Data-driven prediction of dimensionless quantities for semi-infinite target penetration by integrating machine-learning and feature selection methods

This study employs a data-driven methodology that embeds the principle of dimensional invariance into an artificial neural network to automatically identify dominant dimensionless quantities in the penetration of rod projectiles into semi-infinite metal targets from experimental measurements.The derived mathematical expressions of dimensionless quantities are simplified by the examination of the exponent matrix and coupling relationships between feature variables.As a physics-based dimension reduction methodology,this way reduces high-dimensional parameter spaces to descriptions involving only a few physically interpretable dimensionless quantities in penetrating cases.Then the relative importance of various dimensionless feature variables on the penetration efficiencies for four impacting conditions is evaluated through feature selection engineering.The results indicate that the selected critical dimensionless feature variables by this synergistic method,without referring to the complex theoretical equations and aiding in the detailed knowledge of penetration mechanics,are in accordance with those reported in the reference.Lastly,the determined dimensionless quantities can be efficiently applied to conduct semi-empirical analysis for the specific penetrating case,and the reliability of regression functions is validated.

Investigation on the penetration of jacketed rods with striking velocities of 0.9-3.3 km/s into semi-infinite targets

In this study, a combined experimental, numerical and theoretical investigation is conducted on the penetration of semi-infinite 4340 steel targets by a homogeneous 93 W rod and two types of jacketed rods with striking velocities of 0.9-3.3 km/s. The results show that the jacketed rods produced typical“co-erosion” damage at all test velocities, except for the 93 W/1060 Al jacketed rod, which switched from an early “bi-erosion” damage to later “co-erosion” damage at a striking velocity of 936 m/s. However, the homogeneous 93 W rod always forms a large mushroom head during the penetration process. The damage mechanisms of these two types of jacketed rods differ for striking velocities of 0.9-2.0 km/s, but this difference gradually decreases with increased striking velocity. For velocities of 2.0-3.3 km/s, all three types of projectiles exhibit typical hydrodynamic penetration characteristics, and the damage mechanisms of the two types of jacketed rods are almost identical. For the same initial kinetic energy, the penetration performance of the jacketed rods is distinctly superior to that of the homogeneous 93 W rods.Compared with jacket density, jacket strength shows a more significant influence on the damage mechanism and penetration performance of the jacketed rod. Finally, an existing theoretical prediction model of the penetration depth of jacketed rods on semi-infinite targets in the co-erosion mode is modified. It transpires that-in terms of penetration depth-the modified theoretical model is in good agreement with the experimental and numerical observations for 93 W/TC4 and 93 W/1060 Al jacketed rods penetrating semi-infinite 4340 steel targets.

Analytical models for the penetration of semi-infinite targets by rigid,deformable and erosive long rods

A theoretical study is presented herein on the pen- etration of a semi-infinite target by a spherical-headed long rod for Yp 〉 S, where Yp is the penetrator strength and S is the static target resistance. For Yp 〉 S, depending upon initial impact velocity, there exist three types of penetration, namely, penetration by a rigid long rod, penetration by a deforming non-erosive long rod and penetration by an erosive long rod. If the impact velocity of the penetrator is higher than the hydrodynamic velocity （VH）, it will penetrate the target in an erosive mode; if the impact velocity lies between the hydrodynamic velocity （VH） and the rigid body velocity （VR）, it will penetrate the target in a deformable mode; if the impact velocity is less than the rigid body velocity （VR）, it will penetrate the target in a rigid mode. The critical conditions for the transition among these three penetration modes are proposed. It is demonstrated that the present model predictions correlate well with the experimental observations in terms of depth of penetration （DOP） and the critical transition conditions.

Multilevel analysis of the central-peripheral-target organ pathway:contributing to recovery after peripheral nerve injury

