Tissue response, macrophage phenotype, and intrinsic calcification induced by cardiovascular biomaterials: Can clinical regenerative potential be predicted in a rat subcutaneous implant model?

The extent of damage surrounding an implanted electrode in the cerebral cortex is a question of significant importance with regard to attaining consistency and validity of physiological recordings. In order to determine the extent of such tissue changes, 150 micron diameter platinum electrodes were implanted in the cortex of four adult baboons, and after eight days the animals were sacrificed by whole body perfusion with a 3% glutaraldehyde in 0.1M phosphate fixative.The calvarium was carefully removed and the electrode tracts were readily discernible in the firm, glutaraldehyde fixed tissue.Careful dissection of the zone of the electrode tract resulted in a small block which was further sectioned into tip, mid-tract and surface areas. Ultrastructurally, damage extended from the electrode sheath to the greatest extent of from 0.2 to 3.5 mm.

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Comparing the Responses of Osseous Versus Soft-Tissue Metastases of Renal Cell Carcinoma to Receptor Tyrosine Kinase Inhibitors and Immunotherapy

Kidney Cancer ◽

10.3233/kca-200094 ◽

2020 ◽

Vol 4 (3) ◽

pp. 151-158

Author(s):

Katherine Yuxi Tai ◽

Jad M. El Abiad ◽

Carol D. Morris ◽

Mark Christopher Markowski ◽

Adam S. Levin

Keyword(s):

Renal Cell Carcinoma ◽

Soft Tissue ◽

Cell Carcinoma ◽

Receptor Tyrosine Kinase ◽

Renal Cell ◽

Kinase Inhibitors ◽

Tissue Response ◽

Bone Response ◽

Soft Tissue Response ◽

Receptor Tyrosine Kinase Inhibitors

BACKGROUND: Checkpoint inhibitors and receptor tyrosine kinase inhibitors (RTKIs) have changed the standard of care for metastatic renal cell carcinoma (mRCC). Anecdotal evidence suggests these therapies may be less effective for treating bone than soft-tissue metastases. PURPOSE: We performed a retrospective review evaluating the relative clinical responses in soft-tissue and bone metastases in patients undergoing therapy using RTKIs and anti-programmed death-1 (PD-1) agents for mRCC. METHODS: Of the 2,212 patients in our institutional cancer registry with renal cell carcinoma (1997–2017), 68 (82 disease courses) were identified with measurable bone and soft-tissue metastases treated with RTKIs and/or PD-1s. Extent of metastasis was quantified at the time of therapy initiation (baseline) and at 3 months, 6 months, and 1 year. Changes in disease status were categorized as complete response, partial response, stable, mixed, or progression of disease according to RECIST v1.1 and MD Anderson criteria. These categories were further organized into “response to treatment” or “evidence of progression” to generate a generalized linear effects model with soft-tissue response as the independent variable and bone response as the dependent variable. Alpha = 0.05. RESULTS: Soft-tissue response correlated with bone response at 3 months (76 disease courses, p = 0.005) and 6 months (48 disease courses, p = 0.017). Of the patients with controlled soft-tissue disease, only 14 (19%) and 15 (32%) had progression in bone at 3 and 6 months, respectively. CONCLUSION: Contrary to anecdotal reports, osseous metastases do not appear to respond worse than soft-tissue metastases to treatment with these agents.

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Cytocompatibility and Material Properties of Poly-carbonate Urethane/Carbon Nanofiber Composites for Neural Applications

MRS Proceedings ◽

10.1557/proc-774-o7.30 ◽

2003 ◽

Vol 774 ◽

Author(s):

Janice L. McKenzie ◽

Michael C. Waid ◽

Riyi Shi ◽

Thomas J. Webster

Keyword(s):

Mechanical Properties ◽

Carbon Nanofibers ◽

Material Properties ◽

Carbon Nanofiber ◽

Scar Tissue ◽

Tissue Response ◽

Positive Interactions ◽

Weight Percentage ◽

Poly Carbonate

AbstractCarbon nanofibers possess excellent conductivity properties, which may be beneficial in the design of more effective neural prostheses, however, limited evidence on their cytocompatibility properties exists. The objective of the present in vitro study was to determine cytocompatibility and material properties of formulations containing carbon nanofibers to predict the gliotic scar tissue response. Poly-carbonate urethane was combined with carbon nanofibers in varying weight percentages to provide a supportive matrix with beneficial bulk electrical and mechanical properties. The substrates were tested for mechanical properties and conductivity. Astrocytes (glial scar tissue-forming cells) were seeded onto the substrates for adhesion. Results provided the first evidence that astrocytes preferentially adhered to the composite material that contained the lowest weight percentage of carbon nanofibers. Positive interactions with neurons, and, at the same time, limited astrocyte functions leading to decreased gliotic scar tissue formation are essential for increased neuronal implant efficacy.

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Reprogrammed M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 extends lifespan of mice with experimental carcinoma

ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia» ◽

10.25557/0031-2991.2017.02.4-9 ◽

2017 ◽

pp. 4-9

Author(s):

С.В. Калиш ◽

С.В. Лямина ◽

А.А. Раецкая ◽

И.Ю. Малышев

Keyword(s):

Tumor Growth ◽

Culture Medium ◽

Ehrlich Carcinoma ◽

Macrophage Phenotype ◽

M1 Macrophages ◽

M1 Macrophage ◽

Ec Cells ◽

Experimental Carcinoma

Цель исследования. Репрограммирование М1 фенотипа макрофагов с ингибированными факторами транскрипции М2 фенотипа STAT3, STAТ6 и SMAD и оценка их влияния на развитие карциномы Эрлиха (КЭ) in vitro и in vivo. Методика. Рост опухоли иницировали in vitro путем добавления клеток КЭ в среду культивирования RPMI-1640 и in vivo путем внутрибрюшинной инъекции клеток КЭ мышам. Результаты. Установлено, что M1макрофаги и in vitro, и in vivo оказывают выраженный противоопухолевый эффект, который превосходит антиопухолевые эффекты М1, M1, M1 макрофагов и цисплатина. Заключение. М1 макрофаги с ингибированными STAT3, STAT6 и/или SMAD3 эффективно ограничивают рост опухоли. Полученные данные обосновывают разработку новой технологии противоопухолевой клеточной терапии. Objective. Reprogramming of M1 macrophage phenotype with inhibited M2 phenotype transcription factors, such as STAT3, STAT6 and SMAD and assess their impact on the development of Ehrlich carcinoma (EC) in vitro and in vivo . Methods. Tumor growth in vitro was initiated by addition of EC cells in RPMI-1640 culture medium and in vivo by intraperitoneal of EC cell injection into mice. Results. It was found that M1 macrophages have a pronounced anti-tumor effect in vitro , and in vivo , which was greater than anti-tumor effects of M1, M1, M1 macrophages and cisplatin. Conclusion. M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 effectively restrict tumor growth. The findings justify the development of new anti-tumor cell therapy technology.

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