Fabrication of elliptical-silica microfiber for ultrasound detection.

Elliptical shape microfiber enables many higher order modes compared with a circular microfiber. The small difference in the optical path length among many modes enabled multi-resonance peaks with high contrast in Mach-Zehnder (MZI) interferometers, which allows a large dynamic range and minimum detection sensitivity for broadband ultrasound sensing. In this paper, we present the design and fabrication of an ultra-compact elliptical-silica microfiber utilizing off-axis flame-drawing for ultrasound detection. The narrow transmission peak showed high contrast for ultrasensitive ultrasound wave detection. With a major-axis diameter of 6.25 µm, the elliptical-silica microfiber sensor exhibits a broadband ultrasound frequency response spanning from 20 kHz to 38.5 MHz. Furthermore, it achieves a signal-to-noise ratio (SNR) of up to 80 dB at 1 MHz, which is the resonance frequency of the microfiber and the linear response under driving voltages of 3-10 V for the PZT ultrasound generator. This low-cost microfiber sensor offers exceptional sensitivity across a broad ultrasonic bandwidth response, making it an ideal choice for nondestructive testing (NDT) and medical imaging applications. Its compact size and immunity to electric and magnetic fields further enhance its utility in various environments.

Cigarette tar accelerates atherosclerosis progression via RIPK3-dependent necroptosis mediated by endoplasmic reticulum stress in vascular smooth muscle cells.

BACKGROUND: Tar is the main toxic of cigarettes, and its effect on atherosclerosis progression and the underlying mechanisms remain largely unknown. Vascular smooth muscle cells (VSMCs) play a key role in atherogenesis and plaque vulnerability. The present study sought to investigate the mechanism of atherosclerosis progression through tar-induced VSMC necroptosis, a recently described form of necrosis. METHODS: The effect of tar on atherosclerosis progression and VSMC necroptosis was examined in ApoE-/- mice and cultured VSMCs. The role of necroptosis in tar-induced plaque development was evaluated in RIPK3-deletion mice (ApoE-/-RIPK3-/-). The key proteins of necroptosis in carotid plaques of smokers and non-smokers were also examined. Quantitative proteomics of mice aortas was conducted to further investigate the underlying mechanism. Pharmacological approaches were then applied to modulate the expression of targets to verify the regulatory process of tar-induced necroptosis. RESULTS: Tar administration led to increased atherosclerotic plaque area and reduced collagen and VSMCs in ApoE-/- mice. The expression of RIPK1、RIPK3、and MLKL in VSMCs of plaques were all increased in tar-exposed mice and smokers. RIPK3 deletion protected against VSMC loss and plaque progression stimulated by tar. In mechanistic studies, quantitative proteomics analysis of ApoE-/- mice aortas suggested that tar triggered endoplasmic reticulum (ER) stress. PERK-eIF2α-CHOP axis was activated in tar-treated VSMCs and atherosclerotic plaque. Inhibition of ER stress using 4PBA significantly reduced plaque progression and VSMC necroptosis. Further study revealed that ER stress resulted in calcium (Ca2+) release into mitochondria and cytoplasm. Elevated Ca2+ levels lead to mitochondrial dysfunction and excessive reactive oxygen species (ROS) production, which consequently promote RIPK3-dependent necroptosis. In addition, Ca2+/calmodulin-dependent protein kinase II (CaMKII) activated by cytosolic Ca2+ overload binds to RIPK3, accounting for necroptosis. CONCLUSION: The findings revealed that cigarette tar promoted atherosclerosis progression by inducing RIPK3-dependent VSMC necroptosis and identified novel avenues of ER stress and Ca2+ overload.

Association between fasting stress hyperglycemia ratio and contrast-induced acute kidney injury in coronary angiography patients: a cross-sectional study.

