Comparison of Simulated and Measured Power of the Earth-Space Link for Satellite-Based AIS Signals.

This research aims to analyze the impact of the Earth-Space link on the Automatic Identification System (AIS) signals of ships. To achieve this, we established a simulation system that measures the receiving power of AIS signals via satellite platforms. We validated the system by utilizing observation data from Tiantuo-5. Through this simulation, we quantitatively analyzed the effects of ionospheric TEC (Total Electron Content) and space loss on the received power. During the processing of observation data, we construct a geometric propagation model utilizing the measured positions of both the satellite and the ship. We then calculate the antenna gain and remove any system errors. Additionally, we eliminate the deviation of elevation and azimuth angles caused by satellite motion. This allows us to determine the actual power of different ships reaching the receiving platform. Upon comparing the measured power data with the simulated power, it was noted that both exhibited an increasing trend as the elevation angle increased. This led to an RMSE (Root Mean Square Error) result of approximately one, indicating the accuracy of the simulation system. These findings hold significant implications for analyzing interference factors in satellite-ground links.

Hypoxic drive caused type 3 neovascularization in a preclinical model of exudative age-related macular degeneration.

Hypoxia associated with the high metabolic demand of rods has been implicated in the pathology of age-related macular degeneration (AMD), the most common cause of adult blindness in the developed world. The majority of AMD-associated severe vision loss cases are due to exudative AMD, characterized by neovascularization. To further investigate the causes and histopathology of exudative AMD, we conditionally induced hypoxia in a novel preclinical AMD model (Pde6gcreERT2/+;Vhl-/-) by targeting Vhl and used multimodal imaging and immunohistochemistry to track the development of hypoxia-induced neovascularization. In addition to developing a preclinical model that phenocopies exudative AMD, our studies revealed that the photoreceptor hypoxic response initiates and drives type 3 neovascularization, mainly in the outer retina. Activation of the VHL-HIF1a-VEGF-EPO pathway in the adult retina led to long-term neovascularization, retinal hemorrhages and compromised retinal layers. Our novel preclinical model would accelerate the testing of therapies that use metabolomic approaches to ameliorate AMD.

Pretreatment CT and PET radiomics predicting rectal cancer patients in response to neoadjuvant chemoradiotherapy.

BACKGROUND: The purpose of this study was to characterize pre-treatment non-contrast computed tomography (CT) and 18F-fluorodeoxyglucose positron emission tomography (PET) based radiomics signatures predictive of pathological response and clinical outcomes in rectal cancer patients treated with neoadjuvant chemoradiotherapy (NACR T). MATERIALS AND METHODS: An exploratory analysis was performed using pre-treatment non-contrast CT and PET imaging dataset. The association of tumor regression grade (TRG) and neoadjuvant rectal (NAR) score with pre-treatment CT and PET features was assessed using machine learning algorithms. Three separate predictive models were built for composite features from CT + PET. RESULTS: The patterns of pathological response were TRG 0 (n = 13; 19.7%), 1 (n = 34; 51.5%), 2 (n = 16; 24.2%), and 3 (n = 3; 4.5%). There were 20 (30.3%) patients with low, 22 (33.3%) with intermediate and 24 (36.4%) with high NAR scores. Three separate predictive models were built for composite features from CT + PET and analyzed separately for clinical endpoints. Composite features with α = 0.2 resulted in the best predictive power using logistic regression. For pathological response prediction, the signature resulted in 88.1% accuracy in predicting TRG 0 vs. TRG 1-3; 91% accuracy in predicting TRG 0-1 vs. TRG 2-3. For the surrogate of DFS and OS, it resulted in 67.7% accuracy in predicting low vs. intermediate vs. high NAR scores. CONCLUSION: The pre-treatment composite radiomics signatures were highly predictive of pathological response in rectal cancer treated with NACR T. A larger cohort is warranted for further validation.

Modeling precision genomic-based radiation dose response in rectal cancer.

Aim: Genomic-based risk stratification to personalize radiation dose in rectal cancer. Patients & methods: We modeled genomic-based radiation dose response using the previously validated radiosensitivity index (RSI) and the clinically actionable genomic-adjusted radiation dose. Results: RSI of rectal cancer ranged from 0.19 to 0.81 in a bimodal distribution. A pathologic complete response rate of 21% was achieved in tumors with an RSI <0.31 at a minimal genomic-adjusted radiation dose of 29.76 when modeling RxRSI to the commonly prescribed physical dose of 50 Gy. RxRSI-based dose escalation to 55 Gy in tumors with an RSI of 0.31-0.34 could increase pathologic complete response by 10%. Conclusion: This study provides a theoretical platform for development of an RxRSI-based prospective trial in rectal cancer.

