people and pubs update

_bibliography/papers.bib

@@ -1,6 +1,118 @@
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+@ARTICLE{Henthorn2024-gr,
+  title    = "Transcriptional phenotype of the anti-parasitic benzodiazepine
+              meclonazepam on the blood fluke Schistosoma mansoni",
+  author   = "Henthorn, Clair R and McCusker, Paul and Le Clec'h, Winka and
+              Chevalier, Frédéric D and Anderson, Tim J C and Zamanian, Mostafa
+              and Chan, John D",
+  journal  = "bioRxiv",
+  pages    = "2024.10.29.620505",
+  abstract = "There are limited control measures for the disease
+              schistosomiasis, despite the fact that infection with parasitic
+              blood flukes affects hundreds of millions of people worldwide. The
+              current treatment, praziquantel, has been in use since the 1980's
+              and there is a concern that drug resistance may emerge with
+              continued monotherapy. Given the need for additional
+              antischistosomal drugs, we have re-visited an old lead,
+              meclonazepam. In comparison to praziquantel, there has been
+              relatively little work on its antiparasitic mechanism. Recent
+              findings indicate that praziquantel and meclonazepam act through
+              distinct receptors, making benzodiazepines a promising chemical
+              series for further exploration. Previous work has profiled the
+              transcriptional changes evoked by praziquantel treatment. Here, we
+              examine in detail schistosome phenotypes evoked by in vitro and in
+              vivo meclonazepam treatment. These data confirm that meclonazepam
+              causes extensive tegument damage and directly kills parasites, as
+              measured by pro-apoptotic caspase activation. In vivo meclonazepam
+              exposure results in differential expression of many genes that are
+              divergent in parasitic flatworms, as well as several gene products
+              implicated in blood feeding and regulation of hemostasis in other
+              parasites. Many of these transcripts are also differentially
+              expressed with praziquantel exposure, which may reflect a common
+              schistosome response to the two drugs. However, despite these
+              similarities in drug response, praziquantel-resistant parasites
+              retain susceptibility to meclonazepam's schistocidal effects.
+              These data provide new insight into the mechanism of
+              antischistosomal benzodiazepines, resolving similarities and
+              differences with the current frontline therapy, praziquantel.",
+  month    =  nov,
+  year     =  2024,
+  doi      = "10.1101/2024.10.29.620505",
+  language = "en",
+  pdf      = {Henthorn et al. 2024 - Transcriptional phenotype of the anti-parasitic benzodiazepine meclonazepam on the blood fluke Schistosoma mansoni.pdf},
+  preview  = {Henthorn et al. 2024 - Transcriptional phenotype of the anti-parasitic benzodiazepine meclonazepam on the blood fluke Schistosoma mansoni.jpeg}
+
+}
+
+@ARTICLE{Collins2024-dd,
+  title    = "Naturally occurring variation in a cytochrome {P450} modifies
+              thiabendazole responses independent of beta-tubulin",
+  author   = "Collins, J B and Dilks, Clayton M and Hahnel, Steffen R and
+              Rodriguez, Briana and Fox, Bennett W and Redman, Elizabeth and Yu,
+              Jingfang and Cooke, Brittany and Sihuta, Kateryna and Zamanian,
+              Mostafa and Roy, Peter J and Schroeder, Frank C and Gilleard, John
+              S and Andersen, Erik C",
+  journal  = "bioRxiv",
+  pages    = "2024.09. 23.614411",
+  abstract = "AbstractWidespread anthelmintic resistance has complicated the
+              management of parasitic nematodes. Resistance to the benzimidazole
+              (BZ) drug class is nearly ubiquitous in many species and is
+              associated with mutations in beta-tubulin genes. However,
+              mutations in beta-tubulin alone do not fully explain all BZ
+              resistance. We performed a genome-wide association study using a
+              genetically diverse panel ofCaenorhabditis elegansstrains to
+              identify loci that contribute to resistance to the BZ drug
