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M Marin-Padilla

Publications and source records attributed to M Marin-Padilla.

At least 19 recordsLinked to original sources
PubMed1990

Placental hypoechoic-anechoic areas and infarction: sonographic-pathologic correlation.

High-resolution ultrasound (US) and pathologic analysis were used to define the relationship between placental hypoechoic-anechoic areas, frequently seen in the third trimester, and the clinically significant entity of placental infarction. Placentas were obtained from three groups of patients: those prospectively demonstrating one or more placental hypoechoic-anechoic areas greater than or equal to 1 cm in diameter on third-trimester sonograms (n = 14), those with risk factors for vascular disease (n = 12), and control patients without risk factors (n = 16). Pathologic analysis demonstrated significantly more infarcts in patients with risk factors than in control patients (17 vs three, P = .047). Of a total of 22 infarcts from all three groups, 19 (86%) were isoechoic to viable placenta and therefore not detected with US. The three infarcts identified with US contained hypoechoic or anechoic foci of fibrin or hemorrhage. Of 26 placental hypoechoic-anechoic areas 23 (88%) were decidual septal cysts or intervillous thrombosis without infarction. The authors conclude that nonhemorrhagic placental infarction cannot be identified with ex utero US and, by inference, that prenatal US is probably insensitive for detection of placental infarction.

Female↗
PubMed1989

Early neurogenesis of the mouse olfactory nerve: Golgi and electron microscopic studies.

The early neurogenesis of the mouse olfactory nerve, from its exist at the nasal epithelium to its entrance into the embryonic telencephalon, has been investigated by using the rapid Golgi method and electron microscopy. Previously unrecognized anatomical and possible functional interrelationships between developing olfactory nerve axons and their sheath cells have been observed: 1) at their exit from sensory epithelium (nasal compartment), 2) at their contact with the CNS surface (intracranial compartment), and 3) at their entrance into the embryonic telencephalon (central nervous tissue compartment). Based on these observations the anatomy of the mouse olfactory nerve is herein redefined. Exiting olfactory nerve axons and sheath cells from the same regions of the nasal epithelium establish an early association which is maintained up to their terminal glomerular neuropile. No disruptions have been found in either the olfactory nerve axons or in the continuity of their sheath cells from exit at the nasal epithelium to entrance into the developing olfactory bulb. Corresponding olfactory nerve axons with their sheath cells enter together and become incorporated into the developing olfactory bulb as units. Consequently, the cellular envelope of the olfactory glomerulus must be composed of olfactory sheath cells rather than of glial (astroglial) cells from the CNS. With this simple anatomical arrangement, a topographic map of the sensory epithelium could be established progressively in the developing olfactory bulb. Eventually, "regenerating" olfactory nerve axons from different nasal regions could be guided by their specific sheath cell conduits toward their target glomeruli; hence, the olfactory message may be maintained undisturbed throughout the life span of the animal. In addition, olfactory nerve axons establish synaptic-like contacts with their corresponding sheath cells prior to or during the perforation of the CNS surface. Reciprocal recognition between corresponding axons and their sheath cells at this crucial stage in their neurogenesis may play a significant role in the establishment of their terminal glomerulus. This new concept of the anatomy of the mammalian olfactory nerve should provide insights helpful in clarifying some of the still-unresolved questions regarding the structural and functional organizations of this primitive system.

Animals↗
PubMed1989

Triploidy: pregnancy complications and clinical findings in seven cases.

Seven cases of triploidy were encountered by the Prenatal Diagnosis Program at Dartmouth-Hitchcock Medical Center over an 8-year period through associated pregnancy complications. We describe the characteristic findings that facilitate prenatal diagnosis and management. Our experience includes fetuses with major central nervous system abnormalities (spina bifida aperta, holoprosencephaly) and anterior abdominal wall defects, which are detectable with routine prenatal diagnostic screening examinations (ultrasound and AFP). In addition, we stress the importance of recognizing obstetric complications and associated cystic placental changes, which are quite common among triploid conceptuses. Molar changes associated with triploidy have a more benign prognosis than that associated with diploid moles. Such molar changes may relate to the presence of a diploid paternal chromosome complement. The usefulness of cytofluorometric DNA determinations in helping to confirm a clinical suspicion of triploidy is emphasized. These cases are presented in an effort to facilitate prenatal recognition and management of this common cytogenetic condition and prevent unnecessary Caesarean section deliveries.

