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Journal articles on the topic 'Rupture de tolérance immune'

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Published: 25 January 2025

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1

Gapin, Laurent, Jean-Pierre Cabaniols, Ricardo Cibotti, Yolanda Bravo De Alba, Philippe Kourilsky, and Jean Kanellopoulos. "Tolérance et rupture de tolérance." Annales de l'Institut Pasteur / Actualités 7, no. 2 (January 1996): 97–118. http://dx.doi.org/10.1016/s0924-4204(97)85204-3.

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2

Solar cayón, José Ignacio. "Fundamentos filosóficos y jurídicos de la tolerancia religiosa en Europa (siglos XVI-XVIII) : el camino hacia la libertad." Mélanges de la Casa de Velázquez Tome 44, no. 1 (May 1, 2014): 19–44. http://dx.doi.org/10.3917/mcv.441.0019.

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La tolérance est un concept historique, dont la signification varie en fonction du contexte et des problèmes abordés. Cet article traite spécifiquement des fondements de la notion de tolérance religieuse tels qu’ils ont été développés à partir de la rupture de l’unité chrétienne en Europe au xvi e siècle. Dans ce contexte, le débat sur la tolérance constituera les premières formes de réflexion philosophique sur les limites de l’action légitime du pouvoir politique, en engageant un processus d’affirmation de l’autonomie individuelle qui débouchera sur l’idée de la liberté religieuse comme un droit naturel. Toutefois, l’analyse des divers groupes politiques et religieux moteurs de ce processus révèle les différentes racines, philosophies et valeurs qui sous-tendent chacune de ces notions, ainsi que les relations complexes qu’elles entretiennent.
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3

Rothschild, C. "Le jeune hémophile, les inhibiteurs et la tolérance immune." Transfusion Clinique et Biologique 6, no. 3 (June 1999): 191–94. http://dx.doi.org/10.1016/s1246-7820(99)80024-x.

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4

Jeandel, P. Y., E. Delmont, L. Marcq, F. Sanderson, E. Rosenthal, J. G. Fuzibet, and C. Desnuelle. "Efficacité et tolérance du rituximab dans la myasthénie auto-immune." La Revue de Médecine Interne 30 (December 2009): S342. http://dx.doi.org/10.1016/j.revmed.2009.10.053.

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5

GARCIA, C., L. BORDIER, F. BANAL, F. DUTASTA, J. V. MALFUSON, and O. BERETS. "Stratégie diagnostique devant une suspicion de polyendocrinopathie auto-immune." Médecine et Armées Vol. 40 No. 2, Volume 40, Numéro 2 (April 1, 2012): 129–34. http://dx.doi.org/10.17184/eac.6600.

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Les polyendocrinopathies auto-immunes de type 2 correspondent à une association d’au moins deux affections endocriniennes liées à une perturbation de la tolérance du système immunitaire. Nous rapportons l’observation d’une patiente, âgée de 38 ans, chez qui est découverte une maladie d’Addison, deux mois après l’introduction de lévothyroxine dans le traitement d’une thyroïdite à anticorps anti-thyroperoxydase, cette association étant auparavant connue sous l’appellation de syndrome de Schmidt. Ce cas clinique illustre les difficultés diagnostiques des polyendocrinopathies auto-immunes et permet de rappeler les principales associations rencontrées dans les polyendocrinopathie auto-immune de type 2. Enfin les modalités pratiques du dépistage systématique des endocrinopathies associées, non consensuelles, sont discutées.
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Brilland, B., C. Beauvillain, G. Mazurkiewicz, P. Rucay, J. Tabiasco, E. Vinatier, J. Riou, G. Renier, J. F. Subra, and J. F. Augusto. "Rupture de tolérance et dysrégulation lymphocytaire T chez les travailleurs exposés à la silice sans atteinte pulmonaire." Néphrologie & Thérapeutique 15, no. 5 (September 2019): 386–87. http://dx.doi.org/10.1016/j.nephro.2019.07.299.

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7

Lyon, J. A., J. D. Haynes, C. L. Diggs, J. D. Chulay, and J. M. Pratt-Rossiter. "Plasmodium falciparum antigens synthesized by schizonts and stabilized at the merozoite surface by antibodies when schizonts mature in the presence of growth inhibitory immune serum." Journal of Immunology 136, no. 6 (March 15, 1986): 2252–58. http://dx.doi.org/10.4049/jimmunol.136.6.2252.

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Abstract Some immune sera that inhibit erythrocyte invasion by merozoites also agglutinate the merozoites as they emerge from rupturing schizonts. These immune clusters of merozoites (ICM) possess a surface coat that is cross-linked by antibody and is thicker than the surface coat associated with normal merozoites (NM) obtained from cultures containing preimmune serum. Analysis of metabolically labeled ICM and NM performed by using sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed that washed ICM possessed immune complexes containing antigens representative of schizonts and merozoites. Characteristics of the immune complexes included: a) they were not soluble in pH 8 Triton X-100, b) they were soluble at an acid pH, and c) after pH neutralization they were precipitated by using staphylococcal protein A. Merozoite antigens having Mr of 83, 73, and 45 kDa were associated with immune complexes in ICM. The 83 and 73 kDa antigens were recovered in considerably larger quantities from ICM than from NM. Schizont antigens having Mr of 230, 173 (triplet), 152 (doublet), and 31 kDa were associated with immune complexes in ICM, and a 195 kDa antigen(s) from schizonts and merozoites was also present in the immune complexes. In addition, other antigens of Mr 113, 101, 65, and 51 kDa may have been immune complexed. These 15 antigens accounted for less than 30% of the schizont and merozoite antigens recognized by the immune serum. Immune complexes probably formed between antibodies and a) surface antigens of schizont-infected erythrocytes exposed to antibody before schizont rupture, b) surface antigens of merozoites and schizonts exposed during schizont rupture, and c) soluble antigens normally released during schizont rupture. The antibody components of the immune complexes may have prevented rapid degradation or shedding of some antigens from the merozoite surface. Allowing schizonts to rupture in the presence of inhibitory antibodies (to form ICM) is a useful approach to identifying exposed targets of protective immunity against malaria.
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8

Zheng, Lin-Lin, Ya-Ru Wang, Zhen-Rong Liu, Zhi-Hao Wang, Chang-Cheng Tao, Yong-Gang Xiao, Kai Zhang, et al. "High spindle and kinetochore-associated complex subunit-3 expression predicts poor prognosis and correlates with adverse immune infiltration in hepatocellular carcinoma." World Journal of Gastrointestinal Surgery 15, no. 8 (August 27, 2023): 1600–1614. http://dx.doi.org/10.4240/wjgs.v15.i8.1600.

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Tumour rupture of gastrointestinal stromal tumours (GISTs) has been considered to be a remarkable risk factor because of its unfavourable impact on the oncological outcome. Although tumour rupture has not yet been included in the current tumor-node-metastasis classification of GISTs as a prognostic factor, it may change the natural history of a low-risk GIST to a high-risk GIST. Originally, tumour rupture was defined as the spillage or fracture of a tumour into a body cavity, but recently, new definitions have been proposed. These definitions distinguished from the prognostic point of view between the major defects of tumour integrity, which are considered tumour rupture, and the minor defects of tumour integrity, which are not considered tumour rupture. Moreover, it has been demonstrated that the risk of disease recurrence in R1 patients is largely modulated by the presence of tumour rupture. Therefore, after excluding tumour rupture, R1 may not be an unfavourable prognostic factor for GISTs. Additionally, after the standard adjuvant treatment of imatinib for GIST with rupture, a high recurrence rate persists. This review highlights the prognostic value of tumour rupture in GISTs and emphasizes the need to carefully take into account and minimize the risk of tumour rupture when choosing surgical strategies for GISTs.
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9

Noël, E., P. Hardy, E. Laprelle, F. W. Hagena, F. Goebel, and P. Goupille. "Etude prospective de la tolérance et de l'efficacité d'Hylane G-F 20 dans l'omarthrose symptomatique sans rupture de coiffe." Revue du Rhumatisme 73, no. 10-11 (November 2006): 1166–67. http://dx.doi.org/10.1016/j.rhum.2006.10.388.

