Primary Damage Research Articles

Defective Graphene Effects on Primary Displacement Damage and He Diffusion at a Ni–Graphene Interface: Molecular Dynamics Simulations

Ni–graphene nanocomposites with high-density interfaces have enormous potential as irradiation-tolerant materials applied in Gen-IV reactors. Nevertheless, the mechanism wherein the intrinsic and/or irradiation-induced defects of graphene affect the irradiation tolerance of the composites remains poorly understood. Here, we investigate the effects of the two types of defective graphene on the displacement damage and He diffusion of the composites, respectively, using atomistic simulations. The introduction of the intrinsic defects of graphene has a significant effect on the Ni lattice structure near the Ni–graphene interface, especially showing that after displacement cascades, the number of defects gradually increases with the increase in graphene-defective size due to the formation and growth of stacking fault tetrahedra. The existence of the irradiation-induced defects of graphene does not diminish the ability of the interface to trap He atoms/clusters and even may be maintained or improved, mainly reflected in the fact that many isolated He atoms and small clusters can gradually migrate toward the interface and the fraction of He within the interface is up to 37.72% after 1 ns. This study provides an important insight into the understanding of the association relationships of defective graphene with the irradiation tolerance of composites.

Experimental investigation of formation damage during drilling of ultradeep fractured carbonate reservoir

Severe formation damage easily occurs in ultradeep fractured carbonate reservoirs during drilling, yet the formation damage mechanisms have not been studied extensively. This study focused on typical fractured carbonate reservoirs in the Shunbei field, China. The multiscale reservoir space characteristics and core wettability of ultradeep fractured carbonate reservoirs were investigated. The results showed that the reservoirs mainly comprise a fourth-order fracture network. The high-temperature and high-pore-pressure steady-state method also identified fluid sensitivity and phase trapping damage. The fluid sensitivity damage at the formation temperature (170 °C) indicated that this reservoir is affected by water sensitivity, salt sensitivity (critical value: 3/4 formation water salinity (FWS)), alkali sensitivity (critical value: pH 7.5), and liquid phase trapping damage. Particle movement and deposition and liquid phase trapping damage are thought to be the primary damage mechanisms. Furthermore, abnormally low water saturation, mixed wettability, abundant clay minerals, and the fourth-order fracture network contribute to fluid sensitivity and liquid phase trapping damage. Finally, a formation damage control strategy was proposed.

Mitral valve chordal rupture against the background of cardiac SARS-CoV-2 infection. Cases series

In an ever-changing information flow on coronavirus disease 2019 (COVID-19) pandemic, we describe a case series of mitral valve chordal rupture (MVCR) in non-comorbid middle-aged men that occurred over a period of 3 to 5 weeks after Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2) infection. With significant advances in the prevention of acute rheumatic fever, the treatment of bacterial endocarditis and acute coronary syndrome, acute mitral regurgitation has become a relatively rare diagnosis. During the pandemic, there has been a surge in the incidence of spontaneous MVCR, and new data on the problem are accumulating. The presented case series are united by the fact that the infection symptoms were mild, followed by signs of probable endomyocarditis, unrecognized in time, and acute mitral valve regurgitation developed against the background of physical provocation (exercise and cough). Two patients had previously been diagnosed with mitral valve prolapse (myxomatous degeneration and connective tissue disease). Two patients were successfully operated on in different clinics. The described cases emphasize that the consequences of inflammation persistence may be more severe than the primary viral damage, which determines the importance of a comprehensive examination and long-term follow-up. To date, the differential diagnosis of patients with sudden onset of dyspnea and chest pain associated with an infectious process should include MVCR.

Electroacupuncture ameliorates inflammatory response induced by retinal ischemia-reperfusion injury and protects the retina through the DOR-BDNF/Trkb pathway.

