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Nippon Yakurigaku Zasshi. 1979 May;75(4):321-31.
[Behavioral and EEG alterations with brain stem compression and effect of thyrotropin-releasing hormone (TRH) in chronic cats (author's transl)]

[Article in Japanese]

Fukuda N, Saji Y, Nagawa Y.

Behavioral and EEG changes induced by brain stem compression and the effect of TRH were studied. The compression was given for 1 to 6 min by inflating a balloon chronically implanted on the dorsal surface of the cat brain stem in the 4th ventricle via cisterna magna. Within 10 to 36 sec after the start of the compression, the cats turned sideways and became motionless in a spastic extension of four legs, and thereafter all reverted to a normal position, after 45 to 120 min, although slight movements or head-up position was observed in some animals. The cortical EEG patterns observed after the compression were initially a brief rush of low amplitude-fast waves (EEG arousal) followed by a flattened and/or spike pattern, and subsequently these shifted to high amplitude-slow waves with or without an accompanying EEG arousal. These behavioral EEG alterations were remarkably improved by i.v. administration of TRH as follows: eight of 12 cats with 1 mg/kg and one of 4 cats with 0.5 mg/kg promptly changed from the lateral to a crouching or abdominal position, and thereafter never turned sideways again. Partial recovery such as movements of forelegs, struggling or head-up in the lateral position, rolling or slight shift of position was also observed within several min in three cats with 1 mg/kg as well as in two cats with 0.5 mg/kg. Furthermore, TRH induced a dose dependent, persistent EEG arousal in all cats. These results show that TRH ameliorates deterioration in behavior and the EEG, this deterioration being similar to clinical states of disturbance in consciousness induced by compressing the brain stem.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=119693&dopt=Abstract

J Endocrinol Invest. 1979 Oct-Dec;2(4):347-51.
Suppression of clonidine-induced release of growth hormone by thyrotropin releasing hormone in humans.

Zanoboni A, Zanoboni-Muciaccia W, Zanussi C, Baraldi R.

A single oral dose of clonidine (0.15 mg), a selective alpha-adrenergic stimulating agent, was able to increase plasma growth hormone (GH) levels (above 5 ng/ml) in 6 out of 7 normal men tested. This GH increase was independent of the hypotensive effect of the drug and was observed without any modification of plasma prolactin, thyroid stimulating hormone, gonadotropins and glycemia. When oral clonidine administration was associated to a slow thyrotropin releasing hormone (TRH) infusion (1 mg dissolved in 400 ml of 0.9% saline solution, at a constant rate during 150 min) the plasma GH response was significantly inhibited when compared with that observed after clonidine alone. These results suggest that in normal subjects TRH is capable of blocking the effect of an alpha-adrenergic stimulus which is conceivably acting at the level of central nervous system.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=119798&dopt=Abstract

Nippon Ronen Igakkai Zasshi. 2003 Mar;40(2):167-71.
[An elderly case of non-Hodgkin's lymphoma (NHL) with hypercalcemia]

[Article in Japanese]

Ota H, Azuma K, Horiuchi T, Kazama H, Araki A, Hosoi T, Sawabe M, Amizuka N, Orimo H.

Department of Endocrinology, Tokyo Metropolitan Geriatric Medical Center.

A 93 year-old woman was admitted due to anorexia and unconsciousness. Biochemical examination of serum showed hypercalcemia (corrected Ca; 16.6 mg/dl). The level of intact parathyroid hormone (i-PTH) was suppressed, whereas parathyroid hormone-related peptide (PTHrp) was to 5.0 pM (normal range: below 0.6 pM). IL-6 and renal cAMP were also elevated. We started to ameliorate hypercalcemia by saline infusion, furosemide and calcitonin. However, hypercalcemia was not improved and the patient died of DIC and renal failure. Autopsy revealed primary lesion of NHL (diffuse large B cell type) to be in the stomach with infiltration of lymphoma into the liver, pancreas, spleen, adrenal glands, jejunum, and lumbar vertebrae. The results of immunohistochemical examination demonstrated the expression of PTHrP in lymphoma cells. PTHrP was also found in lymphoma cells of the spleen by the RT-PCR technique. These findings indicated that hypercalcemia was caused by overexpression of PTHrP from lymphoma cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12708052&dopt=Abstract

J Endocrinol Invest. 1979 Oct-Dec;2(4):379-83.
Hypothalamic-pituitary function in Cushing's disease.

Le Roith D, Shapiro MS, Gutman A, Spitz IM.

Hypothalamic pituitary function was evaluated in seven patients with Cushing's disease. In all subjects there was an absence of GH elevation following hypoglycemia. Three patients demonstrated basal hyperprolactinemia. Six had an intact PRL rise following TRH. However, four patients failed to show PRL elevation with insulin hypoglycemia and six were unresponsive to chlorpromazine. Five patients showed impaired TSH response to TRH. Many of the subjects had low basal LH and FSH levels. Attenuated or absent gonadotropin responses to LHRH were noted in three females. One male demonstrated an exaggerated FSH response to LHRH. These results indicate that multiple abnormalities of anterior pituitary hormone secretion characterize Cushing's disease.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=119799&dopt=Abstract

J Endocrinol Invest. 1979 Oct-Dec;2(4):395-400.
Clinical application of a cytochemical bioassay for the determination of thyroid stimulating hormone.

Hashimoto T, Dohler KD, Emrich D, von zur Muhlen A.

Thyroid stimulating hormone (TSH) was measured using a highly sensitive cytochemical bioassay (CBA) technique in normal subjects, in patients with Graves' disease (untreated and treated) and in patients with euthyroid goiter and negative thyrotropin-releasing hormone (TRH)-test. Plasma TSH levels of normal subjects and of subjects with untreated Graves' disease were reduced after the plasma had been incubated with a specific antibody to human TSH, indicating that the thyroid stimulating substance measured with this assay was likely to be TSH. Basal TSH levels in patients with Graves' disease and in a special group of patients with euthyroid goiter and negative TRH test were low but detectable. They did not rise after TRH administration. Increased TSH release (4.5- to 10-fold) after TRH stimulation was demonstrated, however, in two formerly hyperthyroid patients after treatment. This increase was not detected by radioimmunoassay (RIA) due to limited sensitivity.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=119800&dopt=Abstract

The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes hair cycle and normally 50-100 hairs randomly fall out a day, which is unnoticeable because lost hair is replaced by as many new hairs springing up daily. Hair loss results from the fall out of hair from the hair follicle. Alopecia or excessive, premature hair loss is the condition caused by many factors. Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs. However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals. The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime. Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.

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