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Introduction/Aims The development and persistence of neurological symptoms following severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection is referred to as “long‐haul” syndrome. We aimed to determine whether small fiber neuropathy (SFN) was associated with SARS‐CoV‐2 infection. Methods We retrospectively studied the clinical features and outcomes of patients who were referred to us between May 2020 and May 2021 for painful paresthesia and numbness that developed during or after SARS‐CoV‐2 infection and who had nerve conduction studies showing no evidence of a large fiber polyneuropathy. Results We identified 13 patients, Eight women and five men with age ranging from 38–67 y. Follow‐up duration ranged from 8 to 12 mo. All patients developed new‐onset paresthesias within 2 mo following SARS‐CoV‐2 infection, with an acute onset in seven and co‐existing autonomic symptoms in seven. Three patients had pre‐existing but controlled neuropathy risk factors. Skin biopsy confirmed SFN in six, all of whom showed both neuropathy symptoms and signs, and two also showed autonomic dysfunction by autonomic function testing (AFT). Of the remaining seven patients who had normal skin biopsies, six showed no clinical neuropathy signs and one exhibited signs and had abnormal AFT. Two patients with markedly reduced intraepidermal nerve fiber densities and one with normal skin biopsy had severe and moderate coronavirus disease 2019 (COVID‐19); the remainder experienced mild COVID‐19 symptoms. Nine patients received symptomatic neuropathy treatment with paresthesias controlled in seven (77.8%). Discussion Our findings suggest that symptoms of SFN may develop during or shortly after COVID‐19. SFN may underlie the paresthesias associated with long‐haul post‐COVID‐19 symptoms.

Introduction Coronavirus disease 2019 (COVID‐19) has rapidly become a global pandemic, but little is known about its potential impact on patients with myasthenia gravis (MG). Methods We studied the clinical course of COVID‐19 in five hospitalized patients with autoimmune MG (four with acetylcholine receptor antibodies, one with muscle‐specific tyrosine kinase antibodies) between April 1, 2020‐April 30‐2020. Results Two patients required intubation for hypoxemic respiratory failure, whereas one required significant supplemental oxygen. One patient with previously stable MG had myasthenic exacerbation. One patient treated with tocilizumab for COVID‐19 was successfully extubated. Two patients were treated for MG with intravenous immunoglobulin without thromboembolic complications. Discussion Our findings suggest that the clinical course and outcomes in patients with MG and COVID‐19 are highly variable. Further large studies are needed to define best practices and determinants of outcomes in this unique population.

BACKGROUND Currently, the prognostic stratification and therapeutic evaluation systems for multiple myeloma (MM) lack specific molecular indicators. OC-STAMP is a new gene and is also highly expressed in MM. METHODS A total of 160 MM patients have been investigated with both quantitative reverse transcription PCR (RT-qPCR), flow cytometry (FCM) and cytogenetic FISH on the same mononuclear cells isolated from bone marrow specimens. RESULTS We found that OC-STAMP mRNA levels were significantly higher in newly diagnosed cases of MM than in healthy donors (median, 0.52% vs. 0.02%, P

About 25% of patients with newly diagnosed acute myeloid leukaemia (AML) have normal cytogenetics and no nucleophosmin 1 (NPM1) mutation or Fms-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD). The prognosis and best therapy for these patients is controversial. We evaluated 158 newly diagnosed adults with this genotype who achieved histological complete remission within two cycles of induction therapy and were assigned to two post-remission strategies with and without an allotransplant. Targeted regional sequencing at diagnosis was performed and data were used to estimate their prognosis, including relapse and survival. In multivariable analyses, having wild-type or mono-allelic mutated CCAAT/enhancer-binding protein alpha (CEBPA) [hazard ratio (HR) 2·39, 95% confidence interval (CI) 1·08-5·30; P = 0·032), mutated NRAS (HR 2·67, 95% CI 1·36-5·25; P = 0·004), mutated colony-stimulating factor 3 receptor (CSF3R) (HR 2·85, 95% CI 1·12-7·27; P = 0·028) and a positive measurable residual disease (MRD)-test after the second consolidation cycle (HR 2·88, 95% CI 1·32-6·30; P = 0·008) were independently correlated with higher cumulative incidence of relapse (CIR). These variables were also significantly associated with worse survival (HR 3·02, 95% CI 1·17-7·78, P = 0·022; HR 3·62, 95% CI 1·51-8·68, P = 0·004; HR 3·14, 95% CI 1·06-9·31, P = 0·039; HR 4·03, 95% CI 1·64-9·89, P = 0·002; respectively). Patients with ≥1 of these adverse-risk variables benefitted from a transplant, whereas the others did not. In conclusion, we identified variables associated with CIR and survival in patients with AML and normal cytogenetics without a NPM1 mutation or FLT3-ITD.

