We developed cobalt-containing Fe3O4 particles, (Co, Fe)3O4, whose particle sizes and magnetic properties were precisely controlled to apply hysteresis-loss heating materials in thermoablation. The crcivity of the (Co, Fe)3O4 particles was adjusted in the range of 19.1 to 42.1 kA/m by changing the content of Co, while the particle size was maintained about 20nm. SiO2-coated (Co, Fe)3O4 particles were dispersed in water. The temperature increase characteristics were examined for the dispersant containing (Co, Fe)3O4 particles with the crcivity of 24.0kA/m by applying a 120kHz ac magnetic field with an amplitude up to 50.1kA/m. The temperature increase ΔT/Δt was proportional to the amplitude of magnetic field, but was not saturated even when a magnetic field of 50.1kA/m was applied. The specific loss power (SLP) calculated from the ΔT/Δt and the particle content of the dispersant did not show a clear dependence on the coercivity, but a maximum value of over 1000W/g was obtained for a dispersant containing (Co, Fe)3O4 particles with a coercivity of 24.0kA/m under an ac magnetic field of 50.1kA/m.
Superior mesenteric venous thrombosis (SMVT) is mostly treated with anticoagulation therapy; however, SMVT can lead to irreversible bowel ischemia and require bowel resection in the acute or subacute phase.
Combined hepatocellular and cholangiocellular carcinomas are rare. Moreover, double cancer cases of hepatocellular carcinoma and cholangiocellular carcinoma are very rare. This report describes a patient with double cancer. A correct clinical diagnosis was made with successful resection, and cutaneous metastases occurred near the exit site of an abdominal drain after the resection of the tumor. The patient, a 66-year-old man with chronic hepatitis C, was admitted to our hospital because he was suspected of having primary liver cancer. Two liver masses in the anteroinferior segment were detected by using angiography, computed tomography during angiography, and computed tomography during arterioportography. These clinical findings indicated that the tumor in the right lobe was hepatocellular carcinoma. A resection of the S5 subsegmentectomy was performed. One mass was diagnosed histologically as hepatocellular carcinoma, and the other mass was diagnosed as cholangiocellular carcinoma. One year after the operation, the patient palpated a hard subcutaneous nodule 4.0 cm in diameter in the right lower abdominal wall. A subcutaneous tumor was excised, and a histological examination revealed moderately differentiated hepatocellular carcinoma. The patient is currently doing well without further recurrence of hepatocellular carcinoma or cholangiocellular carcinoma, 18 months after subsegmentectomy and six months after excision of the subcutaneous tumor.
Abstract Background Primary liposarcoma arising from the liver is exceedingly rare. There have been very few reports documenting primary hepatic liposarcoma, especially of the pleomorphic subtype. Surgery is currently the only established treatment method, and the prognosis remains poor. In this report, we present an unusual case of hepatic liposarcoma of the pleomorphic subtype with literature review. In addition, we discuss theories regarding pathogenesis and the pathological and clinical features of primary hepatic liposarcoma to better outline this rare entity. Case presentation An asymptomatic 65-year-old female was found to have a right hepatic mass on a computed tomography scan 2 years after surgical resection of the left adrenal gland and kidney for adrenocortical carcinoma. Laboratory examinations were unremarkable. Magnetic resonance imaging demonstrated a 16-mm mass in the right hepatic lobe. Adrenocortical carcinoma metastasis was suspected. Laparoscopic partial hepatectomy completely removed the tumor with clear margins. Macroscopically, the surgical specimen contained a nodular, yellow–white mass lesion 20 mm in diameter. On pathologic examination, pleomorphic, spindle-shaped tumor cells containing hypochromatic, irregularly shaped nuclei of various sizes formed fascicular structures. Scattered lipoblasts intervened in varying stages. Mitotic cells were frequent. Ki-67 labeling index was 15%. Immunohistochemically, the tumor cells were diffusely positive for vimentin and focally positive for CD34 and alpha-SMA; lipoblasts were focally positive for S-100. Tumor cells were nonreactive for SF-1, inhibin alpha, desmin, HHF35, HMB45, Melan A, MITF, c-kit, DOG1, cytokeratin AE1/AE3, h-caldesmon, STAT6, CD68, MDM2, CDK4, c17, DHEAST, 3BHSD, CD31, Factor 8, and ERG. From these findings, primary hepatic liposarcoma of pleomorphic subtype was diagnosed. The tumor recurred intrahepatically 3 years later, and the patient died 5 months after recurrence. Conclusions In our report, we discussed the rarity, theories regarding pathogenesis, and a review of the literature of this atypical condition. To the best of our search, this is the 14th case of primary hepatic liposarcoma and the 2nd case of the pleomorphic subtype reported throughout the world. Further research regarding the etiology of this unusual clinical entity is warranted to establish effective diagnostic and management protocols.
