Structural, Optical, and Electrical Parameters of Doped PVA/PVP Blend with TPAI or THAI Salt.

The 70% polyvinyl alcohol/30% polyvinyl pyrrolidone (PVA/PVP) polymer blends, with different weight ratios of tetrapropylammonium iodide (TPAI) or tetrahexylammonium iodide (THAI) salt, were prepared using dimethyl sulfoxide (DMSO) as a solvent. The X-ray diffraction technique was used to trace the crystalline nature of the formed blends. The SEM and EDS techniques were applied to figure out the morphology of the blends. The variation in the FTIR vibrational bands was used to investigate the chemical composition and the effect of different salt doping on the functional groups of the host blend. The influence of the salt type (TPAI or THAI) and its ratio on the linear and nonlinear optical parameters for the doped blends were investigated in detail. Absorbance and reflectance are highly enhanced in the UV region reaching a maximum for the blend with 24% TPAI or THAI; so, it can be employed as shielding materials for UVA and UVB types. The direct (5.1 eV) and indirect (4.8 eV) optical bandgaps were reduced continuously to (3.52, 3.63 eV) and (3.45, 3.51 eV) while increasing the content of TPAI or THAI, respectively. The blend doped with 24% wt TPAI exhibited the highest refractive index (around 3.5 in 400-800 nm). The DC conductivity is affected by the content and type of salt, its dispersion, and blend-salt interaction. The activation energies of different blends were obtained by applying the Arrhenius formula.

Development of Perovskite (MACl)0.33FA0.99MA0.01Pb(I0.99Br0.01)3 Solar Cells via n-Octylammonium Iodide Surface Passivation.

The influence of n-octylammonium iodide (OAI, passive layer) on the types of phases formed in a (MACl)0.33FA0.99MA0.01Pb(I0.99Br0.01)3 perovskite film was studied using X-ray diffraction. Using UV spectrophotometric techniques, it was determined how varied OAI additive layer ratios affected the linear and nonlinear optical characteristics of glass substrates/FTO/compact TiO2/mesoporous TiO2/(MACl)0.33FA0.99MA0.01Pb(I0.99Br0.01)3 films. All films' direct optical bandgap energies were determined to be 1.54 eV. The effects of OAI addition on the films' photoluminescence intensity and emitted colors were also investigated. For the fabricated perovskite solar cells (PSCs) without an OAI passivation layer, the corresponding power conversion efficiency (PCE), open-circuit voltage (VOC), short-circuit current density (JSC), and fill factor (FF) values were 18.8%, 1.02 V, 24.6 mAcm-2, and 75%, respectively. When the concentration of OAI reached 2 mg, the maximum obtained values of PCE, VOC, JSC, and FF were 20.2%, 1.06 V, 24.2 mAcm-2, and 79%, respectively. The decreased trap density and increased recombination resistance were responsible for the improvement in solar cell performance.

Impact of ZnS/Mn on the Structure, Optical, and Electric Properties of PVC Polymer.

The most efficient way to create novel materials that may be used in a variety of optoelectronic applications is thought to be doped mixed polymers with appropriate fillers. Undoped and doped PVC polymers with ZnS/Mn formed at different temperatures were fabricated using the casting method. The Rietveld method was used to discover the structure and microstructure of Zn0.95Mn0.05S prepared at T = 300, 400, and 500 °C. The distribution and existence of the nanofiller over the PVC matrix were determined via XRD, FTIR, EDS, and SEM techniques. The effect of the preparation temperatures of the ZnS/Mn nanofiller on the absorption, transmittance, reflectance, refractive index, extinction coefficient, dielectric constant, AC conductivity, electrical modulus, and DC conductivity activation energy data of the PVC polymer was studied using the diffused reflectance technique. Doping PVC with ZnS/Mn (prepared at 300 °C) lowered the direct and indirect optical band gaps from 5.4 and 4.52 eV to minimum values of 4.55 and 3.63 eV. The fluorescence intensity of pure PVC is greatly enhanced upon loading with ZnS/Mn. The PVC exhibited two near UV peaks, one violet and one blue color, while, in addition, the doped polymers exhibited green and orange colors. The corresponding CIE diagram for all the samples was also determined.

