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Working memory acts as a key bridge between perception, long-term memory, and action. The brain regions, connections, and neurotransmitters that underlie working memory undergo dramatic plastic changes during the life span, and in response to injury. Early life reliance on deep gray matter structures fades during adolescence as increasing reliance on prefrontal and parietal cortex accompanies the development of executive aspects of working memory. The rise and fall of working memory capacity and executive functions parallels the development and loss of neurotransmitter function in frontal cortical areas. Of the affected neurotransmitters, dopamine and acetylcholine modulate excitatory-inhibitory circuits that underlie working memory, are important for plasticity in the system, and are affected following preterm birth and adult brain injury. Pharmacological interventions to promote recovery of working memory abilities have had limited success, but hold promise if used in combination with behavioral training and brain stimulation. The intense study of working memory in a range of species, ages and following injuries has led to better understanding of the intrinsic plasticity mechanisms in the working memory system. The challenge now is to guide these mechanisms to better improve or restore working memory function.

Objectives: Young, athletic patients who sustain a musculoskeletal injury can suffer from major depressive disorder (MDD), either pre-existing the injury, or in response to injury. Depression can have deleterious effects on mental and physical well-being, and can ultimately lead to suicide. In fact, suicide may represent over 7% of deaths in young, high-level athletes. Therefore, it is paramount among surgeons to recognize vulnerable patient populations. The purpose of the present investigation was to determine the prevalence of MDD in patients with shoulder instability and its’ effect on outcomes in patients undergoing primary arthroscopic shoulder stabilization. Methods: Eighty-eight patients undergoing primary arthroscopic shoulder stabilization were prospectively enrolled and queried at 6 weeks, 3 months, 6 months, and 1 year. Depression symptoms were assessed with the Quick Inventory of Depressive Symptomatology (QIDS-SR16). MDD diagnosis was defined as a QIDS-SR16 score ≥6. Shoulder functionality was assessed with the Western Ontario Shoulder Instability Index (WOSI). Patients were grouped based on their MDD symptomatology preoperatively into MDD and Non-MDD groups. T-test analysis was used to compare outcomes between the groups. Results: The average age of patients on the day of surgery was 29.9 years old. Seventy-four (84.1%) participants were male, while 14 (15.9%) were female. Of the 88 patients enrolled, 44 (50%) met MDD criteria. Baseline averaged WOSI scores for the MDD cohort were worse than the non-MDD group (p= 0.016), 64.9% and 55.0%, respectively. Shoulder function, measured via the WOSI score, significantly improved throughout the study except at the 6-week follow-up point; however, the MDD group continued to have worse shoulder function at 6 weeks post-op (p= 0.04), 6 months post-op (p=0.03) and 1 year post-op (p< 0.01). There was no significant difference in mean WOSI score between the MDD and non-MDD group at 3 months (p= 0.16). WOSI scores at 1-year for the MDD and non-MDD cohort were 21.1% and 8.9%, respectively. MDD diagnosis increased at the 6-week time point (p= 0.023); however, it declined during the rest of the study period (p< 0.01). Conclusion: A significant proportion of patients with shoulder instability exhibit depression symptoms (50% in this series). Our results suggest that pre-operative depression negatively correlates with shoulder outcome functionality. Interestingly, arthroscopic shoulder stabilization can lead to post-operative depression; however, by 3-months there is a strong reversal of this effect, with significant reduction of depression symptoms in all patients. This effect may be secondary to the significant physical limitations caused by shoulder immobilization protocols for the first 6 weeks. As patients regain shoulder strength, stability and function, they exhibit less depression symptoms, indicating surgical intervention can significantly decrease depression symptoms that are secondary to musculoskeletal injuries.

Astrocytes are the most abundant cell type in the adult central nervous system (CNS), and their functional diversity in response to injury is now being appreciated. Astrocytes have long been considered the main player in the inhibition of CNS repair via the formation of the gliotic scar, but now it is accepted that astrocyte can play an important role in CNS repair and remyelination. Interest in the relationship between astrocytes and myelination focused initially on attempts to understand how the development of plaques of astroglial scar tissue in multiple sclerosis was related to the failure of these lesions to remyelinate. It is now considered that this is an end stage pathological response to injury, and that normally astrocytes play important roles in supporting the development and maintenance of CNS myelin. This review will focus on how this new understanding may be exploited to develop new strategies to enhance remyelination in multiple sclerosis and other diseases.