Aims: Stress hyperglycemia ratio (SHR), an emerging indicator of critical illness, exhibits a significant association with adverse cardiovascular outcomes. The primary aim of this research endeavor is to evaluate the association between fasting SHR and contrast-induced acute kidney injury (CI-AKI). Methods: This cross-sectional study comprised 3,137 patients who underwent coronary angiography (CAG) or percutaneous coronary intervention (PCI). The calculation of fasting SHR involved dividing the admission fasting blood glucose by the estimated mean glucose obtained from glycosylated hemoglobin. CI-AKI was assessed based on elevated serum creatinine (Scr) levels. To investigate the relationship between fasting SHR and the proportion of SCr elevation, piecewise linear regression analysis was conducted. Modified Poisson's regression analysis was implemented to evaluate the correlation between fasting SHR and CI-AKI. Subgroup analysis and sensitivity analysis were conducted to explore result stability. Results: Among the total population, 482 (15.4%) patients experienced CI-AKI. Piecewise linear regression analysis revealed significant associations between the proportion of SCr elevation and fasting SHR on both sides (≤ 0.8 and > 0.8) [ß = -12.651, 95% CI (-23.281 to -2.022), P = 0.020; ß = 8.274, 95% CI (4.176 to 12.372), P < 0.001]. The Modified Poisson's regression analysis demonstrated a statistically significant correlation between both the lowest and highest levels of fasting SHR and an increased incidence of CI-AKI [(SHR < 0.7 vs. 0.7 ≤ SHR < 0.9) ß = 1.828, 95% CI (1.345 to 2.486), P < 0.001; (SHR ≥ 1.3 vs. 0.7 ≤ SHR < 0.9) ß = 2.896, 95% CI (2.087 to 4.019), P < 0.001], which was further validated through subgroup and sensitivity analyses. Conclusion: In populations undergoing CAG or PCI, both lowest and highest levels of fasting SHR were significantly associated with an increased occurrence of CI-AKI.

A random optical parametric oscillator.

Synchronously pumped optical parametric oscillators (OPOs) provide ultra-fast light pulses at tuneable wavelengths. Their primary drawback is the need for precise cavity control (temperature and length), with flexibility issues such as fixed repetition rates and marginally tuneable pulse widths. Targeting a simpler and versatile OPO, we explore the inherent disorder of the refractive index in single-mode fibres realising the first random OPO - the parametric analogous of random lasers. This novel approach uses modulation instability (χ(3) non-linearity) for parametric amplification and Rayleigh scattering for feedback. The pulsed system exhibits high inter-pulse coherence (coherence time of ~0.4 ms), offering adjustable repetition rates (16.6-2000 kHz) and pulse widths (0.69-47.9 ns). Moreover, it operates continuously without temperature control loops, resulting in a robust and flexible device, which would find direct application in LiDAR technology. This work sets the stage for future random OPOs using different parametric amplification mechanisms.

Apigenin inhibits macrophage pyroptosis through regulation of oxidative stress and the NF-κB pathway and ameliorates atherosclerosis.

Pyroptosis plays an important role in inflammatory diseases such as viral hepatitis and atherosclerosis. Apigenin exhibits various bioactivities, particularly anti-inflammation, but its effect on pyroptosis remains unclear. The aim of this study is to investigate the effect of apigenin on pyroptosis and explore its potential against inflammatory diseases. THP-1 macrophages treated by lipopolysaccharides/adenosine 5'-triphosphate were used as the in vitro pyroptosis model. Western blot was used to detect the expression of NLRP3 inflammasome components and key regulators. Immunofluorescence was used to observe ROS production and intracellular location of p65. The potential of apigenin against inflammatory diseases was evaluated using atherosclerotic mice. Plaque progression was observed by pathological staining. Immunofluorescence was used to observe the expression of NLRP3 inflammasome components in plaques. The results showed that apigenin inhibited NLRP3 inflammasome activation. Apigenin reduced ROS overproduction and inhibited p65 nuclear translocation. Additionally, apigenin decreased the expression of NLRP3 inflammasome components in the plaque. Plaque progression was inhibited by apigenin. In conclusion, apigenin exhibited a preventive effect on macrophage pyroptosis by reducing oxidative stress and inhibiting the NF-κB pathway. Apigenin may alleviate atherosclerosis at least partially by inhibiting macrophage pyroptosis. These findings suggest apigenin to be a promising therapeutic agent for inflammatory diseases.

Combining metabolomics and OCT to reveal plasma metabolic profiling and biomarkers of plaque erosion and plaque rupture in STEMI patients.

OBJECTIVE: Plaque erosion (PE) and plaque rupture (PR) are the main subtypes of ST-segment elevation myocardial infarction (STEMI), the differences of metabolic patterns between PE and PR remain largely unknown. METHODS: 132 STEMI patients were divided into training set (PR, n = 36; PE, n = 36) and test set (PR, n = 30; PE, n = 30), the plasma from patients were analyzed by liquid chromatography quadruple time-of-flight mass spectrometry. RESULTS: We identified 56 and 28 differences in training and test set, respectively. Among these metabolites, it was found that docosahexaenoic acid (DHA), salicylic acid and proline were recognized in both tests. Receiver Operating Characteristic (ROC) analysis showed that the area under curve of docosahexaenoic acid (DHA) was 0.81 and 0.75 in training and test samples, respectively; proline was 0.67 and 0.74 in training and test samples, respectively; salicylic acid was 0.70 and 0.73 in training and test samples, respectively. CONCLUSIONS: DHA, salicylic acid, and proline could be used as non-invasive biomarkers to differentiate PE and PR.

