Surface and thermal properties of synthesized cationic poly(ethylene oxide) gemini surfactants: the role of the spacer

The solubility and heat stability of surfactants are the prerequisites for their oilfield applications. Most commercial surfactants undergo hydrolysis at high temperature and prolonged heating at 40 °C or above leads to decomposition. In this report, three cationic poly(ethylene oxide) gemini surfactants (GSs) containing flexible and rigid spacers were synthesized for oilfield applications. The chemical structures of the GSs were elucidated with the aid of ¹³C NMR, ¹H NMR, FT-IR, and MALDI-TOF MS. The GSs exhibit pronounced solubility in deionized water, seawater, and formation brine and no cloudiness, phase separation, or precipitation were detected after keeping GS solutions in an oven at 90 °C for three weeks. According to thermal gravimetric analysis, the degradation temperature of all the GSs was above 240 °C, which is higher than the existing oilfield temperature (≥90 °C). The critical micelle concentration (CMC) of the synthesized GSs decreases upon increasing the temperature. Additionally, CMC values were observed to increase even further with increasing salinity. The low CMC values of gemini surfactants containing a flexible structure indicate that they create a more closely packed micelle structure compared with gemini surfactants with a rigid structure. The distinct surface and thermal features of the synthesized GSs reveal them to be appropriate materials for high salinity and elevated temperature reservoirs.

Synthesis of new cationic poly(ethylene oxide) gemini surfactants containing flexible and rigid spacer groups to tolerate harsh reservoir condition.     

Elimination of damaged mitochondria through mitophagy reduces mitochondrial oxidative stress and increases tolerance to trichothecenes

Trichothecene mycotoxins are natural contaminants of small grain cereals and are encountered in the environment, posing a worldwide threat to human and animal health. Their mechanism of toxicity is poorly understood, and little is known about cellular protection mechanisms against trichothecenes. We previously identified inhibition of mitochondrial protein synthesis as a novel mechanism for trichothecene-induced cell death. To identify cellular functions involved in trichothecene resistance, we screened the Saccharomyces cerevisiae deletion library for increased sensitivity to nonlethal concentrations of trichothecin (Tcin) and identified 121 strains exhibiting higher sensitivity than the parental strain. The largest group of sensitive strains had significantly higher reactive oxygen species (ROS) levels relative to the parental strain. A dose-dependent increase in ROS levels was observed in the parental strain treated with different trichothecenes, but not in a petite version of the parental strain or in the presence of a mitochondrial membrane uncoupler, indicating that mitochondria are the main site of ROS production due to toxin exposure. Cytotoxicity of trichothecenes was alleviated after treatment of the parental strain and highly sensitive mutants with antioxidants, suggesting that oxidative stress contributes to trichothecene sensitivity. Cotreatment with rapamycin and trichothecenes reduced ROS levels and cytotoxicity in the parental strain relative to the trichothecene treatment alone, but not in mitophagy deficient mutants, suggesting that elimination of trichothecene-damaged mitochondria by mitophagy improves cell survival. These results reveal that increased mitophagy is a cellular protection mechanism against trichothecene-induced mitochondrial oxidative stress and a potential target for trichothecene resistance.Trichothecene mycotoxins are highly toxic secondary metabolites produced by Trichothecium, Myrothecium, Trichoderma, and Fusarium. Fusarium graminearum and Fusarium culmorum cause Fusarium head blight (FHB), which is one of the most damaging diseases of small grain cereals. FHB adversely affects the food supply because trichothecene mycotoxins, such as deoxynivalenol (DON), accumulate in the infected grain, presenting a food safety risk and health hazard to humans and animals (1). Controlling their accumulation in small grains remains a huge challenge. Trichothecenes cause growth retardation, hemorrhagic lesions, immune dysfunction, and emesis (2, 3) and are neurotoxic (4–6). Trichothecene poisoning causes acute gastroenteritis and has been linked to alimentary toxic aleukia (ATA) and Kashin–Beck disease, an endemic and chronic degenerative osteoarthritis (3).Trichothecenes inhibit protein synthesis by targeting ribosomal protein L3 in yeast (7–9). However, their toxicity is not entirely due to inhibition of cytosolic protein synthesis. In mammalian cells, DON induces activation of double-stranded RNA-associated protein kinase (PKR), promotes degradation of 28S rRNA, and up-regulates a number of microRNAs (3, 10). DON exposure stabilizes mRNAs encoding proinflammatory mRNAs (3, 10). In plants, T-2 toxin (T-2) and DON cause oxidative stress damage by increasing reactive oxygen species (ROS) levels (11).Despite the importance of trichothecenes in food safety and chronic environmental exposure, the molecular mechanism of their toxicity is not well-understood and there is a critical gap in our knowledge about the mechanisms that can protect cells against trichothecenes. To understand the trichothecene mechanism of action, we previously carried out a genome-wide screen of Saccharomyces cerevisiae for resistance to trichothecin (Tcin) and showed that the largest group of resistant strains were affected in mitochondrial functions (12). We showed that trichothecenes inhibit mitochondrial translation, before depolarization and fragmentation of the mitochondrial membrane and independent of the cytosolic translation inhibition (12, 13). Previous studies showed a link between ROS generation and mitochondrial translation (14, 15). Yeast mutants with impaired mitochondrial translation exhibited faulty oxidative phosphorylation resulting in toxic levels of ROS, overwhelming the cell’s antioxidant capacity, and causing oxidative stress (14). These results suggested that mitochondrial dysfunction and the resulting oxidative stress might contribute to trichothecene sensitivity. To obtain a comprehensive view of the cellular functions needed for tolerance to trichothecenes, we screened the complete set of viable S. cerevisiae deletion strains for increased sensitivity to Tcin, a representative type B trichothecene that has a similar IC₅₀ for Vero cells (0.5 µM) and yeast grown on nonfermentable media (0.75 µM) (12, 13). Analysis of the identified strains revealed a vital role for mitochondrial oxidative stress in trichothecene sensitivity and provided the first evidence to our knowledge for a prosurvival role for the autophagic degradation of damaged mitochondria or mitophagy in the reduction of trichothecene-mediated mitochondrial oxidative stress.     