Although it is well known that liver allografts are often accepted by recipients, leading to donor-specific tolerance of further organ transplants, the underlying mechanisms remain unclear. We had previously used an in vitro model and showed that mouse liver sinusoidal endothelial cells (LSECs) selectively suppress allospecific T-cells across major histocompatibility complex (MHC) barriers. In the present study, we established an in vivo model for evaluating the immunomodulatory effects of allogeneic LSECs on corresponding T-cells. Allogeneic BALB/cA LSECs were injected intraportally into recombination activating gene 2 γ-chain double-knockout (RAG2/gc-KO, H-2(b)) mice lacking T, B, and natural killer (NK) cells. In order to facilitate LSEC engraftment, the RAG2/gc-KO mice were injected intraperitoneally with monocrotaline 2 days before the adoptive transfer of LSECs; this impaired the host LSECs, conferring a proliferative advantage to the transplanted LSECs. After orthotopic allogeneic LSEC engraftment, the RAG2/gc-KO mice were immune reconstituted intravenously with C57BL/6 splenocytes. After immune reconstitution, mixed lymphocyte reaction (MLR) assay using splenocytes from the recipients revealed that specific inhibition of host CD4(+) and CD8(+) T-cell proliferation was greater in response to allostimulation with irradiated BALB/cA splenocytes rather than to stimulation with irradiated third party SJL/jorllco splenocytes. This inhibitory effect was attenuated by administering anti-programmed death ligand 1 (PD-L1) monoclonal antibody during immune reconstitution in the above-mentioned mice, but not in RAG2/gc-KO mice engrafted with Fas ligand (FasL)-deficient BALB/cA LSECs. Furthermore, engraftment of allogeneic BALB/cA LSECs significantly prolonged the survival of subsequently grafted cognate allogeneic BALB/cA hearts in RAG2/gc-KO mice immune reconstituted with bone marrow transplantation from C57BL/6 mice. In conclusion, murine LSECs have been proven capable of suppressing T-cells with cognate specificity for LSECs in an in vivo model. The programmed death 1/PD-L1 pathway is likely involved in these suppressive effects.
Objectives Experimental data based on cell line–derived xenograft models (cell xenograft) seldom reproduce the clinical situation, and therefore we demonstrated here the superiority of a murine model involving transplantation of human pancreatic cancer tissue fragments (tumor graft), focusing on the histological features and drug delivery characteristics. Methods Tumor pieces from 10 pancreatic cancer patients were transplanted into SCID (severe combined immunodeficient) mice. Histological characteristics of tumor grafts, including morphology, desmoplastic reaction, and vascularization, were compared with those of cell xenografts. Drug delivery was evaluated by quantifying the concentrations of injected drug, and the results were compared with its histological features. Results Eight of the 10 transplanted tumors successfully engrafted. Histological comparisons between tumor grafts and cell xenografts revealed the following: the amount of stroma was more (22.9% ± 11.8% vs 10.8% ± 5.4%; P < 0.05), vessel–cancer cell distance was longer (35.3 ± 39.0 vs 3.9 ± 3.1 μm; P < 0.001), and microvessel density was lower (6.8 ± 1.9 vs 10.8 ± 2.1 vessels/0.4 mm2; P < 0.05) in tumor grafts. Drug concentrations in tumor grafts were lower than those in cell xenografts (3.3 ± 1.2 vs 6.0±0.2 μg/mL; P = 0.003), and the differences were correlated with the histological differences. Conclusions Pancreatic tumor grafts better reproduce the histological nature of clinical cancer and thus provide a more realistic model that is applicable for pharmacokinetic studies.
Abstract Background Muir–Torre syndrome is an autosomal-dominant mutation in mismatch repair genes that gives rise to sebaceous tumors and visceral malignancies over time. Because colorectal and genitourinary cancers are common in Muir–Torre syndrome, duodenal carcinoma diagnoses are often delayed. Case presentation A 58-year-old woman presented with severe emaciation, anorexia, and upper abdominal pain. She had a history of rectal carcinoma, ascending colon carcinoma, and a right shoulder sebaceous carcinoma. Upper gastrointestinal endoscopy and computed tomography examinations suggested duodenal obstruction due to superior mesenteric artery syndrome, leading to long-term observation. Seven months later, she was finally diagnosed with duodenal carcinoma of the third portion. As the papilla of Vater was preservable due to tumor location, she received a partial duodenectomy in lieu of a pancreatoduodenectomy. Pathologically, the tumor was a well-differentiated adenocarcinoma with a classification of T3N0M0 Stage IIA (UICC, 8th edition). The postoperative course was uneventful and her appetite returned. A mutation in mismatch repair gene MSH2 confirmed the diagnosis of Muir–Torre syndrome genetically. Three years later, her nutritional status has fully recovered and she is free from both recurrence and metastasis. Conclusion In patients with comorbid skin sebaceous tumors and gastrointestinal malignancies, genetic screening is strongly recommended. Patients with Muir–Torre syndrome require long-term follow-up, and function-preserving treatment is desirable.