Homocysteine promotes atherosclerosis through macrophage pyroptosis via endoplasmic reticulum stress and calcium disorder.

BACKGROUND: Elevated plasma homocysteine levels, known as hyperhomocysteinemia, have been identified as an independent risk factor for atherosclerosis and related cardiovascular diseases. Macrophage pyroptosis-mediated inflammation is crucial in the development of atherosclerosis, but the underlying mechanisms remain unclear. METHODS: A hyperhomocysteinemia atherosclerotic model with ApoE-/- mice fed with a high-methionine diet was constructed to investigate the role of plasma homocysteine in atherosclerosis. THP-1-derived macrophages were used to investigate the mechanisms by which Hcy regulates pyroptosis. RESULTS: We found that hyperhomocysteinemia resulted in larger atherosclerotic plaques and more secretion of inflammatory cytokines, while these effects were attenuated in Caspase-1 knockdown mice. Likewise, in vitro experiments demonstrated that treatment of macrophages with homocysteine resulted in NLRP3 inflammasome activation and pyroptosis, as evidenced by cleavage of Caspase-1, production of downstream IL-1ß, elevation of lactate dehydrogenase activity, and extensive propidium iodide-positive staining of cells. These were all inhibited by Caspase-1 inhibitor. In addition, excessive generation of reactive oxygen species was associated with mitochondrial dysfunction, characterized by loss of mitochondrial membrane potential and ATP synthesis. Moreover, further experiments revealed that homocysteine induced endoplasmic reticulum stress, enhanced communication between the endoplasmic reticulum and mitochondria, and consequently contributed to calcium disorder. Furthermore, the endoplasmic reticulum stress inhibitor, 4PBA, the calcium chelator, BAPTA, and calcium channel inhibitor, 2-APB significantly improved macrophage pyroptosis. CONCLUSION: Homocysteine accelerates atherosclerosis progression by enhancing macrophages pyroptosis via promoting endoplasmic reticulum stress, endoplasmic reticulum-mitochondria coupling, and disturbing of calcium disorder.

Self-injection locking of a low-noise erbium-doped random fiber laser by a random fiber grating ring.

We demonstrate a self-injection locking (SIL) in an Er-doped random fiber laser by a high quality factor (high-Q) random fiber grating ring (RFGR) resonator, which enables a single-mode narrow-linewidth lasing with ultra-low intensity and frequency noise. The RFGR resonator includes a fiber ring with a random fiber grating to provide random feedback modes and noise suppression filters with self-adjusted peak frequency adaptable to small perturbations allowing single longitudinal mode over 7000 s with frequency jitter below 3.0 kHz. Single-mode operation is accomplished by carefully controlling phase delays and mode coupling of resonant modes between main ring and RFGR with a side-mode suppression ratio of 70 dB and narrow linewidth of 1.23 kHz. The relative intensity noise is -140 dB/Hz above 100 kHz and the frequency noise is 1 Hz/Hz1/2 above 10 kHz.

Orthogonal polarization multi-wavelength Brillouin random fiber laser with triple Brillouin frequency shift space.

A novel multi-wavelength Brillouin random fiber laser with the channel space of triple Brillouin frequency shift and high polarization orthogonality between adjacent wavelengths (TOP-MWBRFL), to the best of our knowledge, is experimentally demonstrated. The TOP-MWBRFL is structured in a ring form by cascading two Brillouin random cavities of single-mode fiber (SMF) and one Brillouin random cavity of polarization-maintaining fiber (PMF). Based on polarization pulling properties of stimulated Brillouin scattering in long-distance SMFs and PMFs, the states of polarization (SOPs) of lasing light from SMF random cavities are linearly bounded to the SOPs of local pump light, whereas the SOP of lasing light from the PMF random cavity is strictly clamped on one of the principal axes of the PMF. Thus, the TOP-MWBRFL can stably emit multi-wavelength light with high polarization extinction ratio (>35d B) between adjacent wavelengths without precise polarization feedback. In addition, the TOP-MWBRFL can also work in one polarization mode to stably lase multi-wavelength light with SOP uniformity as high as 37 dB.