Objectives: Retinal ischemia-reperfusion injury (RIRI) is the common pathological basis of many ophthalmic diseases in the later stages, and inflammation is the primary damage mechanism of RIRI. Our study aimed to assess whether electroacupuncture (EA) has a protective effect against RIRI and to elucidate its related mechanisms. Methods: A high-intraocular pressure (HIOP) model was used to simulate RIRI in Wistar rats. EA was applied to the EA1 group [Jingming (BL1) + Shuigou (GV26)] and the EA2 group [Jingming (BL1) + Hegu (LI4)] respectively for 30 min starting immediately after the onset of reperfusion and repeated (30 min/time) at 12 h and then every 24 h until days 7 after reperfusion. The pathological changes in the retina were observed by H and E staining after HIOP. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was utilized to observe retinal cell apoptosis. The mRNA expression of IL1-β, TNF-α, IL-4, IL-10, δ-opioid receptor (DOR), brain-derived neurotrophic factor (BDNF), and tropomyosin-related kinase B (TrkB) in the retina was measured by quantitative real-time PCR. Results: HIOP caused structural disorders of the retina, decreased RGCs, and increased retinal cell apoptosis. At 1 and 3 days of RIRI, retinal apoptotic cells in the EA group were significantly reduced, while there was no distinct difference in the EA group compared with the HIOP group at 7 days of RIRI. Compared with that in the HIOP group, the expression of anti-inflammatory factors, DOR and TrkB was increased, and the expression of pro-inflammatory factors was decreased in the EA group. In contrast, HIOP had no appreciable effect on BDNF expression. Conclusion: EA at Jingming (BL1) and Shuigou (GV26) or at Jingming (BL1) and Hegu (LI4) may inhibit RIRI induced inflammation through activating the DOR-BDNF/TrkB pathway to protect the retina, especially the pair of Jingming (BL1) and Shuigou (GV26) has better inhibitory effects on inflammation.

Патогенетические и структурно-функциональные изменения в почках после перенесенного COVID-19

There is now a growing evidence of the long-term effects of COVID-19, affecting almost all human systems and organs, including the kidneys. The objective of this paper was to study pathogenetic and structural and functional changes in the kidneys in patients with COVID-19 infection. Materials and methods. Articles were searched in PubMed, Medline, Google Scholar, E-library, Clinical Trial databases using the keywords "post-COVID syndrome," "renal damage (kidney disease)," "COVID-19," "SARS-CoV-2," and "glomerulonephritis" in Russian and English. Databases reporting cases of detectable renal damage following a prior coronavirus infection published by September 28, 2022 were used. This review includes literature reviews, clinical cases, and original studies reporting the confirmed cases of detectable renal damage after confirmed prior COVID-19. The sources that focus only on renal damage during the acute period of coronavirus infection have been excluded. Results. Primary viral damage is carried out through the effect on the receptors of angiotensin-converting enzyme-2 (ACE-2). No less important mechanisms of viral damage are immunological and inflammatory reactions, dysfunctions of the complement system, leading to multiple organ failure. The long-term consequences of coronavirus infection on the kidneys were manifested in a decrease in the estimated glomerular filtration rate (eGFR), an increase in creatinine levels, proteinuria, and microhematuria. Dickkopf-3 protein (uDKK-3) may become a promising marker of kidney damage. Post-COVID renal disease can occur both de novo and with a previous renal complication of COVID-19. The most common morphological variants of kidney damage were tubular lesions and various morphological variants of glomerulonephritis. Conclusion. The association of COVID-19 and kidney damage in the post-COVID period is supported by common mechanisms of pathogenesis, including direct viral damage through ACE-2, inflammatory and immune reactions of the body. These data are confirmed by detectable markers of inflammation and damage to the renal tissue, the morphological picture of necrosis, fibrosis of the renal parenchyma in patients with COVID-19 infection.

Миотубулярная Х-сцепленная миопатия. Клинический случай

Myotubular (centronuclear) myopathy is a rare hereditary disease with primary muscle damage and clinical manifestations of congenital myopathy. The article describes a clinical case of myotubular myopathy in a boy who was observed by us from the age of 2 months to 2 years 5 months at Psychoneurological Department No. 1 of the Children’s Center for Psychoneurology and Epileptology of the Republican Children’s Clinical Hospital in Ufa. The disease was manifested by muscle weakness, hypotension, respiratory failure, peripheral tetraparesis, bulbar disorders, the need for artificial lung ventilation and tube feeding.