Peripheral nerve injury is a common neurological condition that often leads to severe functional limitations and disabilities.Research on the pathogenesis of peripheral nerve injury has focused on pathological changes at individual injury sites,neglecting multilevel pathological analysis of the overall nervous system and target organs.This has led to restrictions on current therapeutic approaches.In this paper,we first summarize the potential mechanisms of peripheral nerve injury from a holistic perspective,covering the central nervous system,peripheral nervous system,and target organs.After peripheral nerve injury,the cortical plasticity of the brain is altered due to damage to and regeneration of peripheral nerves;changes such as neuronal apoptosis and axonal demyelination occur in the spinal cord.The nerve will undergo axonal regeneration,activation of Schwann cells,inflammatory response,and vascular system regeneration at the injury site.Corresponding damage to target organs can occur,including skeletal muscle atrophy and sensory receptor disruption.We then provide a brief review of the research advances in therapeutic approaches to peripheral nerve injury.The main current treatments are conducted passively and include physical factor rehabilitation,pharmacological treatments,cell-based therapies,and physical exercise.However,most treatments only partially address the problem and cannot complete the systematic recovery of the entire central nervous system-peripheral nervous system-target organ pathway.Therefore,we should further explore multilevel treatment options that produce effective,long-lasting results,perhaps requiring a combination of passive(traditional)and active(novel)treatment methods to stimulate rehabilitation at the central-peripheral-target organ levels to achieve better functional recovery.

Research advancements in nanoparticles and cell-based drug delivery systems for the targeted killing of cancer cells

Nanotechnology in cancer therapy has significantly advanced treatment precision,effectiveness,and safety,improving patient outcomes and personalized care.Engineered smart nanoparticles and cell-based therapies are designed to target tumor cells,precisely sensing the tumor microenvironment(TME)and sparing normal cells.These nanoparticles enhance drug accumulation in tumors by solubilizing insoluble compounds or preventing their degradation,and they can also overcome therapy resistance and deliver multiple drugs simultaneously.Despite these benefits,challenges remain in patient-specific responses and regulatory approvals for cell-based or nanoparticle therapies.Cell-based drug delivery systems(DDSs)that primarily utilize the immune-recognition principle between ligands and receptors have shown promise in selectively targeting and destroying cancer cells.This review aims to provide a comprehensive overview of various nanoparticle and cell-based drug delivery system types used in cancer research.It covers approved and experimental nanoparticle therapies,including liposomes,micelles,protein-based and polymeric nanoparticles,as well as cell-based DDSs like macrophages,T-lymphocytes,dendritic cells,viruses,bacterial ghosts,minicells,SimCells,and outer membrane vesicles(OMVs).The review also explains the role of TME and its impact on developing smart DDSs in combination therapies and integrating nanoparticles with cell-based systems for targeting cancer cells.By detailing DDSs at different stages of development,from laboratory research to clinical trials and approved treatments,this review provides the latest insights and a collection of valuable citations of the innovative strategies that can be improved for the precise treatment of cancer.

HNRNPC as a pan-cancer biomarker and therapeutic target involved in tumor progression and immune regulation

Background:Aberrant expression of RNA-binding proteins(RBPs)has been linked to a variety of diseases,including hematological disorders,cardiovascular diseases,and multiple types of cancer.Heterogeneous nuclear ribonucleoprotein C(HNRNPC),a member belonging to the heterogeneous nuclear ribonucleoprotein(hnRNP)family,plays a pivotal role in nucleic acid metabolism.Previous studies have underscored the significance of HNRNPC in tumorigenesis;however,its specific role in malignant tumor progression remains inadequately characterized.Methods:We leveraged publicly available databases,including The Cancer Genome Atlas(TCGA),to explore the potential involvement of HNRNPC across various cancers.Additionally,we performed experimental validation studies focused on liver cancer.Results:Our analysis revealed that HNRNPC is overexpressed in a wide range of common malignancies,including liver and lung cancers,and is strongly linked to unfavorable outcomes.Furthermore,HNRNPC was observed to be closely linked to tumor immunity.Through immune checkpoint analysis and immune cell infiltration assessment,HNRNPC emerged as a potential target for modulating tumor immunotherapy.Notably,silencing of HNRNPC markedly inhibited the proliferation,metastasis,and infiltration of liver cancer cells.Conclusion:In summary,our findings highlight HNRNPC as a prognostic marker in various cancers,including liver cancer,and suggest its involvement in shaping the tumor immune microenvironment.These insights offer potential avenues for improving clinical outcomes in tumors with elevated HNRNPC expression,particularly through immunotherapeutic strategies.

