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Technological advances have made possible the development of high-resolution genetic linkage maps for the mouse. These maps in turn offer exciting prospects for understanding mammalian genome evolution through comparative mapping, for developing mouse models of human disease, and for identifying the function of all genes in the organism.
Sequence data are now available for almost the entire complement of mitochondrial rRNAs from five fungi: Schizosaccharomyces pombe, Saccharomyces cerevisiae, Toropulis glabrata, Aspergillus nidulans and Neurospora crassa. Analysis of these data show that the five mitochondria can be related to a common ancestor. The unusually high similarity between some S. pombe mt tRNAs may be due to a process similar to gene conversion. Using the number of differences between tRNA pairs as a measure of the evolutionary rate the yeast-S. pombe branch has paradoxically a high nuclear rate and a low mt rate of evolution as compared with other branches in the phylogenetic tree. Finally the position of mt tRNA genes in S. pombe is abnormally distinct from gene orders in other mitochondria. All of the above factors must be taken into account when describing the relationship between these mitochondria.
The authors reviewed current criteria on hormone-dependence in functional thyroid cancers, presenting data of compared disease evolution based on the casuistics of thyroid carcinomas from the files of the Fundación Jiménez Díaz, with 5 and 10 year follow-up studies in some of the cases. They found a higher number of survivors among the patients with papilliferous carcinoma in both 5 and 10 year follow-up groups whom, aside total surgical removal of the gland and the administration of thyroid extracts, those who had thyroid residues left were given 100 mc of 131I. Among the patients with follicular adenocarcinoma, under the same comparative conditions, differences were not very clear in the 5 year follow-up group, while the 10 year follow-up group showed marked differences. The authors conclude that an adequate combination of the three therapeutic procedures may allow a higher survival rate.
The genus Rattus has two related families of satellite DNA: Satellite I consists of tandem arrays of a 370 base pair repeat unit which is a dimer of two 185 base pair portions (a, b) which are about 60% homologous. Satellite I' consists of tandem arrays of a 185 base pair repeat unit (a') which is about 85% homologous to a and 60% homologous to b. R. norvegicus contains only satellite I but R. rattus contains both satellites I and I'. We examined certain aspects of satellite DNA evolution by comparing the spacing at which variant repeat units of each satellite have spread among non-variant repeat units in these two species. With but one exception, in R. rattus, 15 different variant repeat units have spread among non-variant repeat units of satellite I, with a spacing equal to the length of the (a,b) dimer. Similarly, fourteen different variant repeat units of the monomeric satellite I' have mixed among non-variant repeat units with a spacing equal to the length of the (a') monomer. These results suggest that a mechanism involving homologous interaction among satellite sequences could account for the spread of variant family members. We also found that a sequence variant present in certain portions of the dimeric repeat unit of satellite I is more efficiently amplified (or less efficiently corrected) than variants occurring in other regions. This was not true for the monomeric repeat unit of satellite I'.
Twenty seven newborn with serious meconial aspiration syndrome are studied. Two groups are stablish weather they require or not mechanical ventilation during evolution. When comparing various perinatal and clinical data, only the Silverman test showed statistically significant differences; pH and gases in blood during the first hours of life did not showed differences. Pneumothorax incidency in both groups was 33%. Twelve newborn required mechanical ventilation. The starting age was 24 hours of life range 3-54 hours. Most frequent indication was hipoxemia and apnea. Use of intermitent positive pressure improved PaCO2 with a light increase in PaO2 though it also increased alveolo-arterial oxygen gradient. Hipoxemia was the most relevant data in evolution of these patients. In seven cases continuous distending pressure was applied, with a light increase in PaO2 only in three patients. No patient suffered pneumothorax during mechanical ventilation. In patients with mechanical ventilation mortality was 25%. The possibility of an addition in certain cases of pulmonary hypertension with right-to-left shunting ductal and atrial is reported.
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.
Recent molecular data indicate that the antigen-specific combinatorial immune response is restricted to jawed vertebrates where it is found in representatives of all class from cartilagenous fishes to mammals. Here, we analyse the relatively rapid emergence of the combinatorial system terms of three stochastic process, with the system reaching essentially full capacity in immunoglobulin recognition elements and diversification and recombination of gene segments in an evolutionary span of time of less than 20 million years. The mechanisms for inducibility were coopted from ancient and widely spread processes in phylogeny for regulation of cell division. The proposed process of formation entailed the evolution of unknown ancestral genes into those specifying bona fide immunoglobulin domains, and the generation of multiple copies of these via a series of events facilitated by horizontal transfer of site-specific recombinases and recombination signal sequences most probably from microbial and fungal sources. The second process is one of rapid "decay" (evolution) which occurred in about 10 million year under stringent selective conditions to generate proper conserved canonical sequences. The third process is that of the long term evolution of these characteristic immunoglobulin domains over the 450 million years since their emergence. As a first approximation the rates of these three processes were computed using first order differential equations. The rate of formation has a magnitude of 10-7 substitutions per site per year, and that of rapid modifications is 10-8 substitutions per site per year. The long term rate of immunoglobulin evolution is comparable to that of other moderately conserved proteins, (1-3) x 10-9 substitutions per site per year). This model is testable by searching for "footprints" of microbial and fungal DNA processing enzymes and recombination mechanisms. The hypothesis raises the general concept that horizontal transfer of genes facilitating rearrangement and duplication can catalyse major steps of macroevolution.