ГЕМОРРАГИЧЕСКИЕ ИНСУЛЬТЫ У ДЕТЕЙ РАННЕГО ВОЗРАСТА

To date, cerebrovascular diseases of childhood are poorly understood. The need to study hemorrhagic strokes in children is due to the high prevalence in early childhood, the difficulty in identifying the causes and the non-specificity of the first signs of pathology. At different stages of child development, the etiological significance of various pathogenic factors is not the same. The purpose of this study - to analyze the results of diagnosis and treatment of intracranial complications in late hemorrhagic disease of the newborn. Methods. 158 cases of treatment of patients with intracranial hemorrhages against the background of vitamin-K dependent hemorrhagic syndrome were chosen as the objects of the study. Among the sick boys prevailed and amounted to 76 percent. At the age of 40 days ± 2, the disease began in 129 (86.6%) patients. The results of treatment were monitored in 158 patients within the period from one to 3 months. Indicators reflecting the results of treatment were subjected to statistical analysis. Results. According to the type of hematoma, the patients were distributed as follows - 64 (41.1%) intracerebral hematoma, 31 (20.2%) were diagnosed with subdural hemorrhage, intraventricular hemorrhage was detected in 6 (3.8%) cases, mixed subduralintracerebral hemorrhage was detected in 15 (9.5%) patients. 43 (26.6%) patients were not operated on: with subarachnoid hemorrhages - 34 (21.4%) and 9 patients (5.7%) - with small intracerebral and suberal hemorrhages. Lethal outcome occurred in 29 children (18.4%), mortality after surgery in 8 (5.1%) cases. In 43% of cases, a follow-up study did not reveal a neurological deficit. Conclusions. Full-term infants with a combination of the following factors are susceptible to the occurrence of hemorrhagic disease of the newborn: lack of prophylactic administration of vitamin K preparations, breastfeeding, and transient cholestasis. Timely surgical treatment in most patients gives positive results, despite the operation in a very difficult general condition of the patient and unstable hemostasis. Residual neurological deficit was noted during the follow-up study mainly in patients with primary gross damage to the brain parenchyma and with late diagnosis of the disease.

MARKERS OF INFLAMMATION IN RATS UNDER TOXIC INJURY AGAINST DIETARY PROTEIN DEFICIENCY

The paper presents studies of biomarkers of the development of inflammatory reactions in the blood serum of rats under the conditions of toxic damage with acetaminophen against the background of dietary protein deficiency. The animals consumed a semi-synthetic diet during the experiment according to the recommendations of the American Institute of Nutrition. In order to simulate alimentary protein deprivation, rats received a low-protein diet containing 1/3 of the standard daily protein requirement daily for 28 days. The animals were modeled acute toxic damage with acetaminophen after four weeks of experimental diet. The administration of the toxin was carried out at doses of 1250 mg/kg animal body weight in suspension in 2 % starch gel solution once a day for 2 days by gavage. Determination of the level of C-reactive protein, procalcitonin, tumor necrosis factor-alpha, interleukin-6 in the blood serum of rats was carried out by the method of immunoenzymatic analysis. We have established that toxic damage by the drug xenobiotic - acetaminophen against the background of dietary protein deficiency is accompanied by a maximum increase in the level of C-reactive protein (15.5 times) and procalcitonin (10 times) in the blood serum of rats compared to the control value, which can be considered as prognostic biomarkers of the systemic inflammatory reaction under these experimental conditions. At the same time, under these experimental conditions, hyperproduction of tumor necrosis factor-alpha and interleukin-6 was registered in the blood serum of experimental groups of rats with maximum values when toxic doses of acetaminophen were administered to protein-deficient animals, which is consistent with changes in the level of C-reactive protein and procalcitonin. The fact we found makes it possible to assume that dietary protein deprivation increases the production of TNF-α and IL-6 as pro-inflammatory mediators in toxic liver damage, thus inducing primary damage to liver parenchymal cells..

The use of antibacterial preparations in COVID-19 patients

SARS-CoV-2 which initially causes an acute respiratory infection with primary damage to the lungs, has shown that it later causes multiple lesions, being considered a systemic disease. Pneumonia caused by the coronavirus is characterized by the development of a marked inflammatory process by direct damage to the pulmonary alveolocytes, as well as by an imbalance of the innate and adaptive immune status, pro-inflammatory and anti-inflammatory cytokines and chemokines, coagulation and fibrinolysis processes. The empirical use of antibacterial preparations has shown an evolution depending on the epidemiological situation, the data of experimental and clinical studies and the accumulated experience. The excessive prescription of antibiotics was determined by of subjective reasons, and with the accumulation of data confirming coinfections and/‌or secondary infections, the administration of antibacterial preparations was redirected. Beta-lactams, macrolides and fluoroquinolones were the most prescribed antibacterial drugs, for which possible antiviral effects were also estimated (azithromycin etc.). The use of antibiotics from the surveillance and reserve groups, according to WHO policy, was one of the major problems during the pandemic due to the aspect of dangerous microbial resistance. The elucidation of the microbial agents involved in the etiology of bacterial infections in COVID-19 has allowed for a more targeted selection of antibiotics, including regarding the danger of threatening microbial resistance.

