Major Insult Research Articles

Possible Models for Multiple Chemical Sensitivity: Conceptual Issues and Role of the Limbic System

Conceivably, chemicals contacting olfactory nerve projections in the nose could either be transported into or relay electrical signals to the limbic region, leading to a vast array of symptoms. Likewise, thought processes and mood states may trigger or interrupt pre-existing limbic activity. At present, however, no evidence suggests that limbic activity triggered by environmental exposures can be entirely overcome by psychologic interventions. One important ramification of a limbic hypothesis, if true, is that no convenient biologic marker for multiple chemical sensitivity may exist at the present time. Ten years from now, we may finally confirm the existence of multiple chemical sensitivities (by careful, blinded challenges) but still have no single mechanism to explain it; that is, after all avenues of biochemical and immunologic inquiry have been exhausted, no single cause or marker for this disorder may be apparent. The theory that adaptation plays a role in MCS is based on the observed responses of patients in a deadapted state who have been housed in an environmental unit. Although adaptation is only an observation at this time, not a mechanism, biologic limits might regulate how much an organism can adapt. Such limits could be highly individual and vary by orders of magnitude. Certainly adaptation occurs at all levels of biologic systems, from enzyme systems to cells, tissues, organs, and even behavior (Fregly, 1969). Theoretically, a major insult or the accumulation of lower-level injuries within these systems could lead to a kind of "overload" or "saturation" effect with respect to adaptive capacity. This might cause an individual to have environmental responses, which, instead of being flexible and fluid, would become fragile and overly responsive. Many MCS patients report that years, and in some cases decades, after the onset of their problems, they have recovered only a portion of their former energies and tolerance for their environment. Their descriptions seem to suggest the loss of an intangible capacity to adapt, parts of which may be temporary and recoverable and other parts of which may not. Perhaps our patients have been telling us the diagnosis.

Clinical Anesthesia in Neurosurgery

Cerebral physiology and evaluation cerebral hemodynamics and metabolism physiology of intracranial pressure electrophysiologic monitoring effects of anesthetic agents on intracranial dynamics anesthetic management for neuroradiologic diagnostic procedures fluid and electrolyte balance in neurosurgical patients neurosurgical and related procedures the management of cerebrovascular disease posterior cranial fossa surgery brain tumours surgery of the spine peripheral nerve surgery pediatric neurologic surgery surgery for seizures pain therapy stereotactic surgery central nervous system trauma the management of head injury cardiovascular effects of severe head injury management of spinal cord trauma anesthetic management of patients with neurologic disease for non-neurosurgical procedures post-operative and intensive care post-anesthetic care neurosurgical intensive care hyperalimentation therapy following major brain insult cerebral death brain death.

Intimal hyperplasia and restenosis after carotid endarterectomy

Intimal hyperplasia and restenosis after carotid endarterectomy

Common injuries in preadolescent and adolescent athletes. Recommendations for prevention.

In general, children and youth sports are safe. The great majority of injuries which are sustained are minor and self-limiting. Fortunately, catastrophic acute injuries such as paraplegia, quadriplegia and major limb insults are rare. The 2 mechanisms of injuries at these age groups are acute traumatic insults and unresolved sequelae of repetitive microtrauma. The latter usually results from inappropriate training and coaching techniques. In the United States, adolescents and children are becoming involved in sport at earlier ages and with higher levels of intensity and competition. Factors which lead to injury include the athlete and his/her own psychobiology, inappropriate equipment, the sports environment (playing surfaces, temperature), training and coaching errors, and parental influences. Preparticipation assessment usually reveals extremely healthy children with rare factors which contribute to non-sports participation. Preventative efforts must be made to provide these children with the appropriate equipment and coaching to limit the number of overuse injuries. Management of acute sports problems and rehabilitation of significant injuries are as important in childhood and youth sports as in those of their older sibs in order to prevent lifelong sequelae of musculoskeletal injury. The appropriate goal of children and youth sports must remain one of enjoyment with acquisition of sport-specific skills.

Teratogens and craniofacial malformations: relationships to cell death.