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10

Noël, E., P. Hardy, F. W. Hagena, E. Laprelle, F. Goebel, C. Faure, L. Favard, et al. "Efficacité et tolérance de l’Hylan GF 20 au cours de l’omarthrose sans rupture de coiffe. Étude ouverte, prospective, multicentrique." Revue du Rhumatisme 76, no. 12 (December 2009): 1327–30. http://dx.doi.org/10.1016/j.rhum.2009.10.025.

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11

Troudi, W., S. Sadkaoui, B. Yacoubi Loueslati, M. Ben Abdallah, W. Ben Ayoub, K. Mrad, F. Ben Ayed, K. Ben Romdhane, and A. Benammar El Gaaied. "Analyse de la rupture de tolérance vis-à-vis de la p53 dans le cancer du sein en Tunisie." Immuno-analyse & Biologie Spécialisée 21, no. 1 (February 2006): 38–44. http://dx.doi.org/10.1016/j.immbio.2005.11.005.

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12

AlMuhsin, Ahmed Mohammed, Antonio Privitera, Ameera Balhareth, and Khalid Sabr. "Spontaneous Splenic Rupture following Colorectal Surgery and Hemodialysis." Case Reports in Surgery 2019 (June 20, 2019): 1–3. http://dx.doi.org/10.1155/2019/8278419.

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Atraumatic splenic rupture is rarely encountered in clinical practice compared to traumatic rupture. General risk factors include hematological, infectious, or malignant splenic diseases, uremic coagulopathy, use of heparin, hypertension, and immune-compromised status. Spontaneous splenic rupture following colorectal surgery has never been reported. Maintaining a high index of suspicion in patients presenting with left upper quadrant pain and tenderness is crucial. Diagnosis can be made with the aid of an ultrasound or CT scan. The management plan should be tailored to the patient’s clinical conditions. The authors present a case of spontaneous splenic rupture in a patient following colectomy for cancer and undergoing postoperative hemodialysis and discuss the possible etiological factors.
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13

Lucke-Wold, Brandon. "212 Differential Immune Cell Recruitment Between Ruptured and Unruptured Intracranial Aneurysms." Neurosurgery 70, Supplement_1 (April 2024): 56. http://dx.doi.org/10.1227/neu.0000000000002809_212.

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INTRODUCTION: Accumulating evidence implicates infiltrating inflammatory cells in intracranial aneurysms. However, few studies have examined immunological differences between aneurysm rupture statuses. METHODS: An established machine-learning deconvolution algorithm was applied on RNA-sequencing data developed from vessel wall tissue of 21 ruptured and 21 unruptured intracranial aneurysms. A validated gene signature matrix of human hematopoietic cell subsets was used to infer the relative fractions of immune cells present within the original aneurysm tissues. RESULTS: Deconvolution of the bulk gene expression data showed significantly increased plasma cells, CD8+ T cells, and activated natural killer cells in unruptured aneurysms compared to ruptured aneurysms. CONCLUSIONS: Specific lymphoid elements may be involved in an inflammatory reaction prior to intracranial aneurysm rupture.
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14

Danlos, F. X., J. M. Michot, A. L. Voisin, E. Routier, J. Haroche, S. Champiat, L. Albiges, et al. "Étude de la tolérance et de l’efficacité des immune checkpoints inhibiteurs en oncologie chez les patients atteints d’une maladie auto-immune ou inflammatoire." La Revue de Médecine Interne 37 (December 2016): A116—A117. http://dx.doi.org/10.1016/j.revmed.2016.10.097.

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15

Biswas, Jayanta K., and Sanjaya K. Gupta. "A rare incidence of averting ‘maternal near-miss’ in a case of spontaneous uterine rupture in shock." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 11, no. 2 (January 28, 2022): 617. http://dx.doi.org/10.18203/2320-1770.ijrcog20220200.

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Uterine rupture is a rare but catastrophic obstetric emergency associated with significant feto-maternal morbidity and mortality. There are various risk factors and wide spectrum of clinical presentations have been identified; previous cesarean delivery being most common risk factor. Spontaneous rupture of unscarred uterus is infrequently encountered, but very dangerous for both mother and fetus as remotely suspected. Usually, spontaneous rupture of primigravida uterus is considered almost immune as it is rare but not unheard of; it may occur before or after onset of labour, at term or preterm and with or without fetal heart rate abnormality. The reported case was such a case of spontaneous unscarred uterine rupture with favourable outcome for both mother and baby.
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16

Chulay, J. D., J. A. Lyon, J. D. Haynes, A. I. Meierovics, C. T. Atkinson, and M. Aikawa. "Monoclonal antibody characterization of Plasmodium falciparum antigens in immune complexes formed when schizonts rupture in the presence of immune serum." Journal of Immunology 139, no. 8 (October 15, 1987): 2768–74. http://dx.doi.org/10.4049/jimmunol.139.8.2768.

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Abstract When Plasmodium falciparum parasites are cultured with some immune sera, merozoites are agglutinated by antibodies to form immune clusters of merozoites and prevent their invasion into erythrocytes. Within these immune clusters of merozoites, several antigens that are normally found in the soluble fraction after detergent extraction accumulate in relatively insoluble immune complexes. From mice immunized with these immune complexes, we obtained hybridomas secreting monoclonal antibodies (mAb) that react with various immune clusters of merozoites antigens, including mAb 3D5, which recognizes a 101-kDa antigen (p101) and mAb, 5E3, which recognizes a 113-kDa antigen (p113). Both mAb reacted with antigens at the surface of schizonts, in the vacuolar space, and at the surface of merozoites before their release from schizont-infected cells. Both p101 and p113 were synthesized by mature trophozoites and young schizonts. In pulse-chase experiments, p113 was processed to 100-, 70-, 55-, and 50-kDa products. Both p101 and p113 appeared in the culture medium when schizont rupture occurred in normal culture medium but were found in immune complexes when schizont rupture occurred in the presence of immune serum. Antibodies in immune complexes, when dissociated with acid and used to probe immunoblots, reacted with affinity-purified p101 and p113. Antigens such as these, which are accessible at the parasite surface and react with antibodies present in immune serum that inhibits parasite invasion, are logical candidates to study in the search for a vaccine against the erythrocytic stages of malaria.
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17

Elias, Heidi, and Kellie Thiessen. "Management of Previable Rupture of Membranes with Prolonged Latency." Canadian Journal of Midwifery Research and Practice 23, no. 1 (October 22, 2024): 104–11. http://dx.doi.org/10.22374/cjmrp.v23i2.17.