Ripasudil alleviated the inflammation of RPE cells by targeting the miR-136-5p/ROCK/NLRP3 pathway.

BACKGROUND: Inflammation of RPE cells led to different kinds of eye diseases and affected the normal function of the retina. Furthermore, higher levels of ROCK1 and ROCK2 induced injury of endothelial cells and many inflammatory diseases of the eyes. Ripasudil, which was used for the treatment of glaucoma, was one kind of the inhibitor of ROCK1 and ROCK2, but whether ripasudil could relieve the LPS-induced inflammation and damage of RPE cells was not clear. METHODS: We used LPS to stimulate ARPE-19 cells, the RPE cell line. After that, we detected the levels of ROCK1 and ROCK2 by western-blotting after the stimulation of LPS and treatment of ripasudil. Then luciferase reporter assays were used to confirm the targeting effect of miR-136-5p on ROCK1 and ROCK2. At last, the levels of NLRP3, ASC, caspase1, IL-1ß and IL-18 were detected with the western-blotting after the knockdown of miR-136-5p. RESULTS: The levels of ROCK1, ROCK2 and miR-136-5p in ARPE-19 cells were promoted after the stimulation of LPS. After the treatment of ripasudil, the expression levels of ROCK1, ROCK2 and miR-136-5p were suppressed. The expression of ROCK1 and ROCK2 was targeted and inhibited by the miR-136-5p. The levels of inflammation related proteins NLRP3, ASC, caspase1, IL-1ß and IL-18 was also inhibited after the treatment of ripasudil. However, the expression of these proteins was rescued after the knockdown of miR-136-5p. CONCLUSION: Ripasudil relieved the inflammatory injury of RPE cells by upregulating miR-136-5p, therefore inhibiting the expression of ROCK1, ROCK2, NLRP3, ASC, caspase1, IL-1ß and IL-18.

Intrinsic radiosensitivity, genomic-based radiation dose and patterns of failure of penile cancer in response to adjuvant radiation therapy.

PURPOSE: Optimal postoperative radiation therapy (PORT) dose is unclear in penile squamous cell carcinoma (PeSCC). Herein, we characterized the radiosensitivity index (RSI) and genomic-adjusted radiation dose (GARD) profiles in a cohort of patients with PeSCC, and assessed the application of GARD to personalize PORT. METHODS: A total of 25 PeSCC samples were identified for transcriptomic profiling. The RSI score and GARD were derived for each sample. A cohort of 34 patients was reviewed for clinical correlation. RESULTS: The median RSI for PeSCC was 0.482 (range 0.215-0.682). The majority (n = 21; 84%) of cases were classified as radioresistant. PeSCC GARD ranged from 9.56 to 38.39 (median 18.25), suggesting variable therapeutic effects from PORT. We further determined the optimal GARD-based RT doses to improve locoregional control. We found that therapeutic benefit was only achieved in 52% of PeSCC lesions with PORT of 50 Gy, in contrast to 84% benefit from GARD-modeled PORT of 66 Gy. In the clinical cohort, the majority of patients presented with pathological N2 or N3 disease (n = 31; 91%) and was treated with adjuvant concurrent platinum-based chemoradiotherapy (CRT, n = 30; 88%). Fourteen of the 34 patients (41%) had locoregional recurrence (LRR), of which half had LRR within six months of completion of PORT. CONCLUSIONS: The majority of PeSCC are intrinsically radioresistant with a low GARD-based therapeutic effect from PORT dose of 50 Gy, consistent with the observed high rate of LRR in the clinical cohort. A GARD-based strategy will allow personalizing PORT dose prescription to individual tumor biology and improve outcomes.

The relationship between HPV status and chemoradiotherapy in the locoregional control of penile cancer.

