Synchronous triple carcinoma of the colon and rectum.

Synchronous multiple colorectal cancers are defined as multiple malignant colorectal tumors that occur simultaneously. All tumors are distant from each other, and none are the result of metastasis from other tumors. Here, we present a case of a 79-year-old man who was admitted to our hospital because of a 3-month history of abdominal pain associated with anemia, loss of appetite, and body weight loss. The patient did not have a family history of cancer. Computed tomography revealed bowel wall thickness and mesentery inflammation at the hepatic flexure of the colon and cecum. Colonoscopy revealed a tumor located 10 cm from the anal verge. Colonoscopic examination of the large bowel was not possible because of bowel obstruction due to the rectal tumor. Synchronous triple adenocarcinoma of the colon and rectum was confirmed by pathologic examination. The tumor was surgically resected by two-segment resection of the colon, low anterior resection, and right hemicolectomy. We used intraoperative colonoscopy to confirm that there were no other lesions after the resection of the three tumors. To the best of our knowledge, this is the first case of synchronous triple carcinoma of the colon and rectum in Taiwan. We consider that comprehensive preoperative study, extensive intraoperative exploration, and radical resection can increase the survival rate of patients with synchronous multiple colorectal cancers.

Interhemispheric lipoma masquerading as pneumocranium in a patient with head injury.

Head injury is very commonly seen in the emergency department (ED) worldwide, and almost, an unenhanced computed tomography scan of the brain suffices for patients seen in the ED presenting after trauma or with a new neurologic deficit. Intracranial lipomas are usually asymptomatic, and they are often an occasional finding. In head injury cases, lipomas are easily to be misdiagnosed as pneumocranium on brain computed tomography with low-density attenuation image. We presented an extremely rare case of interhemispheric lipoma presenting to an ED as a lesion of acute brain insult. The aim of this report is to emphasize the importance of clinical thinking in the differential diagnosis of markedly hypodense lesion on computed tomography imaging of a patient with head injury.

Mortality rates under the care of junior and senior surgery residents in a surgical intensive care unit/neurologic intensive care unit: a 5-year retrospective cohort study at Taoyuan Armed Forces General Hospital.

BACKGROUND: The quality and outcome of health care administered in intensive care units (ICUs) of teaching hospitals are dependent on a myriad of factors; however, few studies have assessed mortality rates and length of stay in surgical intensive care and neurologic intensive care units (SICU/NICU) in relation to the experience of junior and senior surgery residents. OBJECTIVE: The aim of this study was to determine whether there were differences in the outcomes of ICU patients cared for by junior surgery residents or senior surgery residents by assessing mortality rates and length of stay in the SICU/NICU. DESIGN: This was a retrospective cohort analysis. Mortality rates, length of SICU/NICU stay, and baseline characteristics were assessed in 2 patient groups: group 1, patients managed by junior surgical residents; group 2, patients managed by senior surgical residents. Categorical variables were compared by chi(2)/Fisher exact test, and continuous data (age and ICU stay) were compared using the Mann-Whitney U test. Acute Physiology and Chronic Health Evaluation II score was used for ICU prognostic models. SETTING: The Taoyuan Armed Forces General Hospital (Taoyuan, Taiwan, ROC) consists of an 8-bed SICU and an 8-bed NICU. PATIENTS: Data were collected from 2274 patients from January 1, 2002, to December 31, 2006, from the intensive care units (SICU/NICU) of the department of surgery. INTERVENTIONS: None. RESULTS: Significant differences between the 2 groups were found in total patient mortality and the duration of intensive care unit stay. Of 1806 patients in group 1, 446 (24.7%) died, whereas 83 (17.7%) of 468 in group 2 died (P = .002). The major difference of mortality rate was in the division of neurology surgery; 291 (26.6%) of 1092 patients in group 1 died, whereas 55 (19.2%) of 287 in group 2 died (P = .009), with most deaths due to spontaneous intracranial hemorrhage (P = .012) and central nervous system tumors (P = .048). Median length of SICU/NICU stay for group 1 was 3.0 days vs 3.5 days for group 2 (P = .003). CONCLUSIONS: The quality of care of critically ill patients is improved when more experienced residents are providing care. We suggest that residents rotated into the special units such as SICU/NICU for care of critically ill patients should be at least at third year of training.

