Nephrotoxic serum nephritis. I. Chemical, morphologic, and functional changes in the glomerular basement membrane during the evolution of nephritis.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Comparative fine structural studies of amphibian auditory structures in urodeles have been extended to include examination of the papilliform end-organs (amphibian, neglecta and basilar) that variably occur in species selected from three families of caecilians (Gymnophiona). The species investigated were Ichthyophis kohtaoensis (Ichthyophiidae), Dermophis mexicanus (Caeciliidae) and Typhlonectes natans (Typhlonectidae). Ichthyophis is the only form to display all three papillae; both Dermophis and Typhlonectes lack a basilar papilla but all three species show both neglecta and amphibiorum. In these forms, the amphibian papilla contained the most sensory cells with ciliary bundles organized into two proximal and distal groups polarized toward a mid-line papillar axis. The papilla neglecta contained slightly fewer sensory cells and ciliary bundles oriented predominantly posteriorly. In Ichthyophis, the basilar papilla contained the lowest sensory cell counts of any papilla. Here, basilar sensory cilia were unidirectionally polarized away from the saccule. All papillae were overlain by an essentially similar, extracellular tectorial body. When compared to auditory end-organs in the urodeles and anurans, similar conditions in caecilians are suggestive of a common ancestry for the basilar and amphibian papillae; features of the amphibiorum indicate further that it may represent part of a "displaced" papilla neglecta.
The evolution of destructive and restorative alterations was morphologically followed up in 82 tuberculotics that died of non-tiberculous diseases. In the majority of the deceased, the restorative alterations were observed with manifested mesenchymal and immunologic reactions with morphological peculiarities as in the treated with anti tuberculous remedies. The destructive alteration are clearly manifested and the restorative manifestations are depressed in tuberculotics with non-treated diabetes and osteomyelitis treated with cortison. In a negligible part of the patients died of non-tuberculous diseases, a reactivation of the foci developed around the fibrocaseous lung foci, tracheobronchial lymph nodes, kidneys and suprarenals, manifested with filamented neutrophyils in the calcified and caseous matter, fresh necrosis, tubercula, specific granular tissue, friable capsule with appearance of lymphoid cells and specific granular tissue.
The purpose of this paper has been to find out the prevalence of herpetic cervicitis among routine surgical cervical biopsies, categorize the morphological changes and study their evolution. In a 51-month-period, 879 human uterine cervices were examined histologically, 19 percent (168) conforming to predetermined criteria for herpetic cervicitis. These criteria were typed as A through D starting with nuclear homogenization and passing through vesicle formation, bulla formation and finally ulceration. The type D lesion showed an agglomeration of Type A-C morphological changes occurring together, in addition to which focal submucosal haemorrhages were seen with severe congestion. The presence of the Herpes virus was confirmed with the Peroxidase-Antiperoxidase stain and the evolution of the bullae studied by means of the Alcian Blue-Periodic Acid Schiff stain (AB-PAS), Methyl Green-Pyronine (MG-P) stain and the Reticulum stain.
Rapid evolution of reproductive traits has been attributed to sexual selection arising from interaction between the sexes. However, little is known about the nature of selection driving the evolution of interacting sex-specific phenotypes. Using populations of Drosophila melanogaster selected for divergent sperm length or female sperm-storage organ length, we experimentally show that male fertilization success is determined by an interaction between sperm and female morphology. In addition, sperm length evolution occurred as a correlated response to selection on the female reproductive tract. Giant sperm tails are the cellular equivalent of the peacock's tail, having evolved because females evolved reproductive tracts that selectively bias paternity in favor of males with longer sperm.
The adaptive radiation of mammalian clades has involved marked changes in limb morphology that have affected not only the skeleton but also the integumentary structures. For example, didelphid marsupials show distinct differences in nail and claw morphology that are functionally related to the evolution of arboreal, terrestrial, and aquatic foraging behaviors. Vespertilionoid bats have evolved different volar pad structures such as adhesive discs, scales, and skin folds, whereas didelphid marsupials have apical pads covered either with scales, ridges, or small cones. Comparative analysis of pad and claw development reveals subtle differences in mesenchymal and ectodermal patterning underlying interspecific variation in morphology. Analysis of gene expression during pad and claw development reveals that signaling molecules such as Msx1 and Hoxc13 play important roles in the morphogenesis of these integumentary structures. These findings suggest that evolutionary change in the expression of these molecules, and in the response of mesenchymal and ectodermal cells to these signaling factors, may underlie interspecific differences in nail, claw, and volar pad morphology. Evidence from comparative morphology, development, and functional genomics therefore sheds new light on both the patterns and mechanisms of evolutionary change in mammalian limb integumentary structures.
