State of the Art in Burn Treatment

Optimal treatment of burn victims requires deep understanding of the profound pathophysiological changes occurring locally and systemically after injury. Accurate estimation of burn size and depth, as well as early resuscitation, is essential. Good burn care includes also cleansing, debridement, and prevention of sepsis. Wound healing, is of major importance to the survival and clinical outcome of burn patients. An ideal therapy would not only promote rapid healing but would also act as an antiscarring therapy. The present article is a literature review of the most up-to-date modalities applied to burn treatment without overlooking the numerous controversies that still persist.     

Cytokine dysregulation, inflammation and well-being

Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis, health, and well-being. Like the stress response, the inflammatory reaction is crucial for survival and is meant to be tailored to the stimulus and time. A full-fledged systemic inflammatory reaction results in stimulation of four major programs: the acute-phase reaction, the sickness syndrome, the pain program, and the stress response, mediated by the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Common human diseases such as atopy/allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro- versus anti-inflammatory and T helper (Th)1 versus Th2 cytokine balance. Recent evidence also indicates the involvement of pro-inflammatory cytokines in the pathogenesis of atherosclerosis and major depression, and conditions such as visceral-type obesity, metabolic syndrome and sleep disturbances. During inflammation, the activation of the stress system, through induction of a Th2 shift, protects the organism from systemic 'overshooting' with Th1/pro-inflammatory cytokines. Under certain conditions, however, stress hormones may actually facilitate inflammation through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha and C-reactive protein production and through activation of the corticotropin-releasing hormone/substance P-histamine axis. Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression, and atherosclerosis. These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health. These hypotheses require further investigation, but the answers should provide critical insights into mechanisms underlying a variety of common human immune-related diseases.     

Stability of the complexes of some lanthanides with coumarin derivatives. I. Cerium(III)-4-methyl-7-hydroxycoumarin

A complex of cerium(III) with 4-methyl-7-hydroxycoumarin was synthesized by mixing water solutions of cerium(III) nitrate and 4-methyl-7-hydroxycoumarin sodium salt in a metal-to-ligand molar ratio of 1:2. The complex was characterized and identified by elemental analysis, conductometry, IR, 1H and 13C NMR-spectroscopy, mass spectral data, DTA and TGA. Thermal analysis of the complex indicated the formation of a compound of the composition CeR2(OH).5H2O, R standing for the ligand. The reaction of cerium(III) with 4-methyl-7-hydroxycoumarin was studied in detail by the spectrophotometric method. The stepwise formation of two complexes, vis., CeR2+ and CeR2+, was established in the pH region studied. The equilibrium constants for 1:1 and 1:2 complexes were determined to be 10.72 and 9.22, respectively.     

High expressor paraoxonase PON1 gene promoter polymorphisms are associated with reduced risk of vascular disease in younger coronary patients

Human paraoxonase-1 is hypothesised to protect serum lipoproteins from oxidative stress. Decreased serum activity of paraoxonase-1 in animal models is associated with an increased risk of vascular disease and has been linked to the anti-oxidant capacity of the enzyme. Promoter polymorphisms of the human paraoxonase-1 gene strongly influence serum concentrations of the enzyme. The present study examined the hypothesis that promoter polymorphisms may be genetic risk factors for vascular disease in man. Genotypes arising from the promoter C(-907)G polymorphism were analysed in the ECTIM2 population. The global odds ratio for myocardial infarction, comparing the high expressor GG genotype to other genotypes, was 0.77 (0.61-0.97) (P=0.024). The association with the promoter genotype was more pronounced in the youngest age group (odds ratio 0.52 (0.31-0.87), P=0.012) and was progressively lost with age (respectively 50 years to <60 years, P=0.26; >60 years, P=0.45). There was no association between the promoter genotypes and serum lipids. The data are consistent with the high expressor promoter genotype being linked to reduced risk of myocardial infarction. The influence of the genotype may be compromised in older patients.     

Use of neoadjuvant and adjuvant therapy to prevent or delay recurrence of prostate cancer in patients undergoing surgical treatment for prostate cancer

There have been improvements in the outcome of patients with clinically localized prostate cancer treated by radical prostatectomy. However, some patients treated with radical prostatectomy will have clinical or biochemical progression. These men are at increased risk of dying of their disease. Identification of patients with adverse features at the time of radical prostatectomy may permit the use of additional multimodality therapies to improve outcomes. Whether this additional multimodality therapy should be administered in the neoadjuvant or adjuvant setting remains controversial. Further, whether a patient at increased risk for progression after radical prostatectomy requires additional therapy before the development of documented progression remains controversial. This article reviews the potential multimodality approaches to prevent or delay recurrence of prostate cancer in patients undergoing surgical treatment for prostate cancer.     

Treatment of postdiscectomy low back pain by percutaneous posterior lumbar interbody fusion versus open posterior lumbar fusion with pedicle screws

BACKGROUND CONTEXT: Up to a fifth of the patients who had discectomy undergo spinal fusion because of disabling low back pain. PURPOSE: To compare the clinical outcome of percutaneous posterior lumbar interbody fusion (PPLIF) to that of open posterior lumbar fusion (PLF). STUDY DESIGN/SETTING: Two surgical methods that were tried in sequence at a university affiliated hospital. PATIENT SAMPLE: Sixty patients with disabling postdiscectomy low back pain. OUTCOME MEASURES: Pain intensity was scored on a visual analog scale (VAS) and the degree of disability was scored by the Oswestry disability index (ODI). METHODS: Thirty patients were treated by PPLIF. The outcome, after 24 months or more, was compared retrospectively with that of 30 consecutive suitable subjects who had been treated by PLF with pedicle screw fixation by the same surgeons for the same indication. RESULTS: In the PPLIF group, as compared with PLF group, mean operating time was shorter, blood loss was negligible, and mean hospital time was halved. By the last follow-up visit (greater than or equal to 2 years), pain and disability in PLF group had diminished by 31.9% and 20.1%, respectively. The corresponding figures in PPLIF group were 55.4% and 42.7%, respectively. CONCLUSIONS: In the context of postdiscectomy low back pain, PPLIF has proven, thus far, to be a safe procedure with improved clinical results.