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G Moscoso

Publications and source records attributed to G Moscoso.

At least 55 records · Page 3Linked to original sources

Growth of the normal human lower urinary tract from 12 to 21 weeks gestation.

Normal development of the human lower urinary tract was studied between the 14th and 20th week of gestation using 3 modes of fixation. Fixation by direct distension provides a high degree of reproducibility of parameters used to study the growth of the fetal bladder. Using this method, fetuses ranging from 12 to 21 weeks gestation were studied. Results obtained demonstrate that the length of the bladder, the inter-ureteric distance, and the distance between the apex of the trigone and the distal tip of the urethra occur in a linear mode. Furthermore, the rate of growth of the male urethra was evidently higher when compared to that of the female from the 12th week of gestation. Data from this work can be used for a more accurate assessment of cases with abnormal lower urinary tract development.

Female↗

Vasoactive intestinal polypeptide gene expression in the developing human gastrointestinal tract.

Expression of vasoactive intestinal polypeptide has been shown, by immunocytochemistry and biochemical assay, to follow the craniocaudal neural colonization of the mammalian gut. The aim of this study was to use in situ hybridization to see if it could provide more information on vasoactive intestinal polypeptide gene expression in the developing human gut. Immunocytochemistry of vasoactive intestinal polypeptide and, to visualize the total innervation, protein gene product 9.5 was also applied. By 8 weeks of gestation, protein gene product 9.5-immunoreactive neurons had colonized the gut lengthwise (17% of intestinal muscle area) but not transversely. Vasoactive intestinal polypeptide immunoreactivity was first detected at 9 weeks of gestation in a few nerve fibers of the upper gut, the origin of which could not be determined. Vasoactive intestinal polypeptide-immunoreactive ganglion cells were not seen until 18 weeks of gestation, whereas in situ hybridization showed messenger RNA in ganglion cells of the upper gut at 9 weeks. An adultlike pattern of peptide gene products (e.g., 2.5% and 3.1% of intestinal mucosal or muscle area, respectively) was detected by 20 weeks' gestation. The finding that the vasoactive intestinal polypeptide gene is expressed first in the upper human gut is consistent with craniocaudal neuronal colonization and maturation.

Adult↗

Localization of brain and atrial natriuretic peptide in human and porcine heart.

We have compared the localization of brain and atrial natriuretic peptide-like immunoreactivity in human and porcine hearts, using immunohistochemical techniques at both the light and ultrastructural level and specific antisera to amino-(cardiodilatin) and carboxy-terminal regions of the atrial natriuretic precursor molecule and to brain natriuretic peptide. Atrial myocardial cells in human fetal, normal adult and failing explanted hearts, displayed immunoreactivity for both brain and atrial natriuretic peptide-like sequences. At the subcellular level, brain natriuretic peptide-, cardiodilatin- and alpha-atrial natriuretic peptide-like immunoreactivity were co-localized to secretory granules in atrial myocardial cells. Immunoreactivity was also detected in the left (64%) and right ventricular free walls (23%) of 22 failing explanted hearts, but not in donor cardiac tissues. A gradient of natriuretic peptide immunostaining was observed across ventricular free walls and immunoreactivity for both natriuretic peptide sequences co-localized to secretory granules in a subpopulation of myocardial cells, concentrated in subendocardial regions of the ventricular walls. Brain and atrial natriuretic peptide-like immunoreactivity were also demonstrated in porcine atrial myocardium and cells of the ventricular conduction system. The parallel distribution of cardiac brain and atrial natriuretic peptide-like immunoreactivity suggests a dual regulation and co-storage of the natriuretic peptides in human and porcine hearts.

Adolescent↗

Transient expression of neuropeptide Y and its C-flanking peptide immunoreactivities in the spinal cord and ganglia of human embryos and fetuses.

