Osteoclasts are bone-resorbing multinuclear cells derived from hematopoietic stem cells or monocyte/ macrophage lineage cells. Recent identification of RANK/RANKL has provided new insights into the osteoclast differentiation pathway, enabling us to generate osteoclasts without stromal cells, which support osteoclastogenesis. In order to establish a pure osteoclast culture system, we identified the osteoclast precursor cell (c-Kit(+)c-Fms(+)RANK(-) cell), which is a common precursor cell of osteoclasts, macrophages and dendritic cells. Macrophages are induced by M-CSF alone, while a sequential stimulation of M-CSF followed by RANKL effectively induces osteoclast formation. Furthermore, dendritic cells are induced by GM-CSF or GM-CSF plus RANKL. Therefore, we were able to generate pure osteoclasts, macrophages or dendritic cells from the common precursor cell using specific combinations of cytokines. Using this culture system, we found that an adherent condition is critical for osteoclast differentiation. We also found that the osteoclastogenesis induced by M-CSF plus RANKL is completely inhibited by GM-CSF, and that these cells differentiate into a dendritic cell lineage. The osteoclast multinucleation is believed to be induced by cell-cell fusion of mononuclear osteoclasts. Although various molecules have been implicated in the cell-cell fusion of osteoclasts or macrophages, the essential molecule for cell fusion has not been identified. We identified that the dendritic cell-specific transmembrane protein (DC-STAMP) was an essential cell-cell fusion molecule for osteoclasts and foreign body giant cells, and that DC-STAMP deficient mice have no multinuclear osteoclasts. Here I review the osteoclast development from immature precursor cells to multinuclear osteoclasts.
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Gene manipulation by disrupting important genes using homologous recombination in mammals has provided important insights into their function and development with regard to disease. However, many questions related to the genetic pathways that regulate cellular differentiation and function remain to be clarified. In particular, analysis of genetic pathways that control embryonic skeletal development is often hindered by the disruption of critical genes that function in early embryogenesis, thereby leading to embryonic or perinatal death and thus preventing study of the role of these genes in skeletal development and physiology postnatally. To overcome this problem gene-targeting methods, using site- and time-specific recombination based methods with the Cre/loxP system, have been used to delete particular genes in specific tissues and stages during development. Thus, the generation and characterization of transgenic mice expressing Cre recombinase, under the control of a tissue-specific and stage-specific promoter, has become prerequisite for study of the physiology and homeostasis of specific tissues during a specific time frame. In this report, we introduce the principles and methods of site-specific and time-specific recombination using the Cre/loxP and inducible Cre system, and discuss the potential applications for applying this system to the study of the development and physiology of the skeletal system.
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J Korean Endocr Soc. 2006;21(5):373-381. Published online October 1, 2006
BACKGROUND New onset diabetes is a major complication after kidney transplantation. However, the natural course of posttransplantation diabetes mellitus (PTDM) remains unclear. The aim of this study was to demonstrate the detailed natural courses of PTDM according to the onset and persistency of hyperglycemia, and to investigate risk factors for development of different courses of PTDM in renal allograft recipients. METHODS: A total of 77 renal allograft recipients without previously known diabetes were enrolled and performed a serial 75 g oral glucose tolerance test at 0, 1, and 7 years after kidney transplantation. Patients were classified according to the onset and persistency of PTDM: early PTMD (E-PTDM), late PTDM (L-PTDM), persistent PTDM (P-PTDM), transient PTMD (T-PTDM), and non-PTDN (N-PTDM). RESULTS: The incidence of each group was as follows: E-PTDM, 39%; L-PTDM, 11.7%; P-PTDM, 23.4% T-PTDM, 15.6%; N-PTDM, 49.3%. Tacrolimus and female gender were associated with the development of E-PTDM. Among E-PTDM, age at transplantation was a high risk factor for the development of P-PTDM. Higher BMI at year1 was associated with the development of L-PTDM. CONCLUSION: Different risk factors were associated with various natural courses of PTDM. Since old age and female gender are not modifiable risk factors, it may be important to modify immunosuppressive therapy regimens for the prevention of E-PTDM and control of body weight for L-PTDM.
