Digital protractor as an intraoperative guide to cup anteversion in total hip arthroplasty.

INTRODUCTION: To explore if digital protractor could guide the anteversion of acetabular cup during primary THA and make it consistent with preoperative. METHODS: We retrospectively reviewed 172 cases of primary THA with direct anterior approach (DAA) over 2 years. The anteversion of acetabular cup were measured from computed tomography (CT) scan preoperative and de-identified plain radiographs postoperative by two blinded investigators who were not involved in the surgery. The effect of the digital protractor on the anteversion was determined using regression analysis. RESULTS: The mean anteversion for the THAs in digital protractor group was 15.5°and 21.4°in control group (P < 0.01). The mean anteversion bias for the THAs in digital protractor group was 1.59° and 6.63° in control group (P < 0.01).Regression analysis identified a 10.7% difference in anteversion due to the use of digital protractor (P < 0.01), and THAs performed without digital protractor were six times more likely to result in anteversion of > 25°. The correlation coefficient for the interobserver reliability of the measurement of the two investigators was 0.94. CONCLUSION: The digital protractor is a practical tool in the DAA for THA to determine the anteversion of the acetabular prosthesis.

Angelica sinensis polysaccharide improves mitochondrial metabolism of osteoarthritis chondrocytes through PPARγ/SOD2/ROS pathways.

Osteoarthritis (OA) is a common degenerative joint disease, which is characterized by wear of articular cartilage and narrow joint space, resulting in joint movement disorder. At present, accurate molecular mechanisms and effective interventions are still being explored. Here, we propose that angelica sinensis polysaccharide (ASP) alleviates OA progression by activating peroxisome proliferator-activated receptor gamma (PPARγ). Therapeutic effect of ASP improving mitochondrial metabolism of OA chondrocytes was evaluated in vitro and in vivo, respectively. During cell experiments, the concentration and time response of tert butyl hydroperoxide (TBHP) and ASP were determined by cell viability. Apoptosis was detected by flow cytometry. Mitochondrial metabolism was detected by reactive oxygen species (ROS), mitochondrial membrane potential (MMP), release of cytochrome C, adenosine triphosphate (ATP) production, and superoxide dismutase 2 (SOD2) activity. Expressions of Aggrecan, collagen type II (Col2a1), PPARγ, and SOD2 were detected by qRT-PCR and western blot. In animal experiments, we detected cell apoptosis and target protein expression separately through terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) staining and immunohistochemistry. Pretreatment of ASP significantly activated PPARγ and SOD2 in rat chondrocytes incubated with TBHP, cleared ROS, improved mitochondrial metabolism, increased chondrocytes viability, and alleviated chondrocytes apoptosis. In vivo, the administration of ASP could effectively ameliorate cartilage degeneration in OA rats, promote extracellular matrix synthesis, and decelerate the progress of OA. Our research identifies the role of ASP in mitochondrial metabolism of OA chondrocytes through PPARγ/SOD2/ROS pathways, which provides a new idea for the treatment of OA.

Microbially-Induced Calcium Carbonate Precipitation Test on Yellow Sandstone Based on LF-NMR Monitoring.

The microbially-induced calcium carbonate precipitation (MICP) technique has shown great robustness in dealing with soil and groundwater contamination problems. A typical result of the implementation of MICP technique is a change in the pore structure. In this study, the effects of MICP on the pore structure of yellow sandstone from the Zigong area, Sichuan, China under different conditions, (e.g., temperature, pH, and calcium ion concentration) are investigated using LF-NMR resonance. The pore network of yellow sandstone is accurately measured using the peak area of the T2 spectral signal. The distribution of calcium carbonate in the pores of the yellow sandstone is characterized by the magnitude of the T2 signal variation. The results show that the precipitation of calcium carbonate caused by MICP tends to be deposited in relatively large pores. However, the calcium carbonate precipitates in the smaller pores at a higher temperature. A higher pH considerably enhances the precipitation, and the alkaline environment tends to cause the precipitation of the calcium carbonate in the large pores. Although the amount of produced calcium carbonate continuously increases as the MCIP process continues, which is expected, the production efficiency decreases steadily.

Visualization of Flow-Induced Strain Using Structural Color in Channel-Free Polydimethylsiloxane Devices.

