15 research outputs found
Quantitative analysis of vessels with smooth muscle layer in astrocytic tumors: correlation with histological grade and prognostic significance
Angiogenesis plays an important role in the
progression of astrocytic tumors and its evaluation is a
major prognostic factor. Although the form of
proliferating vessels ranges from fine capillaries to welldeveloped
vascular structures with a smooth muscle
layer, the characteristics of vascular smooth muscle cells
(SMCs) are not understood in detail. We therefore
examined the density, size and shape of tumor vessels, as
well as CD34-immunoreactive (CD34-Vs) or α-smooth
muscle actin-immunoreactive (SMA-Vs) vessels in 46
primary astrocytomas (grade II diffuse astrocytomas,
n=11, grade III anaplastic astrocytomas, n=15, grade IV
glioblastomas, n=20) and in normal brain tissues from
10 autopsies. We also examined the expression of high
molecular weight caldesmon (h-CD, a marker of the
contractile phenotype of smooth muscle) and of plateletderived
growth factor receptor ß (PDGFR-ß). The SMAVs
were significantly more dense and larger in grade IV
than grade III, whereas those of CD34-Vs did not differ
between grade III and IV. Changes in the shape of
CD34-Vs and SMA-Vs correlated with histological
grading. The expression of h-CD was reduced, whereas
that of PFGFR-ß was increased in high gradeastrocytomas.
Kaplan-Meier analysis indicated that the
density of SMA-Vs, the size of both CD34 and SMA-Vs
and PDGFR-ß expression were significant prognostic
factors.
These findings suggest that SMA-Vs are
significantly associated with the progression of
astrocytomas and that these vessels provide useful
information for the histological diagnosis and survival of patients with these types of brain tumors
Critical role of von Willebrand factor and platelet interaction in venous thromboembolism
It has been generally considered that platelets
are less important in venous thrombus formation.
However, clinical studies have shown an association
between venous thromboembolism (VTE) and von
Willebrand factor (VWF). We therefore investigated the
contribution of VWF and platelet interaction to the onset
of VTE using tissues from autopsies and from an animal
model. An immunohistochemical study revealed that
glycoprotein (GP) IIb/IIIa, fibrin, glycophorin A
(erythrocyte-specific protein) and VWF were
consistently localized in ilio-femoral venous thrombi and
in pulmonary thromboemboli from 8 autopsied cases
who died of VTE, and VWF was closely associated with
GPIIb/IIIa and fibrin. Venous thrombi and pulmonary
emboli contained significant amounts of GPIIb/IIIa and
VWF, in addition to glycophorin A and fibrin, and the
factors did not significantly differ between them. A
rabbit model of VTE was developed by inserting a
polyethylene tube into the iliac vein. The constituents of
the induced thrombi were quite similar to those of
human VTE. An antibody against VWF (AJW200),
which inhibits interactions between the VWF A1 domain
and platelet GPIb, significantly reduced venous
thrombus formation and pulmonary thromboembolism in
the model. These results suggest that VWF A1-platelet
GPIb interaction plays a significant role in venous
thrombus formation
Associations of intrauterine growth restriction with placental pathological factors, maternal factors and fetal factors; clinicopathological findings of 257 Japanese cases
Intrauterine growth restriction (IUGR) is the
leading cause of fetal mortality and morbidity. As an
etiology, each of placental findings, maternal factors and
fetal factors has been reported to be associated with
IUGR, although a comprehensive approach to examine
all of these parameters as a cause of IUGR has not been
reported. In the present study, therefore, we
comprehensively examined the placental findings and
maternal and fetal factors in the cases of IUGR (n=257,
mean maternal age, 30 years; gestational weeks, 34
weeks) and normal growth pregnancies (n=258, mean
maternal age, 30 years; gestational weeks, 33 weeks),
and determined risk factors for IUGR. The prevalence of
pregnancy hypertension (PHT) (19% vs. 8%, P<0.01),
smoking habit (3% vs. 0.7%, P<0.05) and fetal anomaly
(3.5% vs. 0.8%, P<0.05) were higher in IUGR cases than
normal growth pregnancies. Pathologically, the
prevalence of infarction (33% vs. 14%, P<0.05), fetal
vessel thrombosis (22% vs. 6%, P<0.001) and chronic
villitis (11% vs. 3%, P<0.001) were higher in IUGR
cases than those in normal growth pregnancies. A
multivariable regression analysis revealed that maternal
factors (PHT), fetal factors (anomaly), and placental
findings (infarction, fetal vessel thrombosis, and chronic
villitis) are independently associated with increased risk
of IUGR (all P<0.01)