This study was designed to determine if trauma causes the release of adult-derived blastomere-like stem cells (BLSCs) from skeletal muscle into the circulating blood of adult pigs. Experimental procedures followed the guidelines of Fort Valley State University's Institutional Animal Care and Utilization Committee. Pigs were traumatized by splenectomy followed by pancreatectomy. Blood samples and skeletal muscle biopsies were taken before and after trauma. Adult-derived BLSCs were isolated from skeletal muscle and blood samples following established procedures. Nontraumatized skeletal muscle contained approximately 277 million BLSCs per gram of muscle. After trauma, skeletal muscle contained approximately 2 million BLSCs per gram of muscle. Blood taken before trauma contained approximately 22 million BLSCs per milliliter, whereas approximately 512 million BLSCs per milliliter were present within the blood after trauma. Blood values were statistically significant with a P < 0.05. This report is the first demonstration that trauma causes the release of adult-derived BLSCs from skeletal muscle into blood. Further studies are required to elucidate the roles that adult-derived BLSCs play in the response to injury and in the healing process. Surgeons must take a role in this evolving field.

The systemic inflammatory response syndrome is a well recognized physiological entity being part of our homeostatic mechanisms. It represents the cascade of inflammatory reactions initiated in the immediate aftermath following trauma reflecting the state of alertness that our body undergoes in order to fight for survival. A variety of inflammatory mediators and cellular elements are involved during this process interacting amongst each other. This allows communication between the different organ systems and thus regulating local and systemic responses. We have just begun to characterize and quantify the immuno-inflammatory response to trauma and this has opened new horizons in the way we understand the pathophysiological response to injury. As our knowledge evolves new therapeutic agents and innovative treatment plans will be developed contributing to increased survival rates in patients with multiple injuries.

Systemic inflammatory response syndrome and its progression to multi-organ dysfunction syndrome represent a major challenge in the field of trauma and critical care medicine. This disease state is a product of disorders of the body’s natural response to injury. Attempts to treat this at a molecular level using information from basic science research have been unsuccessful, even detrimental. It is possible that this is due to a failure to account for the nonlinear, complex nature of the inflammatory response in formulating treatment regimes. It is proposed that agent-based computer simulation may be a way to characterize the dynamics of the inflammatory response. This article presents an abstract model of a generic tissue system. Modeling the inflammatory response as a nonlinear complex system may produce simulations that will shed light on the complex nature of the inflammatory response. In the future, more sophisticated simulations may provide a testing framework for designing and evaluating treatment regimes.

Serious trauma in pregnancy is an uncommon event but is particularly challenging to the physician, due to the presence of a potential second patient. Responding to the challenge requires a knowledge of the physiological changes which may alter the maternal response to injury, as well as an understanding of the maternal-fetal relationship. Fetal outcome is dependent on maternal well-being, and thus timely and appropriate resuscitation of the mother is the first priority. Initial management of the pregnant trauma patient includes attention to the airway-breathing-circulation (ABC). Certain injuries are more common in pregnancy and are influenced by the presence of the gravid uterus. The physician needs an awareness of the common complications of pregnancy and additional skills may be required to diagnose and assess fetal viability. The principles of the perimortem section should be understood, as well as the social implications of domestic violence towards pregnant women.

