@CB2 got rid of the black and white ceramic mugs I’ve been eyeing since like high school, I’m gonna need a minute

画力アレなんでわかりにくいですが。中国ロボット「CB2」くんパロのフェンちゃん

#Clemson CB Ashton Hampton (#23) is my early CB2 for the 2027 draft. Super physical, toolsy corner with great length that makes so many plays on ball.

Rb7!! excellent waiting move.And now the Black are lost. What to play: Ca5, Ra1# Ca3, Ra7# Ka3, Ra1# Ka5, Ra7# Any other move of the Knight looses too: For example Cb2, Ra1# or Cb6, Ra7#

THC não tem "a mesma estrutura do estrógeno" e nem se liga aos receptores estrogênicos ERα ou ERβ , ele se liga aos receptores canabinoides cb1 e cb2 do sistema endocanabinoide...

Perso j'aime pas le termes neo cannabinoides il englobe les semi-synthé et synthétique alors que chimiquement ça n'a rien a voir, il n'existe pas de semi-synthé qui sont agoniste complets/sélectifs des récepteurs cb1 et cb2 comparé a ceux synthétique et le risque nest pas moindre

**Endometriosis and migraines are increasingly viewed through the lens of endocannabinoid dysregulation or clinical endocannabinoid deficiency (CECD/CED), where impaired endocannabinoid system (ECS) signaling contributes to chronic pain, inflammation, immune dysfunction, and related symptoms.** This unifying framework highlights how reduced effective ECS tone—due to altered ligand levels, receptor expression, or enzyme activity—underlies key pathological processes in both conditions. ### Endocannabinoid System (ECS) Overview The ECS is a lipid-based signaling network that promotes homeostasis by modulating pain, inflammation, immune responses, neurotransmission, vascular tone, cell proliferation/apoptosis, and reproductive functions. It includes: - **Cannabinoid receptors** (primarily CB1 in nervous and reproductive tissues; CB2 in immune cells).- **Endocannabinoids** like anandamide (AEA) and 2-arachidonoylglycerol (2-AG), produced on-demand. - **Enzymes** for synthesis and breakdown (e.g., FAAH, MAGL). Dysregulation disrupts this balance, leading to heightened nociception, persistent inflammation, and tissue abnormalities. ### Endometriosis as ECS Dysregulation Endometriosis features ectopic endometrial-like tissue that drives chronic inflammation, pelvic pain, dysmenorrhea, and infertility. Research consistently shows ECS alterations: - **Receptor changes**: Decreased CB1 expression in endometrial tissue, stromal cells, and lesions impairs anti-inflammatory and analgesic signaling. Variable CB2 shifts and upregulated TRPV1 (pro-nociceptive) are also noted. - **Ligand and enzyme dynamics**: Often elevated AEA/2-AG in plasma/peritoneal fluid (correlating with pain), yet reduced PEA and overall signaling efficiency due to fewer receptors. This creates a "paradox" of compensatory overproduction amid functional deficiency. Lower synthesis/degradation enzymes in lesions further contribute. - **Pathophysiological roles**: The ECS regulates lesion establishment (migration, proliferation, angiogenesis, apoptosis resistance) and immune modulation (e.g., mast cells, cytokines). Dysregulation promotes survival of ectopic tissue in estrogen-rich inflammatory environments and exacerbates pain via central/peripheral sensitization. Key papers include: - "The Clinical Significance of Endocannabinoids in Endometriosis" (2017): pmc.ncbi.nlm.nih.gov/article… - "Role of the endocannabinoid system in the pathophysiology of endometriosis" (2022): link.springer.com/article/10… - "Endocannabinoids and their receptors modulate endometriosis pathogenesis and immune response" (2024): elifesciences.org/articles/9… - Review on understanding the ECS in endometriosis: endonews.com/understanding-e… Some researchers explicitly describe endometriosis as fitting an endocannabinoid deficiency profile. ### Migraines and CECD Migraines involve neurovascular inflammation, often comorbid with endometriosis (shared menstrual triggers, higher prevalence, overlapping conditions like IBS/fibromyalgia). - **Evidence**: Lower AEA in cerebrospinal fluid/plasma of migraine patients; altered FAAH activity; reduced ECS tone linked to trigeminovascular sensitization, CGRP release, and cortical spreading depression. - **Mechanisms**: ECS normally dampens serotonin dysregulation, neuroinflammation, and pain thresholds. Deficiency lowers the migraine threshold. Foundational work by Ethan Russo positions migraines (with fibromyalgia/IBS) as core CECD examples: - "Clinical Endocannabinoid Deficiency (CECD)" (2004): pubmed.ncbi.nlm.nih.gov/1515… - "Clinical Endocannabinoid Deficiency Reconsidered" (2016): pubmed.ncbi.nlm.nih.gov/2886… (full text often available via PMC) - Additional support: "Emerging Role of (Endo)Cannabinoids in Migraine" (2018): pubmed.ncbi.nlm.nih.gov/2974… ### Shared Spectrum and Comorbidity Both conditions exhibit hormonal-ECS interactions (estrogen modulates ECS components), central sensitization, and inflammatory/immune dysregulation. Higher comorbidity rates suggest a common ECS