+              thiabendazole (TBZ). We identified a quantitative trait locus
+              (QTL) on chromosome V independent of all beta-tubulin genes and
+              overlapping with two promising candidate genes, the cytochrome
+              P450 genecyp-35d1and the nuclear hormone receptornhr-176,
+              identified by another mapping technique. Both genes were
+              previously demonstrated to play a role in TBZ metabolism. NHR-176
+              binds TBZ and induces the expression of CYP-35D1, which
+              metabolizes TBZ. We generated single gene deletions
+              ofnhr-176andcyp-35d1and found that both genes play a role in TBZ
+              response. A predicted high-impact lysine-to-glutamate substitution
+              at position 267 (K267E) in CYP-35D1 was identified in a sensitive
+              parental strain, and reciprocal allele replacement strains in both
+              genetic backgrounds were used to show that the lysine allele
+              conferred increased TBZ resistance. Using competitive fitness
+              assays, we found that neither allele is deleterious, but the
+              lysine allele is selected in the presence of TBZ. Additionally, we
+              found that the lysine allele significantly increased the rate of
+              TBZ metabolism compared to the glutamate allele. Moreover, yeast
+              expression assays showed that the lysine version of CYP-35D1 had
+              twice the enzymatic activity of the glutamate allele. To connect
+              our results to parasitic nematodes, we analyzed fourHaemonchus
+              contortuscytochrome P450 orthologs but did not find variation at
+              the 267 position in fenbendazole-resistant populations. Overall,
+              we confirmed that variation in this cytochrome P450 gene is the
+              first locus independent of beta-tubulin to play a role in BZ
+              resistance.Author SummaryBenzimidazoles (BZs) are the most common
+              drug class used to control parasitic nematodes, but because of
+              overuse, resistance is widespread. The known genetic causes of BZ
+              resistance are associated with mutations in beta-tubulin and are
+              the most well understood of any anthelmintic class. However, BZ
+              response varies significantly and differential levels of
+              resistance likely require mutations in genes independent of
+              beta-tubulin. We used the free-living model nematodeCaenorhabditis
+              elegansto identify and characterize a novel cytochrome P450
+              gene,cyp-35d1, associated with natural resistance to the BZ drug
+              thiabendazole (TBZ). We demonstrated that a lysine at position 267
+              confers TBZ resistance and is selected over multiple generations
+              after TBZ treatment. This allele significantly increased the rate
+              of TBZ metabolism in bothC. elegansand yeast. In conclusion, we
+              have characterized the role of variation in a cytochrome P450 that
+              contributes to TBZ resistance, independent of mutations in
+              beta-tubulin.",
+  month    =  sep,
+  year     =  2024,
+  doi      = "10.1101/2024.09.23.614411",
+  pdf      = {Collins et al. 2024 - Naturally occurring variation in a cytochrome P450 modifies thiabendazole responses independent of beta-tubulin.pdf},
+  preview  = {Collins et al. 2024 - Naturally occurring variation in a cytochrome P450 modifies thiabendazole responses independent of beta-tubulin.jpeg}
+}
+
 @ARTICLE{Mian2024-ch,
   title     = "Development of non-sedating benzodiazepines with in vivo
                antischistosomal activity",

_data/cv.yml

@@ -144,7 +144,7 @@
       orcid:
       github:
       cv_url:
-      portrait: 
+      portrait: cknuese.jpg
       description: 
 
     - title: Natalia Betancourt
@@ -171,6 +171,18 @@
       department: Biology
       portrait: ghiltgen.jpg
 
+    - title: Benjamin Lee
+      location: Singapore
+      year: 2024 - 
+      department: Computer Science
+      portrait: blee.jpg
+
+    - title: Sal Singh
+      location: 
+      year: 2024 - 
+      department: 
+      portrait: ssingh.jpg
+
 
 
 # ALUMNI - Trainees / Staff