Subcellular Fractionation & RNase R Treatment: 3
Purpose: To determine the localization and stability of circ_HECTD1.
Result: Circ_HECTD1 was found mainly in the cytoplasm and resistant to RNase R, indicating its circular nature.
Cell Transfection:
Purpose: To knock down circ_HECTD1 and observe the effects on cell proliferation and apoptosis4.
Result: Knockdown of circ_HECTD1 enhanced cell proliferation and reduced apoptosis in OGD/R-treated HT22 cells5.
EdU & MTT Assays:
Purpose: To assess cell proliferative ability6.
Result: Circ_HECTD1 knockdown increased the number of EdU-positive cells and cell viability, indicating improved cell proliferation.
Flow Cytometry:
Purpose: To analyze cell apoptosis.
Result: Circ_HECTD1 knockdown decreased the apoptosis rate in OGD/R-treated HT22 cells5.
Western Blot:
Purpose: To measure the protein levels related to cell proliferation and apoptosis.
Result: Circ_HECTD1 deficiency led to increased levels of PCNA (a proliferation marker) and Bcl-2 (an anti-apoptotic marker), and decreased levels of Bax and Cleaved PARP (pro-apoptotic markers).
Dual-Luciferase Reporter Assay:1
Purpose: To verify the binding relationship between miR-27a-3p and circ_HECTD1 or FSTL17.
Result: Confirmed that circ_HECTD1 directly interacts with miR-27a-3p and that miR-27a-3p targets FSTL1

RT-qPCR (Reverse Transcription Quantitative Polymerase Chain Reaction):
Purpose: To quantify the expression levels of circ_HECTD1, miR-27a-3p, and FSTL1 mRNA in cells affected by cerebral infarction.
Result: The RT-qPCR results would typically show the relative expression levels of these genes. An increase or decrease in the Ct (Cycle threshold) values would indicate changes in gene expression. For instance, a lower Ct value for circ_HECTD1 might suggest higher expression in cells post-infarction, which could be associated with the cellular response to injury

The article describes several experiments to investigate the role of FSTL1 and miR-125a-3p in adipogenic differentiation and inflammation1. Here’s a summary of the experiments and their results:

Isolation and Differentiation of Preadipocytes: Mouse subcutaneous preadipocytes were isolated and induced to differentiate in vitro2. The study observed morphological changes and lipid accumulation, confirming the suitability of these cells for further experiments.
Plasmid Construction and Luciferase Reporter Assay: A plasmid containing the FSTL1 gene was constructed, and a luciferase reporter assay was performed to validate miR-125a-3p targeting the 3′ UTR region of FSTL134. The assay confirmed that miR-125a-3p could bind to the 3′ UTR of FSTL1, reducing luciferase activity.
Transfection of Plasmids, siRNAs, and miRNAs: The study used transfection techniques to overexpress or silence FSTL1 and miR-125a-3p in preadipocytes5. The results showed that overexpression of FSTL1 inhibited adipogenesis and promoted inflammation, while silencing FSTL1 had the opposite effect67.
Oil Red O Staining and Triglyceride Assay: These assays were used to visualize and quantify lipid accumulation in differentiated adipocytes. Overexpression of FSTL1 reduced lipid droplets, whereas miR-125a-3p promoted lipid accumulation8.
Quantitative Real-Time PCR and Western Blotting: These methods were employed to measure the expression levels of adipogenic and inflammatory genes. The results supported the findings that FSTL1 negatively regulates adipogenesis and promotes inflammation, while miR-125a-3p has the opposite effects6.
Overall, the experiments demonstrated that FSTL1 acts as a pro-inflammatory factor inhibiting adipogenesis, and miR-125a-3p can reverse these effects by targeting FSTL1. This suggests potential therapeutic targets for obesity-related inflammatory diseases.

The article details several experiments conducted to investigate the role of circATP8A1 in gastric cancer progression1. Here’s a summary of the key experiments and their implications:

