No abstract available.
Rehabilitation*

No abstract available.
Primary Health Care*

No abstract available.

No abstract available.
Tuberculosis, Multidrug-Resistant*

No abstract available.
Tuberculosis, Multidrug-Resistant*

No abstract available.
Humans ; Nitric Oxide* ; Tissue Donors*

High septal deformities exert pressure on upper lateral cartilages and nasal bones and cause external deviation of the nose. However, detection of high septal deformities causing deviated noses is very difficult if a detailed intranasal examination is not performed. As well, the high septal border is a difficult area to approach via the endonasal rhinoplasty and is the weakest portion in the septum resulting in much difficulty in correcting deformities and in frequent later recurrence of deviation secondary to the healing process. In order to solve the above problems in 33 cases of deviated nose associated with high septal deformities, the authors evaluated deformities in the high septal border after separation of the septum from upper lateral cartilages and nasal bones. The high septal border is centralized by scoring after resection of the mid or lower-septal portion. And spreader grafts were applied to the convex sides of deviated septal borders to stabilize the high septal border and to prevent long-term recurrence of deviation. Also, to balance the traction force of side walls, the length of both upper lateral cartilages and nasal bones were equalized by resection in the longer side and grafting in the shorter side. Clinical follow-up ranged from 3 to 31 months. There was no surgical or septal complication. Also, there was no incomplete correction, recurrence of deviation, or compromized nasal support. All patients except 2 were satisfied with the aesthetic and functional results. We found that separation of septum from side walls allows detection and correction of higher septal deformities and that spreader graft allows long-term support and prevents later recurrence of deviation.
Cartilage ; Congenital Abnormalities* ; Follow-Up Studies ; Humans ; Nasal Bone ; Nose* ; Recurrence ; Rhinoplasty ; Traction ; Transplants*

We measure left ventricular mass, mitral peak flow velocity and isovolumic relaxation time(IVRT) with M-mode and Doppler echocardiography to evaluate daistolic function of the heart in hypertensive patients, who are seperated into group A(18 patients) with normal electrocardiogram and group B(24 patients) with abnormal electrocardiogram. There is no difference in fractional shortening, which reflects systolic function of the heart,between normal subjects and both groups of patients(36.5+/-6.7% in group B).The left ventricular mass index in group A is higher than in normal subjects(139.8+/-33.6g/m2, 100.2+/-28.8g/m2, respectively, p<0.005). But, that is lower than group B(200.7+/-40.6g/m2, p<0.005). The sensitivity and specificity of electrocardiograohy to detect left ventricular hypertrophy in patient whose left ventricualr mass index is above 160.8g/m2, are 80% and 91%, respectively. The peak flow velocities in early diastolic(PFVE) are 0.67+/-0.15m/sec in normal subjects and 0.60+0.14m/sec in group A (p=not siginificant). In group B, that is lower than normal subjects(0.54+/-0.15m/sec, p<0.005). In both groups, the peak flow velocities in late diastole(PFVA) are higher than normal subjects(0.48+/-0.11m/sec in normal, 0.69+/-0.18m/sec in groups A, 0.71+/-0.16m/sec in group B, p<0.005). The PFVE/PFVA ratio is lower in both groups of patients(1.40+/-0.23 in normal subjects, 0.90+/-0.25 in group A, 0.77+/-0.23 in group B, p<0.005). The IVRT is also prolonged in both groups(85+/-10m/sec in normal, 112+/-16msec in group A, 123+/-23msec in group B, p<0.005). The PFVE/PFVA ratio decreases in relation with the increament of index of IVRT(r=0.60, p<0.01). The IVRT increases in relation to the left ventricular mass index in hypertensive patients(r=0.34, p<0.05), but, the PFVE/PFVA ratio reveals no relation to those. In cocclusion, the impairment of diastolic function develops before the systolic function or electrocardiogram show abnormalities in htpertensive patients.Therefore, it is importment to detect early any abnormalities in the indices of the diastolic function, such as mitral peak flow velocity and isovolumic relaxation time, in the prevention and treatment of hypertensive geart disease.
Echocardiography, Doppler ; Electrocardiography ; Heart ; Humans ; Hypertension* ; Hypertrophy, Left Ventricular ; Relaxation ; Sensitivity and Specificity

No abstract available.
Dermis* ; Skin*

BACKGROUND: It has been known that arteries of hypertensive animals and patients are generally thicker and more rigid than those of normal subjects, resulting from the morphological changes induced by an increased stress on the vessel wall. Factors proposed to be responsible for these changes are smooth muscle hypertrophy, increased amount of collagen, hyperplasia of smooth muscle cell and changes in cross-linkages of the fibrous proteins. The present study was conducted to define whether enalapril, a converting enzyme inhibitor of angiotensin II generation from angiotensin I, can restore the structural alterations of aortic media in spontaneously hypertensive rat(SHR). METHODS: For this purpose, SHR were treated for 22 weeks with 2mg/kg/day enalapril and morphologic changes were compared between enalapril-treated SHR and normotensive Wistar-Kyoto rats. RESULTS: The increased thickness of the aortic media in SHR was reduced and intervening elastic laminae were narrowed by enalapril treatment. Subcellular analysis of cytoplasmic composition and nucleus in the aorta of hypertensive rats revealed some modification with enalapril. Some irregularly arranged collagen fibrils in aortic media of SHR were regularly distributed and the periodic bands of the fibrils which were the fragmented were clearly apparent by enalapril treatmed SHR group. CONCLUSIONS: From the above experimental results, it is concluded that subcellular changes of smooth muscle cells and collage fibrils of aortic media in SHR could be repaired by long-term treatment with enalapril.
Angiotensin I ; Angiotensin II ; Animals ; Aorta ; Arteries ; Collagen ; Cytoplasm ; Enalapril* ; Humans ; Hyperplasia ; Hypertrophy ; Muscle, Smooth ; Myocytes, Smooth Muscle ; Rats ; Rats, Inbred SHR* ; Scleroproteins