Giant-cell tumor is considered one of the benign tumors which is predilected at an ends of a long bone. Although many reports of giant-cell tumor affecting the sacrum have been recentIy presented, the report of the tumor involving coccyx is not comparatively frequent. A case of relatively uncommon giant-cell tumor involving the coccyx is presented with the review of the relevant literature.
Coccyx ; Sacrum

Blood-borne metastatic involvement of the gastric mucosa as a result of cancer is a rare occurrence. The tumors which were most commonly reported to metastasize to the stomach include melanoma, breast carcinoma, and lung carcinoma. Some reports document that large cell carcinoma and squamous cell carcinoma of the lungs have a higher pre- dilection for gastrointestinal tract metastases. Upper gastrointestinal endoscopic findings of metastatic lesions may vary but often produce a characteristic single or multiple bulls eye or target lesion. Therefore, whenever single or multiple target lesions are seen in the stomach on upper gastrointestinal endoscopy or barium study, the examination should include careful radiographic evaluation of the chest. Moreover, when the patient is known to have lung cancer, metastatic disease should be suspected. With a correct diagnosis and proper treatment, relief of symptoms and prolongation of life can sometimes be achieved, A case in reported involving squamous cell lung cancer with stomach metastasis in a 73 year-old woman. The patient was diagnosed by bronchoscopy, upper gastrointestinal endoscopy, chest CT, and abdominal CT. The chest and abdominal CT revealed a poorly marginated, lobulated, and 4 x 3 cm sized mass lesion in the right lower lobe causing obstruction of right lower lobe bronchus with invasion to the left atrium. right inferior pulmonary vein, and superior vena cava. Mediastimal lymph node enlargement and liver metastasis was also detected. Upper gastrointestinal endoscopy showed two "bulls eye" lesions with different sizes and two nodules without tip ulceration.
Aged ; Barium ; Breast Neoplasms ; Bronchi ; Bronchoscopy ; Carcinoma, Large Cell ; Carcinoma, Squamous Cell ; Diagnosis ; Endoscopy, Gastrointestinal ; Female ; Gastric Mucosa ; Gastrointestinal Tract ; Heart Atria ; Humans ; Life Support Care ; Liver ; Lung Neoplasms* ; Lung* ; Lymph Nodes ; Melanoma ; Neoplasm Metastasis* ; Pulmonary Veins ; Stomach* ; Thorax ; Tomography, X-Ray Computed ; Ulcer ; Vena Cava, Superior

The diffuse nodular lung lesion has a diagnostic problem and should be made differential diagnosis. A chest X-ray of 62-year-old male patient with dyspnea showed small-sized scattered multinodular lesion on entire lung field. Bronchoalveolar lavage and transbronchial needle aspiration showed the non-specific findings, so open lung biopsy was done and revealed bronchioloalveolar cell carcinoma.
Biopsy ; Bronchoalveolar Lavage ; Diagnosis, Differential ; Dyspnea ; Humans ; Lung Diseases* ; Lung* ; Male ; Middle Aged ; Needles ; Thorax

Hypertrophic osteoarthropathy(HOA) is a systemic disorder primary affecting the bones, joints, and soft tissues and characterized by several(or all) of the followings ; 1) Clubbing of digits, 2) Persistent new bone formation particulary involving long bones of the distal extremites, 3) Symmetric arthritis-like changes in the joints and periarticular tissue, most commonly the ankles, knees, wrist, and elbows, 4) Increased thickness of the subcutaneous soft tissues in the distal one-third of the arms and legs, and 5) Neurovascular changes of the hands and feet, including chronic erythema, paresthesis, and increase sweating. Most of cases of HOA are secondary to intrathoracic neoplasms, while the remaining few cases are secondary to other disease in the chest or elsewhere. We experienced a case of HOA in association with lung abscess in 26-yr-old male and reported with a review of literatures.
Ankle ; Arm ; Elbow ; Erythema ; Foot ; Hand ; Humans ; Joints ; Knee ; Leg ; Lung Abscess* ; Lung* ; Male ; Osteoarthropathy, Primary Hypertrophic ; Osteoarthropathy, Secondary Hypertrophic* ; Osteogenesis ; Sweat ; Sweating ; Thorax ; Wrist

