Deep network fault diagnosis for imbalanced small-sized samples via a coupled adversarial autoencoder based on the Bayesian method.

Deep network fault diagnosis methods heavily rely on abundant labeled data for effective model training. However, small-sized samples and imbalanced samples often lead to insufficient features, resulting in accuracy degradation and even instability in the diagnosis model. To address this challenge, this paper introduces a coupled adversarial autoencoder (CoAAE) based on the Bayesian method. This model aims to solve the issue of insufficient samples by generating fake samples and integrating them with the original ones. Within the CoAAE framework, the probability density distribution of the original data is captured using an encoder and fake samples are generated by random sampling from this distribution and decoding them. This process is the adversarial interaction between the encoder and a classifier to obtain the prior distribution of the encoder's parameters. The encoder's parameters are updated through the decoder's reconstruction process, leading to the posterior distribution. Concurrently, the decoder is trained to enhance its ability to reconstruct samples accurately. To address the imbalance in the original samples, a parallel coupled network is employed. This network shares the weights of the extraction layer in the encoder, enabling it to learn the joint distribution between fault-related and normal samples. To evaluate the effectiveness of the proposed data augmentation method, experiments were conducted on a bearing database from Case Western Reserve University using ResNet18 as the deep learning diagnosis model representative. The results demonstrate that CoAAE can effectively augment imbalanced datasets and outperform other advanced methods.

An adaptive fully convolutional network for bearing fault diagnosis under noisy environments.

Intelligent diagnostic algorithms based on convolutional neural networks (CNNs) have shown great potential in diagnosing various conditions. However, accurately and robustly diagnosing faults in noisy situations remains challenging. This study presents an adaptive fully convolutional network (AFCN) for identifying bearing defects in noisy environments. First, we use a novel large kernel convolution method for high-frequency noise reduction and wide-area temporal feature extraction. By utilizing a sequence of stacked residual adaptive convolution blocks, the AFCN achieves a selective emphasis on significant features and adaptive adjustment of feature weights at various convolution scales. The experimental results have shown that the AFCN achieves a diagnostic accuracy of over 90% for the faults in the CWRU dataset under the -8 dB noise and over 77% for the PU dataset in the case of -6 dB noise. The comparison results with five advanced baseline models have demonstrated the superiority of the AFCN in feature extraction, noise immunity, and robustness to the noise environment. The AFCN provides a better adaption to noise interference than conventional CNNs and other advanced adaptive networks.

Attapulgite amendment favors the utilization of high cadmium-contaminated soil for Erigeron breviscapus cultivation.

A practical measure of soil pollution can effectively control the utilization of contaminated soil during the remediation process. In this study, Erigeron breviscapus was used as the experimental material. Soil polluted with high concentrations of cadmium (Cd) was used to study the effects of different doses of attapulgite (AP) (0, 10, 20, and 40 kg-1 for AP0, AP10, AP20, and AP40, respectively) on the yield and quality of E. breviscapus (as measured by scutellarin), as well as soil remediation. The results showed that the yield and scutellarin content of E. breviscapus decreased by 33.4% and 78.9%, respectively, in soil contaminated with high concentrations of Cd (AP0) compared with the control soil (without Cd added). Moreover, the yield increased by 48.0% and 10.6% in AP20 and AP40, respectively, compared with AP0, and the scutellarin content increased by a factor of 2.35-2.41 in AP10, AP20, and AP40. Compared with AP0, the soil Cd content decreased by 22.5-26.2% in AP10, AP20, and AP40 and the available Cd content and acid-extractable Cd fraction in the soil also decreased. The catalase, peroxidase, superoxide dismutase activities, chlorophyll, and Fe2+ content were increased in AP10, AP20, and AP40, leading to an increased yield and scutellarin content. Overall, AP20 had the best effect on the yield, quality of E. breviscapus, and soil remediation. This study provides a practical measure to consider for concurrent benefits of pollution remediation and utilization of Cd-contaminated soil.

l-Theanine Inhibits (-)-Epigallocatechin-3-gallate Oxidation via Chelating Copper.