Exosome Isolation and Characterization: Exosomes were isolated from plasma and characterized to confirm their size and presence of specific markers. This established the foundation for studying the role of exosomal circRNAs in gastric cancer2.
circRNA Microarray Analysis: A microarray was used to identify differentially expressed circRNAs in exosomes from gastric cancer patients compared to healthy individuals. This led to the discovery of circATP8A1 as a novel oncogenic circRNA.
Functional Assays: Various in vitro assays (CCK-8, colony formation, and transwell migration/invasion) were performed to assess the effects of circATP8A1 on gastric cancer cell proliferation, colony formation, and invasiveness. The results indicated that circATP8A1 promotes these malignant behaviors.
Macrophage Polarization: The study explored how exosomal circATP8A1 affects macrophage polarization, finding that it induces M2 polarization through the STAT6 pathway, which is associated with tumor progression3.
Molecular Interactions: The interaction between circATP8A1 and miR-1-3p was investigated using FISH, RIP, RNA pull-down, and luciferase reporter assays5. These experiments confirmed that circATP8A1 acts as a sponge for miR-1-3p, affecting the STAT6 pathway and macrophage polarization4.
Animal Models: In vivo experiments with mice models were conducted to study the effects of circATP8A1 on tumor growth and macrophage polarization, further confirming the oncogenic role of circATP8A1 in gastric cancer progression.

The article describes several experiments conducted to investigate the role of circS100A11 in childhood asthma. Here’s a summary of the key experiments and their implications:

Microarray Analysis:
Purpose: To identify differentially expressed circRNAs in PBMCs of children with asthma compared to healthy controls.
Result: 372 circRNAs were found to be differentially expressed, with circS100A11 being significantly upregulated in asthmatic children.
Macrophage Activation Assays:
Purpose: To determine the effect of circS100A11 on M2a macrophage activation.
Result: circS100A11 facilitated M2a macrophage activation by enhancing the translation of its host gene, S100A11.
Murine Asthma Model:
Purpose: To test the role of circS100A11 in lung inflammation in a cockroach allergen extract (CRE)-induced asthma model.
Result: Overexpression of circS100A11 in macrophages exacerbated lung inflammation, while macrophage-specific knockdown of S100A11 alleviated it.
RNA Immunoprecipitation and Chromatin Immunoprecipitation Assays:
Purpose: To explore the mechanism by which circS100A11 promotes S100A11 translation and affects STAT6 expression.
Result: circS100A11 was found to bind competitively to CAPRIN1, reducing its suppression of S100A11 translation, which in turn enhanced STAT6 expression and M2a macrophage activation.
These experiments collectively suggest that circS100A11 and S100A11 play a significant role in promoting M2a macrophage activation and lung inflammation in asthma, making them potential therapeutic and diagnostic targets.

The article discusses a study on the role of circS100A11 in childhood asthma. Here’s a summary of the experiments and their logic:

Expression Analysis: Researchers identified 372 circRNAs differentially expressed in PBMCs of children with asthma. circS100A11 was notably upregulated and mainly expressed in monocytes.
M2a Macrophage Activation: circS100A11 was shown to facilitate M2a macrophage activation by enhancing the translation of its host gene, S100A11, which worsened lung inflammation in a murine asthma model12.
Mechanistic Insights: The study revealed that circS100A11 competitively binds to CAPRIN1, reducing its suppression on S100A11 translation34. S100A11 then promotes SP3 binding to the STAT6 promoter, enhancing STAT6 expression and M2a macrophage activation56.
Therapeutic Potential: Macrophage-specific knockdown of S100A11 alleviated lung inflammation in the murine model, suggesting circS100A11 and S100A11 as potential therapeutic targets for childhood asthma.
The logic connecting these experiments is to demonstrate how circS100A11 contributes to asthma pathogenesis by regulating macrophage activation and to explore potential therapeutic interventions. The study progresses from identifying a key circRNA to understanding its function, mechanism, and therapeutic implications.

我佛了，AI越来越懒了

β-actin, also known as ACTB, is one of the six different actin isoforms identified in humans1. It is a highly conserved protein that plays a crucial role in cell motility, structure, and integrity1. β-actin is a non-muscle cytoskeletal actin, which means it’s involved in forming the cytoskeleton that helps maintain the cell’s shape and provides internal support12.

In addition to its structural role, β-actin participates in various cellular processes such as cell junction assembly, cytoskeleton organization, and membrane organization1. It’s also involved in more complex activities like chromatin remodeling and transcriptional regulation within the nucleus2.

Moreover, β-actin is commonly used as a loading control in Western blotting and as a housekeeping gene standard in quantitative PCR (qPCR) due to its consistent presence across different cell types1. Its molecular weight is approximately 42 kDa1.

In summary, β-actin is a fundamental component of the cellular architecture and is essential for maintaining the cell’s structural integrity and supporting various cellular functions.

