Ionized calcium level predicts in-hospital mortality of severe sepsis patients:A retrospective cross-sectional study

Objective:To evaluate the effect of serum ionized calcium levels on the prognosis of severe sepsis patients.Methods:This retrospective cross-sectional study included sepsis patients who were hospitalized in an intensive care unit between January 2011 and December 2014.The demographic and baseline data of the patients who died and survived were compared.The cutoff value of ionized calcium for in-hospital mortality was determined by the receiver operating characteristics curve(ROC).In-hospital mortalities and the survival rates were compared between patients with different ionized calcium levels.Besides,the risk factor of in-hospital mortality was determined.Results:This study included 145 patients with 113 patients who died in the hospital.The patients who died had significantly lower ionized calcium levels(U=2.25,P=0.034).A cut-off value of 0.93 mmol/L of ionized calcium was determined by the ROC curve.The patients with ionized calcium>0.93 mmol/L showed a significantly lower morality(χ2=9.90,P=0.002)and higher survival rate than with≤0.93 mmol/L(log rank=6.20,P=0.010).Multivariate Cox regression revealed that ionized calcium≤0.93 mmol/L was a risk factor of in-hospital mortality.Conclusions:Ionized calcium level≤0.93 mmol/L was an independent predictor of in-hospital mortality of severe sepsis.

A Study on the Connection between the Incidence of Postherpetic Neuralgia and Serum Ionized Calcium

Herpes zoster （HZ） is an acute virus infectious disease mainly affecting middle-aged and elderly people. The morbidity rates of HZ in the age group of 50-59 years and 60-69 years are, respectively, 46 and 69 （per year, per 10,000 people）. The age groups of 70-79 years and 80-89 years have a much higher rate of 95 and 109 （per year, per 10,000 people）, respectively.

The Study on Intramyocardial Calcium Overload and Apoptosis Induced by Cosackievirus B3

The isolated cardiac myocytes of rats were immediately infected by cosackievirus B3 (CVB3) to investigate the effects of such procedure on the cell cycle, apoptosis and intracellular ionized calcium (Ca 2+ i) of cardiac myocytes. Newborn Balb/c murine cardiac myocytes were cultivated, then infected by CVB3. Intracellular Ca 2+ i was measured by flow cytometer. The calcium in the medium for culturing cardiac myocytes was detected by using atom absorb spectrum test. It was found that CVB3 could markedly inhibit the differentiation and proliferation of the infected cardiac myocytes and induce the apoptosis. The intracellular Ca 2+ i level in the infected group was significantly higher than in the control group (P<0.01). The calcium concentration in the medium for culturing cardiac myocytes in the infected group was significantly lower than in the control group (P<0.05). It was suggested that the apoptosis and intracellular calcium overload of the CVB3-affected cardiac myocytes are likely to play an important role in the pathogenesis of viral myocarditis.

Delayed xenon post-conditioning mitigates spinal cord ischemia/reperfusion injury in rabbits by regulating microglial activation and inflammatory factors

The neuroprotective effect against spinal cord ischemia/reperfusion injury in rats exerted by delayed xenon post-conditioning is stronger than that produced by immediate xenon post-conditioning. However, the mechanisms underlying this process remain unclear. Activated microglia are the main inflammatory cell type in the nervous system. The release of pro-inflammatory factors following microglial activation can lead to spinal cord damage, and inhibition of microglial activation can relieve spinal cord ischemia/reperfusion injury. To investigate how xenon regulates microglial activation and the release of inflammatory factors, a rabbit model of spinal cord ischemia/reperfusion injury was induced by balloon occlusion of the infrarenal aorta. After establishment of the model, two interventions were given： （1） immediate xenon post-conditioning—after reperfusion, inhalation of 50% xenon for 1 hour, 50% N2/50%O2 for 2 hours; （2） delayed xenon post-conditioning—after reperfusion, inhalation of 50% N2/50%O2 for 2 hours, 50% xenon for 1 hour. At 4, 8, 24, 48 and 72 hours after reperfusion, hindlimb locomotor function was scored using the Jacobs locomotor scale. At 72 hours after reperfusion, interleukin 6 and interleukin 10 levels in the spinal cord of each group were measured using western blot assays. Iba1 levels were determined using immunohistochemistry and a western blot assay. The number of normal neurons at the injury site was quantified using hematoxylin-eosin staining. At 72 hours after reperfusion, delayed xenon post-conditioning remarkably enhanced hindlimb motor function, increased the number of normal neurons at the injury site, decreased Iba1 levels, and inhibited interleukin-6 and interleukin-10 levels in the spinal cord.Immediate xenon post-conditioning did not noticeably affect the above-mentioned indexes. These findings indicate that delayed xenon post-conditioning after spinal cord injury improves the recovery of neurological function by reducing microglial activation and the release of interleukin-6 and interleukin-10.

