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Biomedical subjects

M Akhtar

Publications and source records attributed to M Akhtar.

At least 397 records · Page 22Linked to original sources

Application of electron microscopy in the interpretation of fine-needle aspiration biopsies.

A series of 31 fine-needle aspiration biopsies were studied ultrastructurally in order to evaluate the usefulness of electron microscopy in the diagnosis of aspiration biopsies. In seven cases, the electron microscopic findings were crucial to the diagnosis. In the remaining cases, electron microscopy helped to confirm the light microscopic diagnosis. In addition, in a number of cases the diagnosis rendered following electron microscopy was much more precise and specific than was possible with light microscopy alone. It is concluded that electron microscopy has a definite place in the diagnosis of fine-needle aspiration biopsies and should be increasingly utilized on a selective basis.

Adolescent↗

Intra His Purkinje gap phenomenon during retrograde conduction in man.

Ventricular refractory period studies were performed in 24 patients using the ventricular extrastimulus (V2) method at a basic ventricular drive (V1V1). Gap phenomenon confined to the His-Purkinje system (V-H gap) during retrograde conduction was observed in six of 24 patients. In this form of gap, the premature impulse (V2) is initially blocked in the His-Purkinje system (HPS) as recognized by the absence of retrograde His bundle deflection (H2) and atrial depolarization (A2) following V2. At closer V1V2 intervals, V2 resumed conduction to the bundle of His (H2) but not to the atria. The mechanism of this form of gap is similar to the one proposed for the previously described gap phenomena in ventriculoatrial (V-A) conduction and involves proximal delay allowing more time for distal recovery. At shorter V1V2 intervals, V2 resumes conduction to the bundle of His because it encounters sufficient delay in some region below the His bundle. However, this delay may be insufficient to allow recovery of excitability at the A-V node and hence resumption of conduction to the atria is not an integral part of V-H gap. The relation of V-H gaps to the occurrence of reentry within the HPS (V2 phenomenon) is discussed. V-H gaps also explain the failure of some ventricular premature beats (VPBs) to show the effects of concealed conduction in the A-V node. The similarities and differences between V-A and V-H gaps during retrograde conduction are discussed.

Adult↗

Nephrotic syndrome due to preeclamptic nephropathy associated with a transitional mole with coexistence fetus.

An unusual case of nephrotic syndrome secondary to preeclamptic nephropathy is documented. The preeclampsia was associated with a transitional mole with coexistent fetus. A review of the literature revealed only one similar case reported previously. Immuno-pathologic examination of the renal biopsy revealed abundant IgM and fibrinogen within the glomeruli; electron microscopy showed numerous subendothelial and occasional intramesangial deposits of electron-dense material. The significance of these findings with regard to the pathogenesis of preeclamptic nephropathy is briefly discussed.

Adult↗

Role of retrograde His Purkinje block in the initiation of supraventricular tachycardia by ventricular premature stimulation in the Wolff-Parkinson-White syndrome.

The precise mechanisms for paroxysmal reentrant supraventricular tachycardia (PSVT) initiation during right ventricular premature stimulation (V(2) method) were analyzed in 14 consecutive patients with Wolff-Parkinson-White Syndrome in whom the PSVT was inducible during retrograde refractory period studies. 9 patients had left-sided and the remaining 5 of 14 had right-sided ventriculo-atrial (VA) accessory pathway (AP). At the basic cycle lengths (V(1)V(1)) ranging from 550 to 900 ms (mean, 657.1+/-139.5), closely coupled V(2) (mean V(1)V(2), 357.3+/-59.2 ms, range 320-500) produced retrograde His bundle (H(2)) activation via the bundle branches and retrograde atrial (A(2)) activation via the AP. As the V(1)V(2) were further shortened, the V(2) showed a retrograde block in the His Purkinje system (HPS) and conducted to the atria via AP in 9 of 14 cases. Subsequently, the A(2) impulse conducted anterograde over the atrioventricular node-HPS to initiate a PSVT or an atrial echo response in all nine cases. In none of the patients was a PSVT induced by V(2) when the latter produced retrograde H(2) activation via the bundle branches. In 10 of 14 cases, however, the retrograde H(2) was followed by a V(3), due to macroreentry in the HPS. The V(3) in turn blocked retrogradely in the HPS while producing A(3) via the AP to initiate a PSVT or an atrial echo response in 9 of 10 cases. Retrograde block of V(2) and/or V(3) in the HPS resulted in PSVT initiation in 13 of 14 cases, whereas in the remaining 1 case the exact mechanism was not clear. In none of the patients in this series was the PSVT initiated with a retrograde block of V(2) in the atrioventricular node with or without concomitant retrograde A(2) activation via the AP. We conclude that within the ranges of cycle lengths tested, a retrograde block of V(2) and/or V(3) in the HPS is the most common mechanism for initiation of PSVT during ventricular premature stimulation in patients with the Wolff-Parkinson-White Syndrome.