好吧纯纯WB对照组

准确来说loading control

The article describes an experiment investigating the role of Follistatin-like protein 1 (FSTL1) in cigarette smoke-induced Chronic Obstructive Pulmonary Disease (COPD). Here’s a summary of the methods and their intended purposes:

Serum and Lung Specimens: To compare FSTL1 and autophagy protein levels between COPD patients and controls.
Animal Models: To observe the effects of chronic cigarette smoke exposure on wild-type mice, FSTL1 ± mice, and FSTL1 flox/+ mice.
3-Methyladenine (3-MA) Treatment: To assess the impact of autophagy inhibition on cigarette smoke-exposed mice.
ELISA and Western Blotting: To measure the expression of FSTL1 and autophagy-associated proteins.
Immunohistochemistry: To visualize the localization and expression of proteins in lung tissues.
Electron Microscopy: To observe autophagosome formation in lung cells.
Bronchoalveolar Lavage Fluid Analysis: To evaluate airway inflammation by measuring cytokines.
Lung Function Tests: To assess the impact of cigarette smoke and FSTL1 on lung function.
The results indicated that FSTL1 promotes cigarette smoke-induced COPD by modulating autophagy, suggesting that targeting FSTL1 and autophagy could be potential therapeutic strategies for treating COPD. The experiments showed increased FSTL1 and autophagy markers in COPD patients and mice exposed to cigarette smoke, and that inhibiting autophagy reduced airway remodeling and inflammation.

COPD Patients vs. Controls:
FSTL1 and Autophagy Biomarkers: Both FSTL1 and autophagy biomarkers were found to be increased in COPD patients compared to controls.
Serum and Lung Specimens: The study observed higher levels of FSTL1 and autophagy-associated protein expression in the serum and lung specimens of COPD patients.
CS-Exposed WT Mice:
Autophagy Activation: There was an upregulation of autophagy activation in CS-exposed mice, accompanied by airway remodeling and inflammation.
3-MA Intervention: CS-exposed WT mice treated with 3-methyladenine (3-MA) showed similar manifestations to CS-exposed FSTL1 ± mice, suggesting that 3-MA could mitigate the effects of CS exposure.
FSTL1 ± Mice:
CS-Induced Autophagy: FSTL1 ± mice exhibited a lower level of CS-induced autophagy compared to control mice.
Resistance to CS-Induced Effects: These mice also resisted CS-induced inflammatory response, airway remodeling, and impaired lung function.
FSTL1 and Autophagy in COPD Pathogenesis:
FSTL1’s Role: The study suggests that FSTL1 promotes CS-induced COPD by modulating autophagy.
Potential Therapeutic Target: Targeting FSTL1 and autophagy could be a new approach to treating cigarette smoke-induced COPD.
Lung Function Assessment:
3-MA and FSTL1 ± Mice: Both 3-MA pretreated WT mice and FSTL1 ± mice showed attenuated lung function decline in response to CS exposure.
Lung Compliance: The study measured lung compliance and total lung capacity, finding that FSTL1 deficiency could protect against the decline of lung function after CS exposure.
These results collectively indicate that FSTL1 plays a significant role in the development of COPD by regulating autophagy, and that manipulating these pathways could offer new therapeutic strategies for COPD. Remember, these are experimental findings and further research is needed to translate these findings into clinical practice.

3-Methyladenine (3-MA) is widely recognized as an inhibitor of autophagy. It functions by blocking the early stages of the autophagy process, particularly the formation of autophagosomes1. Autophagy is a cellular degradation pathway that involves the lysosomal digestion of damaged organelles, proteins, and other cellular components to maintain cellular homeostasis2.

When 3-MA is applied to cells, it inhibits the class III phosphatidylinositol 3-kinase (PI3K), which is essential for the initiation of autophagosome formation1. By preventing the formation of these autophagic vesicles, 3-MA effectively stops the autophagic flux, leading to the accumulation of autophagy substrates such as p62/SQSTM1, which is a protein often used as a marker to study autophagy dynamics1.