Usefulness of two-dimensional echocardiographic parameters of the left side of the heart to predict right ventricular failure after left ventricular assist device implantation

Right ventricular failure (RVF) after left ventricular assist device (LVAD) placement is associated with increased morbidity and mortality. Echocardiography is a primary imaging method in the assessment of cardiac function; however, visualization of the right-sided heart is often technically difficult in patients with heart failure. We aimed to create a simple and generally applicable scoring system based on "left-sided echocardiographic parameters" to provide complementary information for predicting RVF after LVAD surgery. We reviewed 111 consecutive patients undergoing LVAD surgery from 2007 through 2010. Echocardiograms within 5 days before surgery were analyzed. RVF was defined as an unexpected RV assist devices requirement, nitric oxide inhalation >48 hours, and/or inotropic support >14 days. Thirty-five patients (32%) developed RVF. LV end-diastolic dimension (LVEDD) was smaller, LV ejection fraction was greater, and the left atrial diameter/LVEDD ratio was greater (p < 0.05 for all comparisons) in patients with RVF than in those without RVF. An RVF score (LV echocardiographic RVF score) was determined as a sum of points based on receiver operator characteristics analysis: LVEDD >78, 79 to 70, and <70 mm; LV ejection fraction ≤19%, 19% to 33%, and >33%; and left atrial diameter/LVEDD <0.63, 0.63 to 0.68, and >0.68; each variable was associated with 0 and 1 point and 2 points, respectively. LV echocardiographic RVF score ≥3 was associated with RVF with a sensitivity of 88.6% and score ≥5 with a specificity of 80.3%. In conclusion, patients with relatively small LV size, preserved LV contraction, and dilated left atrium were at higher risk for RVF after LVAD surgery. In conclusion, LV echocardiographic RVF score provides a novel tool to predict RVF after LVAD surgery, which does not involve invasive or technically complicated procedures.     