Circular RNAs (circRNAs) have been established to be involved in numerous processes in the human genome, but their function in vascular aging remains largely unknown. In this study, we aimed to characterize and analyze the function of a circular intronic RNA, ciPVT1, in endothelial cell senescence. We observed significant downregulation of ciPVT1 in senescent endothelial cells. In proliferating endothelial cells, ciPVT1 knockdown induced a premature senescence‐like phenotype, inhibited proliferation, and led to an impairment in angiogenesis. An in vivo angiogenic plug assay revealed that ciPVT1 silencing significantly inhibited endothelial tube formation and decreased hemoglobin content. Conversely, overexpression of ciPVT1 in old endothelial cells delayed senescence, promoted proliferation, and increased angiogenic activity. Mechanistic studies revealed that ciPVT1 can sponge miR‐24‐3p to upregulate the expression of CDK4, resulting in enhanced Rb phosphorylation. Moreover, enforced expression of ciPVT1 reversed the senescence induction effect of miR‐24‐3p in endothelial cells. In summary, the present study reveals a pivotal role for ciPVT1 in regulating endothelial cell senescence and may have important implications in the search of strategies to counteract the development of age‐associated vascular pathologies., We characterized a novel circular intronic RNA ciPVT1, which originates from intron 4 of the PVT1 gene, was markedly reduced in senescent endothelial cells. Further functional and mechanistic investigations revealed that ciPVT1 may act as a competing endogenous RNA (ceRNA) to regulate CDK4 and its downstream gene by decoying miR‐24‐3p, thereby delaying endothelial cell senescence.

Background Published researches have suggested some associations between PPAR‐γ and ischemic stroke (IS) development. This meta‐analysis was conducted to evaluate the association between PPAR‐γ gene polymorphisms and IS risk. Materials and methods A systematic search was conducted in PubMed, Embase, Web of Science, China National Knowledge Infrastructure, and WanFang databases. The pooled association of odd ratios (ORs) and its 95% confidence interval (CI) was calculated to assess the IS risk of PPAR‐γ rs1801282 C/G and rs3856806 C/T polymorphisms. Furthermore, the heterogeneity test, cumulative analyses, sensitivity analyses, and publication bias were conducted. Result Sixteen publications with 3786 cases and 5343 controls were identified. Overall findings indicated that rs1801282 C/G polymorphism may be associated with an increased risk for IS (GG vs. CC: OR = 2.17 95%CI = 1.09–4.35, p = .03, I 2 = 0%; GG vs. CC+CG: OR = 2.15, 95%CI = 1.07–4.32, p = .03, I 2 = 0%). The similar results were also found in the subgroup analysis. In addition, no significant association was observed between rs3856806 C/T polymorphism and IS risk. Conclusion In conclusion, our study showed that PPAR‐γ rs1801282 C/G polymorphism probably plays an important role in IS occurrence. The result should be verified with more studies in the future., Ischemic strokes (IS) are one of the most common diseases resulting in disabilities and death among adults. Our meta‐analysis indicated that the individuals with G mutation of rs1801282 C/G polymorphism would face an increased risk of IS. But there was no significant association between rs3856806 C/T polymorphism and IS risk.

Background Previous studies have shown that the brain‐derived neurotrophic factor (BDNF) rs6265 G > A polymorphism is closely related post‐traumatic stress disorder (PTSD) risk. However, the results were not consistent. We therefore conducted a meta‐analysis to explore the underlying relationships between BDNF rs6265 G > A polymorphism and PTSD risk. Materials and Methods Five online databases were searched, and all related studies were reviewed up to July 1, 2020. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated to examine the statistical power of each genetic model. In addition, heterogeneity, sensitivity accumulative analysis, and publication bias were examined to check the statistical power. Result Overall, 16 publications involving 5,369 subjects were included in this systematic review and 11 case‐control studies were analyses in meta‐analysis. The pooled results indicated an increasing risk of A allele mutations with PTSD risk. Moreover, the sequential subgroup analysis also demonstrated some similar situations in Asian populations and other groups. Conclusion Current meta‐analysis suggests that the BDNF rs6265 G > A polymorphism might be involved in PTSD susceptibility., A meta‐analysis focused on the association between BDNF rs6265 G > A polymorphism and PTSD risk was conducted. 16 publications involving 5,369 subjects were included in this system review and 11 case‐controls were analyses in meta‐analysis. Current meta‐analysis suggests indicated that the BDNF rs6265 G > A polymorphism might be involved in PTSD susceptibility.