In research, 3-MA is commonly used to study the role of autophagy in various physiological and pathological processes by inhibiting this pathway and observing the resulting effects on cells or organisms1. For instance, in the context of neurological diseases, oxidative stress, or atherosclerosis, 3-MA’s inhibition of autophagy can provide insights into how autophagy contributes to these conditions

The article describes a series of experiments to investigate the role of Follistatin-like protein 1 (FSTL1) in asthma. Here’s a summary of the methods and their intended purposes, along with the results:

OVA-Induced Asthma Model: Mice were sensitized and challenged with ovalbumin (OVA) to induce asthma-like symptoms. The control groups received PBS. This model was used to assess the role of FSTL1 in asthma.
Result: Fstl1± mice showed reduced Muc-5AC production and mucus hypersecretion compared to OVA-WT mice1.
Immunohistochemistry & ELISA: These methods were used to detect the protein levels of Muc-5AC, FSTL1, NLRP3, and IL-1β in lung tissues and bronchoalveolar lavage fluid (BALF)2.
Result: Fstl1± mice had decreased levels of these proteins, indicating reduced inflammation.
Western Blot Analysis: This technique was employed to measure the protein expression of NLRP3 and IL-1β in alveolar macrophage cells (MH-S cells)3.
Result: Pretreatment with siFSTL1 or MCC950 reduced the production of NLRP3 and IL-1β induced by OVA or FSTL14.
Cell Culture Experiments: MH-S cells were stimulated with FSTL1 and/or OVA to explore the effect of FSTL1 on the NLRP3/IL-1β signaling pathway.
Result: FSTL1 stimulation increased the expression of NLRP3 and IL-1β, while MCC950 pretreatment inhibited this effect56.
Overall, the study demonstrated that FSTL1 plays a significant role in allergic airway inflammation by activating the NLRP3/IL-1β signaling pathway, and that inhibiting FSTL1 could be a potential therapeutic strategy against asthma78. The experiments collectively aimed to elucidate the mechanisms of FSTL1 in asthma and to explore potential treatments by modulating this protein’s activity.

只能说现在做PPT美观确实很容易，AI确实可以的

The article explains various assays used to assess cell proliferation in the context of papillary thyroid carcinoma (PTC) research:

MTT Assay: This assay measures cell proliferation by adding MTT solution to cells1. MTT is reduced by metabolically active cells, producing a colored formazan product. The intensity of the color, measured by absorbance at 490 nm, correlates with the number of viable cells.
EdU Assay: EdU (5-ethynyl-2’-deoxyuridine) is a nucleoside analog of thymidine and is incorporated into DNA during active DNA synthesis. After labeling cells with EdU, a fluorescent dye is used to detect the incorporated EdU, allowing visualization and quantification of proliferating cells.
Colony Formation Assay: This assay evaluates the ability of a single cell to grow into a colony. Cells are plated at low density and allowed to grow until visible colonies form. The colonies are then fixed, stained, and counted to assess the proliferative potential of the cells.
These assays are utilized in the study to investigate the role of circ_0002111 in PTC cell proliferation and its potential as a therapeutic target2.

Linear PSD3 refers to the linear form of the gene Pleckstrin And Sec7 Domain Containing 3 (PSD3). In the context of this article, PSD3 is the parent gene from which circ_0002111, a circular RNA (circRNA), is derived. The article explains that circ_0002111 is produced from exons 5-9 of the PSD3 gene and has a mature length of 538 base pairs1. Unlike linear RNAs like PSD3, circRNAs like circ_0002111 form a covalently closed continuous loop, which makes them resistant to degradation by RNA exonucleases. This stability allows circRNAs to have regulatory roles in various cellular processes, including acting as microRNA (miRNA) sponges, influencing gene expression, and potentially contributing to diseases such as cancer2. In the case of papillary thyroid carcinoma (PTC), the article discusses the role of circ_0002111 in promoting malignant behaviors by regulating the miR-134-5p/FSTL1 molecular network34. The study uses RT-qPCR to show that linear PSD3 is significantly reduced after RNase R treatment, while circ_0002111 remains stable, highlighting the distinct properties of circRNAs compared to their linear counterparts5.

The Transwell assay, according to this article, is a method used to assess the migration ability of papillary thyroid carcinoma (PTC) cells. Here’s a brief overview:

Purpose: It’s utilized to evaluate the cell migration capability.
Procedure: Cells are placed in the upper chamber of a Transwell chamber, with cell culture medium in the lower chamber. After incubation, migrated cells are stained and counted.
Significance: The assay helps determine the impact of circ_0002111 on PTC cell migration, showing that circ_0002111 knockdown suppresses migration1.
Results Interpretation: Reduced cell migration in the assay indicates the effectiveness of circ_0002111 silencing in inhibiting PTC cell migration.
This assay is part of the experimental methods used to explore the regulatory mechanism of circ_0002111 in PTC progression

incubation
the process of incubating eggs, cells, bacteria, a disease, etc.

