Influence of natural exposure on castor oil based polyurethane reinforced with waste tire rubber.

Waste tire rubber (WTR) has been extensively generated worldwide due to mobility needs growth. About 1.5 billion units are generated annually, constantly discharged in the environment with a few reusability alternatives. Therefore, rubber recovery methods and these residues' transformation into a cost-effective product have gained attention. Aiming to minimize the usage of fossil resources and contributes to a circular economy, it was analyzed the usage of WTR particles (5-20% by weight) in castor oil-based polyurethane foams under natural aging to promote a holistic view of all factors involved in the performance of the foams. Morphological, thermal, chemical, and mechanical properties were determined before and after exposure to open air to observe the impact of photo-oxidation and hydrolysis. The increase in viscosity of pre-polymer during the rubber loading produced greater density foams with smaller cell sizes than neat PU, in which the average cell size increased after the weathering. The rubber contributes to enhancing the compressive behavior in the non-exposed samples. After exposure, the results suggest that degradation may act to increase the crosslinking density even with the presented structural changes such as yellowing and voids. Regarding thermal stability, the rubber promotes a slight decay in the ability to resist a heat flow before and after weathering. Still, the char yield increased, showing a possibility of better fire retardancy for composites. FTIR and UV-vis showed chemical structure changes as Photo-Fries network rearrangement, Norrish I random chain scission, and Norrish II ß-scission. Besides, UV-vis revealed the maximum absorbance in the UVB region, showing that the PU reinforced by WTR can be a promising material for civil coatings.

Long-term weight development after esophagectomy for cancer-comparison between open Ivor-Lewis and minimally invasive surgical approaches.

Esophagectomy is an extensive procedure with severe postoperative effects. It can be assumed that the greater the trauma, the longer the nutritional recovery. This retrospective observational single-center cohort study compared weight development after esophagectomy with open and minimally invasive techniques. Three groups were compared in this study, one representing the first 41 patients who underwent the minimally invasive McKeown esophagectomy (MIMK). The second group included the first 84 consecutive patients operated with the minimally invasive Ivor-Lewis esophagectomy (MIIL). The third group comprised 100 consecutive patients operated with open thoracoabdominal Ivor-Lewis esophagectomy (IL). Virtually all patients submitted to a minimally invasive esophagectomy (MIE) and the majority with an IL had a jejunal catheter inserted during operation for postoperative enteral feeding. All together 225 patients were included in this study. The mean weight loss during the first year was 13.1% (±4.1), 11.2% (±6.1), and 9.6% (±7.5) in the IL, MIIL, and MIMK group, respectively (P = 0.85 and P = 0.95, respectively). The median duration of postoperative enteral nutrition support varied substantially within the groups and was 23.5 days in the IL group (range: 0-2033 days), 54.5 days in those having an MIIL (range: 0-308 days; P ≤ 0.001) and 57.0 days among patients in the MIMK group (range: 0-538 days; P ≤ 0.022). There was no difference in the risk of losing at least 10% of the preoperative weight at 3 or 6 months postoperatively between the groups. However, in patients who suffered severe complications (Clavien-Dindo score ≥ IIIb) after MIIL, there was a nonsignificant trend toward a lower risk of a 10% or greater weight loss, 3 months postoperatively. In conclusion, the greater surgical trauma associated with the traditional open esophagectomy was not followed by more severe weight loss, or other signs of poorer nutritional recovery, when compared to minimal invasive surgical techniques.

Relief of dysphagia during neoadjuvant treatment for cancer of the esophagus or gastroesophageal junction.

