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In coastal areas, transportation infrastructure using reinforced concrete beam structures always works in environmental conditions with high corrosive agents, under the effect of load, the level of corrosion of steel reinforcement in the structure is high. The beam condition becomes more severe, which leads to a decrease in the beam's bending resistance. The level of corrosion of steel reinforcement in reinforced concrete beam structures depends on many influencing factors. These factors need to be seriously researched and evaluated to provide early warning results for designer, construction worker, operater for exploit the project safely and effectively. This article presents the results of research evaluating the influence of concrete strength on the level of corrosion of steel reinforcement in reinforced concrete beam structures, often taking into account the effect of load causing beam bending. Reinforced concrete beam samples were made with concrete at different strength levels: C30, C40 and C50 MPa; Then it was loaded with a yoke system with a loading level equivalent to 0.8Pmax of the destructive strength of the concrete sample. After the yokes were loaded, the beam samples were subjected to accelerated corrosion testing in a highly concentrated salt water environment. concentration equivalent to 3.5% NaCl for a period of 30 days, equivalent to an actual exploitation time of about 35 years. The corrosion rate of steel reinforcement is increased by supplying direct current to create an electrolytic corrosion environment, ensuring that the steel bars are corroded equivalent to the estimated calculated time. Beam samples after accelerated corrosion testing were evaluated for damage in terms of reinforcement volume.

Abstract Background Intervertebral disc degeneration (IDD) is a leading contributor to low back pain (LBP). Autophagy, strongly activated by hypoxia and nutrient starvation, is a vital intracellular quality control process that removes damaged proteins and organelles to recycle them for cellular biosynthesis and energy production. While well‐established as a major driver of many age‐related diseases, autophagy dysregulation or deficiency has yet been confirmed to cause IDD. Methods In vitro, rat nucleus pulposus (NP) cells treated with bafilomycin A1 to inhibit autophagy were assessed for glycosaminoglycan (GAG) content, proteoglycan synthesis, and cell viability. In vivo, a transgenic strain (Col2a1‐Cre; Atg7fl/fl) mice were successfully generated to inhibit autophagy primarily in NP tissues. Col2a1‐Cre; Atg7fl/fl mouse intervertebral discs (IVDs) were evaluated for biomarkers for apoptosis and cellular senescence, aggrecan content, and histological changes up to 12 months of age. Results Here, we demonstrated inhibition of autophagy by bafilomycin produced IDD features in the rat NP cells, including increased apoptosis and cellular senescence (p21CIP1) and decreased expression of disc matrix genes Col2a1 and Acan. H&E histologic staining showed significant but modest degenerative changes in NP tissue of Col2a1‐Cre; Atg7fl/fl mice compared to controls at 6 and 12 months of age. Intriguingly, 12‐month‐old Col2a1‐Cre; Atg7fl/fl mice did not display increased loss of NP proteoglycan. Moreover, markers of apoptosis (cleaved caspase‐3, TUNEL), and cellular senescence (p53, p16INK4a, IL‐1β, TNF‐α) were not affected in 12‐month‐old Col2a1‐Cre; Atg7fl/fl mice compared to controls. However, p21CIP1and Mmp13 gene expression were upregulated in NP tissue of 12‐month‐old Col2a1‐Cre; Atg7fl/fl mice compared to controls, suggesting p21CIP1‐mediated cellular senescence resulted from NP‐targeted Atg7 knockout might contribute to the observed histological changes. Conclusion The absence of overt IDD features from disrupting Atg7‐mediated macroautophagy in NP tissue implicates other compensatory mechanisms, highlighting additional research needed to elucidate the complex biology of autophagy in regulating age‐dependent IDD.

