Diagnosis and treatment of tension pneumothorax under anesthesia: a case report

An 80-year old woman with a history of tracheal stenosis, tracheostomy, and 3 months of increasing respiratory distress underwent tracheal dilatation under general anesthesia with jet ventilation. Tracheal dilatation was successfully performed via suspension laryngoscopy and jet ventilation. During emergence the patient developed decreased oxygen saturation, hypotension, and respiratory distress, requiring intubation and ventilatory support. During tracheostomy, anterior chest subcutaneous emphysema led to a diagnosis of tension pneumothorax. Chest tube placement facilitated tracheostomy and improved ventilatory and circulatory parameters. This article discusses the diagnosis and treatment of a tension pneumothorax under general anesthesia. Jet ventilation, spontaneous rupture of blebs or bullae, surgical trauma, or barotrauma are the 4 most likely explanations for a tension pneumothorax in this patient. Jet ventilation can cause pneumothorax, pneumomediastinum, or subcutaneous emphysema. Chronic obstructive pulmonary disease may cause blebs or bullae, which might rupture when exposed to positive pressure ventilation. Tissue trauma during dilatation or tracheostomy may cause a pneumothorax when positive pressure ventilation is employed. Barotrauma from high peak inspiratory pressure, rigid bronchoscopy, dilatation procedure, or jet ventilation may cause a pneumothorax. Prompt diagnosis and treatment will markedly decrease associated morbidity and mortality.     

Regulation of Nod1 and Nod2 in First Trimester Trophoblast Cells

Problem:  The cytoplasmic pattern recognition receptors, Nod1 and Nod2, are thought to be important for detecting intracellular bacteria. We have previously reported that first trimester trophoblast cells express Nod1 and Nod2, and that trophoblast Nod2 activation triggers an inflammatory response. The objectives of this study were to characterize the effects of Nod1 stimulation, and to determine the regulation of Nod1 and Nod2, in the trophoblast.
Method of Study:  The effect of Nod1 activation on trophoblast cells was determined by analyzing the cytokine response following treatment with γ-D-glutamyl- meso -diaminopimelic acid (iE-DAP). The regulation of Nod1 and Nod2 expression by trophoblast cells was evaluated by RT-PCR.
Results:  Treatment of trophoblast cells with iE-DAP significantly increased their production of cytokines and chemokines. In addition, Nod1 and Nod2 mRNA expression was upregulated following treatment of trophoblast cells with lipopolysaccharide (LPS), and this was significantly reduced by the presence of a NFκB inhibitor and a TLR4-dominant negative (DN).
Conclusion:  This study demonstrates that LPS, through TLR4, increases trophoblast expression of Nod1 and Nod2 via the NFκB pathway; and that Nod1 is functional in the trophoblast. These findings suggest that extracellular recognition of bacterial LPS by TLR4 may prime the trophoblast in preparation for its cytoplasmic recognition of, and response to, bacterial peptides through the Nod proteins.     

Estimated glomerular filtration rate in sickle cell anemia is associated with polymorphisms of bone morphogenetic protein receptor 1B

Renal disease is common in sickle cell anemia. In this exploratory work, we used data from a longitudinal study of the natural history of sickle cell disease to examine the hypothesis that polymorphisms (SNPs) in selected candidate genes are associated with glomerular filtration rate (GFR). DNA samples and clinical and laboratory data were available for 1,140 patients with sickle cell anemia. GFR was estimated using the Cockcroft-Gault and Schwartz formulas for adults and children, respectively. We examined approximately 175 haplotype tagging (ht) SNPs in about 70 genes of the TGFbeta/BMP pathway for their association with GFR using linear regression. Four SNPs in BMPR1B, a bone morphogenetic protein (BMP) receptor gene, yielded statistically significant associations (P values ranging from 0.015 to 0.046). Three haplotypes in this gene were also associated with GFR. The TGF-beta/BMP pathway has been associated with the development of diabetic nephropathy, which has some features in common with sickle cell nephropathy. Our results suggest that, as with other subphenotypes of sickle cell disease, renal function may be genetically modulated.     