Long-term histopathological changes of the nasal mucosa after total laryngectomy: a prospective cohort study.

BACKGROUND: Changes in the nasal function following total laryngectomy resulted in histopathological alterations of the nasal mucosa. We aimed to evaluate the long-term histopathological changes and the mucociliary clearance (MCC) of the nasal mucosa after total laryngectomy. METHODS: We performed a histological examination of inferior turbinate biopsy, and saccharine test to assess the MCC time for patients who were candidates for total laryngectomy before the procedure, 6-12 months after surgery, and at least two years postoperatively. RESULTS: Seventy-five patients scheduled for total laryngectomy were initially enrolled in our study. We excluded patients who received postoperative radiotherapy or were lost during the follow-up period. Eventually, 63 and 54 patients were available for assessment 6-12 months after surgery and at least two years postoperatively, respectively. Except for ciliary and goblet cell destruction, which were significantly reduced 6-12 months postoperatively, there were no statistically significant differences in the histopathological findings of the nasal mucosa before surgery and 6-12 months postoperatively. After two years, the histopathological alterations of the nasal mucosa were statistically more evident than those before surgery and 6-12 months postoperatively; the most common histopathological findings were mononuclear cell infiltration and stromal fibrosis. The mean MCC time preoperatively was 12.56 minutes that statistically significantly decreased to 11.81 minutes 6-12 months after surgery; then, it significantly increased to 20.98 minutes at least two years postoperatively. CONCLUSIONS: After total laryngectomy, the nasal mucosa showed histopathological alterations and early enhancement of the MCC, which was later impaired due to nasal mucosal atrophy and the saprophytic infection.

Third window approach assisted middle meatal antrostomy: prospective cohort study of the two ports technique in management of hard to reach maxillary sinus pathology.

OBJECTIVE: This study aimed to assess the outcomes of a prelacrimal recess approach assisted middle meatal antrostomy in the management of hard to reach maxillary sinus pathologies. METHOD: Twenty-five patients with maxillary sinus pathology underwent prelacrimal recess approach assisted middle meatal antrostomy (with a prelacrimal recess width of more than 3 mm). Patients were prospectively evaluated using both the Arabic version of the Sino-Nasal Outcome Test-22 and nasal endoscopy at least 6 months post-operatively. RESULTS: Our study included 25 maxillary sinuses (13 with antrochoanal polyps, 10 with maxillary fungal ball and 2 with a migrated part of a tooth). At a mean follow-up period of 10.9 months, all patients showed significant improvement in total mean Sino-Nasal Outcome Test-22 score. There was recurrence of one case with antrochoanal polyp and two cases with asymptomatic synechia. Injury to the nasolacrimal duct was not reported. CONCLUSION: A prelacrimal recess approach assisted middle meatal antrostomy is a reliable and safe technique to manage pathologies in hard to reach regions within the maxillary sinus.

Contrasting effects of an Mdm2 functional polymorphism on tumor phenotypes.

MDM2, an E3 ubiquitin ligase, is a potent inhibitor of the p53 tumor suppressor and is elevated in many human cancers that retain wild-type p53. MDM2 SNP309G is a functional polymorphism that results in elevated levels of MDM2 (due to enhanced SP1 binding to the MDM2 promoter) thus decreasing p53 activity. Mdm2SNP309G/G mice are more prone to spontaneous tumor formation than Mdm2SNP309T/T mice, providing direct evidence for the impact of this SNP in tumor development. We asked whether environmental factors impact SNP309G function and show that SNP309G cooperates with ionizing radiation to exacerbate tumor development. Surprisingly, ultraviolet B light or Benzo(a)pyrene exposure of skin shows that SNP309G allele actually protects against squamous cell carcinoma susceptibility. These contrasting differences led us to interrogate the mechanism by which Mdm2 SNP309 regulates tumor susceptibility in a tissue-specific manner. Although basal Mdm2 levels were significantly higher in most tissues in Mdm2SNP309G/G mice compared with Mdm2SNP309T/T mice, they were significantly lower in Mdm2SNP309G/G keratinocytes, the cell-type susceptible to squamous cell carcinoma. The assessment of potential transcriptional regulators in ENCODE ChIP-seq database identified transcriptional repressor E2F6 as a possible negative regulator of MDM2 expression. Our data show that E2F6 suppresses Mdm2 expression in cells harboring the SNP309G allele but not the SNP309T allele. Thus, Mdm2 SNP309G exhibits tissue-specific regulation and differentially impacts cancer risk.

