Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A morphological analysis of 346 biopsy specimens from 140 patients with chronic cystitis permits one to evaluate a nonproliferative and proliferative forms of the disease as well as the squamous-cell metaplasia (leukoplakia) of urothelium as the risk diseases in the development of bladder cancer. Among them only the cases with dysplasia foci of urothelium or the squamous-cell metaplasia with acanthosis or dysplasia from the risk group belonging to bladder precancer. The early ultrastructural signs of urothelial dysplasia are determined; among them the proliferation of the undifferentiated cells with an increased nuclear-cytoplasmic ratio, the disappearance of asymmetrical mutual membrane, vesicular apparatus and cytoplasmic polarity of the superficial cells are to be distinguished.
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PMID:[Morphology of precancerous mucosal changes in the bladder]. 409 93

Dysplasia epiphysealis hemimelica is a condition characterised by asymmetrical and uneven growth of the epiphyses of the long bones of the limbs and of the bones of the tarsus and carpus. The growth disturbance is caused by the development of accessory nuclei that exhibit histological and histochemical features similar to those found in ossifying epiphyseal cartilage and in the ossific centres of developing carpal and tarsal bones. The common histogenesis, as confirmed by the authors, could explain the elective localisations of the disorder.
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PMID:Dysplasia epiphysealis hemimelica. Clinical, histological and histochemical features. 641 54

The authors report their experience of 20 cases of renal artery stenosis in children, seen over the last ten years. The stenosis was latent in 8 of the 20 cases and was usually discovered during investigation for headaches or a complication of hypertension. The search for a renal cause involved the use of urography (which shows the classical signs of asymmetrical kidney size, delayed excretion, very sharp image, asymmetry on the fluid load test) (19 of the 20 cases) and arteriography which, in 5 cases, showed a bilateral lesion. Almost all of the anatomical lesions were situated in the arterial trunk (20 out of 25), 4 lesions were at the bifurcation of the trunk and only one lesion involved a branch. The most common lesions were dysplasia and hyperplasia of the arterial wall. These lesions were treated by aorto-renal by-pass grafting (without any synthetic prosthesis) in 8 cases, by direct re-implantation into the aorta in 5 cases, by spleno-renal anastomosis in 5 cases, by resection and anastomosis in 4 cases, by enlargement venous angioplasty in 1 case and by auto-transplantation in 1 case. The following results were obtained: 9 cures (45%), 3 moderate results (15%) and 8 failures (40%), including 7 cases of early thrombosis and 1 delayed stenosis. The cases treated by direct aorto-renal re-implantation or by resection and end-to-end anastomosis were always successful. The failures occurred in children operated by one of the other techniques of arterial repair. Surgery provided these authors with excellent or satisfactory results in 60% of cases.
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PMID:[Results of reconstructive surgery of renal artery stenosis in children]. 667 80

Eighteen children with unilateral dysplasia of the hip were found to have asymmetrical gluteal folds and an apparent limb-length inequality secondary to pelvic obliquity caused by an abduction contracture of the contralateral hip. The dysplastic hip was on the left in all but one patient. As a result of the pelvic obliquity, the femoral head on the high side of the pelvis was directed superolaterally, stretching the relaxed capsule still farther. The femoral head was then not concentrically reduced, and the pressure it caused on the superior border of the labrum contributed to the development of the acetabular dysplasia. The eighteen dysplastic hips were treated with abduction splinting and stretching exercises of the contralateral hip to decrease the abduction contracture. All of the dysplastic hips returned to a normal roentgenographic appearance with this treatment. Acetabular dysplasia without dislocation of the hip is not always appreciated by clinical examination, but the asymmetry of the gluteal folds and the apparent limb-length inequality that were seen in all of the children in this series were obvious clinical signs. These findings must be differentiated from the anterior thigh-fold asymmetry that is frequently seen without underlying pathology.
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PMID:Hip dysplasia associated with abduction contracture of the contralateral hip. 714 35

