Estimation of economic impacts due to hydatidosis among livestok in Kermanshah Province, western Iran

Abstract

Information about inspection of slaughtered animals is a basic approach to review the epidemiological pattern of infectious diseases. Therefore, this study was aimed to determine the prevalence of hydatidosis as well as estimate of relevant economic losses in livestock slaughtered in Kermanshah Province, western Iran, throughout the years 2010–2015. A total of 539,861 livestock examined; 12,413 (2.29%) were infected with hydatidosis. Overall, 4713 (3.21%) of cattle, 6720 (1.97%) of sheep, and 980 (1.86%) of goats were found to be infected with hydatidosis. The total economic loss was USD 457,582. The direct economic loss in cattle was USD 134,164, in sheep USD 53,908, and in goats USD 7407. Furthermore, the indirect economic loss in cattle, sheep, and goats was USD 220,211, USD 41,197, and USD 695, respectively. Targeted investigations on the prevalence of this disease, especially in endemic areas, as well as continuous and regular actions such as the training of those who deal with livestock, the sanitary condemnation of infected organs, the reduction of stray dog population, and the grazing of livestock on safe pasture can provide a clear horizon for an appropriate solution to minimize the infected cases and prevent huge economic losses due to hydatidosis.

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Advances and Current Concepts in the Medical Management of Gastroenteropancreatic Neuroendocrine Neoplasms

Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) are rare and heterogeneous group of tumors presenting as localised or metastatic disease and in a subset with distinct clinical syndromes. Treatment is aimed at controlling the functional syndrome, eradicating the tumor, and/or preventing further tumor growth. Surgery is the treatment of choice in removing the primary tumor and/or reducing tumor burden but cannot be applied to all patients. Somatostatin analogs (SS-analogs) obtain control of functional syndromes in the majority of GEP-neuroendocrine tumors (NETs); phase III trials have shown that SS-analogs can be used as first-line antiproliferative treatment in patients with slow-growing GEP-NETs. The role of the recently approved serotonin inhibitor, telotristat ethyl, and gastrin receptor antagonist, netazepide, is evolving. Streptozotocin-based chemotherapy has been used for inoperable or progressing pancreatic NENs but the orally administered combination of capecitabine/temozolomide is becoming more popular due to its better tolerability and potential effect in other GEP-NENs. Phase III trials have shown efficacy of molecular targeted therapies in GEP-NETs and of radionuclide treatment in patients with midgut carcinoid tumors expressing somatostatin receptors. Most patients will develop disease progression necessitating further therapeutic options. A combination of currently available treatments along with the molecular signature of each tumor will guide future treatment.

http://ift.tt/2zfZDfm

Retrograde Activation of the Extrinsic Apoptotic Pathway in Spinal-Projecting Neurons after a Complete Spinal Cord Injury in Lampreys

Spinal cord injury (SCI) is a devastating condition that leads to permanent disability because injured axons do not regenerate across the trauma zone to reconnect to their targets. A prerequisite for axonal regeneration will be the prevention of retrograde degeneration that could lead to neuronal death. However, the specific molecular mechanisms of axotomy-induced degeneration of spinal-projecting neurons have not been elucidated yet. In lampreys, SCI induces the apoptotic death of identifiable descending neurons that are "bad regenerators/poor survivors" after SCI. Here, we investigated the apoptotic process activated in identifiable descending neurons of lampreys after SCI. For this, we studied caspase activation by using fluorochrome-labeled inhibitors of caspases, the degeneration of spinal-projecting neurons using Fluro-Jade C staining, and the involvement of the intrinsic apoptotic pathway by means of cytochrome c and V double immunofluorescence. Our results provide evidence that, after SCI, bad-regenerating spinal cord-projecting neurons slowly degenerate and that the extrinsic pathway of apoptosis is involved in this process. Experiments using the microtubule stabilizer Taxol showed that caspase-8 signaling is retrogradely transported by microtubules from the site of axotomy to the neuronal soma. Preventing the activation of this process could be an important therapeutic approach after SCI in mammals.