In biology, “knockdown” refers to an experimental technique used to reduce the expression of one or more genes in an organism. This reduction in gene expression can be achieved through various methods, such as the use of small interfering RNA (siRNA) or short hairpin RNA (shRNA), which bind to mRNA transcripts and prevent them from being translated into proteins. The term can also refer to the genetic modification that leads to a decrease in gene expression without completely eliminating it, which is different from a “knockout” where the gene is completely inactivated1.

Knockdown is often used to study the function of a particular gene by observing the effects of decreased gene expression on the organism. It’s a valuable tool for researchers to understand gene function and to investigate the potential role of genes in diseases and disorders

In summary, knockdown reduces gene expression temporarily without altering the DNA, while knockout permanently removes or inactivates the gene at the DNA level.

AI联想问题正好是我想问的

Here are the key points about OCR and the compounds oligomycin, FCCP, and Rote/AA:

Oxygen Consumption Rate (OCR): OCR is a measure of mitochondrial function and cellular metabolism. It indicates the rate at which cells consume oxygen, which is essential for energy production through oxidative phosphorylation1.
Oligomycin: This compound is an inhibitor of ATP synthase, an enzyme involved in the synthesis of ATP during oxidative phosphorylation. It is used to assess mitochondrial function by blocking ATP production and measuring the resulting changes in OCR2.
FCCP (Carbonyl cyanide-4 (trifluoromethoxy) phenylhydrazone): FCCP is a chemical that uncouples oxidative phosphorylation by transporting protons across the mitochondrial membrane, leading to increased oxygen consumption without ATP production. It is used to determine the maximum respiratory capacity of mitochondria2.
Rotenone/Antimycin A (Rote/AA): These are inhibitors of the mitochondrial electron transport chain. Rotenone inhibits complex I, while Antimycin A inhibits complex III. They are used to measure non-mitochondrial oxygen consumption by shutting down mitochondrial respiration

The Xenograft Tumor Assay in this article refers to an experimental procedure used to study the function of circ_0002111 in tumor growth in vivo13. Here’s a brief overview:

Purpose: To analyze the role of circ_0002111 in promoting tumorigenesis in papillary thyroid carcinoma (PTC).
Method: BALB/c male nude mice were injected subcutaneously with PTC cells that were either untreated or had circ_0002111 knocked down.
Observations: Tumor volume and weight were measured over 4 weeks, and the results showed that tumors in the group with circ_0002111 knockdown were significantly smaller.
Conclusion: The assay demonstrated that circ_0002111 facilitates tumor growth in PTC, indicating its oncogenic role in vivo2.
This experiment supports the overall finding that circ_0002111 acts as a tumorigenic factor in PTC by targeting the miR-134-5p/FSTL1 pathway

好想摆烂啊，有六篇文章但是我还在第一篇打转

The logic behind the statements from the article is as follows:

Circ_0002111 as miR-134-5p Sponge: Circ_0002111 acts as a “natural sponge” for miR-134-5p, meaning it binds to and sequesters miR-134-5p1. This prevents miR-134-5p from performing its normal functions, such as regulating gene expression.
Tumor Progression Inhibition: The si-circ_0002111#1 (a small interfering RNA designed to target circ_0002111) was shown to inhibit tumor progression. However, when miR-134-5p levels were reduced, this inhibition was reversed, indicating that miR-134-5p is essential for the tumor-suppressive effects of si-circ_0002111#1.
FSTL1 as Target Gene: FSTL1 is identified as a target gene for miR-134-5p23. This means that miR-134-5p can bind to the mRNA of FSTL1 and regulate its expression.
The axis confirmation refers to the experimental validation of the interactions between circ_0002111, miR-134-5p, and FSTL14. This was confirmed through various assays such as dual-luciferase reporter assays, RNA pull-down assays, and RT-qPCR, which demonstrated the direct binding and regulatory relationships among these molecules5. These interactions form a regulatory axis that influences the progression of papillary thyroid carcinoma (PTC). The study aimed to elucidate the specific functional mechanism of circ_0002111 in PTC by investigating this molecular network

I’m sorry, but the web page you are referring to seems to be empty or has failed to load, so I cannot provide an explanation based on that article. However, generally speaking, an RNA pull-down assay is a technique used in molecular biology to investigate the interaction between RNA and proteins. It involves binding RNA molecules to a substrate, then “pulling down” the RNA along with any proteins that are bound to it. This allows researchers to identify and study the proteins that interact with specific RNA sequences. If you have another source or article you’d like me to summarize or explain, please let me know!

