Application of stacked autoencoder for identification of bone fracture.

This study presents a stacked autoencoder (SAE)-based assessment method which is one of the unsupervised learning schemes for the investigation of bone fracture. Relatively accurate health monitoring of bone fracture requires considering physical interactions among tissue, muscle, wave propagation and boundary conditions inside the human body. Furthermore, the investigation of fracture, crack and healing process without state-of-the-art medical devices such as CT, X-ray and MRI systems is challenging. To address these issues, this study presents the SAE method that incorporates bilateral symmetry of the human legs and low-frequency transverse vibration. To verify the presented method, several examples are employed with plastic pipes, cadaver legs and human legs. Virtual spectrograms, created by applying a short-time Fourier transform to the differences in vibration responses, are employed for image-based training in SAE. The virtual spectrograms are then classified and the fine-tuning is also carried out to increase the accuracy. Moreover, a confusion matrix is employed to evaluate classification accuracy and training validity.

Diagnostic Accuracy of Microdialysis in Postoperative Flap Monitoring.

Postoperative monitoring plays an important role in achieving success in microvascular free tissue transfer. A systematic review was designed to evaluate the clinical outcomes of microdialysis in flap monitoring and a meta-analysis was conducted for diagnostic accuracies. The search terms "microdialysis" and "flap" were used in a PubMed and Scopus search, resulting in 60 and 78 results, respectively. Among 78 titles, 15 articles were excluded. Among 63 abstracts, 43 abstracts were excluded. From 20 full texts, 7 articles were excluded because they did not have sufficient content (ie, the statistical values in question). A systematic review was conducted of the final 13 articles. The overall sensitivity was 97.24% [95% confidence interval (CI)=93.67%-99.10%]. Eleven of the 13 studies showed 100% sensitivity and 2 studies had 2 and 3 false negative results, resulting in sensitivity values of 85.8% and 95.3%. Specificity ranged from 91.89% to 100%, and the overall value was 98.15% (95% CI=96.80%-99.04%). The positive predictive value ranged from 84.62% to 100%, with an overall value of 93.62% (95% CI=89.33%-96.26%). The negative predictive value ranged from 94.44% to 100%, with an overall value of 99.22% (95% CI=98.17%-99.67%). The overall flap success rate (survival rate) was 93.7% (786/839). The lowest flap survival rate was 86.7% and the highest was 100%. Microdialysis provides excellent diagnostic accuracy and enables the early detection of ischemia in postoperative flap monitoring. Although microdialysis is not the most popular choice among surgeons, it should be considered adjacent to conventional clinical monitoring. Cost-effectiveness, availability, and ease of application remain hurdles.

Experimental study of the effect of the boundary conditions of fractured bone.

Reliable fracture diagnosis monitoring and analyzing low-frequency transverse vibration data can be achieved through an in-depth understanding of the physical interactions between wave propagation and boundary conditions. The present study aims to investigate the effects of the boundary conditions on the low-frequency structural vibrations of bones. Time-frequency domain analysis of transverse vibration signals depending on the boundary conditions of bones is analyzed and investigated. These studies reveal that the responses of fractured or non-fractured bones are different and influenced by the displacement and force boundary conditions. These relationships can be considered in the development of a smart fracture diagnosis system considering the posture and boundary condition. To validate the present observations, the experiments with artificial specimens and cadaver are carried.

Investigation of bone fracture diagnosis system using transverse vibration response.

In this study, a new diagnostic system is developed to easily identify bone fractures in non-medical environments. It is difficult to determine the extent of cracks, fractures, and the healing process inside humans owing to the differences among people and limitations of state-of-the-art medical devices. Thus, various medical techniques, such as X-ray, computed tomography, or fork tuning systems have been developed, and more advanced technologies are emerging in the medical engineering field. In hazardous circumstances, medical devices to detect bone fracture are not available or cannot be easily applied. Thus, there is a need for the rapid detection of bone fractures without medical devices. To this end, this study analyzes the transverse vibration responses of bones because bone fractures cause different mechanical vibration reactions. By comparing the transverse vibration responses of both healthy and fractured bones, the modal assurance criterion can be calculated and applied to detect the existence of bone fractures. The transverse vibration responses at low and high frequencies are different and exhibit different modal assurance criteria depending on whether or not they are abnormal. Then, the virtual spectrogram of the differences between the signals from non-fractured and fractured bones is calculated. With the help of the present criterion with transverse vibration data, this difference can be analyzed quantitatively and effectively. To validate the proposed system, experiments with artificial specimens, animal legs, and a cadaver are performed.