Immunomodulatory effect of decoy receptor 3 on the differentiation and function of bone marrow-derived dendritic cells in nonobese diabetic mice: from regulatory mechanism to clinical implication.

To investigate the regulatory effects of decoy receptor 3 (DcR3) on the differentiation and function of dendritic cells (DCs), bone marrow-derived DCs (BM-DCs) from nonobese diabetic (NOD) mice were cultured with recombinant DcR3.Fc protein. Their differentiating phenotypes and T cell-stimulating functions were then evaluated. Expression of CD11c, CD40, CD54, and major histocompatibility complex I-A(g7) was reduced in cells cultured with additional DcR3.Fc, compared with DCs incubated with granulocyte macrophage-colony stimulating factor and interleukin (IL)-4, indicating that DcR3 interferes with the differentiation and maturation of BM-DCs. One of the most striking effects of DcR3.Fc on the differentiation of DCs was the up-regulation of CD86 and down-regulation of CD80, suggesting a modulatory potential to skew the T cell response toward the T helper cell type 2 (Th2) phenotype. Consistent with this, the proliferation of CD4(+) T cells cocultured with DcR3.Fc-treated DCs was significantly reduced compared with that of T cells stimulated by normal DCs. Moreover, the secretion of interferon-gamma from T cells cocultured with DcR3.Fc-treated DCs was profoundly suppressed, indicating that DcR3 exerts a Th1-suppressing effect on differentiating DCs. Furthermore, adoptive transfer experiments revealed that NOD/severe combined immunodeficiency mice received DcR3.Fc-treated DCs, and subsequently, autoreactive T cells showed delayed onset of diabetes and a decrease in diabetic severity compared with mice that received normal DCs and T cells, suggesting a future therapeutic potential in autoimmune diabetes. Data from two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization-time-of-flight analysis show an up-regulation of some proteins-such as mitogen-activated protein kinase p38 beta, cyclin-dependent kinase 6, and signal-induced proliferation-associated gene 1-and a down-regulation of the IL-17 precursor; tumor necrosis factor-related apoptosis-inducing ligand family member-associated nuclear factor-kappaB activator-binding kinase 1; and Golgi S-nitroso-N-acetylpenicillamine in cells treated with DcR3, further demonstrating its effect on DC differentiation and function.

Anti-4-1BB-based immunotherapy for autoimmune diabetes: lessons from a transgenic non-obese diabetic (NOD) model.

Various therapeutic strategies have been developed to tolerize autoreactive T cells and prevent autoimmune pathology in type 1 diabetes. 4-1BB, a member of the tumor necrosis factor receptor (TNFR) superfamily, is a costimulatory receptor primarily expressed on activated T cells. The administration of an agonistic anti-4-1BB antibody (2A) dramatically reduced the incidence and severity of experimental autoimmune encephalomyelitis (EAE). Treatment with the same antibody in Fas-deficient MRL/lpr mice blocked lymphadenopathy and lupus-like autoimmune processes. Paradoxically, transgenic non-obese diabetic (NOD) mice overexpressing membrane-bound agonistic single-chain anti-4-1BB Fv in pancreatic beta cells developed more severe diabetes than their non-transgenic littermates, with earlier onset, faster diabetic processes, and higher mortality. Forty percent of transgenic mice developed diabetes by 4 weeks of age, compared with their control littermates, which first exhibited diabetes at 14 weeks. The frequency of diabetes in female transgenics reached 70% by 8 weeks of age. Most female transgenic mice died around 12 weeks. Consistent with this, transgenic mice developed earlier and more severe insulitis and showed stronger GAD-specific T-cell responses, compared with age-matched control littermates. Our results indicate an adverse effect of transgenic anti-4-1BB scFv in NOD mice and suggest a potential risk of this anti-4-1BB-based immunotherapy for autoimmune diseases.