CO2 emissions can be transformed into high-added-value commodities through CO2 electrocatalysis; however, efficient low-cost electrocatalysts are needed for global scale-up. Inspired by other emerging technologies, the authors report the development of a gas diffusion electrode containing highly dispersed Ag sites in a low-cost Zn matrix. This catalyst shows unprecedented Ag mass activity for CO production: -614 mA cm-2 at 0.17 mg of Ag. Subsequent electrolyte engineering demonstrates that halide anions can further improve stability and activity of the Zn-Ag catalyst, outperforming pure Ag and Au. Membrane electrode assemblies are constructed and coupled to a microbial process that converts the CO to acetate and ethanol. Combined, these concepts present pathways to design catalysts and systems for CO2 conversion toward sought-after products.

Background Xuanwei district in Yunnan Province has the highest incidence of lung cancer in China, especially among non-smoking women. Cruciferous vegetables can reduce lung cancer risk by prompting a protective mechanism against respiratory tract inflammation caused by air pollution, and are rich in sulforaphane, which can induce changes in gene expression. We investigated the effect of sulforaphane-induced apoptosis in Xuanwei lung adenocarcinoma cell line (XWCL-05) to explore the value of sulforaphane in lung cancer prevention and treatment. Methods Cell growth inhibition was determined by methyl thiazolyl tetrazolium assay; cell morphology and apoptosis were observed under transmission electron microscope; cell cycle and apoptosis rates were detected using flow cytometry; B-cell lymphoma 2 (Bcl-2) and Bcl-2-like protein 4 (Bax) messenger RNA expression were determined by quantitative PCR; and p53, p73, p53 upregulated modulator of apoptosis (PUMA), Bax, Bcl-2, and caspase-9 protein expression were detected by Western blotting. Results Sulforaphane inhibited XWLC-05 cell growth with inhibitory concentration (IC)50 of 4.04, 3.38, and 3.02 μg/mL at 24, 48, and 72 hours, respectively. Sulforaphane affected the XWLC-05 cell cycle as cells accumulated in the G2/M phase. The proportion of apoptotic cells observed was 27.6%. Compared with the control, the sulforaphane group showed decreased Bcl-2 and p53 expression, and significantly increased p73, PUMA, Bax, and caspase-9 protein expression (P Conclusion Sulforaphane induces Xuanwei lung adenocarcinoma cell apoptosis. Its possible mechanism may involve the upregulation of p73 expression and its effector target genes PUMA and Bax in lung cancer cells, downregulation of the anti-apoptotic gene B cl -2, and activation of caspase-9. It may also involve downregulation of the mutant p53 protein.

Genetic ablation or pharmacologic inhibition of CC chemokine receptor type 2 (CCR2) reduced macrophage (MP) infiltration and improved muscle pathology and function in mdx diaphragm muscle at early stages. We addressed whether CCR2 deficiency resulted in sustained improvement of mdx5cv-Ccr2−/− diaphragm. Compared to mdx5cv controls, CCR2 deficiency in mdx5cv-Ccr2−/− mice markedly reduced intramuscular Ly6Chi MPs at all stages, but it reduced Ly6Clow MPs only at early stages (4 and 9 wk). CCR2 deficiency reduced quadriceps and diaphragm muscle damage and fibrosis at 14 wk but not at 6 mo, and it improved diaphragm muscle regeneration and respiratory function at 14 wk but not at 6 mo. Intramuscular MPs in mdx5cv-Ccr2−/− diaphragm expressed a low level of IL-1β, IL-6, and IFN-γ genes, a similar level of TNF-α, TGF-β1, and platelet-derived growth factor α genes, and a high level of IGF-1 and osteopontin genes compared to mdx5cv controls. Diaphragm fibroblasts at 14 wk showed a similar cell number with a similar level of collagen and profibrogenic growth factor gene expression in mdx5cv-Ccr2−/− and mdx5cv mice. Diaphragm MPs from both mdx5cv-Ccr2−/− and mdx5cv mice stimulated collagen gene expression by cocultured fibroblasts. The findings suggest that CCR2 deficiency does not provide a sustained benefit and that Ly6Clow MPs may contribute to the progressive fibrosis and dysfunction of mdx5cv diaphragm.—Zhao, W., Wang, X., Ransohoff, R. M., Zhou, L. CCR2 deficiency does not provide sustained improvement of muscular dystrophy in mdx5cv mice.