Blood Hematological and Biochemical Constituents, Antioxidant Enzymes, Immunity and Lymphoid Organs of Broiler Chicks Supplemented with Propolis, Bee Pollen and Mannan Oligosaccharides Continuously or Intermittently.

This study investigate the effect of bee pollen (BP) and/or propolis (Pro) as an alternative to Mannan oligosaccharides (Bio-MOS, a hydrolyzed yeast with natural and artificial flavors Alltech Inc) when given continuously or intermittently on antioxidant enzymes, immunity, weight and morphology of lymphoid organs of broilers. Thus, 324 unsexed one-day-old Arbor Acres broilers were randomly distributed into nine treatment groups, each replicated 6 times of 6 birds per replicate. The chicks were kept in wire cages and fed the same basal diet and were submitted to the following treatments: control without supplementation (control) or supplemented with BP at 300 mg, Pro at 300 mg, BP+Pro at 300 mg each and Bio-MOS at 0.5 g/kg diet. Each supplemented group was subdivided into two subgroups in which the additives were supplied continuously or intermittently. In the continuously supplemented groups, supplementations were given from one till 36 days of age, and in the intermittently supplemented groups, the administration was only three days before, on the day of and day after vaccination. The BP and Pro supplied continuously or intermittently was equally potent for improving immunity, antioxidant enzymes similar to Bio-MOS. All supplements supplied either continuously or intermittently resulted a significantly higher thymus (P < .04) and bursa weights (P < .001) than the control group. Combining BP with Pro resulted in a further increase in thymus weights and small follicle diameter compared to the control group. In addition, thymus percentage in the group received BP+Pro showed a further increase compared to the control and Pro supplemented intermittently. Bio-MOS, when supplied continuously or intermittently, resulted in the greatest response in splenic lymphoblasts. Supplementation with either BP or Pro intermittently, is adequate to promote health and immune response of broiler chicks, with 40% saving of supplementation costs.

Magnetic resonance imaging features of hip disorders in an Egyptian pediatric population.

Hip disorders in a pediatric population are a diagnostic challenge. The aim of the study is to assess the role of magnetic resonance imaging (MRI) in the evaluation of non-traumatic hip disorders in a series of Egyptian patients and to review the literature on the most common hip conditions. Seventy two consecutive patients [40 males (55.6%) and 32 females (44.4)] with acute onset of hip complaints unrelated to trauma or falls were recruited. All patients underwent an initial full clinical assessment and blood tests as well as contrast enhanced MRI of both hips. The most common diagnosis in this group of Egyptian patients was transient synovitis in 29 (40.3%) cases, followed by seronegative enthesopathy and arthropathy syndrome in 8 (11.1%), septic arthritis in 10 (13.9%), tuberculous arthritis in 4 (5.6%), sickle-cell disease in 7 (9.7%), complicated with septic arthritis in 3 (4.2%), transient bone marrow edema (BME) in 3 (4.2%), osteomyelitis in 2 (2.8%), osteosarcoma in 2 (2.8%), sciatic nerve injury in 1 (1.4%), leukemia with BME in 1 (1.4%), coxa vara of both hips and L5/S1 facet joint ankylosis in 1 (1.4%), and a benign bone cyst in 1 (1.4%). MRI studies showed hip effusion in a total of 51 patients (70.8%), joint space narrowing in 9 (12.5%), and BME in 15(20.8%). MRI is a sensitive tool for assessing hip disorders in a pediatric population and can play an important role in both diagnosis and management of different hip disorders, irrespective of the underlying pathology.

Laser induced infrared spectral shift of the MgB2:Cr superconductor films.

During illumination of the MgB2:Cr2O3 films it was established substantial spectral shift of the infrared spectra in the vicinity of 20-50cm(-1). The excitations were performed by nanosecond Er:glass laser operating at 1.54µm and by microsecond 10.6µm CO2 laser. The spectral shifts of the IR maxima were in opposite spectral directions for the two types of lasers. This one observed difference correlates well with spectral shift of their critical temperatures. The possible explanation is given by performance of DFT calculations of the charge density redistribution and the time kinetics of the photovoltaic response. To understand the kinetics of the photoinduced processes the time kinetics of photoresponse was done for the particular laser wavelengths.