Abstract Background Low back pain (LBP) is a common musculoskeletal condition and a major cause of disability worldwide. Previous studies have found associations of biomarkers with pain and pain-related disability in LBP patients. This study aimed to explore the association between serum biomarkers and pain and disability in patients with acute or subacute axial LBP. Methods This study was ancillary to a parent randomized controlled trial. Enrolled participants were randomized into three intervention groups: one of two types of spinal manipulation or medical care. In the parent study, 107 adults who experienced a new episode of LBP within 3 months prior to enrollment were recruited. For this study, 90 of these 107 participants consented to have blood samples obtained, which were drawn immediately before the beginning of treatment. Seven biomarkers were chosen based on previous literature and analyzed. Clinical outcomes were pain and Oswestry Disability Index (ODI) evaluated at baseline and 4 weeks. Spearman’s |r| was used to study the association of initial levels of each biomarker with pain and ODI scores at baseline and with changes in outcome scores from baseline to 4 weeks (end of treatment) within each intervention group. Results At baseline, 4 of 7 biomarkers had an association with pain that was |r| ≥ .20: neuropeptide Y (NPY) (r = 0.23, p = .028), E-Selectin (r = 0.22, p = .043), vitamin D ((r = − 0.32, p = .002), and c-reactive protein (CRP) (r = 0.37, p = .001). No baseline biomarker had an association with disability that was |r| ≥ 0.20. For the correlations of baseline biomarkers with 4-week change in outcomes, vitamin D showed a correlation with change in disability and/or pain (|r| ≥ 0.20, p > .05) in manipulation-related groups, while CRP, NPY, and E-selectin along with TNFα, Substance P and RANTES showed at least one correlation with change in pain or disability (|r| ≥ 0.20, p > .05) in at least one of the treatment groups. Conclusions In 90 LBP patients, the analyzed biomarkers, especially vitamin D, represent a small set of potential candidates for further research aimed at individualizing patient care. Overall, the associations investigated in the current study are an initial step in identifying the direct mechanisms of LBP and predicting outcomes of manipulation-related treatments or medical care. Trial registration ClinicalTrials.gov Identifier: NCT01211613, Date of Registration: September 29, 2010, https://clinicaltrials.gov/ct2/show/NCT01211613?term=schneider&cond=Low+Back+Pain&cntry=US&state=US%3APA&draw=2&rank=1

Abstract Background The roles of antibody and antigen are indispensable in targeted diagnosis, therapy, and biomedical discovery. On top of that, massive numbers of new scientific articles about antibodies and/or antigens are published each year, which is a precious knowledge resource but has yet been exploited to its full potential. We, therefore, aim to develop a biomedical natural language processing tool that can automatically identify antibody and antigen entities from articles. Results We first annotated an antibody-antigen corpus including 3210 relevant PubMed abstracts using a semi-automatic approach. The Inter-Annotator Agreement score of 3 annotators ranges from 91.46 to 94.31%, indicating that the annotations are consistent and the corpus is reliable. We then used the corpus to develop and optimize BiLSTM-CRF-based and BioBERT-based models. The models achieved overall F1 scores of 62.49% and 81.44%, respectively, which showed potential for newly studied entities. The two models served as foundation for development of a named entity recognition (NER) tool that automatically recognizes antibody and antigen names from biomedical literature. Conclusions Our antibody-antigen NER models enable users to automatically extract antibody and antigen names from scientific articles without manually scanning through vast amounts of data and information in the literature. The output of NER can be used to automatically populate antibody-antigen databases, support antibody validation, and facilitate researchers with the most appropriate antibodies of interest. The packaged NER model is available at https://github.com/TrangDinh44/ABAG_BioBERT.git .

ABSTRACT Infections by pathogenic Acinetobacter species represent a significant burden on the health care system, despite their relative rarity, due to the difficulty of treating infections through oral antibiotics. Multidrug resistance is commonly observed in clinical Acinetobacter infections and multiple molecular mechanisms have been identified for this resistance, including multidrug efflux pumps, carbapenemase enzymes, and the formation of bacterial biofilm in persistent infections. Phenothiazine compounds have been identified as a potential inhibitor of type IV pilus production in multiple Gram-negative bacterial species. Here, we report the ability of two phenothiazines to inhibit type IV pilus-dependent surface (twitching) motility and biofilm formation in multiple Acinetobacter species. Biofilm formation was inhibited in both static and continuous flow models at micromolar concentrations without significant cytotoxicity, suggesting that type IV pilus biogenesis was the primary molecular target for these compounds. These results suggest that phenothiazines may be useful lead compounds for the development of biofilm dispersal agents against Gram-negative bacterial infections. IMPORTANCE Acinetobacter infections are a growing burden on health care systems worldwide due to increasing antimicrobial resistance through multiple mechanisms. Biofilm formation is an established mechanism of antimicrobial resistance, and its inhibition has the potential to potentiate the use of existing drugs against pathogenic Acinetobacter. Additionally, as discussed in the manuscript, anti-biofilm activity by phenothiazines has the potential to help to explain their known activity against other bacteria, including Staphylococcus aureus and Mycobacterium tuberculosis.