Background: There is little information on the molecular factors important in healing and changes that occur in the glenoid labrum in response to injury. Using a novel animal model of acute anterior shoulder dislocation, this study characterizes the factors expressed in the glenoid labrum in response to injury and correlates their expression to glenohumeral stability. Purpose: To study the response of the glenoid labrum to injury both biomechanically and with immunohistochemical testing. Methods: An injury to the anteroinferior labrum was surgically induced in 50 male Lewis rats. Rats were sacrificed at 3, 7, 14, 28, or 42 days. Immunolocalization experiments were performed to localize the expression of growth factors and cytokines. For biomechanical testing, dynamic stiffness for anterior and posterior laxity, load to failure, stiffness, and maximum load were recorded. Statistical differences were determined at P < .05. Study Design: Descriptive laboratory study. Results: Expression of interleukin–1 beta (IL-1β), transforming growth factor–beta 1 (TGF-β1), matrix metalloproteinase 3 (MMP3), and matrix metalloproteinase 13 (MMP13) were increased in injured compared with uninjured specimens. Collagen III expression was increased early and decreased with time. Biomechanical testing verified instability by demonstrating increased anterior displacement and decreased stiffness in injured shoulders at all time points. Conclusion: This novel animal model of acute anterior shoulder dislocation showed increased expression of IL-1β, TGF-β1, MMP3, MMP13, and collagen III in the injured labral tissue at early time points. Increased anterior laxity and decreased stiffness and maximum load to failure were seen after anterior labral injury, supporting the model’s ability to re-create anterior glenohumeral instability. These data provide important information on the temporal changes occurring in a rat model of anterior glenohumeral dislocation. Clinical Relevance: Identification of factors expressed in the anterior capsule and glenoid labrum in response to injury may lead to the development of novel agents that can be used to augment glenoid labrum healing and ultimately improve both surgical and nonsurgical treatment of this common shoulder injury.

Intestinal injury owing to inflammation, severe trauma, and burn is a leading cause of morbidity and mortality. Currently, animal models employed to study the intestinal response to injury and inflammation depend on outdated methods of analysis. Given that these classic intestinal assays are lethal to the experimental animal, there is no ability to study the gut response to injury in the same animal over time. We postulated that by developing an in vivo assay to image intestinal injury using fluorescent dye, it could complement other expensive, time-consuming, and semiquantitative classic means of detecting intestinal injury. We describe a novel in vivo, noninvasive method to image intestinal injury using a charge-coupled device (CCD) camera that allows for serial visual and quantitative analysis of intestinal injury. Our results correlate with traditional, time-consuming, semiquantitative assays of intestinal injury, now allowing the noninvasive, nonlethal assessment of injury over time.

The normal vascular anatomy of the menisci was inves tigated in five dogs by histology and tissue-clearing (Spalteholz) techniques. The vessels were found to originate in the perimeniscal capsular and synovial tis sues and penetrate the peripheral 25% of the meniscal tissues. The vascular response to complete midportion transection of the medial meniscus was evaluated in 15 dogs. This response originated from the peripheral synovial tissues and completely healed the lesion with fibrovascular scar tissue by 10 weeks. Longitudinal incisions in the avascular portion of the meniscus failed to heal. However, when these lesions were connected to the peripheral synovial tissues at their midportion by a vascular access channel, the entire lesion was healed with fibrovascular scar by 10 weeks.

SummaryPeriods of 24, 48 and 72 hours of fasting constantly, though not always significantly, depress the blood-fibrinogen concentration in intact rats.The blood-fibrinogen response to trauma is unaffected by fasting periods of 48 and 72 hours.Simultaneous exposure to cold and fasting significantly reduces the fibrinogen rise induced by trauma.Total adrenalectomy greatly decreases but does not abolish the fibrinogen response to injury. However, the blood-fibrinogen increase following an operation is prolonged in totally adrenalectomized as compared to partially adrenalectomized rats.These observations suggest that the adrenals play an important role in fibrinogen metabolism.

Summary1. Lysozyme is produced in moderately large amounts by the gastrointestinal tract of dogs subjected to chronic stimulation with Mecholyl. The increase in lysozyme is demonstrable in the bloody diarrheal stools of intact animals and in material aspirated from isolated pouches of colon. 2. Cautery of canine rectum stimulates the local production of large amounts of lysozyme within 5 1/2 hours after injury. 3. The rapid production of lysozyme by injured bowel suggests that it is an early accompaniment of the inflammatory reaction and that its presence is a reflection rather than a cause of ulcerative alimentary disease.