ENHANCED FLUORESCENCE IMAGING WITH DMSO-MEDIATED OPTICAL CLEARING

Recent studies have demonstrated that topical application of glycerol on intact skin does not affect its optical scattering properties. Investigators from our research group recently revisited the use of dimethyl sulfoxide (DMSO) as an agent with optical clearing potential. We address the use of optical clearing to enhance quantitation of subsurface fluorescence emission. We employed both in vitro and in vivo model systems to study the effect of topical DMSO application on fluorescence emission. Our in vitro experiments performed on a tissue-simulating phantom suggest that DMSO-mediated optical clearing enables enhanced characterization of subsurface fluorophores. With topical DMSO application, a marked increase in fluorescence emission was observed. After 30 min, the fluorescence signal at the DMSO-treated site was 9× greater than the contralateral saline-treated site. This ratio increased to 13× at 105 min after agent application. In summary, DMSO is an effective optical clearing agent for improved fluorescence emission quantitation and warrants further study in preclinical in vivo studies. Based on outcomes from previous clinical studies on the toxicity profile of DMSO, we postulate that clinical application of DMSO as an optical clearing agent, can be performed safely, although further study is warranted.

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Panel Discussion II: Usefulness of in vitro and in vivo Model Systems for Predicting the Adverse Public Health Outcome for Antimicrobial Drug Residues in Food

Microbial Ecology in Health and Disease ◽

10.1080/08910600050216174 ◽

2000 ◽

Vol 12 (3) ◽

pp. 45-53

Author(s):

Andrew Beaulieu ◽

Jacques Boisseau ◽

Carl Cerniglia ◽

Denis Corpet ◽

A. Haydée Fernández ◽

...

Keyword(s):

Public Health ◽

Health Outcome ◽

Panel Discussion ◽

Antimicrobial Drug ◽

Model Systems ◽

In Vivo Model ◽

Drug Residues ◽

Public Health Outcome

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In Vitro and In Vivo Model Systems for the Study of Allergic and Inflammatory Disorders in Man

CHEST Journal ◽

10.1378/chest.87.5_supplement.162s ◽

1985 ◽

Vol 87 (5) ◽

pp. 162S-164S ◽

Cited By ~ 4

Author(s):

Stephen P. Peters ◽

Robert M. Naclerio ◽

Alkis Togias ◽

Robert P. Schleimer ◽

Donald W. MacGlashan ◽

...

Keyword(s):

Model Systems ◽

In Vivo Model ◽

Inflammatory Disorders

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Development and characterization of catechin-in-cyclodextrin-in-phospholipid liposome to eradicate MRSA-mediated surgical site infection: Investigation of their anti-infective efficacy through in vitro and in vivo studies

International Journal of Pharmaceutics ◽

10.1016/j.ijpharm.2021.121130 ◽

2021 ◽

pp. 121130

Author(s):

Simran Sinsinwar ◽

Vellingiri Vadivel

Keyword(s):

Surgical Site Infection ◽

In Vivo Studies ◽

Site Infection ◽

Phospholipid Liposome

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Diet, Obesity, and Cancer Progression: Are Adipocytes the Link?

Lipid Insights ◽

10.4137/lpi.s10871 ◽

2013 ◽

Vol 6 ◽

pp. LPI.S10871 ◽

Cited By ~ 11

Author(s):

Paul Toren ◽

Benjamin C. Mora ◽

Vasundara Venkateswaran

Keyword(s):

Tumor Microenvironment ◽

Cancer Progression ◽

Tumor Biology ◽

Model Systems ◽

In Vivo Model ◽

Diet Induced Obesity ◽

Breast And Prostate Cancer ◽

Obesity And Cancer

Obesity has been linked to more aggressive characteristics of several cancers, including breast and prostate cancer. Adipose tissue appears to contribute to paracrine interactions in the tumor microenvironment. In particular, cancer-associated adipocytes interact reciprocally with cancer cells and influence cancer progression. Adipokines secreted from adipocytes likely form a key component of the paracrine signaling in the tumor microenvironment. In vitro coculture models allow for the assessment of specific adipokines in this interaction. Furthermore, micronutrients and macronutrients present in the diet may alter the secretion of adipokines from adipocytes. The effect of dietary fat and specific fatty acids on cancer progression in several in vivo model systems and cancer types is reviewed. The more common approaches of caloric restriction or diet-induced obesity in animal models establish that such dietary changes modulate tumor biology. This review seeks to explore available evidence regarding how diet may modulate tumor characteristics through changes in the role of adipocytes in the tumor microenvironment.

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In Vitro and In Vivo Model Systems of Cholangiocarcinoma

Diagnosis and Management of Cholangiocarcinoma ◽

10.1007/978-3-030-70936-5_22 ◽

2021 ◽

pp. 471-494

Author(s):

Giovanni Brandi ◽

Simona Tavolari

Keyword(s):

Model Systems ◽

In Vivo Model

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Unbiased in vivo preclinical evaluation of anticancer drugs identifies effective therapy for the treatment of pancreatic adenocarcinoma

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1920240117 ◽

2020 ◽

Vol 117 (48) ◽

pp. 30670-30678

Author(s):

Olivera Grbovic-Huezo ◽

Kenneth L. Pitter ◽

Nicolas Lecomte ◽

Joseph Saglimbeni ◽

Gokce Askan ◽

...

Keyword(s):

Large Scale ◽

Single Agent ◽

Model Systems ◽

Ductal Adenocarcinoma ◽

In Vivo Model ◽

Cancer Therapies ◽

Hsp90 Inhibition ◽

Dismal Prognosis

Pancreatic ductal adenocarcinoma (PDAC) is typically diagnosed at an advanced stage, which limits surgical options and portends a dismal prognosis. Current oncologic PDAC therapies confer marginal benefit and, thus, a significant unmet clinical need exists for new therapeutic strategies. To identify effective PDAC therapies, we leveraged a syngeneic orthotopic PDAC transplant mouse model to perform a large-scale, in vivo screen of 16 single-agent and 41 two-drug targeted therapy combinations in mice. Among 57 drug conditions screened, combined inhibition of heat shock protein (Hsp)-90 and MEK was found to produce robust suppression of tumor growth, leading to an 80% increase in the survival of PDAC-bearing mice with no significant toxicity. Mechanistically, we observed that single-agent MEK inhibition led to compensatory activation of resistance pathways, including components of the PI3K/AKT/mTOR signaling axis, which was overcome with the addition of HSP90 inhibition. The combination of HSP90(i) + MEK(i) was also active in vitro in established human PDAC cell lines and in vivo in patient-derived organoid PDAC transplant models. These findings encourage the clinical development of HSP90(i) + MEK(i) combination therapy and highlight the power of clinically relevant in vivo model systems for identifying cancer therapies.

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