As a first step toward understanding their mechanism of morphological evolution, we compare the morphology and development of the male genitalia in 10 species of Rhabditidae, the family of nematodes that includes Caenorhabditis elegans. We describe a number of variable morphological characteristics and focus in particular on the differing arrangements of the caudal papillae or rays within the acellular fan. We analyze the development of the ray cells within the epidermis of the last larval stage and identify changes in cell positions and cell contacts that underlie evolutionary changes in the arrangement of the rays. Epidermal cell positions were determined by means of indirect immunofluorescence staining with a monoclonal antibody directed towards adherens junctions. Similarities between the species in the cellular arrangements during the earliest developmental stages allow us to propose homologies between the rays in different species. Evolutionary changes in the positions and order of homologous rays are correlated with shifts in cell positions during development. The results suggest that genes for cell recognition or adhesion proteins, or pattern formation genes that regulate cell recognition or adhesion proteins, may be important foci of evolutionary change affecting morphology.
To explore the extent to which the X chromosome has been conserved during mammalian evolution, we compared six loci that are X-linked in the human genome with the corresponding genes of the North American marsupial, the Virginia opossum (Didelphis virginiana). Our analysis shows that in the opossum genome there are sequences highly homologous to those of human cDNAs for housekeeping genes, glucose-6-phosphoribosyltransferase (HPRT), phosphoglycerate kinase A (PGK1), and alpha-galactosidase A (GLA). However, ornithine transcarbamylase and blood clotting Factor IX--tissue-specific genes that are X-linked in eutherians mammals--have no highly conserved homologs in the marsupial genome. By cloning opossum G6PD and HPRT, we found that these genes are X-linked in the opossum and that homologous sequences are limited to coding regions. As all genomic fragments hybridizing with the human GLA probe show dosage effects, it is likely that the opossum counterpart is X-linked. Finally, the pattern of hybridization suggests that the autosomal pseudogenes of HPRT and PGK1 in the opossum have remained highly homologous to the human X-linked genes.
From 1976 to 1994, we followed 55 children with occult spinal dysraphism (OSD). The average age at diagnosis was 4.5 years (range: 24 days - 21 years). In 13 cases the OSD was associated with anorectal anomalies. Urologic symptoms were present at diagnosis in 24 children (43%), but urinary incontinence affected all patients in the evolution of the OSD. At diagnosis, all children underwent complete neurourologic and urodynamic evaluation. Nine required early neurosurgical correction, before 3 years of age. During follow-up, intermittent clean catheterization was started in all patients. Vesicoureteral reflux was present or developed in 17 patients: 15 underwent endoscopic procedures and 2 required bladder augmentation because of upper-tract and renal-function deterioration. Endoscopic treatment for urinary incontinence was performed in 3 children. At long-term follow-up (6 to 18 years), socially acceptable continence was achieved in 78% of the children; renal failure occurred in 8. The long-term results were analyzed in order to compare the evolution of urinary continence and renal function in children with OSD with or without neurosurgery.
From 1976 to 1994, we followed 55 children with occult spinal dysraphism (OSD). The average age at diagnosis was 4.5 years (range: 24 days - 21 years). In 13 cases the OSD was associated with anorectal anomalies. Urologic symptoms were present at diagnosis in 24 children (43%), but urinary incontinence affected all patients in the evolution of the OSD. At diagnosis, all children underwent complete neurourologic and urodynamic evaluation. Nine required early neurosurgical correction, before 3 years of age. During follow-up, intermittent clean catheterization was started in all patients. Vesicoureteral reflux was present or developed in 17 patients: 15 underwent endoscopic procedures and 2 required bladder augmentation because of upper-tract and renal-function deterioration. Endoscopic treatment for urinary incontinence was performed in 3 children. At long-term follow-up (6 to 18 years), socially acceptable continence was achieved in 78% of the children; renal failure occurred in 8. The long-term results were analyzed in order to compare the evolution of urinary continence and renal function in children with OSD with or without neurosurgery.
