Production of multienzyme by Bacillus aestuarii UE25 using ionic liquid pretreated sugarcane bagasse

The utilization of sugarcane bagasse (SB) in fermentation requires pretreatment processes to render fermentable components available to microorganisms. Pretreatment by using ionic liquids (ILs) is considered promising but the high cost is an impediment in its adoption, therefore, a mixture of IL pretreated and untreated SB was utilized to obtain bacterial multienzyme under solid-state fermentation (SSF). Bacillus aestuarii UE25, a thermophilic strain was utilized for that purpose. Fermentation conditions were optimized by adopting a central composite design. The model showed a good correlation between the predicted and the experimental values for amylase, xylanase, endoglucanase, and β-glucosidase. Volumetric and specific productivity of xylanase (4580 IU ml⁻¹ h⁻¹, 244.25 IU mg⁻¹ substrate, and 50 IU mg⁻¹ protein) were higher than the other enzymes. Changes in lignin content and reduced cellulose crystallinity due to IL pretreatment, followed by fermentation, were visualized by scanning electron microscopy, Fourier transform infrared spectroscopy, and Nuclear magnetic resonance. The strategy adopted by utilizing a mixture of IL pretreated and untreated SB under SSF proved promising to obtain high titers of different enzymes simultaneously. Since the bacterial strain used is thermophilic, therefore, the multienzyme can find its application in commercial processes which are carried out at high temperatures.     

Presentation outside office hours does not negatively influence treatment times for reperfusion therapy for acute ischemic stroke

Journal of Neurology - Treatment outside office hours has been associated with increased workflow times for intravenous thrombolysis (IVT) in acute ischemic stroke (AIS). Limited data suggest that...     

Increased serum levels of quinolinic acid indicate enhanced severity of hepatic dysfunction in patients with liver cirrhosis

Background

The Model for End-Stage Liver Disease (MELD) score is a tool for assessment of the degree of hepatic insufficiency/failure. Quinolinic acid (QuinA) is a tryptophan metabolite produced by activated macrophages. Here we investigate whether the degree of systemic inflammation (QuinA, neopterin, CRP and IL-6) correlates with clinical liver dysfunction according to the MELD Score.

Method

Ninety-four patients with liver cirrhosis were categorized into 2 groups according to baseline MELD score (group I, MELD <20, n = 61, and group II, MELD ?20, n = 33).

Results

Serum levels of QuinA, neopterin, CRP, and IL-6 significantly correlated with MELD score (r = 0.77, 0.75, 0.57, and 0.50; p < 0.0001, respectively). Patients of group II had significantly higher serum levels of QuinA, neopterin, CRP, and IL-6 than group I (p ? 0.0001). ROC curve analysis showed that QuinA and neopterin are more sensitive markers for severity of liver disease than established markers of inflammation such as CRP and IL-6 (sensitivity = 86% and 79%, respectively) (AUC = 0.89 and 0.89, respectively). QuinA provided the most sensitive index with regard to the identification of patients with hepatic encephalopathy.

Conclusion

Serum levels of QuinA reflect the degree of liver dysfunction. Moreover, high levels of QuinA may serve as a sensitive indicator of hepatic encephalopathy.     

Clustering Patterns of Comorbidities Associated with In-Hospital Death in Hospitalizations of US Adults with Venous Thromboembolism

Background: Venous thromboembolism (VTE) is a significant source of mortality, morbidity, disability, and impaired health-related quality of life in the world.Objective: We aimed to evaluate the clustering patterns and associations of 29 comorbidities with in-hospital death among adult hospitalizations with a diagnosis of VTE in the United States by analyzing data from the 2009 Nationwide Inpatient Sample.Methods: This cross-sectional study included 153,124 adult hospitalizations with a diagnosis of VTE. Adjusted rate ratios and 95% confidence intervals (CI) for in-hospital death were generated by using multivariable log-linear regression models to measure independent associations between comorbidities and in-hospital death.Results: We estimated that 44,200 in-hospital deaths occurred in 2009 among 773,273 US adult hospitalizations with a diagnosis of VTE. Subgroups of hospitalizations with comorbidities of “congestive heart failure,” “chronic pulmonary disease,” “coagulopathy,” “liver disease,” “lymphoma,” “fluid and electrolyte disorders,” “metastatic cancer,” “peripheral vascular disorders,” “pulmonary circulation disorders,” “renal failure,” “solid tumor without metastasis,” or “weight loss” were positively and independently associated with 1.07 (95% CI: 1.02-1.12 ) to 2.06 (95% CI: 1.97-2.16) times increased likelihoods of in-hospital death, when compared to those without the corresponding comorbidities. The clustering patterns of these comorbidities by 4 disease categories (i.e., “cancer,” “cardiovascular/respiratory/blood,” “gastrointestinal/urologic,” and “nutritional/bodyweight”) were associated with 2.74 to 10.28 times increased likelihoods of in-hospital death, as compared to hospitalizations without any of these comorbidities. The overall increase in the cumulative number of comorbidities corresponded to significantly elevated risks (P-trend<0.01) for in-hospital death among hospitalizations with a diagnosis of VTE.Conclusion: The presence of multiple comorbidities is ubiquitous among hospitalizations of adults with VTE and among in-hospital deaths with VTE in the United States. The findings of our study further suggest that, among hospitalizations of adults with VTE, the presence of certain comorbidities or clustering of these comorbidities significantly elevates the risk of in-hospital death.     