An immunohistochemical study of spinal cord, dorsal root and sympathetic ganglia of human embryos and fetuses demonstrated that neuropeptide Y and its C-flanking peptide could be detected in seven-week-old embryos but were absent or difficult to demonstrate after the 17th week of gestation. The peptides were found in several structures of the spinal cord, e.g. fibres in the dorsal portion of the lateral funiculus, cell bodies and fibres in the dorsal horn, and motoneurons, and also in numerous primary sensory neurons of dorsal root ganglia. They were also present in sympathetic neurons and since these are the only structures expressing neuropeptide Y and its C-flanking peptide in the adult, it must be concluded that their presence in other neurons is a transient developmental feature. To assist in understanding the relationship of these transient structures with other spinal and sensory neurons, a comparison was made with other neuronal structures showing immunoreactivity for two general neuronal markers, neurofilaments and protein gene product 9.5, and two neuropeptides present in primary sensory afferents, somatostatin and substance P. In the dorsal root ganglia, numerous neuropeptide Y- and C-flanking peptide-immunoreactive neurons were observed before substance P- or somatostatin-immunoreactive cells could be detected. Therefore, neuropeptide Y and its C-flanking peptide could represent a primitive peptidergic system appearing before primary sensory neurons express their characteristic adult phenotype. The fibres of the lateral funiculus showing immunoreactivity for neuropeptide Y and its C-flanking peptide were longitudinally orientated and could be detected at all cephalocaudal levels of the spinal cord. Comparison with the other immunohistochemical markers indicated that they were not primary sensory afferents. At least some of them probably originated from neuropeptide Y- and C-flanking peptide-immunoreactive neurons of the dorsal horn, that may be considered to be a subset of early-appearing interneurons.

Embryo, Mammalian↗

Developmental pattern and distribution of nerve growth factor low-affinity receptor immunoreactivity in human spinal cord and dorsal root ganglia: comparison with synaptophysin, neurofilament and neuropeptide immunoreactivities.

Immunocytochemical expression of the low-affinity nerve growth factor receptor was studied in human fetal and adult tissues using the monoclonal antibody ME20.4. In dorsal root ganglia, a few immunoreactive neurons were first detected in nine-week-old fetuses and many more were found in the following weeks of gestation. However, none was present in adult ganglia. The ME20.4-positive cells were larger than neurons immunostained by substance P, calcitonin gene-related peptide or galanin antibodies. In the spinal cord, fibres immunostained by ME20.4 appeared in a characteristic pattern that differed from the spatial and temporal distributions of synaptophysin- and neurofilament-immunoreactive fibres. Those expressing the low-affinity nerve growth factor receptor were only detected in regions containing collaterals of primary sensory axons: (i) in the dorsal funiculus between seven and 18 weeks of gestation; (ii) in a ventrodorsal bundle reaching the ventral horn from weeks 12-14; (iii) in the medial region of the dorsal horn between weeks 12 and 20; (iv) in the superficial layers and lateral portion of the dorsal horn after the 14th week of gestation and also in adult spinal cord. During the fetal period, ME20.4 immunoreactivity was also found in motoneurons and peripheral nerve fibres in the skin, myotomes and gut. Sheaths of peripheral nerves and the adventitia of blood vessels were stained both in fetal and adult tissues. Thus, the low-affinity nerve growth factor receptor is: (i) strongly expressed in the developing human nervous system; (ii) transiently associated with a subset of large primary sensory neurons and with motoneurons; (iii) transiently and sequentially expressed by various groups of sensory afferents to the spinal cord; (iv) permanently expressed by fibres in the superficial layers of the dorsal horn, Clarke's column, nerve sheaths and the adventitia of blood vessels.

Adult↗

Localisation of endothelin like immunoreactivity in adult and developing human gut.