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Beneficial Effects of 6-Month Supplementation with Omega-3 Acids on Selected Inflammatory Markers in Patients with Chronic Kidney Disease Stages 1–3

Introduction. Chronic kidney disease (CKD) is accompanied by inflammation. The aim of this study was to evaluate the effect of 6-month supplementation with omega-3 acids on selected markers of inflammation in patients with CKD stages 1–3. Methods. Six-month supplementation with omega-3 acids (2 g/day) was administered to 87 CKD patients and to 27 healthy individuals. At baseline and after follow-up, blood was taken for C-reactive protein (CRP) and monocyte chemotactic protein-1 (MCP-1) concentration and white blood cell (WBC) count. Serum concentration of omega-3 acids—eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and alpha-linolenic acid (ALA)—was determined using gas chromatography. And 24-hour urinary collection was performed to measure MCP-1 excretion. Results. After six-month omega-3 supplementation, ALA concentration increased in CKD patients and in the reference group, while EPA and DHA did not change. At follow-up, a significant decrease in urinary MCP-1 excretion in CKD () and in the reference group () was found. CRP, serum MCP-1, and WBC did not change significantly. The estimated glomerular filtration rate (eGFR) did not change significantly in the CKD group. Conclusions. The reduction of urinary MCP-1 excretion in the absence of MCP-1 serum concentration may suggest a beneficial effect of omega-3 supplementation on tubular MCP-1 production. Trial Registration. This study was registered in ClinicalTrials.gov (identifier: NCT02147002).

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Comparative effect of Melissa officinalis aqueous extract, sulfadimidine, and vitamin E–selenium on antioxidant parameters in rabbit experimental coccidiosis

Abstract

This study was undertaken to assess the comparative effect of Melissa officinalis aqueous extract, sulfadimidine, and vitamin E–selenium on some antioxidant parameters in experimental subclinical coccidiosis in rabbit. Forty adult Albino rabbits were alienated into five groups containing eight rabbits in each group. The control animals did not receive any infection or treatment. The remaining groups were inoculated with 1 × 10⁴ infective oocysts of Eimeria perforans. Blood samples were collected before infection and 4, 8, 12, and 16 days post-infection (dpi) to measure antioxidant parameters. The oocyst number per in feces was calculated from 6 to 11 dpi. The results demonstrated a significant drop in antioxidant enzyme activity in the experimentally infected animals; however, these values were increased following treatment with M. officinalis and vitamin E–selenium. High level of malondialdehyde (MDA) in the infected animals was also noticeable which was reduced after treatment with M. officinalis and vitamin E–selenium. Our findings showed that M. officinalis aqueous extract can increase blood level of antioxidant enzymes in coccidiosis but has no direct effect on oocyst shedding.

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Osimertinib in Untreated EGFR-Mutated Advanced Non–Small-Cell Lung Cancer

The current standard of care for patients with locally advanced or metastatic non–small-cell lung cancer (NSCLC) harboring epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI)–sensitizing mutations is treatment with a first-generation or second-generation EGFR-TKI such as…

http://ift.tt/2hzUGTf

Collection of Post-mating Semen from the Female Reproductive Tract and Measurement of Semen Liquefaction in Mice

Semen liquefaction is required for sperm to be liberated from the seminal gel. This study provides the procedures for collecting semen from the female reproductive tract post-coitus, and measuring semen liquefaction time.

http://ift.tt/2mGaXeI

Visualizing Multiciliated Cells in the Zebrafish Through a Combined Protocol of Whole Mount Fluorescent In Situ Hybridization and Immunofluorescence

Cilia development is vital to proper organogenesis. This protocol describes an optimized method to label and visualize ciliated cells of the zebrafish.