A series of monodispersed silica microspheres with favourable sphericity and different diameters in the range 180–380 nm were prepared by adjusting the concentrations of tetraethylorthosilicate, ammonia, and deionised water by the Stober method. In different self-assembly conditions, the quality of silica photonic crystals on a polyester fabric substrate was investigated by field-emission scanning electron microscopy for the morphology of the crystal structures and by spectrometry for their stop band intensities. High-quality silica photonic crystals with a face-centred cubic (fcc) array on polyester fabrics were produced at a low evaporation rate by adopting a high-relative-humidity controlled condition with a medium mass fraction of colloidal silica, and exhibited brilliant and variable structural colours, depending on the photonic band gap regulated by the spherical size of the silica microspheres and the viewing angles.

Laboratory testing plays a major role in hepatitis C virus (HCV) diagnosis and patient follow-up. The high false positive rates of HCV screening tests require confirmation through a supplementary test. According to the 2003 CDC guidelines, recombinant immunoblot assay (RIBA) is indispensible to confirm positive screening results and differentiate biologic false positivity from true HCV exposure. However, RIBA has been permanently discontinued since 2011. In the 2013 update of its guidelines, CDC called for further studies on HCV laboratory testing without RIBA. In this study, we analyzed the applicability of quantitative real-time PCR (qPCR) as a supplementary HCV diagnostic test. By comparing our HCV testing performances before and after RIBA discontinuation, we found that omitting RIBA has no significant effect on the accurate and efficient identification of HCV infection, provided that HCV antibody signal-to-cutoff ratio is considered. Furthermore, we proposed a new HCV testing algorithm that incorporates semiquantitative assessment of HCV antibody positivity and HCV viral load measurement by qPCR. By following the algorithm, we were able to address confirmation of positive HCV screening results and to provide useful information generally required by clinicians, including the needs of further laboratory testing or clinical follow-up, as well as HCV viral titers.

Adequate inflammatory response predominated by macrophage infiltration is essential to acute skeletal muscle injury repair. The majority of intramuscular macrophages express the chemokine receptor CX3CR1. We studied the role of CX3CR1 in regulating intramuscular macrophage number and function in acute injury repair by using a loss-of-function approach. Muscle injury repair was delayed in CX3CR1GFP/GFP mice as compared with wild-type (WT) controls. CX3CR1 was predominantly expressed by macrophages but not by myogenic cells or capillary endothelia cells in injured muscles. Intramuscular macrophage number and subset composition were not altered by CX3CR1 deficiency. Intramuscular macrophage phagocytosis function was impaired by CX3CR1 deficiency as demonstrated by increased number of necrotic fibers (+115%) and percentage of necrotic area (+204%) at 7 d, increased number of intramuscular neutrophils at 3 (+89%) but not 1 d, reduced number of phagocytosing macrophages (−12%) and phagocytosed beads within macrophages (−15%) in CX3CR1GFP/GFP mice as compared with WT controls. The mRNA expression of CD36 (−50%), CD14 (−43%), IGF-1 (−53%), and IL-6 (−40%) was reduced in CX3CR1-deficient macrophages as compared with WT controls. We conclude that CX3CR1 is important to acute skeletal muscle injury repair by regulating macrophage phagocytosis function and trophic growth factor production.—Zhao, W., Lu, H., Wang, X., Ransohoff, R. M., Zhou, L. CX3CR1 deficiency delays acute skeletal muscle injury repair by impairing macrophage functions.

A facile method was developed for the synthesis of nitrogen-doped porous carbon-gold (NPCAu) hybrid nanocomposite. The NPCAu modified gold electrode has been prepared for the electrochemical determination of ultratrace mercury(II) in drinking water through square wave anodic stripping voltammetry (SWASV). Under optimized conditions, the NPCAu modified electrode shows a sensitive detection to Hg(II) ion present in concentrations of 0.001∼1 μM, with a detection limit of 0.35 nM (S/N=3), which was much lower than the guideline values in drinking water given by the World Health Organization.

