We filtered cells with fewer than 500 genes or more than 20% mitochondrial reads. In the pancreas datasets, we filtered cells with the same thresholds used in Butler et al7 : 1750 genes for CelSeq, 2500 genes for CelSeq2, no filter for Fluidigm C1, 2500 genes for SmartSeq2, and 500 genes for inDrop. We then library normalized each cell to 10,000 reads, by multiplicative scaling, then log scaled the normalized data. We then identified the top 1000 variable genes, ranked by coefficient of variation, within in each dataset. We pooled these genes to form the variable gene set of the analysis. Using only the variable genes, we mean centered and variance 1 scaled the genes across the cells. Note that this was done in the aggregate matrix, with all cells, rather than within each dataset separately. With these values, we performed truncated SVD keeping the top 30 eigenvectors. Finally, we multiplied the cell embeddings by the eigenvalues to avoid giving eigenvectors equal variance.
Pancreas
It produces enzymes that aid in the breakdown of food, as well as hormones such as insulin and glucagon that regulate blood sugar levels.
Pancreatic disorders can lead to conditions like pancreatitis, diabetes, and pancreatic cancer, making it an importamnt area of medical research.
Optimizing pancreas research through tools like PubCompare.ai can enhance reproducibility, accuracy, and the identification of effective protocols and methods.
Most cited protocols related to «Pancreas»
We filtered cells with fewer than 500 genes or more than 20% mitochondrial reads. In the pancreas datasets, we filtered cells with the same thresholds used in Butler et al7 : 1750 genes for CelSeq, 2500 genes for CelSeq2, no filter for Fluidigm C1, 2500 genes for SmartSeq2, and 500 genes for inDrop. We then library normalized each cell to 10,000 reads, by multiplicative scaling, then log scaled the normalized data. We then identified the top 1000 variable genes, ranked by coefficient of variation, within in each dataset. We pooled these genes to form the variable gene set of the analysis. Using only the variable genes, we mean centered and variance 1 scaled the genes across the cells. Note that this was done in the aggregate matrix, with all cells, rather than within each dataset separately. With these values, we performed truncated SVD keeping the top 30 eigenvectors. Finally, we multiplied the cell embeddings by the eigenvalues to avoid giving eigenvectors equal variance.
Most recents protocols related to «Pancreas»
Example 1
1) Tucaresol
Tucaresol (0-1200 μM) is exposed for 72 hours to a panel of human liquid, hematological, and solid tumors such as multiple myeloma, leukemia, colorectal, non-small cell lung cancer (squamous and adenocarcinoma), hepatocellular, renal, pancreatic and breast cancer cell lines, and human non-tumor such as HUVEC, PBMC, skin fibroblast cells lines. Tucaresol is studied either alone or in combination with standard-of-care agents (1-100 μM). All cell lines are grown in standard serum-containing media with an exposure time of 24-144 hours. Cell viability is measured using, for example, the Cell TiterGlo® Viability Assay. The potency (IC50) and efficacy (% cell kill) are determined from the percent cell growth of the vehicle control.
2) Tucaresol Plus PD-1 Antibody
Tucaresol (0-1200 μM) in the presence of a PD-1 antibody is exposed for 72 hours to a panel of human liquid, hematological, and solid tumor such as multiple myeloma, leukemia, colorectal, non-small cell lung cancer (squamous and adenocarcinoma), hepatocellular, renal, pancreatic and breast cancer cell lines, and human non-tumor such as HUVEC, PBMC, skin fibroblast cells lines, and the viability of the cell lines are measured as described above. The viability of the cell lines in the presence of tucaresol plus PD-1 antibody is compared to the viability of the cell lines in the presence of a CTLA-4 antibody plus the PD-1 antibody or PD-1 antibody alone.
3) CTLA-4 Antibody Plus PD-1 Antibody
CTLA-4 antibody in the presence of a PD-1 antibody is exposed for 72 hours to a panel of human liquid, hematological, and solid tumor such as multiple myeloma, leukemia, colorectal, non-small cell lung cancer (squamous and adenocarcinoma), hepatocellular, renal, pancreatic and breast cancer cell lines, and human non-tumor such as HUVEC, PBMC, skin fibroblast cells lines, and the viability of the cell lines are measured as described above.