Pyroptosis,ferroptosis,and autophagy in spinal cord injury:regulatory mechanisms and therapeutic targets

Regulated cell death is a form of cell death that is actively controlled by biomolecules.Several studies have shown that regulated cell death plays a key role after spinal cord injury.Pyroptosis and ferroptosis are newly discovered types of regulated cell deaths that have been shown to exacerbate inflammation and lead to cell death in damaged spinal cords.Autophagy,a complex form of cell death that is interconnected with various regulated cell death mechanisms,has garnered significant attention in the study of spinal cord injury.This injury triggers not only cell death but also cellular survival responses.Multiple signaling pathways play pivotal roles in influencing the processes of both deterioration and repair in spinal cord injury by regulating pyroptosis,ferroptosis,and autophagy.Therefore,this review aims to comprehensively examine the mechanisms underlying regulated cell deaths,the signaling pathways that modulate these mechanisms,and the potential therapeutic targets for spinal cord injury.Our analysis suggests that targeting the common regulatory signaling pathways of different regulated cell deaths could be a promising strategy to promote cell survival and enhance the repair of spinal cord injury.Moreover,a holistic approach that incorporates multiple regulated cell deaths and their regulatory pathways presents a promising multi-target therapeutic strategy for the management of spinal cord injury.

Targeting capabilities of engineered extracellular vesicles for the treatment of neurological diseases

Recent advances in research on extracellular vesicles have significantly enhanced their potential as therapeutic agents for neurological diseases.Owing to their therapeutic properties and ability to cross the blood–brain barrier,extracellular vesicles are recognized as promising drug delivery vehicles for various neurological conditions,including ischemic stroke,traumatic brain injury,neurodegenerative diseases,glioma,and psychosis.However,the clinical application of natural extracellular vesicles is hindered by their limited targeting ability and short clearance from the body.To address these limitations,multiple engineering strategies have been developed to enhance the targeting capabilities of extracellular vesicles,thereby enabling the delivery of therapeutic contents to specific tissues or cells.Therefore,this review aims to highlight the latest advancements in natural and targeting-engineered extracellular vesicles,exploring their applications in treating traumatic brain injury,ischemic stroke,Parkinson's disease,Alzheimer's disease,amyotrophic lateral sclerosis,glioma,and psychosis.Additionally,we summarized recent clinical trials involving extracellular vesicles and discussed the challenges and future prospects of using targeting-engineered extracellular vesicles for drug delivery in treating neurological diseases.This review offers new insights for developing highly targeted therapies in this field.

Subretinal fibrosis secondary to neovascular age-related macular degeneration:mechanisms and potential therapeutic targets

Subretinal fibrosis is the end-stage sequelae of neovascular age-related macular degeneration.It causes local damage to photoreceptors,retinal pigment epithelium,and choroidal vessels,which leads to permanent central vision loss of patients with neovascular age-related macular degeneration.The pathogenesis of subretinal fibrosis is complex,and the underlying mechanisms are largely unknown.Therefore,there are no effective treatment options.A thorough understanding of the pathogenesis of subretinal fibrosis and its related mechanisms is important to elucidate its complications and explore potential treatments.The current article reviews several aspects of subretinal fibrosis,including the current understanding on the relationship between neovascular age-related macular degeneration and subretinal fibrosis;multimodal imaging techniques for subretinal fibrosis;animal models for studying subretinal fibrosis;cellular and non-cellular constituents of subretinal fibrosis;pathophysiological mechanisms involved in subretinal fibrosis,such as aging,infiltration of macrophages,different sources of mesenchymal transition to myofibroblast,and activation of complement system and immune cells;and several key molecules and signaling pathways participating in the pathogenesis of subretinal fibrosis,such as vascular endothelial growth factor,connective tissue growth factor,fibroblast growth factor 2,platelet-derived growth factor and platelet-derived growth factor receptor-β,transforming growth factor-βsignaling pathway,Wnt signaling pathway,and the axis of heat shock protein 70-Toll-like receptors 2/4-interleukin-10.This review will improve the understanding of the pathogenesis of subretinal fibrosis,allow the discovery of molecular targets,and explore potential treatments for the management of subretinal fibrosis.

A novel detection method for warhead fragment targets in optical images under dynamic strong interference environments

A measurement system for the scattering characteristics of warhead fragments based on high-speed imaging systems offers advantages such as simple deployment,flexible maneuverability,and high spatiotemporal resolution,enabling the acquisition of full-process data of the fragment scattering process.However,mismatches between camera frame rates and target velocities can lead to long motion blur tails of high-speed fragment targets,resulting in low signal-to-noise ratios and rendering conventional detection algorithms ineffective in dynamic strong interference testing environments.In this study,we propose a detection framework centered on dynamic strong interference disturbance signal separation and suppression.We introduce a mixture Gaussian model constrained under a joint spatialtemporal-transform domain Dirichlet process,combined with total variation regularization to achieve disturbance signal suppression.Experimental results demonstrate that the proposed disturbance suppression method can be integrated with certain conventional motion target detection tasks,enabling adaptation to real-world data to a certain extent.Moreover,we provide a specific implementation of this process,which achieves a detection rate close to 100%with an approximate 0%false alarm rate in multiple sets of real target field test data.This research effectively advances the development of the field of damage parameter testing.