BACKGROUND: Penile cancer (PeCa) is a rare, aggressive malignancy often associated with the human papillomavirus (HPV). The practice of a personalized risk-adapted approach is not yet established. This study is to assess the relationship between HPV tumor status and chemoradiotherapy (CRT) in PeCa locoregional control (LRC). METHODS: We retrospectively identified patients with HPV status who were diagnosed with squamous cell carcinoma of the penis and treated with surgical resection between 1999 and 2016. The relationship between tumor/treatment characteristics and LRC were analyzed with univariate and multivariate Cox proportional hazard regression analysis (UVA and MVA, respectively). Time-to-event outcomes were estimated with Kaplan-Meier curves and compared via log-rank tests. RESULTS: Fifty-one patients were identified. The median follow-up was 36.6 months. Patients were primarily HPV-negative (HPV-) (n = 28, 55%), and pathologic node positive (pN+) (55%). The 2 year LRC rate was 54%. pN+ patients had a significantly lower 2 year LRC (37 vs. 81%, p = 0.002). In the subgroup analysis of pN+ patients (n = 28), there was a LRC benefit associated with the addition of CRT (HR 0.19; 95% CI 0.05-0.70, p = 0.012) and HPV-positive (HPV+) disease (HR 0.18; 95% CI 0.039-0.80, p = 0.024) using MVA. HPV+ patients treated with CRT had improved 2 year LRC compared to HPV- patients (83 vs. 38%, p = 0.038). CONCLUSIONS: Adjuvant CRT and HPV+ disease independently predicted for improved LRC in pN+ PeCa. In HPV+ PeCa, the LRC benefit was primarily observed in patients treated with adjuvant CRT. Prospective investigation of HPV+ and CRT is required to further delineate their roles in optimizing PeCa treatment.

[Genetic analysis of a pedigree affected with inherited thrombocytopenia caused by a novel mutation of MYH9 gene].

OBJECTIVE: To study genetic mutations and clinical features of a pedigree affected with MYH9-related disorders from Guangxi. METHODS: Blood platelets were counted with a hemocytometer. Blood smear was carried out to detect the inclusion body in peripheral blood neutrophils. DNA and mRNA samples were extracted from blood samples from the members of the pedigree. Fragments of the MYH9 gene were amplified with PCR and directly sequenced. RESULTS: The affected individuals presented with a triad of giant platelets, decreased platelet count and inclusion bodies in the neutrophils with variable expressivity. A heterozygous deletional mutation (c.5803delG) in exon 41 of the MYH9 gene was found in all of the 8 affected individuals, which led to a frame-shift and change of 26 amino acids at the C-end of the tail domain of nonmuscle myosin heavy chain IIA (NMMHC-IIA) (p.Ala1935Profs*12). The same mutation was not found among healthy members of the pedigree. CONCLUSION: The c.5803delG mutation probably underlies the MYH9-related disorders in this pedigree. The mutation has altered the C-end of the tail domain of the NMMHC-IIA protein, resulting in mild clinical symptoms in the affected individuals.

Histone deacetylase 10 regulates DNA mismatch repair and may involve the deacetylation of MutS homolog 2.

MutS homolog 2 (MSH2) is an essential DNA mismatch repair (MMR) protein. It interacts with MSH6 or MSH3 to form the MutSα or MutSß complex, respectively, which recognize base-base mispairs and insertions/deletions and initiate the repair process. Mutation or dysregulation of MSH2 causes genomic instability that can lead to cancer. MSH2 is acetylated at its C terminus, and histone deacetylase (HDAC6) deacetylates MSH2. However, whether other regions of MSH2 can be acetylated and whether other histone deacetylases (HDACs) and histone acetyltransferases (HATs) are involved in MSH2 deacetylation/acetylation is unknown. Here, we report that MSH2 can be acetylated at Lys-73 near the N terminus. Lys-73 is highly conserved across many species. Although several Class I and II HDACs interact with MSH2, HDAC10 is the major enzyme that deacetylates MSH2 at Lys-73. Histone acetyltransferase HBO1 might acetylate this residue. HDAC10 overexpression in HeLa cells stimulates cellular DNA MMR activity, whereas HDAC10 knockdown decreases DNA MMR activity. Thus, our study identifies an HDAC10-mediated regulatory mechanism controlling the DNA mismatch repair function of MSH2.

Ubiquitinated sirtuin 1 (SIRT1) function is modulated during DNA damage-induced cell death and survival.

