Strain/strain rate imaging of impaired left atrial function in patients with metabolic syndrome.

Left ventricular (LV) dysfunction has been demonstrated in patients with metabolic syndrome (MetS). However, alterations in left atrial (LA) function in MetS are unknown. We aimed to use strain/strain rate (SR) imaging to investigate the effect of MetS on LA function. A total of 177 MetS patients and 156 normal subjects underwent echocardiography. Strain and SR tissue Doppler imaging values were used to evaluate LA function. Partial correlation and multiple stepwise regression analyses were used to determine the risk factors for impaired LA function. Compared with the controls, the MetS patients showed significantly lower levels of mean strain, mean peak systolic SR and mean peak early diastolic SR (P<0.001 for all), with no difference in the mean peak late diastolic SR. Central obesity, hypertension, dyslipidemia and LV diastolic abnormality were independent risk factors for impaired LA function. LA function was impaired in patients with MetS as a result of metabolic disturbance and LV diastolic abnormality. SR imaging is reliable in assessing LA function in MetS patients.

Effect of dexamethasone on the incidence of post-dural puncture headache after spinal anesthesia: a randomized, double-blind, placebo-controlled trial and a meta-analysis.

The effect of dexamethasone on post-dural puncture headache (PDPH) after spinal anesthesia has not been well elucidated. This randomized, double-blind, placebo-controlled trial was carried out in patients undergoing a cesarean at the Qilu Hospital, Shandong University. The subjects were randomly divided into a placebo and a dexamethasone group. The incidences of PDPH on the first, second, third and seventh postoperative day were studied, and the severity of PDPH was assessed using a visual analog scale. Studies in PubMed, Embase and the Cochrane Library database were searched and included in the present meta-analysis. Summary estimates of weighted mean differences and 95 % confidence intervals (CIs) were obtained using random-effects models. We included 307 participants in the dexamethasone group and 309 in the placebo group for analysis. The results indicated that prophylactic administration of 8 mg dexamethasone did not have any protective effect against PDPH (31 vs. 18, P = 0.054) and even increased the incidence of PDPH in the first 24 h in parturient patients (25 vs. 11, P = 0.016). Furthermore, the meta-analysis also showed that dexamethasone did not prevent the incidence of PDPH in the postoperative follow-up days (RR 1.05; 95 % CI 0.46-2.38; P = 0.91) and may even have increased the trend in the first 24 h. Prophylactic administration of 8 mg dexamethasone does not have any protective effect against PDPH and may even increase the incidence of PDPH in the first 24 h in patients with spinal anesthesia.

Recombinant human erythropoietin attenuates neuronal apoptosis and cognitive defects via JAK2/STAT3 signaling in experimental endotoxemia.

BACKGROUND: Septic encephalopathy is characterized by changes in mental status and an increase in neuronal apoptosis. Accumulating evidence has shown that recombinant human erythropoietin (rhEPO) protects brain against ischemia and hypoxia injury. However, whether rhEPO exerts neuroprotective effects on septic encephalopathy remains unclear. We designed the current study to evaluate possible neuroprotection of rhEPO in a model of sepsis. METHODS: For this in vitro study, we determined hippocampal neuronal apoptosis by lactate dehydrogenase release, cell counting kit-8 assay, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining after treatment with lipopolysaccharide. We transfected the signal transducer and activator of transcription 3 (STAT3) short hairpin RNA at 14 d in vitro for 48 h. For the in vivo study, we performed cecal ligation and peroration surgery. We detected the expression of phospho-Janus-activated kinase 2 (JAK2), total JAK2, phospho-STAT3, total STAT3, Bax and Bcl-XL by Western blot, and examined behavior using the Morris water maze. RESULTS: Treatment with rhEPO reduces apoptosis and increases cell viability in lipopolysaccharide-treated neuronal cultures. In cecal ligation and peroration rats, rhEPO attenuated the inhibition of phospho-JAK2 and phospho-STAT3. In addition, rhEPO enhanced the expression of Bcl-XL, but depressed Bax, which was abolished by additional administration of inhibitor of JAK2/STAT3 signaling 2-cyano-3-(3,4-dihydroxyphenyl)-N-(benzyl)-2-propenamide,2-cyano-3-(3,4-dihydroxyphenyl)-N-(phenylmethyl)-2-propenamide or (E)-3(6-bromopyridin-2-yl)-2-cyano-N-([S0-1-phenylethyl]acrylamide)in vivo, and was ameliorated by STAT3 short hairpin RNA transfection in vitro. Alternatively, we confirmed the neuronal protective effect of rhEPO by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelingstaining. For the Morris water maze study, rhEPO improved learning and memory disorders without an alternation in locomotor activity. CONCLUSIONS: These results indicated that rhEPO improves brain dysfunction by reducing neuronal apoptosis, and JAK2/STAT3 signaling is likely to be involved. Application of rhEPO may serve as a potential therapy for the treatment of septic encephalopathy.