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Preterm prelabor rupture of membranes at pre-viable gestations (<23–24 weeks) complicates approximately 0.1–0.8% of pregnancies. Few cases of pre-viable preterm prelabor rupture of membranes (pPPROM) have resulted in term delivery, and even fewer have experienced no complications. The case presented sustained a 21-week (147-day) latency period after confirmed pPPROM at 18+6 weeks gestation, resulting in term delivery with exceptional outcomes for both mother and baby. Expectant management with minimal intervention, due to the client’s decline of more invasive options, makes this case unique. A focused literature review was conducted to identify other rare cases of pPPROM. We were particularly interested in understanding the different approaches to managing two similar cases with prolonged latency. We highlight the variations and outcomes of expectant management of pPPROM. Despite the demonstrated benefits of recommended interventions in the expectant management of pPPROM cases, the potential side effects and outcomes of these interventions may be undesirable for patients, leading to their decline. This case underscores the importance of careful counseling regarding management options and the individualization of care based on client risk tolerance. RÉSUMÉLa rupture prématurée des membranes avant travail à des stades de gestation pré-viables (<23-24 semaines) complique environ 0,1-0,8% des grossesses. Peu de cas ont connu une rupture prématurée des membranes avant travail (RPMT), qui aboutit à un accouchement à terme, et encore moins de cas n’ont pas eu de complications. Le cas présenté a connu une période de latence de 21 semaines (147 jours) après une RPPM confirmée à 18+6 semaines de gestation et s’est soldé par un accouchement à terme avec des résultats exceptionnels pour la mère et le bébé. La gestion de l’attente avec une intervention minimale en raison du déclin de la cliente rend cette gestion de cas unique. Une analyse documentaire ciblée a été réalisée afin d’identifier d’autres cas rares de pPPROM. Nous voulions en particulier comprendre les différentes approches de la gestion de deux cas similaires avec une latence prolongée. Nous soulignons ensuite les variations et les résultats de la prise en charge attendue de la pPPROM. Malgré les avantages démontrés des interventions recommandées dans la prise en charge des cas de pPPROM, les effets secondaires potentiels et les résultats des interventions peuvent être indésirables pour les patients et entraîner leur déclin. Ce cas souligne l’importance d’un conseil attentif sur les options de prise en charge et de l’individualisation des soins en fonction de la tolérance au risque du client.
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Mitsui, Kazuha, Taichi Ikedo, Yoshinobu Kamio, Hajime Furukawa, Michael T. Lawton, and Tomoki Hashimoto. "TLR4 (Toll-Like Receptor 4) Mediates the Development of Intracranial Aneurysm Rupture." Hypertension 75, no. 2 (February 2020): 468–76. http://dx.doi.org/10.1161/hypertensionaha.118.12595.

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Inflammation is emerging as a critical factor in the pathophysiology of intracranial aneurysm. TLR4 (toll-like receptor 4) contributes not only to the innate immune responses but also to the inflammatory processes associated with vascular disease. Therefore, we examined the contribution of the TLR4 pathway to the development of the rupture of intracranial aneurysm. We used a mouse model of intracranial aneurysm. TLR4 inhibition significantly reduced the development of aneurysmal rupture. In addition, the rupture rate and levels of proinflammatory cytokines were lower in TLR4 knockout mice than the control littermates. Macrophage/monocyte-specific TLR4 knockout mice had a lower rupture rate than the control littermate mice. Moreover, the deficiency of MyD88 (myeloid differentiation primary-response protein 88), a key mediator of TLR4, reduced the rupture rate. These findings suggest that the TLR4 pathway promotes the development of intracranial aneurysmal rupture by accelerating inflammation in aneurysmal walls. Inhibition of the TLR4 pathway in inflammatory cells may be a promising approach for the prevention of aneurysmal rupture and subsequent subarachnoid hemorrhage.
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Østergaard, John R., Bent Ø. Kristensen, Sven-Erik Svehag, Børge Teisner, and Tomislav Miletic. "Immune complexes and complement activation following rupture of intracranial saccular aneurysms." Journal of Neurosurgery 66, no. 6 (June 1987): 891–97. http://dx.doi.org/10.3171/jns.1987.66.6.0891.

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✓ Circulating immune complexes (CIC) and complement activation (plasma C3d levels) were monitored during a 2-week period in patients with ruptured cerebral aneurysms and also in patients with cerebral hematoma unrelated to saccular aneurysms. Thirteen of 18 aneurysm patients were found to have CIC on admission as compared to three of 21 healthy blood donors (p < 0.001). The presence of CIC in aneurysm patients was associated with a poor prognosis. Eight of nine patients who developed angiographic vasospasm had CIC on admission compared with one of four without vasospasm. Patients with vasospasm showed a twofold increase in plasma C3d levels at the time when the spasm occurred, whereas no significant changes in the C3d concentration could be demonstrated in aneurysm patients without spasm or in patients with hematoma unrelated to aneurysm rupture. These findings suggest that immunological processes involving complement-activating immune complexes are involved in the pathogenesis of cerebral vasospasm following rupture of saccular aneurysms.
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20

Lakehal, Redha, Soumaia Bendjaballah, Radouane Boukarroucha, Farid Aimer, Rabeh Bouharagua, Amine Amrous, Khacha Khaled, Baya Aziza, and Abdelmalek Bouzid. "Cardiac hydatic cyst ruptured in the pericardium complicated tamponade. A case report." Batna Journal of Medical Sciences (BJMS) 7, no. 1 (May 2, 2020): 50–52. http://dx.doi.org/10.48087/bjmscr.2020.7112.

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Introduction. La localisation cardiaque de la maladie hydatique est rare (< 3%) même dans les pays endémiques. C’est une affection caractérisée par une longue tolérance fonctionnelle et un grand polymorphisme clinique et para clinique. L’hydatitose cardiaque est grave à cause du risque de rupture imposant une chirurgie semi urgente. Le diagnostic repose sur la sérologie et l’échocardiographie. Le but de cette observation est de montrer un cas de rupture d’un kyste hydatique du ventricule gauche dans le péricarde donnant un tableau de tamponnade. Observation. Nous rapportons l’observation un homme âgé de 22 ans présentant un tableau de tamponnade avec turgescence des veines jugulaires et orthopnée suite à la rupture brutale du kyste hydatique du VG dans le péricarde. En préopératoire : dyspnée stade II de la NYHA. Radiographie pulmonaire : ICT : 0,65. ECG : RRS. Echocardiographie : épanchement péricardique compressif avec collapsus de l’OD, compression du VD, présence d’image kystique de la paroi postéro-inferieur du VG rompu dans le péricarde avec images écho gènes intra péricardique VG : 59/37 mm, VD : 18 mm, FE : 75%. TDM thoracique : KHC rompu dans le péricarde. Le patient a subi une ponction évacuatrice avant l’intervention chirurgicale. L’exploration per opératoire : épanchement péricardique de grande abondance avec liquide eau de roche, membrane kystique flottant en intra péricardique ainsi que les vésicules filles. Le geste : prélèvement péricardique, ablation de la membrane et les vésicules filles, stérilisation par du sérum salé hypertonique de la cavité péricardique et la cavité kystique résiduelle et enfin résection d’une partie du péri kyste et capitonnage de la cavité résiduelle. Les suites post opératoires étaient simples. Conclusion. Les progrès de l’imagerie font de l’échographie l’examen de choix dans la détection du kyste hydatique du cœur. L’indication opératoire est formelle dans tous les cas du kyste du cœur car l’évolution spontanée est mortelle a plus ou moins brève échéance. En fait le véritable traitement de la maladie parasitaire et sa prophylaxie la lutte contre l’échinococcose repose sur des mesures de prévention.
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Venger, Benjamin H., and Alfonso E. Aldama. "Mycotic vasculitis with repeated intracranial aneurysmal hemorrhage." Journal of Neurosurgery 69, no. 5 (November 1988): 775–79. http://dx.doi.org/10.3171/jns.1988.69.5.0775.

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✓ A case of repeated intracranial aneurysmal rupture occurring despite successful treatment of infective endocarditis is reported. While the valvular source of emboli was eradicated and serial angiograms documented no further aneurysms after resection of the primary lesion, the formation and rupture of multiple septic aneurysms occurred 9 months later in the opposite hemisphere. A relationship to damage of the cerebral vasculature by immune complexes is suggested as one possible explanation for this unusual occurrence. This implies that some patients with infective endocarditis may be at permanent risk for the formation and rupture of mycotic intracranial aneurysms, despite successful treatment of the primary cardiac lesion.
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Guitton, Z., O. Robineau, L. Surgers, A. Cheret, C. Fontier, L. Deconinck, P. Bataille, and H. Bazus. "Éfficacité et tolérance des traitements immunosupresseurs chez les personnes vivant avec le VIH présentant une pathologie auto-immune." Médecine et Maladies Infectieuses 49, no. 4 (June 2019): S150—S151. http://dx.doi.org/10.1016/j.medmal.2019.04.363.