The Level of Serum Osmolarity at Admission in Prognosis of Nosocomial Mortality in Patients with Severe Brain Trauma.

Traumatic brain injury (TBI) is a leading cause of death among patients in developed countries. The patients' prognosis depends on the trauma-induced primary damage as well as the secondary brain damage, including electrolyte disturbances. Therefore, prevention, diagnosis, and timely treatment lead to better prognosis. Herein, the aim is to prognosticate about the mortality in patients with TBI through serum osmolarity at admission. In this cross-sectional study, 141 patients with TBI were assigned through convenience sampling. The level of serum osmolarity was examined once the patients were admitted to emergency department and later, the outcome was recorded. Finally, we analyzed the relationship between osmolarity level and patient outcome in age groups. The mean serum osmolarity in the age group of under 18 years, 18 to 60 years, and more than 60 years was equal to 295.3 ± 10.02 mOsm/L, 297.2 ± 6.5 mOsm/L, and 301.6 ± 7.6 mOsm/L, respectively (P-value <0.001). Osmolarity with a cut-off point of more than 298.90 and sensitivity and specificity of 70.49 and 62.86, respectively, had appropriate diagnostic value for predicting mortality in these patients (P-value <0.001). According to the results of this study, serum osmolarity can have an appropriate diagnostic value in predicting mortality in patients with TBI. In addition, in different age categories, the osmolarity serum in the mortality of these patients was significantly different. Therefore, due to the high importance of serum osmolarity in the mortality of patients, careful monitoring of fluid therapy status of trauma patients should be implemented to prevent the development of hyperosmolarity for the patient with irreversible outcomes.

Genome-Wide Binding Analysis of DNA Repair Protein APE1 in Tumor Cells by ChIP-Seq.

The base excision repair (BER) is the primary damage repair pathway for repairing most of the endogenous DNA damage including oxidative base lesions, apurinic/apyrimidinic (AP) sites, and single-strand breaks (SSBs) in the genome. Repair of these damages in cells relies on sequential recruitment and coordinated actions of multiple DNA repair enzymes, which include DNA glycosylases (such as OGG1), AP-endonucleases (APE1), DNA polymerases, and DNA ligases. APE1 plays a key role in the BER pathway by repairing the AP sites and SSBs in the genome. Several methods have been developed to generate a map of endogenous AP sites or SSBs in the genome and the binding of DNA repair proteins. In this chapter, we describe detailed approaches to map genome-wide occupancy or enrichment of APE1 in human cells using chromatin immunoprecipitation followed by next-generation sequencing (ChIP-seq). Further, we discuss standard bioinformatics approaches for analyzing ChIP-seq data to identify APE1 enrichment or binding peaks in the genome.

Primary radiation damage in bone evolves via collagen destruction by photoelectrons and secondary emission self-absorption

X-rays are invaluable for imaging and sterilization of bones, yet the resulting ionization and primary radiation damage mechanisms are poorly understood. Here we monitor in-situ collagen backbone degradation in dry bones using second-harmonic-generation and X-ray diffraction. Collagen breaks down by cascades of photon-electron excitations, enhanced by the presence of mineral nanoparticles. We observe protein disintegration with increasing exposure, detected as residual strain relaxation in pre-stressed apatite nanocrystals. Damage rapidly grows from the onset of irradiation, suggesting that there is no minimal ‘safe’ dose that bone collagen can sustain. Ionization of calcium and phosphorous in the nanocrystals yields fluorescence and high energy electrons giving rise to structural damage that spreads beyond regions directly illuminated by the incident radiation. Our findings highlight photoelectrons as major agents of damage to bone collagen with implications to all situations where bones are irradiated by hard X-rays and in particular for small-beam mineralized collagen fiber investigations.

Molecular Mechanisms in the Vascular and Nervous Systems following Traumatic Spinal Cord Injury.

