An acute coronary syndrome in Antarctica

Cruise tourism to Antarctica is constantly growing. Passengers and crewmembers may experience illnesses or injuries while traveling to remote areas with harsh weather conditions from where prompt evacuation is mostly unavailable. While a small explorer ship was at Wilhelmina bay (64°39’ South and 62°08’ West) in the Antarctic Peninsula, a 73-year-old male passenger presented with acute chest pain after two short excursions off the vessel in cold weather conditions. He was treated on board and remained clinically stable until the ship reached Ushuaia at the end of the cruise which was 5 days after the symptoms onset.

Cruise ship pathologies in remote regions

Background: Navigations on cruise ships are rising and tend to spread to remote areas like polar regions. Our aim was to assess the prevalence of pathologies encountered on a cruise ship navigating in remote areas including Polar Seas. Materials and methods: A prospective observational, descriptive and cross-sectional study was conducted aboard a cruise ship with an overall capacity of 200–264 passengers and 140 crewmembers, sailing in remote areas as the Arctic Ocean and the Antarctic Peninsula over a period of 205 days. The database was built on all first consultations for passengers and crewmembers done by the onboard physician. Each symptom and diagnosis was coded according to the “International Classification of Primary Care, 2nd edition”. For statistical analysis, the quantitative data were expressed as mean ± standard deviation and qualitative data as percentages. The percentages were compared using a c2 test corrected according to the Yates’ method or by a Fisher test when appropriate. Results: A total of 446 diagnoses were studied on the 910 consultations originally included (13.7% of the people on board). The median age for the passengers and the crewmembers was respectively 68 (age ranging from 12 to 90) years and 31 (18–62) years. Likewise, the sex ratio (male/female) was 0.98 and 3.23. Infectious diseases were predominant (prevalence of 43.7%). Among them, respiratory infections were the most common and gastroenteritis seemed to be more frequent in passengers (prevalence of 11.5% vs. 5%, p = 0.10). Cutaneous pathologies were more frequent in crewmembers (prevalence of 26.6% vs. 18.7%, p = 0.04) and allergic dermatitis was the second most frequent in this group of patients (prevalence of 7.2%). Cardiovascular diseases, more common in passengers (p = 0.05), represented 4% of all diagnoses. Two cases of phlebitis, one stroke and one subacute heart failure were diagnosed. Among traumatic injuries, cutaneous traumas were the commonest (prevalence of 76.5%). Musculoskeletal traumas were more common in passengers (p = 0.04). An acute gastrointestinal haemorrhage required a medical evacuation from the Antarctic Peninsula. Conclusions: The physician should be prepared to face emergency cases by developing personal expertise specific to maritime medicine in remote areas. Highlighting the particularity of cases handled in remote areas, our results should also pave the way of the development of medical protocols for ships lacking physician

Anion gap, anion gap corrected for albumin, base deficit and unmeasured anions in critically ill patients: implications on the assessment of metabolic acidosis and the diagnosis of hyperlactatemia

Abstract Background Base deficit (BD), anion gap (AG), and albumin corrected anion gap (ACAG) are used by clinicians to assess the presence or absence of hyperlactatemia (HL). We set out to determine if these tools can diagnose the presence of HL using cotemporaneous samples. Methods We conducted a chart review of ICU patients who had cotemporaneous arterial blood gas, serum chemistry, serum albumin (Alb) and lactate(Lac) levels measured from the same sample. We assessed the capacity of AG, BD, and ACAG to diagnose HL and severe hyperlactatemia (SHL). HL was defined as Lac > 2.5 mmol/L. SHL was defined as a Lac of > 4.0 mmol/L. Results From 143 patients we identified 497 series of lab values that met our study criteria. Mean age was 62.2 ± 15.7 years. Mean Lac was 2.11 ± 2.6 mmol/L, mean AG was 9.0 ± 5.1, mean ACAG was 14.1 ± 3.8, mean BD was 1.50 ± 5.4. The area under the curve for the ROC for BD, AG, and ACAG to diagnose HL were 0.79, 0.70, and 0.72, respectively. Conclusion AG and BD failed to reliably detect the presence of clinically significant hyperlactatemia. Under idealized conditions, ACAG has the capacity to rule out the presence of hyperlactatemia. Lac levels should be obtained routinely in all patients admitted to the ICU in whom the possibility of shock/hypoperfusion is being considered. If an AG assessment is required in the ICU, it must be corrected for albumin for there to be sufficient diagnostic utility.</p

The ArcA regulon and oxidative stress resistance in Haemophilus influenzae

Haemophilus influenzae transits between niches within the human host that are predicted to differ in oxygen levels. The ArcAB two-component signal transduction system controls gene expression in response to respiratory conditions of growth and has been implicated in bacterial pathogenesis, yet the mechanism is not understood. We undertook a genome-scale study to identify genes of the H. influenzae ArcA regulon. Deletion of arcA resulted in increased anaerobic expression of genes of the respiratory chain and of H. influenzae's partial tricarboxylic acid cycle, and decreased anaerobic expression levels of genes of polyamine metabolism, and iron sequestration. Deletion of arcA also conferred a susceptibility to transient exposure to hydrogen peroxide that was greater following anaerobic growth than after aerobic growth. Array data revealed that the dps gene, not previously assigned to the ArcA modulon in bacteria, exhibited decreased expression in the arcA mutant. Deletion of dps resulted in hydrogen peroxide sensitivity and complementation restored resistance, providing insight into the previously uncharacterized mechanism of arcA-mediated H2O2 resistance. The results indicate a role for H. influenzae arcA and dps in pre-emptive defence against transitions from growth in low oxygen environments to aerobic exposure to hydrogen peroxide, an antibacterial oxidant produced by phagocytes during infection

Regulation of mTORC1 Signaling by pH

BACKGROUND: Acidification of the cytoplasm and the extracellular environment is associated with many physiological and pathological conditions, such as intense exercise, hypoxia and tumourigenesis. Acidification affects important cellular functions including protein synthesis, growth, and proliferation. Many of these vital functions are controlled by mTORC1, a master regulator protein kinase that is activated by various growth-stimulating signals and inactivated by starvation conditions. Whether mTORC1 can also respond to changes in extracellular or cytoplasmic pH and play a role in limiting anabolic processes in acidic conditions is not known. METHODOLOGY/FINDINGS: We examined the effects of acidifying the extracellular medium from pH 7.4 to 6.4 on human breast carcinoma MCF-7 cells and immortalized mouse embryo fibroblasts. Decreasing the extracellular pH caused intracellular acidification and rapid, graded and reversible inhibition of mTORC1, assessed by measuring the phosphorylation of the mTORC1 substrate S6K. Fibroblasts deleted of the tuberous sclerosis complex TSC2 gene, a major negative regulator of mTORC1, were unable to inhibit mTORC1 in acidic extracellular conditions, showing that the TSC1-TSC2 complex is required for this response. Examination of the major upstream pathways converging on the TSC1-TSC2 complex showed that Akt signaling was unaffected by pH but that the Raf/MEK/ERK pathway was inhibited. Inhibition of MEK with drugs caused only modest mTORC1 inhibition, implying that other unidentified pathways also play major roles. CONCLUSIONS: This study reveals a novel role for the TSC1/TSC2 complex and mTORC1 in sensing variations in ambient pH. As a common feature of low tissue perfusion, low glucose availability and high energy expenditure, acidic pH may serve as a signal for mTORC1 to downregulate energy-consuming anabolic processes such as protein synthesis as an adaptive response to metabolically stressful conditions