Measuring flow of gases is of fundamental importance yet is typically done with complex equipment. There is, therefore, a longstanding need for a simple and inexpensive means of flow measurement. Here, gas flow is measured using an extremely simple device that consists of an Ar plasma-treated polydimethylsiloxane (PDMS) slab adhered on a glass substrate with a tight seal. This device does not even have a channel, instead, gas can flow between the PDMS and the glass by deforming the PDMS wall, in other words, by making an interstice as a temporary path for the flow. The formation of the temporary path results in a compressive bending stress at the inner wall of the path, which leads to the formation of well-ordered wrinkles, and hence, the emergence of structural color that changes the optical transmittance of the device. Although it is very simple, this setup works sufficiently well to measure arbitrary gases and analyzes their flow rates, densities, and viscosities based on the change in color. It is also demonstrated that this technique is applicable to the flow-induced display of a pattern such as a logo for advanced applications.

Characterization and pre-clinical assessment of a proposed biosimilar to its originator Omalizumab.

Omalizumab is an anti-IgE monoclonal antibody (mAb) approved for the treatment of moderate-to-severe asthma. Herein, we report physicochemical, biological, pharmacological, and toxicological characteristics of an Omalizumab biosimilar mAb named KA. We show that KA and its originator present only minimum differences. Their charge heterogeneity and primary, secondary structures are similar. The two molecules are comparable regarding in vitro activity, including molecular binding and cell-based inhibition. Pharmacological and toxicological properties were assessed using a mouse model of allergy and cynomolgus monkeys, and we determined that the efficacy, safety, and pharmacokinetic characteristics of KA are comparable to its originator. Our data, which demonstrated that KA has similar activity to the Omalizumab reference product in relevant preclinical models, calls for a clinical evaluation of its bio-similarity.

Preclinical pharmacology and toxicology evaluation of an anti-CD52 monoclonal antibody produced by perfusion fermentation process.

Anti-cluster of differentiation 52 (CD52) monoclonal antibody (mAb) has been employed in the treatment of chronic lymphoblastic leukemia and multiple sclerosis. Previously we developed a perfusion process to produce the biosimilar mAb named "Mab-TH." A series of quality assessments was conducted in the fields of structural identification, purity analysis, and activity measurement. After these quality researches, this report laid emphasis on preclinical pharmacology and toxicology evaluation. Mab-TH was characterized in biological, pharmacological, and toxicological properties in comparison with the original drug, alemtuzumab. Binding activity and immune-dependent toxicity as in vitro activity were evaluated. Severe immunodeficient mice transplanted with a human leukemia cell line were also used as an in vivo pharmacological model and a 4-week repeated dosing study in cynomolgus monkeys was conducted to evaluate the safety differences. Our results demonstrated that Mab-TH, the anti-CD52 antibody generated by a perfusion process, had high similarity in in vitro and in vivo activities compared with alemtuzumab in relevant preclinical models. The results supported it as a biosimilar candidate for clinical evaluation.

PPARγ Attenuates Interleukin-1ß-Induced Cell Apoptosis by Inhibiting NOX2/ROS/p38MAPK Activation in Osteoarthritis Chondrocytes.

INTRODUCTION: Reactive oxygen species (ROS) induced by extracellular cytokines trigger the expression of inflammatory mediators in osteoarthritis (OA) chondrocyte. Peroxisome proliferator-activated receptor gamma (PPARγ) exerts an anti-inflammatory effect. The aim of this study was to elucidate the role of PPARγ in interleukin-1ß- (IL-1ß-) induced cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) expression through ROS generation in OA chondrocytes. METHODS: IL-1ß-induced ROS generation and chondrocyte apoptosis were determined by flow cytometry. Contents of NADPH oxidase (NOX), caspase-3, and caspase-9 were evaluated by biochemical detection. The involvement of NOX2 and mitogen-activated protein kinases (MAPKs) in IL-1ß-induced COX-2 and PGE2 expression was investigated using pharmacologic inhibitors and further analyzed by western blotting. Activation of PPARγ was performed by using a pharmacologic agonist and was analyzed by western blotting. RESULTS: IL-1ß-induced COX-2 and PGE2 expression was mediated through NOX2 activation/ROS production, which could be attenuated by N-acetylcysteine (NAC; a scavenger of ROS), GW1929 (PPARγ agonist), DPI (diphenyleneiodonium chloride, NOX2 inhibitor), SB203580 (p38MAPK inhibitor), PD98059 (extracellular signal-regulated kinase, ERK inhibitor), and SP600125 (c-Jun N-terminal kinase, JNK inhibitor). ROS activated p38MAPK to enter the nucleus, which was attenuated by PPARγ. CONCLUSION: In OA chondrocytes, IL-1ß induced COX-2 and PGE2 expression via activation of NOX2, which led to ROS production and MAPK activation. The activation of PPARγ exerted protective roles in the pathogenesis of OA.