Neuroprotective effects of hydrogen inhalation in an experimental rat intracerebral hemorrhage model.

OBJECTIVE: Hydrogen inhalation has been found to be neuroprotective and anti-oxidative in several brain injury models. Building on these studies, we investigated potential neuroprotective effects of hydrogen inhalation in a rat model of intracerebral hemorrhage (ICH), focusing on apoptosis and inflammation. METHODS: Forty-five 8-week-old male Sprague-Dawley rats were randomly divided into three groups (n = 15 per each group): a sham group, ICH group, and ICH + hydrogen group. Induction of ICH was performed via injection of 0.23 U of bacterial collagenase type IV into the left striatum. Hydrogen was administered via spontaneous inhalation. Mortality and neurologic deficits were investigated at 6, 24, and 48 h after ICH. To investigate the antioxidative activity of hydrogen gas, the expression of malondialdehyde was measured. Real-time polymerase chain reaction analyses of TNF-a, IL-1b, BDNF, and caspase-3 expression were used to detect anti-inflammatory and anti-apoptotic effects. Neuroprotective effect was evaluated by immunohistochemical and TUNEL staining. RESULT: At 6, 24 and 48 h post-intracerebral hemorrhage, animals showed brain edema and neurologic deficits, accompanied by up-regulation of TNF-a, IL-b, BDNF, and caspase-3, which is indicative of neuroinflammation, neuroprotection, and apoptosis. Hydrogen treatment significantly reduced the level of oxidative stress, neuroinflammation, neuronal damage, and apoptosis-related genes. This was accompanied by increased neurogenesis and expression of growth factor-related genes at <24 h, but not 48 h, after ICH. CONCLUSION: H2 gas administration exerted a neuroprotective effect against early brain injury after ICH through anti-inflammatory, neuroprotective, anti-apoptotic, and antioxidative activity.

Gα12 overexpression induced by miR-16 dysregulation contributes to liver fibrosis by promoting autophagy in hepatic stellate cells.

BACKGROUND & AIMS: Hepatic stellate cells (HSCs) have a role in liver fibrosis. Guanine nucleotide-binding α-subunit 12 (Gα12) converges signals from G-protein-coupled receptors whose ligand levels are elevated in the environment during liver fibrosis; however, information is lacking on the effect of Gα12 on HSC trans-differentiation. This study investigated the expression of Gα12 in HSCs and the molecular basis of the effects of its expression on liver fibrosis. METHODS: Gα12 expression was assessed by immunostaining, and immunoblot analyses of mouse fibrotic liver tissues and primary HSCs. The role of Gα12 in liver fibrosis was estimated using a toxicant injury mouse model with Gα12 gene knockout and/or HSC-specific Gα12 delivery using lentiviral vectors, in addition to primary HSCs and LX-2 cells using microRNA (miR) inhibitors, overexpression vectors, or adenoviruses. miR-16, Gα12, and LC3 were also examined in samples from patients with fibrosis. RESULTS: Gα12 was overexpressed in activated HSCs and fibrotic liver, and was colocalised with desmin. In a carbon tetrachloride-induced fibrosis mouse model, Gα12 ablation prevented increases in fibrosis and liver injury. This effect was attenuated by HSC-specific lentiviral delivery of Gα12. Moreover, Gα12 activation promoted autophagy accompanying c-Jun N-terminal kinase-dependent ATG12-5 conjugation. In addition, miR-16 was found to be a direct inhibitor of the de novo synthesis of Gα12. Modulations of miR-16 altered autophagy in HSCs. In a fibrosis animal model or patients with severe fibrosis, miR-16 levels were lower than in their corresponding controls. Consistently, cirrhotic patient liver tissues showed Gα12 and LC3 upregulation in desmin-positive areas. CONCLUSIONS: miR-16 dysregulation in HSCs results in Gα12 overexpression, which activates HSCs by facilitating autophagy through ATG12-5 formation. This suggests that Gα12 and its regulatory molecules could serve as targets for the amelioration of liver fibrosis. LAY SUMMARY: Guanine nucleotide-binding α-subunit 12 (Gα12) is upregulated in activated hepatic stellate cells (HSCs) as a consequence of the dysregulation of a specific microRNA that is abundant in HSCs, facilitating the progression of liver fibrosis. This event is mediated by c-Jun N-terminal kinase-dependent ATG12-5 formation and the promotion of autophagy. We suggest that Gα12 and its associated regulators could serve as new targets in HSCs for the treatment of liver fibrosis.