Downstream signaling of physiological and pathological cell responses depends on post-translational modification such as ubiquitination. The mechanisms regulating downstream DNA damage response (DDR) signaling are not completely elucidated. Sirtuin 1 (SIRT1), the founding member of Class III histone deacetylases, regulates multiple steps in DDR and is closely associated with many physiological and pathological processes. However, the role of post-translational modification or ubiquitination of SIRT1 during DDR is unclear. We show that SIRT1 is dynamically and distinctly ubiquitinated in response to DNA damage. SIRT1 was ubiquitinated by the MDM2 E3 ligase in vitro and in vivo. SIRT1 ubiquitination under normal conditions had no effect on its enzymatic activity or rate of degradation; hypo-ubiquitination, however, reduced SIRT1 nuclear localization. Ubiquitination of SIRT1 affected its function in cell death and survival in response to DNA damage. Our results suggest that ubiquitination is required for SIRT1 function during DDR.

Post-processing of fused silica and its effects on damage resistance to nanosecond pulsed UV lasers.

HF-based (hydrofluoric acid) chemical etching has been a widely accepted technique to improve the laser damage performance of fused silica optics and ensure high-power UV laser systems at designed fluence. Etching processes such as acid concentration, composition, material removal amount, and etching state (etching with additional acoustic power or not) may have a great impact on the laser-induced damage threshold (LIDT) of treated sample surfaces. In order to find out the effects of these factors, we utilized the Taguchi method to determine the etching conditions that are helpful in raising the LIDT. Our results show that the most influential factors are concentration of etchants and the material etched away from the viewpoint of damage performance of fused silica optics. In addition, the additional acoustic power (∼0.6 W·cm-2) may not benefit the etching rate and damage performance of fused silica. Moreover, the post-cleaning procedure of etched samples is also important in damage performances of fused silica optics. Different post-cleaning procedures were, thus, experiments on samples treated under the same etching conditions. It is found that the "spraying + rinsing + spraying" cleaning process is favorable to the removal of etching-induced deposits. Residuals on the etched surface are harmful to surface roughness and optical transmission as well as laser damage performance.

Overexpression p21WAF1/CIP1 in suppressing retinal pigment epithelial cells and progression of proliferative vitreoretinopathy via inhibition CDK2 and cyclin E.

BACKGROUND: P21 is one kind of cyclin-dependent kinase inhibitor that can prevent cells from going through the G1/S phase checkpoint and inhibit cell proliferation. Proliferative vitreoretinopathy (PVR) is a proliferative response in the eye. The aim of this study was to determine whether p21Waf1/Cip1 (p21) suppresses the proliferation and migration of retinal pigment epithelial (RPE) cells in vitro and controls PVR development in vivo. METHODS: Cell cycle analyses and transwell assays were conducted to assess cell proliferation characteristics and the migration ability of RPE cells after transfection with p21. Western blot and reverse-transcription polymerase chain reaction technologies were used to detect the expression of p21, CDK2 and cyclinE in RPE cells and rabbit retinal tissues. The impact of increasing p21 expression on PVR development was conducted by implantation of an adenovirus vector containing rabbit p21 (rAd-p21) in a PVR rabbit model. The prevalence of PVR and retinal detachment was determined by indirect ophthalmoscopy on days 3, 7, 14, and 21 after the injection of rAd-p21 into the vitreous. B scans and hematoxylin-eosin staining were employed to check rabbit retinas on day 21. RESULTS: Cell cycle analyses and transwell assays showed that p21 inhibited the proliferation and migration of RPE cells. Increased expression of p21 was detected in cultured RPE cells and rabbit retinas after transfection with the p21 gene, whereas levels of CDK2 and cyclinE were decreased. The increase in p21 expression effectively suppressed the development of PVR in a rabbit model. CONCLUSIONS: The increase in p21 expression in RPE cells not only inhibits the proliferation and migration of RPE cells in vitro, but also suppresses the development of PVR in vivo, which indicates its therapeutic potential in treating PVR.

[Analysis of SCA3/MJD3 gene mutation and genetic polymorphism in a guangxi family with spinocerebellar ataxia 3].