Traumatic spinal cord injury (SCI) induces various complex pathological processes that cause physical impairment and psychological devastation. The two phases of SCI are primary mechanical damage (the immediate result of trauma) and secondary injury (which occurs over a period of minutes to weeks). After the mechanical impact, vascular disruption, inflammation, demyelination, neuronal cell death, and glial scar formation occur during the acute phase. This sequence of events impedes nerve regeneration. In the nervous system, various extracellular secretory factors such as neurotrophic factors, growth factors, and cytokines are involved in these events. In the vascular system, the blood-spinal cord barrier (BSCB) is damaged, allowing immune cells to infiltrate the parenchyma. Later, endogenous angiogenesis is promoted during the subacute phase. In this review, we describe the roles of secretory factors in the nervous and vascular systems following traumatic SCI, and discuss the outcomes of their therapeutic application in traumatic SCI.

Co-exposure to urban particulate matter and aircraft noise adversely impacts the cerebro-pulmonary-cardiovascular axis in mice

Worldwide, up to 8.8 million excess deaths/year have been attributed to air pollution, mainly due to the exposure to fine particulate matter (PM). Traffic-related noise is an additional contributor to global mortality and morbidity. Both health risk factors substantially contribute to cardiovascular, metabolic and neuropsychiatric sequelae. Studies on the combined exposure are rare and urgently needed because of frequent co-occurrence of both risk factors in urban and industrial settings. To study the synergistic effects of PM and noise, we used an exposure system equipped with aerosol generator and loud-speakers, where C57BL/6 mice were acutely exposed for 3d to either ambient PM (NIST particles) and/or noise (aircraft landing and take-off events). The combination of both stressors caused endothelial dysfunction, increased blood pressure, oxidative stress and inflammation. An additive impairment of endothelial function was observed in isolated aortic rings and even more pronounced in cerebral and retinal arterioles. The increase in oxidative stress and inflammation markers together with RNA sequencing data indicate that noise particularly affects the brain and PM the lungs. The combination of both stressors has additive adverse effects on the cardiovascular system that are based on PM-induced systemic inflammation and noise-triggered stress hormone signaling. We demonstrate an additive upregulation of ACE-2 in the lung, suggesting that there may be an increased vulnerability to COVID-19 infection. The data warrant further mechanistic studies to characterize the propagation of primary target tissue damage (lung, brain) to remote organs such as aorta and heart by combined noise and PM exposure.

Improved methods for calculating electron, positron, and photon radiation-induced displacement damage cross sections

Radiation damage is a key challenge for materials. Accurate evaluation of radiation damage is a starting point for investigating the behaviors of materials used in a radiation environment. The present work proposes improved methods for calculating the primary radiation damage cross sections induced by light particles, including electrons, positrons, and photons. The main improvements compared with previous methods are: (1) accurate Mott cross section rather than the McKinley-Feshbach analytical approach is used for electron and positron scattering; (2) data and methods recommended by the International Commission on Radiation Unit and measurements (ICRU) are systematically applied for computing the stopping powers of electron and positron; (3) accurate differential cross section by combining different models instead of some simple approaches is used for pair production. The electron, positron, and photon irradiation-induced displacement cross sections for various important elements covering a large range of atomic numbers (from Li to U) are computed with the improved methods for energy up to 100 MeV. The calculated displacement cross sections are also tabulated so that they can be simply used for further applications.

A machine-learning interatomic potential to understand primary radiation damage of silicon

Harsh radiation environments cause displacement damages in semiconductor components, resulting in performance degradation. Molecular simulations provide a unique approach to study the dynamic processes of radiation-induced defect production, clustering, and evolution to design and reinforce novel semiconductor components. In this paper, we developed a more efficient machine learning (ML) potential with DFT accuracy to investigate the radiation damage in silicon material. The accuracy of the potential was verified by comparing the static properties, defect formation energy, and threshold displacement energy with experiments and DFT data. By simulating the excitation of a single PKA we found that with the ML potential PKA has an impact over a larger spatial area compared to the empirical potentials. Finally, by simulating multiple PKA excitations in sequence, we found that the first several excited PKAs produce an amorphous region. For the later excited PKAs, the energies are dissipated when they cross through the amorphous region, resulting in a 36% decrease in newly generated defects.

Experimental Study of the Propagation Process of Dissection Using an Aortic Silicone Phantom.

