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At least 19 recordsLinked to original sources

Quantitation of localized abnormal deformation in asymmetric nonobstructive hypertrophic cardiomyopathy: a velocity, strain rate, and strain Doppler myocardial imaging study.

We report a case of a 10-year-old child with nonobstructive hypertrophic cardiomyopathy in whom two-dimensional echocardiography showed asymmetric septal hypertrophy with a localized thickening in the mid-septal segment. Systolic regional longitudinal motion and deformation indices were quantified by the new ultrasound-based parameters velocity, strain rate, and strain. Regional longitudinal myocardial function indices were normal for the basal and apical septal segments. The deformation parameters strain rate and strain (not the regional velocity profile) were abnormal only in the hypertrophied mid-septal segment with myofibril disarray. The concepts and advantages and clinical implications behind this quantitative approach to localizing and quantifying areas of abnormal deformation related to such myocardial disarray in localized hypertrophy are discussed.

Biomechanical Phenomena↗

[The childhood ankle joint. Deformities, abnormalities and clinical variations].

The ankle joint unites high functionality with high load on a small surface. Congenital as well as acquired variations lead to a derangement of the complex concerted action of tendons, ligaments and joints. This causes dysfunction and the development of typical deformities. It is necessary to discriminate physiological variants, congenital, posttraumatic and tumoral variations for the differential diagnosis. In most instances this is only possible with the aid of radiological clarification. Congenital malformations in the region of the upper and lower ankle joint are generally rare. One disease is club foot, with malposition and deformity in the upper and lower ankle joint. Extreme malposition can also be found in talus verticalis and congenital hypoplasias and aplasias of fibula and tibia. A rather frequently found disease, which first occurs in the adolescence, is osteochondrosis dissecans.

Adolescent↗

Spectacle fitting with ear, nose and face deformities or abnormalities.

Spectacle frame selection and dispensing remain significant components of optometry. Occasionally, we encounter patients who are unable to wear conventional spectacles due to abnormalities or deformities following injury and/or surgery to their nose, ears or head. In these cases, spectacle frame fitting may be more complex and customized frame adjustments may be required to account for the anatomical variations. A patient with a microtia (hypoplastic pinna) was fitted with a tailored spectacle frame. The details are presented together with a summary of different frames and modifications available for ears, nose and face abnormalities.

Adolescent↗

Systemic atrioventricular valve regurgitation in corrected transpositon of the great vessels. Angiographic differentiation of operable and nonoperable valve deformities.

Abnormalities of the systemic atrioventricular (A-V) valve are frequently present in patients with corrected transposition. Systemic A-V valve regurgitation is usually present and may be amenable to operative correction with valve replacement if the regurgitation is caused by normally positioned but deformed valve leaflets or a dilated valve ring, or both. Systemic A-V valve regurgitation secondary to the more common Ebstein-type malformation of the inverted tricuspid valve is an inoperable conditon at present. Displacement of the valve leaflets below the level of the valve ring may be seen in the angiocardiograms of patients with this finding and is the differentiating feature between the two lesions. Ten cases of systemic A-V valve regurgitation in patients with corrected transposition are reviewed to illustrate these features.

Adolescent↗

Abnormal myocardial deformation properties in obese, non-hypertensive children: an ambulatory blood pressure monitoring, standard echocardiographic, and strain rate imaging study.

