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  1. Article ; Online: Incorporating diversity, equity, and inclusion concepts in pharmacy education and experiential training.

    Yang, Tianrui / Linn, Becky S / Bennis, Jane

    American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists

    2023  Volume 81, Issue 8, Page(s) 275–278

    MeSH term(s) Humans ; Diversity, Equity, Inclusion ; Curriculum ; Problem-Based Learning ; Education, Pharmacy ; Schools, Pharmacy ; Students, Pharmacy
    Language English
    Publishing date 2023-11-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 1224627-x
    ISSN 1535-2900 ; 1079-2082
    ISSN (online) 1535-2900
    ISSN 1079-2082
    DOI 10.1093/ajhp/zxad279
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Evaluation of a polymer-coated nanoparticle cream formulation of resiniferatoxin for the treatment of painful diabetic peripheral neuropathy.

    Baskaran, Padmamalini / Mohandass, Adithya / Gustafson, Noah / Bennis, Jane / Louis, Somaja / Alexander, Brenda / Nemenov, Mikhail I / Thyagarajan, Baskaran / Premkumar, Louis S

    Pain

    2022  Volume 164, Issue 4, Page(s) 782–790

    Abstract: Abstract: Painful diabetic peripheral neuropathy (PDPN) is one of the major complications of diabetes. Currently, centrally acting drugs and topical analgesics are used for treating PDPN. These drugs have adverse effects; some are ineffective, and ... ...

    Abstract Abstract: Painful diabetic peripheral neuropathy (PDPN) is one of the major complications of diabetes. Currently, centrally acting drugs and topical analgesics are used for treating PDPN. These drugs have adverse effects; some are ineffective, and treatment with opioids is associated with use dependence and addiction. Recent research indicates that transient receptor potential vanilloid 1 (TRPV1) expressed in the peripheral sensory nerve terminals is an emerging target to treat pain associated with PDPN. Block of TRPV1 ion channel with specific antagonists, although effective as an analgesic, induced hyperthermia in clinical trials. However, TRPV1 agonists are useful to treat pain by virtue of their ability to cause Ca 2+ influx and subsequently leading to nerve terminal desensitization. Here, we report the effectiveness of an ultrapotent TRPV1 agonist, resiniferatoxin (RTX) nanoparticle, in a topical formulation (RTX-cream; RESINIZIN) that alleviates pain associated with DPN in animal models of diabetes. Resiniferatoxin causes nerve terminal depolarization block in the short term, which prevents pain during application and leading to nerve terminal desensitization/depletion in the long term resulting in long-lasting pain relief. Application of RTX cream to the hind limbs suppresses thermal hyperalgesia in streptozotocin-induced diabetic rats and mini pigs without any adverse effects as compared with capsaicin at therapeutic doses, which induces intense pain during application. Resiniferatoxin cream also decreases the expression of TRPV1 in the peripheral nerve endings and suppresses TRPV1-mediated calcitonin gene-related peptide release in the skin samples of diabetic rats and mini pigs. Our preclinical data confirm that RTX topical formulation is an effective treatment option for PDPN.
    MeSH term(s) Swine ; Rats ; Animals ; Diabetic Neuropathies/drug therapy ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/drug therapy ; Swine, Miniature/metabolism ; Pain ; Diterpenes/therapeutic use ; Analgesics/therapeutic use ; Capsaicin/pharmacology ; TRPV Cation Channels/metabolism
    Chemical Substances resiniferatoxin (A5O6P1UL4I) ; Diterpenes ; Analgesics ; Capsaicin (S07O44R1ZM) ; TRPV Cation Channels
    Language English
    Publishing date 2022-08-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 193153-2
    ISSN 1872-6623 ; 0304-3959
    ISSN (online) 1872-6623
    ISSN 0304-3959
    DOI 10.1097/j.pain.0000000000002765
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Assessment of Pharmacology, Safety, and Metabolic activity of Capsaicin Feeding in Mice.

    Baskaran, Padmamalini / Markert, Laurel / Bennis, Jane / Zimmerman, Liesl / Fox, Jonathan / Thyagarajan, Baskaran

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 8588

    Abstract: Capsaicin (CAP) activates transient receptor potential vanilloid subfamily 1 (TRPV1) to counter high-fat diet (HFD)-induced obesity. Several studies suggest that CAP induces the browning of white adipocytes in vitro or inguinal white adipose tissue (iWAT) ...