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23

Paumier, Manon, Kévin Bigaut, Aleksandra Nadaj-Pakleza, Jérôme de Sèze, and Laurent Kremer. "Efficacité et tolérance du rituximab chez des patients atteints de myasthénie auto-immune dans une une cohorte strasbourgeoise." Revue Neurologique 180 (April 2024): S118. http://dx.doi.org/10.1016/j.neurol.2024.02.230.

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24

Martin, M., A. M. Knapp, L. Vallat, C. Schleiss, D. Ghergus, A. S. Korganow, F. Gros, S. Jung, P. Soulas-Sprauel, and T. Martin. "Expression de ZAP-70 par les lymphocytes B non tumoraux : une nouveau mécanisme de rupture de tolérance B ? Résultats préliminaires in vivo." La Revue de Médecine Interne 39 (June 2018): A67—A68. http://dx.doi.org/10.1016/j.revmed.2018.03.293.

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25

Maciejowski, John, and Emily M. Hatch. "Nuclear Membrane Rupture and Its Consequences." Annual Review of Cell and Developmental Biology 36, no. 1 (October 6, 2020): 85–114. http://dx.doi.org/10.1146/annurev-cellbio-020520-120627.

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The nuclear envelope is often depicted as a static barrier that regulates access between the nucleus and the cytosol. However, recent research has identified many conditions in cultured cells and in vivo in which nuclear membrane ruptures cause the loss of nuclear compartmentalization. These conditions include some that are commonly associated with human disease, such as migration of cancer cells through small spaces and expression of nuclear lamin disease mutations in both cultured cells and tissues undergoing nuclear migration. Nuclear membrane ruptures are rapidly repaired in the nucleus but persist in nuclear compartments that form around missegregated chromosomes called micronuclei. This review summarizes what is known about the mechanisms of nuclear membrane rupture and repair in both the main nucleus and micronuclei, and highlights recent work connecting the loss of nuclear integrity to genome instability and innate immune signaling. These connections link nuclear membrane rupture to complex chromosome alterations, tumorigenesis, and laminopathy etiologies.
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Danlos, F. X., A. L. Voisin, V. Dyevre, J. M. Michot, E. Routier, S. Champiat, C. Massard, et al. "Tolérance et efficacité des anticorps anti immune check-point inhibiteurs (anti PD-1/PD-L1) chez les patients atteints d’une maladie auto-immune ou inflammatoire." La Revue de Médecine Interne 38 (December 2017): A107—A108. http://dx.doi.org/10.1016/j.revmed.2017.10.415.

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27

Antonios, Joseph Paul, Tanyeri Barak, Batur Gultekin, Kanat Yalcin, Nana Adenu-Mensah, Nanthiya Sujijantarat, Andrew B. Koo, et al. "306 Endothelial Infiltrating Regulatory B Cells and NK T Cells Precipitate Inflammatory Cascade That Leads to Aneurysmal Rupture." Neurosurgery 70, Supplement_1 (April 2024): 88–89. http://dx.doi.org/10.1227/neu.0000000000002809_306.

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INTRODUCTION: Current literature examining the mechanisms delineating intracranial aneurysm development and subsequent rupture is sparse. Studies from decades prior defined the aneurysm model as being one largely driven by flow changes. However, the scope of these models is limited and does not fully explain why only a subset of patients with existing intracranial aneurysms subsequently go on to rupture. METHODS: We obtained aneurysm endothelial lining from 20 patients with ruptured, unruptured, sentinel hemorrhage, and recurrent aneurysms during endovascular coil embolization, which were processed and analyzed using mass spectrometry. RESULTS: Compared to unruptured aneurysms, ruptured aneurysms had significantly increased infiltrating populations of NK cells (5.5% vs 1.4%, p < 0.01), regulatory B cells (27.6% vs 16.0%, p < 0.05), and cytotoxic CD8 T cells (23.7% vs 13.5%, p < 0.05). To understand whether these cells were recruited at the time of rupture or whether they were present prior to the ictus event, we examined aneurysms that were treated after presenting with sentinel hemorrhages – again these patients had that same population of early-NK cells (7.5%, p = 0.2), suggesting that these cells were present at the nexus point immediately prior to rupture. Further, the regulatory B cells were even more prominent in the sentinel population, (45.6%, p < 0.01). CONCLUSIONS: These findings all point to a complex, coordinated immune response that is driving the remodeling of the aneurysm vessel wall. We interpret the results to suggest that regulatory B cell driven destabilization of the aneurysmal wall leads to a series of events; namely the recruitment of NK cells, subsequent inflammatory cascade, and ultimate rupture. While there remains much to be understood about this multi-faceted picture, these findings provide the basis for further studies looking at targets for adjunctive immune therapies in both our unruptured and ruptured patient populations.
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Jaquier, Joanne, and Jean-Luc Kuenlin. "Biosphères : mesure de résilience à visée d’insertion sociale et professionnelle en nature et sur le marché du travail réel en faveur des jeunes en difficulté." Cortica 1, no. 2 (September 20, 2022): 332–54. http://dx.doi.org/10.26034/cortica.2022.3184.

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Comment agir sur la motivation des jeunes à s’en sortir, s’émanciper et prendre place en société ? Constat : il existe des jeunes pris dans la spirale de la marginalisation sociale et professionnelle à risque de dépendance chronique des systèmes de protection sociale (aide sociale, AI et autres). Problématique : Les jeunes en situation de grande difficulté d’insertion ne voient pas d’issues à leur situation complexe et se sentent, tout comme les professionnels qui les accompagnent, démunis. À force d’échecs successifs, ils perdent espoir et confiance en eux. Ils ne voient plus de sens à l’avenir. Souvent, pour se protéger ou en lien avec des difficultés personnelles, ils ont tendance à se couper de leurs propres émotions qu’ils vont mettre à distance par des comportements et des consommations à risque (drogue, alcool). Ils activent des mécanismes de défense (croyances limitantes, trouble du comportement) et finissent pas se distancer ou être distancé des systèmes d’intégration sociale (travail, famille, formation, société) qui révèlent ses failles. Lorsqu’on leur donne la parole, ils disent avoir besoin d’être attendus quelque part par quelqu’un, pour une activité sociale ou professionnelle valorisante et valorisée, qui procure un statut et une fonction sociale. En bref, ces jeunes ont besoin d’appartenance. C’est pourquoi, souvent, ils se rapprochent des milieux marginaux dans lesquels ils ont une place et sont reconnus par les pairs qui partagent la même réalité de « mise à la marge ». Enjeux : Comment amener les jeunes en (risque de) rupture d’insertion sociale et à la prise de conscience de leur capacité d’agir sur soi ? Depuis 2020, la Fondation de Fribourg pour la jeunesse élabore un concept d’accompagnement spécifique aux jeunes en (risque de) rupture d’insertion sociale et professionnelle, intitulé : « mentorat à haut seuil de tolérance en nature et sur le marché du travail réel ».
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Hu, Zeyang, Hang Chen, Hongxiang Li, Shuguang Xu, Yinyu Mu, Qiaoling Pan, Jingtao Tong, and Guodong Xu. "Lysosome-related genes: A new prognostic marker for lung adenocarcinoma." Medicine 102, no. 35 (September 1, 2023): e34844. http://dx.doi.org/10.1097/md.0000000000034844.

