Surface magnetic canting in a ferromagnet

The surface magnetic canting (SMC) of a semi-infinite film with ferromagnetic exchange interaction and competing bulk and surface anisotropies is investigated via a nonlinear mapping formulation of mean-field theory previously developed by our group [L. Trallori et al., Int. J. Mod. Phys. B 10, 1935-1988 (1996)], and extended to the case where an external magnetic field is applied to the system. When the field H is parallel to the film plane, the condition for SMC is found to be the same as that recently reported by Popov and Pappas [Phys. Rev. B 64, 184401 (2001)]. The case of a field H applied perpendicularly to the film plane is also investigated. In both cases, the zero-temperature equilibrium configuration is easily determined by our theoretical approach.Comment: 4 pages, 3 figure

Surface spin-flop transition in a uniaxial antiferromagnetic Fe/Cr superlattice induced by a magnetic field of arbitrary direction

We studied the transition between the antiferromagnetic and the surface spin-flop phases of a uniaxial antiferromagnetic [Fe(14 \AA)/Cr(11 \AA]$_{\rm x20}$ superlattice. For external fields applied parallel to the in-plane easy axis, the layer-by-layer configuration, calculated in the framework of a mean-field one-dimensional model, was benchmarked against published polarized neutron reflectivity data. For an in-plane field $H$ applied at an angle $\psi \ne 0$ with the easy axis, magnetometry shows that the magnetization $M$ vanishes at H=0, then increases slowly with increasing $H$. At a critical value of $H$, a finite jump in $M(H)$ is observed for $\psi<5^{\rm o}$, while a smooth increase of $M$ $vs$ $H$ is found for $\psi>5^{\rm o}$. A dramatic increase in the full width at half maximum of the magnetic susceptibility is observed for $\psi \ge 5^{\rm o}$. The phase diagram obtained from micromagnetic calculations displays a first-order transition to a surface spin-flop phase for low $\psi$ values, while the transition becomes continuous for $\psi$ greater than a critical angle, $\psi_{\rm max} \approx 4.75^{\rm o}$. This is in fair agreement with the experimentally observed results.Comment: 24 pages, 7 figure

Survival after laparoscopic and open surgery for colon cancer: a comparative, single-institution study

BACKGROUND: Some recent studies have suggested that laparoscopic surgery for colorectal cancer may provide a potential survival advantage when compared with open surgery. This study aimed to compare cancer-related survivals of patients who underwent laparoscopic or open resection of colon cancer in the same, high volume tertiary center. METHODS: Patients who had undergone elective open or laparoscopic surgery for colon cancer between January 2002 and December 2010 were analyzed. A clinical database was prospectively compiled. Survival analysis was calculated by using the Kaplan-Meier method. RESULTS: A total of 460 resections were performed. There were no significant differences between the laparoscopic (n = 227) and the open group (n = 233) apart from tumor stage: stage I tumors were more frequent in the laparoscopic group whereas stage II tumors were more frequent in the open group. The mean number of harvested lymph nodes was significantly higher in the laparoscopic than in the open group (20.0 ± 0.7 vs 14.2 ± 0.5, P < 0.01). The 5-year cancer-related survival for patients undergoing laparoscopic resection was significantly higher than that following open resections (83.1% vs 68.5%, P = 0.01). By performing a stage-to-stage comparison, we found that the improvement in survival in the laparoscopic group occurred mainly in patients with stage II tumors. CONCLUSIONS: Our study shows a survival advantage for patients who had undergone laparoscopic surgery for stage II colon cancer. This may be correlated with a higher number of harvested lymph nodes and thus a better stage stratification of these patients

4-Hydroxy-3-nitro-5-ureido-benzenesulfonamides selectively target the tumor-associated carbonic anhydrase isoforms IX and XII showing hypoxia-enhanced anti-proliferative profiles.

Human carbonic anhydrases (CA, EC, 4.2.1.1) IX and XII are overexpressed in cancer cells as adaptive response to hypoxia and acidic conditions characteristic of many tumors. In addition, hypoxia facilitates the activity of specific oxido-reductases that may be exploited to selectively activate bioreductive prodrugs. Here, new selective CA IX/XII inhibitors, as analogues of the antitumor phase II drug SLC-0111 are described, namely ureido-substituted benzenesulfonamides appended with a nitro-aromatic moiety to yield an antiproliferative action increased by hypoxia. These compounds were screened for the inhibition of the ubiquitous hCA I/II and the target hCA IX/XII. Six X-ray crystallographies with CA II and IX/mimic allowed for the rationalization of the compounds inhibitory activity. The effects of some such compounds on the viability of HT-29, MDA-MB-231, and PC-3 human cancer cell lines in both normoxic and hypoxic conditions were examined, providing the initiation toward the development of hypoxia-activated antitumor CAIs

Characterization of tumor antigen peptide-specific T cells isolated from the neoplastic tissue of patients with gastric adenocarcinoma.