Abstract Background In vitro studies using nucleus pulposus (NP) cells are commonly used to investigate disc cell biology and pathogenesis, or to aid in the development of new therapies. However, lab‐to‐lab variability jeopardizes the much‐needed progress in the field. Here, an international group of spine scientists collaborated to standardize extraction and expansion techniques for NP cells to reduce variability, improve comparability between labs and improve utilization of funding and resources. Methods The most commonly applied methods for NP cell extraction, expansion, and re‐differentiation were identified using a questionnaire to research groups worldwide. NP cell extraction methods from rat, rabbit, pig, dog, cow, and human NP tissue were experimentally assessed. Expansion and re‐differentiation media and techniques were also investigated. Results Recommended protocols are provided for extraction, expansion, and re‐differentiation of NP cells from common species utilized for NP cell culture. Conclusions This international, multilab and multispecies study identified cell extraction methods for greater cell yield and fewer gene expression changes by applying species‐specific pronase usage, 60–100 U/ml collagenase for shorter durations. Recommendations for NP cell expansion, passage number, and many factors driving successful cell culture in different species are also addressed to support harmonization, rigor, and cross‐lab comparisons on NP cells worldwide.

Abstract Background Intervertebral disc degeneration contributes to low back pain. The avascular intervertebral disc consists of a central hypoxic nucleus pulpous (NP) surrounded by the more oxygenated annulus fibrosus (AF). Lactic acid, an abundant end-product of NP glycolysis, has long been viewed as a harmful waste that acidifies disc tissue and decreases cell viability and function. As lactic acid is readily converted into lactate in disc tissue, the objective of this study was to determine whether lactate could be used by AF cells as a carbon source rather than being removed from disc tissue as a waste byproduct. Methods Import and conversion of lactate to tricarboxylic acid (TCA) cycle intermediates and amino acids in rabbit AF cells were measured by heavy-isotope (13C-lactate) tracing experiments using mass spectrometry. Levels of protein expression of lactate converting enzymes, lactate importer and exporter in NP and AF tissues were quantified by Western blots. Effects of lactate on proteoglycan (35S-sulfate) and collagen (3H-proline) matrix protein synthesis and oxidative phosphorylation (Seahorse XFe96 Extracellular Flux Analyzer) in AF cells were assessed. Results Heavy-isotope tracing experiments revealed that AF cells imported and converted lactate into TCA cycle intermediates and amino acids using in vitro cell culture and in vivo models. Addition of exogenous lactate (4 mM) in culture media induced expression of the lactate importer MCT1 and increased oxygen consumption rate by 50%, mitochondrial ATP-linked respiration by 30%, and collagen synthesis by 50% in AF cell cultures grown under physiologic oxygen (2-5% O2) and glucose concentration (1-5 mM). AF tissue highly expresses MCT1, LDH-H, an enzyme that preferentially converts lactate to pyruvate, and PDH, an enzyme that converts pyruvate to acetyl-coA. In contrast, NP tissue highly expresses MCT4, a lactate exporter, and LDH-M, an enzyme that preferentially converts pyruvate to lactate. Conclusions These findings support disc lactate-dependent metabolic symbiosis in which lactate produced by the hypoxic, glycolytic NP cells is utilized by the more oxygenated AF cells via oxidative phosphorylation for energy and matrix production, thus shifting the current research paradigm of viewing disc lactate as a waste product to considering it as an important biofuel. These scientifically impactful results suggest novel therapeutic targets in disc metabolism and degeneration.