Our recent study showed that glutamate can inhibit dopamine oxidation via chelating copper. l-Theanine is an amino acid analogue of glutamate, whereas tea (-)-epigallocatechin-3-gallate (EGCG) is similar to dopamine in avidly undergoing oxidation. We thus hypothesized that l-theanine could also restrain EGCG oxidation via chelating copper. The current study scrutinized influences of l-theanine on EGCG oxidation in vitro and in vivo. The in vitro results showed that l-theanine and copper formed an l-theanine-copper complex with impaired redox activity of copper. Accordingly, l-theanine effectively suppressed copper-facilitated EGCG oxidation, hydroxyl radical production, and DNA damage; inhibited EGCG autoxidation which in essence involves catalysis of transition metals such as copper; and reduced EGCG oxidation-associated formation of a quinone adduct with proteins known as quinoproteins. Consistently, l-theanine significantly increased hepatic EGCG levels and reduced hepatic quinoprotein levels and liver injury in mice treated with EGCG. These lines of evidence together suggest that tea l-theanine can protect against tea catechin oxidation.

Prooxidant activity-based guideline for a beneficial combination of (-)-epigallocatechin-3-gallate and chlorogenic acid.

In the current study, the prooxidant activities of (-)-epigallocatechin-3-gallate (EGCG) and chlorogenic acid (CGA) were systematically compared both in multiple in vitro models and in mice. At equimolar concentrations in vitro and in vivo, EGCG displayed powerful prooxidant effects though CGA exhibited none. In vitro, though CGA and EGCG synergistically produced hydrogen peroxide, CGA was able to scavenge hydroxyl radicals generated by EGCG/copper. Consistent with the selective modulation of reactive oxygen species produced from EGCG, CGA lowered hepatotoxicity but did not perturb hepatic AMPK activation nor the increase of hepatic Nrf2-associated proteins induced by high-dose EGCG. CGA, along with low-dose EGCG, synergistically activated hepatic AMPK and increased hepatic Nrf2-associated proteins without causing toxicity in mice. This proof-of-principle study suggests that polyphenols with potent prooxidant activities (e.g., EGCG) together with antioxidant polyphenols with noticeably low prooxidant activities (e.g., CGA) may yield health benefits with a low risk of side effects.

Evaluation of Epidural Analgesia Use During Labor and Infection in Full-term Neonates Delivered Vaginally.

Importance: Quantification of potential consequences associated with the use of epidural analgesia during labor could help to improve the safety and quality of labor and delivery care for parturient women. Objective: To evaluate the association between epidural analgesia use during labor and neonatal infection in a large cohort of parturient women. Design, Setting, and Participants: This propensity score-matched cohort study was conducted at a university-affiliated hospital in Shanghai, China. Women at full-term pregnancy undergoing vaginal delivery between January 2013 and October 2018 were included in the study. Parturient women who were parous, experiencing premature delivery (gestational age <37 weeks), were pregnant with more than 1 fetus, or had experienced a stillbirth were excluded. Data were analyzed from October 2019 to June 2020. Exposures: The use of epidural analgesia during labor. Main Outcomes and Measures: The primary outcome was the incidence of neonatal infection, including neonatal sepsis, neonatal uncharacterized infection, neonatal pneumonia, and neonatal necrotizing enterocolitis reported in the medical record. Secondary outcomes included the incidence of maternal intrapartum fever and histologic chorioamnionitis. Results: Among 37 786 parturient women included (mean [SD] age, 29.5 [3.0] years), 19 968 (52.8%) received epidural analgesia during labor. In the propensity score-matched cohort (including 15 401 parturient women in each group), use of epidural analgesia was associated with a higher incidence of neonatal infection (absolute risk difference, 2.6%, 95% CI, 2.2%-3.0%; relative risk [RR], 2.43; 95% CI, 2.11-2.78), including higher incidence of sepsis (absolute risk difference, 0.1%, 95% CI, 0.1%-0.2%; RR, 3.50; 95% CI, 1.73-7.07) and uncharacterized infection (absolute risk difference, 2.2%, 95% CI, 1.9% to 2.6%; RR, 2.69; 95% CI, 2.30-3.15), compared with no epidural analgesia use. Use of epidural analgesia was also associated with greater incidence of maternal intrapartum fever (RR, 4.12; 95% CI, 3.78-4.50) and histologic chorioamnionitis (RR, 4.08; 95% CI, 3.59-4.64) compared with no epidural analgesia use. Conclusions and Relevance: This cohort study found that use of epidural analgesia in full-term nulliparous women undergoing vaginal delivery was associated with an increased risk of neonatal infection, pending further investigation. These findings support efforts to further improve safety and quality of labor and delivery care for parturient women.