Polysaccharide from Angelica sinensis attenuates SNP-induced apoptosis in osteoarthritis chondrocytes by inducing autophagy via the ERK1/2 pathway.

OBJECTIVE: Chondrocyte apoptosis plays a vital role in osteoarthritis (OA) progression. Angelica sinensis polysaccharide (ASP), a traditional Chinese medicine, possesses anti-inflammatory and anti-apoptotic properties in chondrocytes. This study aimed to determine the protective role of ASP on sodium nitroprusside (SNP)-induced chondrocyte apoptosis, and explore the underlying mechanism. METHOD: Human primary chondrocytes isolated from the articular cartilage of OA patients were treated with SNP alone or in combination with different doses of ASP. Cell viability and apoptosis were assessed, and apoptosis-related proteins including Bcl-2 and Bax were detected. Autophagy levels were evaluated by light chain 3 (LC3) II immunofluorescence staining, mRFP-GFP-LC3 fluorescence localization, and western blot (LC3II, p62, Beclin-1, Atg5). Meanwhile, activation of the ERK 1/2 pathway was determined by western blot. The autophagy inhibitors, 3-methyladenine (3-MA), chloroquine (CQ), and a specific inhibitor of ERK1/2, SCH772984, were used to confirm the autophagic effect of ASP. RESULTS: The results showed that SNP-induced chondrocyte apoptosis was significantly rescued by ASP, whereas ASP alone promoted chondrocyte proliferation. The anti-apoptotic effect of ASP was related to the enhanced autophagy and depended on the activation of the ERK1/2 pathway. CONCLUSION: ASP markedly rescued SNP-induced apoptosis by activating ERK1/2-dependent autophagy in chondrocytes, and it made ASP as a potential therapeutic supplementation for OA treatment.

Oxidative Stress Induces Chondrocyte Apoptosis through Caspase-Dependent and Caspase-Independent Mitochondrial Pathways and the Antioxidant Mechanism of Angelica Sinensis Polysaccharide.

INTRODUCTION: Chondrocyte apoptosis is considered one of the pathogenic factors of osteoarthritis (OA), but its importance in the pathogenesis of OA remains unclear. Recent research adds progress to the knowledge that the mitochondrial signaling pathway mediates chondrocyte apoptosis in OA. METHOD: Rat chondrocyte exposed to H2O2 was used as the experimental oxidative stress model. Chondrocyte viability was tested by cell counting kit-8 (CCK-8) assay. Cell apoptosis and ROS were tested by flow cytometry. Contents of malondialdehyde (MDA), catalase (CAT), caspase-3, caspase-9, cytochrome C, superoxide dismutase (SOD)-2, and adenosine triphosphate (ATP) were evaluated by biochemical detection. The expressions of related genes and proteins were assessed by quantitative polymerase chain reaction (qPCR) and western blot. RESULTS: H2O2 provokes oxidative stress and decreases the viability of chondrocyte, which leads to the release of cytochrome C and inhibition of SOD-2 activity. The damage of mitochondrion disturbs the energy metabolism of chondrocyte and eventually induces chondrocyte apoptosis through the mitochondrial pathway. Furthermore, pretreated with anglicasinensis polysaccharide (ASP) or caspase inhibitors increase the expression of Bcl-2 and Bcl-xL but do not work for the expression of Bax and Bad. CONCLUSION: Oxidative stress induces chondrocyte apoptosis through caspase-dependent and caspase-independent mitochondrial pathways. ASP protects chondrocyte from H2O2-induced oxidative stress and subsequent cell injury through its antioxidant effect by inhibiting the caspase pathway.

LncRNA LUADT1 regulates miR-34a/SIRT1 to participate in chondrocyte apoptosis.

It is known that miR-34a can promote the apoptosis of chondrocytes, which directly contribute to osteoarthritis (OA). Through bioinformatics analysis, we found that long noncoding RNA LUADT1 may interact with miR-34a. We, therefore, further investigate the interactions between them in osteoarthritis. We found that LUADT1 was downregulated, while miR-34a was upregulated in OA synovial fluid. Correlation analysis revealed no significant correlation between them. Overexpression experiment also revealed no significant effects of LUADT1 and miR-34a on the expression of each other. However, the dual-luciferase assay showed that LUADT1 and miR-34a can directly interact with each other. Moreover, LUADT1 overexpression led to the upregulation of SIRT1, which is a downstream target of miR-34a. Cell apoptosis showed that LUADT1 and SIRT1 overexpression led to decreased, while miR-34a led to increased apoptotic rates of chondrocytes. Therefore, LUADT1 regulates miR-34a/SIRT1 to participate in chondrocyte apoptosis.

