Digitum Colección:http://hdl.handle.net/10201/177322024-03-28T18:35:45Z2024-03-28T18:35:45ZAnalytical histopathological diagnosis of small hepatocellular nodules in chronic liver diseasesNakanuma, Y.Hirata, K.Terasaki, S.Ueda, K.Matsui, O.http://hdl.handle.net/10201/191252020-02-10T00:15:12Z1998-01-01T00:00:00ZTítulo: Analytical histopathological diagnosis of small hepatocellular nodules in chronic liver diseases
Autor/es principal/es: Nakanuma, Y.; Hirata, K.; Terasaki, S.; Ueda, K.; Matsui, O.
Resumen: Due to the recent progress in radiology and
increased clinical and pathological interest, small
hepatocellular nodules about 1 cm in size are frequently
being detected in patients with chronic liver disease,
particularly liver cirrhosis. Two new types of small
hepatocellular nodules are now known: low-grade
hepatocellular carcinomas (HCC) and dysplastic
nodules, in addition to the previously known HCC
(classical) and regenerative nodules. Ultrasound-guided
needle biopsies from these nodules are routinely used
for the differential diagnosis. For comparison, a
simultaneous needle biopsy from the liver remote from
the nodule is strongly recommended. Low-grade HCC,
which are different from classical HCC in their
morphological atypia and also biological behaviors,
show local invasion into the portal tracts and
surrounding hepatic parenchyma, but not intrahepatic or
extrahepatic metastasis. Dysplastic nodules show mild
cellular and structural atypia, a finding which is not
sufficient for making a diagnosis of malignancy. An
increased nuclear/cytoplasmic (N/C) ratio and nuclear
crowding, small cell-dysplasia, increased cytoplasmic
staining, clear cell change, pseudogland formation, and
fatty change of hepatocytes are variably seen in these
nodules. Nuclear changes, local invasion to the portal
tract and surrounding liver, and loss of the reticulum
fibers along the hepatocytes are useful markers favoring
low-grade HCC rather than dysplastic nodules. These
low-grade HCC and dysplastic nodules should also be
distinguished from classical HCC as well as large-sized
regenerative nodules. A comparative analysis of the
histological findings observed in individual nodules is a
reasonable approach to differential diagnosis at present.
The recognition and analysis of these two new
hepatocellular nodules may augur a new horizon in the
study of hepatocellular neoplasm.1998-01-01T00:00:00ZMolecular changes in human melanoma metastasisLuca, M.R.Bar-Eli, M.http://hdl.handle.net/10201/191242020-02-10T00:15:10Z1998-01-01T00:00:00ZTítulo: Molecular changes in human melanoma metastasis
Autor/es principal/es: Luca, M.R.; Bar-Eli, M.
Resumen: The molecular changes associated with the
transition of melanoma cells from radial growth phase to
vertical growth phase (metastatic phenotype) are not
well defined. Our recent studies have demonstrated that
the two tumor suppressor genes, p53 and p16/CDKN2,
do not play a major role in the acquisition of the
metastatic phenotype in human melanoma. Mutations in
p53 are infrequent and do not correlate with the
metastatic potential of human melanoma cells while
p161CDKN2 abnormalities are frequent, but are not prerequisite
for the acquistion of the metastatic phenotype.
On the other hand, the tyrosine-kinase receptor c-KIT
and the cell adhesion molecule MCAMIMUC-18 play
active roles in the progression of human melanoma.
Metastatic melanoma cells overexpress MCAM and do
not express the c-KIT receptor. Enforced c-KIT
expression in metastatic cells significantly inhibited their
growth and metastatic potential in nude mice.
Furthermore, exposure of c-KIT-positive melanoma cells
in vitro and in vivo to stem cell factor (SCF), the ligand
for c-KIT, triggered apoptosis of these cells but not of
normal melanocytes. Ectopic expression of MCAM into
primary cutaneous melanoma cells enhanced their
tumorigenicity and met$static ability in vivo. We found
that both genes, c-KIT and MCAM, are regulated by the
transcription factor AP-2 and that metastatic melanoma
cells do not express AP-2. We therefore propose that loss
of AP-2 might be a crucial event in the progression of
human melanoma.1998-01-01T00:00:00ZMorphological changes associated with long-term potentiationAgnihotri, N.Lopez-Garcia, J.C.Hawkins, R.D.Arancio, O.http://hdl.handle.net/10201/191232020-02-10T00:15:09Z1998-01-01T00:00:00ZTítulo: Morphological changes associated with long-term potentiation
Autor/es principal/es: Agnihotri, N.; Lopez-Garcia, J.C.; Hawkins, R.D.; Arancio, O.
Resumen: Long-term potentiation (LTP) is a longlasting
form of synaptic plasticity induced by brief
repetitive afferent stimulation that is thought to be
associated with learning and memory. It is most
commonly studied in the hippocampus where it may last
for several weeks, and involves the synthesis of new
proteins that might play a structural role. In this review
we summarize the evidence in favor of modifications of
neuronal architecture during LTP. We focus our attention
on changes occurring at the level of single synapses,
including components of postsynaptic dendrites
(dendritic spines, the postsynaptic density, and synaptic
curvature), of presynaptic terminals, and the formation
of new synapses. We conclude that although many
morphological changes at various sites have been
observed during LTP, there is no definitive proof in favor
of structural changes associated with LTP. However,
morphological modifications remain a valid candidate
for mechanisms of learning and memory.1998-01-01T00:00:00ZMyenteric plexus in the gastrointestinal tract of non-obese diabetic miceSpangeus, A.El-Salhy, M.http://hdl.handle.net/10201/191222020-02-10T00:15:07Z1998-01-01T00:00:00ZTítulo: Myenteric plexus in the gastrointestinal tract of non-obese diabetic mice
Autor/es principal/es: Spangeus, A.; El-Salhy, M.
Resumen: The myenteric plexus was investigated in the
gastrointestinal tract of pre-diabetic and diabetic nonobese
diabetic (NOD) mice. The plexus was immunostained
by the avidin-biotin complex method, using a
general marker for nerve elements, namely protein geneproduct
9.5. The nerve fibres were quantified by pointcounting
and the number of ganglia and their area were
determined by image analysis. The relative volume
density of the nerve fibres in duodenal muscularis
propria was found to be significantly reduced in of both
pre-diabetic and diabetic NOD mice. There was no
statistical difference between controls and NOD mice
regarding relative volume density of nerve fibres in
antral and colonic muscularis propria. The number of
myenteric ganglialmm baseline was significantly
decreased in the duodenum of diabetic NOD mice, and
showed a non-statistically significant tendency to
decrease in pre-diabetic mice. In the antrum and colon,
there was no difference between the controls and NOD
mice regarding the number of ganglialmm baseline. Nor
was there any significant difference between controls
and NOD mice in the area of myenteric ganglia in either
antrum, duodenum or colon. It is concluded that the
changes in the duodenal myenteric plexus of NOD mice
are prior to the onset of diabetes. It is suggested that the
absence of changes in the antral and colonic myenteric
plexus when using a general marker for neuroelements
does not preclude a possible change in cholinergic,
adrenergic or peptidergic innervation.1998-01-01T00:00:00Z