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BACKGROUND Peripheral vascular disease (PVD) is a primary risk factor of foot amputation. In patients with diabetes mellitus (DM), the frequency of PVD is twice that of the general population. The ankle-brachial index (ABI) is a valuable diagnostic test for PVD. In this study, we investigated the relationship between the ABI and PVD, as well as the cutoff value of ABI in the diagnosis of PVD, and analyzed whether the ABI can be used as a predictor for amputation. METHODS: Fifty-two type 2 DM patients (31 males, 21 females) underwent peripheral angiography. PVD was defined as the complete obstruction of arteries and/or significant luminal narrowing, with collateral vessels formation, using peripheral angiography. The ABI was calculated by measurement of the segmental pressure using the Doppler method. RESULTS: Significant differences were observed between PVD and non-PVD patients in terms of age, systolic pressure and total cholesterol (each P < 0.05). The ABI was significantly lower in legs with PVD (P < 0.01) and an ABI less than 0.90 was adequate for diagnosing PVD. The risk of amputation was significantly increased in relation to the ABI level, and the risk of amputation was 21.5 times greater in a leg with an ABI less than 0.40 compared to 0.90 (P = 0.021). CONCLUSION: ABI is a good diagnostic test for PVD and a good predictor of the need for amputation.
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BACKGROUND The prevalence of palpable thyroid nodules in the general population is about 5%, and is 3~5 times higher in women than in men. However, much higher prevalence, up to 50%, was reported from autopsy data. Recently, the use of high resolution ultrasonography for routine check-up has resulted in much more detection of non-palpable thyroid nodules. We studied the prevalence of thyroid nodules in healthy adults without history of thyroid disease, and compared the prevalence in relation to palpability, age and gender. METHODS: The prevalence of thyroid nodules was studied in adults aged from 20 to 79 years who had visited the health promotion center at Asan Medical Center, Seoul, Korea, from Jan 2002 to Dec 2003. Subjects with previous thyroid disease were excluded. 7,440 subjects (6,168 female, 1,272 men) were included in this study. Thyroid palpation was performed and followed by ultrasonography using a 12-MHz real-time scanner. RESULTS: Thyroid nodules were detected in 3,040 of the 7,440 subjects (41%). Palpable nodules were present in 213 (3%), and non-palpable, but ultrasonographically detected thyroid nodules were present in 2,827 (38%). Thyroid nodules were present in 2,602 women (42.2%) and 370 men (29%). Among them, 159 women (2.6%) and 54 men (4.2%) had palpable thyroid nodules and 2,443 women (39.6%) and 316 men (24.8%) had non-palpable but ultrasonographically detected nodules. A significant linear trend was found between age and the prevalence of thyroid nodules. CONCLUSIONS: The prevalence of ultrasonographically detected thyroid nodules in adults with no previous history of thyroid disease was 41%. The prevalence of palpable nodules and non-palpable, but ultrasonographically detected nodules were 3% and 38%, respectively. Thyroid nodules were detected in 42.2% of women and 29% of men, showing that thyroid nodules are very common in healthy adults, even in men.
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BACKGROUND Polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism and chronic anovulation, and this is a common disorder in premenopausal women. However, the pathogenesis is still uncertain. There has been no studies about PCOS-related genetic abnormalities in Korea. In this study, we examined the frequency of the adiponectin and ghrelin genotypes in Korean women with PCOS. METHODS: Fifty four women with PCOS and 174 regular cycling healthy women were recruited for the study, and their reproductive hormones and metabolic profiles were measured. The polymorphisms of the ghrelin and adiponectin genes were analyzed. RESULTS: The frequency of ghrelin gene polymorphism was not different between the women with PCOS and the controls. The frequency of the TG adiponectin genotype was higher and the frequency of the TT genotype was lower in the women with PCOS compared to the controls (P < 0.05). For the PCOS women with GG adiponectin genotype, their triglycerides levels were significantly higher compared to the PCOS women with the TT and TG genotypes even after adjusting for the BMI. CONCLUSION: Adiponectin gene polymorphism is associated with presence of PCOS and it is responsible for the dyslipidemia seen in PCOS. Yet further study is required to confirm the role of this genetic polymorphism in the susceptibility to PCOS and the associated metabolic features.
Pheochromocytoma arises from chromaffin cells of the paraganglionic system. Urinary bladder pheochromocytoma is very rare tumor that accounts for less than 0.06% of all urinary bladder tumors and it is less than 1% of all pheochromocytoma. Urinary bladder pheochromocytoma usually arises from the sympathetic nervous system of the bladder wall. Paroxysmal headache and palpitation precipitated by micturition are common specific symptoms of this tumor. The paroxysm commonly persists or the patients relapse in a few days or months. Herein, we report a case of urinary bladder pheochromocytoma with a long asymptomatic period.
