A Study of Sepsis in Surgical Wounds

Published records of the frequency of wound sepsis are often unreliable sources of information on the general frequency of this complication because of unstandardized methods of reporting and because of the various views of different investigators as to what constitutes sepsis. A method of infection reporting, its study and analysis are outlined. A survey of postoperative infections by this method for the years 1959, 1960 and 1961 revealed infection rates of 2.02%, 1.20% and 1.14%, respectively. For the same period the percentages of wound infections caused by Staph. aureus were 83.06%, 69.8% and 51.8%, respectively. The most prevalent phage types were 55/53/54 and 52/80/81/82, although types 80/81/82 and 80 were also involved. Infections with Gram-negative organisms were encountered more often in 1961 than in 1959. The majority of these were of mixed type, and followed abdominal surgery.There is need for more comprehensive study and analysis of postoperative wound sepsis and its complications. It was apparent from this study that, statistically, a relatively low rate of postoperative infections may mask a high rate following a specific surgical procedure.     

Pasteurella Pseudotuberculosis Infection in Man

Pasteurella pseudotuberculosis has been considered a widespread animal pathogen for many years, but only within the last decade has its capacity to cause human disease been recognized. Two forms of human disease have been established—acute septicemia and mesenteric lymphadenitis. Because mesenteric adenitis is frequently indistinguishable from acute appendicitis, blood serum was obtained from 66 consecutive patients who underwent operation for appendicitis and was examined for agglutinins to seven serotype strains of P. pseudotuberculosis. Agglutinins were obtained in 21.2% of this series. Titres of over 1/100 were found in three of three cases of mesenteric lymphadenitis, one of 11 with no apparent disease, and one of 46 with appendicitis. P. pseudotuberculosis was isolated from a lymph node in the latter case. Two to four follow-up samples of sera in each of these five cases had increasing and then decreasing titres, indicative of active disease. Titres of 1/15 or less were found in five of the cases of appendicitis, in one case of salpingitis, and in three with no apparent disease. The occurrence of these nine cases with low titres may be indicative of previous contact with the organism.Human infection with P. pseudotuberculosis is not unusual in the Edmonton region and is responsible for at least some cases of mesenteric lymphadenitis.     

A Model of Genome Size Dynamics During Speciation

A model developed for the evolving size of the repetitive part of the eukaryote genome during speciation was subjected to analytical and computer treatment. The basic assumption of the model was that two classes of repetitive DNA contribute mainly to macroevolutionary changes in genome size: arrays of tandem repeats (ATR) changing through unequal crossover and mobile genetic elements (MGE) changing presumably through an integration mechanism of the Tn- and Is-kind operating in bacteria. Within the framework of this model, the macroevolution of the MGE size is formally equivalent to that of the ATR in the particular case when shifts of chromatids have only one repeat out of register. This allowed us to consider genome size as a large set of various ATRs. The results obtained are as follows. If the duplication and deletion of repeats have unequal fixation probabilities during each speciation act, the predicted species distributions of genome size significantly deviate from the real ones; if they have equal fixation probabilities, there is a conformance between calculated and real distributions. In the latter case, the model reproduces the salient features of real distributions upon acceptance of 1) upper selective boundary nonspecifically limiting increase in genome size within the evolving taxonomic group and 2) non-neutrality of variability in genome size with respect to speciation.     

A Software Architecture for Multi-Cellular System Simulations on Graphics Processing Units

The first aim of simulation in virtual environment is to help biologists to have a better understanding of the simulated system. The cost of such simulation is significantly reduced compared to that of in vivo simulation. However, the inherent complexity of biological system makes it hard to simulate these systems on non-parallel architectures: models might be made of sub-models and take several scales into account; the number of simulated entities may be quite large. Today, graphics cards are used for general purpose computing which has been made easier thanks to frameworks like CUDA or OpenCL. Parallelization of models may however not be easy: parallel computer programing skills are often required; several hardware architectures may be used to execute models. In this paper, we present the software architecture we built in order to implement various models able to simulate multi-cellular system. This architecture is modular and it implements data structures adapted for graphics processing units architectures. It allows efficient simulation of biological mechanisms.     

Absence of Intraspinal Sprouting in Dorsal Root Axons Caudal to a Partial Spinal Hemisection: A Horseradish Peroxidase Transport Study

Primary afferent sprouting in the spinal cord was evaluated by comparing the central projection of horseradish peroxidase (HRP)-labeled sciatic nerve afferent axons in nonlesioned control rats, and in rats subjected to acute or chronic partial spinal hemisections as adults. The lesions were performed at various levels from T₁₀ to L₃, and removed supraspinal and varying amounts of descending propriospinal afferents to lumbar segments receiving the maximal sciatic projection. The hemisections typically involved all but the dorsal column, although in some cases a portion of the dorsal column, including the corticospinal tract, was also transected.

The distribution pattern and density of spinal HRP reaction product was not significantly different in experimental and control preparations in any segment below the lesion, regardless of the quantity of denervation, or the density of the normal sciatic projection in a given terminal region. These results, together with our previous finding concerning an absence of primary afferent sprouting following long-term dorsal root ganglionectomies, suggest that current concepts concerning collateral sprouting as a factor in functional plasticity in the mature mammalian spinal cord warrant re-evaluation.     

Lifelong choline supplementation ameliorates Alzheimer’s disease pathology and associated cognitive deficits by attenuating microglia activation

Currently, there are no effective therapies to ameliorate the pathological progression of Alzheimer's disease (AD). Evidence suggests that environmental factors may contribute to AD. Notably, dietary nutrients are suggested to play a key role in mediating mechanisms associated with brain function. Choline is a B‐like vitamin nutrient found in common foods that is important in various cell functions. It serves as a methyl donor and as a precursor for production of cell membranes. Choline is also the precursor for acetylcholine, a neurotransmitter which activates the alpha7 nicotinic acetylcholine receptor (α7nAchR), and also acts as an agonist for the Sigma‐1 R (σ1R). These receptors regulate CNS immune response, and their dysregulation contributes to AD pathogenesis. Here, we tested whether dietary choline supplementation throughout life reduces AD‐like pathology and rescues memory deficits in the APP/PS1 mouse model of AD. We exposed female APP/PS1 and NonTg mice to either a control choline (1.1 g/kg choline chloride) or a choline‐supplemented diet (5.0 g/kg choline chloride) from 2.5 to 10 months of age. Mice were tested in the Morris water maze to assess spatial memory followed by neuropathological evaluation. Lifelong choline supplementation significantly reduced amyloid‐β plaque load and improved spatial memory in APP/PS1 mice. Mechanistically, these changes were linked to a decrease of the amyloidogenic processing of APP, reductions in disease‐associated microglial activation, and a downregulation of the α7nAch and σ1 receptors. Our results demonstrate that lifelong choline supplementation produces profound benefits and suggest that simply modifying diet throughout life may reduce AD pathology.