Hepcidin inhibits Smad3 phosphorylation in hepatic stellate cells by impeding ferroportin-mediated regulation of Akt.

Hepatic stellate cell (HSC) activation on liver injury facilitates fibrosis. Hepatokines affecting HSCs are largely unknown. Here we show that hepcidin inhibits HSC activation and ameliorates liver fibrosis. We observe that hepcidin levels are inversely correlated with exacerbation of fibrosis in patients, and also confirm the relationship in animal models. Adenoviral delivery of hepcidin to mice attenuates liver fibrosis induced by CCl4 treatment or bile duct ligation. In cell-based assays, either hepcidin from hepatocytes or exogenous hepcidin suppresses HSC activation by inhibiting TGFß1-mediated Smad3 phosphorylation via Akt. In activated HSCs, ferroportin is upregulated, which can be prevented by hepcidin treatment. Similarly, ferroportin knockdown in HSCs prohibits TGFß1-inducible Smad3 phosphorylation and increases Akt phosphorylation, whereas ferroportin over-expression has the opposite effect. HSC-specific ferroportin deletion also ameliorates liver fibrosis. In summary, hepcidin suppresses liver fibrosis by impeding TGFß1-induced Smad3 phosphorylation in HSCs, which depends on Akt activated by a deficiency of ferroportin.

Neonatal diffusion tensor brain imaging predicts later motor outcome in preterm neonates with white matter abnormalities.

BACKGROUND: White matter (WM) abnormalities associated with prematurity are one of the most important causes of neurological disability that involves spastic motor deficits in preterm newborns. This study aimed to evaluate regional microstructural changes in diffusion tensor imaging (DTI) associated with WM abnormalities. METHODS: We prospectively studied extremely low birth weight (ELBW; <1000 g) preterm infants who were admitted to the Neonatal Intensive Care Unit of Hanyang University Hospital between February 2011 and February 2014. WM abnormalities were assessed with conventional magnetic resonance (MR) imaging and DTI near term-equivalent age before discharge. Region-of-interests (ROIs) measurements were performed to examine the regional distribution of fractional anisotropy (FA) values. RESULTS: Thirty-two out of 72 ELBW infants underwent conventional MR imaging and DTI at term-equivalent age. Ten of these infants developed WM abnormalities associated with prematurity. Five of ten of those with WM abnormalities developed cerebral palsy (CP). DTI in the WM abnormalities with CP showed a significant reduction of mean FA in the genu of the corpus callosum (p = 0.022), the ipsilateral posterior limb of the internal capsule (p = 0.019), and the ipsilateral centrum semiovale (p = 0.012) compared to normal WM and WM abnormalities without CP. In infants having WM abnormalities with CP, early FA values in neonatal DTI revealed abnormalities of the WM regions prior to the manifestation of hemiparesis. CONCLUSIONS: DTI performed at term equivalent age shows different FA values in WM regions among infants with or without WM abnormalities associated with prematurity and/or CP. Low FA values of ROIs in DTI are related with later development of spastic CP in preterm infants with WM abnormalities.

Changes in Neuroglial Activity in Multiple Spinal Segments after Caudal Epidural Pulsed Radiofrequency in a Rat Model of Lumbar Disc Herniation.