Dysphagia is the main symptom of cancer of the esophagus and gastroesophageal junction and causing nutritional problems and weight loss, often counteracted by insertion of self-expandable metal stents or nutrition via an enteral route. Clinical observations indicate that neoadjuvant therapy may effectively and promptly alleviate dysphagia, making such nutrition supportive interventions redundant before surgical resection. The objective of the current study was to carefully study the effects of induction neoadjuvant therapy on dysphagia and its subsequent course and thereby investigate the actual need for alimentary gateways for nutritional support. Thirty-five consecutive patients scheduled for neoadjuvant therapy were recruited and assessed regarding dysphagia and appetite at baseline, after the first cycle of preoperative treatment with either chemotherapy alone or with chemoradiotherapy and before surgery. Platinum-based therapy in combination with 5-fluorouracil was administered intravenously days 1-5 every 3 weeks and consisted of three treatments. Patients receiving combined chemoradiotherapy started radiotherapy on day one of second chemotherapy cycle. They received fractions of 2 Gy/day each up to a total dose of 40 Gy. Watson and Ogilvie dysphagia scores were used to assess dysphagia, while appetite was assessed by the Edmonton Assessment System Visual analogue scale-appetite questionnaire. Patients were evaluated at regular outpatient clinic visits or by telephone. The histological tumor response in the surgical specimen was assessed using the Chirieac scale. Ten patients scheduled for neoadjuvant chemotherapy and 25 patients scheduled for chemoradiotherapy were included in the analysis. There was a significant improvement in dysphagia in both treatment groups, according to both scales, already from baseline to the completion of the first chemotherapy cycle which remained to the end of the neoadjuvant treatment (P < 0.001). Appetite also improved after the first chemotherapy cycle (P = 0.03). Body weight did not change during any type of neoadjuvant therapy. We were unable to demonstrate any association between relief of dysphagia and the degree of histological response to neoadjuvant therapy in the surgical specimen. The present study shows that a platin - 5FU-based neoadjuvant chemotherapy, with or without concomitant radiotherapy, effectively and promptly relieves dysphagia in patients presenting with cancers of the esophagus or gastroesophageal junction already after the first cycle.

Large-diameter (30-35 mm) pneumatic balloon dilatation of the pylorus in patients with gastric outlet obstruction symptoms after esophagectomy.

BACKGROUND AND AIMS: Functional gastric outlet obstruction is a common problem after esophagectomy. The aim of this study was to evaluate the safety and efficacy of treating this group of patients with pneumatic dilatation of the pyloric sphincter region using a large-diameter (30-35 mm) balloon. MATERIAL AND METHODS: A review of all patients who had undergone pneumatic dilatation of the pylorus sphincter because of gastric outlet obstruction symptoms after esophagectomy at the Karolinska University Hospital from 2006-2011 was completed. Main outcomes were recordings of nausea, regurgitation and bloating. RESULTS: A total of 13 patients received pneumatic dilatation after an esophagectomy. The median time between esophagectomy and the first dilatation was 100 days, and the patients underwent a total of 21 dilatations (1-3 per patient) to a final median diameter of 30 mm. No procedure-related complications occurred. The median follow-up time was 205 days, and nausea and regurgitation improved significantly (p < 0.001, Fisher's test). CONCLUSIONS: Pneumatic dilatation of the pylorus using a large-diameter pneumatic balloon seems to be a safe and effective method for treating symptoms suggestive of gastric outlet obstruction after esophagectomy. To document its true effectiveness, a randomized and sham-controlled study is needed.

The influence of cone-beam computed tomography and periapical radiographic evaluation on the assessment of periapical bone destruction in dog's teeth.

OBJECTIVE: The aim of this study was to determine the influence of periapical radiographs, cone beam computed tomography (CBCT) sections, and cone beam volumetric data on the determination of periapical bone destruction in endodontically treated distal root canals of premolar canine teeth. Nontreated mesial roots were used as controls. STUDY DESIGN: Enterococcus faecalis strain (ATCC 29212) was inoculated into 30 root canals of 2 mongrel dogs to induce apical periodontitis. After 60 days, the root canals of the distal roots of the 11 mandibular and 4 maxillary premolars were endodontically treated (n = 15). The mesial root canals were used as controls (no treatment). The bone destruction was evaluated after 6 months by 5 evaluators using periapical radiographs and by CBCT (coronal and sagittal sections). After the experimental period, the area of the lesions in periapical radiographs and CBCT sections were measured in mm(2) using the ImageTool software. A single evaluator measured the volumetric data using the OsiriX software. The comparison between the diagnosis methods in treated root canals and controls was performed using parametric and nonparametric criteria. The Pearson correlation coefficient was computed between radiographic values and CBCT volumetric data in treated root canals and controls. RESULTS: The results showed the presence of chronic apical periodontitis in every inoculated tooth. After 6 months, periapical radiographs, coronal CBCT sections, and volumetric data showed lower bone destruction in endodontically treated teeth in comparison with the control group (P < .05). The 5 evaluators found no differences between the apical periodontitis area of treated teeth and controls when CBCT sagittal sections were used (P > .05). No correlation was found between x-ray and CBCT volumetric values in treated root canals. CONCLUSIONS: Although selected CBCT sagittal sections showed similar values of bone destruction in endodontically and nontreated root canals, volumetric CBCT data showed that periapical lesions of endodontically treated root canals had half of the volume of periapical lesions in nontreated root canals. No relationship could be found between the periapical values of bone destruction and volumetric data found in CBCT of treated rood canals.