http://ift.tt/2hL3RnJ

The function of the cellular prion protein in health and disease

Abstract

The essential role of the cellular prion protein (PrP^C) in prion disorders such as Creutzfeldt–Jakob disease is well documented. Moreover, evidence is accumulating that PrP^C may act as a receptor for protein aggregates and transduce neurotoxic signals in more common neurodegenerative disorders, such as Alzheimer's disease. Although the pathological roles of PrP^C have been thoroughly characterized, a general consensus on its physiological function within the brain has not yet been established. Knockout studies in various organisms, ranging from zebrafish to mice, have implicated PrP^C in a diverse range of nervous system-related activities that include a key role in the maintenance of peripheral nerve myelination as well as a general ability to protect against neurotoxic stimuli. Thus, the function of PrP^C may be multifaceted, with different cell types taking advantage of unique aspects of its biology. Deciphering the cellular function(s) of PrP^C and the consequences of its absence is not simply an academic curiosity, since lowering PrP^C levels in the brain is predicted to be a powerful therapeutic strategy for the treatment of prion disease. In this review, we outline the various approaches that have been employed in an effort to uncover the physiological and pathological functions of PrP^C. While these studies have revealed important clues about the biology of the prion protein, the precise reason for PrP^C's existence remains enigmatic.

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Contributors

Publication date: December 2017
Source:Seminars in Spine Surgery, Volume 29, Issue 4





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Forthcoming/Previous Issues

Publication date: December 2017
Source:Seminars in Spine Surgery, Volume 29, Issue 4





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Table of Contents

Publication date: December 2017
Source:Seminars in Spine Surgery, Volume 29, Issue 4





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Masthead

Publication date: December 2017
Source:Seminars in Spine Surgery, Volume 29, Issue 4





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Parkinson’s disease: experimental models and reality

Abstract

Parkinson's disease (PD) is a chronic, progressive movement disorder of adults and the second most common neurodegenerative disease after Alzheimer's disease. Neuropathologic diagnosis of PD requires moderate-to-marked neuronal loss in the ventrolateral substantia nigra pars compacta and α-synuclein (αS) Lewy body pathology. Nigrostriatal dopaminergic neurodegeneration correlates with the Parkinsonian motor features, but involvement of other peripheral and central nervous system regions leads to a wide range of non-motor features. Nigrostriatal dopaminergic neurodegeneration is shared with other parkinsonian disorders, including some genetic forms of parkinsonism, but many of these disorders do not have Lewy bodies. An ideal animal model for PD, therefore, should exhibit age-dependent and progressive dopaminergic neurodegeneration, motor dysfunction, and abnormal αS pathology. Rodent models of PD using genetic or toxin based strategies have been widely used in the past several decades to investigate the pathogenesis and therapeutics of PD, but few recapitulate all the major clinical and pathologic features of PD. It is likely that new strategies or better understanding of fundamental disease processes may facilitate development of better animal models. In this review, we highlight progress in generating rodent models of PD based on impairments of four major cellular functions: mitochondrial oxidative phosphorylation, autophagy-lysosomal metabolism, ubiquitin–proteasome protein degradation, and endoplasmic reticulum stress/unfolded protein response. We attempt to evaluate how impairment of these major cellular systems contribute to PD and how they can be exploited in rodent models. In addition, we review recent cell biological studies suggesting a link between αS aggregation and impairment of nuclear membrane integrity, as observed during cellular models of apoptosis. We also briefly discuss the role of incompetent phagocytic clearance and how this may be a factor to consider in developing new rodent models of PD.

http://ift.tt/2AZoKAd

Downregulation of DUSP4 enhances cell proliferation and invasiveness in colorectal carcinomas

Abstract

It is widely accepted that aberrant activation of the Wnt signaling pathway is responsible for the development of precursor lesions of colorectal cancer (CRC). However, the molecular mechanisms involved in the process of progression from these precursor lesions to invasive lesions of CRC are not fully understood. Recently, we reported that constitutive activation of MAPK accompanied by downregulation of dual-specificity phosphatase 4 (DUSP4), a MAPK phosphatase, contributes to the progression of precursor lesions in the pancreas. In this study, we found that downregulation of DUSP4 was related to constitutive activation of extracellular signal-regulated kinases (ERKs) in CRC cells. Restoration of DUSP4 resulted in inactivation of ERKs, leading to suppression of both proliferation and invasiveness, as shown by treatment with a MEK inhibitor. Furthermore, immunohistochemistry revealed that DUSP4 expression was upregulated in the superficial region of CRC tissue, whereas it was significantly downregulated in the deep region. On the other hand, ERKs in the deep region were markedly hyper-activated compared to those in the superficial region. These results suggest that activation of the MAPK signaling pathway caused by downregulation of DUSP4 is responsible for progression of CRCs and would be a promising therapeutic target.