Targeted maintenance therapy for a young woman with cervical rhabdomyosarcoma:A case report and review of literature

BACKGROUND Rhabdomyosarcoma of the uterine cervix is a rare form of soft-tissue sarcoma predominantly affecting young women,with no established standard treatment protocol.CASE SUMMARY This report presents a case of a 17-year-old female patient presenting with in-termittent,non-cyclical vaginal bleeding and associated lower abdominal pain.Pelvic magnetic resonance imaging and additional examinations led to the dia-gnosis of cervical rhabdomyosarcoma.The primary treatment options for uterine cervical rhabdomyosarcoma include surgery,with or without adjuvant chemo-therapy and radiotherapy.This patient underwent surgery followed by a posto-perative chemotherapy regimen of gemcitabine combined with docetaxel and bevacizumab.After 19 months of follow-up,the patient showed no signs of re-currence and maintained good overall health.Given the rarity of cervix rhab-domyosarcoma,this case is presented to provide insights into the diagnosis and treatment of this condition.CONCLUSION This suggests that bevacizumab may demonstrate potential efficacy in the treat-ment of cervical rhabdomyosarcoma.In the future,targeted therapy is expected to play an increasingly significant role in the management of rhabdomyosarcoma.

Tankyrase 2 as a therapeutic target in non-small cell lung cancer: Implications for apoptosis and migration

This letter addresses Wang and Zhang's investigation into the role of tankyrase 2(TNKS2)as a pivotal driver of malignancy in non-small cell lung cancer(NSCLC)through mechanisms including apoptosis inhibition,enhanced cellular migration,andβ-catenin pathway activation.Their study in NSCLC cell lines demonstrates that TNKS2 overexpression stabilizesβ-catenin,subsequently triggering onco-genic gene expression and facilitating cellular migration-key attributes of meta-static potential.These insights position TNKS2 as a compelling target for therapy and a potential prognostic marker in NSCLC.Nevertheless,translating these in vitro findings to clinical practice requires validation in in vivo models.Addi-tionally,further research should investigate TNKS2 expression in patient samples and assess its implications in therapy resistance and combination treatment strategies.

Real-world cost-effectiveness of targeted temperature management in out-of-hospital cardiac arrest survivors: results from an academic medical center

BACKGROUND: Targeted temperature management(TTM) is a common therapeutic intervention, yet its cost-effectiveness remains uncertain. This study aimed to evaluate the real-world cost-effectiveness of TTM compared with that of conventional care in adult out-of-hospital cardiac arrest(OHCA) survivors using clinical patient-level data.METHODS: We conducted a retrospective cohort study at an academic medical center in the USA to assess the cost-effectiveness of TTM in adult non-traumatic OHCA survivors between 1 January, 2019 and 30 June, 2023. The primary outcome was survival to hospital discharge. Incremental cost-effectiveness ratios(ICERs) were calculated and compared with various decision makers' willingness to pay. Cost-effectiveness acceptability curves were utilized to evaluate the economic attractiveness of TTM. Uncertainty about the incremental cost and effect was explored with a 95% confidence ellipse.RESULTS: Among 925 non-traumatic OHCA survivors, only 30(3%) received TTM. After adjusting for potential confounders, the TTM group did not demonstrate a significantly lower cost(delta cost-$5,141, 95% confidence interval [95% CI]: $-35,347 to $25,065, P=0.79) and higher survival to hospital discharge(delta effect 6%, 95% CI:-11% to 23%, P=0.41). Additionally, a 95% confidence ellipse indicated uncertainty reflected by evidence that the true value of the ICER could be in any of the quadrants of the cost-effectiveness plane.CONCLUSION: Although TTM did not demonstrate a clear survival benefit in this study, its potential cost-effectiveness warrants further investigation with larger sample sizes. These findings highlight the need for additional research to optimize TTM use in OHCA care and inform resource allocation decisions.