Adolescent↗
PubMed1989

Abnormal Purkinje cell morphogenesis in human renal agenesis. A Golgi study.

The prenatal histogenesis of the human cerebellum in renal agenesis has been studied in four fetuses (32-, 33-, 33-, and 36-week-old) using the rapid Golgi method. A fundamental anomaly involving the developing Purkinje cell has been found. The normal histogenesis of this neuron is aborted about the 32nd-33rd week of gestation. Subsequently, the neuron undergoes a progressive transformation acquiring an abnormal dendritic morphology in only four weeks. The perikaryal basal dendrites are retained rather than disappear, and they continue to grow spreading horizontally through the ganglionic plate and into the internal granular layer. Progressively the basal dendrites become hypertrophic and long and give off accessory apical branches that penetrate into the molecular layer. Concomitantly, the development of the apical dendrites is impeded, and their size and number are progressively reduced. The structure of the transformed Purkinje cell as well as the distribution of its dendrites contrast sharply with those of normal neurons. This transformation reflects a remarkable degree of plasticity of developing neurons and implies structural reorganizations of the local circuitry which could result in functional anomalies. Similar Purkinje cell dendritic anomalies have been described in renal dysplasia and the infantile type of polycystic kidney. The cause of this cerebellar anomaly, or its relationship to congenital renal disorders, remains unexplained. Failure of climbing fiber/Purkinje cell normal interactions is proposed as a possible explanation for the abnormal Purkinje cell histogenesis.

Fetus↗
PubMed1987

The chandelier cell of the human visual cortex: a Golgi study.

The size, location, distribution, and spatial orientation of the chandelier cell of the human visual cortex are described for the first time. The rapid Golgi method has been utilized to study the structural features of these inhibitory interneurons. The human chandelier cell is a small stellate interneuron with prominent idiodendritic and idioaxonic arborizations. These arborizations are distributed within a narrow rectangular tissue slab that measures approximately 300 X 200 X 100 microns. This relatively small and narrow functional territory is oriented perpendicular to the pial surface and to the long axis of the gyrus. The territory of distribution of its axon is larger than and encloses that of its dendrites. The number of specific axonic terminals (candles) per chandelier cell is also relatively small, ranging from 60 to 80 units. These axonic terminals represent the functional units of the neuron and reflect the number of pyramidal cell axons contacted by it. The chandelier cell of the human visual cortex possibly represents the smallest neuron of this kind described to date. The size of its functional territory and the number of its specific axonic terminals are among the smallest of any neuron of this kind thus far described. It is postulated herein that in the course of mammalian phylogeny the chandelier cell shows a tendency toward a progressive reduction in the size of its functional territory and in the number of its functional units (candles), as well as a tendency toward a more "idio" pattern of distribution for its axonic and dendritic arborizations. Perhaps, these progressive evolutionary modifications could reflect a tendency of this type of interneuron toward an increasing specialization. The possible existence of a relationship between the progressive transformation of the chandelier cell and the increasing visual acuity, dexterity, and skillfulness in the course of mammalian phylogeny should be explored.

Female↗
PubMed1987

Bilateral renal agenesis in three consecutive siblings.

We report here an unusual recurrence of bilateral renal agenesis (BRA) in three consecutive siblings. Chromosome analysis was normal, as were renal ultrasound studies on both parents and their surviving child. Ultrasound was employed prenatally to diagnose Potter's syndrome in both of the recurrences, and autopsy confirmed BRA in otherwise normal fetuses. Recurrence of BRA points to the usefulness of ultrasound in monitoring subsequent pregnancies in couples who have had one such occurrence. Ultrasound studies should also be performed in non-affected family members to detect the presence of asymptomatic anomalies of the genitourinary system, but a negative family study does not preclude recurrence of BRA.

Abnormalities, Multiple↗
PubMed1987

Malignant melanoma arising in an ovarian cystic teratoma in pregnancy.

Ovarian cystic teratoma is a common neoplasm, but malignant melanoma arising within such a tumor is exceedingly rare. The small number of previous cases generally occurred in older individuals, usually with a poor outcome. The patient presented herein is remarkable for her youth and an optimistic prognosis. Hers is also the first such case to be associated with pregnancy. The relevant literature is briefly reviewed.

