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Klippel-Trenaunay Syndrome (KTS) is a rare congenital disorder, characterized by venous and lymphatic malformations of the skin, soft tissue, and bone, causing limb hypertrophy. Although, a ruptured hemorrhagic corpus luteum is a rare condition in women of reproductive age, it can result in lethal outcomes. Here, we have described a patient with KTS and hypofibrinogenemia who went through recurrent lethal postoperative bleeding due to a ruptured hemorrhagic corpus luteum. This case suggested that conservative therapy might be the first choice and effective therapy for the patients with KTS, who suffered from bleeding complications of surgical therapy.

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Cardiac hypertrophy is a compensatory response in reaction to mechanical load that reduces wall stress by increasing wall thickness. Chronic hypertrophic remodeling involves cardiac dysfunction that will lead to heart failure and ultimately death. Studies have been carried out on cardiac hypertrophy for years, whereas the mechanisms have not been well defined. Tamarixetin (TAM), a natural flavonoid derivative of quercetin, have been demonstrated possessing anti-oxidative and anti-inflammatory effects on multiple diseases. However, little is known about the function of TAM on the development of cardiac hypertrophy. Here, we found TAM could alleviate pressure-overload-induced cardiac hypertrophy in transverse aortic constriction (TAC) mouse model, assessed by ventricular weight/body weight, lung weight/body weight, echocardiographic parameters, as well as myocyte cross-sectional area and the expression of ANP, BNP and Myh7. In vitro, TAM showed a dose dependent inhibitory effect on phenylephrine-induced hypertrophy in H9c2 cardiomyocytes. Furthermore, TAM reversed cardiac remodeling of stress overloaded heart by suppressing apoptosis and the expression of fibrotic-related genes, reduced oxidative stress and ROS production both in vivo and in vitro. In addition, TAM could negatively modulate TAC-induced nuclear translocation of NFAT and the activation of PI3K/AKT signaling pathways. Therefore, these data indicate for the first time that TAM has a protective effect on experimental cardiac hypertrophy and might be a novel candidate for the treatment of cardiac hypertrophy in clinic.

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OBJECTIVE: To Compare the clinical efficacy and safety of meropenem with a 3-hour extended infusion or conventional 30-minute infusion regimen in treatment of hospital acquired pneumonia (HAP) in intensive care unit (ICU) patients. METHODS: An open-label randomized controlled clinical trial was conducted. 100 HAP patients, admitted to ICU of Qilu Hospital of Shandong University, who needed meropenem therapy were enrolled from September 1st, 2012 to September 30th, 2013. The patients were randomly divided into two groups. Patients who did not conform to the study protocol were excluded. A total of 78 patients were included for the study of clinical efficacy evaluation, with 38 cases in study group, and 40 in control group. The patients in study group received intravenous 1 g of meropenem (dissolved in 40 mL saline) within 10 minutes, and followed by the remaining 750 mg by continuous intravenous infusion for 3 hours, and the treatment was repeated every 8 hours. The patients in control group received meropenem by injection of 1 g (dissolved in 40 mL saline), i.e. by intravenous infusion within 30 minutes every 8 hours. This regime was carried out for at least 7 days. Clinical efficacy, bacterial clearance rate, improvement of critical illness scoring, and safety were observed and compared after meropenem withdrawal between two groups. RESULTS: Compared with control group, the clinical cure rate and 28-day survival rate in study group were significantly increased [clinical cure rate: 71.1% (27/38) vs. 42.5% (17/40), χ² = 6.461, P=0.011; survival rate: 81.6% (31/38) vs. 60.0% (24/40), χ² = 4.364, P=0.037]. The improvement of clinical pulmonary infection score (CPIS) and sequential organ failure assessment (SOFA) score in study group were more marked than those in control group (difference of CPIS score: -3.47 ± 2.48 vs. -1.50 ± 2.48, t=-3.513, P=0.001; difference of SOFA score: -2.10 ± 2.38 vs. -1.00 ± 2.21, t=-0.800, P=0.037). There were no significant differences in duration of meropenem treatment, acute physiology and chronic health evaluation II (APACHEII) score, procalcitonin (PCT), duration of mechanical ventilation, ICU stay days, secondary infection, and bacterial clearance rate between two groups. The main adverse reactions observed were transient elevation of liver enzymes and diarrhea in both groups, but no significant difference in their incidence was found between study and control groups [elevated liver enzymes: 28.9% (11/38) vs. 30.0% (12/40), χ² = 0.010, P=0.919; diarrhea: 7.9% (3/38) vs. 10.0% (4/40), χ² = 0.000, P=1.000]. CONCLUSIONS: Compared with conventional regime of 30-minute infusion of meropenem in the treatment of HAP in ICU patients, the clinical efficacy can be improved, the severity of the disease can be reduced, the recovery of organ failure and long-term prognosis can be improved with 3 hour extended infusion of meropenem.