The morphological, ecological, and clinical diversity among ascomycete fungi that are pathogenic to humans suggest that the potential for pathogenicity may have arisen multiple times within these higher fungi. We have obtained 18S ribosomal DNA sequences from a diverse group of human pathogenic fungi in order to determine their evolutionary origins. The fungi studied include a skin pathogen that is confined to humans (Trichophyton rubrum) and three systemic, facultative parasites that cause histoplasmosis (Histoplasma capsulatum), blastomycosis (Blastomyces dermatitidis) and coccidioidomycosis (Coccidioides immitis) in humans and other higher animals. Also included in our analysis are representatives of non-pathogenic fungi, as well as two opportunistic pathogens, Pneumocystis carinii and Candida albicans, that cause severe disease in immunocompromised individuals, especially those with AIDS. Two of the fungi we sequenced, T. rubrum and C. immitis, are limited to asexual modes of reproduction and therefore lack the sexual structures that are most useful for evolutionary comparison as well as being essential for classification among the higher fungi. Coccidioides immitis is particularly problematic owing to its contradictory and confusing asexual morphologies, which have caused it to be placed in three fungal classes and the protista. Our analysis shows that the specialized, superficial parasite and the systemic, facultative parasites, including C. immitis, are closely related ascomycetes, which clearly demonstrates the power of molecular characters to compensate for missing or confusing reproductive morphology. Analysis also shows that the opportunistic pathogens are more distantly related, with the likely explanation that pathogenicity has arisen more than once within the Ascomycetes.
Genetic relationships among 25 species of Central and South American Bufo and among representative North, Central, and South American, Asian, and African Bufo were probed, using the quantitative immunological technique of microcomplement fixation (MC'F) which indicated a clear separation of North, Central, and South American lineages of Bufo. The South American lineage likely diverged from the Central and North American lineages in the Eocene; the latter two lineages diverged later, probably in the mid-Oligocene. Some species groups of South American toads, defined on the basis of traditional morphological studies, are genetically quite similar within groups, whereas others are genetically divergent. The amount of albumin evolution does not appear to parallel the amount of karyotypic, morphological, ecological, or behavioral evolution documented. Comparisons suggest that the African lineages separated from the American and Asian lineages in the late Cretaceous, corresponding to the time of the final separation of Gondwanaland, the southern supercontinent including the modern continents of South America, Africa, Australia, Antarctica, and India. The Asian lineages diverged from the lineage giving rise to all of the American species in the early Paleocene.
How new discrete states of morphological traits evolve is poorly understood. One possibility is that single-gene changes underlie the evolution of new discrete character states and that evolution is dependent on the occurrence of new single-gene mutations. Another possibility is that multiple-gene changes are required to elevate an individual or population above a threshold required to produce the new character state. A prediction of the latter model is that genetic variation for the traits should exist in natural populations in the absence of phenotypic variation. To test this idea, we studied traits that are phenotypically invariant within teosinte and for which teosinte is discretely different from its near relative, maize. By employing a QTL mapping strategy to analyze the progeny of a testcross between an F(1) of two teosintes and a maize inbred line, we identified cryptic genetic variation in teosinte for traits that are invariant in teosinte. We argue that such cryptic genetic variation can contribute to the evolution of novelty when reconfigured to exceed the threshold necessary for phenotypic expression or by acting to modify or stabilize the effects of major mutations.
