We present images of an 83-year-old female with a history of osteoporosis and bilateral total knee replacement arthroplasty, referred for bone scintigraphy and single-photon emission computed tomography (SPECT)/computed tomography (CT), owing to left knee pain. No trauma to, or intense exercise of, the kneewas reported. The bone scan and SPECT/CT revealed a focally increased Tc-99m methylene diphosphonate (MDP) uptake in the medial cortex of the left femoral diaphysis with matched linear radiolucency on CT images. This was misinterpreted as atypical femoral stress fracture; however, focal stress reaction injury to the nutrient foramen was confirmed on contrast-enhanced magnetic resonance imaging.
Aged, 80 and over ; Arthroplasty ; Arthroplasty, Replacement, Knee ; Diaphyses ; Female ; Fractures, Stress ; Humans ; Knee ; Magnetic Resonance Imaging ; Osteoporosis ; Radionuclide Imaging ; Technetium Tc 99m Medronate ; Tomography, Emission-Computed ; Tomography, Emission-Computed, Single-Photon

We present images of an 83-year-old female with a history of osteoporosis and bilateral total knee replacement arthroplasty, referred for bone scintigraphy and single-photon emission computed tomography (SPECT)/computed tomography (CT), owing to left knee pain. No trauma to, or intense exercise of, the kneewas reported. The bone scan and SPECT/CT revealed a focally increased Tc-99m methylene diphosphonate (MDP) uptake in the medial cortex of the left femoral diaphysis with matched linear radiolucency on CT images. This was misinterpreted as atypical femoral stress fracture; however, focal stress reaction injury to the nutrient foramen was confirmed on contrast-enhanced magnetic resonance imaging.

BACKGROUND/OBJECTIVES: Dietary behavior and life stress in adolescence is related to growth rate and learning ability. This study was conducted to identify the relations between dietary habits, dietary attitude nutritional knowledge and life stress among high school girls in Korea and China. SUBJECTS/METHODS: The subjects of this study were 221 high school girls in Korea and 227 high school girls in China. The questionnaire were about dietary habits, dietary attitude, nutritional knowledge and life stress. RESULTS: The dietary habits of chinese girls were healthier than those of Korean girls with a significant difference (P < .001). There was no significant difference in dietary attitude between Korean girls and Chinese girls. Korean girls had more nutritional knowledge than Chinese girls with a significant difference (P < .001). Korean girls did less physical exercise but spent more time watching TV and using PCs, compared to Chinese girls. Korean girls' degree of confidence in nutrition information that they had learned and their performance in their real lives were low. Also, they had a low level of awareness of the need for nutritional education. There was no significant difference in life stress between the two groups. Dietary habits had a significantly negative correlation with life stress in both Korean and Chinese girls (P < .01, P < .001). As for Chinese students, dietary attitude had a negative correlation with life stress with a significant difference (P < .05). As for Korean girls, nutritional knowledge had a negative correlation with life stress with a significant difference (P < .05), which means as life stress was less, dietary habits were better. CONCLUSIONS: This study shows that effective nutrition education programs should include components that encourage application of learned nutrition information to real life, increase physical exercise and reduce life stress.
Adolescent ; Asian Continental Ancestry Group* ; China ; Education ; Exercise ; Female* ; Food Habits ; Humans ; Korea ; Learning ; Surveys and Questionnaires ; Stress, Psychological*

Wnt signaling is known to be important for diverse embryonic and post-natal cellular events and be regulated by the proteins Dishevelled and Axin. Although Dishevelled is activated by Wnt and involved in signal transduction, it is not clear how Dishevelled-mediated signaling is turned off. We report that guanine nucleotide binding protein beta 2 (Gnb2; Gbeta2) bound to Axin and Gbeta2 inhibited Wnt mediated reporter activity. The inhibition involved reduction of the level of Dishevelled, and the Gbeta2gamma2 mediated reduction of Dishevelled was countered by increased expression of Axin. Consistent with these effects in HEK293T cells, injection of Gbeta2gamma2 into Xenopus embryos inhibited the formation of secondary axes induced either by XWnt8 or Dishevelled, but not by beta-catenin. The DEP domain of Dishevelled is necessary for both interaction with Gbeta2gamma2 and subsequent degradation of Dishevelled via the lysosomal pathway. Signaling induced by Gbeta2gamma2 is required because a mutant of Gbeta2, Gbeta2 (W332A) with lower signaling activity, had reduced ability to downregulate the level of Dishevelled. Activation of Wnt signaling by either of two methods, increased Frizzled signaling or transient transfection of Wnt, also led to increased degradation of Dishevelled and the induced Dishevelled loss is dependent on Gbeta1 and Gbeta2. Other studies with agents that interfere with PLC action and calcium signaling suggested that loss of Dishevelled is mediated through the following pathway: Wnt/Frizzled-->Gbetagamma-->PLC-->Ca+2/PKC signaling. Together the evidence suggests a novel negative feedback mechanism in which Gbeta2gamma2 inhibits Wnt signaling by degradation of Dishevelled.
Adaptor Proteins, Signal Transducing/genetics/*metabolism ; Animals ; Blastomeres/cytology/*metabolism ; Cell Line ; Embryonic Development/genetics ; *Feedback, Physiological ; Frizzled Receptors/genetics/metabolism ; GTP-Binding Proteins/genetics/*metabolism ; Gene Expression Regulation, Developmental ; Humans ; Mutation ; Phosphoproteins/genetics/*metabolism ; Protein Binding ; RNA, Small Interfering/genetics ; Repressor Proteins/genetics/metabolism ; Transfection ; Wnt Proteins/*genetics/metabolism ; Xenopus ; Xenopus Proteins/*genetics/metabolism