Craniofacial dysplasia is a term covering all types of skeletal anomalies. Craniofacial surgery has made possible the movement of any bone of the face or skull to correct such deformities. Such surgery is a new and separate subspecialty and should be limited to a few regional centers. There are numerous osteotomies available. The common ones are the Le Fort I, II, and III for advancement of different segments of the midface, orbital hypertelorism correction converting each orbit into a box, which moves medially together with the eyeball, and advancement of the forehead to correct premature coronal synostosis in infancy or forehead recession in Crouzon's or Apert's syndrome. In hemifacial microsomia, the asymmetrical skeleton is rotated about the facial midline to produce symmetry, and the mandibular ascending ramus and temporomandibular joint are constructed if absent. Combinations of the various osteotomies are possible, depending upon the type of deformity as assessed by the craniofacial team. Psychosocial study indicates that surgical correction should be undertaken as early as is technically feasible. The four main complications are death, blindness, brain damage, and infection.
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PMID:Current surgery of craniofacial anomalies. 725 37

A case of early epileptic encephalopathy (EIEE) with suppression-bursts or Ohtahara's syndrome, associated with focal cortical dysplasia is reported. Infantile spasms and brief tonic unilateral seizures began on the fifth day of life. Interictal EEG demonstrated an asymmetrical "suppression-burst" pattern with no wake or sleep cycling. Seizures were refractory to all antiepileptic drug (AED) and steroid therapy. Magnetic resonance imaging (MRI) showed right frontotemporal cortical thickening. After three weeks of an ineffective medical treatment a preoperative evaluation with single photon emission computed tomography (SPECT) and electrocorticography (ECoG) was performed to characterize epileptogenic focus. Surgical resection of the precentral area was performed at age 1 month. Neuropathologic examinations confirmed diagnosis of focal cortical dysplasia by identifying cytoarchitectural disarray and ectopic neurons located deep in subcortical white matter. During follow-up, 1-year postoperative the child had a single febrile seizure. Neurologic examination showed minor developmental delay and slight left-sided weakness.
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PMID:Surgical treatment of an early epileptic encephalopathy with suppression-bursts and focal cortical dysplasia. 800 6

One hundred and fifty-one cases of primary glenohumeral osteoarthritis were analyzed both clinically and radiographically with CT scanning. There were 76% females in this series, and the mean age at operation was 66.8 years. The diagnosis was made only with true anteroposterior views of the shoulder which show the narrowing of the glenohumeral joint and the presence of osteophytes. The arthrogram showed a supra-spinatus tear in 10% of the cases that extended to the infra-spinatus in 2.6%. Glenoid retroversion averaged 15.4 degrees. However, measurements of glenoid retroversion with CT-scan do not distinguish posterior wear from glenoid dysplasia. Posterior subluxation of the humeral head was observed in 45% of the cases. We describe a classification of the glenoid morphology in three types: Type A (53.5%) is characterized by an equal balance of forces acting on the glenoid and a centralized humeral head. Type B (39.5%) has asymmetrical posterior force distribution on the glenoid and a posterior subluxation of the humeral head. Type C (5%) is arbitrarily defined as glenoid retroversion greater than 25 degrees. Posterior subluxation of the proximal humeral head did not correlate with either glenoid retroversion or humeral retroversion. However, subluxation of the humeral head may be responsible for the posterior glenoid erosion and possibly for the biconcave appearance of the glenoid observed in primary glenohumeral osteoarthritis. The posterior subluxation of the humeral head may still be present after shoulder arthroplasty and may be responsible for glenoid loosening due to a "horizontal rocking-horse effect".
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PMID:Primary glenohumeral osteoarthritis: clinical and radiographic classification. The Aequalis Group. 992 29