A 58-year-old man was investigated for his complaints of chronic frontal headache. The endocrinologic hormone studies were compatible with diabetes insipidus and suggestive of panhypopituitarism. Sellar MRI showed a cystic sellar lesion with peripheral rim enhancement after contrast injection, and this led to an initial diagnosis of pituitary adenoma with hemorrhagic necrosis. He underwent an operation via the transsphenoidal approach to access the pituitary gland. During the operation, purulent materials were obtained and no tumor or other associated lesions were detected. There was no evidence of current or previous septicemic illness, meningitis, cavernous sinus thrombosis or sinus infection. All the cultures we obtained were negative. He was put on antibiotics and discharged after 4 weeks. Now, 18 months after treatment, he is doing well.
Jae Youn Park, Seoung Young Kim, Jin Nam Kim, Seo Jung Yang, Ju Ri Park, Bo Sung Kwan, Dong Jin Kim, Kye Won Lee, Kyung Mook Choi, Sei Hyun Baik, Moon Kyoung Joo, Jin Soo Chang
J Korean Endocr Soc. 2006;21(5):414-418. Published online October 1, 2006
Mayer-Rokitansky-Kuster-Hauser (MRKH) syndrome is the second frequent cause of primary amenorrhea. There have been several reports concerning gynecologic disease in MRKH syndrome, but there has been no case about a colon cancer in a patient with this condition. A 43 years old woman, who reported primary amenorrhea with sexual infantilism, was evaluated in our department because of lower abdominal pain: she presented with a suprapubic mass. To evaluate the suprapubic abdominal mass and primary amenorrhea, abdominal MRI, colonoscopy and endocrine tests were done. She had no gynecologic organs, and she finally was diagnosed as having colon cancer with the atypical form of MRKH syndrome (bilateral gonadal agenesis 46 XX). To the best of our knowledge this is the first case concerning primary colon cancer in a patient with MRKH syndrome.
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Patients with adrenocortical carcinoma (ACC) present with evidence of excessive adrenal steroid hormone in approximately 60% of cases, in which rapidly progressing Cushing's syndrome with or without virilization is the most frequent presentation. Some patients experience an increase or a decline in cortisol production through the progression of their ACC. We report on an unusual case of a cortisol-producing ACC, and the patient presented with a decline in cortisol production, followed by an increase in cortisol production, through the progression of the tumor. A 65-year-old woman who manifested with facial edema and weight gain was diagnosed with Cushing's syndrome, caused by cortisol producing ACC. The patient was treated with adrenalectomy. However, 8 months later, a metastatic hepatic tumor of recurred ACC was detected. At that time, the hormonal evaluation revealed that the liver mass did not produce any hormones. The patient was treated with metastatectomy. Four months later, a relapsed tumor was detected. Increased cortisol production was observed at that time. We speculate there was a change in the clonal dominance within the ACC and this change might cause such a difference. This is the first case report of ACC that showed variable hormone production during progression.
Although the spontaneous rupture of a pheochromocytoma is rare, it can be fatal if not promptly diagnosed. Hemorrhagic necrosis of the tumor will require an emergency operation, as this causes intraperitoneal hemorrhaging. Excessive vasoconstriction, tachycardia and labile blood pressure are the signs of a ruptured pheochromocytoma. The standard diagnostic tool of such a condition is an abdominal computed tomographic scan. Although the exact mechanism of the rupture is still unknown, a hemorrhage inside the tumor or a high intra-cortical pressure, due to rapid growth of the tumor, is known to play a major role in the pathogenesis. Herein is reported the case of a 53-year old male patient with a pheochromocytoma and an acute abdomen. The CT scan showed a left adrenal gland mass, with a hemorrhage in the left perirenal space. The patient underwent an emergency adrenalectomy, with the final histopathological diagnosis being that of a pheochromocytoma. Prompt recognition and early surgical intervention can improve outcome.
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Jae Ho Park, Ji Hoon Ahn, Mi Hee Kang, Jong Chul Won, Kyung Wook Lee, Yeo Joo Kim, Ji Oh Mok, Hyeong Kyu Park, Chul Hee Kim, Sang Jin Kim, Dong Won Byun, Kyo Il Suh, Myung Hi Yoo
J Korean Endocr Soc. 2006;21(5):428-432. Published online October 1, 2006
Antithyroid hormone autoantibodies can be present in the sera of patients with thyroid and non-thyroid disorders. Antithyroid hormone autoantibodies in a patient's serum interfere with radioimmunoassay of thyroid hormones. Clinically, this interference can result in discordance between the serum thyroid hormone levels and the clinical features of the patient, which can lead to misdiagnosis or inappropriate treatment. We experienced a woman who had primary hypothyroidism with unexpectedly high concentrations of serum total triiodothyronine (T(3)) and free T(3), and she had been treated for Graves' disease in the past. Through the use of a polyethylene glycol precipitation method, we detected the anti-triiodothyronine autoantibodies in her serum. We report on this case along with a review of the related literature.
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