Loss of epithelial p53 and αv integrin cooperate through Akt to induce squamous cell carcinoma yet prevent remodeling of the tumor microenvironment.

Most of the squamous cell carcinomas (SCCs) of the skin and head and neck contain p53 mutations. The presence of p53 mutations in premalignant lesions suggests that they represent early events during tumor progression and additional alterations may be required for SCC development. Here we show that codeletion of the p53 and αv integrin genes in mouse stratified epithelia induced SCCs in 100% of the mice, more frequently and with much shorter latency than deletion of either gene alone. The SCCs that lacked p53 and αv in the epithelial tumor cells exhibited high Akt activity, lacked multiple types of infiltrating immune cells, contained a defective vasculature and grew slower than tumors that expressed p53 or αv. These results reveal that loss of αv in epithelial cells that lack p53 promotes SCC development, but also prevents remodeling of the tumor microenvironment and delays tumor growth. We observed that Akt inactivation in SCC cells that lack p53 and αv promoted anoikis. Thus, tumors may arise in these mice as a result of the increased cell survival induced by Akt activation triggered by loss of αv and p53, and by the defective recruitment of immune cells to these tumors, which may allow immune evasion. However, the defective vasculature and lack of a supportive stroma create a restrictive microenvironment in these SCCs that slows their growth. These mechanisms may underlie the rapid onset and slow growth of SCCs that lack p53 and αv.

Imaging findings of head and neck dermatofibrosarcoma protuberans.

BACKGROUND AND PURPOSE: Dermatofibrosarcoma protuberans is a rare, locally aggressive sarcoma of the skin in children and adults, usually involving the trunk and extremities and less commonly the head and neck. Despite clinical reports in the literature on the management of dermatofibrosarcoma protuberans, there are limited articles describing its imaging features. MATERIALS AND METHODS: We retrospectively reviewed the demographics and imaging findings in all 24 patients with pathologically proven dermatofibrosarcoma protuberans of the head and neck seen at a tertiary cancer center between 2001 and 2010. RESULTS: Twenty-two of the 24 lesions were nodular and well circumscribed; 19 of the 24 were located on the scalp. On imaging, all 24 lesions involved subcutaneous tissues. The lesions ranged in size from 0.6-9.5 cm (mean, 3.7 cm; standard deviation, 2.3 cm). Twelve lesions involved the soft tissues either at or extending directly to the midline. Thirteen lesions were associated with bulging of the skin surface. Fourteen lesions were imaged with CT and 14 with MR imaging. Whereas variable enhancement patterns were noted on CT and MR imaging, dermatofibrosarcoma protuberans was usually T2-hyperintense and demonstrated marked enhancement. None of the lesions was associated with bone invasion, perineural spread, or nodal/distant metastasis. CONCLUSIONS: Knowledge of the imaging characteristics of dermatofibrosarcoma protuberans may alert neuroradiologists to include dermatofibrosarcoma protuberans in the differential diagnosis of lesions about the head and neck with similar imaging characteristics.

IR laser induced spectral kinetics of AgGaGe3Se8:Cu chalcogenide crystals.

The possibility to operate by optical spectra near the absorption edge gap was discovered for the AgGaGe3Se8:Cu semiconducting chalcogenide crystals under influence of microsecond CO2 laser with pulse energy 60 mJ operating at wavelength 10.6 µm. An occurrence of substantial photoinduced optical density was observed at wavelengths in the spectral range of 610-620 nm. Introducing of Cu ions leads to substantial spectral asymmetry in the observed spectra. The process achieves its maximum value after the 80-120 s of CO2 laser treatment and relaxes with almost irreversible changes after the same time. The contribution of thermo heating did not exceed 5-6%. Only the irreversible changes of the sample's surface topography were observed during the CO2 laser treatment, which do not influence the treatment. So the surface states do not play a principal role and the effect is prevailingly originated from the. The observed effect may be used for control of the CO2 laser power density.

Urban legends series: oral leukoplakia.