Pb enamel biomarker: deposition of pre- and postnatal Pb isotope injection in reconstructed time points along rat enamel transect.

Exposure to lead (Pb) as well as other heavy metals in the environment is still a matter of public health concern. The development of the enamel biomarker for heavy metal exposure assessment is designed to improve studies of dose-effect relationships to developmental anomalies, particularly embryonic dysfunctions, and to provide a time-specific recount of past exposures. The work presented in this paper demonstrates maternal transfer across the placental barrier of the enriched isotope (206)Pb tracer to the enamel of the rat pup. Likewise, injections of (204)Pb-enriched tracer in the neonate rat resulted in deposition of the tracer in the enamel histology as measured by secondary ion microprobe spectrometry. Through enamel, we were able to observe biological removal and assimilation of prenatal and postnatal tracers, respectively. This research demonstrates that enamel can be used as a biomarker of exposure to Pb and may illustrate the toxicokinetics of incorporating Pb into fetal and neonatal steady-state system processes. The biomarker technique, when completely developed, may be applied to cross-sectional and longitudinal epidemiological research.

Orphan nuclear receptor Nurr1 is essential for Ret expression in midbrain dopamine neurons and in the brain stem.

The orphan nuclear receptor Nurr1 is essential for development of midbrain dopamine (DA) cells. In Nurr1-deficient mice, DA precursor cells fail to migrate normally, are unable to innervate target areas, and only transiently express DA cell marker genes. In the search for Nurr1-regulated genes that might explain this developmental phenotype, we found that expression of the receptor tyrosine kinase Ret is deregulated in these cells of Nurr1-deficient embryos. In addition, our analyses establish Nurr1 as an early marker for the dorsal motor nucleus (DMN) of the vagus nerve. Interestingly, Ret expression is absent also in these cells in Nurr1-targeted mice. Neuronal innervation of vagus nerve target areas appeared normal apart from a subtle disorganization of the DMN-derived nerve fibers. In conclusion, regulation of Ret by Nurr1 in midbrain DA neurons and in the DMN has implications for both embryonal development and adult physiology in which signaling by neurotrophic factors plays important roles.

Different levels of repressor activity assign redundant and specific roles to Nkx6 genes in motor neuron and interneuron specification.

Specification of neuronal fate in the vertebrate central nervous system depends on the profile of transcription factor expression by neural progenitor cells, but the precise roles of such factors in neurogenesis remain poorly characterized. Two closely related transcriptional repressors, Nkx6.2 and Nkx6.1, are expressed by progenitors in overlapping domains of the ventral spinal cord. We provide genetic evidence that differences in the level of repressor activity of these homeodomain proteins underlies the diversification of interneuron subtypes, and provides a fail-safe mechanism during motor neuron generation. A reduction in Nkx6 activity further permits V0 neurons to be generated from progenitors that lack homeodomain proteins normally required for their generation, providing direct evidence for a model in which progenitor homeodomain proteins direct specific cell fates by actively suppressing the expression of transcription factors that direct alternative fates.

Rapid detection of the methicillin-resistance gene, mecA, in coagulase-negative Staphylococci.