The distribution of immunoreactivity for the potent vasoconstrictor endothelin-1 was studied in adult and developing human gut using antisera to endothelin-1 (1-21) and the C terminus of big endothelin-1. The coexistence of these peptides with other neuropeptides was investigated using comparative immunocytochemistry. Endothelin-1 like immunoreactivity was detected in extracts of adult (range 20-60 fmol/g wet weight) and fetal (33 fmol/g) gastrointestinal tract and was shown by chromatography to be the predominant isoform of endothelin present in both. It was localised by immunocytochemistry to ganglion cells in the submucous and myenteric plexuses and to scattered nerves, whereas big endothelin-1 like immunoreactivity was found in the submucous plexus only. Colocalisation studies showed immunoreactivity for both endothelin-1 and vasoactive intestinal peptide in the same ganglion cells of the submucous plexus. Although endothelin-1 immunoreactivity was not detected by immunocytochemistry in the fetal human gut until the 32nd week of gestation, big endothelin-1 was found as early as 11 weeks in the developing neural structures and epithelial cells. The latter were shown to be endocrine cells by their immunoreactivity for chromogranin. Our results indicate that endothelin is a neuropeptide found in adult human gut which shows transient expression in endocrine cells during development.

Adult↗

Detection of myosin gene expression in the developing heart using probes derived by polymerase chain reaction.

The polymerase chain reaction provides a rapid method for the molecular cloning of DNA probes suitable for the detection of specific messenger RNA. We have used this approach to prepare probes specific for human cardiac myosin messenger RNA and demonstrate here the use of such probes in the analysis of human cardiac development by hybridization in situ to sections of fetal tissue. This combination of techniques is suitable for the detection of any messenger RNA for which sequence data are available, and offers a powerful new approach to the analysis of cardiac development.

Fetal Heart↗

Placental vascular anomaly with diffuse mesenchymal stem villous hyperplasia. A new clinico-pathological entity?

Diffuse mesenchymal hyperplasia of placental stem villi produces a pathological increase of placental volume, gives images of partial hydatidiform mola on ultrasound examination and is associated with elevated levels of alpha feto-protein. On gross examination, the placenta is enlarged, the vessels on the fetal plate show aneurysmal and varicose dilatations, and the stem villi appear as distinct, semitranslucent lobulated structures. At microscopy level, stem villi show excessive proliferation of mesenchymatous tissue with foci of myxoid degeneration and large macrophages containing alcian blue positive material within cytoplasmic vacuoles. Involved areas show blood vessels with abnormally thin walls, which are negative to factor VIII and alpha feto-protein immunohistochemical reactions. Pathological trophoblastic proliferation or stromal trophoblastic inclusions are not part of this condition. Although there is a clear predominance of a female genotype in this cases, the true sex incidence in placental vascular anomalies with diffuse mesenchymal stem villus hyperplasia has yet to be defined.

Adult↗

Sudden death caused by unsuspected pulmonary arterial hypertension, 10 years after surgery for extrahepatic biliary atresia.

A case of extrahepatic biliary atresia presenting with an acute respiratory episode and rapid deterioration, 10 years after a successful portoenterostomy and a very active life, was the setting of unsuspected severe pulmonary arterial hypertension leading to sudden death. The pulmonary arteries showed widespread plexiform lesions, thickening of the muscular media, and subendothelial proliferation. Occasionally, eccentric arterial obstructive lesions and fibrinous thrombi were observed. There was marked reduction of preacinar arterioles with a consequent increase in the alveolar/arterial ratio. The pulmonary veins showed arterialization of their walls. There was marked hypertrophy of myocardial fibres in the right ventricle together with foci of myocardial degeneration and fibrosis. Areas of endocardial thickening were observed in both ventricles. The absence of clinical indicators of pulmonary arterial hypertension at any but the terminal stages of the disease precluded any form of conservative management. Lung-heart and presumably liver transplantation might have been the only option. Prospective assessment of pulmonary function and haemodynamic studies should be considered in cirrhotic patients with portal hypertension.

Biliary Atresia↗

Localization of endothelin binding sites and endothelin-like immunoreactivity in human fetal heart.