OBJECTIVES: To compare the evolution of stenoses responsible for acute coronary events with those not associated with acute coronary syndromes. METHODS AND RESULTS: We prospectively studied angiographic stenosis progression in 190 stable angina patients, with single vessel disease, who were awaiting non-urgent coronary angioplasty. Sixty four patients had a previous history of unstable angina (Group 1) and 126 patients had no history of unstable angina (Group 2). Culprit stenoses were classified as "complex' or "smooth'. At restudy, 8 +/- 4 months after the first angiogram, 12 of 63 culprit stenoses in Group 1 had progressed and seven of 125 in Group 2 (19% vs 6%, P = 0.0044). Thirteen of 68 complex culprit stenoses had progressed, compared with only 6 of 120 smooth culprit stenoses (19% vs 5%, P = 0.003). Coronary events occurred in 12 Group 1 patients and nine Group 2 patients (P = 0.02). CONCLUSIONS: In patients with stable angina, stenoses associated with previous episodes of unstable angina are more likely to progress than stenoses not associated with previous unstable angina. Unstable coronary atherosclerotic plaques, even those that have been clinically stable for more than 3 months, may retain the potential for rapid progression to total occlusion.
We accessed the potential impact of diabetes mellitus and hyperglycemia on early prognosis in a study of 109 cases of CT proved brain infarction. Main end-points of this study were 30-days case-fatality rates and the probability of early discharge or prolonged hospitalization. Proportions of patients exhibiting diverse evolutions were compared by Fisher's test and, when the number of observations permitted, by chi-square test. Diabetes mellitus was diagnosed by history in 15.6% (17 patients). In 86 cases analysed within 72 hours of admission, hyperglycemia (glucose level higher than 110 mg/dL) was detected in 67.4% (including all 14 diabetic patients (35.3% vs 21.7%; p = 0.18), but these patients probably were discharged early less frequently (23.5% vs 51.1%; p = 0.06). Compared to the normoglycemic patients, hyperglycemic patients also fared worse, when considering altogether the early discharge and case fatality rates and the need for prolonged hospitalization (p = 0.06). They also exhibited a nonsignificant increase in early case fatality rate (31% vs 15.4%; p = 0.21) and a markedly reduced chance of obtaining early hospital discharge (37.9% vs 65.4%; p = 0.03). Case fatality rates were maximal in diabetic hyperglycemic patients (42.9%) and seemed intermediate in non-diabetic hyperglycemic patients (27.3%). Considering the three end-points evaluated, the apparent differences between non-diabetic hyper and normoglycemic patients did not reach statistical significance (p = 0.19). These results suggest that both diabetes mellitus and hyperglycemia "per se" have deleterious effects on the clinical evolution of patients with cerebral infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
Walker's 256 carcinosarcoma a transplantable tumor of the rate changes its behaviour as a consequence of various factors. In this paper we compare the evolution of 2 lines of the tumor: WM 16 (muscular) and Christ Hospital (ascitic) both inoculated intramuscularly. Animals receiving line WM 16 had a severe rapidly progressive evolution dying around day 14 after inoculation with diffuse metastases to lymph nodes (65% of animals), kidneys (53%), spleen (50%), lungs (46.5%), liver (45%), bone marrow (44.8%), in 56% of the animals there were circulating tumoral cells. Animals receiving Christ Hospital line survived up to 40 days, metastases were limited do lungs (48.7%) and lymph nodes (31.7%) and only in 2 of 45 animals circulating tumoral cells were observed.
The cDNAs encoding the catfish prepro-gonadotropin-releasing hormone and the chicken prepro-gonadotropin-releasing hormone II of the African catfish (Clarias gariepinus) have been isolated and sequenced. The catfish gonadotropin-releasing-hormone precursor and the chicken gonadotropin-releasing-hormone-II precursor have the same overall architecture as other gonadotropin-releasing-hormone precursors identified so far; each is composed of a signal peptide, gonadotropin-releasing hormone and a gonadotropin-releasing-hormone-associated peptide which is connected to gonadotropin-releasing hormone and chicken gonadotropin-releasing hormone II, in combination with the Gly-Lys-Arg sequence, are highly conserved during evolution when compared with the corresponding regions of mammalian, avian (chicken gonadotropin-releasing hormone I) and other fish gonadotropin-releasing-hormone precursors. However, the gonadotropin-releasing-hormone-associated peptide regions are markedly divergent. Northern-blot analysis revealed the presence of a single catfish gonadotropin-releasing-hormone mRNA species of about 470 bases, and the presence of a single chicken gonadotropin-releasing-hormone-II mRNA species of about 650 bases in the African catfish brain. In situ hybridization revealed catfish gonadotropin-releasing-hormone cell bodies rostro-caudally scattered in the olfactory nerve, along both sides of the midline of the telencephalon, in the preoptic area of the ventral hypothalamus, and in the infundibular stalk close to the pituitary. Chicken gonadotropin-releasing-hormone-II cell bodies, however, were exclusively found in the midbrain tegmentum.