The rat and turtle differ markedly in major structural features of the corticocerebellorubrospinal circuitry. Although both species have a well-developed cerebellorubrospinal system, they differ in that a direct cerebral cortical input to the red nucleus is present only in the rat. The aim of the present study was to compare features of the soma and dendritic morphology of rubrospinal neurons that receive cortical input, as in rats, with those that do not, as in turtles. Intracellular Lucifer Yellow injections of neurons retrogradely labeled with Fast Blue in the rat or activity-dependent sulforhodamine-labeled neurons in the turtle were used to fill rubrospinal neurons in 150-200-microm-thick fixed sections. Images of filled neurons were imported into a computer to analyze quantitatively soma and dendritic morphology. The results show that rubrospinal soma size is slightly larger in the rat than in the turtle. However, analysis of the dendritic morphology, including total dendritic length, length of primary, secondary, and tertiary dendritic branches, and a Scholl analysis of dendritic branch intersections across concentric rings, demonstrated no significant differences between the two species. These findings suggest that the basic dendritic morphology of rubrospinal neurons may have been established early in phylogeny, preceding the evolution of cortical inputs. Alternatively, similar dendritic morphologies may have arisen due to the presence of other synapses in the turtle that occupy the sites of the cortical input in the rat. This comparative approach provides insights into the information processing capabilities of cortically versus subcortically controlled motor systems.
A morphological association between genitalia and ejaculates could provide insight into the function and evolution of genitalia. In this study, the morphologies of the ejaculates and male genitalia of 15 species of Pterostichini and two species of Platynini (Coleoptera: Carabidae) are described. All the species examined formed a spermatophore, the morphology of which could be classified into three types based on its relative volume in the female vaginal cavity and the presence or absence of a pluglike conformation. Male genital morphology could be divided into two types by the direction of the endophallus and gonopore. Species with a strongly bent endophallus invariably formed a pluglike spermatophore. The results suggest that the peculiar shape of endophallus found in some species of Pterostichini may function in forming the pluglike structure of the spermatophore.
Lung morphology in ARDS reflects the rapid evolution from interstitial and alveolar edema to end-stage fibrosis consequent to injury of the alveolocapillary unit. This morphologic progression, termed diffuse alveolar damage, has been subdivided into sequentially occurring exudative, proliferative, and fibrotic phases. Pulmonary lesions correlate with the phase of alveolar damage rather than its specific cause. The pathologic features are consistent with the effects of a host of injurious stimuli and the complex interaction of inflammatory mediators on alveolar epithelial and capillary endothelial cells. Although ARDS frequently culminates in "interstitial" fibrosis, the organization of intraluminal exudate dominates the histologic picture in the proliferative phase and establishes the framework for subsequent fibrous remodeling of the lung. Involvement of the pulmonary vasculature is an important aspect of ARDS, from the initial phase of edema to the terminal stage of intractable pulmonary hypertension. Vascular lesions include thrombotic, fibroproliferative, and obliterative changes that, like the parenchymal lesions, correlate with the temporal phase of DAD. Although ARDS is characterized by extensive bilateral lung involvement, alveolar damage can also affect the lung in a localized fashion. RAD is associated with the same clinical risk factors as DAD, suggesting that there is a spectrum in the extent of lung involvement and disease severity in patients at risk for ARDS. The factors that govern which patients will develop the fulminant syndrome are poorly understood. It must be re-emphasized that the lung is stereotyped in its response to injury and, consequently, descriptive, or even quantitative, studies of lung morphology can only provide clues regarding the initiating factors and pathogenetic mechanisms of ARDS. Progress in understanding the pathogenesis of ARDS and development of rational approaches to therapy will ultimately depend on careful clinical and experimental studies and the application of immunohistochemical and molecular biology techniques to unravel basic mechanisms of cellular injury and response.
The genetic coupling of morphology and behaviour means that the evolution of the two types of traits will not be independent: changes in behaviour will result in changes in morphology and vice versa. This might explain nonadaptive differences in morphology through indirect selection on correlated characters of other categories. Genetic correlations between morphology and behaviour are also the basis for some models of sympatric speciation and of the stability of polymorphisms. Morphology and behaviour are often correlated in nature and a genetic basis for such couplings has been demonstrated. I present here evidence that colour pattern and antipredator behaviour are genetically coupled in natural populations of the garter snake Thamnophis ordinoides. Similar phenotypic correlations between pattern and behaviour exist among species of North American snakes, indicating that selection for particular combinations of traits may help to maintain genetic covariances and colour polymorphism in Thamnophis ordinoides.
