Pathology and laboratory medicine

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Archive for June, 2010


Why do people die if they have their throat cut ? I thought if it happened,
you could put your hand or something over the cut to help you breathe.

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"Adverse Obstetric Outcomes" due to short interval following first pregnancy possibly explained…

"Interpregnancy Interval and Risk of Preterm Birth and Neonatal Death" (Smith,
et al., BMJ 2003; 327: 313 )

Explanation May be Due to Reduced DHEA Postpartum Following a First Pregnancy

(Copyright 2003, James Michael Howard, Fayetteville, U.S.A., At bottom of: )

Smith, et al., conclude in their report in the British Medical Journal that: "A
short interpregnancy interval is an independent risk factor for preterm delivery
and neonatal death in the second birth." (The abstract is available below.) I
suggest these "adverse obstetric outcomes" result from a single phenomenon which
should not go unacknowledged vis-à-vis the tremendous burdens in emotional
suffering and medical costs. These conditions may be ameliorated by monitoring
low levels of, and supplementation with, dehydroepiandrosterone (DHEA) in women
who become pregnant again, soon after a first pregnancy.

DHEA has been determined to decline in women "only after a first pregnancy" for
remain low sometimes up to 150 months (J Clin Endocrinol Metab. 1987; 64:
111-8). This finding was repeated: "A previous paper in this journal reported
that first pregnancy was followed by a marked decrease in dehydroepiandrosterone
sulfate (DH[E]AS) and dehydroepiandrosterone (DH[E]A) levels. We report here
confirmatory observations from cross-sectional measurements in 460 women. In
premenopausal subjects (n = 306), the mean DH[E]AS level was 21% lower (P =
0.005) and the mean DH[E]A level was 32% lower (P less than 0.001) in parous
than in nulliparous women." (J Clin Endocrinol Metab. 1990; 70: 1651-3). I
suggest these low levels of DHEA are directly connected with "adverse obstetric
outcomes" in pregnancies of short intervals following a first pregnancy.

In order to understand the connection of this low DHEA with "adverse obstetric
outcomes," in pregnancies following first pregnancies without sufficient time
for DHEA to rebound, I have to explain two ideas about DHEA. In 1985, I
copyrighted my explanation of the "fight or flight" mechanism. I suggested that
the major adrenal steroid, dehydroepiandrosterone (DHEA), was "selected" by
evolution because it "optimizes" replication and transcription of DNA.
Therefore, DHEA is involved in every tissue, especially nervous tissue, the
brain. It follows that DHEA in sufficiently available levels will be involved in
increasing, or optimizing, aggression between combatants. Combatants who fight
to death or maiming reduce the probability of continuance of a species. DHEA
levels would be positively involved in "impulses" or "motivation." I suggest the
other major adrenal steroid, cortisol, was selected by evolution to counteract
the effects of DHEA. As you may know, cortisol is the "stress" hormone, produced
when we experience stress. I suggest cortisol levels are negatively involved in
impulses or motivation. The ratio of cortisol to DHEA will be directly tied to
our personalities as well as actions. When cortisol is high, we flee, when DHEA
is high, we fight. Cortisol antagonizes the effects of DHEA and the ratio of
cortisol to DHEA is important in many physiological phenomena, including
obstetric outcomes. Too much cortisol for extended periods, especially in low
DHEA conditions, may produce very negative effects in all tissues.

Also, one should know that the very abundant source of DHEA in our blood exists
as a "sulfated" form. This is known as DHEAS or DHEAsulfate. The active
molecule, DHEA, is derived from DHEAS. Now, this is not well known. Therefore,
sometimes, when DHEAS levels are measured and found to be high, this literally
indicates that abundant DHEA is readily available. However, sometimes when DHEAS
levels are measured as high, this also may mean that DHEA is not being produced
from DHEAS. Since this is not well known, one has to look at the pattern of this
ratio and interpret it in terms of potential pathology. So, sometimes high DHEAS
may indicate negative or adverse conditions. I suggest this is the case in the
following citations which connect high levels of DHEAS with preterm delivery.