Phenotypical methods are routinely used to detect methicillin resistance in Staphylococci. These methods are time-consuming and there are difficulties in detecting all resistant strains carrying the mecA gene. We detected methicillin-resistant Staphylococci in biological samples by PCR amplification of mecA, without the time-consuming step of identifying a bacterial isolate. Methicillin-resistant Staphylococci isolates were also detected by screening on agar supplemented with oxacillin. The biological samples were collected from the hands of 17 healthcare workers at the Department of Paediatrics at the University Hospital of Tromsø. mecA was amplified in 12 of the 17 samples. The gene was verified by DNA sequencing of the PCR amplicon. Using the phenotypical method, methicillin-resistant Staphylococci were isolated from 6 of the samples. In all 6 of these samples, mecA was amplified by PCR. We conclude that PCR is a sensitive and specific method for detecting methicillin resistance in Staphylococci. The PCR detection of mecA is rapid, fairly simple and can easily be assimilated into the routines of a clinical microbiological laboratory.

Measurements of manganese with respect to calcium in histological enamel cross sections: toward a new manganese biomarker.

Airborne Mn may become an important route of exposure if the use of Mn-containing gasoline additives becomes more widespread. We report on the measurement of manganese and calcium in histological cross sections of shed deciduous tooth enamel of three human subjects. The goal of this research was to measure Mn in tooth enamel for use as a biomarker in assessing manganese exposure in cross-sectional and longitudinal studies. The histological locations can be time-specific (analogous to examining growth rings in trees). This technique, which may identify critical windows of exposure, can be important for evaluating potential vulnerability of the fetus and neonate to inhaled or ingested Mn.

An investigation of environmental racism claims: testing environmental management approaches with a geographic information system.

The purpose of this research was to explore the concept of an environmental racism claim through the use of several environmental management tools. The EPAs Toxics Release Inventory, Cumulative Exposure Project, and the Los Angeles County Department of Health Services' Hot Zone Census Tract Assessment were combined with racial and socioeconomic data to test claims that minorities in South Central Los Angeles are disproportionately exposed to environmental lead. Multivariate analysis indicated that race is strongly associated with the number of cases of elevated blood lead levels in South Central, irrespective of poverty status. Proximity to point sources, a common focal point for studies of environmental racism, was not a contributing factor to health outcomes. Proximity to transportation corridors was consistently the strongest indicator of environmental lead exposure, while median home values were significantly and positively related to elevated blood lead levels. Implications for environmental justice advocates and social and environmental scientists are discussed.

Groucho-mediated transcriptional repression establishes progenitor cell pattern and neuronal fate in the ventral neural tube.

The pattern of neuronal specification in the ventral neural tube is controlled by homeodomain transcription factors expressed by neural progenitor cells, but no general logic has emerged to explain how these proteins determine neuronal fate. We show that most of these homeodomain proteins possess a conserved eh1 motif that mediates the recruitment of Gro/TLE corepressors. The eh1 motif underlies the function of these proteins as repressors during neural patterning in vivo. Inhibition of Gro/TLE-mediated repression in vivo results in a deregulation of cell pattern in the neural tube. These results imply that the pattern of neurogenesis in the neural tube is achieved through the spatially controlled repression of transcriptional repressors-a derepression strategy of neuronal fate specification.

Specification of neuronal fates in the ventral neural tube.

The generation of distinct classes of neurons at defined positions is a fundamental step in the development of the vertebrate central nervous system. Recent work has begun to reveal the extracellular signals and transcriptional mediators that direct the pattern of generation of distinct neuronal subtypes in the neural tube. This work has provided a framework to understand the patterning of the ventral neural tube and is permitting molecular analyses of the assembly of functional neuronal circuits.

Enamel lead biomarker for prenatal exposure assessment.

The development of the enamel biomarker for heavy metal exposure assessment is designed to improve studies of dose-effect relationships to embryonic anomalies, particularly neurotoxic dysfunction. This report documents initial demonstrations of ambient lead (Pb) relative to calcium (Ca) in histological cross sections of deciduous tooth enamel of three human subjects, by use of ion mass spectrometry. The goal of this research was to measure Pb and Ca in tooth enamel for use as a temporal biomarker in assessing prenatal and postnatal exposure. This involves measurement of these heavy metals in enamel at high spatial resolution along histological transects following the temporal pattern of enamel growth. The technique may be applied when completely developed to cross-sectional and longitudinal research.

Ventral neural patterning by Nkx homeobox genes: Nkx6.1 controls somatic motor neuron and ventral interneuron fates.