This article is protected by copyright. All rights reserved.

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I thought he was going to set our house on fire

Abstract

Recently the wife of an octogenarian suffering from dementia brought her husband to the emergency department stating, "I can't take care of him anymore. He is becoming more aggressive. I thought he was going to set our house on fire last night". She recounted finding her husband in the kitchen at the range turning the dials.

This article is protected by copyright. All rights reserved.

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Patient-level Factors and the Quality of Care Delivered in Pediatric Emergency Departments

Abstract

Objective

Quality of care delivered to adult patients in the emergency department (ED) is often associated with demographic and clinical factors such as a patient's race/ethnicity and insurance status. We sought to determine whether the quality of care delivered to children in the ED was associated with a variety of patient-level factors.

Methods

This was a retrospective, observational cohort study. Pediatric patients (<18 years) who received care between January 2011 and December 2011 at one of twelve EDs participating in the Pediatric Emergency Care Applied Research Network (PECARN) were included. We analyzed demographic factors (including age, sex, and payment source) and clinical factors (including triage, chief complaint, and severity of illness). We measured quality of care using a previously validated implicit review instrument using chart review with a summary score that ranged from 5 to 35. We examined associations between demographic and clinical factors and quality of care using a hierarchical multivariable linear regression model with hospital site as a random effect.

Results

In the multivariable model, among the 620 ED encounters reviewed, we did not find any association between patient age, sex, race/ethnicity, and payment source and the quality of care delivered. However, we did find that some chief complaint categories were significantly associated with lower than average quality of care, including fever (-0.65 points in quality, 95% CI: -1.24, -0.06) and upper respiratory symptoms (-0.68 points in quality, 95% CI: -1.30, -0.07).

Conclusion

We found that quality of ED care delivered to children among a cohort of 12 EDs participating in the PECARN network was high and did not differ by patient age, sex, race/ethnicity, and payment source, but did vary by the presenting chief complaint.

This article is protected by copyright. All rights reserved.

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A Family Reunion

Abstract

She had arrived from home via ambulance for back pain in the middle of the night; elderly patients with back pain are always cases that concern me - nothing chronic seems amenable to satisfying treatment and nothing acute ends well. The paramedics' report was clear: she was the acute type.

This article is protected by copyright. All rights reserved.

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Significance of prostate-specific antigen kinetics after three-dimensional conformal radiotherapy with androgen deprivation therapy in patients with localized prostate cancer

Abstract

Background

To evaluate the relationship between biochemical recurrence and post-radiation prostate-specific antigen (PSA) kinetics in patients with localized prostate cancer treated by radiotherapy with various durations of androgen deprivation therapy (ADT).

Methods

We reviewed our single-institution, retrospectively maintained data of 144 patients with T1c-T3N0M0 prostate cancer who underwent three-dimensional conformal radiotherapy (3D-CRT) between December 2005 and December 2015 and 113 patients were fulfilled the inclusion criteria. In this cohort, 3D-CRT was delivered with a dose in the range from 70.0 to 72.0 Gy with ADT. All patients received ADT as concurrent regimens. Biochemical recurrence was defined on the basis of the following: "PSA nadir + 2.0 ng/ml or the clinical judgement of attending physicians". Kaplan–Meier, log-rank, and Cox regression analyses were carried out.

Results

The median follow-up period was 54.0 months. The median duration of ADT was 17 months (interquartile range, 10–24 months). There was a trend toward statistical significant correlation between post-radiation PSA decline rate of ≥ 90% and PSA recurrence (p = 0.056). The same correlation could be observed in D'Amico high-risk patients (p = 0.036). However, it was not observed between PSA nadir and PSA recurrence (p = 0.40) in univariate analysis. Furthermore, multivariate analysis showed that post-radiation PSA decline rate of ≥ 90% was a significant predictor of biochemical recurrence in patients who received radiotherapy with various durations of ADT (p = 0.044).

