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At least 37 records · Page 2Linked to original sources
PubMed1991

Localization of ectopic ventricular depolarization by ISPECT-radionuclide ventriculography and by magnetocardiography. ISPECT and MCG for ectopic mapping.

Since catheter or surgical techniques for ablating the arrhythmogenic substrate in patients with SVT due to accessory pathways or those with VT are now available, exact localization of the substrate is mandatory. We report preliminary results of two new non-invasive techniques for localizing either the site of earliest ventricular contraction using ISPECT, or the site of initial ventricular depolarization by magnetocardiography (MCG) in WPW syndrome and in VT patients. Thirteen patients with WPW syndrome and 8 patients with sustained VTs were studied with ISPECT. In 9/13, comparative catheter mapping data were available. Two patients had two Kent bundles. 13/15 Kent bundles could be localized by ISPECT. In 5/9 patients the area of Kent bundle insertion was identical with ISPECT and catheter mapping, in 3 correlation was fair, and in 2 patients with 2 Kent bundles ISPECT failed to localize their insertion. In 3/8 patients with VT catheter mapping could not be performed for hemodynamic reasons. In 2/5 patients the area of VT focus was identical with both methods, in one patient it was adjacent to each other, and in 2/5 patients a larger anatomic distance of the focus was found with both methods. In 3/7 patients with WPW the MCG showed the site of Kent bundle insertion, which was identical to that seen by catheter mapping. In one patient the area was adjacent, and in 3 more distant from the site determined by catheter mapping. In 1/2 patients with 2 Kent bundles, one of these could be detected by MCG. In 1/3 patients with VT, the site of VT focus was identical with both methods, but in the remaining two a distance of 3-4 cm was observed between the area seen with MCG and that with catheter mapping. In 4 further VT patients with stable and uniform ventricular late potentials, ventricular late magnetic activity was found with different QRS lengths within the single MCG channels. From our results we conclude that both ISPECT and MCG seem to become very promising non-invasive techniques for localizing ectopic ventricular depolarization in WPW syndrome and VT patients. However, these methods have to be refined, improved and validated by further systematical studies.

Action Potentials↗
PubMed2000

Ectopic prostatic tissue in the uterine cervix: a report of four cases and review of ectopic prostatic tissue.

We report four examples of prostatic tissue occurring in the uterine cervix of patients aged 22, 25, 31, and 77 years. Three were incidental findings in loop excisions (two patients) and cone biopsy (one patient) of the cervix for high-grade squamous dysplasia. One presented as a cervical mass, clinically suspected to represent a fibroid. The prostatic tissue consisted of ducts and acini, some of which had papillary or cribriform patterns. Squamous metaplasia was prominent in all cases. No Wolffian duct tissue was present. The glandular epithelium in all cases was positive for prostatic acid phosphatase and prostate-specific antigen. High molecular weight keratin, performed in two cases, highlighted basal cells in a manner similar to the normal prostate. These unusual cases, only one of which is documented previously, further complicate the often-challenging area of interpretation of benign glandular lesions of the cervix. The unusual phenomenon of ectopic prostate tissue in general is reviewed.

Adult↗
PubMed1986

Acromegaly due to ectopic growth hormone (GH)-releasing hormone (GHRH) production: dynamic studies of GH and ectopic GHRH secretion.

Dynamic studies of GH and GH-releasing hormone (GHRH) secretion were performed in a man with a GHRH-producing carcinoid tumor and acromegaly. Insulin hypoglycemia stimulated and metoclopramide inhibited both GH and GHRH acutely. Bromocriptine suppressed GH both acutely and chronically without altering circulating GHRH levels and also blunted the GH response to exogenous GHRH. TRH acutely stimulated GH, but not GHRH, secretion, and iv bolus doses of synthetic GHRH-(1-40) stimulated GH release acutely. Somatostatin infusion decreased both GH and GHRH concentrations and blunted the GH responses to TRH and GHRH-(1-40). We conclude that prolonged exposure of the pituitary gland to high concentrations of GHRH is associated with chronic GH hypersecretion and may be accompanied by a preserved acute GH response to exogenous GHRH; a paradoxical response of GH to TRH may be mediated at the pituitary level, consequent to prolonged pituitary exposure to GHRH; bromocriptine suppression of GH in acromegaly is due to a direct pituitary effect of the drug; and somatostatin inhibits both ectopic GHRH secretion as well as GH responsiveness to GHRH in vivo. Since GH secretory responses in patients with somatotroph adenomas are similar to those in this patient, augmented GHRH secretion may play a role in development of the "classic" form of acromegaly.

Acromegaly↗
PubMedDate not supplied

Synthesis of fast myosin induced by fast ectopic innervation of rat soleus muscle is restricted to the ectopic endplate region.

Skeletal muscle fibres, long multinucleated cells, arise by fusion of mononucleated myoblasts to form a myotube that matures into the adult fibre. The two major types of mature fibre, fast and slow fibres, differ physiologically in their rate of isotonic shortening. At the molecular level these type-specific physiological properties are ascribed to different isoforms of myosin, a major protein involved in shortening. Differentiation of fast and slow fibres seems to be under the control of motoneurones, and mature fibres are innervated by only one motoneurone. When rat soleus muscle (SOL, a slow muscle) is dually innervated with a fast nerve, it acquires some properties of a fast muscle, that is, low sensitivity to caffeine and high glycogen content. We report here that in dually innervated soleus muscle the foreign fast nerve induces synthesis of fast isoforms of myosin, but only in the segment of the muscle fibre that is close to the foreign endplate. The localized influence of the nerve endplates suggest that factors controlling the phenotypic expression of the muscle fibre have a short range of activity.

Animals↗
PubMed2000

Ectopic expression of c-myc fails to overcome downregulation of telomerase activity induced by herbimycin A, but ectopic hTERT expression overcomes it.

Telomerase plays a key role in the maintenance of chromosomal stability in tumors, but the mechanism regulating telomerase activity is still unclear. Recent studies have suggested that c-myc may be vital for regulation of hTERT mRNA expression and telomerase activity. In this study, we investigated the changes of telomerase activity and telomerase-related genes induced by herbimycin A in K562 human chronic myelogeous leukemic cells. Telomerase activity showed a biphasic pattern in herbimycin A-treated K562 cells. Initially, the telomerase activity decreased along with the decline of cells in S and G2/M phases, but it recovered slightly at the end of treatment. Expression of mRNA for the telomerase catalytic subunit (hTERT) was decreased before the decline of telomerase activity, and increased slightly before the reactivation of telomerase activity. During herbimycin A treatment, both c-myc and cyclin D1 mRNA showed transient downregulation before the increase of G1 cells. Herbimycin A treatment caused the downregulation of both telomerase activity and hTERT mRNA in cyclin D1-transfected K562 cells, while telomerase activity was partially restored in c-Myc-transfected cells. In contrast, hTERT-transfected K562 cells maintained a high level of telomerase activity during herbimycin A treatment. Neither the template RNA component of telomerase (hTERC) nor telomerase-associated protein (TEP-1) were altered in any of the transfected K562 cells. These results indicate that telomerase activity is mainly regulated by hTERT, and that c-Myc protein is one of the positive regulators of hTERT in leukemic cells but is not enough to counteract the downregulation of telomerase activity by herbimycin A completely.

Benzoquinones↗