BioResearch Open Access最新文献

Outbreaks of transboundary animal diseases (TADs) have the potential to cause significant detriment to animal, human, and environmental health; severe economic implications; and national security. Challenges concerning data sharing, model development, decision support, and disease emergence science have recently been promoted. These challenges and recommendations have been recognized and advocated in the disciplines intersecting with outbreak prediction and forecast modeling regarding infectious diseases. To advance the effective application of computation and risk communication, analytical products ought to follow a collaboratively agreed common plan for implementation. Research articles should seek to inform and assist prioritization of national and international strategies in developing established criteria to identify and follow best practice standards to assess risk model attributes and performance. A well-defined framework to help eliminate gaps in policy, process, and planning knowledge areas would help alleviate the intense need for the formation of a comprehensive strategy for countering TAD outbreak risks. A quantitative assessment that accurately captures the risk of introduction of a TAD through various pathways can be a powerful tool in guiding where government, academic, and industry resources ought to be allocated, whether implementation of additional risk management solutions is merited, and where research efforts should be directed to minimize risk. This review outlines a part of a process for the development of quantitative risk analysis to collect, analyze, and communicate this knowledge. A more comprehensive and unabridged manual was also developed. The framework used in supporting the application of aligning computational tools for readiness continues our approach to apply a preparedness mindset to challenges concerning threats to global biosecurity, secure food systems, and risk-mitigated agricultural economies.

The microbiome of the human body represents a symbiosis of microbial networks spanning multiple organ systems. Bacteria predominantly represent the diversity of human microbiota, but not to be forgotten are fungi, viruses, and protists. Mounting evidence points to the fact that the "microbial signature" is host-specific and relatively stable over time. As our understanding of the human microbiome and its relationship to the health of the host increases, it is becoming clear that many and perhaps most chronic conditions have a microbial involvement. The oral and gastrointestinal tract microbiome constitutes the bulk of the overall human microbial load, and thus presents unique opportunities for advancing human health prognosis, diagnosis, and therapy development. This review is an attempt to catalog a broad diversity of recent evidence and focus it toward opportunities for prevention and treatment of debilitating illnesses.

The atrial natriuretic peptide (ANP) hormone is secreted by cardiac atrial myocytes and acts to regulate blood pressure homeostasis in humans. Previous research indicates ANP treatment significantly decreases the proliferation of human prostate cancer cells, pancreatic adenocarcinoma, and breast cancer cells. Minimal studies have been conducted with regard to ANP regulating tumor suppressor genes and steroid hormone receptors in breast cancer cells. Our study analyzed the effects of ANP in combination with 17β-estradiol (E₂) and antiestrogen treatments on p53 and ERα levels in T-47D breast cancer cells. Preliminary studies through Western blot analysis showed that ANP treatment decreases p53 and ERα expression levels in a concentration-dependent (10-100 nM) manner. Treatment with ANP alone, at a 100 nM concentration, causes a decrease of p53 and ERα expression compared with Cs (control stripped), but with E₂ and antiestrogen combinations, expression of both protein levels decreased compared with treatments without ANP. Combined treatment with E₂, an estrogen antagonist, and ANP decreased cellular proliferation compared with treatments without ANP, except in the case of raloxifene (RAL). Our studies indicate that ANP has potential as a therapeutic breast cancer treatment and should inspire further studies on the molecular mechanism of ANP in T-47D breast cancer cells.