Continuous cardiovascular hemodynamics monitoring with pressure recording analytical method in patients under spinal anesthesia for elective cesarean section: a pilot study.

BACKGROUND: Pressure recording analytical method (PRAM) of MOSTCARE is a minimally invasive system based on mathematical analysis of arterial pressure profile changes and allows continuous recording of hemodynamic measurements. Herein, we aimed to use the MostCare system to investigate the hemodynamics of patients receiving spinal anesthesia during elective cesarean section. METHODS: In this observational study, we recruited 17 patients scheduled for elective cesarean section. For each patient, we acquired continuous recordings of hemodynamic parameters at 14 key timepoints: surgical admission (two baseline parameters), immediately after the administration of spinal anesthesia, six subsequent time points (2, 4, 6, 8, 10, and 12 min after anesthesia), during peritoneum and uterine incision, during delivery, following the administration of oxytocin, and after surgery had been completed. Statistical analysis was carried out by repeated measures analysis of variance (ANOVA). RESULTS: During a twelve min period after spinal anesthesia, we observed significant reductions in mean arterial pressure (MAP), dicrotic pressure (Pdic), cardiac index (CI), stroke volume index (SVI), dP/dtmax, and cardiac cycle efficiency (CCE) (P<0.05 for all). However, systemic vascular resistance index (SVRI) was reversely correlated to CI and increased significantly after spinal anesthesia (P<0.05). These hemodynamic parameters return to near basal values after peritoneum incision. Furthermore, there were significant fluctuations in MAP, Pdic and CI after oxytocin administration (P<0.05). CONCLUSIONS: PRAM of MostCare system revealed significant changes in key hemodynamic parameters undergoing cesarean section with spinal anesthesia. It enables clinicians gain a much better understanding of hemodynamics of parturients and optimize clinical management strategies. TRIAL REGISTRATION: This study was registered at http://www.chictr.org.cn on 16, July, 2019. No. ChiCTR1900024566.

Activation of PGC-1α and Mitochondrial Biogenesis Protects Against Prenatal Hypoxic-ischemic Brain Injury.

Survivals after prenatal hypoxia-ischemia (HI) usually suffer long-lasting cognitive defects. Reduced blood-oxygen supplies and the following reperfusion cause mitochondrial injury. Damaged mitochondria could be replaced by mitochondrial biogenesis program and peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) is the specific up-regulator. The objective of this study was to determine whether PGC-1α and mitochondrial biogenesis participate in the resistant responses of an immature brain to prenatal HI. We used a pregnant rat model of transient occlusion of uterine perfusion to induce intrauterine HI associated brain injury. SH-SY5Y cells exposed to oxygen-glucose deprivation was used to investigate the HI induced reactions in vitro. PGC-1α and its downstream signaling pathway (NRF-1 and TFAM) were examined by Western blot and quantitative Real-time PCR. Mitochondrial respiratory enzyme COX-IV was investigated by Western blot and immunohistochemistry. Mitochondrial density and morphology was detected by transmission electron microscopy. The hippocampal injury and cognitive function were examined. We found that the intrauterine HI triggered PGC-1α-NRF-1-TFAM pathway in both protein and mRNA levels. COX-IV expression significantly increased after HI injury. Intrauterine HI induced both mitochondrial impairment and mitochondrial biogenesis. Postnatal administration of pioglitazone further promoted PGC-1α and mitochondrial biogenesis, alleviated hippocampal injury, and improved performance in the behavioral tasks after intrauterine HI. Our investigation implicated activation of PGC-1α, and mitochondrial biogenesis is a neuroprotective mechanism against brain injury caused by systemic prenatal HI. Promotion of PGC-1α by pioglitazone might be a potential treatment for protecting against hippocampal injury and cognitive defects after intrauterine HI.

Association of lymphocyte count and incidence of maternal fever in epidural analgesia-involved labor.