Environmental agents including ethanol, 13-cis retinoic acid (RA, Accutane), the antimetabolite methotrexate, periods of hypoxia, ionizing radiation or hyperthermic stress, when administered acutely to pregnant experimental animals, induce stage-dependent craniofacial malformations comparable to those in corresponding human teratogen syndromes. Acute treatment regimens have allowed analysis of cell populations initially affected and subsequent dysmorphogenetic sequences as well as speculation relative to mechanisms of teratogenesis. In rodent models, ethanol and RA appear to affect similar cell populations and comparable malformations can be induced by both agents. When administered during gastrulation they cause a major insult to the anterior neural plate which results in characteristic ocular, brain and facial malformations comparable to those seen in the fetal alcohol syndrome. Exposure to these drugs at a time just prior to and during neural crest cell migration into the craniofacial and cervical regions results in malformations comparable to those seen in the Di-George sequence and/or retinoic acid embryopathy. Slightly later, at the time that the epibranchial placodes are active, insult results in mandibulofacial dysostosis-like syndromes. We propose that the pattern of these malformations is related to the particular vulnerability of cells in the vicinity of normal programmed cell death. Cell death is also associated with ionizing radiation and hyperthermia-induced malformations. Both of these teratogens are particularly damaging to the early development of the eye and central nervous system. Teratogenic temperature elevations result in arrest of mitotic activity and death of cells in mitosis. Hypoxia is also associated with cell death in specific regions and subsequent malformation. For example, death of cells in the invaginating olfactory placode has recently been associated with cleft lip formation. The relationship of hypoxia-induced cell death to energy requirements is being explored. Acute treatment with methotrexate results in frontonasal dysplasia (median facial clefts). Combined effects of fluid imbalance, lack of proliferation or death of frontonasal mesenchyme appear to be involved. Although the mechanisms of craniofacial malformation are complex, a common feature for many is excessive cell death for which the embryo may be unable to compensate. Excessive cell death in regions of programmed cell death represents an important, yet little appreciated, mechanism of teratogenesis.

A response to trauma and infection: metabolic changes and immunologic consequences.

The protein catabolic response to injury or illness is often associated with reduction in nutrient intake, since major physical insult often diminishes the patient's ability to consume food. Consequently, the injured patient is in a state of starvation as well as stress. When starvation is superimposed on stress, the metabolic consequences differ substantially from those of simple starvation without stress. These differences will be discussed in greater detail, as will the effects of these metabolic changes on the immunologic responsiveness of injured patients.

Anaesthetic considerations for major thermal injury.

Extensive thermal injury represents a major insult to body homeostasis. The anaesthetist, while providing anaesthesia for a multitude of debridement and reconstructive procedures, is also likely to assist in initial resuscitation and stabilization and subsequent intensive care management. A thorough understanding of the major systemic and end-organ effects after a major burn allow for a better appreciation of the many pertinent considerations for anaesthesia during the immediate post-burn phase as well as the later period of reconstruction and rehabilitation.

Mechanism of bleomycin action: [formula omitted] studies

The cytotoxic activity of bleomucin results from DNA cleavage, which is also accomplished in vitro by reaction mixtures containing Fe(II), drug and O 2. Bleomycin forms a complex with Fe(II) and O 2 in the presence or absence of DNA. The species attacking DNA forms rapidly from this complex. The nature of the attacking species and of the primary lesion(s) to DNA are not yet known, but two major insults to DNA have been characterized. They are the release of free bases from their glycosidic linkages and, at other residues, the cleavage of the polymer backbone at the deoxyribose C3-C4 bond.

Cold injury of the newborn.

COLD injury of the newborn is a well described entity in the European literature,1 2 3 4 but there are only scattered case reports of this problem in the United States, and then only in the immediate newborn period.5 , 6 In this country, hospital delivery and central heating probably prevent the immediate newborn and later neonatal environmental cold stress that appears to be the major cause of this syndrome. Nevertheless, recognition of cold stress as the major insult in infants usually thought to be suffering from sepsis can be extremely important in the choice of specific treatment directed at the severe hypothermia. Three cases . . .