Fredagsmix

Piedmont Triad (Triad benämnt) har klivit in på Topp-10 listan över USA,s främsta center för life science forskning / utbildning och samlingsplats för över 150 Biotech-företag.Triad kommer sig av den medicinska termen för 3 olika symptom inom samma sjukdom. I detta kluster finns Wake Forest/ReMDO och naturligtvis PHI med eget kontor.  

Triad ranks in top 10 U.S. markets with most life sciences construction

Mar 27, 2024

The Triad has outdone historical life science metros like Boston and San Francisco, coming in at No. 1 for how much its life sciences spaces will grow.

The Piedmont Triad Regenerative Medicine Engine, based in Winston-Salem, will tap the world’s largest regenerative medicine cluster to create and scale breakthrough clinical therapies, contributing to a growing industry that is key to healthcare delivery.

Vår vän Mr ReMDO, Joshua Hunsberger, som nyligen aviserade sin övergång till The Piedmont Triad Regenerative Medicine Engine premiärade igår med den första hearingen av 3 i att samla styrkorna och starta kommersialiseringsfasen.Hearingen har på morgonen lagts ut och vill man se den klickar man här.

Triad klustret utökades nyligen med ännu en större BioTech-aktör.

Winston-Salem’s Charter Medical grows with new laboratory space in Innovation Quarter

With more than 170 employees, Charter Medical is the 10th-largest life sciences firm in the Triad.

Min kommentar
Att befinna sig mitt i detta epicentrum av Biotech-aktörer (som PHI gör) öppnar naturligtvis upp för nya möjligheter när klustret har ökat sin attraktionsgrad och alltfler aktörer söker sig dit. Är PHI på tårna kan det innebära nya samarbeten och naturligtvis chans att kränga X antal HoloMonitor.

I anslutning till min kommentar i gårdagens inlägg har Oscar mejlat över en ny forskningsrapport. Tack Oscar.

11 ungerska forskare har fått sina studier om tjock- och ändtarmscancer publicerade. 

Lectin-Based Immunophenotyping and Whole Proteomic Profiling of CT-26 Colon Carcinoma Murine Model

Published: 4 April 2024

Abstract

A murine colorectal carcinoma (CRC) model was established. CT26 colon carcinoma cells were injected into BALB/c mice’s spleen to study the primary tumor and the mechanisms of cell spread of colon cancer to the liver. The CRC was verified by the immunohistochemistry of Pan Cytokeratin and Vimentin expression. Immunophenotyping of leukocytes isolated from CRC-bearing BALB/c mice or healthy controls, such as CD19+ B cells, CD11+ myeloid cells, and CD3+ T cells, was carried out using fluorochrome-labeled lectins. The binding of six lectins to white blood cells, such as galectin-1 (Gal1), siglec-1 (Sig1), Sambucus nigra lectin (SNA), Aleuria aurantia lectin (AAL), Phytolacca americana lectin (PWM), and galectin-3 (Gal3), was assayed. Flow cytometric analysis of the splenocytes revealed the increased binding of SNA, and AAL to CD3 + T cells and CD11b myeloid cells; and increased siglec-1 and AAL binding to CD19 B cells of the tumor-bearing mice. The whole proteomic analysis of the established CRC-bearing liver and spleen versus healthy tissues identified differentially expressed proteins, characteristic of the primary or secondary CRC tissues. KEGG Gene Ontology bioinformatic analysis delineated the established murine CRC characteristic protein interaction networks, biological pathways, and cellular processes involved in CRC. Galectin-1 and S100A4 were identified as upregulated proteins in the primary and secondary CT26 tumor tissues, and these were previously reported to contribute to the poor prognosis of CRC patients. Modelling the development of liver colonization of CRC by the injection of CT26 cells into the spleen may facilitate the understanding of carcinogenesis in human CRC and contribute to the development of novel therapeutic strategies.

Kortfattat berättar studien att denna cancerform,som är den 3e vanligaste,att drabbade alldeles för sent får signaler till dess uppkomst.Det ger sämre möjligheter att bota då tidsfaktor från upptäckt till insats är så viktig.Forskarna berättar även att denna cancerform inte sällan ger upphov till levermetastaser. 
Med dessa konstateranden utgick forskarna till att söka svar på hur sätta in behandling och vilken typ av läkemedel som fungerar under dessa förutsättningar. Läs mer om hur de gick tillväga.

Materials and Methods (urval)

4.8. Lectin Agglutination Test

To obtain the best results, we had to know whether each lectin was capable of cell agglutination, and we had to exclude them from the experiments. After euthanizing the animals, the spleens were removed and homogenized freshly on a cell strainer (70 μm pore size, Merck Millipore, Burlington, MA, USA) using the piston of a syringe and sterile PBS. Cells were pelleted by centrifugation at 1500 rpm for 5 min. The pellet was resuspended in 5 mL ACK lysis buffer for 5 min. Samples were loaded on a cell strainer (70 μm in pore size) and washed with 20 mL PBS. Cells were counted using a Bürker chamber and trypan blue viability dye (Thermo Fischer Scientific, Waltham, MA, USA), and 100.000 cells were plated on 96-well plates (Corning, New York, NY, USA) for a lectin agglutination assay and microscopic evaluation (HoloMonitor™ M3). The agglutination assay consisted of four different concentrations (0,1 µg/mL; 1 µg/mL; 10 µg/mL and 50 µg/mL) in RPMI (GIBCO, Life Technologies, Paisley, UK). Lectins were diluted in sterile PBS with 0,1% sodium azide (Sigma-Aldrich, Saint Louis, MO, USA). The lectins involved in the study were used in a lower concentration than the concentration with the agglutination activity of leukocytes.

                                               Mvh the99

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