Mazor, et al., reported that "Maternal plasma DHEA-S concentrations were
significantly higher in women with preterm labor who delivered preterm than in
those who delivered at term." (Arch Gynecol Obstet. 1996; 259: 7-12). Now, if
DHEAS is working normally, the relationship of cortisol ratio becomes important
as an indication that cortisol is too high and antagonizing the effects of DHEA.
(Remember the connection of cortisol to DHEA above.) Yoon, et al., found this in
1998: "An elevation in fetal plasma cortisol but not dehydroepiandrosterone
sulfate was followed by the onset of spontaneous preterm labor in patients with
preterm premature rupture of the membranes." (Am J Obstet Gynecol. 1998; 179:

I suggest the "adverse obstetric outcomes" connected with a short interval
between a first pregnancy and a subsequent pregnancy may result from
insufficient DHEA in the mother. These conditions may be ameliorated by
monitoring low levels of, and supplementation with, dehydroepiandrosterone
(DHEA) in women who become pregnant again, soon after a first pregnancy.

British Medical Journal 2003; 327: 313.

 Interpregnancy interval and risk of preterm birth and neonatal death:
retrospective cohort study.

Smith GC, Pell JP, Dobbie R.

OBJECTIVE: To determine whether a short interval between pregnancies is an
independent risk factor for adverse obstetric outcome. DESIGN: Retrospective
cohort study. SETTING: Scotland. SUBJECTS: 89 143 women having second births in
1992-8 who conceived within five years of their first birth. MAIN OUTCOME
MEASURES: Intrauterine growth restriction (birth weight less than the 5th
centile for gestational age), extremely preterm birth (24-32 weeks), moderately
preterm birth (33-36 weeks), and perinatal death. RESULTS: Women whose
subsequent interpregnancy interval was less than six months were more likely
than other women to have had a first birth complicated by intrauterine growth
restriction (odds ratio 1.3, 95% confidence interval 1.1 to 1.5), extremely
preterm birth (4.1, 3.2 to 5.3), moderately preterm birth (1.5, 1.3 to 1.7), or
perinatal death (24.4, 18.9 to 31.5). They were also shorter, less likely to be
married, and more likely to be aged less than 20 years at the time of the second
birth, to smoke, and to live in an area of high socioeconomic deprivation. When
the outcome of the second birth was analysed in relation to the preceding
interpregnancy interval and the analysis confined to women whose first birth was
a term live birth (n = 69 055), no significant association occurred (adjusted
for age, marital status, height, socioeconomic deprivation, smoking, previous
birth weight vigesimal, and previous caesarean delivery) between interpregnancy
interval and intrauterine growth restriction or stillbirth. However, a short
interpregnancy interval (< 6 months) was an independent risk factor for
extremely preterm birth (adjusted odds ratio 2.2, 1.3 to 3.6), moderately
preterm birth (1.6, 1.3 to 2.0), and neonatal death unrelated to congenital
abnormality (3.6, 1.2 to 10.7). The adjusted attributable fractions for these
associations were 6.1%, 3.9%, and 13.8%. The associations were very similar when
the analysis was confined to married non-smokers aged 25 and above. CONCLUSIONS:
A short interpregnancy interval is an independent risk factor for preterm
delivery and neonatal death in the second birth.

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pulmonary acariasis

I am interested in mites in sputum and am looking for a pathologist
with an interest in this area.


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marketing a practice

I am working for a pathology practice in Denver, and we are looking
for a firm to help us with market research, as well as with marketing
in general.

Does anyone have any suggestions?

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weird but interesting question…

why do grown dogs get stomachaches when they drink milk and grown cats
It is known that lack of lactase, the enzyme that breaks down lactose,
produces stomachahces in humans. The other thing is that when puppies
drink milk nothing happens to them, but as they grow older and stop
producing the enzyme, they get stomachaches. The same hapens with
cats, so why dont they get stomachaches as they also lack the enzyme?
I would appreciate any kind of help/guidance on this topic. PLease,
prove me wrong if i am!
Thank you before hand.

Yuri Sylvester

ps: i couldnt find any vet group so i guessed pathology would have
some explanation for this =)

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liver fibrosis / alcohol / iron

Alcohol. 2003 Jun;30(2):121-9.  Related Articles, Links  

Iron-induced oxidant stress in alcoholic liver fibrogenesis.

Pietrangelo A.

