ABSTRACT
Secondary osteomyelitis pubis is rare, particularly when it arises due to genitourinary postoperative infections, such as those occurring after vulvar cancer surgeries. Diagnosis and treatment of secondary osteomyelitis pubis are challenging. Here, we report on two cases of osteomyelitis pubis caused by Pseudomonas aeruginosa secondary to surgical site infections after of vulvar cancer surgeries. Both patients were in their 80 s and underwent vulvectomy and vulvar reconstructive surgery using skin flaps. The patients were discharged from the hospital after postoperative antimicrobial treatment for surgical site infections and continued self-cleaning of the wound dehiscence. Both patients presented, respectively, with gait disturbance due to pain in the pubic bone postoperatively at 24 and 7 weeks. Computed tomography (CT) and magnetic resonance imaging (MRI) were performed to confirm the diagnosis of osteomyelitis pubis. The patients underwent pubic bone debridement, and tissue culture revealed the presence of Pseudomonas aeruginosa that required several months of antimicrobial therapy. Pubic pain and gait disturbance improved with treatment, and no osteomyelitis pubis relapse has been observed in both cases 12 and 9 months since treatment initiation. CT and MRI were useful in diagnosing osteomyelitis pubis. Early debridement helped identify the causative organism and appropriate antibiotics selection.
ABSTRACT
OBJECTIVE: Obesity is a major risk factor of atherosclerotic cardiovascular disease. Circulating free fatty acid levels are known to be elevated in obese individuals and, along with dietary saturated fatty acids, are known to associate with cardiovascular events. However, little is known about the molecular mechanisms by which free fatty acids are linked to cardiovascular disease. APPROACH AND RESULTS: We found that administration of palmitate, a major saturated free fatty acid, to mice markedly aggravated neointima formation induced by carotid artery ligation and that the neointima primarily consisted of phenotypically modulated smooth muscle cells (SMCs). In cultured SMCs, palmitate-induced phenotypic modulation was characterized by downregulation of SMC differentiation markers, such as SM α-actin and SM-myosin heavy chain, and upregulation of mediators involved in inflammation and remodeling of the vessel wall, such as platelet-derived growth factor B and matrix metalloproteinases. We also found that palmitate induced the expression of proinflammatory genes via a novel toll-like receptor 4/myeloid differentiation primary response 88/nuclear factor-κB/NADPH oxidase 1/reactive oxygen species signaling pathway: nuclear factor-κB was activated by palmitate via toll-like receptor 4 and its adapter, MyD88, and once active, it transactivated Nox1, encoding NADPH oxidase 1, a major reactive oxygen species generator in SMCs. Pharmacological inhibition and small interfering RNA-mediated knockdown of the components of this signaling pathway mitigated the palmitate-induced upregulation of proinflammatory genes. More importantly, Myd88 knockout mice were resistant to palmitate-induced exacerbation of neointima formation. CONCLUSIONS: Palmitate seems to promote neointima formation by inducing inflammatory phenotypes in SMCs.
Subject(s)
Carotid Artery Injuries/metabolism , Fatty Acids/metabolism , Myocytes, Smooth Muscle/metabolism , Neointima/metabolism , Obesity/metabolism , Palmitates/metabolism , Animals , Carotid Artery Injuries/pathology , Disease Models, Animal , Fatty Acids/pharmacology , Ligation , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Myeloid Differentiation Factor 88/genetics , Myocytes, Smooth Muscle/cytology , NADH, NADPH Oxidoreductases/genetics , NADH, NADPH Oxidoreductases/metabolism , NADPH Oxidase 1 , Neointima/chemically induced , Obesity/pathology , Palmitates/pharmacology , Phenotype , Reactive Oxygen Species/metabolism , Signal Transduction/physiology , Toll-Like Receptor 4/metabolismABSTRACT
Consumption of foods high in saturated fatty acids (FAs) as well as elevated levels of circulating free FAs are known to be associated with T2D. Though previous studies showed inflammation is crucially involved in the development of insulin resistance, how inflammation contributes to ß cell dysfunction has remained unclear. We report here the saturated FA palmitate induces ß cell dysfunction in vivo by activating inflammatory processes within islets. Through a combination of in vivo and in vitro studies, we show ß cells respond to palmitate via the TLR4/MyD88 pathway and produce chemokines that recruit CD11b(+)Ly-6C(+) M1-type proinflammatory monocytes/macrophages to the islets. Depletion of M1-type cells protected mice from palmitate-induced ß cell dysfunction. Islet inflammation also plays an essential role in ß cell dysfunction in T2D mouse models. Collectively, these results demonstrate a clear mechanistic link between ß cell dysfunction and inflammation mediated at least in part via the FFA-TLR4/MyD88 pathway.
Subject(s)
Inflammation/metabolism , Inflammation/pathology , Insulin-Secreting Cells/metabolism , Insulin-Secreting Cells/pathology , Palmitic Acids/pharmacology , Signal Transduction/drug effects , Toll-Like Receptor 4/metabolism , Animals , CD11b Antigen/metabolism , Cell Communication/drug effects , Chemokines/genetics , Chemokines/metabolism , Gene Expression Regulation/drug effects , Insulin-Secreting Cells/drug effects , Macrophages/drug effects , Macrophages/metabolism , Macrophages/pathology , Mice , Monocytes/drug effects , Monocytes/metabolism , Monocytes/pathology , Myeloid Differentiation Factor 88/metabolism , Palmitic Acids/administration & dosageABSTRACT
A recent study in Molecular Cell (Tsukahara et al., 2010) identifies cyclic phosphatidic acid (CPA) as a naturally occurring PPARgamma antagonist that can be generated from lysophospholipids by signal-dependent activation of phospholipase D2. This endogenous CPA regulates PPARgamma functions required for adipogenesis, glucose homeostasis, and vascular wall biology.
ABSTRACT
To clarify the magnetic resonance (MR) characteristics of primary uterine malignant lymphoma, we identified 4 patients with primary uterine lymphoma in the MR database of our institute from 1994 to 2005 and evaluated their clinical and MR findings for tumor extension, size, shape, and signal intensity, multinodular growth pattern, preservation of normal endometrium, and lymphadenopathy. In all 4 patients, tumors extended to the uterus and vagina or parametrium, and uterine tumors showed relatively homogeneous intensity on both T(1)- and T(2)-weighted MR imaging. Two patients showed multinodular tumor growth; three revealed pelvic lymphadenopathy; and none had intact endometrium or normal uterine zonal structure. Thus, large tumors with relatively homogeneous signal intensity seemed to be a specific MR finding of uterine lymphoma, and findings of multinodular growth were considered a possible characteristic suggesting the uterine involvement of malignant lymphoma.
Subject(s)
Image Enhancement/methods , Lymphoma/diagnosis , Magnetic Resonance Imaging/methods , Uterine Neoplasms/diagnosis , Aged , Female , Humans , Sensitivity and SpecificityABSTRACT
The authors reported a case of fundal-type adenomyomatosis in which mural stratification corresponding to histopathological findings was clearly demonstrated with MR imaging. Single-shot fast spin echo images for MR cholangiopancreatography clearly visualized Rokitansky-Aschoff sinuses (RAS), which are a diagnostic clue for this disease. However, mural stratification comprising RAS with muscular proliferation, massive fibrosis and subserosal fat deposition was more precisely demonstrated in T(2)-weighted images obtained with fast spin echo.
