Intraperitoneal photodynamic therapy causes a capillary-leak syndrome.

BackgroundIn patients undergoing intraperitoneal (IP) photodynamic therapy (PDT), the combination of aggressive surgical debulking and light therapy causes an apparent systemic capillary-leak syndrome that necessitates significant intensive care unit (ICU) management after surgery.MethodsFrom May 1997 to May 2001, 65 patients underwent surgical debulking and PDT as part of an ongoing phase II trial for disseminated IP cancer. Perioperative data were reviewed retrospectively, and statistical analyses were performed to determine whether any identifiable factors were associated with the need for mechanical ventilation for longer than 1 day and with the occurrence of postoperative complications.ResultsForty-three women and 22 men (mean age, 49 years) were treated. Operative time averaged 9.8 hours, and mean estimated blood loss was 1450 mL. The mean crystalloid requirement for the first 48 hours after surgery was 29.3 L, and 49 patients required blood products. Twenty-four patients were intubated for longer than 24 hours, with a mean of 8.3 days for those intubated longer than 1 day. The median ICU stay was 4 days. Overall, 110 complications developed in 45 (69%) of the 65 patients. Significant complications included 6 patients with acute respiratory distress syndrome, 28 patients with infectious complications, and 4 patients with anastomotic complications. Statistical analyses revealed that surgery-related factors were significantly associated with these complication outcomes.ConclusionsPatients who undergo surgical debulking and IP PDT develop a significant capillary-leak syndrome after surgery that necessitates massive volume resuscitation, careful ICU monitoring, and, frequently, prolonged ventilatory support

Against the Odds: Psychomotor Development of Children Under 2 years in a Sudanese Orphanage.

Providing abandoned children the necessary medical and psychological care as possible after their institutionalization may minimize developmental delays. We describe psychomotor development in infants admitted to an orphanage in Khartoum, Sudan, assessed at admission and over an 18-month follow-up. Psychological state and psychomotor quotients were determined using a simplified Neonatal Behavior Assessment Scale (NBAS), the Brunet-Lezine and Alarm distress baby (ADBB) scale. From May-September 2005, 151 children were evaluated 2, 4, 9, 12 and 18 months after inclusion. At admission, ∼15% of children ≤1 month had a regulation impairment according to the NBAS, and 33.8% presented a distress state (ADBB score >5). More than 85% (129/151) recovered normal psychomotor development. The results of the program reinforce the importance of early detection of psychological disorders followed by rapid implementation of psychological case management to improve the development of young children in similar institutions and circumstances

Analysis of a Large Sample of Neutrino-Induced Muons with the ArgoNeuT Detector

ArgoNeuT, or Argon Neutrino Test, is a 170 liter liquid argon time projection chamber designed to collect neutrino interactions from the NuMI beam at Fermi National Accelerator Laboratory. ArgoNeuT operated in the NuMI low-energy beam line directly upstream of the MINOS Near Detector from September 2009 to February 2010, during which thousands of neutrino and antineutrino events were collected. The MINOS Near Detector was used to measure muons downstream of ArgoNeuT. Though ArgoNeuT is primarily an R&D project, the data collected provide a unique opportunity to measure neutrino cross sections in the 0.1-10 GeV energy range. Fully reconstructing the muon from these interactions is imperative for these measurements. This paper focuses on the complete kinematic reconstruction of neutrino-induced through-going muons tracks. Analysis of this high statistics sample of minimum ionizing tracks demonstrates the reliability of the geometric and calorimetric reconstruction in the ArgoNeuT detector

Single Nucleotide Polymorphisms in Selected Apoptotic Genes and BPDE-Induced Apoptotic Capacity in Apparently Normal Primary Lymphocytes: A Genotype-Phenotype Correlation Analysis

Apoptotic capacity (AC) in primary lymphocytes may be a marker for cancer susceptibility, and functional single nucleotide polymorphisms (SNPs) in genes involved in apoptotic pathways may modulate cellular AC in response to DNA damage. To further examine the correlation between apoptotic genotypes and phenotype, we genotyped 14 published SNPs in 11 apoptosis-related genes (i.e., p53, Bcl-2, BAX, CASP9, DR4, Fas, FasL, CASP8, CASP10, CASP3, and CASP7) and assessed the AC in response to benzo[a]pyrene-7,8-9,10-diol epoxide (BPDE) in cultured primary lymphocytes from 172 cancer-free subjects. We found that among these 14 SNPs, R72P, intron 3 16-bp del/ins, and intron 6 G>A in p53, −938C>A in Bcl-2, and I522L in CASP10 were significant predictors of the BPDE-induced lymphocytic AC in single-locus analysis. In the combined analysis of the three p53 variants, we found that the individuals with the diplotypes carrying 0-1 copy of the common p53 R-del-G haplotype had higher AC values compared to other genotypes. Although the study size may not have the statistical power to detect the role of other SNPs in AC, our findings suggest that some SNPs in genes involved in the intrinsic apoptotic pathway may modulate lymphocytic AC in response to BPDE exposure in the general population. Larger studies are needed to validate these findings for further studying individual susceptibility to cancer and other apoptosis-related diseases

A phenomenological approach to the simulation of metabolism and proliferation dynamics of large tumour cell populations

A major goal of modern computational biology is to simulate the collective behaviour of large cell populations starting from the intricate web of molecular interactions occurring at the microscopic level. In this paper we describe a simplified model of cell metabolism, growth and proliferation, suitable for inclusion in a multicell simulator, now under development (Chignola R and Milotti E 2004 Physica A 338 261-6). Nutrients regulate the proliferation dynamics of tumor cells which adapt their behaviour to respond to changes in the biochemical composition of the environment. This modeling of nutrient metabolism and cell cycle at a mesoscopic scale level leads to a continuous flow of information between the two disparate spatiotemporal scales of molecular and cellular dynamics that can be simulated with modern computers and tested experimentally.Comment: 58 pages, 7 figures, 3 tables, pdf onl