Abstract Introduction Intervertebral disc degeneration (IDD) is closely related to heightened inflammation in the annulus fibrosis (AF) and nucleus pulposus (NP) cells in the intervertebral disc. An imbalanced matrix homeostasis has been shown to contribute to disc degeneration and associated discogenic low back pain. Metformin, a diabetes medication, has been noted to exhibit anti‐inflammatory properties through upregulation of the AMPK pathway, leading to various anti‐inflammatory‐related responses in hepatocytes. However, it is still unclear how metformin influences disc cellular response to inflammatory stress and the corresponding mechanism. Hence, the objective of this study is to elucidate the effects of metformin on expression of key pro‐inflammatory, catabolic, and anabolic factors within rat AF cells in response to inflammatory stimulation and mechanical tensile stress. Methods Five Fischer 344 rats were sacrificed and their spines isolated. AF cells were cultured and plated in flexible silicone membrane‐based six‐well plates. Wells were split into eight groups and subjected to metformin, IL‐1β, mechanical stretch, and combined treatments. Relative gene expressions of MMP‐13, COX‐2, iNOS, AGC, and Col1 were assessed with quantitative real‐time polymerase chain reaction (qRT‐PCR), and downstream prostaglandin E2 (PGE2) production was quantified with enzyme‐linked immunosorbent assay (ELISA). NF‐kB nuclear translocation was also quantified. Results Metformin in the presence of the combined stress treatments (M + IL/S) significantly increased Col1, COX‐2, and MMP‐13 gene expression, decreased PGE2 production compared to IL/S conditions alone. Metformin treatment of cultured rat annulus fibrosus cells significantly reduced the nuclear translocation of NF‐κB after 4 h of IL‐1β treatment from 43.1% in case of IL‐1β treatment down to 26.2% in the case of metformin + IL‐1β treatment. Discussion The lack of metformin‐mediated suppression of inflammatory response in the nonstretch groups indicates that metformin may be enacting its effects through a stretch‐dependent manner. These results suggest a foundation for pursuing further research into metformin's potential role as an anti‐inflammatory agent for curtailing intervertebral disc degeneration.

Abstract Background Given the central role of radiology in patient care, it is important that radiological research is grounded in reproducible science. It is unclear whether there is a lack of reproducibility or transparency in radiologic research. Purpose To analyze published radiology literature for the presence or lack of key indicators of reproducibility. Methods This cross-sectional retrospective study was performed by conducting a search of the National Library of Medicine (NLM) for publications contained within journals in the field of radiology. Our inclusion criteria were being MEDLINE indexed, written in English, and published from January 1, 2014, to December 31, 2018. We randomly sampled 300 publications for this study. A pilot-tested Google form was used to record information from the publications regarding indicators of reproducibility. Following peer-review, we extracted data from an additional 200 publications in an attempt to reproduce our initial results. The additional 200 publications were selected from the list of initially randomized publications. Results Our initial search returned 295,543 records, from which 300 were randomly selected for analysis. Of these 300 records, 294 met inclusion criteria and 6 did not. Among the empirical publications, 5.6% (11/195, [3.0–8.3]) contained a data availability statement, 0.51% (1/195) provided clear documented raw data, 12.0% (23/191, [8.4–15.7]) provided a materials availability statement, 0% provided analysis scripts, 4.1% (8/195, [1.9–6.3]) provided a pre-registration statement, 2.1% (4/195, [0.4–3.7]) provided a protocol statement, and 3.6% (7/195, [1.5–5.7]) were pre-registered. The validation study of the 5 key indicators of reproducibility—availability of data, materials, protocols, analysis scripts, and pre-registration—resulted in 2 indicators (availability of protocols and analysis scripts) being reproduced, as they fell within the 95% confidence intervals for the proportions from the original sample. However, materials’ availability and pre-registration proportions from the validation sample were lower than what was found in the original sample. Conclusion Our findings demonstrate key indicators of reproducibility are missing in the field of radiology. Thus, the ability to reproduce studies contained in radiology publications may be problematic and may have potential clinical implications.