Gastric cancer is a significant cause of morbidity and mortality worldwide. Surgical resection remains the primary curative treatment for gastric adenocarcinoma, but the poor (15-35%) survival rate at 5 years has prompted many studies for new therapeutic strategies, such as specific immunotherapy. The aim of this study was to analyze the functional properties of the T cell response to different antigen peptides related to gastric cancer in patients with gastric adenocarcinoma. To this purpose, we have cloned and characterized tumor-infiltrating T cells (TILs) isolated from the neoplastic gastric tissue samples. A T cell response specific to different peptides of gastric cancer antigens tested was documented in 17 out of 20 patients, selected for their HLA-A02 and/or -A24 alleles. Most of the cancer peptide-specific TILs expressed a Th1/Tc1 profile and cytotoxic activity against target cells. The effector functions of cancer peptide-specific T cells obtained from the peripheral blood of the same patients were also studied. The majority of peripheral blood peptide-specific T cells also expressed the Th1/Tc1 functional profile. In conclusion, in most of the patients with gastric adenocarcinoma, a specific type-1 T cell response to gastric cancer antigens was detectable and would have the potential of hamper tumor cell growth. However, in order to get tumor cell killing in vivo, the activity and the number of cancer peptide-specific Th1/Tc1 cells probably need to be enhanced by vaccination with the appropriate cancer antigenic peptides or by injection of the autologus tumor peptide-specific T cells expanded in vitro

Divergent patterns of total and cancer mortality in ulcerative colitis and Crohn’s disease patients: the Florence IBD study 1978–2001

Background and aims: Two divergent patterns of mortality for smoking related diseases in ulcerative colitis and Crohn’s disease patients were suggested in a previous population based study in Florence, Italy. Long term follow up (median 15 years) was completed to re-evaluate mortality in this Mediterranean cohort. Patients and methods: Overall, 920 patients with inflammatory bowel disease were followed until December 2001 or death, with seven patients (0.8%) lost to follow up. A total of 14 040 person years were available for analysis; 118 deaths were observed (81/689 in ulcerative colitis and 37/231 in Crohn’s disease). Expected deaths were estimated using age, sex, and calendar specific national and local mortality rates; standardised mortality ratios (SMR) and 95% confidence interval (CI) were calculated. Results: Among Crohn’s disease patients, mortality was strongly increased for gastrointestinal diseases (SMR 4.49 (95% CI 1.80–9.25)), all cancers (SMR 2.10 (95% CI 1.22–3.36)), and lung cancer (SMR 4.00 (95% CI 1.60–8.24)), leading to a significant 50% excess total mortality. Ulcerative colitis patients showed a significantly reduced total mortality because of lower cardiovascular (SMR 0.67 (95% CI 0.45–0.95)) and lung cancer (SMR 0.32 (95% CI 0.07–0.95)) mortality. No significant excess for colorectal cancer mortality was evident in this extended follow up. Conclusions: These clearly divergent patterns of mortality correlate with documented differences in smoking habits between Crohn’s disease and ulcerative colitis patients. Family doctors and gastroenterologists should consider stopping cigarette smoking a specific priority for Crohn’s disease patients; the latter should be offered free participation in structured programmes for smoking cessation, with the aim of reducing smoking related excess mortality. Overall, no evidence of an increased mortality for large bowel cancer emerged in this series

The relationship between heritability and smoking habits in Crohn&apos;s disease

OBJECTIVE: In Crohn's disease (CD), the relationship between genetic predisposition and smoking has not been well defined. The aim of this study was to compare the smoking habits at the time of the diagnosis of CD patients having familial occurrence of inflammatory bowel disease (IBD) with those of some control groups. METHODS: In a multicenter study, 136 CD patients with a relative with IBD, 272 healthy controls matched for sex and age, 500 CD patients without familial occurrence of IBD, and 84 ulcerative colitis patients (UC) with familial occurrence of IBD were personally interviewed about their smoking habits. In addition, data for 35 healthy siblings of patients with familial CD were collected by interviewing the patients' relatives. RESULTS: The prevalence of smokers was found significantly higher in CD patients with a family history for IBD than in healthy controls and in familial UC patients (OR 2.28 CI 1.5-3.48 and OR 5.81 CI 3.15-10.75, respectively). No significant difference was found either in the percentage of smokers or in the number of cigarettes smoked per day between familial and sporadic CD patients. Among all siblings of CD patients, 72% of affected siblings and 34% of healthy siblings were smokers, concordant with their relatives. CONCLUSIONS: In CD patients with familial occurrence of IBD, the percentage of smokers is elevated. It is possible that in a genetically predisposed population, smoking could be an important environmental factor in determining CD or expressing this disease instead of UC