Faculty Opinions recommendation of Dopamine agonist administration causes a reduction in endometrial implants through modulation of angiogenesis in experimentally induced endometriosis.

Numbers of immunological approach have been made to the amyloidosis through the variety of predisposing human diseases and the experimentally induced animals by the greater number of agents. The results suggest an important role of impaired immunity involving both humoral and cell-mediated aspects.Recently the author has succeeded in producing amyloidosis in the rabbits and mice by the injections of immune complex of heat denatured DNA.The aim of this report is to demonstrate the details of the ultrastructure of the amyloidosis induced by heterologous insoluble immune complex. Eleven of twelve mice, dd strain, subcutaneously injected twice a week with Freund's complete adjuvant and four of seven animals intraperitonially injected developed systemic amyloidosis two months later from the initial injections. The spleens were electron microscopically observed.

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The effect of bromocriptine on mammary-gland ultrastructure of hyperprolactinemic rats

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100111136 ◽

1984 ◽

Vol 42 ◽

pp. 204-205

Author(s):

I.C. Murray

Keyword(s):

Mammary Gland ◽

Dopamine Agonist ◽

Alveolar Epithelium ◽

Mammary Glands ◽

Female Rats ◽

Control Group ◽

Cell Hyperplasia ◽

Once Daily ◽

Long Evans

In women, hyperprolactinemia is often due to a prolactin (PRL)-secreting adenoma or PRL cell hyperplasia. RRL excess stimulates the mammary glands and causes proliferation of the alveolar epithelium. Bromocriptine, a dopamine agonist, inhibits PRL secretion and is given to women to treat nonpuerperal galactorrhea. Old female rats have been reported to have PRL cell hyperplasia or adenoma leading to PRL hypersecretion and breast stimulation. Herein, we describe the effect of bromocriptine and consequently the reduction in serum PRL levels on the ultrastructure of rat mammary glands.Female Long-Evans rats, 23 months of age, were divided into control and bromocriptine-treated groups. The control animals were injected subcutaneously once daily with a 10% ethanol vehicle and were later divided into a normoprolactinemic control group with serum PRL levels under 30 ng/ml and a hyperprolactinemic control group with serum PRL levels above 30 ng/ml.

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Effects of Experimentally Induced Pain on Mismatch Negativity

Journal of Psychophysiology ◽

10.1027/0269-8803.20.1.21 ◽

2006 ◽

Vol 20 (1) ◽

pp. 21-31 ◽

Cited By ~ 6

Author(s):

Bruce D. Dick ◽

John F. Connolly ◽

Michael E. Houlihan ◽

Patrick J. McGrath ◽

G. Allen Finley ◽

...

Keyword(s):

Cognitive Processing ◽

Mismatch Negativity ◽

Event Related Potentials ◽

Disruptive Effect ◽

Ischemic Pain ◽

Active Attention ◽

Early Processing ◽

Related Potentials ◽

Healthy Participants ◽

Experimentally Induced

Abstract: Previous research has found that pain can exert a disruptive effect on cognitive processing. This experiment was conducted to extend previous research with participants with chronic pain. This report examines pain's effects on early processing of auditory stimulus differences using the Mismatch Negativity (MMN) in healthy participants while they experienced experimentally induced pain. Event-related potentials (ERPs) were recorded using target and standard tones whose pitch differences were easy- or difficult-to-detect in conditions where participants attended to (active attention) or ignored (passive attention) the stimuli. Both attention manipulations were conducted in no pain and pain conditions. Experimentally induced ischemic pain did not disrupt the MMN. However, MMN amplitudes were larger to difficult-to-detect deviant tones during painful stimulation when they were attended than when they were ignored. Also, MMN amplitudes were larger to the difficult- than to the easy-to-detect tones in the active attention condition regardless of pain condition. It appears that rather than exerting a disruptive effect, the presence of experimentally induced pain enhanced early processing of small stimulus differences in these healthy participants.

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