
크론병 진단 수년 전부터 혈액 내 항체의 특정 당쇄 변화가 감지되며, 이는 향후 크론병 발병을 예측할 수 있는 생물학적 표지자로 활용될 수 있다.


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The altered antibody, detectable in blood, may initiate inflammation up to 6 years before symptom onset.

Altered Antibody Predicts Crohn's Years Before Diagnosis

크론병-진단-수년-전부터-감지되는-변형된-항체


크론병 진단 수년 전부터 감지되는 변형된 항체


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생물의학 분야에서 연구 자원(데이터, 소프트웨어, 도구 등)이 급증하고 있지만 이들이 분산되어 있어 접근과 재사용이 어려운 문제를 해결하기 위해 대규모 연구 자원 데이터베이스(RRD-Bio)를 구축하였다.


생물의학-분야를-위한-통합-연구-자원-데이터베이스-구축


생물의학 분야를 위한 통합 연구 자원 데이터베이스 구축



이 논문은 생물의학 분야에서 인과 관계 학습을 위한 표준화된 합성 데이터셋을 제공합니다. 이 데이터셋은 크렙스 사이클을 시뮬레이션하여 생성되었으며, 선형 및 비선형 인과 관계, 잠재 변수, 시계열 데이터 등 다양한 특성을 포함하고 있습니다.


인과-관계-학습을-위한-생물의학-벤치마크-데이터셋


인과 관계 학습을 위한 생물의학 벤치마크 데이터셋



초기 간헐적 고지혈증은 동맥 내 대식세포의 수와 항상성 표현형을 변화시켜 동맥경화증 진행을 가속화한다.


Early intermittent hyperlipidaemia alters tissue macrophages to fuel atherosclerosis - Nature

초기-간헐적-고지혈증이-동맥경화증-진행을-가속화하는-조직-대식세포의-변화


초기 간헐적 고지혈증이 동맥경화증 진행을 가속화하는 조직 대식세포의 변화



신장암 전이 과정에서 미토콘드리아 복합체 I의 기능이 중요한 역할을 한다.


Studying changes in the&nbsp;metabolic properties of kidney cancer in patients reveals an increased need for mitochondrial metabolism as tumors metastasize from the kidney to distant organs.

Mitochondrial complex I promotes kidney cancer metastasis - Nature

신장암-전이에-있어-미토콘드리아-복합체-i의-역할


신장암 전이에 있어 미토콘드리아 복합체 I의 역할



종양 세포와 stromal 세포 간의 상호작용, 대사 환경 변화에 따른 전이성 특징의 직접적 관찰


Metabolic conditions such as hypoxia, nutrient starvation, and media acidification, together with interactions with stromal cells are critical drivers of metastasis. Since these conditions arise deep within tumor tissues with poor access to the bloodstream, the observation of nascent metastases in vivo is exceedingly challenging. On the other hand, conventional cell culture studies cannot capture the complex nature of metastatic processes. We thus designed and implemented an ex vivo model of the tumor microenvironment to study the emergence of metastatic features in tumor cells in their native 3-dimensional (3D) context. In this system, named 3MIC, tumor cells spontaneously create ischemic-like conditions, and it allows the direct visualization of tumor-stroma interactions with high spatial and temporal resolution. We studied how 3D tumor spheroids evolve in the 3MIC when cultured under different metabolic environments and in the presence or absence of stromal cells. Consistent with previous experimental and clinical data, we show that ischemic environments increase cell migration and invasion. Importantly, the 3MIC allowed us to directly observe the emergence of these pro-metastatic features with single-cell resolution allowing us to track how changes in tumor motility were modulated by macrophages and endothelial cells. With these tools, we determined that the acidification of the extracellular media was more important than hypoxia in the induction of pro-metastatic tumor features. We also illustrate how the 3MIC can be used to test the effects of anti-metastatic drugs on cells experiencing different metabolic conditions. Overall, the 3MIC allows us to directly observe the emergence of metastatic tumor features in a physiologically relevant model of the tumor microenvironment. This simple and cost-effective system can dissect the complexity of the tumor microenvironment to test perturbations that may prevent tumors from becoming metastatic.

### Competing Interest Statement

The 3MIC is an embodiment of a patent filed by NYU where CC-F is the inventor.