Lung morphology in ARDS reflects the rapid evolution from interstitial and alveolar edema to end-stage fibrosis consequent to injury of the alveolocapillary unit. This morphologic progression, termed diffuse alveolar damage, has been subdivided into sequentially occurring exudative, proliferative, and fibrotic phases. Pulmonary lesions correlate with the phase of alveolar damage rather than with its specific cause. As suggested by experimental models of acute lung injury, the pathologic features seen in humans are consistent with the effects of a host of injurious stimuli and the complex interaction of inflammatory mediators on alveolar epithelial and capillary endothelial cells. Although ARDS frequently culminates in "interstitial" fibrosis, the organization of intraluminal exudate dominates the histologic picture in the proliferative phase and establishes the framework for subsequent fibrous remodeling of the lung. Involvement of the pulmonary vasculature is an important aspect of ARDS, from the initial phase of edema to the terminal stage of intractable pulmonary hypertension. Vascular lesions include thrombotic, fibroproliferative, and obliterative changes, which, like the parenchymal lesions, correlate with the temporal phase of diffuse alveolar damage. Although ARDS is characterized by extensive bilateral lung involvement, alveolar damage can affect the lung in a localized fashion. "Regional alveolar damage" is associated with the same clinical risk factors as diffuse damage, suggesting that there is a spectrum in the extent of lung involvement and disease severity in patients at risk for ARDS. The factors that govern which patients will develop the fulminant syndrome are poorly understood. It must be re-emphasized that the lung is stereotyped in its response to injury, and, consequently, descriptive, or even quantitative, studies of lung morphology can only provide clues regarding the initiating factors and pathogenetic mechanisms of ARDS. Progress in understanding the pathogenesis of ARDS and the devising of rational approaches to therapy will ultimately depend on careful clinical and experimental studies that unravel basic mechanisms of cellular injury and response. The course of these investigations must be guided by and constantly correlated with the pathologic features that occur in humans.
Oncomelania snails are the intermediate hoste of Schistosoma japonicum in Asian countries. In order to understand the genetic and morphological variation of Oncomelania snails in mainland China, field snails from 31 localities were collected and investigated by means of allele enzyme electrophoresis and numerical taxonomical technics. Results demonstrated that out of 17 loci examined, seven polymorphic loci were presented. Genetic distance (Nei, 1978) among the populations varied from 0.03 to 0.27. The phenogenetic tree based on UPGMA cluster analysis showed that genetic diversity corresponded to geographic distribution along the Yangtze River, which provided supplementary genetic data about the evolution of Oncomelania spp. A morphological study showed that Mahalanobis' morphological distance ranged from 1.53 to 346.7. Both genetic and morphological data indicated that the diversity among populations of smooth shelled snails was higher than that among populations of ribbed shelled snails. A positive correlation (r = 0.80) between Mahalanobis' morphological distance and genetic distance supports the hypothesis that the different shell phenotypes represent different species or subspecies.
The recent findings that key developmental genes are conserved across animal phyla have led to descriptions of evolutionary change in development based on the recruitment of these few molecules. This approach, however, encounters problems in assigning homology across long evolutionary distances. By contrast, reproducibility of the cell lineage of free-living soil nematodes (order Rhabditida) and conservation of larval blast cells across nematode species permit evolutionary comparisons of developmental mechanisms among nematodes at the cellular level. Such comparative studies uncover an unexpected flexibility of developmental mechanisms: Large evolutionary differences have been described between invariant and noninvariant lineages, in the cellular mechanisms specifying a given cell (for instance, the gonadal anchor cell), in the subcellular events leading to asymmetric divisions (for instance, the first division of the egg), and in redundant networks of cell interactions (for instance, those specifying the centered pattern of vulva precursor fates). Interestingly, redundancy of developmental mechanisms favored by selective pressure allows in turn for evolution of these mechanisms. Such evolutionary changes in developmental mechanisms specifying cell fates can occur in the absence of obvious morphological change, which rather correlates with evolution of cell fates per se: death, division, migration, and differentiation (for instance, in the reduction of the posterior gonadal arm in monodelphic species or in change in vulva position).
The architecture of gene action during development is relevant to phenotypic evolution as it links genotype to morphological phenotype. Analysis of development at the level of cell fate specification mechanisms illuminates some of the properties of developmental evolution. In this article, we first review examples of evolutionary change in mechanisms of cell fate specification, with an emphasis on evolution in the dependence on inductive signaling and on evolution of the mechanisms that result in spatial asymmetries. We then focus on properties of development that bias possible phenotypic change and present how the distribution of phenotypes that are available by mutational change of the starting genotype can be experimentally tested by systematic mutagenesis. We finally discuss ways in which selection pressures on phenotypes can be inferred from a comparison of the phenotypic spectrum found on mutation with that found in the wild.