The effects of testosterone on the pituitary growth hormone (GH) response directly and to hypothalamic growth hormone-releasing hormone (GHRH) were evaluated in vitro using a male pituitary cell monolayer culture system. Wistar male rats were gonadectomized at 22 days of age, and 21 days later their anterior pituitaries were removed and trypsinized for cell dispersion. Testosterone 0, 0.1, 1.0, 10.0 nM was added to the medium for 1 day and GH amounts in media were measured. In another experiment, testosterone 1, 0.1, 1.0, 5.0, 10,0 nM was added to the medioum for 3 days, and subsequently 5 nM GHRH was added for 1 day, thereafter GH amounts in media were measured. The results were as follows: 1) The increase of GH response after testosterone administration to the cultured rat pituitary cell was not significant. 2) The rat pituitary cell response to GHRH was augmented after pretreatment with testosterone. These results are suggested that testosterone has no direct effect on GH secretion, but by increasing the pituitary cell response to GHRH, contributes to the regulation of GH secretion in vitro.
Animals ; Growth Hormone* ; Growth Hormone-Releasing Hormone ; Humans ; Male ; Rats* ; Testosterone* ; Trypsin

No abstract available.
Growth Hormone* ; Testosterone*

Non-alcoholic fatty liver disease (NAFLD), the most common liver disease, represents a spectrum of disease including steatohepatitis, fibrosis, and irreversible cirrhosis. Although a "benign" condition, NAFLD is a risk factor eventually leading to fibrosis and to non-alcoholic steatohepatitis (NASH). A number of evidences support an association between NAFLD/NASH and metabolic syndrome. The pathogenesis of NAFLD/NASH and metabolic syndrome seems to have common pathophysiological mechanisms, with focus on insulin resistance as a key factor. This review discusses the new aspects of NAFLD/NASH pathogenesis, and anticipate that such knowledge will eventually serve to the deveolpment of novel treatment strategies for this disease.
Risk Factors

No abstract available.

This is to report the technique of reversed iliac leg stent-graft in endovascular treatment for isolated internal iliac artery (IIA) aneurysm, which had significant size discrepancy between the common iliac artery (CIA) and external iliac artery (EIA) in 3 patients from different hospitals. Three patients were a 85- and two 82-year-old men. Treated were right IIA aneurysms, sized 6.5x6.2 cm, 5.0x4.0 cm, and 4.1 cm in longest diameter, respectively. The diameters of the right CIA and right EIA measured 21 mm/11 mm, 15 mm/11 mm, and 20 mm/10 mm, respectively. In all cases, reversed iliac leg stent-grafts were prepared on-site; unsheathed and mounted upside-down manually, and deployed in each right CIA. Post-stent-graft angiograms showed complete exclusion of the aneurysms, except for minimal type 1 endoleak in one case. This technique is a useful treatment option in patients with isolated IIA aneurysm.
Aged, 80 and over ; Aneurysm* ; Endoleak ; Endovascular Procedures ; Humans ; Iliac Aneurysm ; Iliac Artery* ; Leg* ; Male

BACKGROUND: Metformin, a well-known anti-diabetic drug, has gained interest due to its association with the reduction of the prevalence of cancer in patients with type 2 diabetes and the anti-proliferative effect of metformin in several cancer cells. Here, we investigated the anti-proliferative effect of metformin with respect to apoptosis and autophagy in H4IIE hepatocellular carcinoma cells. METHODS: H4IIE rat cells were treated with metformin in glucose-free medium for 24 hours and were then subjected to experiments examining the onset of apoptosis and/or autophagy as well as the related signaling pathways. RESULTS: When H4IIE cells were incubated in glucose-free media for 24 hours, metformin and 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) reduced the viability of cells. Inhibition of AMP-activated protein kinase (AMPK) by compound C significantly blocked cell death induced by metformin or AICAR. Pro-apoptotic events (nuclear condensation, hydrolysis of intact poly ADP ribose polymerase and caspase-3) were stimulated by metformin and then suppressed by compound C. Interestingly, the formation of acidic intracellular vesicles, a marker of autophagy, was stimulated by compound C. Although the deprivation of amino acids in culture media also induced apoptosis, neither metformin nor compound C affected cell viability. The expression levels of all of the autophagy-related proteins examined decreased with metformin, and two proteins (light chain 3 and beclin-1) were sensitive to compound C. Among the tested inhibitors against MAP kinases and phosphatidylinositol-3-kinase/mammalian target of rapamycin, SB202190 (against p38MAP kinase) significantly interrupted the effects of metformin. CONCLUSION: Our data suggest that metformin induces apoptosis, but suppresses autophagy, in hepatocellular carcinoma cells via signaling pathways, including AMPK and p38 mitogen-activated protein kinase.
Amino Acids ; AMP-Activated Protein Kinases ; Animals ; Apoptosis* ; Autophagy* ; Carcinoma, Hepatocellular* ; Cell Death ; Cell Survival ; Culture Media ; Humans ; Hydrolysis ; Metformin* ; Phosphotransferases ; Poly(ADP-ribose) Polymerases ; Prevalence ; Protein Kinases ; Rats ; Sirolimus