Autosomal dominant cerebellar ataxias (ADCAs) comprise a group of genetically heterogeneous neurodegenerative disorders among which spinocerebellar ataxia type 3 (SCA3) represents the most common form of SCAs worldwide. The fragments of SCA3/MJD gene,which is the member of family GXPL1,were amplified by polymerase chain reaction (PCR). The PCR products of SCA3/MJD gene were detected with capillary electrophoresis (CE) and sequencing to evaluate the size of CAG repeats, feature in the transmission and the mutation in the family with SCA3 in Guangxi province. The results showed that the exon 10 of the SCA3/MJD gene contains 64-71 CAG repeats in all of the affected individuals and three asymptomatic carriers of the family. The number of the CAG repeats during transmission in the normal individuals carrying CGG allele remains consistent, suggesting that CGG allele could have no effect on intergenerational stability of CAG repeats in normal individuals. In addition, two novel point mutations were identified: IVS9-113 T > C in the intronic region and a missense mutation 220 G > A (Glu > Gly) in the encoding region. These two novel point mutations have not been reported and the effect of the mutations on the phenotype of SCA3 is not clear.

Effects of Low-Frequency (0.5 Hz) and High-Frequency (10 Hz) Repetitive Transcranial Magnetic Stimulation on Neurological Function, Motor Function, and Excitability of Cortex in Ischemic Stroke Patients.

BACKGROUND: Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive neuromodulation technique. The purpose of our study is to explore the effects of low-frequency (0.5 Hz) and high-frequency (10 Hz) rTMS on neurological function, motor function, and excitability of cortex in Chinese ischemic stroke patients. MATERIALS AND METHODS: A total of 240 ischemic stroke patients were collected. The National Institutes of Health Stroke Scale (NIHSS), modified Rankin Scale (mRS), motor-evoked potential (MEP) cortical latency, central motor conduction time (CMCT), Fugel-Meyer assessment (FMA), Berg balance scale (BBS), and modified Barthel index (MBI) scores were recorded. RESULTS: After treatment, the NIHSS, mRS, MEP cortical latency, CMCT, FMA, BBS, and MBI scores of the high-frequency group and low-frequency group were significantly improved than the sham stimulation group, and the changes in the low-frequency group were more significant (adjusted P <0.05). Compared with the sham stimulation group, high-frequency stimulation reduced the NIHSS score by 9.5%, mRS score by 12.6%, MEP latency by 2.5%, and CMCT by 5.8%, and increased the upper limb FMA scale by 16.4%, lower limb FMA scale by 8.8%, BBS by 26.3%, and MBI by 9.3%, while low-frequency stimulation reduced the NIHSS score by 23.8%, mRS score by 25.3%, MEP Latency by 11.7%, and CMCT by 9.1%, and increased the upper limb FMA scale by 24.1%, lower limb FMA scale by 18.4%, BBS by 27.4%, and MBI by 23.7% in our cohort. CONCLUSIONS: Low-frequency rTMS is better than high-frequency rTMS stimulation in improving neurological function, motor function, and excitability of cortex in ischemic stroke.

Fabrication of SiC Porous Ceramics by Foaming Method.

In this work, hierarchically porous SiC ceramics were prepared via the foaming method. Porous ceramics with tunable, uniform, and bimodal pore structures were successfully fabricated in a facile way. The formation mechanisms of the 1st and 2nd modal macropores are the H2O2 foaming process and SiC particle overlap, respectively. The effect of pore-foaming agent amount, foaming temperature, and surfactant was investigated. According to the results, with increasing H2O2 amount, the porosity, pore size, and interconnectivity of the 1st modal pores increased, whereas bulk density and strength decreased. The porosity increased while the strength decreased as the foaming temperature increased. Surfactants increased pore interconnectivity and porosity. When the foaming temperature was 85 °C, and the addition of H2O2 was 5 wt.%, the porosity, bulk density, flexural strength, and compressive strength were 56.32%, 2.8301 g/cm3, 11.94 MPa, and 24.32 MPa, respectively. Moreover, SiC porous ceramics exhibited excellent corrosion resistance to acids and alkalis.

Diffuse auroral precipitation driven by lower-band chorus second harmonics.

Diffuse aurora at the Earth's high latitude regions is mainly caused by the low-energy (0.1-30 keV) electron precipitation which carries the major energy flux into the nightside upper atmosphere. Previous studies have demonstrated that combined scattering by the upper- and lower- band chorus waves acts as the dominant cause of diffuse auroral precipitation, but that is not necessarily the case as these two types of waves do not always occur simultaneously, with the lower-band more often. Here we report that the lower-band chorus satisfying the preferred condition can generate their second harmonics so as to trigger the diffuse auroral electron precipitation. We find that the lower-band chorus alone can only cause the precipitation of electrons greater than 4 keV, while the self-consistently generated second harmonic is weak but still able to result in the electron precipitation below 4 keV. The combined effect of those modes results in the observed pancake electron distributions and the diffuse aurora. Our results clearly demonstrate an alternative but universal mechanism of chorus-driven diffuse aurora in the Earth, which may also apply to the auroral formation in other planetary magnetospheres.