Bone morphogenetic proteins (BMPs) are members of the TGF-β superfamily signaling factors. Expression of several BMPs (BMP2, BMP4, and BMP7) is correlated to poor prognosis in gastric cancer patients. The function of BMP9, the latest discovered and most powerful osteogenetic factor, in gastric cancer is relatively unclear. In this report, we investigated the expression, function and underlying molecular mechanisms of BMP9 in gastric cancer. The results show that BMP9 expression was markedly decreased in gastric cancer tissues and cell lines. Enforced BMP9 expression in the gastric cancer cell lines SGC-7901 and MNK-45 increased apoptosis and reduced viability and migration. The in vivo function of BMP9 was evaluated in a xenograft mouse model. Tumors derived from SGC-7901 cells with enforced BMP9 expression (SGC-7901/BMP9) showed significantly reduced size and weight compared to that from control cells. Enforced BMP9 expression resulted in decreased Akt activity shown as lower levels of phosphorylation at Ser473 and Thr308 in Akt. The PI3K/Akt inhibitor LY294002 potentiated BMP9's viability and migration suppression, and apoptosis induction, which was associated with reduced expression of snail and VEGF and increased expression of E-cadherin. In addition, tumors derived from SGC-7901/BMP9 showed reduced Akt activity and VEGF expression, and increased E-cadherin expression. Therefore, our studies reveal for the first time that inhibition of the PI3K-Akt pathway is involved in the tumor suppressor effects of BMP9 in gastric cancer.

In view of the low solubility of thiourea dioxide in water and its inertia to most chemical reagents, a novel non-aqueous medium, decamethylcyclopentasiloxane, was introduced to replace water in the grinding process for better dispersibility and discharge stability. In this study, the effects of different grinding methods on the particle size distribution and surface appearance of thiourea dioxide were studied. The influences of aqueous and decamethylcyclopentasiloxane media on the discharge stability of thiourea dioxide in discharge paste were compared. The whiteness, handle, and the tensile strength of the discharge-printed fabric were evaluated. The results showed that the wet grinding process endowed thiourea dioxide with smaller particle sizes and narrower size distributions in the presence of dispersants. Decamethylcyclopentasiloxane as a non-aqueous medium was beneficial in maintaining good discharge stability of thiourea dioxide for a longer time. The fabrics discharged by the prepared thiourea dioxide printing paste had favourable whiteness, good handle, and acceptable tensile strength.

Introduction: Meralgia paresthetica is a focal neuropathy caused by compression of the lateral femoral cutaneous nerve (LFCN). The disease can be difficult to assess by neurophysiological or imaging studies. Methods: We studied 5 patients who presented to our neuromuscular clinic from April 2012 to December 2014 with a clinical suspicion of meralgia paresthetica and had skin biopsies with intraepidermal nerve fiber density (IENFD) evaluation. Results: The mean age at onset was 37.2 (range 21–59) years. There were 4 women and 1 man. Two were obese, 2 wore tight jeans, and 1 had mild diabetes mellitus. IENFD was reduced in the symptomatic proximal thigh in all 5 patients and was also reduced in the asymptomatic thigh in 2 patients. It was normal in the distal leg in 4 patients. Conclusion: Meralgia paresthetica is associated with loss of small intraepidermal nerve fibers. Skin biopsy with IENFD evaluation may be a useful diagnostic tool for this disease. Muscle Nerve 53: 641–643, 2016

Introduction Carpal tunnel syndrome (CTS) is a common clinical syndrome seen in the outpatient setting that is easily confirmed by electrodiagnostic testing. Methods We describe the case of a patient who presented with the classic symptoms and neurological examination for CTS, but had a normal nerve conduction study and electromyogram. Results Neuromuscular ultrasound of the median nerve on the symptomatic side revealed penetration of the nerve by a persistent median artery and vein in the mid-forearm, with a positive sonographic Tinel sign over this spot. This finding is an anatomical variation that has been described sparingly in the literature, mostly in cadavers. It has not been reported previously to be a mimic of CTS. Conclusions This case demonstrates the diagnostic utility of neuromuscular ultrasound and the importance of considering an anatomical variation involving the median nerve in the differential diagnosis of CTS.