Estrogen deficiency accelerates postmenopausal atherosclerosis by inducing endothelial cell ferroptosis through inhibiting NRF2/GPX4 pathway.

Oxidative stress and lipid metabolism disorder caused by estrogen deficiency are regarded as the main causes of postmenopausal atherosclerosis, but the underlying mechanisms remain still unclear. In this study, ovariectomized (OVX) female ApoE-/- mice fed with high-fat diet were used to imitate postmenopausal atherosclerosis. The atherosclerosis progression was significantly accelerated in OVX mice, accompanied by the upregulation of ferroptosis indicators, including increased lipid peroxidation and iron deposition in the plaque and the plasma. While both estradiol (E2) and ferroptosis inhibitor ferrostatin-1 alleviated atherosclerosis in OVX mice, with the inhibition of lipid peroxidation and iron deposition, as well as the upregulation of xCT and GPX4, especially in endothelial cells. We further investigated the effects of E2 on ferroptosis in endothelial cells induced by oxidized-low-density lipoprotein or ferroptosis inducer Erastin. It was found that E2 exhibited anti-ferroptosis effect through antioxidative functions, including improving mitochondrial dysfunction and upregulating GPX4 expression. Mechanistically, NRF2 inhibition attenuated the effect of E2 against ferroptosis as well as the upregulation of GPX4. Our findings revealed that endothelial cell ferroptosis played a pivotal role in postmenopausal atherosclerosis progression, and the NRF2/GPX4 pathway activation contributed to the protection of E2 against endothelial cell ferroptosis.

Cigarette tar mediates macrophage ferroptosis in atherosclerosis through the hepcidin/FPN/SLC7A11 signaling pathway.

Despite the known promotional effects of cigarette smoking on progression of atherosclerosis (AS), tar as the most dominant toxic component in cigarette smoking has been little studied. Understanding the potential role and mechanisms of tar in AS may be a prerequisite for future reductions in cardiovascular morbidity and mortality. Male ApoE-/- mice were fed with high-fat diet and injected intraperitoneally with cigarette tar (40 mg/kg/day) for 16 weeks. The results showed that cigarette tar significantly promoted the formation of lipid-rich plaques with larger necrotic cores and less fibrous, and caused severe iron overload and lipid peroxidation in AS lesions. Moreover, tar significantly upregulated the expression of hepcidin and downregulated FPN and SLC7A11 of macrophages in AS plaques. Ferroptosis inhibitor (FER-1 and DFO) treatment, hepcidin-knockdown or SLC7A11-overexpression reversed above changes, thereby delaying the progression of atherosclerosis. In vitro, the use of FER-1, DFO, si-hepcidin, and ov-SLC7A11 increased cell viability and inhibited iron accumulation, lipid peroxidation and GSH depletion in tar treated macrophages. These interventions also inhibited the tar induced upregulation of hepcidin, and increased the expression of FPN, SLC7A11, and GPX4. Furthermore, NF-κB inhibitor reversed the regulatory effect of tar on hepcidin/FPN/SLC7A11 axis, and then inhibiting macrophage ferroptosis. These findings indicated that cigarette tar promotes atherosclerosis progression by inducing macrophage ferroptosis via NF-κB-activated hepcidin/FPN/SLC7A11 pathway.

Distributed Impact Wave Detection in Steel I-Beam with a Weak Fiber Bragg Gratings Array.

In this paper, acoustic, dynamic and static strain variations along a steel I-beam generated by an impact load are reconstructed simultaneously within a single measurement. Based on the chirped pulse φ-OTDR system with the single-shot measurement technique, both a higher strain-sensing resolution and a higher measurable vibration frequency are achieved. In addition, a weak fiber Bragg gratings array (WFBGA) with enhanced Rayleigh reflection is employed as a sensor, providing high signal-to-noise ratio Rayleigh traces, resulting in lower measurement uncertainty. In the experiments, the damping constant and fundamental frequency of the damped harmonic oscillator could then be measured based on the recovered strain variation profile for further structural health analysis. Compared with commercial strain gauges, linear potentiometers, and OFDR systems, the proposed sensing system ensures a distributed, quantitative, and high-frequency sensing ability, with an extensive range of potential applications.