A Type-Curve Method for the Analysis of Pumping Tests with Piecewise-Linear Pumping Rates.

Aquifer hydraulic parameters are commonly inferred from constant-rate pumping tests, while variable pumping rates are frequently encountered in actual field conditions. In this study, we propose a generally applicable dimensionless form of the analytical solution for variable-rate pumping tests in confined aquifers. In particular, we adopt a piecewise-linear fitting of variable pumping rates and propose a new type-curve method for estimating the hydraulic conductivity (K) and specific storage (Ss ) of the investigated confined aquifer. For each test, a series of type curves, which depend on the variable pumping rates, the location of observation wells and the introduced first dimensionless inflection time, need to be provided for matching the observed drawdown data on a log-log graph. We first demonstrate the applicability and robustness of this method through a synthetic pumping test. Subsequently, we apply this method to analyze drawdown data from four pumping tests conducted within a multilayered aquifer/aquitard system in Wuxi city, Jiangsu Province, China. The parameter estimates are then compared with those reported by PEST. The K and Ss values estimated by the new type-curve method are found to be quite close to PEST-based estimates. Parameter estimation results demonstrate the difference in K and Ss values between observation wells. The difference could be attributed to the spatial heterogeneity in K and Ss . A future research topic may focus on the characterization of K and Ss heterogeneity with the currently available drawdown data from variable-rate pumping tests.

FSTL1 promotes nitric oxide-induced chondrocyte apoptosis via activating the SAPK/JNK/caspase3 signaling pathway.

OBJECTIVE: Previous studies have shown that follistatin-like protein 1 (FSTL1) is elevated in the synovial fluid of osteoarthritis and is associated with disease activity. The experiment was performed to stuy the effect and mechanism of FSTL1 on chondrocyte apoptosis in osteoarthritis. DESIGN: After the isolation of human normal and osteoarthritis (OA) chondrocytes, the expression of FSTL1 was detected by Q-PCR and western blot analyses. Chondrocytes were pre-transfected with FSTL1 overexpression plasmids then treated with SNP, and chondrocyte viability and apoptosis levels were detected by MTS and flow cytometry, respectively. Cartilage matrix gene expression was measured by Q-PCR and signal pathway-related proteins were assessed by western blot. RESULTS: The expression of FSTL1 in OA chondrocytes was markedly up-regulated compared with normal human chondrocytes (P < 0.05). The apoptosis rate of chondrocytes in the FSTL1 overexpression groups was highly elevated in the comparison with the negative control groups (P < 0.05). Additionally, FSTL1 potentiated protein abundances of MMP1, MMP3, MMP-9, and Bax as well as reduced Coll2a1 and Aggrecan and Bcl-2 expression. Furthermore, western blot results showed that the SAPK/JNK/Caspase3 signal pathway was significantly activated and the Ac-DEVD-FMK impaired FSTL1 induced chondrocyte apoptosis. CONCLUSION: FSTL1 promoted SNP-induced chondrocytes apoptosis by activating the SAPK/JNK/Caspase3 signal pathway.

A Plasmon-Mediated Electron Emission Process.

Light-driven electron emission plays an important role in modern optoelectronic devices. However, such a process usually requires a light field with either a high intensity or a high frequency, which is not favorable for its implementations and difficult for its integrations. To solve these issues, we propose to combine plasmonic nanostructures with nanoelectron emitters of low work function. In such a heterostructure, hot electrons generated by plasmon resonances upon light excitation can be directly injected into the adjacent emitter, which can subsequently be emitted into the vacuum. Electron emission of high efficiency can be obtained with light fields of moderate intensities and visible wavelengths, which is a plasmon-mediated electron emission (PMEE) process. We have demonstrated our proposed design using a gold-on-graphene (Au-on-Gr) nanostructure, which can have electron emission with light intensity down to 73 mW·cm-2. It should be noted that the field electron emission is not involved in such a PMEE process. This proposal is of interest for applications including cold-cathode electron sources, advanced photocathodes, and micro- and nanoelectronic devices relying on free electrons.

PI3K/Akt and caspase pathways mediate oxidative stress-induced chondrocyte apoptosis.