Complications of radiofrequency ablation of varicose veins

Radiofrequency ablation (RFA) has become a valued weapon in the phlebologist's armoury. It offers ease of use and reproducibility with good outcomes. However, as with all interventions, complications arise. In this review we examine the complications inherent with RFA and their relative risk, with their avoidance measures if available. Overall, we find that RFA offers a very safe procedure with rare severe complications.     

Congenital heart defects in recurrent reciprocal 1q21.1 deletion and duplication syndromes: Rare association with pulmonary valve stenosis

Microdeletion 1q21.1 (del 1q21.1) and the reciprocal microduplication 1q21.1 (dup 1q21.1) are newly recognized genomic disorders, characterized by developmental delay, dysmorphic features and congenital malformations. Congenital heart defect (CHD) is a major feature of del 1q21.1, and has been occasionally reported in dup 1q21.1. We report here a family segregating del 1q21.1 in 3 members. Two of the affected family members had CHD, including the proband with syndromic atrial septal defect, pulmonary valve stenosis (PVS), and muscular ventricular septal defects, and the maternal uncle with non-syndromic PVS. This finding prompted investigation of the role of recurrent rearrangements of chromosome 1q21.1 in the pathogenesis of PVS. We gathered 38 patients with PVS (11 syndromic and 27 non-syndromic), and searched for genomic rearrangements of 1q21.1. A dup 1q21.1 was detected in a single sporadic non-syndromic patient. Review of the CHDs in published del 1q21.1 and dup 1q21.1 subjects showed a great heterogeneity in anatomic types. In conclusion, the present family illustrates recurrent CHD in del 1q21.1, expressing either as syndromic in one family member or as non-syndromic in the another one. The spectrum of CHDs associated with del 1q21.1 and dup 1q21.1 can occasionally include PVS.     

Endoscopic Management for Delayed Diagnosis of a Foreign Body Penetrating the Esophagus into the Lung

A 31-year-old male presented with chest pain started after eating chicken about 2 weeks earlier. Upper endoscopy and Computed tomography scan of the chest revealed a sharp chicken bone penetrating the esophageal wall into the right lung. The foreign body was removed endoscopically using a rat-tooth forceps, followed by prophylactic placement of a metal stent across the esophageal perforation site. Foreign body-induced perforation is one of the common etiologies of benign esophageal perforations. Although the primary treatment is surgery, endoscopic therapy may be appropriate in individualized cases like our patient.     

The Association of Metabolic Syndrome, Insulin Resistance and Non-alcoholic Fatty Liver Disease in Overweight/Obese Children

Background/Aim:

To study the prevalence of metabolic syndrome (MS), insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) in overweight/obese children with clinical hepatomegaly and/or raised alanine aminotransferase (ALT).

Patients and Methods:

Thirty-three overweight and obese children, aged 2-13 years, presenting with hepatomegaly and/or raised ALT, were studied for the prevalence of MS, IR and NAFLD. Laboratory analysis included fasting blood glucose, serum insulin, serum triglycerides (TG), total cholesterol, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c) and liver biochemical profile, in addition to liver ultrasound and liver biopsy.

Results:

Twenty patients (60.6%) were labeled with MS. IR was present in 16 (48.4%). Fifteen (44%) patients had biopsy-proven NAFLD. Patients with MS were more likely to have NAFLD by biopsy (P=0.001). Children with NAFLD had significantly higher body mass index, waist circumference, ALT, total cholesterol, LDL-c, TG, fasting insulin, and lower HDL-c compared to patients with normal liver histology (P< 0.05) and fitted more with the criteria of MS (80% vs. 44%). IR was significantly more common among NAFLD patients (73% vs. 28%).

Conclusion:

There is a close association between obesity, MS, IR and NAFLD. Obese children with clinical or biochemical hepatic abnormalities are prone to suffer from MS, IR and NAFLD.