We would like to correct the paragraph on page 207.

The mesentery is a structure comprising a double peritoneal layer that attaches the bowel to the abdominal wall. Mesenteric disease can cause various non-specific clinical symptoms in adults and is sometimes found incidentally during unrelated diagnostic imaging studies. CT plays an essential role in the diagnosis of mesenteric disease, which can present with various radiologic features, including a solid mass, cystic mass, or local or diffuse infiltration on CT. Some mesenteric diseases present with distinctive characteristics, while others share similar findings, thereby complicating their differential diagnosis. Therefore, understanding the radiological findings of mesenteric disease is important for accurate diagnosis and appropriate treatment.

PURPOSE: The purpose of this study was to evaluate the ultrasonographic features of pure ductal carcinoma in situ (DCIS) of the breast and to evaluate the correlations of ultrasonographic features with pathologic and biological features. METHODS: A total of 141 lesions in 138 women with pure DCIS who underwent preoperative breast ultrasonography were retrospectively reviewed. Ultrasonographic features were analyzed using the American College of Radiology Breast Imaging Reporting and Data System (BI-RADS) ultrasonography lexicon and the diagnostic criteria of the Japan Society of Ultrasonics in Medicine. Pathologic features including the nuclear grade and presence of comedonecrosis were evaluated. Biological markers including estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (HER2) status, as well as the Ki-67 index, were recorded. Ultrasonographic features were compared with pathologic findings and biological markers using the chi-square test. P-values of < 0.05 were considered to indicate statistical significance. RESULTS: Of the 141 lesions, 75 (53.2%) were mass lesions, 56 (39.7%) were non-mass lesions, and 10 (7.1%) were not visible. The most common feature of the mass pattern was a mass with irregular shape (32.6%), an indistinct margin (27.7%), and hypoechogenicity (37.6%). Microcalcifications were observed in 48 cases (36.6%) as an associated feature. Calcifications outside of a mass were more common than calcifications within a mass. Ultrasonographic microcalcifications and ductal changes were frequently observed in non-mass lesions. Ultrasonographic non-mass lesions were associated with high-grade DCIS (P=0.004) and the presence of comedonecrosis (P=0.006). Microcalcifications were significantly associated with high-grade DCIS (P < 0.001), the presence of comedonecrosis (P < 0.001), an elevated Ki-67 (P < 0.001), and HER2 positivity (P=0.003). CONCLUSION: The most common ultrasonographic feature of pure DCIS was an irregular, hypoechoic mass with an indistinct margin. Ultrasonographic microcalcifications and ductal changes were more frequent in non-mass lesions, which were correlated with poor prognostic factors, such as a high nuclear grade, comedonecrosis, HER2 positivity, and an elevated Ki-67 index.
Biomarkers* ; Breast* ; Carcinoma, Ductal* ; Carcinoma, Intraductal, Noninfiltrating* ; Estrogens ; Female ; Humans ; Information Systems ; Japan ; Pathology ; Receptor, Epidermal Growth Factor ; Receptors, Progesterone ; Retrospective Studies ; Ultrasonics ; Ultrasonography ; Ultrasonography, Mammary