Introduction: Polyneuropathy evaluation in older patients is often challenging due to conflicting data regarding normative values for peripheral nerve testing. Methods: We characterized the results of sural nerve conduction studies, intraepidermal nerve fiber density (IENFD), and quantitative sudomotor axon reflex testing (QSART) in a prospective study of 50 healthy subjects aged ≥60 years. Results: Of the 50 subjects, 48 (96%) had an obtainable sural sensory nerve action potential (SNAP). Using quantile regression, we estimated the lower limit of normal (LLN) for sural amplitudes to be 3 μV for patients 60–70 years, 1 μV for those 70–74 years, and

This paper concerns the design of a robust discrete-time observer-based repetitive-control system for a class of linear plants with periodic uncertainties. A discrete two-dimensional model is built that partially uncouples the control and learning actions of a repetitive-control system, enabling their preferential adjustment. The combination of a singular-value decomposition of the output matrix and Lyapunov stability theory is used to derive a linear-matrix-inequality-based design algorithm that determines the control and state-observer gains. A numerical example illustrates the main advantage of the method: easy, preferential adjustment of control and learning by means of two tuning parameters in an linear-matrix-inequality-based condition.

The high-temperature degumming technology of cotton stalk bark fiber was studied, and the effects of the caustic soda concentration on the constituents, structure, and thermal degradation of the cotton stalk bark fiber were examined. The morphology, structure, and thermal degradation of the cotton stalk bark fiber after high-temperature degumming were investigated through scanning electron microscopy, Fourier transform infrared (FTIR) spectroscopy, wide-angle X-ray diffraction, and thermogravimetric analysis. The results indicate that the high-temperature degumming process was effective for removing hemicelluloses and lignin and could improve the thermal stability of the cellulose. The raw and degummed cotton stalk bark fibers both showed the structure of cellulose I, according to the FTIR spectroscopy and X-ray diffraction results. It was interesting to note that the crystallinity and crystallinity index were related to the caustic soda concentration. © 2012 Wiley Periodicals, Inc. J Appl Polym Sci, 2012

Introduction Muscle fibrosis is a prominent pathological feature that directly causes muscle dysfunction in Duchenne muscular dystrophy (DMD). The DMD mouse models, mdx mice and mdx mice with haploinsufficiency of the utrophin gene (mdx/utrn+/−), display progressive diaphragm fibrosis.

A retrospective study of autopsy cases was conducted at the Department of Forensic Medicine, Tongji Medical College (DFM-TMC), in Hubei, China to describe the characteristics of poisoning deaths from 1999 to 2008. A total of 212 poisoning deaths were investigated by DFM-TMC during the 10-year period. The poisoning deaths ranged from 17 cases in 1999 to 27 cases in 2008. Of the 212 cases, 82 deaths (38.7%) were from pesticides, 36 deaths (17.0%) from carbon monoxide, 34 deaths (16.0%) from drugs, 22 deaths (10.4%) from alcohol, 17 deaths (8.0%) from other chemicals, 15 deaths (7.1%) from poisonous plants and animals, and six deaths (2.8%) from heavy metals. Of the 82 pesticide poisoning deaths, 43 (52.4%) cases were caused by rodenticides, mainly tetramine (N = 39). The majority of poisoning deaths were accidents (63.7%), followed by suicides (25.9%) and homicides (3.8%). The manner of death could not be determined in 14 cases (6.6%).

CC chemokine receptor 2 (CCR2) is essential to acute skeletal muscle injury repair. We studied the subpopulation of inflammatory cells recruited via CCR2 signaling and their cellular functions with respect to muscle regeneration. Mobilization of monocytes/macrophages (MOs/MPs), but not lymphocytes or neutrophils, was impaired from bone marrow to blood and from blood to injured muscle in Ccr2−/− mice. While the Ly-6C+ but not the Ly-6C− subset of MOs/MPs was significantly reduced in blood, both subsets were drastically reduced in injured muscle of Ccr2−/− mice. Expression of insulin-like growth factor-1 (IGF-I) was markedly up-regulated in injured muscle of wild-type but not Ccr2−/− mice. IGF-I was strongly expressed by macrophages within injured muscle, more prominently by the Ly-6C− subset. A single injection of IGF-I, but not PBS, into injured muscle to replace IGF-I remarkably improved muscle regeneration in Ccr2−/− mice. CCR2 was not detected in myogenic cells or capillary endothelial cells in injured muscle to suggest its direct involvement in muscle regeneration or angiogenesis. We conclude that CCR2 is essential to acute skeletal muscle injury repair primarily by recruiting Ly-6C+ MOs/MPs. Within injured muscle, these cells conduct phagocytosis, contribute to accumulation of intramuscular Ly-6C− macrophages, and produce a high level of IGF-I to promote muscle regeneration.—Lu, H., Huang, D., Saederupm, N., Charo, I. F., Ransohoff, R. M., Zhou, L. Macrophages recruited via CCR2 produce insulin-like growth factor-1 to repair acute skeletal muscle injury.