Conclusions

Post-radiation PSA decline rate of ≥ 90% was a prognostic factor for biochemical recurrence in localized prostate cancer patients received 3D-CRT with various durations of ADT.

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HPLC-DAD, ESI - MS/MS and NMR of Lycopene isolated from P. guajava L. and its Biotechnological applications

Abstract

Psidium guajava L. has been reported to be a rich source of antioxidant compounds. Its carotenoids have been highlighted by their high antioxidant capacity, which offers several benefits for human health. In this sense, lycopene isomers need to be identified. In this work, the comprehensive chemical characterization, by HPLC-DAD, MS/MS and NMR, of lycopene isolated from P. guajava L., antioxidant and antimicrobial activity of lycopene extracts and isolated lycopene were evaluated. The FTIR results reported a structure with Z configuration, confirmed by UV-Vis, with λmax = 448, 473 and 505 nm for 5-Z lycopene. Furthermore, MS/MS positive ionization showed one fragment m/z 309 [M – 227]⁺, relatively abundant for isolated lycopene. Experimental and Theoretical NMR studies revealed that guava may contain 5-Z lycopene because of the similarity found among the peaks. Lycopene extracts presented higher antioxidant activity than isolated lycopene, from both P. guajava L. and tomato, when measured by ABTS and ORAC (r² = 0.9995 and r² = 0.9992, respectively). In addition, lycopene extract showed antibacterial efficacy against E. coli, S. aureus and L. innocua, presenting MBC values of 20 mg.mL⁻¹. These results suggest that lycopene extract has potential applicability for food, cosmetics and pharmaceutical industry.

Practical Applications: Lycopene from P. guajava L. was characterized by HPLC-DAD, MS, NMR, FTIR and X-Ray, presented antioxidant capacity by ORAC and antibacterial efficacy against food pathogens.

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Optic disc segmentation for glaucoma screening system using fundus images

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Deactivation of cisplatin-resistant human lung/ovary cancer cells with pyropheophorbide-α methyl ester-photodynamic therapy

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LncRNA CCAT1/miR-130a-3p axis increases cisplatin resistance in non-small-cell lung cancer cell line by targeting SOX4

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The roles of vasohibin and its family members: Beyond angiogenesis modulators

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The IGF-1R/AKT pathway has opposing effects on Nutlin-3a-induced apoptosis

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How does p53 induce apoptosis and how does this relate to p53-mediated tumour suppression?

How does p53 induce apoptosis and how does this relate to p53-mediated tumour suppression?

Cell Death Differ. 2017 Nov 17;:

Authors: Aubrey BJ, Kelly GL, Janic A, Herold MJ, Strasser A

Abstract
The tumour suppressor gene TP53 is mutated in ~50% of human cancers. In addition to its function in tumour suppression, p53 also plays a major role in the response of malignant as well as nontransformed cells to many anticancer therapeutics, particularly those that cause DNA damage. P53 forms a homotetrameric transcription factor that is reported to directly regulate ~500 target genes, thereby controlling a broad range of cellular processes, including cell cycle arrest, cell senescence, DNA repair, metabolic adaptation and cell death. For a long time, induction of apoptotic death in nascent neoplastic cells was regarded as the principal mechanism by which p53 prevents tumour development. This concept has, however, recently been challenged by the findings that in striking contrast to Trp53-deficient mice, gene-targeted mice that lack the critical effectors of p53-induced apoptosis do not develop tumours spontaneously. Remarkably, even mice lacking all mediators critical for p53-induced apoptosis, G1/S boundary cell cycle arrest and cell senescence do not develop any tumours spontaneously. In this review we discuss current understanding of the mechanisms by which p53 induces cell death and how this affects p53-mediated tumour suppression and the response of malignant cells to anticancer therapy.Cell Death and Differentiation advance online publication, 17 November 2017; doi:10.1038/cdd.2017.169.

PMID: 29149101 [PubMed - as supplied by publisher]

http://ift.tt/2zMrmDH

Exploiting a new strategy to induce immunogenic cell death to improve dendritic cell-based vaccines for lymphoma immunotherapy.