BACKGROUND: Herniated lumbar discs can induce sciatica by mechanical compression and/or chemical irritation. It was recently reported that neuroglial cellular activity after pulsed radiofrequency (PRF) application to a single dorsal root ganglion (DRG) attenuated neuroglial activity at the corresponding spinal dorsal horn. Recently, caudal epidural PRF has been used to manage neuropathic pain, but evidence of molecular changes after the administration of caudal epidural PRF to attenuate neuropathic pain is lacking, and it has not been determined whether caudal epidural PRF affects neuroglial activity at different spinal levels. OBJECTIVES: Using immunohistochemical methods in a rat model of lumbar disc herniation, the authors investigated the effects of caudal epidural PRF administration on pain-related behavior, on the activations of microglia and astrocytes in spinal cord, and on the expressions of calcitonin gene-related peptide (CGRP) and Transient receptor potential vanilloid 1(TRPV1) in the DRG at the L3, L4, L5, L6, and S1 levels. STUDY DESIGN: Controlled animal trial. SETTING: University hospital laboratory. METHODS: Forty-five Sprague-Dawley rats were randomly assigned to a sham-operated group (n = 10) or a nucleus pulposus (NP)-exposed group (n = 35). Rats in the NP-exposed group were further subdivided into a NP-exposed with sham stimulation group (the NP-nonPRF group; n = 13) or a NP exposed with caudal epidural PRF stimulation group (the NP-PRF group; n = 22). Pulsed radiofrequency was administered on postoperative day 10 (POD 10) by placing an electrode in the caudal epidural space through the sacral hiatus and administering 5 Hz of PRF current for 600 seconds (maximum tip temperature 42°C). Rats were tested for mechanical allodynia on POD 10 and on days 7 and 14 after caudal epidural PRF administration (post-PRF). At 14 days post-PRF, sections of the spinal cord from L3, L4, L5, L6, and S1 were immunostained for ionized calcium-binding adapter molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP), and DRGs from the same levels were immunostained for CGRP and TRPV1. RESULTS: Mechanical withdrawal thresholds increased at 7 days post-PRF (P = 0.04), and the immunohistochemical expression of Iba1 in the L5 spinal dorsal horn and of CGRP in the L5 DRG were quantitatively reduced (P < 0.001) at 14 days post-PRF. Furthermore, the upregulations of Iba1 at L3, L4, L6, and S1 dorsal horns and CGRP at L6 DRG were also attenuated by caudal epidural PRF (P < 0.001). LIMITATION: We examined molecular changes only in ipsilateral lumbar regions and at 14 days post-PRF. CONCLUSION: Caudal epidural PRF reduced mechanical allodynia and downregulated microglia activity and CGRP expression at the lumbar disc herniated level and in adjacent lumbar spinal levels in a rat model of lumbar disc herniation.Key words: Caudal, pulsed radiofrequency, multisegmental, lumbar disc herniation, microglia, calcitonin gene-related peptide.

Changes in the Expressions of Iba1 and Calcitonin Gene-Related Peptide in Adjacent Lumbar Spinal Segments after Lumbar Disc Herniation in a Rat Model.

Lumbar disc herniation is commonly encountered in clinical practice and can induce sciatica due to mechanical and/or chemical irritation and the release of proinflammatory cytokines. However, symptoms are not confined to the affected spinal cord segment. The purpose of this study was to determine whether multisegmental molecular changes exist between adjacent lumbar spinal segments using a rat model of lumbar disc herniation. Twenty-nine male Sprague-Dawley rats were randomly assigned to either a sham-operated group (n=10) or a nucleus pulposus (NP)-exposed group (n=19). Rats in the NP-exposed group were further subdivided into a significant pain subgroup (n=12) and a no significant pain subgroup (n=7) using mechanical pain thresholds determined von Frey filaments. Immunohistochemical stainings of microglia (ionized calcium-binding adapter molecule 1; Iba1), astrocytes (glial fibrillary acidic protein; GFAP), calcitonin gene-related peptide (CGRP), and transient receptor potential vanilloid 1 (TRPV1) was performed in spinal dorsal horns and dorsal root ganglions (DRGs) at 10 days after surgery. It was found immunoreactivity for Iba1-positive microglia was higher in the L5 (P=0.004) dorsal horn and in the ipsilateral L4 (P=0.009), L6 (P=0.002), and S1 (P=0.002) dorsal horns in the NP-exposed group than in the sham-operated group. The expression of CGRP was also significantly higher in ipsilateral L3, L4, L6, and S1 segments and in L5 DRGs at 10 days after surgery in the NP-exposed group than in the sham-operated group (P<0.001). Our results indicate that lumbar disc herniation upregulates microglial activity and CGRP expression in many adjacent and ipsilateral lumbar spinal segments.

Ideal or Young-Looking Brow Height and Arch Shape Preferred by Koreans.

The aim of this study is to see which brow height and arch shape is preferred as ideal or young-looking by Koreans. A survey was conducted between June and Dec 2014 on 186 women who visited the brow bar ("Benefit" of Incheon city). They were asked to choose which they believed ideal and youngest amongst the 3 brow archetypes according to their height and 4 types of modification of Anastasia (rotation of medial and lateral arms), which was illustrated. Approximately half (52.5%) of the respondents answered that their brow matches them very well or well. Most (81.2%) believed there might be a method to yield an ideal brow archetype and almost all (97.3%) would change the brow shape if the expert advised. The most preferred ideal brow height was of a middle height (63.2%, the distance from the lateral canthus to the lateral end of eyebrow, which was 2/3 of the eye width). The most preferred ideal brow arch shape was the arched type (57.6% arches on a line drawn from the center of the nose through the center of the pupil). The most preferred young-looking brow height was of an upper height (46.2%, the distance from the lateral canthus to the lateral end of eyebrow was 3/4 of the eye width) followed by a middle height (39.7%). The most preferred young-looking brow arch shape was the head-up position (53.3%, medial arm of the brow was rotated upward to the horizontal plane). The result of this study might be useful in facial rejuvenation surgeries as well as in brow esthetics or tattooing of the eyebrows.