To date, the term oral leukoplakia (OL) should be used to recognize 'predominantly white plaques of questionable risk, having excluded (other) known diseases or disorders that carry no increased risk of cancer'. In this review, we addressed four controversial topics regarding oral leukoplakias (OLs): (i) Do tobacco and alcohol cause OLs?, (ii) What percentage of OLs transform into oral squamous cell carcinoma (OSCC)?, (iii) Can we distinguish between premalignant and innocent OLs?, and (iv) Is proliferative verrucous leukoplakia (PVL) a specific entity or just a form of multifocal leukoplakia? Results of extensive literature search suggest that (i) no definitive evidence for direct causal relationship between smoked tobacco and alcohol as causative factors of OLs, (ii and iii) the vast majority of OLs follow a benign course and do not progress into a cancer, and no widely accepted and/or validated clinical and/or biological factors can predict malignant transformation, and (iv) the distinction between multifocal/multiple leukoplakias and PVL in their early presentation is impossible; the temporal clinical progression and the high rate of recurrences and development of cancer of PVL are the most reliable features for diagnosis.

TrkC signaling is activated in adenoid cystic carcinoma and requires NT-3 to stimulate invasive behavior.

Treatment options for adenoid cystic carcinoma (ACC) of the salivary gland, a slowly growing tumor with propensity for neuroinvasion and late recurrence, are limited to surgery and radiotherapy. Based on expression analysis performed on clinical specimens of salivary cancers, we identified in ACC expression of the neurotrophin-3 receptor TrkC/NTRK3, neural crest marker SOX10, and other neurologic genes. Here, we characterize TrkC as a novel ACC marker, which was highly expressed in 17 out of 18 ACC primary-tumor specimens, but not in mucoepidermoid salivary carcinomas or head and neck squamous cell carcinoma. Expression of the TrkC ligand NT-3 and Tyr-phosphorylation of TrkC detected in our study suggested the existence of an autocrine signaling loop in ACC with potential therapeutic significance. NT-3 stimulation of U2OS cells with ectopic TrkC expression triggered TrkC phosphorylation and resulted in Ras, Erk 1/2 and Akt activation, as well as VEGFR1 phosphorylation. Without NT-3, TrkC remained unphosphorylated, stimulated accumulation of phospho-p53 and had opposite effects on p-Akt and p-Erk 1/2. NT-3 promoted motility, migration, invasion, soft-agar colony growth and cytoskeleton restructuring in TrkC-expressing U2OS cells. Immunohistochemical analysis demonstrated that TrkC-positive ACC specimens also show high expression of Bcl2, a Trk target regulated via Erk 1/2, in agreement with activation of the TrkC pathway in real tumors. In normal salivary gland tissue, both TrkC and Bcl2 were expressed in myoepithelial cells, suggesting a principal role for this cell lineage in the ACC origin and progression. Sub-micromolar concentrations of a novel potent Trk inhibitor AZD7451 completely blocked TrkC activation and associated tumorigenic behaviors. Pre-clinical studies on ACC tumors engrafted in mice showed efficacy and low toxicity of AZD7451, validating our in vitro data and stimulating more research into its clinical application. In summary, we describe in ACC a previously unrecognized pro-survival neurotrophin signaling pathway and link it with cancer progression.

Somatic SF3B1 mutation in myelodysplasia with ring sideroblasts.

BACKGROUND: Myelodysplastic syndromes are a diverse and common group of chronic hematologic cancers. The identification of new genetic lesions could facilitate new diagnostic and therapeutic strategies. METHODS: We used massively parallel sequencing technology to identify somatically acquired point mutations across all protein-coding exons in the genome in 9 patients with low-grade myelodysplasia. Targeted resequencing of the gene encoding RNA splicing factor 3B, subunit 1 (SF3B1), was also performed in a cohort of 2087 patients with myeloid or other cancers. RESULTS: We identified 64 point mutations in the 9 patients. Recurrent somatically acquired mutations were identified in SF3B1. Follow-up revealed SF3B1 mutations in 72 of 354 patients (20%) with myelodysplastic syndromes, with particularly high frequency among patients whose disease was characterized by ring sideroblasts (53 of 82 [65%]). The gene was also mutated in 1 to 5% of patients with a variety of other tumor types. The observed mutations were less deleterious than was expected on the basis of chance, suggesting that the mutated protein retains structural integrity with altered function. SF3B1 mutations were associated with down-regulation of key gene networks, including core mitochondrial pathways. Clinically, patients with SF3B1 mutations had fewer cytopenias and longer event-free survival than patients without SF3B1 mutations. CONCLUSIONS: Mutations in SF3B1 implicate abnormalities of messenger RNA splicing in the pathogenesis of myelodysplastic syndromes. (Funded by the Wellcome Trust and others.).