Chondrocyte apoptosis is closely related to the development and progression of osteoarthritis (OA); however, the underlying mechanisms remain enigmatic. Previous studies have confirmed that cell apoptosis is one of the main pathological alterations during oxidative stress, and chondrocyte apoptosis induced by oxidative stress plays an important role in the development of OA. Rat chondrocytes exposed to hydrogen peroxide (H2O2) were used as the experimental oxidative stress model. We assessed cell viability, cell apoptosis, levels of intracellular reactive oxygen species (ROS), nitric oxide (NO) production, gene relative expression level of inducible nitric oxide synthase (iNOS), and expressions of iNOS, PI3K, phospho-Akt, caspase-9, and caspase-3. With the rising of intracellular ROS and increasing iNOS synthesis, producing a large amount of NO in chondrocytes, H2O2 decreased the cell viability and induced cell apoptosis of chondrocytes. Furthermore, the levels of caspase-9 and caspase-3 protein expression were significantly elevated as well as the level of p-Akt protein expression when induced by oxidative stress. These findings suggest that oxidative stress-induced chondrocyte apoptosis occurred via activating both PI3K/Akt and caspase pathways in the early stage in these processes.

Effects of Hesperidin on H2O2-Treated Chondrocytes and Cartilage in a Rat Osteoarthritis Model.

BACKGROUND The purpose of this research was to investigate the effects of hesperidin on hydrogen peroxide (H2O2)-induced chondrocytes injury and cartilage degeneration in a rat model of osteoarthritis (OA). MATERIAL AND METHODS Chondrocytes were isolated from rat knee joints and treated with hesperidin alone or combined with H2O2. Then, Cell Counting Kit-8 (CCK-8) assay was used to assess cell viability. Activity of reactive oxygen species (ROS) and levels of malondialdehyde (MDA) were estimated. Cell apoptosis was assessed by flow cytometry assay. In addition, gene expression levels were measured for caspase 3, tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1ß), collagen type II (Col2a1), aggrecan, (sex-determining region Y)-box 9 (SOX9), matrix metalloproteinase (MMP)-13, and inducible nitric oxide synthase (iNOS) through quantitative real-time polymerase chain reaction (qPCR). To examine the effects on cartilage destruction in vivo, hesperidin or vehicle control were orally administrated in a surgically-induced osteoarthritis (OA) model. RESULTS The results indicated that hesperidin pretreatment of chondrocytes reduce H2O2-induced cytotoxicity and apoptosis. Hesperidin pretreatment decreased the formation of MDA and intracellular ROS, including chondrocyte apoptosis. Hesperidin also reversed the activity of H2O2 on inhibiting the Col2a1, aggrecan, and SOX9 gene expression and increasing the gene expression of caspase 3, IL-1ß, TNFα, iNOS, and MMP13. In addition, hesperidin administration markedly attenuated cartilage destruction and reduced IL-1ß and TNF-α levels in a surgically-induced OA model. CONCLUSIONS Our study suggests that hesperidin can prevent H2O2-induced chondrocytes injury through its antioxidant effects in vitro and reduce cartilage damage in a rat model of OA.

Medical Applications of Collagen and Hyaluronan in Regenerative Medicine.

In order to develop and commercialize for the regenerative medicinal products, smart biomaterials with biocompatibility must be needed. In this chapter, we introduce collagen and hyaluronic acid (HA) as extracellular matrix as well as deal with the molecular mechanism as microenvironment, mechanistic effects, and gene expression. Application of collagen and HA have been reviewed in the area of orthopedics, orthopedics, ophthalmology, dermatology and plastic surgery. Finally, the ongoing and commercial products of collagen and HA for regenerative medicine have been introduced.

Plasmonic Sensing Characteristics of Gold Nanorods with Large Aspect Ratios.

Plasmonic gold nanorods play important roles in nowadays state-of-the-art plasmonic sensing techniques. Most of the previous studies and applications focused on gold nanorods with relatively small aspect ratios, where the plasmon wavelengths are smaller than 900 nm. Gold nanorods with large aspect ratios are predicted to exhibit high refractive-index sensitivity (Langmir 2008, 24, 5233⁻5237), which therefore should be promising for the development of high-performance plasmonic chemical- and bio-sensors. In this study, we developed gold nanorods with aspect ratios over 7.9, which exhibit plasmon resonances around 1064 nm. The refractive index (RI) sensitivity of these nanorods have been evaluated by varying their dielectric environment, whereby a sensitivity as high as 473 nm/RIU (refractive index unit) can be obtained. Furthermore, we have demonstrated the large-aspect-ratio nanorods as efficient substrate for surface enhanced Raman spectroscopy (SERS), where an enhancement factor (EF) as high as 9.47 × 108 was measured using 4-methylbenzenethiol (4-MBT) as probe molecule. Finally, a type of flexible SERS substrate is developed by conjugating the gold nanorods with the polystyrene (PS) polymer. The results obtained in our study can benefit the development of plasmonic sensing techniques utilized in the near-infrared spectral region.