AIMS: The prevalence of obesity is increasing among children in the developed world. The association of obesity and abnormal cardiac function is still debated. The reported changes may reflect the role of comorbidities that contribute to ventricular dysfunction. Obese children, without arterial hypertension, may be a unique clinical opportunity to evaluate the effect of obesity, per se, on myocardial function, excluding the influence of possible comorbidities. We sought to define the preclinical effects of obesity on the cardiovascular system, of healthy children with excess weight who have no other clinically appreciable cause of heart disease, using the more sensitive ultrasonic-derived strain and strain rate (SR) imaging. METHODS AND RESULTS: We studied 300 subjects divided into two groups: (i) obese children (Group O: n=150; age, 12+/-3 years); (ii) healthy lean children comparable for age, sex, and pubertal stage (Referents: n=150; mean age, 12+/-3 years). Systolic (SBP) and diastolic blood pressure (DBP), as well as 24 h-SBP and 24 h-DBP were comparable between groups. Left ventricular (LV) mass/height(2.7) was increased (P<0.0001) in Group O (46+/-12 g/m(2.7)) when compared with Referents (31+/-14 gm(2.7)). Standard echocardiographic indices of global systolic function were similar in the two groups. Intima-media thickness measured at the common carotid artery was not significantly different (P=0.4) in obese children (0.46+/-0.09 mm) when compared with Referents (0.45+/-0.07 mm). Obese children showed regional longitudinal peak systolic myocardial deformation properties (SR=-1.4+/-0.7 s(-1)) lower (P<0.0001) than those of Referents (SR=-2.2+/-0.5) in both left and right ventricle. In multivariable analysis, average peak systolic SR was significantly correlated with homeostasis model assessment of insulin resistance (P<0.01; coefficient, 0.02; SE, 0.011), and insulin serum concentration (P<0.01; coefficient, 0.05; SE, 0.023). Average LV peak systolic strain was significantly correlated with body mass index (P=0.0001; coefficient, 0.06; SE, 0.016), LVM/H(2.7) (P=0.006; coefficient, 0.016; SE, 0.018). CONCLUSIONS: Our study demonstrated that obesity, in absence of hypertension, is associated with significant reduction in systolic myocardial deformation properties already in childhood involving both right and left ventricle. Obesity not only is a risk factor for later cardiovascular disease, but also is associated with contemporaneous and significant impairment of longitudinal myocardial deformation properties.

Blood Pressure↗

Analysis of the size variability of the human normal and cleft palate fetal nasal capsule by means of three-dimensional computer reconstruction of histologic preparations.

As part of an ongoing study of cleft palate fetal morphology, normal and dysmorphic development of the human fetal nasal capsule was studied in a cross-sectional sample of 29 human fetuses (20 "normal" and 9 cleft), ranging in age from 8 to 21 postmenstrual weeks. The specimens were celloidin embedded, sectioned at 20 microns, and every tenth section stained with hematoxylin and eosin. A computer reconstruction technique was applied to produce three-dimensional representations of the nasal capsule, nasal septal cartilage, and nasal airway. Qualitatively, the cleft palate nasal capsule exhibited gross abnormalities including cartilaginous nasal septum deformities, abnormal septal volume and hypertrophy, reduced nasal airway and capsule volumes, and abnormal spatial relationships between the nasal capsule components. These results suggest that the reduced nasal airways, noted clinically in cleft perinates, may be a function of an interaction of nasal capsule deficiency and nasal septum hypertrophy. However, when lengths and volumes were plotted against fetal postmenstrual age, producing fetal "growth" curves, no significant differences (p greater than 0.05) were noted for growth rates (slopes) or nasal capsule size between the normal and cleft palate fetal samples. Curvilinear regression analysis revealed that both normal and cleft palate nasal capsule and septum lengths changed in a sigmoidal fashion, with the steepest increases from 13 to 17 weeks. In contrast, nasal capsule, airway, and septum volumes changed curvilinearly, showing slow relative growth rates from 8 to 17 weeks, which increased sharply from 18 to 21 weeks. Results suggest that from 8 to 21 weeks prenatally, normal and cleft palate specimens exhibited a similar pattern of fetal nasal capsule development that was characterized by an initial anteroposterior elongation followed by circumferential (i.e., volumetric) growth.

Cleft Palate↗

Decreased survival in vivo of diamide-incubated dog erythrocytes. A model of oxidant-induced hemolysis.