KiSS1 mediates platinum sensitivity and metastasis suppression in head and neck squamous cell carcinoma.

Although surgery and radiotherapy have been the standard treatment modalities for head and neck squamous cell carcinoma (HNSCC), the integration of cisplatin (CDDP)-based therapy has led to improvements in local and regional control of disease for patients. However, many trials show that only 10-20% of patients benefit from this treatment intensification, which can result in profound treatment-associated morbidity and mortality. Moreover, the marginal survival improvement suggests that CDDP resistance is an innate characteristic of HNSCC. To elucidate the biological mechanisms underpinning CDDP resistance in HNSCC, we utilized an experimental model of CDDP resistance in this disease. We first observed significant enhancements in local tumor growth and metastasis, as well as adverse survival, in CDDP-resistant (CR) tumors compared with sensitive tumors. To elucidate the molecular mechanisms of this phenotype, we undertook a systems biology-based approach utilizing high-throughput PCR arrays, and we identified a significant suppression of KiSS1 mRNA and protein expression in the CR cells, but no significant regions of genomic loss with array comparative genomic hybridization. Genetic suppression of KiSS1 in CDDP-sensitive cell lines rendered them CR, an observation that was mechanistically linked to alterations in glutathione S-transferase-π expression and function. We next confirmed that, in human HNSCC tumors, loss of KiSS1 expression was associated with metastatic human HNSCC tumors compared with non-metastatic tumors. Genetic reconstitution of KiSS1 in CR cells abrogated cellular migration and induced CDDP sensitivity. To confirm these findings in a murine model, either CR or KiSS1-transfected CR cells were studied in an orthotopic model of HNSCC, or survival studies revealed significant improvement in survival of the mice bearing CR-KiSS1 tumors. Mechanistically, alterations in apoptotic pathways and CDDP metabolism contributed to KiSS1-associated chemotherapy sensitization. These studies provided further direct evidence for the role of KiSS1 loss in biologically aggressive HNSCC and suggest potential targets for therapy in CR cancers.

TrkB induces EMT and has a key role in invasion of head and neck squamous cell carcinoma.

Head and neck squamous cell carcinoma (HNSCC) remains a significant public health problem, accounting for over 5% of all cancer-related deaths, and these deaths primarily result from metastatic disease. The molecular processes involved in HNSCC pathogenesis and progression are poorly understood, and here we present experimental evidence for a direct role of the cell surface receptor tyrosine kinase, TrkB, in HNSCC tumor progression. Using immunohistochemical analysis and transcriptional profiling of archival HNSCC tumor specimens, we found that TrkB and its secreted ligand, brain-derived neurotrophic factor (BDNF), are expresses in greater than 50% of human HNSCC tumors, but not in normal upper aerodigestive tract (UADT) epithelia. Studies with HNSCC cell lines reveal that in vitro stimulation with BDNF, the ligand for TrkB, upregulates the migration and invasion of HNSCC cells, and both transient and stable suppressions of TrkB result in significant abrogation of constitutive and ligand-mediated migration and invasion. Furthermore, enforced overexpression of TrkB results in altered expression of molecular mediators of epithelial-to-mesenchymal transition (EMT), including downregulation of E-cadherin and upregulation of Twist. Using an in vivo mouse model of HNSCC, we were able to show that downregulation of TrkB suppresses tumor growth. These results directly implicate TrkB in EMT and the invasive behavior of HNSCC, and correlate with the in vivo overexpression of TrkB in human HNSCC. Taken together, these data suggest that the TrkB receptor may be a critical component in the multi-step tumor progression of HNSCC, and may be an attractive target for much needed new therapies for this disease.