The implication of nitric oxide in the process of bacterial translocation

Since there is increasing evidence indicating nitric oxide [NO] would play a role in sepsis, we decided to investigate whether this multifaceted mediator is directly implicated in the process of bacterial translocation. A total of 48 rats received intraperitoneal either Zymosan A (group Z) for systemic inflammation production or sodium chloride solution (controls); they were then further subdivided into three groups of eight animals each, being given, through the tail vein: L-NAME (N-nitro-L-arginine] for inhibition of NO production; SNP (sodium nitroprusside) as NO donor; or sodium chloride as control. After 2 h, the mesenteric lymph node complex was excised, under sterile conditions, and, using standard bacteriological techniques, bacterial translocation was assessed as colony forming units per gram of tissue (CFU/g). Statistical evaluation of the bacteriological data revealed a significant increase of bacterial translocation in all rats subjected to systemic inflammation (group Z) versus controls (P = 0.01) Control rats that were subjected to L-NAME treatment exhibited a statistically significant increase (P = 0.001) in CFU/g compared to sodium chloride treated rats, while SNP treatment revealed no difference in relation to sodium chloride treated rats. Group Z rats, subjected to L-NAME treatment, similarly exhibited a statistically significant increase (P = 0.01) in CFU/g compared to sodium chloride treated rats, while SNP treatment led to a statistical increase of bacterial translocation in relation to sodium chloride treated rats (P = 0.05). The results of this study lead us to suggest that NO appears to participate in the process of bacterial translocation.     

Leukocyte and Platelet-Rich Fibrin Have Same Effect as Blood Clot in the 3-Dimensional Alveolar Ridge Preservation. A Split-Mouth Randomized Clinical Trial

1. Download : Download high-res image (317KB)
2. Download : Download full-size image

     

The Sequential Relation Between Changes in Catastrophizing and Changes in Posttraumatic Stress Disorder Symptom Severity

Catastrophizing has been discussed as a cognitive precursor to the emergence of posttraumatic stress disorder (PTSD) symptoms following the experience of stressful events. Implicit in cognitive models of PTSD is that treatment-related reductions in catastrophizing should yield reductions in PTSD symptoms. The tenability of this prediction has yet to be tested. The present study investigated the sequential relation between changes in a specific form of catastrophizing—symptom catastrophizing—and changes in PTSD symptom severity in a sample of 73 work-disabled individuals enrolled in a 10-week behavioral activation intervention. Measures of symptom catastrophizing and PTSD symptom severity were completed at pre-, mid-, and posttreatment assessment points. Cross-sectional analyses of pretreatment data revealed that symptom catastrophizing accounted for significant variance in PTSD symptom severity, β = .40, p < .001, sr = .28 (medium effect size), even when controlling for known correlates of symptom catastrophizing, such as pain and depression. Significant reductions in symptom catastrophizing and PTSD symptoms were observed during treatment, with large effect sizes, ds = 1.42 and 0.94, respectively, ps < .001. Cross-lagged analyses revealed that early change in symptom catastrophizing predicted later change in PTSD symptoms; early changes in PTSD symptom severity did not predict later change in symptom catastrophizing. These findings are consistent with the conceptual models that posit a causal relation between catastrophizing and PTSD symptom severity. The clinical implications of the findings are discussed.     

Long-term male-specific chronic pain via telomere- and p53‑mediated spinal cord cellular senescence

Mice with experimental nerve damage can display long‑lasting neuropathic pain behavior. We show here that 4 months and later after nerve injury, male but not female mice displayed telomere length (TL) reduction and p53‑mediated cellular senescence in the spinal cord, resulting in maintenance of pain and associated with decreased lifespan. Nerve injury increased the number of p53‑positive spinal cord neurons, astrocytes, and microglia, but only in microglia was the increase male‑specific, matching a robust sex specificity of TL reduction in this cell type, which has been previously implicated in male‑specific pain processing. Pain hypersensitivity was reversed by repeated intrathecal administration of a p53‑specific senolytic peptide, only in male mice and only many months after injury. Analysis of UK Biobank data revealed sex-specific relevance of this pathway in humans, featuring male‑specific genetic association of the human p53 locus (TP53) with chronic pain and a male-specific effect of chronic pain on mortality. Our findings demonstrate the existence of a biological mechanism maintaining pain behavior, at least in males, occurring much later than the time span of virtually all extant preclinical studies.     

Postmastectomy radiation in patients with four or more positive nodes

Postmastectomy radiotherapy (PMR), a local therapeutic modality, is recommended to treat breast cancer patients with multiple involved axillary lymph nodes (a marker of increased systemic risk). Bothered by this conceptually flawed treatment approach we evaluated the impact of PMR on the treatment of women with four or more involved axillary lymph nodes. We identified 1164 patients treated from 1982 through 1999 with mastectomy. We reviewed the records of the 223 who demonstrated four or more positive axillary lymph nodes. Of these 128 were treated by mastectomy only and 95 by PMR. The mastectomy-only group demonstrated a mean tumor size of 3.5 cm, a median of seven axillary nodes involved, and a median of 24.9 nodes harvested. The PMR group had a mean tumor size of 4.3 cm with nine positive nodes out of a median total of 23.3 harvested. The difference in mean tumor size was statistically significant (P = 0.01). The locoregional recurrence (10.9% vs 12.6%), distant recurrence rates (42.2% vs 35.8%), and 5-year survival (51% vs 55%) were not statistically different between the mastectomy-only group versus the PMR group, respectively. Adding PMR to breast cancer treatment demonstrated no improvement in outcome. Despite limitations of this retrospective study the results strongly support evaluation of PMR by a high-quality randomized prospective trial.     

Reducing unintentional injuries on the nation's highways: research and program policy to increase seat belt use

Death, disability, and injury from motor vehicle accidents constitute a public health crisis. The goal of this paper is to describe how Meharry Medical College's Center for Community Based Research plans to address this problem. A model of how high-risk groups are influenced to engage in behaviors that increase risk for traffic crashes is articulated. Five strategies for reducing risk for motor vehicle morbidity and mortality are identified: 1) influencing the individual at the point of decision; 2) mobilizing communities and coalitions to support individual and systems changes; 3) modifying environmental factors to modify behaviors; 4) changing laws and public policy; and 5) working towards the elimination of underlying causes. The Center for Community Based Research's promotion of seat belt use, based on each of these five strategies, is described. Addressing the public health crisis resulting from death and injury on the nation's roads and the excess risk faced by minority groups in this country will require the coordinated efforts of many groups. This work must be driven by research, the outcome of which will be a reduction in preventable injury, disability and premature death.