OBJECTIVES: We sought to compare the evolution of complex and smooth stenoses within the same coronary tree in patients with stable coronary artery disease. BACKGROUND: Progression of coronary stenosis has prognostic significance and may be influenced by local and systemic factors. Stenosis morphology is a determinant of disease progression, but no previous study has systematically assessed progression of complex and smooth stenoses within the same patient. METHODS: We studied 50 men with stable angina who 1) had one complex coronary stenosis and one smooth stenosis in different noninfarct-related coronary vessels at initial coronary angiography, and 2) had a second angiogram after a median interval of 9 months (range 3 to 24). Patients with lesions > or = 10 mm long, at a major branching point or with > 85% diameter reduction were not included. Coronary lesions were measured quantitatively from comparable end-diastolic frames. Stenosis morphology was determined qualitatively by two independent observers. RESULTS: All patients remained in stable condition during follow-up. Progression, defined as an increase in diameter stenosis by > or = 15% was seen in only eight complex stenosis (16%) but in no smooth lesions (p < 0.01). The severity of complex stenoses changed more than that of corresponding smooth stenoses (mean +/- 1 SD 5.8 +/- 13% vs. -0.06 +/- 6%, p < 0.01). On average, the annual rate of growth was 11.4 +/- 28% and 1.5 +/- 14% for complex and smooth lesions, respectively (p < 0.01). CONCLUSIONS: Few coronary stenoses progress rapidly in stable angina. Complex and smooth coronary stenoses progress at different rates within the same coronary tree. complex stenosis morphology itself is an important determinant of progression of stenosis in patients with apparently clinically stable coronary artery disease.
Many statistics demonstrate a definite improvement of myocardial infarction during hospitalization, especially a decrease in the mortality. It appears tempting to credit that improvement to the numerous modifications of the treatment of this dangerous disease in the last few decades. The study reported here indicates, however, that other factors must be taken into account. We compared the evolution of two groups of patients hospitalized for acute myocardial infection, 10 years apart: The first group (G1) of 731 patients corresponds to years 1970-1975; the second group (G2) of 729 patients, corresponds to the years 1984-85-86. During these ten years, mortality decreased by 38 p. cent, from 19.2 p. cent (G1) to 11.9 p. cent (G2). This decrease remains significant regardless of age and sex, except in two subgroups with the least number of patients, i.e. women under the age of 65 and men over 65. It should be noted that rhythm disorders occur with the same frequency in both sub-groups while atrio-ventricular blocks seem to have decreased. The difference in the mortality cannot be attributed to the patient's selection. In fact, in both groups, they are comparable regarding the men/women ratio, the age distribution and the presence of main risk factors (tobacco abuse, dyslipidemia, arterial hypertension, diabetes, heredity). The treatment results in many alterations especially concerning diuretics which seem to be used in approximately 30 p. cent of the patients in both groups. On the contrary, steroids, prescribed in 25.3 p. cent of G1 patients are abandoned; electro-systolic stimulation established in 21.2 p. cent of G1 patients, concerned only 4 p. cent of G2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
In discussions about the relative rate of molecular evolution, intraspecific variability in rate is rarely considered. An underlying assumption is that intraspecific sequence differences are small, and thus variations in rate would be difficult to detect or would not affect comparisons among distantly related taxa. However, several studies on mammalian mitochondrial DNA (mtDNA) have revealed considerable intraspecific sequence divergence. In this report, we test for differences in the rate of intraspecific evolution by comparing mtDNA sequences, as inferred from restriction site polymorphisms and direct sequencing, between mtDNA genotypes of the eastern African black-backed jackal, Canis mesomelas elongae, and those of two other sympatric jackal species. Our results are unusual for several reasons. First, mtDNA sequence divergence within several contiguous black-backed jackal populations is large (8.0%). Previous intraspecific studies of terrestrial mammals have generally found values of less than 5% within a single population, with larger divergence values most often occurring among mtDNA genotypes from geographically distant or isolated localities. Second, only 4 mtDNA genotypes were present in our sample of 64 jackals. The large sequence divergence observed among these mtDNA genotypes suggests there should be many more genotypes of intermediate sequence divergence if they had evolved in sympatry. Finally, estimates of the rate of mtDNA sequence evolution differ by approximately 2- to 4-fold among black-backed jackal mtDNA genotypes, thus indicating a substantial heterogeneity in the rate of sequence evolution. The results are difficult to reconcile with ideas of a constant molecular clock based on random fixation of selectively neutral or nearly neutral mtDNA sequence mutations.