4) Tucaresol Plus Plinabulin
Tucaresol (0-1200 μM) in the presence of Plinabulin is exposed for 72 hours to a panel of human liquid, hematological, and solid tumor such as multiple myeloma, leukemia, colorectal, non-small cell lung cancer (squamous and adenocarcinoma), hepatocellular, renal, pancreatic and breast cancer cell lines, and human non-tumor such as HUVEC, PBMC, skin fibroblast cells lines, and the viability of the cell lines are measured as described above.
The viability of the cell lines in the presence of tucaresol, tucaresol plus PD-1 antibody, CTLA-4 antibody plus the PD-1 antibody, and tucaresol plus plinabulin are compared.
Example 3
Lung cancer cell line A549 and squamous cell carcinoma cell line H10 expressing inducible SEQ ID NO: 1-HA vector were established as described previously. SEQ ID NO: 1 expression was detected by qPCR (
To evaluate the effects of SEQ ID NO: 1 on proliferation, A549 and H10 cells transduced with SEQ ID NO: 1-HA vector or control vector were monitored for 14 days. Growth curves show that cells overexpressing micropeptide SEQ ID NO: 1 have a consistently lower growth rate compared to the control (
Example 7
Five groups including tucaresol, tucaresol plus PD-1 or PD-L1 antibody, tucaresol plus CTLA-4 antibody, CTLA-4 antibody plus PD-1 or PD-L1 antibody, and tucaresol plus plinabulin are tested to determine their effect in an animal xenograft model.
The combined treatment with tucaresol and the checkpoint inhibitor(s) is tested in comparison with the treatment with tucaresol alone, the treatment with checkpoint inhibitor alone, or combination of checkpoint inhibitors. The tests are performed using seven to ten-week old athymic (nu/nu) mice that were injected subcutaneously with human tumor cell lines (of either solid or liquid tumor origin, for example of breast, lung, colon, brain, liver, leukemia, myeloma, lymphoma, sarcoma, pancreatic or renal origin). Six to ten testing groups are prepared, and each group includes 10 mice.
Each treatment starts at tumor size between 40-150 mm3 and continues until Day 24-56, when the animals are necropsied. To determine the efficacy of each treatment, the following data are collected: mortality; the body weight of the mice assessed twice weekly both prior to treatments; the rate of tumor growth as determined by the tumor size measurement (twice every week); the tumor growth index; overall survival rate; the tumor weight at necropsy; and the time required to increase tumor size 10 fold.
Example 9
In vivo PET/CT imaging was conducted in NCr nude mice bearing bxpc3 (human pancreatic adenocarcinoma cell line) and 4T1 (a murine breast cancer cell line that overexpresses integrin αvβ3 and CD13) tumor xenografts.
Mice were injected with bxpc3 cells (1 million cells in 150 μL PBS) into the subcutaneous flank of the right shoulder and 4T1 cells (1 million cells in 150 μL PBS) into the subcutaneous flank of the left shoulder. Either the CNGRC-(68Ga)NOTA-RGDyK heterodimer (“CNGRC” disclosed as SEQ ID NO: 1), (68Ga)NOTA(CNGRC) (“CNGRC” disclosed as SEQ ID NO: 1), or (68Ga)NOTA(RGDyK) were injected into the bloodstream via tail vein injection. Blocking studies were conducted for the heterodimer studies by co-injecting 100 times of cyclo(CNGRC) (“CNGRC” disclosed as SEQ ID NO: 1) and cyclo(RGDyK). Small animal PET/CT was performed at 1 hour post injection of tracers (
Example 16
The antitumor activity of exemplary MEK inhibitor compounds is evaluated in vivo using human cell line derived xenografts (CDX) grown in immunodeficient mice. For these studies, AsPC1 (pancreatic cell line with KRAS G12D mutation), NCI-H2122 (lung cell line with KRAS G12C mutation), and 5637 (bladder cell line with CRAF amplification) models are used. In addition, HCT-116 (colorectal cell line with KRAS G13D mutation), SKM-1 (AML cell line with KRAS K117N mutation), and OCI-AML-3 (AML cell line with NRAS Q61L mutation) models are used. The tumor cell lines (AsPC-1, NCI-H2122, 5637, and HCT-116 cells) are maintained in vitro as monolayer culture in medium at 37° C. in an atmosphere of 5% CO2 in air. The tumor cell lines (SKM-1 and OCI-AML-3 cells) are maintained in vitro as a suspension in medium at 37° C. in an atmosphere of 5% CO2 in air. The tumor cells are routinely sub-cultured before confluence by trypsin-EDTA treatment, not to exceed 4-5 passages. The cells growing in an exponential growth phase are harvested for tumor inoculation. AsPC1, NCI-H2122, and OCI-AML-3 tumors are implanted into Balb/c nude mice. HCT-116 tumors are implanted into Nu/Nu mice. 5637 and SKM-1 tumors are implanted into NOG mice. Each mouse is inoculated subcutaneously on the right flank with tumor cells in a 1:1 mixture with matrigel. Tumors are allowed to grow to approximately 150-200 mm3. At this time, mice are assigned to groups such that the mean tumor volume is the same for each treatment group. The MEK inhibitor compound treatments are administrated to the tumor-bearing mice via oral gavage. Throughout the study, mouse body weight and tumor volume are recorded. The measurement of tumor size is conducted twice weekly with a caliper and recorded. The tumor volume (mm3) is estimated using the formula: TV=a×b2/2, where “a” and “b” are long and short diameters of a tumor, respectively.