Impact of setting distinct target blood glucose levels on endogenous insulin suppression and pharmacodynamics of insulin preparations

BACKGROUND Insulin therapy plays a crucial role in managing diabetes.Regulatory guidelines mandate assessing the pharmacokinetics(PK)and pharmacodynamics(PD)of new insulin formulations with euglycemic clamp techniques before entry into the market.Typically,blood glucose(BG)levels are maintained at 5%below baseline to suppress endogenous insulin secretion in healthy volunteers.However,in scenarios where BG baseline is relatively low,maintaining it at 5%below baseline can increase hypoglycemic risk.Consequently,we adjusted to maintain it at 2.5%below a baseline of<4.00 mmol/L.It remains uncertain whether this adjustment impacts endogenous insulin inhibition or the PD of study insulin.AIM To evaluate and compare the PD and C-peptide status using two different target BG setting methods.METHODS Data came from euglycemic clamp trials assessing the PK/PD of insulin aspart(IAsp)in healthy participants.Target BG was set at 2.5%below baseline for those with a basal BG of<4.00 mmol/L(group A),and at 5%below baseline for others(group B).The area under the curve(AUC)of IAsp(AUC_(IAsp,0-8 h))and GIR from 0 to 8 hours(AUCGIR,0-8 h)was used to characterize the PK and PD of IAsp,respectively.The C-peptide reduction and PK/PD of IAsp were compared between the two groups.RESULTS Out of 135 subjects,15 were assigned to group A and 120 to group B;however,group B exhibited higher basal Cpeptide(1.59±0.36 vs 1.32±0.42 ng/mL,P=0.006).Following propensity score matching to adjust for basal Cpeptide differences,71 subjects(15 in group A and 56 in group B)were analyzed.No significant differences were observed in demographics,IAsp dosage,or clamp quality.Group B showed significantly higher baseline(4.35±0.21 vs 3.91±0.09 mmol/L,P<0.001),target(4.13±0.20 vs 3.81±0.08 mmol/L,P<0.001),and clamped(4.10±0.17 vs 3.80±0.06 mmol/L,P<0.001)BG levels.Both groups exhibited comparable C-peptide suppression(32.5%±10.0%vs 35.6%±12.1%,P=0.370)and similar IAsp activity(AUCGIR,0-8 h:1433±400 vs 1440±397 mg/kg,P=0.952)under nearly equivalent IAsp exposure(AUC_(IAsp,0-8 h):566±51 vs 571±85 ng/mL×h,P=0.840).CONCLUSION Maintaining BG at 2.5%below a baseline of<4.00 mmol/L did not compromise the endogenous insulin suppression nor alter the observed pharmacodynamic effects of the study insulin.

Synergistic inhibition of colorectal cancer progression by silencing Aurora A and the targeting protein for Xklp2

BACKGROUND Unraveling the pathogenesis of colorectal cancer(CRC)can aid in developing prevention and treatment strategies.Aurora kinase A(AURKA)is a key participant in mitotic control and interacts with its co-activator,the targeting protein for Xklp2(TPX2)microtubule nucleation factor.AURKA is associated with poor clinical outcomes and high risks of CRC recurrence.AURKA/TPX2 co-overexpression in cancer may contribute to tumorigenesis.Despite its pivotal role in CRC development and progression,the action mechanism of AURKA remains unclear.Further research is needed to explore the complex interplay between AURKA and TPX2 and to develop effective targeted treatments for patients with CRC.AIM To compare effects of AURKA and TPX2 and their combined knockdown on CRC cells.METHODS We evaluated three CRC gene datasets about CRC(GSE32323,GSE25071,and GSE21510).Potential hub genes associated with CRC onset were identified using the Venn,search tool for the retrieval of interacting genes,and KOBAS platforms,with AURKA and TPX2 emerging as significant factors.Subsequently,cell models with knockdown of AURKA,TPX2,or both were constructed using SW480 and LOVO cells.Quantitative real-time polymerase chain reaction,western blotting,cell counting kit-8,cell cloning assays,flow cytometry,and Transwell assays were used.RESULTS Forty-three highly expressed genes and 39 poorly expressed genes overlapped in cancer tissues compared to controls from three datasets.In the protein-protein interaction network of highly expressed genes,AURKA was one of key genes.Its combined score with TPX2 was 0.999,and their co-expression score was 0.846.In CRC cells,knockdown of AURKA,TPX2,or both reduced cell viability and colony number,while blocking G0/G1 phase and enhancing cell apoptosis.Additionally,they were weakened cell proliferation and migration abilities.Furthermore,the expression levels of B-cell lymphoma-2-Associated X,caspase 3,and tumor protein P53,and E-cadherin increased with a decrease in B-cell lymphoma-2,N-cadherin,and vimentin proteins.These effects were amplified when both AURKA and TPX2 were concurrently downregulated.CONCLUSION Combined knockdown of AURKA and TPX2 was effective in suppressing the malignant phenotype in CRC.Coinhibition of gene expression is a potential developmental direction for CRC treatment.