Zika virus infection of Hofbauer cells

Recent studies have linked antenatal infection with Zika virus (ZIKV) with major adverse fetal and neonatal outcomes, including microcephaly. There is a growing consensus for the existence of a congenital Zika syndrome (CZS). Previous studies have indicated that non‐placental macrophages play a key role in the replication of dengue virus (DENV), a closely related flavivirus. As the placenta provides the conduit for vertical transmission of certain viruses, and placental Hofbauer cells (HBCs) are fetal—placental macrophages located adjacent to fetal capillaries, it is not surprising that several recent studies have examined infection of HBCs by ZIKV. In this review, we describe congenital abnormalities associated with ZIKV infection, the role of HBCs in the placental response to infection, and evidence for the susceptibility of HBCs to ZIKV infection. We conclude that HBCs may contribute to the spread of ZIKV in placenta and promote vertical transmission of ZIKV, ultimately compromising fetal and neonatal development and function. Current evidence strongly suggests that further studies are warranted to dissect the specific molecular mechanism through which ZIKV infects HBCs and its potential impact on the development of CZS.     

Association of klotho, bone morphogenic protein 6, and annexin A2 polymorphisms with sickle cell osteonecrosis

In patients with sickle cell disease, clinical complications including osteonecrosis can vary in frequency and severity, presumably due to the effects of genes that modify the pathophysiology initiated by the sickle mutation. Here, we examined the association of single nucleotide polymorphisms (SNPs) in candidate genes (cytokines, inflammation, oxidant stress, bone metabolism) with osteonecrosis in patients with sickle cell disease. Genotype distributions were compared between cases and controls using multiple logistic regression techniques. An initial screen and follow-up studies showed that individual SNPs and haplotypes composed of several SNPs in bone morphogenic protein 6, annexin A2, and klotho were associated with sickle cell osteonecrosis. These genes are important in bone morphology, metabolism, and vascular disease. Our results may provide insight into the pathogenesis of osteonecrosis in sickle cell disease, help identify individuals who are at high risk for osteonecrosis, and thus allow earlier and more effective therapeutic intervention.     

Association of longer telomeres with better health in centenarians

Prior animal model studies have demonstrated an association between telomere length and longevity. Our study examines telomere length in centenarians in good health versus poor health. Using DNA from blood lymphocytes, telomere length was measured by quantitative polymerase chain reaction in 38 sex- and age-matched centenarians (ages 97-108). "Healthy" centenarians (n = 19) with physical function in the independent range and the absence of hypertension, congestive heart failure, myocardial infarction, peripheral vascular disease, dementia, cancer, stroke, chronic obstructive pulmonary disease, and diabetes were compared to centenarians with physical function limitations and >/=2 of the above conditions (n = 19). Healthy centenarians had significantly longer telomeres than did unhealthy centenarians (p =.0475). Our study demonstrated that investigations of the association between telomere length and exceptional longevity must take into account the health status of the individuals. This raises the possibility that perhaps it is not exceptional longevity but one's function and health that may be associated with telomere length.     

Returning to work following curative chemotherapy: a qualitative study of return to work barriers and preferences for intervention

Purpose

This study aimed to explore barriers to return to work (RTW) and preferences for intervention and support for cancer patients treated with curative intent from the perspectives of cancer survivors and oncology health professionals.

Methods

Participants attended a focus group (N?=?24) or an individual interview (N?=?14). A topic guide and a semi-structured recorded interview format were used to gather data, which were later transcribed and analysed for global themes and subthemes.

Results

With regard to barriers, the global theme ‘work capacity’ captured an array of barriers encompassing financial pressure, preparedness for work, lack of confidence as well as other key physical, practical and psychosocial barriers. Participants expressed a preference for RTW models that focus on objective and structured assessment whilst allowing for flexibility to address individual needs.

Conclusions

Cancer survivors perceive multiple barriers when attempting to RTW. These barriers were perceived to impact upon work capacity, where ‘capacity’ was defined broadly to include practical, physical and psychosocial concerns. RTW is an important concern for cancer survivors and structured RTW interventions should be incorporated into the care of cancer survivors.