Skin tension related to tension reduction sutures.

The aim of this study was to compare the skin tension of several fascial/subcutaneous tensile reduction sutures. Six upper limbs and 8 lower limbs of 4 fresh cadavers were used. At the deltoid area (10 cm below the palpable acromion) and lateral thigh (midpoint from the palpable greater trochanter to the lateral border of the patella), and within a 3 × 6-cm fusiform area of skin, subcutaneous tissue defects were created. At the midpoint of the defect, a no. 5 silk suture was passed through the dermis at a 5-mm margin of the defect, and the defect was approximated. The initial tension to approximate the margins was measured using a tensiometer.The tension needed to approximate skin without any tension reduction suture (S) was 6.5 ± 4.6 N (Newton). The tensions needed to approximate superficial fascia (SF) and deep fascia (DF) were 7.8 ± 3.4 N and 10.3 ± 5.1 N, respectively. The tension needed to approximate the skin after approximating the SF was 4.1 ± 3.4 N. The tension needed to approximate the skin after approximating the DF was 4.9 ± 4.0 N. The tension reduction effect of approximating the SF was 38.8 ± 16.4% (2.4 ± 1.5 N, P = 0.000 [ANOVA, Scheffé]). The tension reduction effect of approximating the DF was 25.2% ± 21.9% (1.5 ± 1.4 N, P = 0.001 [ANOVA, Scheffé]). The reason for this is thought to be that the SF is located closely to the skin unlike the DF. The results of this study might be a basis for tension reduction sutures.

Discovery of an integrative network of microRNAs and transcriptomics changes for acute kidney injury.

The contribution of miRNA to the pathogenesis of acute kidney injury (AKI) is not well understood. Here we evaluated an integrative network of miRNAs and mRNA data to discover a possible master regulator of AKI. Microarray analyses of the kidneys of mice treated with cisplatin were used to extract putative miRNAs that cause renal injury. Of them, miR-122 was mostly downregulated by cisplatin, whereas miR-34a was upregulated. A network integrating dysregulated miRNAs and altered mRNA expression along with target prediction enabled us to identify Foxo3 as a core protein to activate p53. The miR-122 inhibited Foxo3 translation as assessed using an miR mimic, an inhibitor, and a Foxo3 3'-UTR reporter. In a mouse model, Foxo3 levels paralleled the degree of tubular injury. The role of decreased miR-122 in inducing Foxo3 during AKI was strengthened by the ability of the miR-122 mimic or inhibitor to replicate results. Increase in miR-34a also promoted the acetylation of Foxo3 by repressing Sirt1. Consistently, cisplatin facilitated the binding of Foxo3 and p53 for activation, which depended not only on decreased miR-122 but also on increased miR-34a. Other nephrotoxicants had similar effects. Among targets of p53, Phlda3 was robustly induced by cisplatin, causing tubular injury. Consistently, treatment with miR mimics and/or inhibitors, or with Foxo3 and Phlda3 siRNAs, modulated apoptosis. Thus, our results uncovered an miR integrative network regulating toxicant-induced AKI and identified Foxo3 as a bridge molecule to the p53 pathway.

Effects of DA-9701, a novel prokinetic agent, on phosphorylated extracellular signal-regulated kinase expression in the dorsal root ganglion and spinal cord induced by colorectal distension in rats.

BACKGROUND/AIMS: DA-9701, a standardized extract of Pharbitis Semen and Corydalis Tuber, is a new prokinetic agent that exhibits an analgesic effect on the abdomen. We investigated whether DA-9701 affects visceral pain induced by colorectal distension (CRD) in rats. METHODS: A total of 21 rats were divided into three groups: group A (no CRD+no drug), group B (CRD+no drug), and group C (CRD+DA-9701). Expression of pain-related factors, substance P (SP), c-fos, and phosphorylated extracellular signal-regulated kinase (p-ERK) in the dorsal root ganglion (DRG) and spinal cord was determined by immunohistochemical staining and Western blotting. RESULTS: The proportions of neurons in the DRG and spinal cord expressing SP, c-fos, and p-ERK were higher in group B than in group A. In the group C, the proportion of neurons in the DRG and spinal cord expressing p-ERK was lower than that in group B. Western blot results for p-ERK in the spinal cord indicated a higher level of expression in group B than in group A and a lower level of expression in group C than in group B. CONCLUSIONS: DA-9701 may decrease visceral pain via the downregulation of p-ERK in the DRG and spinal cord.