**Cannabidiol (CBD) Exhibits Dose-Dependent Anti-Cancer Effects Across Multiple Cancer Types** Research demonstrates that cannabidiol (CBD) consistently produces dose-dependent reductions in cancer cell viability, proliferation, migration, invasion, and tumor growth while inducing apoptosis and cell cycle arrest in various preclinical models. Below is a compilation of key studies highlighting these effects across different cancers, with specific dose ranges and outcomes. ### Breast Cancer **CBD Induces Concentration-Dependent Apoptosis and Reduces Viability in Breast Cancer Cell Lines** CBD treatment (0–10 μM for 24 hours) significantly decreased cell viability in both estrogen receptor-positive (e.g., MCF-7, T-47D) and triple-negative (e.g., MDA-MB-231) breast cancer lines in a concentration-dependent manner. It triggered apoptosis (measured by Annexin V staining) and inhibited survival pathways independently of CB1/CB2 receptors at lower doses, with partial CB2 involvement at higher concentrations. Higher doses enhanced pro-apoptotic proteins like p53, Caspase-3, and Bax. **CBD and THC Mixture Shows Dose- and Time-Dependent Anti-Proliferative and Pro-Apoptotic Effects in Breast Cancer** In MDA-MB-231 and MCF-7 cells, CBD/THC (3:1 ratio, 12.5–17.5 μg/mL) inhibited proliferation dose- and time-dependently over 24–48 hours, reducing viability by up to 86% at higher doses. It increased apoptotic cells (Annexin V/PI staining) and altered cell cycle progression, with stronger effects in triple-negative lines. ### Colorectal Cancer **CBD Represses Viability and Induces G1 Arrest and Apoptosis in Colorectal Cancer Cells** CBD (0–40 μM for 24–48 hours) reduced viability in multiple human colorectal cancer lines (e.g., HCT116, SW480) in a dose-dependent manner, with IC50 values ranging from 4.7–20 μM. It caused G1-phase cell cycle arrest, elevated apoptosis markers, and endoplasmic reticulum stress. **CBD Reduces Viability and Enhances Apoptosis in p53-Dependent Colorectal Cancer Models** In HCT116 (p53 wild-type and knockout) and other lines, CBD (5–20 μM for 24–48 hours) lowered viability dose-dependently (IC50 7.9–24.3 μM). Sensitivity was higher in p53 wild-type cells, with increased ROS, mitochondrial disruption, and caspase activation at higher doses. ### Glioma/Glioblastoma **CBD Is Cytotoxic and Perturbs Mitochondrial Function in Glioma Cells** CBD (0–20 μg/mL for 96 hours) inhibited proliferation and induced cytotoxicity in human (U87MG, U373MG) and canine glioma lines in a dose-dependent manner (IC50 4.9–8.2 μg/mL). It reduced oxygen consumption and ATP production dose-dependently within 2 hours, leading to swollen mitochondria and apoptosis (rescued by apoptosis inhibitors). **CBD Suppresses Glioma Cell Viability in Combination Contexts** CBD and BCNU each produced dose-dependent suppression of T98G glioma cell viability, with CBD enhancing overall anti-tumor activity through apoptotic pathways. ### Prostate Cancer **CBD Decreases Viability and Induces Apoptotic Cell Death in Prostate Cancer Cells** In PC3 cells, CBD (0.03–10 μM for 48 hours) reduced viability dose-dependently (up to 37% at higher doses) and activated caspase-3/7 pathways, increasing DNA fragmentation, ROS, and pro-apoptotic Bax while altering mitochondrial potential. ### Lung Cancer and Other Solid Tumors **CBD Inhibits Long-Term Survival in Multiple Cancer Cell Lines Including Lung Carcinoma** CBD showed dose-dependent killing in large cell lung carcinoma (H460, IC50 8.47 μM), metastatic breast (MDA-MB-231, IC50 8.35 μM), melanoma (A375, IC50 2.45 μM), cervical carcinoma, and osteosarcoma lines after 7–10 days. Apoptosis was confirmed via PARP cleavage, with ER stress as a key mechanism. **CBD Reduces Proliferation, Migration, and Invasion in Head and Neck Squamous Cell Carcinoma** CBD treatment decreased HNSCC cell viability, migration, and invasion dose- and t