The localization of [125I]endothelin-1 ([125I]ET-1) and [125I]endothelin-3 ([125I]ET-3) binding sites, as well as ET-like immunoreactivity, was investigated in sections of human fetal heart, using in vitro autoradiographic and immunohistochemical techniques. High-affinity [125I]ET-1 binding sites showed a tissue-specific distribution pattern, with high-density binding to the atria, ventricles (77-100 amol/mm2), and cardiac valve cusps (120.6 +/- 2.6 amol/mm2). Specific high-density binding of [125I]ET-3 was also exhibited on valve cusps (143.2 +/- 2 amol/mm2), whereas a much lower density of binding was displayed on atria and ventricles (10-15 amol/mm2). Microautoradiographic examination demonstrated binding sites on the wall of the aorta, pulmonary and coronary arteries, myocardium, ventricular conduction system, endocardium, and endothelial lining of valve cusps. Regional differences in the density and affinity of ET binding sites suggest that subpopulations of receptors are present in the human fetal heart. ET-like immunoreactivity was localized to a heterogeneous population of endothelial, endocardial, and epicardial mesothelial cells. The concordant localization of specific binding sites and ET-like immunoreactive cells indicates that locally released peptide might have a paracrine or autocrine role, possibly influencing cardiovascular development and function.

Autoradiography↗

Distribution of endothelin-like immunoreactivity and mRNA in the developing and adult human lung.

Localization and characterization of endothelin-producing cells in the developing (fetal and postnatal) and adult human lung was investigated using the technics of immunocytochemistry and in situ hybridization. Immunoreactivity for endothelin was seen mainly in pulmonary endocrine cells of developing human lung. Immunoreactivity was also seen in the airway epithelium in fewer cases (about 50%) of human adults. In situ hybridization with 35S- or 32P-labeled RNA probes complementary to endothelin-1, -2, and -3, showed that endothelin mRNAs were expressed in a number of cells that were in similar sites to endocrine cells. Immunocytochemistry and in situ hybridization employed on pairs of reverse-face serial sections showed the presence of endothelin immunoreactivity and mRNAs in the same endocrine cell. Correlative studies revealed that endothelin is co-localized with general endocrine markers (synaptophysin, chromogranin, protein gene product 9.5) and regulatory peptides (e.g., gastrin-releasing peptide). The density (cells/mm2) of endocrine cells containing immunoreactivity or mRNAs was highest during fetal life and started to decline before birth, and was minimal in adults. Endothelin-like immunoreactivity and mRNAs were also expressed in endothelial cells. From these results, it is concluded that endothelin is synthesized in endocrine cells of human lung and the change of developmental expression of this peptide suggests it may play a part in growth regulation in addition to its putative vasoconstrictor role in human lung.

Adult↗

Islet amyloid polypeptide in proliferating pancreatic B cells during development, hyperplasia, and neoplasia in humans and mice.

The occurrence of islet amyloid polypeptide (IAPP) immunoreactivity was investigated in fetal pancreas, islet cell hyperplasia, and tumors in humans and mice. Transgenic mice heritably developing endocrine tumors of the pancreas (AVP/SV40, Rip 1 Tag2/Rip2PyST1 and Glu2-Tag strains) were used as murine models of islet cells proliferative disease. In the mouse, IAPP immunoreactivity was found in B cells at embryonic day 12 (E12), paralleling the onset of insulin immunoreactivity. In hyperplastic/dysplastic islets and in B-cell tumors of transgenic mice (n = 16), IAPP immunoreactivity was localized consistently to insulin-immunoreactive cells. Ultrastructural single- and double-immunogold labeling of transgenic mice B-cell tumors (n = 3) showed insulin and IAPP to be colocalized in beta granules. In human fetuses, IAPP immunoreactivity was found in insulin-immunoreactive B cells, but at a later gestational age than the onset of insulin immunoreactivity. In pancreatic specimens of infantile/neonatal persistent hyperinsulinemic hypoglycemia (11 cases) and in pancreatic endocrine tumors (21 cases, 10 of which were functioning insulinomas), IAPP immunoreactivity was found consistently in insulin-immunoreactive B cells. Congo-red-positive amyloid deposits present in tumors also were IAPP immunoreactive. Ultrastructural single and double immunogold labeling of infantile/neonatal persistent hyperinsulinemic hypoglycemia cases (n = 3) and functioning insulinomas (n = 2) showed IAPP and insulin to be colocalized in beta granules. In addition, IAPP immunoreactivity was observed in amyloidlike fibrils. These findings indicate that IAPP is a constitutive component of B cells. Possible relationships between IAPP and insulin expression and interspecies differences are suggested and discussed.