There is growing evidence that sonic hedgehog (Shh) signaling regulates ventral neuronal fate in the vertebrate central nervous system through Nkx-class homeodomain proteins. We have examined the patterns of neurogenesis in mice carrying a targeted mutation in Nkx6.1. These mutants show a dorsal-to-ventral switch in the identity of progenitors and in the fate of postmitotic neurons. At many axial levels there is a complete block in the generation of V2 interneurons and motor neurons and a compensatory ventral expansion in the domain of generation of V1 neurons, demonstrating the essential functions of Nkx6.1 in regional patterning and neuronal fate determination.

A homeodomain protein code specifies progenitor cell identity and neuronal fate in the ventral neural tube.

Distinct classes of neurons are generated at defined positions in the ventral neural tube in response to a gradient of Sonic Hedgehog (Shh) activity. A set of homeodomain transcription factors expressed by neural progenitors act as intermediaries in Shh-dependent neural patterning. These homeodomain factors fall into two classes: class I proteins are repressed by Shh and class II proteins require Shh signaling for their expression. The profile of class I and class II protein expression defines five progenitor domains, each of which generates a distinct class of postmitotic neurons. Cross-repressive interactions between class I and class II proteins appear to refine and maintain these progenitor domains. The combinatorial expression of three of these proteins--Nkx6.1, Nkx2.2, and Irx3--specifies the identity of three classes of neurons generated in the ventral third of the neural tube.

Cloning and DNA-binding properties of the rat pancreatic beta-cell-specific factor Nkx6.1.

The homeodomain (HD) protein Nkx6.1 is the most beta-cell-specific transcription factor known in the pancreas and its function is critical for the formation of the insulin-producing beta-cells. However, the target genes, DNA-binding site, and transcriptional properties of Nkx6.1 are unknown. Using in vitro binding site selection we have identified the DNA sequence of the Nkx6.1 binding site to be TTAATTG/A. A reporter plasmid containing four copies of this sequence is activated by an Nkx6.1HD/VP16 fusion construct. Full-length Nkx6.1 fails to activate this reporter plasmid in spite of robust interaction with the binding site in vitro. Stable expression of Nkx6.1 in the glucagon-producing alpha-cell-like MSL-G-AN cells induces expression of the endogenous insulin gene in a subset of the cell population. The expression of other known beta-cell-specific factors such as Pax4, Pax6, Pdx1, GLUT2 and GLP1-R is unchanged by the introduction of Nkx6.1.

The specification of neuronal identity by graded Sonic Hedgehog signalling.

During the development of vertebrate nervous system, distinct classes of motor neurons and interneurons are generated at distinct dorsoventral positions in the ventral neural tube. The differentiation of these neuronal subtypes is directed by the secreted protein Sonic Hedgehog (Shh). Shh acts in a graded manner to establish different neural progenitor cell populations, defined by the expression of homeodomain transcription factors. These factors are critical for the interpretation of graded Shh signalling and act initially both to refine progenitor domain boundaries and to maintain their integrity. Subsequently, these factors direct the expression of genes that confer neuronal subtype identity to post-mitotic neurons.

Homeobox gene Nkx2.2 and specification of neuronal identity by graded Sonic hedgehog signalling.

During vertebrate development, the specification of distinct cell types is thought to be controlled by inductive signals acting at different concentration thresholds. The degree of receptor activation in response to these signals is a known determinant of cell fate, but the later steps at which graded signals are converted into all-or-none distinctions in cell identity remain poorly resolved. In the ventral neural tube, motor neuron and interneuron generation depends on the graded activity of the signalling protein Sonic hedgehog (Shh). These neuronal subtypes derive from distinct progenitor cell populations that express the homeodomain proteins Nkx2.2 or Pax6 in response to graded Shh signalling. In mice lacking Pax6, progenitor cells generate neurons characteristic of exposure to greater Shh activity. However, Nkx2.2 expression expands dosally in Pax6 mutants, raising the possibility that Pax6 controls neuronal pattern indirectly. Here we provide evidence that Nkx2.2 has a primary role in ventral neuronal patterning. In Nkx2.2 mutants, Pax6 expression is unchanged but cells undergo a ventral-to-dorsal transformation in fate and generate motor neurons rather than interneurons. Thus, Nkx2.2 has an essential role in interpreting graded Shh signals and selecting neuronal identity.