In the AsPC-1 model, exemplary MEK inhibitor I-2 was treated at 3 mg/kg QD and a percent TGI (tumor growth inhibition) on Day 21 of 83.4% was observed. The average body weight gain observed on Day 21 was 2.4%.
In the NCI-H2122 model, exemplary MEK inhibitor 1-2 was treated at 3 mg/kg QD and a percent TGI on Day 31 of 104% was observed. The average body weight loss observed on Day 31 was 1.5%.
In the 5637 model, exemplary MEK inhibitor I-2 was treated at 3 mg/kg QD and a percent TGI on Day 21 of 111% was observed. The average body weight loss observed on Day 21 was 6.8%.
In the HCT-116 model, exemplary MEK inhibitor I-2 was treated at 2 mg/kg QD, 3 mg/kg QOD or 6 mg/kg QOD and a percent TGIs on Day 20 of 102.9%, 98.1%, and 98%, respectively, were observed. The average body weight gain observed on Day 20 was 4%, 5.5%, and 12.1%, respectively.
In the SKM-1 model, exemplary MEK inhibitor I-2 was treated at 1 mg/kg QD, 3 mg/kg QD or 6 mg/kg QOD and venetoclax was treated at 100 mg/kg QD and a percent TGIs on Day 22 of 97.7%, 98.4%, 96.2%, and 46.6% respectively, were observed. The average body weight loss observed on Day 22 for the 3 mg/kg QD group was 1.2%, whereas weight gain was observed in 1 mg/kg QD, 6 mg/kg QOD and venetoclax groups (1.2%, 3.9, and 7.5%, respectively).
In the OCI-AML-3 model, exemplary MEK inhibitor I-2 was treated at 1 mg/kg QD, 3 mg/kg QD or 6 mg/kg QOD, and venetoclax was treated at 100 mg/kg QD and a percent TGIs on Day 15 of 94.8, 98.6, 95.2, and 13% respectively, were observed. The average body weight loss observed on Day 15 for the 1 and 3 mg/kg QD group was 2.9% and 7.8%, respectively, whereas weight gain was observed in 6 mg/kg QOD and venetoclax groups (3.3% and 8.3%, respectively).
Top products related to «Pancreas»
More about "Pancreas"
This glandular structure, situated behind the stomach, is responsible for producing essential enzymes that aid in the breakdown of food, as well as hormones like insulin and glucagon that regulate blood sugar levels.
Pancreatic disorders can lead to various health conditions, including pancreatitis, diabetes, and pancreatic cancer, making it a key area of medical research and investigation.
Optimizing pancreas research is essential, and tools like PubCompare.ai can help enhance reproducibility, accuracy, and the identification of effective protocols and methods.
PubCompare.ai's powerful platform allows researchers to easily locate the best protocols, pre-prints, and patents from the literature, streamlining the research process.
When studying the pancreas, researchers often utilize various cell lines, such as FBS, PANC-1, BxPC-3, AsPC-1, and MIA PaCa-2, which are derived from pancreatic cancer cells.
These cell lines are commonly cultured in DMEM media, supplemented with penicillin/streptomycin and other essential components, such as collagenase P, to maintain their growth and viability.
By leveraging the capabilities of PubCompare.ai, researchers can seamlessly navigate the vast array of pancreas-related information, identify the most effective methods and products, and enhance the overall efficiency and quality of their research.
The platform's user-friendly interface and cutting-edge technology ensure a streamlined and productive experience for scientists working to advance the understanding and treatment of pancreatic disorders.