Adenoma, Islet Cell↗

Early sonographic diagnosis of body stalk anomaly.

Ultrasonographic features of a fetus at 18 weeks of gestation suggesting a body stalk anomaly are presented. These included a large abdominal anterior wall defect in apparent continuity with the placenta, severe kyphoscoliosis of the lower spine, the absence of one kidney, and a very short umbilical cord with only one umbilical artery. The amniotic fluid was reduced and the fetus was almost immobile at short-interval ultrasound examinations. The pregnancy was terminated and autopsy of the fetus showed abnormalities compatible with maldevelopment of both cephalic and caudal embryonic folds.

Abdominal Muscles↗

Ultrasonographic diagnosis of a large placental intervillous thrombosis associated with elevated maternal serum alpha-fetoprotein level.

A placental lesion associated with elevated maternal serum alpha-fetoprotein level and a positive Kleihauer-Betke test is reported. Serial ultrasonograms showed a progressive increase in the echogenicity of the lesion that corresponded to a large intervillous thrombosis after delivery. This case illustrates the importance of detailed ultrasonographic and pathologic placental investigations in pregnancies with unexplained elevated levels of alpha-fetoprotein.

Adult↗

Correlation of ultrasound and pathologic findings of placental anomalies in pregnancies with elevated maternal serum alpha-fetoprotein.

Twenty pregnancies with elevated maternal serum alpha-fetoprotein (MSAFP), a normal fetus and unusual or abnormal placental/cord sonographic features are reported. These include: (A) gigantic enlargement with multiple sonolucent spaces of different size and shape (n = 2; Swiss cheese); (B) placental masses of variable echogenicity (n = 5); (C) cord masses with central echo-dense zone and peripheral hypoechoic areas (n = 2); (D) enlarged placentas with patchy decrease of echogenicity (n = 6; jelly-like); and (E) large sonolucent spaces with turbulent blood flow surrounded by normal placental tissue (n = 5; placental lakes). After delivery, these ultrasound features were compared with pathologic findings. Diffuse mesenchymal hyperplasia of the stem villi were found in the gigantic placentas (n = 2). The placental masses corresponded to chorioangiomas (n = 3), infarct (n = 1) or subamniotic hematoma (n = 1) and the cord masses to angiomyxomas (n = 2). The 'jelly-like' placentas were related to subchorial thrombosis (n = 2), massive fibrin deposition (n = 1) or hypertrophy with no obvious abnormalities (n = 3). Large subchorial thrombosis (n = 2), or no obvious abnormalities (n = 3) were observed in placentas with large lakes. These findings suggest that a large range of placental and cord anomalies are associated with elevated MSAFP and are potentially diagnosable by routine sonographic examination at the time of AFP screening.

Female↗

Variations in microscopic anatomy and ultrastructure of human embryonic hearts subjected to three different modes of fixation.

The external form and the internal contour of the ventricular surfaces were studied in human embryonic hearts following three modes of fixation: A) simple immersion fixation, B) indirect ventricular perfusion through the umbilical vein and C) high flow-low pressure ventricular perfusion-inflation. Fixation artifacts, resulting in distortion of the external form of the heart together with distortion of the internal contour of the ventricular cavities, were observed in specimens submitted to modes A and B of fixation. By contrast, hearts fixed by direct ventricular perfusion-inflation (C), showed less distortion in their external form, and the various intraventricular components maintained their spatial relationship among themselves and with the great arteries. Thus, reproducible developmental anatomical features at organ and tissue levels were readily available for study. The relevance of a direct ventricular perfusion-fixation method is discussed in relation to the value of human cardiac developmental data obtained in the past, after using simple immersion, or other modes of fixation.

Heart↗