Association between the polymorphisms of CALM1 gene and osteoarthritis risk: a meta-analysis based on observational studies.

The existing studies on the association between polymorphisms of Calmodulin 1 (CALM1) gene and the risk of osteoarthritis (OA, a complex multifactorial disease and a major degenerative form of arthritis) in different populations have yielded conflicting findings. Therefore, we conducted a meta-analysis by systematically searching PubMed, Embase, Medline, Cochrane Library and Google Scholar, and assessing this association by calculating pooled odds ratios with 95% confidence intervals. Subgroup analyses stratified by ethnicity, OA type, and genotype were also conducted. Six studies (2752 cases and 3259 controls) involving six single nucleotide polymorphisms were included. Our data suggested that the T allele and genotype TT of the rs12885713 polymorphism, and the C allele of the rs2300496 polymorphism in the CALM1 gene all increased the risk of OA. The pooled results revealed no significant association between the CALM1 rs3213718 polymorphism and the risk of OA. Stratification analyses by ethnicity and OA type showed that the rs12885713 polymorphism increased the risk of OA among Asians and in knee OA, respectively. In conclusion, the rs12885713 and rs2300496 polymorphisms of the CALM1 gene may both increase the risk of OA. Owing to the limitations of the present study, this finding should be further confirmed in future well-designed studies.

Improved osteogenic differentiation of human dental pulp stem cells in a layer-by-layer-modified gelatin scaffold.

Dental pulp stem cell is a new type of mesenchymal stem cell that has a potential for tissue regeneration. Gelatin sponges are often used for hemostasis in dental surgery. In this study, we aimed to evaluate the dental pulp stem cells' proliferation and osteogenic differentiation in different layer-by-layer-modified gelatin sponge scaffolds including the G, G + P (gelatin sponge+ poly-l-lysine modification), G + M (gelatin sponge + mineralization modification), and G + M + P (gelatin sponge + mineralization modification + poly-l-lysine modification) groups in vitro and assessed them in vivo. The results showed that dental pulp stem cells had a great potential for osteogenic differentiation. In vitro, the G + M + P group not only enhanced the adhesion and proliferation of dental pulp stem cells but also facilitated their osteogenic differentiation. However, alkaline phosphatase activity was prohibited after modification. In vivo, both dental pulp stem cells and cells from nude mice grew well on the scaffold, and G + M and G + M + P groups could promote the mineralization deposit formation and the expression of osteocalcin in osteogenic differentiation of dental pulp stem cells. In conclusion, the combination of dental pulp stem cells and G + M + P scaffold has a great potential for bone tissue engineering.

Essential thrombocythemia during treatment of acute myeloid leukemia with JAK2 V617F mutation: A case report of a CARE-compliant article.

RATIONALE: The JAK2 V617F mutation is frequently found in ET, while it is rare in de novo AML. ET has a low frequency of leukemic transformation. Both secondary AML (sAML) from ET and AML with JAK2 V617F mutation have poor prognoses. Because of the low incidence of JAK2 mutation in acute myeloid leukemia (AML), the clinical features of AML with JAK2 mutation are rarely reported so far, either transformed from essential thrombocythemia (ET) or de novo AML. PATIENT CONCERNS: In this article, we present a pediatric AML patient with the JAK2 V617F mutation. DIAGNOSES: A diagnosis of acute megakaryoblastic leukemia was made and sAML was ruled out. INTERVENTIONS: The patient underwent chemotherapy. OUTCOMES: In the first two complete remission periods, we found significantly increased numbers of platelets and bone marrow megakaryocytes, which are characteristic of ET. After the third chemotherapy phase, the disease relapsed; the platelet count was reduced and continued to decrease. When disease relapsed, her family abandoned treatment. LESSONS: These observations of our case raise two possibilities: either transient posttreatment thrombocythemia is a feature of AML with JAK2 V617F mutation, or this was a case of secondary AML. Additional information is required to reach better conclusions on the connection between AML and JAK2 mutations.