Sirtuin 1 (SIRT1) is a mammalian NAD+-dependent protein deacetylase that regulates cellular metabolism and inflammatory response. The organ-specific deletion of SIRT1 induces local inflammation and insulin resistance in dietary and genetic obesity. Macrophage-mediated inflammation contributes to insulin resistance and metabolic syndrome, however, the macrophage-specific SIRT1 function in the context of obesity is largely unknown. C57/BL6 wild type (WT) or myeloid-specific SIRT1 knockout (KO) mice were fed a high-fat diet (HFD) or normal diet (ND) for 12 weeks. Metabolic parameters and markers of hepatic steatosis and inflammation in liver were compared in WT and KO mice. SIRT1 deletion enhanced HFD-induced changes on body and liver weight gain, and increased glucose and insulin resistance. In liver, SIRT1 deletion increased the acetylation, and enhanced HFD-induced nuclear translocation of nuclear factor kappa B (NF-kappaB), hepatic inflammation and macrophage infiltration. HFD-fed KO mice showed severe hepatic steatosis by activating lipogenic pathway through sterol regulatory element-binding protein 1 (SREBP-1), and hepatic fibrogenesis, as indicated by induction of connective tissue growth factor (CTGF), alpha-smooth muscle actin (alpha-SMA), and collagen secretion. Myeloid-specific deletion of SIRT1 stimulates obesity-induced inflammation and increases the risk of hepatic fibrosis. Targeted induction of macrophage SIRT1 may be a good therapy for alleviating inflammation-associated metabolic syndrome.
Acetylation ; Actins ; Animals ; Collagen ; Connective Tissue Growth Factor ; Diet ; Diet, High-Fat ; Fibrosis ; Glucose ; Inflammation* ; Insulin Resistance ; Liver ; Macrophages ; Metabolism ; Mice* ; NF-kappa B ; Obesity ; Sirtuin 1 ; Sterol Regulatory Element Binding Protein 1 ; Weight Gain

Excessive immune responses induced by ischemia-reperfusion injury (IRI) are known to lead to necrotic and apoptotic cell death, and calcineurin plays a major role in this process. Calcineurin dephosphorylates the nuclear factor of activated T-cells (NFAT), permitting its translocation into the nucleus. As a result, calcineurin promotes the release of pro-inflammatory cytokines, such as tumor necrosis factor-alpha. The overproduction of pro-inflammatory cytokines causes renal cell death. Calcineurin activity is regulated by calpain, a cysteine protease present in the nucleus. Calpain-mediated proteolysis increases the phosphatase activity of calcineurin, resulting in NFAT dephosphorylation. This process has been studied in cardiomyocytes but its role in renal IRI is unknown. Thus, we examined whether calpain regulates calcineurin in renal tubule nuclei. We established an in vivo renal IRI model in mice and identified the protective role of a calcineurin inhibitor, FK506, in this process. Calcineurin is expressed in the nucleus, where it is present in its calpain-cleaved form. FK506 reduced nuclear expression of calcineurin and prevented calcineurin-mediated NFAT activation. Our study shows clearly that FK506 reduces calpain-mediated calcineurin activity. Consequently, calcineurin could not maintain NFAT activation. FK506 reduced renal cell death by suppressing the transcription of pro-inflammatory cytokine genes. This study provides evidence that FK506 protects against inflammation in a renal IRI mouse model. We also provided a mechanism of calcineurin action in the nucleus. Therefore, FK506 could improve renal function by decreasing calcineurin activity in both the cytoplasm and the nucleus of renal tubule cells.
Animals ; Calcineurin* ; Calpain ; Cell Death ; Cysteine Proteases ; Cytokines ; Cytoplasm* ; Inflammation ; Mice ; Myocytes, Cardiac ; Proteolysis ; Reperfusion Injury ; T-Lymphocytes ; Tacrolimus* ; Tumor Necrosis Factor-alpha

Excessive immune responses induced by ischemia-reperfusion injury (IRI) are known to lead to necrotic and apoptotic cell death, and calcineurin plays a major role in this process. Calcineurin dephosphorylates the nuclear factor of activated T-cells (NFAT), permitting its translocation into the nucleus. As a result, calcineurin promotes the release of pro-inflammatory cytokines, such as tumor necrosis factor-alpha. The overproduction of pro-inflammatory cytokines causes renal cell death. Calcineurin activity is regulated by calpain, a cysteine protease present in the nucleus. Calpain-mediated proteolysis increases the phosphatase activity of calcineurin, resulting in NFAT dephosphorylation. This process has been studied in cardiomyocytes but its role in renal IRI is unknown. Thus, we examined whether calpain regulates calcineurin in renal tubule nuclei. We established an in vivo renal IRI model in mice and identified the protective role of a calcineurin inhibitor, FK506, in this process. Calcineurin is expressed in the nucleus, where it is present in its calpain-cleaved form. FK506 reduced nuclear expression of calcineurin and prevented calcineurin-mediated NFAT activation. Our study shows clearly that FK506 reduces calpain-mediated calcineurin activity. Consequently, calcineurin could not maintain NFAT activation. FK506 reduced renal cell death by suppressing the transcription of pro-inflammatory cytokine genes. This study provides evidence that FK506 protects against inflammation in a renal IRI mouse model. We also provided a mechanism of calcineurin action in the nucleus. Therefore, FK506 could improve renal function by decreasing calcineurin activity in both the cytoplasm and the nucleus of renal tubule cells.
Animals ; Calcineurin* ; Calpain ; Cell Death ; Cysteine Proteases ; Cytokines ; Cytoplasm* ; Inflammation ; Mice ; Myocytes, Cardiac ; Proteolysis ; Reperfusion Injury ; T-Lymphocytes ; Tacrolimus* ; Tumor Necrosis Factor-alpha