Bundle of His↗

Hormonal control of uterine growth: the effect of hypothyroidism on estrogen-stimulated cell division.

The increase in mitotic indices of uterine luminal epithelium, stroma, and myometrium were determined as a function of time after the administration of a single dose of 17 beta-estradiol to euthyroid and hypothyroid rats. Hypothyroidism reduced the increase in the mitotic index 5-fold in the luminal epithelium, 6-fold in the stroma, and 9-fold in the myometrium. In addition to reducing mitotic indices, hypothyroidism also produced a shift of 12 h in the time course of estrogen-stimulated cell division of all uterine cell types relative to euthyroid animals. This shift in the time course of cell division was preceded by a shift in the time course of uterine DNA synthesis measured by tritiated thymidine incorporation. In contrast, hypothyroidism did not alter the magnitude or the time course of synthesis of 2-deoxyglucose-6-phosphate from 2-deoxyglucose after estrogenic stimulation. These results indicate that hypothyroidism decreases the ability of all major uterine cell types to undergo cell division in response to acute administration of estradiol, and also shifts the time course of the uterine growth response to the hormone.

Animals↗

Mechanistic and stereochemical studies on 3-oxo steroid delta 4-delta 5-isomerase from human placenta.

The mechanism of isomerization of delta 5-3-ox steroids to delta 4-3-oxo steroids was examined by using the membrane-bound 3-oxo steroid delta 4-delta 5-isomerase (EC 5.3.3.1) and the 3 beta-hydroxy steroid dehydrogenase present in the microsomal fraction obtained from full-term human placenta. (1) Methods for the preparation of androst-5-ene-3 beta, 17 beta-diol specifically labelled at the 4 alpha-, 4 beta- or 6-positions are described. (2) Incubations with androst-5-ene-3 beta, 17 beta-diol stereospecifically 3H-labelled either in the 4 alpha- or 4 beta-position showed that the isomerization reaction occurs via a stereospecific elimination of the 4 beta hydrogen atom. In addition, the complete retention of 3H in the delta 4-3-oxo steroids obtained from [4 alpha-3H]androst-5-ene-3 beta, 17 beta-diol indicates that the non-enzymic contribution to these experiments was negligible. (3) To study the stereochemistry of the insertion of the incoming proton at C-6, the [6-3H]androst-4-ene-3, 17-dione obtained from the oxidation isomerization of [6-3H]androst-5-ene-3 beta, 17 beta-diol was enzymically hydroxylated in the 6 beta-position by the fungus Rhizopls stolonifer. Retention of 3H in the 6 alpha-position of the isolated 6 beta-hydroxyandrost-4-ene-3, 17-dione indicates that in the isomerase-catalysed migration of the C(5) = C(6) double bond, the incoming proton from the acidic group on the enzyme must enter C-6 from the beta-face, forcing the existing 3H into the 6 alpha-position.

Androstenediol↗

Multilocular cyst of kidney with embryonic tissue.

A case of a multilocular cyst in a child is documented, and a brief review of reported cases of multilocular cysts in pediatric age groups is presented. These cases can be divided into two subgroups based on the presence or absence of embryonic tissue within the cysts. The significance of this embryonic tissue with regard to histogenesis and prognosis of the multilocular cysts is discussed.

Follow-Up Studies↗

Lepromatous leprosy presenting as orchitis.

Two patients with lepromatous leprosy presenting initially because of lepromatous orchitis are reported. These cases are unusual because they were diagnosed as lepromatous orchitis at a stage when no other evidence of leprosy was present. Generalized skin lesions characteristic of lepromatous leprosy subsequently developed in one of these patients. It is suggested that lepromatous orchitis should be actively considered in the differential diagnosis of orchitis and infertility.

Adult↗

A proton-magnetic-resonance study of N-trifluoroacetyl-L-alanyl-L-phenylalaninal binding to alpha-chymotrypsin.

Cross-saturation NMR studies have shown that the dipeptide aldehyde N-trifluoroacetyl-L-alanyl-L-phenylalaninal forms a hemiacetal complex with alpha-chymotrypsin. The free aldehyde resonance was seen to broaden upon addition of alpha-chymotrypsin and a detailed analysis has identified the enzyme-bound hemiacetal as the species which was in slow exchange with the free aldehyde and so gave rise to the perturbation. The line broadening was found to be dependent on p2H and this behaviour could be adequately described by the ionisation of a single group on the free enzyme (pKa2H7.6) with the alkaline form being required for hemiacetal formation. The pH dependence of alpha-chymotrypsin-induced catalysis around neutral pH correlates well with the observed p2H dependence of hemiacetal formation, indicating that it is an intermediate in the catalytic mechanism.

Binding Sites↗