Rapid GFAP and Iba1 expression changes in the female rat brain following spinal cord injury

Evidence suggests that rapid changes to supporting glia may predispose individuals with spinal cord injury(SCI) to such comorbidities. Here, we interrogated the expression of astrocyte-and microglial-specific markers glial fibrillary acidic protein(GFAP) and ionized calcium binding adaptor molecule 1(Iba1) in the rat brain in the first 24 hours following SCI. Female Sprague-Dawley rats underwent thoracic laminectomy;half of the rats received a mild contusion injury at the level of the T10 vertebral body(SCI group), the other half did not(Sham group). Twenty-four hours post-surgery the amygdala, periaqueductal grey, prefrontal cortex, hypothalamus, lateral thalamus, hippocampus(dorsal and ventral) in rats were collected. GFAP and Iba1 m RNA and protein levels were measured by real-time quantitative polymerase chain reaction and Western blot. In SCI rats, GFAP m RNA and protein expression increased in the amygdala and hypothalamus. In contrast, gene and protein expression decreased in the thalamus and dorsal hippocampus. Interestingly, Iba1 transcripts and proteins were significantly diminished only in the dorsal and ventral hippocampus, where gene expression diminished. These findings demonstrate that as early as 24 hours post-SCI there are region-specific disruptions of GFAP and Iba1 transcript and protein levels in higher brain regions. All procedures were approved by the University of Technology Sydney Institutional Animal Care and Ethics Committee(UTS ACEC13-0069).

Effect of Lipoxin A_4 on IL-1β Production of Monocytes and Its Possible Mechanism in Severe Preeclampsia

This study examined in vitro effect of lipoxin A 4 (LXA 4) on interleukin-1β (IL-1β) production of monocytes and its possible mechanism in severe preeclampsia (PE).Peripheral venous blood was drawn from 15 patients with severe preeclampsia (PE group) and 20 normal pregnant women (control group) to prepare monocytes which were then treated with LXA 4 at different concentrations of 0,10,100 nmol/L respectively.IL-1β level in the supernatant of monocytes was detected by enzyme linked immunoassay.The [Ca 2+ ] i of monocytes was measured by laser scanning confocal microscopy.The results showed that the IL-1β level and the [Ca 2+ ] i of monocytes in the PE group were significantly higher than those in the control group.LXA 4 significantly decreased the generation of IL-1β in a dose-dependent manner in the PE group.After treatment with 100-nmol/L LXA 4,in the PE group,the [Ca 2+ ] i concentration of monocytes was significantly reduced.It was concluded that LXA 4 may inhibit the IL-1β production of monocytes from severe preeclampsia women by inhibiting extracellular calcium influx.

A New Type of Double-Lumen Catheter to Replace Current One in RCA

Objective: To replace the peripheral venous puncture for blood sampling with taking blood samples extracorporally from arterial line before predilution during RCA-CRRT performed. Methods: A new type of double-lumen femoral catheter was used instead of the current tubes. The new type of double-lumen tube had a greater distance from the inner venous ports to the inner arterial ports than current tubes. The minimum distance from the venous port to the arterial port was greatly lengthened. Replacement solution contained citrate, zero Ca2+, zero bicarbonate, low Na+. Blood samples were synchronously collected from the arterial line before the infusion of citrate replacement fluid and from the peripheral vein. The iCa concentration data of two groups were analyzed to observe the difference between iCa concentration levels in the arterial line and in peripheral vein;the anticoagulant effect of RCA and possible complications were observed, such as bleeding, clottings and hypocalcaemia. Results: 28 times of RCA-CRRT were performed on17 AKI and CRF patients with active bleeding or at the high risk of bleeding;336 blood samples were collected. Statistics showed that the difference of iCa concentration between arterial line group and the peripheral vein group was not significant (P = 0.9), there is a high degree of similarity between the iCa concentration of arterial line blood and the peripheral venous blood. None of the patients developed citrate toxicity or metabolic alkalosis. None induced bleeding, or bleeding aggravated. No obvious clotting occurred. Systemic calcium concentration was achieved in the ideal range. Conclusion: In clinical practice, the data of iCa concentration from arterial line can be used to replace that from peripheral vein when the new type of double-lumen femoral catheter is placed in femoral vein. RCA-CRRT therapy is safe and effective.