Erythrocytes from patients with chronic hemolytic variants of glucose-6-phosphate dehydrogenase (G-6-PD) deficiency have structural membrane protein abnormalities accompanied by decreased cell membrane deformability which we postulate represent the consequences of oxidant-induced membrane injury. To evaluate the pathophysiologic significance of oxidant-induced membrane injury, we studied the in vitro and in vivo effects of the thiol-oxidizing agent, diamide, on dog erythrocytes. In vitro incubation of dog erythrocytes with 0.4 mM diamide in Tris-buffered saline for 90 min at 37 degrees C resulted in depletion of GSH, formation of membrane polypeptide aggregates (440,000 and > 50,000,000 daltons) and decreased cell micropipette deformability, abnormalities similar to those observed in the erythrocytes of patients with chronic hemolytic variants of G-6-PD deficiency. In addition, diamide-incubated cells had increased viscosity and increased membrane specific gravity, but no change in ATP. Reinjection of 51Cr-labeled, diamide-incubated cells was followed by markedly shortened in vivo survival and splenic sequestration. Further incubation of diamide-incubated cells in 4 mM dithiothreitol reversed the membrane polypeptide aggregates, normalized micropipette deformability, decreased cell viscosity, prolonged in vivi survival, and decreased splenic sequestration. These studied demonstrate that diamide induces a partially reversible erythrocyte lesion which is a useful model of oxidant-induced membrane injury. They suggest that oxidant-induced erythrocyte membrane injury plays an important role in the pathophysiology of chronic hemolysis which accompanies some G-6-PD variants.

Adenosine Triphosphate↗

[The expression of red blood cell deformability in micropore filtration tests].

For the purpose of evaluating and comparing RBC deformability quantitatively with micropore filtration method, the precise meanings and applicability of physical parameters and defined indices expressing RBC deformability are discussed and analyzed in detail. The mean transit time (or the relative transit resistance) and the proportion of pore-clogging cells are found to be appropriate for representing the average deformability and the clogging characteristic of RBCs respectively. To eliminate the effects of clogging on filtration, previous studies were conducted filtration with as less clogging as possible. Investigations on experimental results from various filtration methods, however, reveal that the clogging property of RBCs contains important information on the RBC deformability. It reflects a different aspect of the RBC deformability besides the average deformability and is more sensitive to the abnormal deformability induced by physical, chemical, especially pathological factors.

Erythrocyte Deformability↗

Observations on the structure and levels of expression of murine spermatozoan abnormalities with special reference to tail deformations.

Spermatozoan abnormalities have been studied by light and electron microscopy in the cauda epididymidis of 3 month old Balb/c and C57Bl mice. A qualitative account of the different abnormality-types at both levels of microscopy is given, with special emphasis on tail-defects which have so far received little attention. Quantitative data by light microscopy are also provided in an attempt to correlate structural abnormalities with the difference in fertility between these strains.

Animals↗

Influence of tumor burden on red blood cell deformability in small cell lung cancer patients.

Red blood cell deformability was measured in 54 newly diagnosed patients with small cell bronchogenic carcinoma and in 22 normal hospital employees. Twenty-one small cell cancer patients had disease confined to one hemithorax plus draining lymph nodes (one organ system), 15 had involvement of one additional metastatic site (two organ systems), 12 had two metastatic sites (three organ systems) and 6 patients had 4 organ systems involved. Patients with one or two organ system involvement had red cell deformability results comparable to the normal control group. Patients with tumor extension to 3 or 4 organ systems had significantly decreased deformability relative to patients with lesser tumor burdens. Based on the lowest deformability results in the control population small cell cancer patients were divided into those with normal or impaired red blood cell deformability. The latter patients were significantly more anemic and had higher red cell mean corpuscular volumes than their normal counterparts. Patients with impaired deformability also had significantly elevated blood glucose levels and significantly lower serum inorganic phosphorus and iron binding capacity. Since red cell deformability is the principal determinant of capillary blood flow abnormal deformability may result in decreased tumor oxygenation and decreased, and non-uniform, delivery of chemotherapeutic agents to tumor tissue.

Adolescent↗

Erythrocyte rheology in acute cerebral thrombosis. Effects of ABO blood groups.

Within a few hours after a cerebral thrombosis in 220 patients, the flow-properties of the red blood cells (RBC) were analyzed by a filtration test that expresses quantitatively the deformability and aggregability of the RBC by the filtration indexes pT. Abnormal deformability of the RBC washed clean of plasma was found in 27.5% of the patients. Aggregability disorders, caused by the plasma trapped between the unwashed RBC, were found in 78.6% of the patients: computation of correlation coefficients between pT indexes and fibrinogen, which was found abnormally high in 88.2% of cases, demonstrated significantly that in the patients with A and B blood groups these aggregability disorders were due to fibrinogen and that they were caused by other components of plasma in patients with O and AB blood groups. All these disorders can account for blood hyperviscosity.

ABO Blood-Group System↗