BACKGROUND: Evidence showed that the use of epidural analgesia increased the risk of maternal fever during labor, and the potential mechanisms involved inflammation. Lymphocyte played a role in the inflammatory responses, and lymphopenia predicted adverse outcomes for patients. The aim of this study was to investigate whether lymphocyte count was associated with the incidence of intrapartum fever in nulliparous women undergoing vaginal delivery. METHODS: In this retrospective cohort study, electronic medical record data at the International Peace Maternity and Child Health Hospital (IPMCH, Shanghai, China) between 2012 and 2017 were extracted. The primary outcome of this study was baseline lymphocyte count in febrile and afebrile parturients who received labor epidural analgesia. Other confounding factors associated with the development of intrapartum fever were analyzed using multivariable logistic regression. RESULTS: The final study population consisted of 36,562 parturients, of whom 18,952 (51.8%) received labor epidural analgesia. Labor epidural analgesia was associated with an increased risk of maternal fever [relative risk: 4.55; 95% confidence interval (CI): 4.16-4.98; P<0.001]. Among the parturients who received epidural analgesia, both baseline lymphocyte count and lymphocyte percentage were lower in the febrile patients than those in the afebrile patients (P<0.001; P=0.015). The lower (<1.1×109/L) baseline lymphocyte was associated with a higher risk of maternal fever (adjusted odds ratio: 1.30, 95% CI: 1.14-1.48; P<0.001). CONCLUSIONS: Our results suggested that lower lymphocyte baseline indicated an increased risk of maternal fever during epidural analgesia-involved labor. Further studies are needed to confirm the findings and determine the potential mechanisms.

Antioxidant and Pro-Oxidant Activities of Melatonin in the Presence of Copper and Polyphenols In Vitro and In Vivo.

Melatonin is a well-documented antioxidant. Physicochemical analysis using the density functional theory suggests that melatonin is a copper chelating agent; however, experimental evidence is still in demand. The present study investigated the influence of melatonin on reactive oxygen species (ROS) generated from polyphenol autoxidation in the presence of copper. Surprisingly, we found that melatonin paradoxically enhanced ROS formation in a redox system containing low concentrations of copper and quercetin (Que) or (-)-epigallocatechin-3-gallate (EGCG), due to reduction of cupric to cuprous ion by melatonin. Addition of DNA to this system inhibited ROS production, because DNA bound to copper and inhibited copper reduction by melatonin. When melatonin was added to a system containing high concentrations of copper and Que or EGCG, it diminished hydroxyl radical formation as expected. Upon addition of DNA to high concentrations of copper and Que, this pro-oxidative system generated ROS and caused DNA damage. The DNA damage was not prevented by typical scavengers of hydroxyl radical DMSO or mannitol. Under these conditions, melatonin or bathocuproine disulfonate (a copper chelator) protected the DNA from damage by chelating copper. When melatonin was administered intraperitoneally to mice, it inhibited hepatotoxicity and DNA damage evoked by EGCG plus diethyldithiocarbamate (a copper ionophore). Overall, the present study demonstrates the pro-oxidant and antioxidant activities of melatonin in the redox system of copper and polyphenols. The pro-oxidant effect is inhibited by the presence of DNA, which prevents copper reduction by melatonin. Interestingly, in-vivo melatonin protects against copper/polyphenol-induced DNA damage probably via acting as a copper-chelating agent rather than a hydroxyl radical scavenger. Melatonin with a dual function of scavenging hydroxyl radical and chelating copper is a more reliable DNA guardian than antioxidants that only have a single function of scavenging hydroxyl radical.

Effects of Propofol General Anesthesia on Olfactory Relearning.

How general anesthesia interferes with sensory processing to cause amnesia remains unclear. Here, we show that activation of a learning-associated immediate early gene in rat olfactory cortices is uninterrupted by propofol, an intravenous general anesthetic with putative actions on the inhibitory GABAA receptors. Once learned under anesthesia, a novel odor can no longer re-activate the same high-level transcription programming during subsequent conscious relearning. Behavioral tests indicate that the animals' ability to consciously relearn a pure odorant, first experienced under general anesthesia, is indeed compromised. In contrast, when a mixture of two novel odorants is first experienced under anesthesia and then relearned consciously in pairs with one of the components, the animals show a deficit in relearning only the component but not the mixture. Our results reveal a previously unknown mechanism of unconscious memory due to irreplaceable neuronal commitment under general anesthesia and support the notion that general anesthesia acts at stages beyond cellular coding to disrupt sensory integration for higher-order association.

Immune Modulation by Volatile Anesthetics.