Clinical Characteristics and Prognosis of MINOCA Caused by Atherosclerotic and Nonatherosclerotic Mechanisms Assessed by OCT.

BACKGROUND: Myocardial infarction with nonobstructive coronary artery (MINOCA) is a heterogeneous syndrome caused by different pathophysiologic mechanisms. There is limited evidence regarding prognosis of patients with MINOCA caused by different mechanisms. OBJECTIVES: The present study aimed to assess the underlying mechanisms of MINOCA by optical coherence tomography (OCT) and to correlate with clinical outcomes. METHODS: Patients with MINOCA were divided into 2 groups based on OCT findings: atherosclerotic MINOCA (Ath-MINOCA) and nonatherosclerotic MINOCA (non-Ath-MINOCA). Major adverse cardiac events (MACE) were defined as cardiac death, nonfatal MI, target lesion revascularization, stroke, and rehospitalization for unstable or progressive angina. RESULTS: Among 7,423 patients with a clinical diagnosis of MI who underwent angiography, 190 of 294 MINOCA were studied using OCT. The causes of Ath-MINOCA (n = 99, 52.1%) were plaque erosion (n = 64, 33.7%), plaque rupture (n = 33, 17.4%), and calcified nodule (n = 2, 1.1%) whereas the causes of non-Ath-MINOCA (n = 91, 47.9%) were spontaneous coronary artery dissection (n = 8, 4.2%), coronary spasm (n = 9, 4.7%), and unclassified cause (n = 74, 38.9%). The 1-year MACE was 15.3% for Ath-MINOCA vs 4.5% for non-Ath-MINOCA (P = 0.015). An atherosclerotic cause was an independent predictor of MACE (HR: 5.36 [95% CI: 1.08-26.55]; P = 0.040), mainly driven by target lesion revascularization and rehospitalization, despite the composite endpoint including cardiac death and MI showing no difference. CONCLUSIONS: OCT identified a cause in 61.1% of MINOCA, in which Ath-MINOCA represents an important and distinct MINOCA subset. Ath-MINOCA were more common and associated with worse outcomes. (Incidence Rate of Heart Failure After Acute Myocardial Infarction With Optimal Treatment; NCT03297164; Paradigm Shift in the Treatment of Patients With ACS; NCT02041650).

Oxidative Stress-Mediated Programmed Cell Death: a Potential Therapy Target for Atherosclerosis.

Nowadays, as a type of orderly and active death determined by genes, programmed cell death (PCD), including apoptosis, pyroptosis, ferroptosis, and necroptosis, has attracted much attention owing to its participation in numerous chronic cardiovascular diseases, especially atherosclerosis (AS), a canonical chronic inflammatory disease featured by lipid metabolism disturbance. Abundant researches have reported that PCD under distinct internal conditions fulfills different roles of atherosclerotic pathological processes, including lipid core expansion, leukocyte adhesion, and infiltration. Noteworthy, emerging evidence recently has also suggested that oxidative stress (OS), an imbalance of antioxidants and oxygen free radicals, has the potential to mediate PCD occurrence via multiple ways, including oxidization and deubiquitination. Interestingly, more recently, several studies have proposed that the mediating mechanisms could effect on the atherosclerotic initiation and progression significantly from variable aspects, so it is of great clinical importance to clarify how OS-mediated PCD and AS interact. Herein, with the aim of summarizing potential and sufficient atherosclerotic therapy targets, we seek to provide extensive analysis of the specific regulatory mechanisms of PCD mediated by OS and their multifaceted effects on the entire pathological atherosclerotic progression.

Stabilizing Brillouin random laser with photon localization by feedback of distributed random fiber grating array.

Strong scattering random media can localize light and extend photon lifetime through multiple scattering, which offers opportunities for stabilizing random lasers. Here, we demonstrate a frequency stabilized Brillouin random laser with high coherence enabled by photon localization in random fiber grating array (RFGA). Photon trapping is realized due to wave interference in multi-scattering Fabry-Pérot (FP) cavities between random fiber gratings enabling light localization to prolong photon lifetime. The formation of the high finesse peaks of RFGA suppresses multi-longitudinal modes, which offers single-mode operation at high pump power. The RFGA distributed feedback-based Brillouin random fiber laser (BRFL) maintains a small frequency drift with the pump laser (a phase-locked laser with a linewidth of 100 Hz) at 51 kHz/s for a total change of 620 kHz over 12 s. Note there is no locking between the two lasers, and the beat frequency is measured by the optical heterodyne method. The correlation coefficient change of the measured optical beat frequency is maintained at 4.5%. This indicates that the BRFL is capable of maintaining a small optical frequency difference with the phase-locked pump laser over 12 s thanks to the RFGA capable of trapping photons in the same path, which is a remarkable feature for a random fiber laser. Furthermore, we confirm the single-mode lasing with a long lifetime in the stabilizing BRFL by the replica symmetry behavior and ultralow intensity noise at high pump power. Our findings explore a new approach to stabilize the frequency of Brillouin random lasers passively without commonly used active phase locking laser themes, which makes a simple and cost-effective system.