Interaction between many parallel screw dislocations and a semi-infinite crack in a magnetoelectroelastic solid

Based on the fundamental equations of magnetoelectroelastic material and the analytic theory, and using the Muskhelishvili-introduced well-known elastic techniques combined with the superposition principle, the closed form solution of the generalized stress field of the interaction between many parallel screw dislocations and a semi-infinite crack in an infinite magnetoelectroelastic solid is obtained, on the assumption that the surface of the crack is impermeable electrically and magnetically. Besides, the Peach-Koehler formula of n parallel screw dislocations is given. Numerical examples show that the generalized stress varies with the position of point z and is related to the material constants. The results indicate that the stress concentration occurs at the dislocation core and the tip of the crack. The result of interaction makes the system stay in a lower energy state.

ASYMPTOTIC APPROXIMATION METHOD AND ITS CONVERGENCE ON SEMI-INFINITE PROGRAMMING

The aim of this article is to discuss an asymptotic approximation model and its convergence for the minimax semi-infinite programming problem. An asymptotic surrogate constraints method for the minimax semi-infinite programming problem is presented by making use of two general discrete approximation methods. Simultaneously, the consistence and the epi-convergence of the asymptotic approximation problem are discussed.

Interaction between infinitely many dislocations and a semi-infinite crack in one-dimensional hexagonal quasicrystal

By means of analytic function theory, the problems of interaction between infinitely many parallel dislocations and a semi-infinite crack in one-dimensional hexagonal quasicrystal are studied. The analytic solutions of stress fields of the interaction between infinitely many parallel dislocations and a semi-infinite crack in one-dimensional hexagonal quasicrystal are obtained. They indicate that the stress concentration occurs at the dislocation source and the tip of the crack, and the value of the stress increases with the number of the dislocations increasing. These results are the development of interaction among the finitely many defects of quasicrystals, which possesses an important reference value for studying the interaction problems of infinitely many defects in fracture mechanics of quasicrystal.

Exact solutions of two semi-infinite collinear cracks in piezoelectric strip

Using the complex variable function method and the conformal mapping technique, the fracture problem of two semi-infinite collinear cracks in a piezoelectric strip is studied under the anti-plane shear stress and the in-plane electric load on the partial crack surface. Analytic solutions of the field intensity factors and the mechanical strain energy release rate are derived under the assumption that the surfaces of the crack are electrically impermeable. The results can be reduced to the well-known solutions for a purely elastic material in the absence of an electric load. Moreover, when the distance between the two crack tips tends to infinity, analytic solutions of a semi-infinite crack in a piezoelectric strip can be obtained. Numerical examples are given to show the influence of the loaded crack length, the height of the strip, the distance between the two crack tips, and the applied mechanical/electric loads on the mechanical strain energy release rate. It is shown that the material is easier to fail when the distance between two crack tips becomes shorter, and the mechanical/electric loads have greater influence on the propagation of the left crack than those of the right one.

Anti-plane analysis of semi-infinite crack in piezoelectric strip

Using the complex variable function method and the technique of the conformal mapping, the fracture problem of a semi-infinite crack in a piezoelectric strip is studied under the anti-plane shear stress and the in-plane electric load. The analytic solutions of the field intensity factors and the mechanical strain energy release rate are presented under the assumption that the surface of the crack is electrically impermeable. When the height of the strip tends to infinity, the analytic solutions of an infinitely large piezoelectric solid with a semi-infinite crack are obtained. Moreover, the present results can be reduced to the well-known solutions for a purely elastic material in the absence of the electric loading. In addition, numerical examples are given to show the influences of the loaded crack length, the height of the strip, and the applied mechanical/electric loads on the mechanical strain energy release rate.