Volatile general anesthetics continue to be an important part of clinical anesthesia worldwide. The impact of volatile anesthetics on the immune system has been investigated at both mechanistic and clinical levels, but previous studies have returned conflicting findings due to varied protocols, experimental environments, and subject species. While many of these studies have focused on the immunosuppressive effects of volatile anesthetics, compelling evidence also exists for immunoactivation. Depending on the clinical conditions, immunosuppression and activation due to volatile anesthetics can be either detrimental or beneficial. This review provides a balanced perspective on the anesthetic modulation of innate and adaptive immune responses as well as indirect effectors of immunity. Potential mechanisms of immunomodulation by volatile anesthetics are also discussed. A clearer understanding of these issues will pave the way for clinical guidelines that better account for the impact of volatile anesthetics on the immune system, with the ultimate goal of improving perioperative management.

Inhibition of PARP-1 participates in the mechanisms of propofol-induced amnesia in mice and human.

Poly(ADP-ribose) polymerase 1 (PARP-1) has emerged as an important regulator in learning and memory. Propofol leads to amnesia, however, the mechanism remains unclear. The present study was designed to examine whether and how PARP-1 plays a role in propofol-induced amnesia. Mice were injected intraperitoneally with propofol before acquisition training. Cognitive function was evaluated by object recognition test. PARP-1 and PAR expression was determined through Western blot. The protein and mRNA levels of Arc and c-Fos were detected by Western blot and real-time PCR. Thirty volunteers were assigned to three groups according to codon 762 variation of PARP-1 gene (rs1136410). They learned word lists awake and during propofol sedation. Their cognitive traits were evaluated through fMRI. Rodent data demonstrated that propofol inhibited acquisition-induced increase in PARP-1 and PAR, thereby suppressing Arc and c-Fos, which impaired object recognition 24h after learning. Consistent with this, carriers of a low-catalyzing function PARP-1 variant (Val762Ala) exhibited decreased retrieval-induced hippocampal reactivity 24h after learning under propofol-sedative condition. These findings suggested that inhibition of PARP-1 might participate in the mechanism of propofol-induced amnesia in mice and human. More generally, our approach illustrated a potential translational research bridging animal models and human studies.

Location- and Subunit-Specific NMDA Receptors Determine the Developmental Sevoflurane Neurotoxicity Through ERK1/2 Signaling.

It is well established that developmental exposure of sevoflurane (an inhalational anesthetic) is capable of inducing neuronal apoptosis and subsequent learning and memory disorders. Synaptic NMDA receptors activity plays an essential role in cell survival, while the extra-synaptic NMDA receptors activation is usually associated with cell death. However, whether synaptic or extra-synaptic NMDA receptors mediate developmental sevoflurane neurotoxicity is largely unknown. Here, we show that developmental sevoflurane treatment decreased NR2A, but increased NR2B subunit expression both in vitro and in vivo. Sevoflurane-induced neuronal apoptosis was attenuated by synaptic NMDA receptors activation or low dose of exogenous NMDA in vitro. Interestingly, these effects could be abolished by NR2A inhibitor PEAQX, but not NR2B inhibitor Ifenprodil in vitro. In contrast, activation of extra-synaptic NMDA receptors alone had no effects on sevoflurane neurotoxicity. In the scenario of extra-synaptic NMDA receptors stimulation, however, sevoflurane-induced neuronal apoptosis could be prevented by addition of Ifenprodil, but not by PEAQX in vitro. In addition, sevoflurane neurotoxicity could also be rescued by memantine, an uncompetitive antagonist for preferential blockade of extra-synaptic NMDA receptors both in vitro and in vivo. Furthermore, we found that developmental sevoflurane-induced phospho-ERK1/2 inhibition was restored by synaptic NMDA receptor activation (in vitro), low dose of NMDA (in vitro) or memantine (in vivo). And the neuroprotective role of synaptic NMDA activity was able to be reversed by MEK1/2 inhibitor U0126 in vitro. Finally, administration of memantine or NMDA significantly improved spatial learning and memory dysfunctions induced by developmental sevoflurane exposure without influence on locomotor activity. These results indicated that activation of synaptic NR2A-containing NMDA receptors, or inhibition of extra-synaptic NR2B-containing NMDA receptors contributed to the relief of sevoflurane neurotoxicity, and the ERK1/2 MAPK signaling may be involved in this process.

Propofol Provides More Effective Protection for Circulating Lymphocytes Than Sevoflurane in Patients Undergoing Off-Pump Coronary Artery Bypass Graft Surgery.