Generation of reactive oxygen species (ROS) is associated with final stages of follicular development and ovulation in mammals. The human chorionic gonadotropin (hCG) mimics the action of luteinizing hormone and triggers follicular development and ovulation. However, it remains unclear whether hCG induces generation of ROS, if yes, whether hCG-mediated increased level of ROS could induce meiotic exit and/or apoptosis in rat oocytes. For this purpose, cumulus-oocyte complexes (COCs) were collected from ovary of experimental rats injected with 20 IU pregnant mare's serum gonadotropin for 48 h followed by 20 IU hCG for 0, 7, 14, and 21 h. The morphological changes in COCs, meiotic status of oocyte, total ROS, hydrogen peroxide (H₂O₂), inducible nitric oxide synthase (iNOS), nitric oxide (NO), Bax, Bcl-2, cytochrome c, telomerase reverse transcriptase (TERT) expression levels, and DNA fragmentation were analyzed in COCs. Our data suggest that hCG surge increased total ROS as well as H₂O₂ levels but decreased iNOS expression and total NO level in oocytes. The hCG-mediated increased level of ROS was sufficient to induce meiotic cell cycle resumption in majority of oocytes as evidenced by meiotic exit from diplotene as well as metaphase-II (M-II) arrest and their meiotic status. However, increase of ROS level due to hCG surge was not sufficient to trigger Bax and cytochrome c expression levels and DNA fragmentation in COCs. In addition, increased TERT activity was observed in oocytes collected 21 h post-hCG surge showing onset of oocyte aging. Taken together, these results suggest that hCG induces generation of ROS sufficient to trigger meiotic exit from diplotene, as well as M-II arrest, but not good enough to induce apoptosis in rat oocytes.

Environmental endocrine disrupting chemicals (EDCs), including bisphenol A (BPA), induce DNA methylation errors and oxidative stress, and alter fertility. Animal studies have demonstrated that supporting the one-carbon cycle (1-CC) with appropriate dietary supplements can reduce the effects of EDCs. Anti-Mullerian hormone (AMH), a marker of ovarian functionality, has been tested in subfertile female patients, to control this hypothesis in humans. Fifty-five women with a history of 3-7 years of infertility, with at least two assisted reproductive technology (ART) treatment failures, and low serum levels of AMH were enrolled in the study. Before starting any further ART treatment, they were tested for AMH and for follicular count. A urinary control of BPA was proposed. Then a support of the 1-CC, already tested in other clinical studies, was initiated and continued for 4 months. At the end of this period, antral follicle count and serum AMH levels were re-evaluated. The AMH levels before and after treatment were compared using the Wilcoxon test (nonparametric test, non-Gaussian population). Out of the 55 patients, 35 accepted a BPA dosage in the urine. No correlation was found between BPA and serum AMH concentrations. Forty-nine patients followed the full treatment with 1-CC supplements, which resulted in increased AMH levels, independent of initial AMH levels and maternal age (in the range studied), p = 0.0001. Eight patients spontaneously conceived ongoing pregnancies within 3 months, at the end of the protocol. A support of the 1-CC can partly alleviate metabolic derangements induced by environment, as observed in animal models, and improve endocrine background in women.

To assess the prevalence of osteoporosis and osteopenia among Jordanian postmenopausal women attending the National Center for Diabetes, Endocrinology, and Genetics (NCDEG), and to determine the potential associated risk factors. A cross-sectional study was conducted at (NCDEG) in Amman, Jordan. A total of 1079 Jordanian postmenopausal women aged between 45 and 84 years were included in this study that was conducted during the period between April 2013 and December 2014. All patients underwent bone mineral density measurement through dual-energy X-ray absorptiometry (DEXA) scan. DEXA scan was interpreted in terms of T score as per World Health Organization guidelines. The overall prevalence of osteoporosis and osteopenia was 37.5% and 44.6%, respectively. The maximum prevalence of osteoporosis was observed at the lumbar spine (32.4%) followed by the left femoral neck (14.4%), while the maximum prevalence of osteopenia was observed at the left femoral neck (56.1%) followed by the lumbar spine (41.3%). Patients with longer menopausal duration, normal or overweight body mass index, high parity, physical inactivity, positive family history of osteoporosis, inadequate sun exposure, high daily caffeine intake, low daily calcium intake, and delay in the age of menarche were all positively associated with osteoporosis. On the other hand, women with type 2 diabetes mellitus had lower risk of osteoporosis. There is a high prevalence of osteoporosis and osteopenia among Jordanian postmenopausal women. Necessary steps are needed for more public education and a wider dissemination of information about osteoporosis and its prevention.

We evaluated recently published articles relevant to the biological effects of titanium dioxide (TiO₂) particles on local endogenous cells required for normal bone homeostasis, repair, and implant osseointegration. Structural characteristics, size, stability, and agglomeration of TiO₂ particles alter the viability and behavior of multiple bone-related cell types. Resulting shifts in bone homeostasis may increase bone resorption and lead to clinical incidents of osteolysis, implant loosening, and joint pain. TiO₂ particles that enter cells (through endocytosis or Trojan horse mechanism) may further disrupt implant retention. We propose that cellular responses to titanium-based nanoparticles contribute to pathological mechanisms underlying the aseptic loosening of titanium-based metal implants.