Distributed birefringence sensing at 10-9 accuracy over ultra-long PMF by optical frequency comb and distributed Brillouin amplifier.

Brillouin dynamic gratings (BDG) can measure the distributed birefringence of polarization-maintaining fibers (PMF), however, its sensing range is limited by both stimulated Brillouin scattering depletion and fiber losses in PMF, which are significantly higher than those in standard single-mode fibers. In this work, we theoretically and experimentally verify that BDG can be sustained over ultra-long distances when assisted by distributed Brillouin amplification, significantly extending the distributed birefringence measurement distance. Using an optical frequency comb pumped by a narrow linewidth laser to both generate and interrogate the amplified BDG, a birefringence measurement accuracy of 7.5 × 10-9 was achieved over 7 km sensing length, more than double the longest range reported. This opens a new opportunity to investigate small birefringence changes due to nonlinear optics effects and monitoring fiber network security from eavesdropping.

A novel anti-atherosclerotic mechanism of quercetin: Competitive binding to KEAP1 via Arg483 to inhibit macrophage pyroptosis.

Natural antioxidants represented by quercetin have been documented to be effective against atherosclerosis. However, the related mechanisms remain largely unclear. In this study, we identified a novel anti-atherosclerotic mechanism of quercetin inhibiting macrophage pyroptosis by activating NRF2 through binding to the Arg483 site of KEAP1 competitively. In ApoE-/- mice fed with high fat diet, quercetin administration attenuated atherosclerosis progression by reducing oxidative stress level and suppressing macrophage pyroptosis. At the cellular level, quercetin suppressed THP-1 macrophage pyroptosis induced by ox-LDL, demonstrated by inhibiting NLRP3 inflammasome activation and reducing ROS level, while these effects were reversed by the specific NRF2 inhibitor (ML385). Mechanistically, quercetin promoted NRF2 to dissociate from KEAP1, enhanced NRF2 nuclear translocation as well as transcription of downstream antioxidant protein. Molecular docking results suggested that quercetin could bind with KEAP1 at Arg415 and Arg483. In order to verify the binding sites, KEAP1 mutated at Arg415 and Arg483 to Ser (R415S and R483S) was transfected into THP-1 macrophages, and the anti-pyroptotic effect of quercetin was abrogated by Arg483 mutation, but not Arg415 mutation. Furthermore, after administration of adeno associated viral vector (AAV) with AAV-KEAP1-R483S, the anti-atherosclerotic effects of quercetin were almost abolished in ApoE-/- mice. These findings proved quercetins suppressed macrophage pyroptosis by targeting KEAP1/NRF2 interaction, and provided reliable data on the underlying mechanism of natural antioxidants to protect against atherosclerosis.

Generation of high performance optical chirped pulse for distributed strain sensing application with high strain accuracy and larger measurement range.

A photonic approach for generating low frequency drifting noise, arbitrary and large frequency chirping rate (FCR) optical pulses based on the Kerr effect in the nonlinear optical fiber is theoretically analyzed and experimentally demonstrated. Due to the Kerr effect-induced sinusoidal phase modulation in the nonlinear fiber, high order Kerr pulse with a large chirping rate is generated. In the concept-proof experiments, the FCR of the mth Kerr pulse has been significantly improved by a factor of 2m+1. In addition, dynamic strain measurement along with a random fiber grating array (RFGA) sensor by using different order Kerr pulse is carried out for demonstrating a large strain measurement range with lower uncertainty sensing capability. Benefiting from the use of a single laser source and large FCR Kerr pulse, the system exhibits a 3.9 µÉ› static strain measurable range, 0.24 µÉ› measurement uncertainty by using -4th order Kerr pulse that has an FCR up to 0.8 GHz/ns. Note that the FCR of the chirped pulse could be further enhanced by using larger FCR chirped pulse seed or choosing higher order Kerr pulses.