OBJECTIVES: To compare the effects of propofol, sevoflurane, and the combination of the 2 on circulating lymphocytes in patients undergoing off-pump coronary artery bypass graft (OPCAB) surgery. DESIGN: A prospective, randomized study. SETTING: A university hospital. PARTICIPANTS: One hundred five patients undergoing elective OPCAB surgery. INTERVENTIONS: Participants were randomized to receive sevoflurane (group S), propofol (group P), or coadministration (group C) of sevoflurane- and propofol-maintained anesthesia. MEASUREMENTS AND MAIN RESULTS: Blood samples were obtained before, during, and after surgery. Caspase-3 and apoptosis-inducing factor in lymphocytes were evaluated by Western blot. During surgery, 5 minutes after revascularization of the left anterior descending artery, 5 minutes after all anastomoses (T4), and after the sternal closure (T5), caspase-3 expression of group S was higher than that of group P (p = 0.02) and group C (p = 0.02). At T4 and T5, expression of active apoptosis-inducing factor in group S was higher than that in the other 2 groups (p = 0.03 and p = 0.04, respectively). 24 hours after surgery, the lymphocyte count of group S (0.55/nL) was lower than that of group P (0.73/nL, p = 0.02) and group C (0.73/nL, p = 0.03). Intensive care unit stay of group S (3.0 days) was longer than that of the other 2 groups (2.2 days, p = 0.02 and 2.1 days, p = 0.01). CONCLUSIONS: OPCAB surgery was associated with postoperative lymphopenia. Regarding a protective effect for circulating lymphocytes, propofol and the combination of sevoflurane- and propofol-maintained anesthesia were both superior to sevoflurane-maintained anesthesia.

Inhibition of aberrant cyclin-dependent kinase 5 activity attenuates isoflurane neurotoxicity in the developing brain.

Aberrant CDK5 activity is implicated in a number of neurodegenerative disorders. Isoflurane exposure leads to neuronal apoptosis, and subsequent learning and memory defects in the developing brain. The present study was designed to examine whether and how CDK5 activity plays a role in developmental isoflurane neurotoxicity. Rat pups and hippocampal neuronal cultures were exposed to 1.5% isoflurane for 4 h. The protein and mRNA levels of CDK5, p35 and p25 were detected by western blot and QReal-Time PCR. CDK5 activity was evaluated in vitro using Histone H1 as a substrate. Roscovitine (an inhibitor of CDK5) was applied before isoflurane treatment, cleaved Caspase-3, Bcl-2, Bax, MEF2 and phospho-MEF2A-Ser-408 expressions were determined. Dominant-Negative CDK5 was transfected before isoflurane treatment. Neuronal apoptosis was evaluated by Flow cytometry (FCM) and TUNEL-staining. Cognitive functions were assessed by Morris water maze. We found that isoflurane treatment led to an aberrant CDK5 activation due to its activator p25 that was cleaved from p35 by calpain. Inhibition of CDK5 activity with Roscovitine enhanced Bcl-2, and decreased cleaved Caspase-3 and Bax expressions. In addition, isoflurane exposure resulted in a decrease of MEF2 and increase of phospho-MEF2A-Ser-408, which were rescued by Roscovitine or Dominant-Negative CDK5 transfection. Dominant-Negative CDK5 transfection also decreased the percentage of TUNEL-positive cells in isoflurane neurotoxicity. Moreover, Roscovitine remarkably alleviated the learning and memory deficits induced by postnatal isoflurane exposure. These results indicated that aberrant CDK5 activity-dependent MEF2 phosphorylation mediates developmental isoflurane neurotoxicity. Inhibition of CDK5 overactivation contributes to the relief of isoflurane neurotoxicity in the developing brain.

Using small RNA sequences to diagnose, sequence, and investigate the infectivity characteristics of vegetable-infecting viruses.

In a virus-infected plant, small interfering RNAs (siRNAs) corresponding to the viral genome form a large proportion of the small RNA population. It is possible to reassemble significant portions of the virus sequence from overlapping siRNA sequences and use these to identify the virus. We tested this technique with a resistance-breaking and a non-resistance-breaking strain of tomato spotted wilt virus (TSWV). We were able to assemble contigs covering 99% of the genomes of both viruses. The abundance of TSWV siRNAs allowed us to detect TSWV at early time points before the onset of symptoms, at levels too low for conventional detection. Combining traditional and bioinformatic detection methods, we also measured how replication of the resistance-breaking strain differed from the non-resistance-breaking strain in susceptible and resistant tomato varieties. We repeated this technique in identification of a squash-infecting geminivirus and also used it to identify an unspecified tospovirus.