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I F Hussain

Publications and source records attributed to I F Hussain.

5 recordsLinked to original sources

Pressure-flow study as an evaluating method of neurogenic urethral relaxation failure.

Voiding difficulty is a common feature in neurological diseases, which can be attributed to dysfunction of the urethral sphincter and the detrusor. Electromyography (EMG)-cystometry can reveal the presence of detrusor-external sphincter dyssynergia (DESD), however, internal sphincter function on voiding is not easily evaluated. Pressure-flow study is widely used to diagnose benign outlet obstruction due to prostatic hypertrophy. We applied pressure-flow study in neurological patients in order to evaluate neurogenic urethral relaxation failure. We recruited 71 patients with neurological diseases. All were men under 60 years, with mean age of 44 years, ranging from 18 to 59 years. None had abnormal finding of digital examination or ultrasound echography of the prostate. Standard cystometry showed detrusor hyperreflexia in 33 patients and residual urine was noted in 36. DESD was noted in seven of 43 patients. Pressure-flow relation curve and a detrusor pressure (P(det)) at the point of maximum flow rate (Q(max)) (i.e., P(det)Q(max)) were obtained by urodynamic computers. The Abram-Griffiths (AG) number (P(det)Q(max)-2Q(max)), showing outlet obstruction particularly over 40, was also obtained. The points of P(det)Q(max) of the patients fell into three categories of the AG nomogram, showing obstruction in 19.7%, equivocal in 52.1% and unobstructed in 28.2%. Patients with DESD had AG number over 40 more commonly (57.1%) than those without DESD (8.4%) (p<0.05). The mean AG number was 46.4 in patients with DESD, which was larger than 17.1 in patients without DESD (p<0.01). Patients with detrusor hyperreflexia had AG number over 40 more commonly (42.4%) than those with normal cystometric curve (0%) (p<0.01). The mean AG number was 30.6 in patients with detrusor hyperreflexia, which was larger than 13.6 in patients with normal cystometric curve (p<0.01). The results showed that 19.7% of patients with neurological diseases had obstructive pattern (high pressure voiding), evidence of urethral relaxation failure with relatively preserved detrusor contraction. DESD is a factor contributing to the urethral relaxation failure of the patients. The results also indicated a relationship between detrusor hyperreflexia and obstructed pattern, probably reflecting co-occurrence of detrusor hyperreflexia with DESD or detrusor-internal sphincter dyssynergia.

Adolescent

The immunohistochemical heterogeneity of atheroma macrophages: comparison with lymphoid tissues suggests that recently blood-derived macrophages can be distinguished from longer-resident cells.

We studied the antigenic markers of macrophages (Mphs) in atherosclerotic human arteries by immunohistochemistry and compared them with the patterns in Mph subpopulations of tonsil and lymph node, which are also described. The staining of atheroma intimal Mphs was assessed semiquantitatively in the subendothelial, mid, and outer intima. Three patterns of reactivity with Mph antibodies were recognized. (a) Pan-Mph (antibodies HAM56, EBM11, and CD14 group). Staining was maximal in the mid-intimal zone. (b) Subendothelial Mphs (anti-muramidase, anti-alpha-1-antitrypsin and MAC387). In lymphoid tissue, sinusoidal Mphs and a few inflammatory Mphs were stained, as well as blood monocytes. This group of antibodies recognizes Mphs that are likely to be recently blood-derived (RBD-Mphs). (c) Antibodies reactive with various histiocyte populations in lymphoid tissues (anti-Factor XIII; anti-HLA Class II and LN2) also gave maximal staining in the mid-intimal zone, but differences between lesion types suggest that they are recognizing heterogeneous subpopulations of Mphs. These observations demonstrate the heterogeneity of tissue Mphs and suggest that an insight into the dynamics of tissue Mphs can be obtained from the cell phenotype. They indicate that all stages of atherosclerosis can have an outward traffic of Mphs from the blood through the arterial intima.

Antibodies, Monoclonal