    Abstract Capsaicin (CAP) activates transient receptor potential vanilloid subfamily 1 (TRPV1) to counter high-fat diet (HFD)-induced obesity. Several studies suggest that CAP induces the browning of white adipocytes in vitro or inguinal white adipose tissue (iWAT) in vivo. However, there is a lack of data on the dose-response for CAP to inhibit HFD-induced obesity. Therefore, we first performed experiments to correlate the effect of various doses of CAP to prevent HFD-induced weight gain in wild-type (WT) mice. Next, we performed a subchronic safety study in WT mice fed a normal chow diet (NCD ± CAP, 0.01% in NCD) or HFD ± CAP (0.01% in HFD) for eight months. We analyzed the expression of adipogenic and thermogenic genes and proteins in the iWAT from these mice, conducted histological studies of vital organs, measured the inflammatory cytokines in plasma and iWAT, and evaluated liver and kidney functions. The dose-response study showed that CAP, at doses above 0.001% in HFD, countered HFD-induced obesity in mice. However, no difference in the anti-obesity effect of CAP was observed at doses above 0.003% in HFD. Also, CAP, above 0.001%, enhanced the expression of sirtuin-1 and thermogenic uncoupling protein 1 (UCP-1) in the iWAT. Safety analyses suggest that CAP did not cause inflammation. However, HFD elevated plasma alanine aminotransferase and creatinine, caused iWAT hypertrophy and hepatic steatosis, and CAP reversed these. Our data suggest that CAP antagonizes HFD-induced metabolic stress and inflammation, while it does not cause any systemic toxicities and is well tolerated by mice.
    MeSH term(s) Animals ; Body Weight/drug effects ; Capsaicin/adverse effects ; Capsaicin/pharmacology ; Cytokines/blood ; Diet, High-Fat ; Disease Models, Animal ; Feeding Behavior ; Female ; Gene Expression Regulation/drug effects ; Heart Function Tests ; Inflammation Mediators/blood ; Metabolism/drug effects ; Mice, Knockout ; Neuromuscular Junction/drug effects ; Obesity/blood ; Obesity/genetics ; Organ Size/drug effects ; Thermogenesis/genetics
    Chemical Substances Cytokines ; Inflammation Mediators ; Capsaicin (S07O44R1ZM)
    Language English
    Publishing date 2019-06-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-45050-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Binding Efficacy and Thermogenic Efficiency of Pungent and Nonpungent Analogs of Capsaicin.

    Baskaran, Padmamalini / Covington, Kyle / Bennis, Jane / Mohandass, Adithya / Lehmann, Teresa / Thyagarajan, Baskaran

    Molecules (Basel, Switzerland)

    2018  Volume 23, Issue 12

    Abstract: 1) Background: Capsaicin, a chief ingredient of natural chili peppers, enhances metabolism and energy expenditure and stimulates the browning of white adipose tissue (WAT) and brown fat activation to counter diet-induced obesity. Although capsaicin and ... ...

    Abstract (1) Background: Capsaicin, a chief ingredient of natural chili peppers, enhances metabolism and energy expenditure and stimulates the browning of white adipose tissue (WAT) and brown fat activation to counter diet-induced obesity. Although capsaicin and its nonpungent analogs are shown to enhance energy expenditure, their efficiency to bind to and activate their receptor-transient receptor potential vanilloid subfamily 1 (TRPV1)-to mediate thermogenic effects remains unclear. (2) Methods: We analyzed the binding efficiency of capsaicin analogs by molecular docking. We fed wild type mice a normal chow or high fat diet (± 0.01% pungent or nonpungent capsaicin analog) and isolated inguinal WAT to analyze the expression of thermogenic genes and proteins. (3) Results: Capsaicin, but not its nonpungent analogs, efficiently binds to TRPV1, prevents high fat diet-induced weight gain, and upregulates thermogenic protein expression in WAT. Molecular docking studies indicate that capsaicin exhibits the highest binding efficacy to TRPV1 because it has a hydrogen bond that anchors it to TRPV1. Capsiate, which lacks the hydrogen bond, and therefore, does not anchor to TRPV1. (4) Conclusions: Long-term activation of TRPV1 is imminent for the anti-obesity effect of capsaicin. Efforts to decrease the pungency of capsaicin will help in advancing it to mitigate obesity and metabolic dysfunction in humans.
    MeSH term(s) Adipose Tissue, White/drug effects ; Adipose Tissue, White/metabolism ; Animals ; Capsaicin/chemistry ; Capsaicin/metabolism ; Capsaicin/pharmacology ; Capsicum/chemistry ; Energy Metabolism/drug effects ; Mice ; Obesity/drug therapy ; Obesity/metabolism ; TRPV Cation Channels/metabolism ; Thermogenesis/drug effects
    Chemical Substances TRPV Cation Channels ; TRPV1 protein, mouse ; Capsaicin (S07O44R1ZM)
    Language English
    Publishing date 2018-12-04
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1413402-0
    ISSN 1420-3049 ; 1431-5165 ; 1420-3049
    ISSN (online) 1420-3049
    ISSN 1431-5165 ; 1420-3049
    DOI 10.3390/molecules23123198
    Database MEDical Literature Analysis and Retrieval System OnLINE

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