Sciatic nerve injury after stretching exercise is uncommon. We report a case of an 18-year-old female trained dancer who developed sciatic neuropathy primarily involving the tibial division after routine stretching exercise. The patient presented with dysesthesia and weakness of the right foot during dorsiflexion and plantarflexion. The mechanism of sciatic nerve injury could be thought as hyperstretching alone, not caused by both hyperstretching and compression. Electrodiagnostic tests and magnetic resonance imaging revealed evidence of the right sciatic neuropathy from the gluteal fold to the distal tibial area, and partial tear of the left hamstring origin and fluid collection between the left hamstring and ischium without left sciatic nerve injury. Recovery of motor weakness was obtained by continuous rehabilitation therapy and some evidence of axonal regeneration was obtained by follow-up electrodiagnostic testing performed at 3, 5, and 12 months after injury.
Adolescent ; Axons ; Female ; Follow-Up Studies ; Foot ; Humans ; Ischium ; Lower Extremity ; Magnetic Resonance Imaging ; Muscle Stretching Exercises ; Paresthesia ; Regeneration ; Rehabilitation ; Sciatic Nerve* ; Sciatic Neuropathy

BACKGROUND: FSH is a heterodimeric glycoprotein and is composed of alpha and beta subunits. alpha subunit is common to FSH and LH, while an unique beta subunit determines the biological specificity of each hormone. The synthesis of beta subunit is the primary rate-limiting step in the synthesis of each hormone. Although FSH plays a pivotal role in folliculogenesis and ovulation, very little studies have been performed on the regulation of FSH beta gene expression. Therefore, the present study attempted to examine the effect of GnRH or activin on the expression of FSH beta mRNA as well as FSH release and signaling pathway involved in their actions. METHODS: The primary cultures of rat anterior pituitary were used for this study. To determine FSH beta mRNA levels, northern blotting method was used. The concentration of FSH in the culture medium was evaluated by using a specific radioimmunoassay for rat FSH. RESULTS: PMA, an activator of PKC, increased FSH beta mRNA levels and FSH release, whereas forskolin, an activator of adenylate cyclase, showed no effect. The application of GnRH augmented FSH release, but not FSH beta mRNA levels. However, the administration of activin increased FSH beta mRNA levels as well as FSH release. Staurosporine, an inhibitor of PKC, suppressed activin-induced increment of FSH beta mRNA levels and FSH release. CONCLUSION: The present study demonstrated that activin rather than GnRH is a major regulator for FSH beta mRNA expression, and suggest that PKC-dependent pathway is also involved in the action of activin on the expression of FSH beta mRNA and FSH release.
Activins ; Adenylyl Cyclases ; Animals ; Blotting, Northern ; Colforsin ; Female ; Follicle Stimulating Hormone ; Follicle Stimulating Hormone, beta Subunit ; Gene Expression* ; Glycoproteins ; Gonadotropin-Releasing Hormone ; Ovulation ; Radioimmunoassay ; Rats* ; RNA, Messenger ; Sensitivity and Specificity ; Staurosporine

To know recent status and the point at issue of postmortem investigation in Jeju, the southernmost island in Korea has short history of forensic practice, we analyzed unnatural deaths investigated in Jeju during the five years of 1988 through 2002 inclusively. Of the total number of unnatural deaths (1, 118), 349 of the deceased (31.2%) were studied by autopsy in this period. Advisably, the annual autopsy rate was increased gradually with an increase of unnatural deaths. Drowning occupied large proportion (25.6%) of unnatural deaths. A sudden increase of thermal injury and intoxication in 2002 has attracted attention. Postmortem investigation conducted by prosecutor without participation of expert witness involves a lot of risk and that is one of the current nationwide issue as well as in Jeju. In conclusion, the role of forensic specialist in scene investigation and necessity of administrative support for improvement of medicolegal investigation system in Jeju. is emphasized.
Autopsy ; Drowning ; Expert Testimony ; Korea ; Specialization

BACKGROUND: It is well known that growth hormone (GH) stimulates animal growth, but studies on metabolic effects of growth hormone have recently been increasing. The purpose of this study was to clarify the effects of growth hormone treatment on body composition and glucose metabolism in hypophysectomized growth hormone-deficient rats. METHODS: The 20-week-old rnale Sprague-Dawley rats were hypophysectomized and replaced with cortisol and thyroxine for 8 weeks, then administered with recombinant human growth hormone for 2 weeks. Group 1 consisted of intact controls (n 15), while group 2 consisted of hypophysectomized controls (n 12), and group three consisted of those with GH treatment (n 13). The body weights, body composition, blood glucose levels, plasma insulin-like growth factor-I (IGF-I) levels, euglycemic hyperinsulinemic clamp test, and glycogen synthase activities in gastrocnemius muscle were measured before and after growth hormone treatment. RESULTS: Plasma IGF-I levels in GH-treated group increased to intact control group levels after 2 weeks of GH treatment. There were significant changes in body composition after the treatment (fat mass significantly decreased and lean body mass significantly increased). There were no changes in glucose metabolism in peripheral tissue after 2 weeks of GH treatment. CONCLUSION: Human GH treatment (4 IU/kg/day) in adult hypophysectomized GH-deficient rats changed the body composition, but did not alter the glucose metabolism in peripheral tissue.
Adult* ; Animals ; Blood Glucose ; Body Composition* ; Body Weight ; Glucose* ; Glycogen Synthase ; Growth Hormone* ; Human Growth Hormone ; Humans ; Hydrocortisone ; Insulin-Like Growth Factor I ; Metabolism* ; Muscle, Skeletal ; Plasma ; Rats* ; Rats, Sprague-Dawley ; Thyroxine