Splicing Measurement and Compensation of Straightness Errors for Ultra-Precision Guideways.

The straightness error of guideways is one of the key indicators of an ultra-precision machine, which plays an important role in the machining accuracy of a workpiece. In order to measure the straightness error of a long-distance ultra-precision guideway accurately, a splicing measurement for the straightness error of a guideway using a high-precision flat mirror and displacement sensor was proposed in this paper, and the data splicing processing algorithm based on coordinate transformation was studied. Then, comparative experiments on a splicing measurement and direct measurement of the straightness error were carried out on a hydrostatic guideway grinder. The maximum difference between the two measurements was 0.3 µm, which was far less than the straightness error of 5.8 µm. The experiment demonstrated the correctness of the proposed splicing measurement method and data processing algorithm. To suppress the influence of the straightness error on machining accuracy, a straightness error compensation algorithm based on error rotation transformation and vertical axis position correction was proposed, and the grinding experiment of a plane optics with a size of 1400 mm × 500 mm was carried out. Without error compensation grinding, the flatness error of the element was 7.54 µm. After error compensation grinding, the flatness error was significantly reduced to 2.98 µm, which was less than the straightness errors of the guideways. These results demonstrated that the straightness error of the grinding machine had been well suppressed.

Clinical Observation of Anatomical and Visual Outcomes of Macular Hole after Inverted Internal Limiting Membrane Flap in Patients with Idiopathic Macular.

Objective: To investigate anatomical and visual outcomes of macular hole (MH) after inverted internal limiting membrane (ILM) flap technique for idiopathic macular hole (IMH). Methods: A total of 13 IMH cases diagnosed in Shanxi Eye Hospital between January 2015 and June 2016 were included in the study. All patients underwent vitrectomy combined with indocyanine green-assisted inverted ILM flap technique. The MH closure rate, best-corrected visual acuity (BCVA), changes of ellipsoid zone (EZ), and external limiting membrane (ELM) were examined before operation and one, three, and six months after operation. Furthermore, 488 nm fundus autofluorescence (FAF) and spectral domain optical coherence tomography (SD-OCT) were used to observe the dynamic changes in function of macular area after surgery. Results: One month after the surgery, the MH closure rate was 100% and the visual acuity (VA) was stable, with no recurrence. Additionally, the average logMAR BCVA before operation was 1.208 ± 0.158, and this value became 0.877 ± 0.105 one month after the operation, showing a significant decrease. Three months after surgery, the average logMAR BCVA was 0.792 ± 0.103, which was significantly lower than the level one month after the surgery but much higher than that six months after surgery (0.708 ± 0.131). Besides, the diameter of the EZ defect of the postoperative one month, three months, and six months was (1377.46 ± 198.65) µm, (964.62 ± 336.26) µm, and (817.08 ± 442.99) µm, respectively. In postoperative one month, three months, and six months, the diameter of the ELM defect diameter was (969.62 ± 189.92) µm, (649.92 ± 413.15) µm, and (557.62 ± 412.50) µm, respectively. The diameter of both EZ and ELM defects was significantly reduced with the passage of time after surgery. Conclusion: Inverted ILM flap technique can reconstruct macular anatomical structure and improve VA. This technique is effective for the treatment of IMH with large MH minimum diameter and base diameter.

Observational evidence of accelerating electron holes and their effects on passing ions.

As a universal structure in space plasma, electron holes represent an obvious signature of nonlinear process. Although the theory has a 60-year history, whether electron hole can finally accelerate ambient electrons (or ions) is quite controversial. Previous theory for one-dimensional holes predicts that net velocity change of passing electrons (or ions) occurs only if the holes have non-zero acceleration. However, the prediction has not yet been demonstrated in observations. Here, we report four electron holes whose acceleration/deceleration is obtained by fitting the spatial separations and detection time delays between different Magnetospheric Multiscale spacecraft. We find that electron hole acceleration/deceleration is related to the ion velocity distribution gradient at the hole's velocity. We observe net velocity changes of ions passing through the accelerating/decelerating holes, in accordance with theoretical predictions. Therefore, we show that electron holes with non-zero acceleration can cause the velocity of passing ions to increase in the acceleration direction.