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Currently, a reliable early prognostic marker has not been identified for lung adenocarcinoma (LUAD), the most common malignancy. Recent studies demonstrated that lysosomal rupture is involved in cancer migration, progression, and immune microenvironment formation. We performed a bioinformatics analysis of lysosomal rupture to investigate whether lysosome-related genes (LRGs) are key in LUAD. The analysis identified 23 LRGs. Cytoscape visualization identified 10 core genes (CCNA2, DLGAP5, BUB1B, KIF2C, PBK, CDC20, NCAPG, ASPM, KIF4A, ANLN). With the 23 LRGs, we established a new risk scoring rule to classify patients with LUAD into high- and low-risk groups and verified the accuracy of the risk score by receiver operating characteristic curves and established a nomogram to evaluate clinical patients. Immunotherapy effectiveness between the high- and low-risk groups was evaluated based on the tumor mutational burden and analyses of immune cell infiltration and drug sensitivity. Pathway enrichment analysis revealed that lysosomes were closely associated with glucose metabolism, amino acid metabolism, and the immune response in patients with LUAD. Lysosomes are a likely new therapeutic target and provide new directions and ideas for treating and managing patients with LUAD.
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Ropp, Laurent. "Des tueries horribles ? Les violences religieuses dans la France du XVIe siècle selon les mémorialistes." Source(s) – Arts, Civilisation et Histoire de l’Europe, no. 14-15 (October 19, 2022): 39–57. http://dx.doi.org/10.57086/sources.158.

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Des tueries horribles ? Les violences religieuses dans la France du XVIe siècle selon les mémorialistes – Les mémoires rédigés par des témoins des affrontements confessionnels du XVIe siècle français constituent des sources particulièrement adaptées pour saisir les seuils de tolérances de contemporains aux massacres religieux. Ils livrent un large éventail de réactions, de la ferme condamnation d’abus à la justification de violences, en passant par un certain malaise vis-à-vis des tueries. Lorsque celles-ci sont dénoncées, les narrateurs mettent en valeur leur caractère extrême et la malheureuse rupture de la paix que les actes de brutalité engendrent. Mais les réactions différenciées des mémorialistes face à des massacres commis dans des circonstances similaires suggère l’existence d’autres facteurs permettant d’expliquer pourquoi ces gestes apparaissent comme des horreurs. L’étude comparative des mémoires révèle le rôle de l’identité religieuse de l’auteur, plus ou moins affirmée, et de la période de rédaction : les textes qui expriment un dépassement du seuil de tolérance directement lié à la confession des victimes sont rédigés pendant les affrontements et marqués par la piété de leurs auteurs tandis que les mémoires plus tardifs et composés par des individus dont l’ardeur religieuse paraît plus faible livrent des condamnations de tueries qui ne sont pas orientées par une logique confessionnelle.
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Montecucco, Fabrizio, Sabine Steffens, and François Mach. "The Immune Response Is Involved in Atherosclerotic Plaque Calcification: Could the RANKL/RANK/OPG System Be a Marker of Plaque Instability?" Clinical and Developmental Immunology 2007 (2007): 1–8. http://dx.doi.org/10.1155/2007/75805.

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Atherogenesis is characterized by an intense inflammatory process, involving immune and vascular cells. These cells play a crucial role in all phases of atherosclerotic plaque formation and complication through cytokine, protease, and prothrombotic factor secretion. The accumulation of inflammatory cells and thus high amounts of soluble mediators are responsible for the evolution of some plaques to instable phenotype which may lead to rupture. One condition strongly associated with plaque rupture is calcification, a physiopathological process orchestrated by several soluble factors, including the receptor activator of nuclear factor NFκB ligand (RANKL)/receptor activator of nuclear factor NFκB (RANK)/osteoprotegerin (OPG) system. Although some studies showed some interesting correlations with acute ischemic events, at present, more evidences are needed to evaluate the predictive and diagnostic value of serum sRANKL and OPG levels for clinical use. The major limitation is probably the poor specificity of these factors for cardiovascular disease. The identification of tissue-specific isoforms could increase the importance of sRANKL and OPG in predicting calcified plaque rupture and the dramatic ischemic consequences in the brain and the heart.
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Korostynski, Michal, Rafal Morga, Marcin Piechota, Dzesika Hoinkis, Slawomir Golda, Tomasz Dziedzic, Agnieszka Slowik, Marek Moskala, and Joanna Pera. "Inflammatory Responses Induced by the Rupture of Intracranial Aneurysms Are Modulated by miRNAs." Molecular Neurobiology 57, no. 2 (October 25, 2019): 988–96. http://dx.doi.org/10.1007/s12035-019-01789-1.

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Abstract Influence of an intracranial aneurysm (IA) rupture on the expression of miRNAs and the potential significance of the resulting changes remains poorly understood. We aimed to characterize the response to the IA rupture through the analysis of miRNAs in peripheral blood cells. Expression of small RNAs was investigated using deep transcriptome sequencing in patients in the acute phase of an IA rupture (first 72 h), in the chronic phase (3–15 months), and controls. A functional analysis and the potential interactions between miRNAs and target genes were investigated. We also measured the levels of proteins that were influenced by regulated miRNAs. We found that 106 mature miRNAs and 90 miRNA precursors were differentially expressed among the groups. The regulated miRNAs were involved in a variety of pathways, and the top pathway involved cytokine-cytokine receptor interactions. The identified miRNAs targeted the inflammatory factors HMGB1 and FASLG. Changes in their expression were detected at the mRNA and protein levels. IA rupture strongly influences the transcription profiles in peripheral blood cells. The regulated miRNAs were involved in the control of immune cell homeostasis. In summary, these results may aid in the elucidation of the molecular mechanisms that orchestrate the inflammatory response to IA rupture.
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Hachulla, E., G. Solé, M. Hamidou, C. Desnuelle, J. P. Azulay, G. Besson, L. Swiader, M. Gauthier-Darnis, and S. Puget. "Résultats d’une étude évaluant la tolérance de Tégéline® administrée à domicile chez des patients atteints de maladie auto-immune." La Revue de Médecine Interne 31 (December 2010): S344. http://dx.doi.org/10.1016/j.revmed.2010.10.017.

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Ricciardelli, Ashley R., Ariadna Robledo, Jason E. Fish, Peter T. Kan, Tajie H. Harris, and Joshua D. Wythe. "The Role and Therapeutic Implications of Inflammation in the Pathogenesis of Brain Arteriovenous Malformations." Biomedicines 11, no. 11 (October 24, 2023): 2876. http://dx.doi.org/10.3390/biomedicines11112876.

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Brain arteriovenous malformations (bAVMs) are focal vascular lesions composed of abnormal vascular channels without an intervening capillary network. As a result, high-pressure arterial blood shunts directly into the venous outflow system. These high-flow, low-resistance shunts are composed of dilated, tortuous, and fragile vessels, which are prone to rupture. BAVMs are a leading cause of hemorrhagic stroke in children and young adults. Current treatments for bAVMs are limited to surgery, embolization, and radiosurgery, although even these options are not viable for ~20% of AVM patients due to excessive risk. Critically, inflammation has been suggested to contribute to lesion progression. Here we summarize the current literature discussing the role of the immune system in bAVM pathogenesis and lesion progression, as well as the potential for targeting inflammation to prevent bAVM rupture and intracranial hemorrhage. We conclude by proposing that a dysfunctional endothelium, which harbors the somatic mutations that have been shown to give rise to sporadic bAVMs, may drive disease development and progression by altering the immune status of the brain.
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Kwon, Mijung, Mitchell L. Leibowitz, and Jae-Ho Lee. "Small but mighty: the causes and consequences of micronucleus rupture." Experimental & Molecular Medicine 52, no. 11 (November 2020): 1777–86. http://dx.doi.org/10.1038/s12276-020-00529-z.