The mortality of acute aortic dissection (AD) can reach 65~70%. However, it is challenging to follow the progress of AD formation. The purpose of this work was to observe the process of dissection development using a novel tear-embedded silicone phantom. Silicone phantoms were fabricated by embedding a torn area and primary tear feature on the inner layer. CT scanning and laser lightening were conducted to observe the variations in thickness and volume of the true lumen (TL) and false lumen (FL) during development. The model with a larger interlayer adhesion damage required a lower pressure to trigger the development of dissection. At the initiation stage of dissection, the volume of TL increased by 25.5%, accompanied by a 19.5% enlargement of tear size. The force analysis based on the change of tear size verified the deduction of the process of interlaminar separation from the earlier studies. The primary tear and the weakening adhesion of the vessel layers are key factors in AD development, suggesting that some forms of primary damage to the arterial wall, in particular, the lumen morphology of vessels with straight inner lumen, should be considered as early risk predictors of AD.

Molecular Dynamics Simulations of Primary Radiation Damage in Silicon Carbide

Molecular Dynamics Simulations of Primary Radiation Damage in Silicon Carbide

Tomography features of the lamina cribrosa and its scleral canal in different types and stages of the diabetic optic neuropathy

AbstractLamina cribrosa morphology is ever changing in health and disease, and its changes might cause primary optic nerve damage and secondary damage due to decreasing of blood supplying and axoplasmic transport. Anatomical narrowing of the lamina cribrosa scleral canal may be a precondition of optic nerve and retina damage in diabetes mellitus (DM).Purpose: to define the tomography changes of lamina cribrosa (LC) and its scleral canal depending on type and stage of diabetic optic neuropathy (DON).Methods: 575 patients (1150 eyes) with type 2 DM and 50 non‐diabetic control persons (100 eyes) aged 55.9 ± 7.8 years were examined. LC thickness was measured with optical coherent tomography (OCT) using LC_Thickness_programm.m and main_low_noise_filters_programm.m. The area of LC scleral canal was measured with SD OCT using the LC_cut_position_programm.m and LC_diameter_calculation_programm.m.Results: A correlation between type and stage of DON and LC thickness in diabetic patients was found. An average index of LC thickness in diabetic patients without DON was 1.4 times higher than in controls; in subclinical stage of axial DON – 1.9 times higher, in initial stage – 2.1 times higher, in severe stage of axial DON and diabetic papillopathy – 2.6 times higher, in anterior ischemic DON – 2.7 times higher, in dystrophic stage – 3.1 times higher than in controls (303 ± 56 μm) (р &lt; 0.001). Scleral canal area in diabetic papillopathy was 35% less and in anterior ischemic DON was 21.6% less than that in controls. A direct correlation between the area of LC scleral canal and the state of optic nerve head was found in diabetic papillopathy and ischemic DON (r = 0.89, р &lt; 0.001 and r = 0.93, р &lt; 0.001 соrrespondingly).Conclusions: A direct correlation between type and stage of DON and scleral LC thickness in patients with DM was revealed. Narrowing of LC scleral canal and thickening of LC were found to change in diabetic papillopathy and ischemic DON.

Mode of action of astrocytes in pain: From the spinal cord to the brain.

Chronic pain is a maladaptive condition affecting 7%-10% of the population worldwide and can be accompanied by depression, anxiety, and insomnia. In particular, chronic pain is becoming more common due to the increasing incidence of diabetes mellitus, cancer, systemic (body-wide) autoimmune, trauma, and infections that attack nerve tissues with an aging global population. Upon stimuli, pain responses are evoked from nociceptive primary sensory neurons in the peripheral nervous system (PNS). Still, pathological changes leading to central sensitization of the pain circuitry in the central nervous system (CNS) is a key mechanism underlying pain maintenance. In humans, chronic pain can last for years, even after the observable signs and symptoms of the primary inflammation or damage have resolved. It is clear that astrocytes, the most abundant cell type in the CNS, are highly involved in regulating pain signaling under health and disease. Multiple astrocyte subsets and diversified activation states driven by intrinsic and extrinsic cues have recently been identified in the spinal cord and brain, playing complex roles in pain development and resolution. Targeting detrimental astrocyte subtypes and activity is considered a promising pain management strategy. Here, we integrate the latest findings to review differential astrocytes activities in distinct regions of the CNS during pain pathophysiology and discuss the underlying molecular mechanisms that control their mode of action in beneficial or/and harmful aspects of pain. Finally, we provide a translational overview of current progress for pain therapies via modulating astrocytic activity.