines
occur at least once a week are more than 4 times as likely to have a
stroke as women who do not have migraines.

Women with migraine with aura who have migraines less than once a
month were more than twice as likely to have a MI and nearly twice as
likely to have had heart procedures such as coronary artery bypass
surgery or angioplasty.

In contrast, women who had migraines with aura once a month had no
increased risk of stroke or heart problems.

"These results should be interpreted with caution, since the number of
migraine and migraine features were self-reported and there were
relatively low numbers of stroke and heart problems in the large study
group," said study author and Tobias Kurth, MD, Brigham and Women’s
Hospital, and Harvard Medical School, Boston, Massachusetts.

"Nonetheless, more research is needed to determine how and why these
differences occur and whether preventing migraines could reduce the
risk of stroke and heart problems."

The Women’s Health Study involved 27,798 US women health professionals
aged 45 years and older. The women had no heart or cerebrovascular
problems at the start of the study and were followed for about 12
years.

During that time, 706 women (2.5%) had cerebrovascular events,
including 305 MIs and 310 strokes. In addition, 655 women had heart
procedures such as bypass surgery.

Of the 3,568 women with migraine at the start of the study, 75% had
migraines less than once a month, 20% had them once a month, and 5%
had migraines at least once a week. A total of 1,428 had migraine with
aura.

SOURCE: American Academy of Neurology

———————–
"Increased iron concentrations"

 Migraine is associated with an increased risk of deep
white matter lesions, subclinical posterior circulation
infarcts and brain iron accumulation: the population-based
MRI CAMERA study.
Kruit M, van Buchem M, Launer L, Terwindt G, Ferrari M.
Department of Radiology, Leiden University Medical Centre,
Leiden, The Netherlands.

Previous studies have suggested that migraine is a risk factor
for brain lesions, but methodological issues hampered drawing
definite conclusions.
Therefore, we initiated the magnetic resonance imaging (MRI)
‘CAMERA’ (Cerebral Abnormalities in Migraine, an Epidemiological
Risk Analysis) study.
We summarize our previously published results.
A total of 295 migraineurs and 140 controls were randomly selected
from a previously diagnosed population-based sample (n = 6039),
who underwent an interview, physical examination and a brain MRI
scan.
Migraineurs, notably those with aura, had higher prevalence of
subclinical infarcts in the posterior circulation [odds ratio (OR)
13.7; 95% confidence interval (CI) 1.7, 112].
Female migraineurs were at independent increased risk of white
matter lesions (WMLs; OR 2.1; 95% CI 1.0, 4.1), and migraineurs
had a higher prevalence of brainstem hyperintense lesions
(4.4% vs. 0.7%, P = 0.04).
We observed a higher lifetime prevalence of (frequent) syncope and
orthostatic insufficiency in migraineurs; future research needs to
clarify whether autonomic nervous system dysfunction could explain
(part of) the increased risk of WMLs in female migraineurs.
Finally, in migraineurs aged < 50 years, compared with controls,
we found evidence of increased iron concentrations in putamen
(P = 0.02), globus pallidus (P = 0.03) and red nucleus (P = 0.03).
Higher risks in those with higher attack frequency or longer disease
duration were found consistent with a causal relationship between
migraine and lesions.
This summary of our population-based data illustrates that migraine
is associated with a significantly increased risk of brain lesions.
Longitudinal studies are needed to assess whether these lesions are
progressive and have relevant (long-term) functional correlates.

PMID: 19515125

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