Background: Uncoupling protein 1 (UCP1) is a proton uncoupler located across the mitochondrial membrane gener‑ ally involved in thermogenesis of brown adipose tissues. Although UCP1 is known to be strongly expressed in brown adipocytes, recent evidence suggest that white adipocytes can also express UCP1 under certain circumstances such as cold- or β-adrenergic receptor-stimulation, allowing them to acquire brown adipocyte-like features thereby becoming ’beige’ adipocytes. Results: In this study, we report that UCP1 can be expressed in adipose-tissue macrophages (ATM) lacking func‑ tional hypoxia-inducible factor-1 (HIF-1) and this does not require cold- nor β-adrenergic receptor activation. By using myeloid-specific Hif-1α knockout (KO) mice, we observed that these mice were protected from diet-induced obesity and exhibited an improved thermogenic tolerance upon cold challenge. ATM isolated from white adipose tissues (WAT) of these mice fed with high fat diet exhibited significantly higher M2-polarization, decreased gly‑ colysis, increased mitochondrial functions and acetyl-CoA levels, along with increased expression of Ucp1, peroxisome proliferator activated receptor-gamma co-activator-1a, and others involved in histone acetylation. Consistent with the increased Ucp1 gene expression, these ATM produced a significant amount of heat mediating lipolysis of cocultured adipocytes liberating free fatty acid. Treating ATM with acetate, a substrate for acetyl-CoA synthesis was able to boost the heat production in wild-type or Hif-1α-deficient but not UCP1-deficient macrophages, indicating that UCP1 was necessary for the heat production in macrophages. Lastly, we observed a significant inverse correlation between the number of UCP1-expressing ATM in WAT and the body mass index of human individuals. Conclusions UCP1-expressing ATM produce the heat to mediate lipolysis of adipocytes, indicating that this can be a novel strategy to treat and prevent diet-induced obesity.

Background: Uncoupling protein 1 (UCP1) is a proton uncoupler located across the mitochondrial membrane gener‑ ally involved in thermogenesis of brown adipose tissues. Although UCP1 is known to be strongly expressed in brown adipocytes, recent evidence suggest that white adipocytes can also express UCP1 under certain circumstances such as cold- or β-adrenergic receptor-stimulation, allowing them to acquire brown adipocyte-like features thereby becoming ’beige’ adipocytes. Results: In this study, we report that UCP1 can be expressed in adipose-tissue macrophages (ATM) lacking func‑ tional hypoxia-inducible factor-1 (HIF-1) and this does not require cold- nor β-adrenergic receptor activation. By using myeloid-specific Hif-1α knockout (KO) mice, we observed that these mice were protected from diet-induced obesity and exhibited an improved thermogenic tolerance upon cold challenge. ATM isolated from white adipose tissues (WAT) of these mice fed with high fat diet exhibited significantly higher M2-polarization, decreased gly‑ colysis, increased mitochondrial functions and acetyl-CoA levels, along with increased expression of Ucp1, peroxisome proliferator activated receptor-gamma co-activator-1a, and others involved in histone acetylation. Consistent with the increased Ucp1 gene expression, these ATM produced a significant amount of heat mediating lipolysis of cocultured adipocytes liberating free fatty acid. Treating ATM with acetate, a substrate for acetyl-CoA synthesis was able to boost the heat production in wild-type or Hif-1α-deficient but not UCP1-deficient macrophages, indicating that UCP1 was necessary for the heat production in macrophages. Lastly, we observed a significant inverse correlation between the number of UCP1-expressing ATM in WAT and the body mass index of human individuals. Conclusions UCP1-expressing ATM produce the heat to mediate lipolysis of adipocytes, indicating that this can be a novel strategy to treat and prevent diet-induced obesity.

Background: Uncoupling protein 1 (UCP1) is a proton uncoupler located across the mitochondrial membrane gener‑ ally involved in thermogenesis of brown adipose tissues. Although UCP1 is known to be strongly expressed in brown adipocytes, recent evidence suggest that white adipocytes can also express UCP1 under certain circumstances such as cold- or β-adrenergic receptor-stimulation, allowing them to acquire brown adipocyte-like features thereby becoming ’beige’ adipocytes. Results: In this study, we report that UCP1 can be expressed in adipose-tissue macrophages (ATM) lacking func‑ tional hypoxia-inducible factor-1 (HIF-1) and this does not require cold- nor β-adrenergic receptor activation. By using myeloid-specific Hif-1α knockout (KO) mice, we observed that these mice were protected from diet-induced obesity and exhibited an improved thermogenic tolerance upon cold challenge. ATM isolated from white adipose tissues (WAT) of these mice fed with high fat diet exhibited significantly higher M2-polarization, decreased gly‑ colysis, increased mitochondrial functions and acetyl-CoA levels, along with increased expression of Ucp1, peroxisome proliferator activated receptor-gamma co-activator-1a, and others involved in histone acetylation. Consistent with the increased Ucp1 gene expression, these ATM produced a significant amount of heat mediating lipolysis of cocultured adipocytes liberating free fatty acid. Treating ATM with acetate, a substrate for acetyl-CoA synthesis was able to boost the heat production in wild-type or Hif-1α-deficient but not UCP1-deficient macrophages, indicating that UCP1 was necessary for the heat production in macrophages. Lastly, we observed a significant inverse correlation between the number of UCP1-expressing ATM in WAT and the body mass index of human individuals. Conclusions UCP1-expressing ATM produce the heat to mediate lipolysis of adipocytes, indicating that this can be a novel strategy to treat and prevent diet-induced obesity.