The induced pluripotent stem cell (iPSC) was first described more than 10 years ago and is currently used in various basic science and clinical research fields. The aim of this report is to examine the trends in research using iPSCs over the last 10 years. The 2006-2016 PubMed database was searched using the MeSH term "induced pluripotent stem cells." Only original research articles were selected, with a total of 3323 articles. These were classified according to research theme into reprogramming, differentiation protocols for specific cells and/or tissues, pathophysiological research on diseases, and discovery of new drugs, and then the trends over the years were analyzed. We also focused on 232 research publications on the pathophysiological causes of diseases and drug discovery with impact factor (IF; Thomson Reuters) of six or more. The IF of each article was summed up by year, by main target disease, and by country, and the total IF score was expressed as trends of research. The trends of research activities of reprogramming and differentiation on specific cells and/or tissues reached maxima in 2013/2014. On the other hand, research on pathophysiology and drug discovery increased continuously. The 232 articles with IF ≥6 dealt with neurological, immunological/hematological, cardiovascular, and digestive tract diseases, in that order. The majority of articles were published from the United States, followed by Japan, Germany, and United Kingdom. In conclusion, iPSCs have become a general tool for pathophysiological research on disease and drug discovery.

The aim of this study was to identify and analyze the top 50 most cited articles in cartilage regeneration. The impact of a scientific journal can be gauged by the total number of citations it has accrued. The top 50 most cited articles involving cartilage regeneration represent the most quoted level of evidence among this new subspecialty. This study aims to identify and analyze the 50 most cited articles in cartilage regeneration. The Web of Science™ citation indexing service was utilized to determine the most frequently cited articles published after 1956 containing "cartilage regeneration" in the "topic" or "title." The 50 most cited articles were included. The number of citations, year of publication, country of article origin, article institution, journal of publication, publication format, and authorship were then calculated for each article. The span of citations ranged from 1287 to 203 citations, with a mean of 361.02 citations per article in question. The articles originated from 11 countries, with the United States contributing 34 articles, followed by Japan with 5 articles. The articles were distributed across 34 high-impact journals. Biomaterials was the journal with the highest number of publications (seven articles) followed by the Journal of Orthopaedic Research (three articles). Of the 50 articles, 2 were clinical observational studies, 47 concerned basic science, and 1 was review article. The most cited articles involving cartilage regeneration are detected in both experimental and clinical research fields. The high ratio of basic science to clinical articles reflects the infancy of this relatively new specialty and that further clinical research is required in this area.

Healing of rotator cuff (RC) injuries with current suture or augmented scaffold techniques fails to regenerate the enthesis and instead forms a weaker fibrovascular scar that is prone to subsequent failure. Regeneration of the enthesis is the key to improving clinical outcomes for RC injuries. We hypothesized that the utilization of our tissue-engineered tendon to repair either an acute or a chronic full-thickness supraspinatus tear would regenerate a functional enthesis and return the biomechanics of the tendon back to that found in native tissue. Engineered tendons were fabricated from bone marrow-derived mesenchymal stem cells utilizing our well-described fabrication technology. Forty-three rats underwent unilateral detachment of the supraspinatus tendon followed by acute (immediate) or chronic (4 weeks retracted) repair by using either our engineered tendon or a trans-osseous suture technique. Animals were sacrificed at 8 weeks. Biomechanical and histological analyses of the regenerated enthesis and tendon were performed. Statistical analysis was performed by using a one-way analysis of variance with significance set at p < 0.05. Acute repairs using engineered tendon had improved enthesis structure and lower biomechanical failures compared with suture repairs. Chronic repairs with engineered tendon had a more native-like enthesis with increased fibrocartilage formation, reduced scar formation, and lower biomechanical failure compared with suture repair. Thus, the utilization of our tissue-engineered tendon showed improve enthesis regeneration and improved function in chronic RC repairs compared with suture repair. Clinical Significance: Our engineered tendon construct shows promise as a clinically relevant method for repair of RC injuries.