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OBJECTIVE: Alternating hemiplegia of childhood (AHC) is a rare neurodevelopmental syndrome of uncertain etiology. Although the use of magnetic resonance spectroscopy (MRS) for the study of neurologic diseases has grown rapidly over the past decade, its use for AHC patients is quite new. This study was aimed at investigating changes of brain metabolites in patients with alternating hemiplegia of childhood (AHC) during the hemiplegic ictal phases and interictal phases by proton magnetic resonance spectroscopy ((1)H-MRS). METHODS: (1)H-MRS was used in AHC patients during the hemiplegic ictal phases and interictal phases to evaluate functional activity in certain brain regions. A total of 10 unmedicated, healthy volunteers served as controls. RESULTS: N-acetylaspartate (NAA)/Creatine(Cr) ratio of the frontal lobes, basal ganglia, and temporal lobes in contralateral hemiplegic hemisphere of AHC patients during the ictal phases was significantly lower than that in AHC patients during interictal phases and control subjects. Significantly increased choline-containing compounds (Cho)/Cr were obtained in corresponding regions. CONCLUSIONS: These findings suggest neuronal metabolic dysfunctions in frontal lobes, temporal lobes and basal ganglia in AHC patients during ictal phases that perhaps are involved in the pathogenesis of AHC.

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OBJECTIVE: To evaluate the value of the AKIN criteria of acute kidney injury (AKI) in the incidence and prognoses in critically ill patients, and to further identify risk factors associated with the prognoses of the critically ill patients. METHODS: We retrospectively studied 544 adult patients hospitalized for ≥24 h to a comprehensive ICU with 16 beds in teaching hospital from January 2008 to December 2009. Based on AKIN criteria, these patients were classified into four groups: NAKI (no AKI), AKII, AKIII, and AKIIII respectively. RESULTS: (1) Of the patients, 191 (35.5%) fulfilled the criteria for AKI (14.8% had AKI I 8.2% had AKI II and 11.9% had AKIIII). (2) Mortality in the ICU was much higher in patients with AKI than in patients with no AKI (48% vs 11%, OR 7.48, 95%CI 4.831-11.587, P<0.001). The mortality rate was 37% for AKII group, 51% for AKIII group and 60% for AKIIII group. (3) In multivariate analysis, each AKIN category was independently associated with ICU mortality. The other independent risk factors for ICU mortality included internal medical diseases, septic shock, pre-existing chronic illness, APACHEII score, the number of failed organs, mechanical ventilation and CRRT. CONCLUSIONS: The AKIN category closely relates to the prognoses in critically ill patients, even the mild degree of AKI with a much higher mortality rate than the patients without AKI. The AKIN criteria has some direction significance to the early detection and classification of AKI and to the prediction of clinical outcomes in critically ill patients.

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OBJECTIVE: To study and quantify the relationship between dynamic lactic acid monitoring indexes and prognosis of critically ill patients in intensive care unit (ICU). METHODS: One hundred and one critically ill patients with elevated blood lactic acid level were included in this study and divided into death group (n=50) and survival group (n=51). Differences in their lactic acid indexes (including: lactic acid level, duration of lacticemia, lactic clearance), acute physiology and chronic health evaluation II (APACHEII) score, and other clinical indicators which reflected organ/system status were compared, and prognostic significant lacticemia indexes were formulated by multi-variable logistic analysis. Subsequently, patients were grouped by significant lactic indexes separately and compared with incidence of shock/multiple organ dysfunction syndrome (MODS), APACHE II score and mortality. RESULTS: Differences in lactic acid level, peak lactic acid level, 12-hour and 24-hour lactic acid clearance between death group and survival group showed statistically significant difference (P<0.05 or P<0.01). Peak lactic acid level, 12-hour lactic clearance, APACHE II score and blood pH had significant correlation with prognosis, odds ratios (OR) were 1.466, 0.922, 1.208, 0.032, respectively. Patients with peak lactic acid value> or =10 mmol/L or 12-hour lactic clearance< or =10% had significantly higher mortality: 77.8% and 70.6%, respectively (P<0.05 and P<0.01). Although patients with lacticemia>24 hours had higher mortality, there was no statistically significant difference. CONCLUSION: Peak lactic acid level, 12-hour lactic clearance, APACHE II score and blood pH are good indicators to evaluate patients' prognosis. Peak lactic acid value> or =10 mmol/L or 12-hour lactic clearance< or =10% is an alert of extremely bad prognosis. Prognosis value of duration of lacticemia is limited.

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Approximately 20-30% of patients with epilepsy continue to have seizures despite carefully monitored treatment with antiepileptic drugs. The mechanisms that underlie why some patients are responsive and others prove resistant to antiepileptic drugs are poorly understood. Increasing evidence supports a role for altered mitochondrial function in the pathogenesis of epilepsy. To gain greater molecular insight in the pathogenesis of intractable epilepsy, we undertook a global analysis of protein expressions in a pharmacoresistant epileptic model selected by phenytoin in electrical amygdala-kindled rats by using two-dimensional gel electrophoresis coupled with matrix-assisted laser desorption/ionization time of flight (MALDI-TOF-TOF). We identified five increased proteins and 14 decreased proteins including voltage-dependent anion channel 1 (VDAC1) with a 2.82-fold increased level (P < 0.05) and voltage-dependent anion channel 2 (VDAC2) with a 3.97-fold decreased level (P < 0.05) in hippocampus of pharmacoresistant rats. The increased VDAC1 and decreased VDAC2 were confirmed by Western blot analysis and immunohistochemistry. Vascular mitochondria and apoptosis neurons were observed through electron microscopy. Energy contents, the adenine nucleotides, were measured by high-performance liquid chromatography (HPLC). The correlation analyses were carried out between VDAC and the energy charge. These findings indicate that the increase of VDAC1 and the decrease of VDAC2 play an important role during the process and provide new molecular evidence in understanding mechanism of refractory epilepsy.

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