Background Predatory journals fail to fulfill the tenets of biomedical publication: peer review, circulation, and access in perpetuity. Despite increasing attention in the lay and scientific press, no studies have directly assessed the perceptions of the authors or editors involved. Objective Our objective was to understand the motivation of authors in sending their work to potentially predatory journals. Moreover, we aimed to understand the perspective of journal editors at journals cited as potentially predatory. Methods Potential online predatory journals were randomly selected among 350 publishers and their 2204 biomedical journals. Author and editor email information was valid for 2227 total potential participants. A survey for authors and editors was created in an iterative fashion and distributed. Surveys assessed attitudes and knowledge about predatory publishing. Narrative comments were invited. Results A total of 249 complete survey responses were analyzed. A total of 40% of editors (17/43) surveyed were not aware that they were listed as an editor for the particular journal in question. A total of 21.8% of authors (45/206) confirmed a lack of peer review. Whereas 77% (33/43) of all surveyed editors were at least somewhat familiar with predatory journals, only 33.0% of authors (68/206) were somewhat familiar with them (P<.001). Only 26.2% of authors (54/206) were aware of Beall’s list of predatory journals versus 49% (21/43) of editors (P<.001). A total of 30.1% of authors (62/206) believed their publication was published in a predatory journal. After defining predatory publishing, 87.9% of authors (181/206) surveyed would not publish in the same journal in the future. Conclusions Authors publishing in suspected predatory journals are alarmingly uninformed in terms of predatory journal quality and practices. Editors’ increased familiarity with predatory publishing did little to prevent their unwitting listing as editors. Some suspected predatory journals did provide services akin to open access publication. Education, research mentorship, and a realignment of research incentives may decrease the impact of predatory publishing.
Liver metastatic disease is the main cause of death in colorectal cancer (CRC) patients. During metastatic spread of the disease an imbalance in the oxidative stress and inflammation plays a crucial role in tumor progression. In order to improve the efficacy of current therapies, new complementary therapeutic approaches are being analyzed including biologically active compounds with low side effects. The anti-inflammatory and anti-oxidant properties of Ocoxin® oral solution (OOS) prompt us to analyze its effect on the metastatic development of CRC to the liver. First, in vitro effect of OOS in tumor cell viability and migration was analyzed. Second, in vivo effect of different dosage patterns and concentrations in the development of hepatic metastasis was analyzed by intrasplenic inoculation of C26 colon carcinoma cells in Balb/c mice. Third, the expression of alpha smooth muscle actin, caspase-3 and Ki-67 expression was quantified by immunohistochemistry, then gene expression levels of inflammatory factors were measured by quantitative RT-PCR. According to our results, OOS reduced tumor cell viability and migration in vitro. Moreover, in vivo daily administration of OOS from the 7th day after tumor cell inoculation decreased the total area and size of metastatic foci in the liver. Furthermore, cell proliferation and fibroblast recruitment was decreased in tumor foci while a higher number of apoptotic cells were observed. Finally, RNA levels for the inflammatory mediators COX-2, IFNγ, IL1β, IL6 and TNFα were reduced in total liver. In conclusion, OOS reduced the metastatic development of colorectal cancer to the liver by increasing apoptosis, and decreasing tumor cell proliferation and fibroblast recruitment in the tumor foci, as well as the expression of inflammatory mediators in total liver. These results point out OOS as a potential supplement to be applied as complementary therapy for the treatment of liver metastasis from colorectal cancer.
Purpose Complementary and alternative medicine (CAM) use is common amongst cancer patients. However, there is growing concern about its safety and efficacy. Online crowdfunding campaigns represent a unique avenue to understand the cancer patient's perspective for using CAM or declining conventional cancer therapy (CCT). Methods Five hundred GoFundMe campaigns from 2012 to 2019 detailing financial need for cancer treatment were randomly selected and reviewed for endorsement of CAM use, reasons for using CAM, and reasons for declining CCT. Descriptive statistics were used to compare patient and campaign characteristics between 250 CAM users and 250 non-CAM users. Results Compared to non-CAM users, CAM users were more likely to be female (70% vs. 54%, p < 0.01), to report more stage IV cancer (54% vs. 12%, p < 0.01), and to have a history of delayed, missed, or misdiagnosis (10% vs. 4%, p < 0.01). Reasons for using CAM include endorsing curative/therapeutic effects 212 (85%), pain/stress reduction 137 (55%), and dissatisfaction with current or past medical treatment options 105 (42%). 87 (35%) CAM users that declined CCT reported that they wanted to try to fight off cancer using CAM first 57 (61%), that CCT was too "toxic" to the body 39 (42%), and cancer was already too advanced, so that CCT would be futile or too aggressive 25 (27%). Conclusion Cancer patients on GoFundMe using CAM highly value quality of life, comfort, and autonomy. Physicians should educate themselves on CAM to set realistic expectations and provide comprehensive counseling of the risks and benefits of CAM usage to patients who choose to use CAM to either augment or completely replace CCT.
Multiple sclerosis (MS) is an inflammatory disease of the central nervous system characterized by myelin loss and neuronal dysfunction. Although the majority of patients do not present familial aggregation, Mendelian forms have been described. We performed whole-exome sequencing analysis in 132 patients from 34 multi-incident families, which nominated likely pathogenic variants for MS in 12 genes of the innate immune system that regulate the transcription and activation of inflammatory mediators. Rare missense or nonsense variants were identified in genes of the fibrinolysis and complement pathways ( PLAU , MASP1 , C2 ), inflammasome assembly ( NLRP12 ), Wnt signaling ( UBR2 , CTNNA3 , NFATC2 , RNF213 ), nuclear receptor complexes ( NCOA3 ), and cation channels and exchangers ( KCNG4 , SLC24A6 , SLC8B1 ). These genes suggest a disruption of interconnected immunological and pro-inflammatory pathways as the initial event in the pathophysiology of familial MS, and provide the molecular and biological rationale for the chronic inflammation, demyelination and neurodegeneration observed in MS patients.
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