Mitigation of carbon tetrachloride-induced hepatic injury by methylene blue, a repurposed drug, is mediated by dual inhibition of GSK3ß downstream of PKA.

BACKGROUND AND PURPOSE: Methylene blue (MB) has recently been considered for new therapeutic applications. In this study, we investigated whether MB has antioxidant and mitochondria-protecting effects and can prevent the development of toxicant-induced hepatitis. In addition, we explored the underlying basis of its effects. EXPERIMENTAL APPROACH: Blood biochemistry and histopathology were assessed in mice injected with CCl4 (0.5 mL·kg(-1)) following MB administration (3 mg·kg(-1) ·day(-1), 3 days). Immunoblottings were performed to measure protein levels. Cell survival, H2 O2 , and mitochondrial superoxide and membrane permeability transition were determined in HepG2 cells. KEY RESULTS: MB protected cells from oxidative stress induced by arachidonic acid plus iron; it restored GSH content and decreased the production of H2 O2 . It consistently attenuated mitochondria dysfunction, as indicated by inhibition of superoxide production and mitochondrial permeability transition. MB inhibited glycogen synthase kinase-3ß (GSK3ß) and protected the liver against CCl4. Using siRNA, the inhibition of GSK3ß was shown to depend on AMPK. MB increased the activation of AMPK in vitro (3-24 h) and in vivo. MB also increased the phosphorylation of liver kinase B1 (LKB1) via cAMP-dependent PKA. SiRNA knockdown of LKB1 eliminated phosphorylation of AMPK and inhibited MB activation of AMPK. In addition, MB treatment (≤1 h) facilitated PKA-mediated GSK3ß serine phosphorylation independently of AMPK. CONCLUSIONS AND IMPLICATIONS: MB has antioxidant and mitochondria-protecting effects and protects the liver from toxicants, which results from the dual inhibition of GSK3ß by AMPK downstream of PKA-activated LKB1, and PKA itself. Our findings reveal a novel pharmacological effect of MB and its molecular basis.

Changes in pain behavior and glial activation in the spinal dorsal horn after pulsed radiofrequency current administration to the dorsal root ganglion in a rat model of lumbar disc herniation: laboratory investigation.

OBJECT: Herniated discs can induce sciatica by mechanical compression and/or chemical irritation caused by proinflammatory cytokines. Using immunohistochemistry methods in the dorsal horn of a rat model of lumbar disc herniation, the authors investigated the effects of pulsed radiofrequency (PRF) current administration to the dorsal root ganglion (DRG) on pain-related behavior and activation of microglia, astrocytes, and mitogen-activated protein kinase. METHODS: A total of 33 Sprague-Dawley rats were randomly assigned to either a sham-operated group (n = 10) or a nucleus pulposus (NP)-exposed group (n = 23). Rats in the NP-exposed group were further subdivided into NP exposed with sham stimulation (NP+sham stimulation, n = 10), NP exposed with PRF (NP+PRF, n = 10), or euthanasia 10 days after NP exposure (n = 3). The DRGs in the NP+PRF rats were exposed to PRF waves (2 Hz) for 120 seconds at 45 V on postoperative Day 10. Rats were tested for mechanical allodynia 10 days after surgery and at 8 hours, 1 day, 3 days, 10 days, 20 days, and 40 days after PRF administration. Immunohistochemical staining of astrocytes (glial fibrillary acidic protein), microglia (OX-42), and phosphorylated extracellular signal-regulated kinases (pERKs) in the spinal dorsal horn was performed at 41 days after PRF administration. RESULTS: Starting at 8 hours after PRF administration, mechanical withdrawal thresholds dramatically increased; this response persisted for 40 days (p < 0.05). After PRF administration, immunohistochemical expressions of OX-42 and pERK in the spinal dorsal horn were quantitatively reduced (p < 0.05). CONCLUSIONS: Pulsed radiofrequency administration to the DRG reduced mechanical allodynia and downregulated microglia activity and pERK expression in the spinal dorsal horn of a rat model of lumbar disc herniation.