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

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.

No abstract available.
Growth Hormone* ; Testosterone*

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

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

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

BACKGROUND: Multi-drug resistant (MDR) Acinetobacter baumannii has emerged as a significant infectious agent in hospitals worldwide. The purpose of this study was to determine the molecular characterization of MDR A. baumannii clinical isolates. METHODS: Two hundred eighty-five strains of non-duplicated A. baumannii collected from March to November 2011 from a university hospital laboratory located in the Wonju area of the Gangwon province of Korea were analyzed for MDR genes. RESULTS: All of the 285 imipenem-resistant A. baumannii isolates were encoded by a blaOXA-23-like gene, and all isolates with the blaOXA-23-like gene had the upstream element ISAba1. The 16S rRNA methylase gene armA was detected in 153 (50.2%) clinical isolates, but rmtA, rmtB, rmtC, rmtD and npmA were not detected in any isolates in the present study. The gene encoding aac(6')-Ib was the most prevalent aminoglycoside-modifying enzyme. The sequencing data for the quinolone resistance-determining region of gyrA and parC revealed the presence of Ser (TCA) 83 to Leu (TTA) and Ser (TCG) 80 to Leu (TTG) substitutions. All but one of the 285 A. baumannii isolates showed similar band patterns on repetitive extragenic palindromic-PCR profiles. CONCLUSION: The molecular characteristics of the resistance genes of MDR A. baumannii isolates obtained from the Wonju area of Gangwon province were similar to those of other areas in Korea.
Acinetobacter ; Acinetobacter baumannii ; beta-Lactamases ; Genes, MDR ; Imipenem ; Korea ; Laboratories, Hospital ; Methyltransferases

A 44-year-old man, who had a history of myocardial infarction (MI) due to thrombotic occlusion of right coronary artery (RCA) aneurysm, visited emergency department presenting with ST-segment elevation myocardial infarction (STEMI). The patient had been on oral anticoagulant therapy (warfarin) from the first thrombotic event, but the medication had been recently changed to aspirin 4 months before the second event. Emergent coronary angiography revealed thrombotic total occlusion of RCA with heavy thrombotic burden from middle RCA to the ostium of the posterior descending branch. Combination pharmacotherapy was performed with anticoagulants (heparin), fibrinolytics (urokinase), and Glycoprotein IIb/IIIa antagonists (abciximab), in addition to mechanical thrombosuction. However, on hospital day 2, the patient complained recurrent chest pain and again underwent coronary angiography, which revealed distal embolization of large thrombus to the posterior lateral branch. Coronary flow was recovered after repeated mechanical thrombosuction was performed. This case has shown the importance of aggressive combination drug therapy, accompanied by mechanical thrombosuction in patient with myocardial infarction due to thrombotic occlusion of coronary artery aneurysm and the importance of unceasing life-long anticoagulant therapy in those particular patients.
Adult ; Aneurysm* ; Anticoagulants ; Aspirin ; Chest Pain ; Coronary Aneurysm ; Coronary Angiography ; Coronary Occlusion* ; Coronary Vessels* ; Drug Therapy ; Drug Therapy, Combination ; Emergency Service, Hospital ; Glycoproteins ; Humans ; Myocardial Infarction* ; Thrombectomy ; Thrombosis ; Warfarin*