Centre for the Study of Iron Disorders, Department of Internal Medicine,
University of Modena and Reggio Emilia, Policlinico, Via del Pozzo 71, 41100,
Modena, Italy

Iron is an essential micronutrient. However, because human beings have no means
to control iron excretion, excess iron, regardless of the route of entry,
accumulates in parenchymal organs and threatens cell viability. Indeed, when
iron-buffering capability is overwhelmed, oxidative stress-induced cell damage
and fibrogenesis may arise, mainly in the liver, the main storage site for iron
in the body. Results of recent studies have clearly shown that these pathologic
events are induced by iron-generated reactive oxygen species and lipid
peroxidation by-products. Hepatic fibrosis, characterized by excessive
accumulation of extracellular matrix components in the liver, is a dynamic
process, from chronic liver damage to end-stage liver cirrhosis. Iron-induced
oxidant stress is involved in this process (1) as the primary cause of
parenchymal cell necrosis or (2) as activator of cells that are effectors
[e.g., hepatic stellate cells, (myo)fibroblasts] or key mediators (e.g.,
Kupffer cells) of hepatic fibrogenesis (or through both mechanisms). Beyond
their effect as direct cytotoxic agents, iron and free radicals may trigger
increased synthesis of collagen in myofibroblast-like cells as well as activate
granulocytes and Kupffer cells, resulting in an increased formation of
cytokines and eicosanoids and further reactive oxygen species. This may
constitute a cascade of amplifying loops, which perpetuate the fibrogenic
process. The fibrogenic potential of iron is even more dramatic when iron acts
in concert with other hepatotoxins such as alcohol. In this instance, even if
tissue iron levels are only slightly elevated, the toxic effect of alcohol or
its metabolites may be amplified and propagated with rapid acceleration of the
liver disease. At the molecular level, the presence of catalytically active
"free iron" may (1) contribute directly to the hepatotoxicity of alcohol or (2)
enhance the generation of cytokine and fibrogenic mediators from resident
Kupffer cells (or be involved in both ways). A challenge for future research is
to develop therapeutic tools able to block "redox-active" free iron in the

PMID: 12957296 [PubMed - in process]


Who loves ya.
Jesus Was A Vegetarian!
Man Is A Herbivore!

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autoimmune encephalomyelitis

J Nutr. 2003 Aug;133(8):2635-8.  Links

Iron-deficient mice fail to develop autoimmune encephalomyelitis.

Grant SM, Wiesinger JA, Beard JL, Cantorna MT.

Department of Nutrition, The Pennsylvania State University, 126 South
Henderson, University Park, PA 16802, USA.

Determinations of the effects of iron status on the immune system are
complicated by the fact that microorganisms and immune cells both utilize iron.
To determine the role of iron in immune function, we utilized a model
[experimental autoimmune encephalomyelitis (EAE)] in which a strong
antigen-specific CD4+ T-cell response develops in the absence of infection. EAE
is an autoimmune disease frequently used as a model for the human disease
multiple sclerosis (MS). EAE was induced in B10.PL mice fed low iron (1 mg/kg),
normal iron (10 mg/kg) or high iron (160 mg/kg) diets that were replete in all
other nutrients. Liver iron measurements verified iron status, i.e., low iron
mice had 1.9 micro mol/g tissue, normal iron mice, 3.27 micro mol/g tissue and
high iron mice, 5.35 micro mol/g tissue. EAE symptoms were most severe in
normal iron mice, and EAE did not develop in low iron mice. The incidence of
EAE was 71% in normal iron mice, 62% in iron-overloaded mice and 0% in
iron-deficient mice. Two of seven mice in the normal iron group developed
severe EAE and were euthanized. None of the iron-overloaded mice developed
severe EAE. Other measures of EAE severity were similar in the normal and
iron-overloaded mice. The data suggest that iron deficiency provides protection
from the development of EAE and that iron excess with its potential
contribution to free radical formation was not an important factor. The
mechanism of EAE inhibition in iron-deficient mice likely involves the delivery
and metabolism of iron for optimal CD4+ T-cell development.

PMID: 12888650 [PubMed - in process]


Who loves ya.
Jesus Was A Vegetarian!
Man Is A Herbivore!

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Toxicity of 2,4-diamino-6-alkyl-s-triazines

Can you give me some information about toxicity of
2,4-diamino-6-alkyl-s-triazines or at least indicate some literature
about it?

Many thanks! With best regards

José M. Santos

Ciba Spezialitäten Chemie
Coating Effects (CE 703)
R-1049 3.58
P.O. Box 4002
Basel – Switzerland
Tfn:00416163622667 (Intern: 622667)
mail to : jose_manuel.santos_pica…

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why is it that mosquitoes and other insects only seem to be vectors
for a rather limited number of diseases?  for instance, why can’t they
transmit aids?

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Alternative more natural product than Golytely, Colyte, polyethylene glycol

What more natural products are available for people who use natural foods
than the Golytely, Colyte, polyethylene glycol used in the day before
preparation for a routine colonoscopy colon screening?…

Something that is as effective…

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