Adult↗
PubMed1985

Early vascularization of the embryonic cerebral cortex: Golgi and electron microscopic studies.

Two developmental aspects in the establishment of the vasculature of the embryonic cerebral cortex have been analyzed: the vascular perforation of the external basal lamina and marginal glia by leptomeningeal capillaries and their early intracortical angiogenesis. Electron microscopic and rapid Golgi preparations have been used in this study. Four phases have been identified in the vascular perforation of the cortex. First, the leptomeningeal capillary approaches and establishes direct contact with the external basal lamina and marginal glia of the cerebral cortex. Second, the leading endothelium of the glia-touching capillary undergoes considerable membrane activity forming many filopodia and pseudopodia. Some filopodia of this activated endothelium perforate the vascular and cortical basal laminae and penetrate into the neural tissue. This filopodial perforation is accompanied by swelling and disintegration of the subadjacent marginal glial endfeet. Third, the original perforation enlarges progressively and allows an entire endothelial cell (or cells) to penetrate into the neural tissue. Fourth, proliferation and progressive canalization of penetrated endothelial cells result in the formation of a new cortical capillary in situ. Its proximal wall becomes surrounded by perivascular glial processes which appear to replace the degenerated ones. Thus a vasculoglial barrier is formed around the growing capillary, isolating it from the neural tissue, while the filopodia at its leading edge are still growing among the neural elements without recognizable basal lamina. The formation of a shallow pial-funnel at the capillary entrance can also be recognized at this time. This funnel contains the fine processes of leptomeningeal cells, a few collagen fibers, and the basal laminae of the penetrating vessel and of the perivascular glia. It represents an early stage in the formation of the Virchow-Robin space. The intracortical embryonic vasculature is characterized by both capillary angiogenesis and regression and by the formation of anastomotic plexuses. While capillary angiogenesis and reabsorption are found everywhere and appear as random phenomena, the location of the anastomotic plexuses is specific and always associated with actively growing cortical regions.

Animals↗
PubMed1985

Neurogenesis of the climbing fibers in the human cerebellum: a Golgi study.

The prenatal and early postnatal neurogenesis of the human climbing fibers of the lateral cerebellar hemispheres have been studied, with the rapid Golgi method, and correlated with the developmental stages of Purkinje cells. A transitional phase has been established in the neurogenesis of the human Purkinje cell between the second and third stages of Cajal. This phase coincides with the arrival of the climbing fibers. It is characterized by the reabsorption and subsequent transformation of Purkinje cell's basal dendrites into somatic spines. Following the arrival of the climbing fibers and the establishment of contacts, the Purkinje cell is progressively transformed from an immature stellate and nonoriented cell into a monopolar and spatially oriented one which acquires all of its mature morphological and functional features. The human climbing fibers arrive at the Purkinje cell plate by the 28th week of gestation and establish a transient paraganglionic plexus before contacts with these neurons can be recognized. They start to form pericellular nests by the 29th week, and by the 31st week of gestation all Purkinje cells of the lateral hemispheres have pericellular nests around their bodies. These pericellular nests are progressively and rapidly transformed into supracellular "capuchones" which themselves are also short-lived because the climbing process starts readily in them. Supracellular "capuchones" are recognized by the 34th seek and their fibrils start to climb the dendrites of Purkinje cells (young climbing phase) by the 36th week of gestation. The process of climbing the dendrites of the Purkinje cells will continue through late prenatal and early postnatal life. The human climbing fibers are distributed, in the internal granular layer, within narrow and long vertical territories which are transverse to the long axis of the follium. A single climbing fiber is (1) able to establish contacts with many Purkinje cells located within its narrow territory of distribution; (2) has a tendency to establish contacts with small groups of Purkinje cells rather than with isolate neurons; (3) able to send collaterals to several contiguous cerebellar folia; and (4) able to send collaterals to the internal granular layer and to form pericellular nests in it. The human cerebellum may be considered to be subdivided into a series of parallel, narrow, and transverse structural/functional planes, each one characterized by the distribution of a climbing fiber.(ABSTRACT TRUNCATED AT 400 WORDS)

Axons↗
PubMed1984

Newborn puppy cerebral acid-base regulation in experimental asphyxia and recovery.