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AbstractMicronuclei are small DNA-containing nuclear structures that are spatially isolated from the main nucleus. They are frequently found in pathologies, including cancer. It was recently shown that these nuclear structures are not only biomarkers of disease but also play an active role in tumor biology. Many consequences of micronucleus formation on tumor biology are dependent on the frequent and irreversible rupture of their nuclear envelopes, which results in the exposure of their DNA contents to the cytoplasm. In this review, we discuss models of defective nuclear envelope deposition on missegregated chromosomes that lead to nuclear envelope rupture. Furthermore, we expound upon the various downstream consequences of micronucleus nuclear envelope rupture on cells. These consequences include a massive DNA rearrangement phenomenon called chromothripsis and activation of the cGAS-STING innate immune signaling pathway, which can be a double-edged sword with tumorigenesis and tumor prevention functions. Although micronuclei are small structures, the impact they have on cells and their microenvironment is quite large.
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Amadi, Margherita, Silvia Visentin, Francesca Tosato, Paola Fogar, Giulia Giacomini, Giulia Res, Luca Bonadies, et al. "Neonatal lymphocyte subpopulations analysis and maternal preterm premature rupture of membranes: a pilot study." Clinical Chemistry and Laboratory Medicine (CCLM) 59, no. 10 (June 7, 2021): 1688–98. http://dx.doi.org/10.1515/cclm-2021-0375.

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Abstract Objectives Preterm premature rupture of membranes (pPROM) causes preterm delivery, and increases maternal T-cell response against the fetus. Fetal inflammatory response prompts maturation of the newborn’s immunocompetent cells, and could be associated with unfavorable neonatal outcome. The aims were (1) to examine the effects of pPROM on the newborn’s and mother’s immune system and (2) to assess the predictive value of immune system changes in neonatal morbidity. Methods Mother-newborn pairs (18 mothers and 23 newborns) who experienced pPROM and controls (11 mothers and 14 newborns), were enrolled. Maternal and neonatal whole blood samples underwent flow cytometry to measure lymphocyte subpopulations. Results pPROM-newborns had fewer naïve CD4 T-cells, and more memory CD4 T-cells than control newborns. The effect was the same for increasing pPROM latency times before delivery. Gestational age and birth weight influenced maturation of the newborns’ lymphocyte subpopulations and white blood cells, notably cytotoxic T-cells, regulatory T-cells, T-helper cells (absolute count), and CD4/CD8 ratio. Among morbidities, fewer naïve CD8 T-cells were found in bronchopulmonary dysplasia (BPD) (p=0.0009), and more T-helper cells in early onset sepsis (p=0.04). Conclusions pPROM prompts maturation of the newborn’s T-cell immune system secondary to antigenic stimulation, which correlates with pPROM latency. Maternal immunity to inflammatory conditions is associated with a decrease in non-major histocompatibility complex (MHC)-restricted cytotoxic cells.
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Galaz, Jose, Roberto Romero, Rebecca Slutsky, Yi Xu, Kenichiro Motomura, Robert Para, Percy Pacora, et al. "Cellular immune responses in amniotic fluid of women with preterm prelabor rupture of membranes." Journal of Perinatal Medicine 48, no. 3 (March 26, 2020): 222–33. http://dx.doi.org/10.1515/jpm-2019-0395.

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Abstract Background Preterm birth is the leading cause of perinatal morbidity and mortality. Preterm prelabor rupture of membranes (pPROM) occurs in 30% of preterm births; thus, this complication is a major contributor to maternal and neonatal morbidity. However, the cellular immune responses in amniotic fluid of women with pPROM have not been investigated. Methods Amniotic fluid samples were obtained from women with pPROM and a positive (n = 7) or negative (n = 10) microbiological culture. Flow cytometry was performed to evaluate the phenotype and number of amniotic fluid leukocytes. The correlation between amniotic fluid immune cells and an interleukin-6 (IL-6) concentration or a white blood cell (WBC) count in amniotic fluid was calculated. Results Women with pPROM and a positive amniotic fluid culture had (1) a greater number of total leukocytes in amniotic fluid, including neutrophils and monocytes/macrophages and (2) an increased number of total T cells in amniotic fluid, namely CD4+ T cells and CD8+ T cells, but not B cells. The numbers of neutrophils and monocytes/macrophages were positively correlated with IL-6 concentrations and WBC counts in amniotic fluid of women with pPROM. Conclusion Women with pPROM and a positive amniotic fluid culture exhibit a more severe cellular immune response than those with a negative culture, which is associated with well-known markers of intra-amniotic inflammation.
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38

Mausoléo, A., R. Praliaud, S. Audia, J. Fadlallah, L. Languille, E. Crickx, B. Bonnotte, B. Godeau, M. Michel, and M. Mahevas. "Nouvelles données d’efficacité et de tolérance de l’association bortezomib et dexaméthasone dans l’anémie hémolytique auto-immune réfractaire à auto-anticorps chauds." La Revue de Médecine Interne 45 (June 2024): A72—A73. http://dx.doi.org/10.1016/j.revmed.2024.04.359.

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Konyshev, Ilya V., Olga D. Novikova, Olga Yu Portnyagina, and Andrey A. Byvalov. "Immunochemical activity of <i>Yersinia pseudotuberculosis</i> ompF and ompC porins evaluated by optical trapping." Russian Journal of Infection and Immunity 12, no. 6 (December 30, 2022): 1163–68. http://dx.doi.org/10.15789/2220-7619-iao-2007.

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Introduction. Study of features for interacting antigen-antibody system is of great importance for developing new modern tools for diagnostics and therapy of infectious diseases. In this regard, it is of great interest to study the rupture force between bacterial antigens and antibodies using modern biophysical methods including optical trapping. The importance of surface antigens in the immunochemical activity of Yersinia pseudotuberculosis assessed by such method has not been evaluated yet. In this work we examined an opportunity to evaluate the interaction of hydrophobic Y. pseudotuberculosis porins OmpF and OmpC with specific antibodies using optical trapping method. Materials and methods. Polystyrene microspheres (d = 1 m) were coated by passive adhesion with purified preparations of OmpF and OmpC porins; microsphere sensitization was verified by enzyme immunoassay. Antibodies from mouse sera were adsorbed onto the glass surface by chemical linking. The rupture force in the porins-antibodies system was determined using a laser trap according to the previously developed algorithm. Results. Using a model system including polystyrene microspheres sensitized with the proteins and aminated glass substrate coated with immune or nonimmune serum, significant differences in binding strength of OmpF and OmpC porins to homologous immune versus nonimmune sera were detected. The average forces of interaction with immune sera was 60 pN for OmpF microspheres (control 40 pN) and 69 pN for OmpC microspheres (control 49 pN). The proportion of irreversible substrate binding of the microspheres coated by the antigens to the treated with immune vs. non-immune sera was significantly higher. The results of assessing the average interaction force, as well as the predominance of the proportion of irreversible binding of antigen-coated microspheres with sera-treated substrates, indicates that specific interactions contribute significantly to the force of interaction. The aforementioned method can be used to evaluate the forces of intermolecular interaction in similar model systems using other microbial antigens.
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KÜÇÜKBAŞ, Gökçe Naz, and Arzu YAVUZ. "Systemic immune inflammation indices: novel predictors for preterm premature rupture of membranes and associated complications." Journal of Medicine and Palliative Care 4, no. 5 (October 27, 2023): 516–23. http://dx.doi.org/10.47582/jompac.1348845.

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Aim: This study aimed to investigate the relationship between systemic immune inflammation (SII) and response indices (SIRI), which are new markers of systemic inflammation derived from immune cells, and preterm premature rupture of membranes (PPROM), as well as adverse pregnancy outcomes. Materials and Methods: The retrospective study included 75 singleton pregnancies complicated with PPROM between 24 and 34 gestational weeks and 75 healthy pregnant women who delivered at term (control group). Inflammation indices were calculated based on neutrophil (N), platelet (P), lymphocyte (L), and monocyte (M) counts as follows: The neutrophil-to-lymphocyte ratio (NLR) = N/L; the platelet-to-lymphocyte ratio (PLR) = P/L; SII = (N×P)/L; and SIRI = (N×M)/L. Results: The median NLR (4.8 vs. 3.5, p
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Швец, E. Shvets, Горлов, A. Gorlov, Голубова, and T. Golubova. "Prospects of the use of new tablet hydrodynamic technology for rehabilitation in the traumatology." Journal of New Medical Technologies. eJournal 8, no. 1 (November 5, 2014): 0. http://dx.doi.org/10.12737/7235.