Inhibition of hepatic stellate cell activation following Yinchenhao decoction administration to dimethylnitrosamine-treated rats

Aim: In an effort to investigate the mechanism by which Yinchenhao decoction (YCHD) acts on liver injury, we investigated the potential antifibrogenic effects of YCHD in an experimental liver fibrosis rat model, with special focus on the mechanisms inhibiting the activation and promoting apoptosis of hepatic stellate cells (HSC). Methods: The rats were initially randomized into two groups: the control (n = 10) and dimethylnitrosamine‐treated (DMN; n = 30) groups. DMN (10 mg/kg body weight) was administered intraperitoneally to the DMN‐treated rats for three consecutive days each week. At the end of the second week, three rats from the control and six rats from the DMN‐treated groups were killed for the fibrosis development assessment. The remaining DMN rats were further randomized into two groups: the DMN–water group (n = 12) and the DMN–YCHD group (n = 12). Both groups continued to receive weekly DMN treatment for another 2 weeks in addition to daily administration of either water or YCHD, which were given intragastrically at a dose of 0.418 g/100 g body weight. Results: Hepatic hydroxyproline content decreased and had improved histopathology in the DMN–YCHD rats. Compared to the DMN group, α‐smooth muscle actin (SMA) and CD68 expression in the DMN–YCHD group was reduced significantly; however, α‐SMA‐positive HSC apoptosis was not observed by confocal microscopy; Fibrogenic proteins (tissue inhibitor matrix proteinases‐1 and 2 and matrix metalloproteinase [MMP]‐2/14) and cytokines (tumor necrosis factor‐α and transforming growth factor‐β₁) were decreased; MMP‐9 was significantly upregulated. Conclusion: Yinchenhao administration attenuates liver fibrosis at least in part by inhibiting HSC activation directly, rather than promoting cell apoptosis of activated HSC, and the suppressive activation of Kupffer cells.     

Therapy with cardiac contractility modulation electrical signals improves left ventricular function and remodeling in dogs with chronic heart failure.

OBJECTIVES: This study examined the effects of long-term delivery of cardiac contractility modulation (CCM) electric signals on left ventricular (LV) function and global, cellular, and molecular remodeling in dogs with chronic heart failure (HF). BACKGROUND: Acute studies in dogs with experimentally induced HF showed that CCM signals applied to the failing myocardium during the absolute refractory period improved LV function without increasing myocardial oxygen consumption. METHODS: In one study, dogs with intracoronary microembolization-induced HF were randomized to 3 months of active CCM monotherapy or to a sham-operated control group. In another study, 19 HF dogs were randomized to 3 months chronic monotherapy with extended release metoprolol succinate (MET-ER), MET-ER with CCM, or no therapy at all (control group). RESULTS: In CCM-only treated dogs, LV ejection fraction (EF) increased (27 +/- 1% vs. 33 +/- 1%, p < 0.0001) compared with a decrease in sham-operated control animals (27 +/- 1% vs. 23 +/- 1%, p < 0.001). The increase in EF seen with CCM-treated dogs was accompanied by reduced LV volumes, improved myocardial structure, reversal of the maladaptive fetal gene program, and an improvement in sarcoplasmic reticulum calcium cycling proteins. Dogs treated with a combination of MET-ER and CCM showed a greater increase in LV EF and a greater reversal of LV global, structural, and biochemical remodeling compared with dogs treated with MET-ER alone. CONCLUSIONS: In dogs with HF, long-term CCM therapy improves LV systolic function. The improvements are additive to those seen with beta-blockers. These findings are further strengthened by the concomitant benefits of CCM therapy on LV global, cellular, and biochemical remodeling.