Objective Low back pain is frequently treated with nonsteroidal anti-inflammatory drugs (NSAIDs), but little is known about intervertebral disc metabolism of the prostaglandins that are diminished by these drugs. Hence, this study aimed at delineating prostaglandin actions in cytokine activated disc cells by comparing the response of nucleus pulposus (NP) cells to the pro-inflammatory cytokine interleukin (IL)-1β with and without cyclooxygenase 2 (COX-2) inhibition. Methods NP cells cultured in alginate beads were activated with IL-1β ± the COX-2 inhibitor Sc-58125. Media harvested from cultured cells were analyzed for prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2α), IL-6, and matrix metalloproteinase (MMP)-3 by enzyme-linked immunosorbent assay and nitric oxide by Griess Reaction. Gene expression along with proteoglycan, collagen, and total protein synthesis were also measured. Results IL-1β increased culture media PGE2 and PGF2α, but decreased proteoglycan and collagen syntheses as well as mRNA expression of the matrix genes aggrecan, versican, collagen I, and collagen II. COX-2 inhibition partially rescued proteoglycan and collagen syntheses and collagen I mRNA, but decreased collagen II mRNA IL-1β activated NP cells. COX-2 inhibition initially enhanced and subsequently reduced IL-1β induced inducible nitric oxide synthase, without altering medium nitrite. IL-1β induction of MMP-3 mRNA was increased by COX-2 inhibition at 24 and 48 hours. Conclusion COX-2 inhibition alters the response of NP cells to IL-1β, suggesting IL-1β action on disc cells is mediated at least in part through COX-2 and its prostaglandins. COX-2 inhibition produces minimal effects on several key catabolic mediators, with the exception of MMP-3. Blocking COX-2 might be beneficial for maintaining disc matrix since it provides an overall rescue of IL-1 induced loss of matrix protein synthesis.

Abstract Mice have been increasingly used as preclinical model to elucidate mechanisms and test therapeutics for treating intervertebral disc degeneration (IDD). Several intervertebral disc (IVD) histological scoring systems have been proposed, but none exists that reliably quantitate mouse disc pathologies. Here, we report a new robust quantitative mouse IVD histopathological scoring system developed by building consensus from the spine community analyses of previous scoring systems and features noted on different mouse models of IDD. The new scoring system analyzes 14 key histopathological features from nucleus pulposus (NP), annulus fibrosus (AF), endplate (EP), and AF/NP/EP interface regions. Each feature is categorized and scored; hence, the weight for quantifying the disc histopathology is equally distributed and not driven by only a few features. We tested the new histopathological scoring criteria using images of lumbar and coccygeal discs from different IDD models of both sexes, including genetic, needle‐punctured, static compressive models, and natural aging mice spanning neonatal to old age stages. Moreover, disc sections from common histological preparation techniques and stains including H&E, SafraninO/Fast green, and FAST were analyzed to enable better cross‐study comparisons. Fleiss's multi‐rater agreement test shows significant agreement by both experienced and novice multiple raters for all 14 features on several mouse models and sections prepared using various histological techniques. The sensitivity and specificity of the new scoring system was validated using artificial intelligence and supervised and unsupervised machine learning algorithms, including artificial neural networks, k‐means clustering, and principal component analysis. Finally, we applied the new scoring system on established disc degeneration models and demonstrated high sensitivity and specificity of histopathological scoring changes. Overall, the new histopathological scoring system offers the ability to quantify histological changes in mouse models of disc degeneration and regeneration with high sensitivity and specificity.

Abstract Introduction Ubiquitously found in all life forms, inorganic polyphosphates (polyP) are linear polymers of repeated orthophosphate units. Present in intervertebral disc tissue, polyP was previously shown to increase extracellular matrix production in nucleus pulposus (NP) cells. However, the effects of polyP on human annulus fibrosus (hAF) cell metabolism is not known. Methods and Results Here, hAF cells cultured in the presence of 0.5 to 1 mM polyP, chain length 22 (polyP‐22), showed an increase in glycosaminoglycan content, proteoglycan and collagen synthesis, and aggrecan and collagen type 1 gene expression. Gene expression level of matrix metalloproteinases 1 was reduced while matrix metalloproteinases 3 level was increased in hAF cells treated with 1 mM polyP. Adenosine triphosphate (ATP) synthesis was also significantly increased in hAF cell culture 72 hours after the exposure to 1 mM polyP‐22. Conclusions PolyP thus has both anabolic and bioenergetic effects in AF cells, similar to that observed in NP cells. Together, these results suggest polyP as a potential energy source and a metabolic regulator of disc cells.