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The purpose of this work was to evaluate the effectiveness of hydrodynamic tablet technology methods in a post-traumatic rehabilitation of patients after surgery knee injuries with rupture of the cruciate ligament. The patients were divided into 2 groups. In the control group standard rehabilitation complex was used. In the main group (n=4) in addition to standard complex hydrodynamic tablet technology was used for influence on the lower limbs with the same parameters of exposure (daily tablet hydrodynamic procedure lasting 10 minutes, 10 procedures per treatment). There were evaluated such criteria as pain (Richie index), the mobility of the joints, the severity of edema by a simple measurement of the joint circumference. Hemodynamics was evaluated by using the method of rheovasography. Assessment of immunological parameters were performed by using the method of indirect immune-fluorescence and enzyme-linked immune-sorbent assay with reagents «Diaclone». It was proved that in the conditions of post-traumatic rehabilitation (in case of the cruciate ligament rupture in the late postoperative period) hydrodynamic tablet technology technique possesses the properties to stimulate recovery significantly, the pathogenic basis of which is an intensification of blood flow and, as a result – improvement the trophic tissues.
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Jara, Luis J., Carmen Navarro, Gabriela Medina, Olga Vera-Lastra, and Francisco Blanco. "Immune-Neuroendocrine Interactions and Autoimmune Diseases." Clinical and Developmental Immunology 13, no. 2-4 (2006): 109–23. http://dx.doi.org/10.1080/17402520600877059.

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The relationship between immune-neuroendocrine system is firmly established. The messengers of this connection are hormones, neuropeptides, neurotransmitters and cytokines. The immune-neuroendocrine system have the capacity to synthesize and release these molecules, which, in turn, can stimulate or suppress the activity of immune or neuroendocrine cells by binding to receptors. In fact, hormones, neuropeptides and neurotransmitters participate in innate and adaptive immune response.Autoimmune rheumatic diseases (ARD) are characterized by aberrant production of pro-inflammatory cytokines, which are a potent activator of the HPA axis. In consequence, high levels of pro-inflammatory hormones such as estrogens and prolactin, and low levels of glucocorticoids, an anti-inflammatory hormone, have been described in the active phase of ARD. In addition, high levels of pro-inflammatory hormones and cytokines have also been frequently detected in organ involvement of patients with ARD, suggesting an abnormal local neuroendocrine immune interaction. There is evidence that hormonal changes may appear before the symptomatic phase of the disease. Therefore, it is possible that a pro-inflammatory hormone favors the rupture of tolerance, which is a key feature of autoimmune diseases. The interactions between the immune-neuroendocrine system have a major impact on our understanding of the pathogenic mechanisms, diagnosis and therapy of ARD.
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Anderson, Leif Stefan, Rens Braster, Gerrit Sitters, Andrea Candelli, Ton N. Schumacher, and Wouter Scheper. "Measuring T-cell avidity and enrichment using acoustic force-based technology." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e14010-e14010. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14010.

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e14010 Background: The key driver for effective immune cell therapies is the overall binding strength of the immune cell and the target cell (e.g. tumor cells). The overall strength is known as ‘avidity’, a parameter reflecting interaction efficiency. The key to success for immune cell therapies is generating effective and long-lasting immune responses. The avidity of an immune cell to its target is predicative of its function, but current techniques to measure avidity are low-throughput and ineffective. Herein, we describe the use of acoustic forces to discriminate immune cells based on their avidity to tumor cells. The force required to separate a cell from its target is called the ‘rupture force’, and in this study, we were able to identify the rupture forces of tumor specific and non-specific T cells and enrich these different populations for downstream characterization. Methods: T cells from a healthy donor were transduced with either a non-relevant, or a melanoma recognizing T cell receptor and selected with puromycin resistance. Melanoma cells were seeded in the flow cell and allowed to adhere overnight to form a monolayer. For confocal experiments CFSE and Cell Trace far red stained T cells were mixed in a 1:1 ratio before co-culturing them in the flow cell. An acoustic force ramp was applied within the flow cell and cell detachment was monitored. Results: T cells engineered with a melanoma antigen-recognizing T-cell receptor needed 6 times more force than non-specific T cells to be separated from the melanoma target cells. Furthermore, 1.4 to 3.6-fold enrichment of high-avidity T cells was obtained from a mixed population of specific and non-specific T cells using acoustic forces. Conclusions: These findings indicate that melanoma-specific T cells bind with a higher avidity than non-specific T cells and that they can be separated with this approach. In conclusion, we demonstrate a novel method to measure cell avidity and sort cells by utilizing acoustic forces.
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Gauthier, Benoit R., Petra I. Lorenzo, and Valentine Comaills. "Physical Forces and Transient Nuclear Envelope Rupture during Metastasis: The Key for Success?" Cancers 14, no. 1 (December 24, 2021): 83. http://dx.doi.org/10.3390/cancers14010083.

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During metastasis, invading tumor cells and circulating tumor cells (CTC) face multiple mechanical challenges during migration through narrow pores and cell squeezing. However, little is known on the importance and consequences of mechanical stress for tumor progression and success in invading a new organ. Recently, several studies have shown that cell constriction can lead to nuclear envelope rupture (NER) during interphase. This loss of proper nuclear compartmentalization has a profound effect on the genome, being a key driver for the genome evolution needed for tumor progression. More than just being a source of genomic alterations, the transient nuclear envelope collapse can also support metastatic growth by several mechanisms involving the innate immune response cGAS/STING pathway. In this review we will describe the importance of the underestimated role of cellular squeezing in the progression of tumorigenesis. We will describe the complexity and difficulty for tumor cells to reach the metastatic site, detail the genomic aberration diversity due to NER, and highlight the importance of the activation of the innate immune pathway on cell survival. Cellular adaptation and nuclear deformation can be the key to the metastasis success in many unsuspected aspects.
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Mammel, Anna E., Heather Z. Huang, Amanda L. Gunn, Emma Choo, and Emily M. Hatch. "Chromosome length and gene density contribute to micronuclear membrane stability." Life Science Alliance 5, no. 2 (November 17, 2021): e202101210. http://dx.doi.org/10.26508/lsa.202101210.

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Micronuclei are derived from missegregated chromosomes and frequently lose membrane integrity, leading to DNA damage, innate immune activation, and metastatic signaling. Here, we demonstrate that two characteristics of the trapped chromosome, length and gene density, are key contributors to micronuclei membrane stability and determine the timing of micronucleus rupture. We demonstrate that these results are not due to chromosome-specific differences in spindle position or initial protein recruitment during post-mitotic nuclear envelope assembly. Micronucleus size strongly correlates with lamin B1 levels and nuclear pore density in intact micronuclei, but, unexpectedly, lamin B1 levels do not completely predict nuclear lamina organization or membrane stability. Instead, small gene-dense micronuclei have decreased nuclear lamina gaps compared to large micronuclei, despite very low levels of lamin B1. Our data strongly suggest that nuclear envelope composition defects previously correlated with membrane rupture only partly explain membrane stability in micronuclei. We propose that an unknown factor linked to gene density has a separate function that inhibits the appearance of nuclear lamina gaps and delays membrane rupture until late in the cell cycle.
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Dyatlova, Larisa Ivanovna, Aleksandr Viktorovich Mikhaylov, Nina Pavlovna Chesnokova, Yelena Vyacheslavovna Ponukalina, and Tatyana Nikolayevna Glukhova. "Laws of changes of immune status of mother and child at pregnancy prolongation, complicated by premature rupture of amniotic membranes." Journal of obstetrics and women's diseases 63, no. 2 (June 15, 2014): 35–41. http://dx.doi.org/10.17816/jowd63235-41.