Exploiting a new strategy to induce immunogenic cell death to improve dendritic cell-based vaccines for lymphoma immunotherapy.

Oncoimmunology. 2017;6(11):e1356964

Authors: Montico B, Lapenta C, Ravo M, Martorelli D, Muraro E, Zeng B, Comaro E, Spada M, Donati S, Santini SM, Tarallo R, Giurato G, Rizzo F, Weisz A, Belardelli F, Dolcetti R, Dal Col J

Abstract
Although promising, the clinical benefit provided by dendritic cell (DC)-based vaccines is still limited and the choice of the optimal antigen formulation is still an unresolved issue. We have developed a new DC-based vaccination protocol for aggressive and/or refractory lymphomas which combines the unique features of interferon-conditioned DC (IFN-DC) with highly immunogenic tumor cell lysates (TCL) obtained from lymphoma cells undergoing immunogenic cell death. We show that treatment of mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL) cell lines with 9-cis-retinoic acid and IFNα (RA/IFNα) induces early membrane exposure of Calreticulin, HSP70 and 90 together with CD47 down-regulation and enhanced HMGB1 secretion. Consistently, RA/IFNα-treated apoptotic cells and -TCLs were more efficiently phagocytosed by DCs compared to controls. Notably, cytotoxic T cells (CTLs) generated with autologous DCs pulsed with RA/IFNα-TCLs more efficiently recognized and specifically lysed MCL or DLBCL cells or targets loaded with several HLA-A*0201 cyclin D1 or HLA-B*0801 survivin epitopes. These cultures also showed an expansion of Th1 and Th17 cells and an increased Th17/Treg ratio. Moreover, DCs loaded with RA/IFNα-TCLs showed enhanced functional maturation and activation. NOD/SCID mice reconstituted with human peripheral blood lymphocytes and vaccinated with autologous RA/IFNα-TCL loaded-IFN-DCs showed lymphoma-specific T-cell responses and a significant decrease in tumor growth with respect to mice treated with IFN-DC unpulsed or loaded with untreated TCLs. This study demonstrates the feasibility and efficacy of the use of RA/IFNα to generate a highly immunogenic TCL as a suitable tumor antigen formulation for the development of effective anticancer DC-based vaccines.

PMID: 29147614 [PubMed]

http://ift.tt/2mEgN04

Extending antigen release from particulate vaccines results in enhanced antitumor immune response.

Extending antigen release from particulate vaccines results in enhanced antitumor immune response.

J Control Release. 2017 Nov 13;:

Authors: Kapadia CH, Tian S, Perry JL, Sailer D, Christopher Luft J, DeSimone JM

Abstract
Tumor-specific CD8(+) cytotoxic T lymphocytes (CTLs) play a critical role in an anti-tumor immune response. However, vaccination intended to elicit a potent CD8(+) T cell responses employing tumor-associated peptide antigens, are typically ineffective due to poor immunogenicity. Previously, we engineered a polyethylene glycol (PEG) hydrogel-based subunit vaccine for the delivery of an antigenic peptide and CpG (adjuvant) to elicit potent CTLs. In this study, we further examined the effect of antigen release kinetics on their induced immune responses. A CD8(+) T cell epitope peptide from OVA (CSIINFEKL) and CpG were co-conjugated to nanoparticles utilizing either a disulfide or a thioether linkage. Subsequent studies comparing peptide release rates as a function of linker, determined that the thioether linkage provided sustained release of peptide over 72h. Ability to control the release of peptide resulted in both higher and prolonged antigen presentation when compared to disulfide-linked peptide. Both NP vaccine formulations resulted in activation and maturation of bone marrow derived dendritic cells (BMDCs) and induced potent CD8(+) T cell responses when compared to soluble antigen and soluble CpG. Immunization with either disulfide or thioether linked vaccine constructs effectively inhibited EG7-OVA tumor growth in mice, however only treatment with the thioether linked vaccine construct resulted in enhanced survival.

PMID: 29146244 [PubMed - as supplied by publisher]

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