Objectives As much as 50%–90% of research is estimated to be irreproducible, costing upwards of $28 billion in USA alone. Reproducible research practices are essential to improving the reproducibility and transparency of biomedical research, such as including preregistering studies, publishing a protocol, making research data and metadata publicly available, and publishing in open access journals. Here we report an investigation of key reproducible or transparent research practices in the published oncology literature.Design We performed a cross-sectional analysis of a random sample of 300 oncology publications published from 2014 to 2018. We extracted key reproducibility and transparency characteristics in a duplicative fashion by blinded investigators using a pilot tested Google Form.Primary outcome measures The primary outcome of this investigation is the frequency of key reproducible or transparent research practices followed in published biomedical and clinical oncology literature.Results Of the 300 publications randomly sampled, 296 were analysed for reproducibility characteristics. Of these 296 publications, 194 contained empirical data that could be analysed for reproducible and transparent research practices. Raw data were available for nine studies (4.6%). Five publications (2.6%) provided a protocol. Despite our sample including 15 clinical trials and 7 systematic reviews/meta-analyses, only 7 included a preregistration statement. Less than 25% (65/194) of publications provided an author conflict of interest statement.Conclusion We found that key reproducibility and transparency characteristics were absent from a random sample of published oncology publications. We recommend required preregistration for all eligible trials and systematic reviews, published protocols for all manuscripts, and deposition of raw data and metadata in public repositories.

OBJECTIVE: To investigate the effects of proteins products of endothelial cells (ECs) on the annulus fibrosus (AF) cell metabolism in an in vitro culture.METHODS:Human AF cells were expanded in monolayer cultures and treated with proteins from the medium of cell line HMEC-1 (Human Microvascular Endothelial Cells) (125µg/ml). After 72h of treatment RNA was isolated from AF cells for analysis of gene expression and the culture medium was collected for protein expression analysis.RESULTS: The qRT-PCR analysis demonstrated increased gene expression of matrix metalloproteinases (MMPs) in AF cells treated with protein products of endothelial cells compared with cells from control group of AF cells: MMP-1 243.10 times (pCONCLUSIONS: In this study, we observed that the proteins produced by ECs induced the MMPs expression and suppressed the TIMPs as well as the aggrecan in primary cells of the human intervertebral disc, targeting the development of potential treatments for intervertebral disc degeneration and associated discogenic pain.

Introduction: This study aimed to evaluate the status, resource use, and challenges of the capture-based hatchery of black tiger shrimp (Penaeus monodon) (BTS). Methods: Data was obtained through the investigation of 15 broodstock fishing boats and 60 capture-based BTS broodstock hatcheries. Resource use index (RUI) of the capture-based BTS hatchery, calculated from 1,000 female brooders to produce 15-day-old post-larvae (PL15) (production efficiency of PL15, or PEPL15), was analysed. Results: The results indicated that the fishing boats captured an average of 5,900 brooders.boat-1.year-1, 20,856 kg of by catch.boat-1.year-1, and the PE-PL15 production of 937 million for 1,000 female brooders. In the hatchery stage, the use of larger body weight female brooders had benefits in terms of higher survival rate and better efficiency of labour use, Artemia cyst, and probiotic products, but it reduced the efficiency use of chemicals, pellets, and total tank volume of the hatchery. Discussion: There is increasing use of domesticated brooder sources, but wildcaught brooders still play an important role in producing low-cost PL15 for traditional shrimp farming systems, accounting for most farmed BTS production. Therefore, the certification of good practices should be implemented to capture-based BTS hatcheries for the reasonable use of this brooder resource to sustain BTS farming in Vietnam. [ABSTRACT FROM AUTHOR]

The bacterial wilt disease in tomato caused by Ralstonia solanacearum results in harvest losses of up to 90% and significant economic loss to farmers. In this study, 11 R. solanacearum strains were isolated in the largest tomato-growing province in Vietnam. These strains belonged to 3 different groups, and 9/11 strains showed different disease rates in experimental tomato plants. A BHDTSo81 phage specific to R. solanacearum was isolated from a soil sample. Morphological analysis indicated that BHDTSo81 had podovirus morphology and was classified into the Autographiviridae family. The latent period and burst size of BHDTSo81 were calculated to be approximately 145 min and 8.6 ±1.8 virions per infected cell, respectively. In a test of 26 bacterial strains, BHDTSo81 infected 7/11 R. solanacearum strains, while none of the other bacteria tested were susceptible to the phages. R. solanacearum was also challenged in vitro and was inactivated by BHDTSo81 for 40 h in broth. The genome of BHDTSo81 is 41,296 bp long with a total GC content of 63% and contains 46 predicted protein-encoding CDSs (coding sequences). No virulence factor or antibiotic resistance gene was found in the genome. Thus, the initial characteristics of phage BHDTSo81 indicate its potential utility as a control agent against R. solanacearum. [ABSTRACT FROM AUTHOR]