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Purpose and tasks: to establish new prognostic criteria of date of prolongation of pregnancy with premature discharge of amniotic fluid on the basis of performance monitoring of cell immunity of mother in the dynamics of observation and the child at the time of completion childbirth. Material and methods. A clinical and laboratory examination of 50 pregnant women, the pregnancy of women was complicated by premature rupture of membranes at 22-34 weeks of gestation. The control group consisted of 40 women with normal pregnancy with the same time of gestation. The traditional methods of clinical and laboratory examination were used to assess the status of pregnant women. The study of peripheral blood was performed with hematological analyzer BC- 3000+. Subpopulations of peripheral blood lymphocytes was studied by cytometry using monoclonal antibodies (apparatus «FAC SCalibur» company «BectonDickinson», USA). Results. The development of leukocytosis with absolute and relative lymphopenia, reduction of CD16+56+lymphocytes and CD19 B lymphocytes were revealed in pregnant women with premature rupture of membranes. The failure of proliferative activity CD3+4+ T-helper cells, the increase of level of CD3+8+ cytotoxic T lymphocytes were revealed at the time of onset of labor after the prolongation of pregnancy. Prolongation of pregnancy at patients with premature rupture of membranes combined with the development of leukocytosis in the fetus, as well as the mother in the same period of observation. At the same time, unlike the parent organism, activation of B-lymphocyte proliferation and humoral immunity at fetus were occurred.
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Berrocal, José Ramón García, and Rafael Ramírez-Camacho. "Sudden Sensorineural Hearing Loss: Supporting the Immunologic Theory." Annals of Otology, Rhinology & Laryngology 111, no. 11 (November 2002): 989–97. http://dx.doi.org/10.1177/000348940211101107.

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Sudden deafness constitutes a diagnostic challenge. Classically, 2 causes, viral and vascular, are considered in the origin of idiopathic sudden hearing loss. More recently added to the list of possibilities are rupture of the membranous labyrinth and immune-mediated sensorineural hearing loss. The latter can be either primary and localized to the inner ear or, in perhaps fewer than one third of cases, secondary to generalized systemic autoimmune disease. The purpose of the present review is to define immune-mediated sudden sensorineural hearing loss as a distinctive entity, on the basis of clinical, immunologic, and pathological findings, and suggest a profile of the typical patient.
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48

Sadighpour, Tella, Celeste Cagnazzo, Shahrzad Alimohammadi, Anahita Emami, Azadeh Khayyat, and Mohammad Ali EsmaeilPour. "Immune-related adverse kidney events by immune checkpoint inhibitors; a narrative review on current studies." Journal of Nephropharmacology 10, no. 2 (June 1, 2021): e22-e22. http://dx.doi.org/10.34172/npj.2021.22.

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Chemotherapy-associated renal injury is considered one of the major concerns among nephrological and oncological practice. The use of novel anti-neoplastic therapies that target carcinomas has helped in the detection of this form of renal injury. Immune checkpoint inhibitors (ICPIs) are a group of monoclonal antibodies targeting inhibitory receptors that exist on tumor cells and T cells. ICPIs are able to suppress tumors that might have escaped from the immune surveillance. Meanwhile, although ICPIs have shown promising efficacy in cancer treatment, their immune-related side effects limit their widespread use in cancer therapy schedules. One of the major side effects limiting ICPIs’ usage is nephrotoxicity. Glomerular disease, acute interstitial nephritis (AIN), and acute tubular necrosis (ATN) are considered different infusion-related adverse events. Infiltration of eosinophils, T lymphocytes, and plasma cells, as well as interstitial inflammation and edema, leading to acute tubulointerstitial nephritis (ATIN). It is conceivable that the rupture of self-tolerance by ICPIs induces an autoimmune reaction against some specific self-antigens in the organs including kidneys. The exact nature of the antigen is unclear; however, it is possible that it is found in the renal tubular cells, as indicated by a greater frequency of ATIN in kidney biopsies. The current review paper discusses the relationship between ICPIs therapy and kidney disorders or more specifically, their possible role in renal damage along with renal toxicity profile in the setting of ICPIs treatment.
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Ordoñez-Granja, Jaime, José Chávez-Monter, Viridiana Chávez-Gómez, and Carlos Castillo-Rangel. "Racemose Neurocysticercosis of the Silviano Valley with Inflammatory Aneurysm of the Right Middle Cerebral Artery. Case Report." International Journal of Medical and Surgical Sciences 3, no. 4 (October 27, 2018): 1009–12. http://dx.doi.org/10.32457/ijmss.2016.037.

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Neurocysticercosis (NCC) is the most common parasitic disease of the brain, has a wide variety of patterns of presentation and can mimic many diseases. We report a patient with inflammatory aneurysm, and found only 5 cases reported in the literature, and only one has histopathological report. This is a case report of a patient with diabetes and arterial hypertension condition which started with sim- plesecondarygeneralizedpartialseizures. Thestudy reported the patient was diagnosed with neurocysticercosis racemosa, resection of lesions was performed with secondary inflammatory rupture intraoperative aneurysm clipping successful NCC, inflammatory changes in the literature described in the aneurysm wall and the dependent artery, secondary to immune process with vasculitis associated with a chronic inflammatory process, these changes in the aneurysm wall increase the possibility of intraoperative rupture. Histopathological report was conclusive with neurocysticercosis.
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50

Samuel, Nardin, and Ivan Radovanovic. "Genetic basis of intracranial aneurysm formation and rupture: clinical implications in the postgenomic era." Neurosurgical Focus 47, no. 1 (July 2019): E10. http://dx.doi.org/10.3171/2019.4.focus19204.

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OBJECTIVEDespite the prevalence and impact of intracranial aneurysms (IAs), the molecular basis of their pathogenesis remains largely unknown. Moreover, there is a dearth of clinically validated biomarkers to efficiently screen patients with IAs and prognosticate risk for rupture. The aim of this study was to survey the literature to systematically identify the spectrum of genetic aberrations that have been identified in IA formation and risk of rupture.METHODSA literature search was performed using the Medical Subject Headings (MeSH) system of databases including PubMed, EMBASE, and Google Scholar. Relevant studies that reported on genetic analyses of IAs, rupture risk, and long-term outcomes were included in the qualitative analysis.RESULTSA total of 114 studies were reviewed and 65 were included in the qualitative synthesis. There are several well-established mendelian syndromes that confer risk to IAs, with variable frequency. Linkage analyses, genome-wide association studies, candidate gene studies, and exome sequencing identify several recurrent polymorphic variants at candidate loci, and genes associated with the risk of aneurysm formation and rupture, including ANRIL (CDKN2B-AS1, 9p21), ARGHEF17 (11q13), ELN (7q11), SERPINA3 (14q32), and SOX17 (8q11). In addition, polymorphisms in eNOS/NOS3 (7q36) may serve as predictive markers for outcomes following intracranial aneurysm rupture. Genetic aberrations identified to date converge on posited molecular mechanisms involved in vascular remodeling, with strong implications for an associated immune-mediated inflammatory response.CONCLUSIONSComprehensive studies of IA formation and rupture have identified candidate risk variants and loci; however, further genome-wide analyses are needed to identify high-confidence genetic aberrations. The literature supports a role for several risk loci in aneurysm formation and rupture with putative candidate genes. A thorough understanding of the genetic basis governing risk of IA development and the resultant aneurysmal subarachnoid hemorrhage may aid in screening, clinical management, and risk stratification of these patients, and it may also enable identification of putative mechanisms for future drug development.
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