Background: Uncoupling protein 1 (UCP1) is a proton uncoupler located across the mitochondrial membrane gener‑ ally involved in thermogenesis of brown adipose tissues. Although UCP1 is known to be strongly expressed in brown adipocytes, recent evidence suggest that white adipocytes can also express UCP1 under certain circumstances such as cold- or β-adrenergic receptor-stimulation, allowing them to acquire brown adipocyte-like features thereby becoming ’beige’ adipocytes. Results: In this study, we report that UCP1 can be expressed in adipose-tissue macrophages (ATM) lacking func‑ tional hypoxia-inducible factor-1 (HIF-1) and this does not require cold- nor β-adrenergic receptor activation. By using myeloid-specific Hif-1α knockout (KO) mice, we observed that these mice were protected from diet-induced obesity and exhibited an improved thermogenic tolerance upon cold challenge. ATM isolated from white adipose tissues (WAT) of these mice fed with high fat diet exhibited significantly higher M2-polarization, decreased gly‑ colysis, increased mitochondrial functions and acetyl-CoA levels, along with increased expression of Ucp1, peroxisome proliferator activated receptor-gamma co-activator-1a, and others involved in histone acetylation. Consistent with the increased Ucp1 gene expression, these ATM produced a significant amount of heat mediating lipolysis of cocultured adipocytes liberating free fatty acid. Treating ATM with acetate, a substrate for acetyl-CoA synthesis was able to boost the heat production in wild-type or Hif-1α-deficient but not UCP1-deficient macrophages, indicating that UCP1 was necessary for the heat production in macrophages. Lastly, we observed a significant inverse correlation between the number of UCP1-expressing ATM in WAT and the body mass index of human individuals. Conclusions UCP1-expressing ATM produce the heat to mediate lipolysis of adipocytes, indicating that this can be a novel strategy to treat and prevent diet-induced obesity.

Background: Uncoupling protein 1 (UCP1) is a proton uncoupler located across the mitochondrial membrane gener‑ ally involved in thermogenesis of brown adipose tissues. Although UCP1 is known to be strongly expressed in brown adipocytes, recent evidence suggest that white adipocytes can also express UCP1 under certain circumstances such as cold- or β-adrenergic receptor-stimulation, allowing them to acquire brown adipocyte-like features thereby becoming ’beige’ adipocytes. Results: In this study, we report that UCP1 can be expressed in adipose-tissue macrophages (ATM) lacking func‑ tional hypoxia-inducible factor-1 (HIF-1) and this does not require cold- nor β-adrenergic receptor activation. By using myeloid-specific Hif-1α knockout (KO) mice, we observed that these mice were protected from diet-induced obesity and exhibited an improved thermogenic tolerance upon cold challenge. ATM isolated from white adipose tissues (WAT) of these mice fed with high fat diet exhibited significantly higher M2-polarization, decreased gly‑ colysis, increased mitochondrial functions and acetyl-CoA levels, along with increased expression of Ucp1, peroxisome proliferator activated receptor-gamma co-activator-1a, and others involved in histone acetylation. Consistent with the increased Ucp1 gene expression, these ATM produced a significant amount of heat mediating lipolysis of cocultured adipocytes liberating free fatty acid. Treating ATM with acetate, a substrate for acetyl-CoA synthesis was able to boost the heat production in wild-type or Hif-1α-deficient but not UCP1-deficient macrophages, indicating that UCP1 was necessary for the heat production in macrophages. Lastly, we observed a significant inverse correlation between the number of UCP1-expressing ATM in WAT and the body mass index of human individuals. Conclusions UCP1-expressing ATM produce the heat to mediate lipolysis of adipocytes, indicating that this can be a novel strategy to treat and prevent diet-induced obesity.