RNA Pull-Down Assay:

Purpose: It’s a technique used to determine the interaction between RNA and other molecules, such as proteins or microRNAs (miRNAs).
Process: Involves using a probe (like circ_0002111) to capture target miRNAs from cell extracts, which are then identified and quantified.
Application: This study used RNA pull-down to confirm that circ_0002111 binds to miR-134-5p, indicating a regulatory interaction in papillary thyroid carcinoma (PTC).
Significance: Helps understand the molecular mechanisms in diseases like PTC by revealing how circRNAs like circ_0002111 can regulate miRNA levels and affect gene expression.

The article verifies that circS100A11 enhances M2a macrophage activation through several key experiments:1

Expression Analysis: circS100A11 was found to be dominantly expressed in monocytes and significantly upregulated in children with asthma23.
Functional Assays: Knockdown of circS100A11 in THP-1-derived human macrophages resulted in reduced expression of M2a macrophage marker genes, while overexpression led to increased marker gene expression.
Protein Interaction: circS100A11 was shown to promote the translation of its host gene, S100A11, by competitively binding to CAPRIN1, which decreases the suppression of CAPRIN1 upon S100A11 translation45.
In Vivo Model: A cockroach allergen extract (CRE)-induced murine asthma model with macrophage-specific overexpression of circS100A11 exhibited exacerbated lung inflammation, confirming the role of circS100A11 in vivo.

今天：
问老板购买质粒的事宜
去实验室和师姐学习养细胞
去买一辆小电驴
晚上看执医技能视频，刷儿科的题

养完细胞了，啥都没记住，回去上网学
下一步去买小电驴

问了老板购买质粒事宜，我发现我就是害怕等消息回复，所以会拖延找老板，这次拖延了整一天

克服了消费冲动，在1600和2200选了便宜的，电池里程足够用了

晚上还有哪些事情：
在网上看一看养细胞的流程细节
找一下实验室某个型号的离心机怎么配平
还有执医
明天要看论文，细化预实验实验步骤，列出每一步需要的试剂，发给实验室的老师核对哪些有哪些没有

Cultivating COS-7 cells is a meticulous process that requires careful attention to aseptic techniques to prevent contamination. Here’s a detailed guide to help you with the cultivation process:

COS-7 Cell Cultivation Instructions:
Prepare the Growth Medium: Use Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% Fetal Bovine Serum (FBS).
Incubation: Maintain the cells at 37°C in a humidified atmosphere containing 5% CO2.
Subculturing:
Rinse cells with sterile 1x PBS to remove all traces of media containing FBS.
For a T75 flask, add 2 mL of Trypsin-EDTA and observe cell layer detachment using an inverted microscope. Detachment should occur within 3-15 minutes.
If cells do not detach, incubate the flask to increase enzymatic activity. Avoid agitation during this process.
After detachment, add 8 mL of complete medium to neutralize the trypsin.
Use the appropriate split ratio aliquot of the cell suspension to transfer to a new culture flask.
Confluency: Maintain culture at a confluency between 30-90%. The doubling time for COS-7 cells is approximately 35-48 hours.
Long-term Storage: For storing COS-7 cells long-term, use the complete growth medium with 5% (v/v) DMSO and store in the vapor phase of liquid nitrogen12.
Using an Alcohol Lamp for Aseptic Techniques:
The alcohol lamp is used for flame sterilization, which is a part of aseptic technique. Here are the key points when you should use an alcohol lamp:

Before Starting: Sterilize all tools and work surfaces.
Preparing Culture Medium: Properly sterilize and cool the medium before use.
Aseptic Transfer: Flame sterilize the neck of the culture vessel to ensure no contaminants enter.
Remember, the use of an alcohol lamp should be part of your routine to maintain a sterile environment. It’s typically used before any procedure that requires opening of culture vessels or transferring cultures to prevent microbial contamination345.

Keep in mind that while using an alcohol lamp, you should work in a well-ventilated area and keep all flammable materials away from the flame. Always practice good personal hygiene, such as washing hands before and after handling cultures, and wear appropriate protective equipment.

I hope this helps you with your cell culture practice! If you need more assistance or have other questions, feel free to ask.

今天todolist
帮老板审批我的项目采购(？)
把信息发给厂商客服
上次没查的离心机怎么配平
查询TPH-1细胞培养出现细胞聚集正常吗
最重要:查文献细化预实验方案

周四前还要做好主任教学查房的PPT