We hypothesized that part of the newborn tolerance of asphyxia involves strong ion changes that minimize the cerebral acidosis and hasten its correction in recovery. After exposure of newborn puppies to 15 or 30 min experimental asphyxia (inhalation of gas with fractional concentration of CO2 and of O2 in inspired gas = 0.07-0.08 and 0.02-0.03, respectively), blood lactate increased to 13.2 and 23.4 mmol/l, respectively, brain tissue lactate increased to 14.4 and 19.7 mmol/kg, and cerebrospinal fluid (CSF) lactate increased to 7.6 and 14.4 mmol/l. We presume that the tissue lactate increase reflects increases in brain cell and extracellular fluid lactate concentration. The lactate increase, a change that will decrease the strong ion difference (SID), [HCO3-], and pH, was accompanied by increases in Na+ (plasma, CSF, brain), K+ (plasma, CSF), and osmolality without change in Cl-. After 60-min recovery, plasma and brain lactate decreased significantly, but CSF lactate remained unchanged. [H+] recovery was more complete than that of the strong ions due to hyperventilation-induced hypocapnia. We conclude that during asphyxia-induced lactic acidosis, changes in strong ions occur that lessen the decrease in SID and minimize the acidosis in plasma and CSF. To the extent that the increase in brain tissue sodium reflects increases in intra-and extracellular fluid sodium concentration, the decrease in SID will be less in these compartments as well. In recovery, CSF ionic values change little; plasma and brain tissue lactate decrease with a similar time course, and the [H+] is rapidly returned toward normal by hypocapnia even while the SID is below normal.

Acid-Base Equilibrium↗
PubMed1977

Erythrophagocytosis by epithelial cells of a breast carcinoma.

Erytrophagocytosis by epithelial tumor cells has been observed in metastases of ductal carcinoma of the female breast. Some malignant cells of this tumor seem to be capable of phagocytizing and digesting extravasated red blood cells with for formation of residual hemosiderin probably from their hemoglobin content. Erythrophagocytosis has been observed only in hemorrhagic areas of the tumor. Erythrophagocytosis has been observed only in hemorrhagic areas of the tumor. Although the nature of this phenomenon is unknown, it is postulated that acquired hematological disturbancess during the natural course of the malignant disease affect the surface of the red blood cells making them vulnerable to phagocytosis by the malignant cells. This case seems to represent the second time such a phenomenon has been reported in an epithelial neoplasm in man. However, it has been more frequently observed in reticulo-endothelial malignancies. The possible occurence of this phenomenon should alert pathologists to search for it in primary and metastatic epithelial tumors and in living patients to correlate pertinent hematological studies in an attempt to elucidate its possible significance.

Adult↗
PubMed1977

Developmental abnormalities of the occipital bone in human chondrodystrophies (achondroplasia and thanatophoric dwarfism).

Specific developmental malformations have been demonstrated in the occipital bone of two chondrodysplastic disorders (achondroplasia and thanatophoric dwarfism). Analysis of these malformations indicates that the occipital bone is primary affected in these disorders. In both cases, the endochondral-derived components of the occipital bone (the basioccipital, the two lateral parts, and the planum nuchale of the squama occipitalis) have failed to grow properly and are smaller and shorter than normal. On the other hand, the planum occipitalis of the squama, which derives from intramembranous ossification, is unaffected. In addition, the nature of these abnormalities indicates that the occipital synchondroses, together with the epiphyseal plates of other bones, are primarily affected in these two chondrodysplasias. The components of the occipital bone formed between the affected synchondroses failed to grow normally. The resulting malformation of the occipital bone is undoubtedly the cause of the shortening of the posterior cerebral fossa and of the considerable narrowing of the foramen magnum often described in these chondrodysplasias. It is postulated that growth disturbances between the affected occipital bone and the unaffected central nervous system results in the inadequacy of the posterior cerebral fossa and the foramen magnum to accommodate the growing brain. Consequently, compression of the brain at the posterior cerebral fossa or the foramen magnum levels could occur and thus lead to neurologic complications such as hydrocephalus and compression of the brain stem. It is suggested that the surgical removal of the fused posterior border of the lateral parts of the occipital bone (partial nuchalectomy) for the purpose of enlarging the narrow foramen magnum may be indicated in those chondrodysplastic children who develop these types of neurologic complications.

Achondroplasia↗