First: based off the structure of that last sentence I dont think you should be questioning someone's intelligence. Second: how is nearly 1 thousand less yard keeping up? Mind you AJ Brown drew CB1's weekly and Smith went up against CB2's My point stands....

【CBGはなぜ「日中向き」と言われるのか？】 CBGは「明るくなる」「集中できる」「頭が整う」と口コミやレビューでよく見れますが、実はCB1・CB2受容体への作用はかなり弱いです。 それでも体感が語られる理由は、CBGが“その他の受容体”に強く働きかける可能性にあります。 ① α-2アドレナリン受容体（α2AR） CBGはこの受容体に非常に強く作用するとされています。α2ARは血圧を下げ、交感神経の過剰な興奮を抑える働きがあり、「落ち着きながら集中できる」「ノイズが減る」感覚に関与している可能性があります。 ② セロトニン5-HT1A受容体 CBGはこの受容体の強力な拮抗薬（ブロッカー）として作用。その結果、間接的に ・セロトニン（安心感・幸福感） ・ノルアドレナリン（覚醒・集中） ・ドーパミン（やる気・モチベーション） が増える可能性が示唆されています。 ③ PPAR（ペルオキシソーム増殖因子活性化受容体） 代謝・炎症・脂質や糖の調整に関与する受容体。 CBGはこの受容体への親和性も高く、メタボや代謝系への可能性も研究されています。 CBGは「この受容体＝この効果」と断定できる段階ではありません。しかし、これらの受容体作用を総合するとCBGが「日中向き」「集中・覚醒・安定感がある」と言われる理由は、決して根拠のない噂ではないことが見えてきます。 CBGは、神経調節・集中・気分・代謝まで幅広い可能性を持つカンナビノイド。今後の研究がさらに期待される成分です。

40歳キーパーMomで草。 cb2枚にガチの拍手だわ90分集中途切れず守りきってすごい

サウジアラビア謎サッカーでアルゼンチン倒した実績あるからなぁ。てかカーボベルデはここまでやるなら謎CB2枚相手破壊して1点くらい決めろや。引き分け1番おもんないねん

テスセン14回受けた私が思う今の指標 【言語】 7 抜き出し字数制限なし、CB2問 6 抜き出し5字以内、CB2問 5 抜き出し2字以内 4 長文、抜き出し・CBなし 【非言語】 7 推論6割、CB3問以上 6 推論6割、CB2問 5 推論5割、CB1問 4 CBなし

Cb1 being traction, cb2 being distraction, cb3 line them up like fractions oh bawcarbie stans rise

어제 그냥 Crate and Barrel 가봤는데 뭐가 별루 없더라구요 ㅠㅠ cb2 모아둔 매장을 가봐야하나…