Prevalence of progressive sensorineural hearing loss in childhood seems to be extremely variable, as percentages reported range from 4 to 30%. Differences in the criteria employed for identifying the deterioration, in the groups of patients, and the age range, could explain this wide range of reported figures. The etiology of the progressive sensorineural hearing loss in infants can be hereditary or acquired. Hereditary causes are divided into syndromic and non-syndromic, whereas the acquired causes include congenital or acquired infection (syphilis, cytomegalovirus, rubella virus and toxoplasma infections, bacterial meningitis and acquired viral infections) and congenital inner ear anomalies (Mondini's dysplasia, large vestibular aqueduct, large cochlear aqueduct). Other acquired causes such as disorders of the metabolism, chronic use of ototoxic drugs, autoimmune diseases, perilymphatic fistula and head or acoustic trauma are less common. The age of onset of deterioration shows a great variability because even the congenital hearing losses may occur late after birth. The progressive evolution seems to be binaural in most patients, but more commonly it presents interaural differences, and when the hearing deficit is initially asymmetrical the deterioration is usually greater in the ear which appeared least affected in the first audiogram. Furthermore, at the different frequencies, there is a tendency to a greater deterioration at the frequencies initially least affected, but some authors are not in agreement because they report a uniform pattern of progression in the range of 0.5 to 4 kHz with no modification of the audiometric shape in most of the examined patients.
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PMID:[Progressive sensorineural hearing loss in childhood]. 1020 28

Otomandibular dysplasia are characterised by a combination of anomalies of the ear and the mandible. From the surgical point of vue, facial dysostosis is prominent and focus the attention. For the geneticist it is a group of different entities, familial or sporadic. Familial history, detailed clinical examination looking for extra-facial associated malformations, characteristics of the facial dysostosis, unilaterality or bilaterality and biological or radiological findings allow sometimes to identify a known syndrome. A bilateral and symetric dysostosis with predominant zygomatic and malar hypoplasia suggest the diagnosis of Treacher-Collins or Franceschetti syndrome or mandibulofacial dysostosis, particularly in the presence of positive familial history. Acral anomalies associated with facial dysostosis allow the distinction between Treacher-Collins syndrome and acrofacial dysostosis (Nager and Miller syndromes). Unilateral and bilateral asymmetrical anomalies, namely facioauriculovertebral syndrome, hemifacial microsomia, otomandibular dysostosis, no. 7 cleft, first branchial arch syndrome, Goldenhar syndrome were lumping together by Gorlin in 1990, who proposed to use the term "oculoauriculovertebral spectrum". This classification is the first step before genetic studies, who need homogeneous group of patients. Lastly recurrence risk can be evaluated and genetic counselling can be done only if a precise genetic diagnosis is known.
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PMID:[Oto-mandibular dysplasias: genetics and nomenclature of syndromes]. 1177 Apr 50

To describe the poorly known characteristics of epilepsy during infancy in focal cortical dysplasia (FCD), one of the most frequent cause of infantile epilepsy. All 28 patients with FCD referred to two specialized centres were retrospectively studied regarding seizure characteristics, psychomotor evaluation, and response to medical and surgical treatment. All patients presented with early partial seizures. Semiology, but not the age of onset, depended on the topography of the dysplasia, with abnormal eye movements in all cases of posterior FCD. Eleven patients also developed infantile spasms (IS), mainly asymmetrical. IS were easily controlled with Vigabatrin or ACTH, but no partial seizures could be medically controlled except in one patient. All patients except one had abnormal neuropsychological findings. Fifteen patients had surgery, eight became seizure free, and seven were significantly improved regarding psychomotor development. Very early and refractory partial seizures, but easily controlled IS are the main characteristics of FCD in infancy. Only the focal ictal semiology may help differentiate the localization of FCD. Its intrinsic epileptogenicity could sustain this clinical pattern. Since the chances for medical control and normal neurodevelopment are poor, surgical treatment should be considered early in infants with FCD.
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PMID:Characteristics of epilepsy in focal cortical dysplasia in infancy. 1235 Mar 89


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