Direct visualization of emergent metastatic features within an ex vivo model of the tumor microenvironment

종양-미세환경-ex-vivo-모델-내에서-관찰되는-전이성-특징의-직접적-시각화


종양 미세환경 ex vivo 모델 내에서 관찰되는 전이성 특징의 직접적 시각화



혈우병 환자의 관절에서 반복적인 출혈은 혈우병성 관절병증을 유발하며, 이는 연골의 심각한 손상을 특징으로 한다. 이 연구에서는 혈우병성 관절병증 연골에서 DNA 메틸화 변화와 TNXB 발현 감소가 관찰되었으며, TNXB 억제가 연골세포 세포사와 세포외기질 분해를 촉진시켜 관절 퇴행을 악화시킨다는 것을 밝혔다.


Recurrent joint bleeding in hemophilia patients frequently causes hemophilic arthropathy (HA). Drastic degradation of cartilage is a major characteristic of HA, but its pathological mechanisms has not yet been clarified. In HA cartilages, we found server matrix degradation and increased expression of DNA methyltransferase proteins. We thus performed genome-wide DNA methylation analysis on human HA (N = 5) and osteoarthritis (N = 5) articular cartilages, and identified 1228 differentially methylated regions (DMRs) associated with HA. Functional enrichment analyses revealed the association between DMR genes (DMGs) and extracellular matrix (ECM) organization. Among these DMGs, Tenascin XB (TNXB) expression was down-regulated in human and mouse HA cartilages. The loss of Tnxb in F8-/- mouse cartilage provided a disease-promoting role in HA by augmenting cartilage degeneration and subchondral bone loss. Tnxb knockdown also promoted chondrocyte apoptosis and inhibited phosphorylation of AKT. Importantly, AKT agonist showed chondroprotective effects following Tnxb knockdown. Together, our findings indicate that exposure of cartilage to blood leads to alterations in DNA methylation, which is functionally related to ECM homeostasis, and further demonstrate a critical role of TNXB in HA cartilage degeneration by activating AKT signaling. These mechanistic insights allow development of potentially new strategies for HA cartilage protection.

### Competing Interest Statement

The authors have declared no competing interest.

Aberrant methylation and expression of TNXB promote chondrocyte apoptosis and extracullar matrix degradation in hemophilic arthropathy via AKT signaling

혈우병성-관절병증에서-tnxb의-비정상적인-메틸화와-발현이-akt-신호전달을-통해-연골세포-세포사와-세포외기질-분해를-촉진시킨다


혈우병성 관절병증에서 TNXB의 비정상적인 메틸화와 발현이 AKT 신호전달을 통해 연골세포 세포사와 세포외기질 분해를 촉진시킨다



당뇨병성 발기부전 환자의 해면체 조직에서 혈관주위세포의 기능 저하가 발기부전의 주요 원인임을 밝혔다.


Erectile dysfunction (ED) affects a significant proportion of men aged 40-70 and is caused by cavernous tissue dysfunction. Presently, the most common treatment for ED is phosphodiesterase 5 inhibitors; however, this is less effective in patients with severe vascular disease such as diabetic ED. Therefore, there is a need for development of new treatment, which requires a better understanding of the cavernous microenvironment and cell-cell communications under diabetic condition. Pericytes are vital in penile erection; however, their dysfunction due to diabetes remains unclear. In this study, we performed single-cell RNA sequencing to understand the cellular landscape of cavernous tissues and cell type-specific transcriptional changes in diabetic ED. We found a decreased expression of genes associated with collagen or extracellular matrix organization and angiogenesis in diabetic fibroblasts, chondrocytes, myofibroblasts, valve-related lymphatic endothelial cells, and pericytes. Moreover, the newly identified pericyte-specific marker, Limb Bud-Heart (Lbh), in mouse and human cavernous tissues, clearly distinguishing pericytes from smooth muscle cells. Cell-cell interaction analysis revealed that pericytes are involved in angiogenesis, adhesion, and migration by communicating with other cell types in the corpus cavernosum; however, these interactions were highly reduced under diabetic conditions. Lbh expression is low in diabetic pericytes, and overexpression of LBH prevents erectile function by regulating neurovascular regeneration. Furthermore, the LBH-interacting proteins (Crystallin Alpha B and Vimentin) were identified in mouse cavernous pericytes through LC-MS/MS analysis, indicating that their interactions were critical for maintaining pericyte function. Thus, our study reveals novel targets and insights into the pathogenesis of ED in patients with diabetes.

### Competing Interest Statement

The authors have declared no competing interest.

Single cell transcriptome analysis of cavernous tissues reveals the key roles of pericytes in diabetic erectile dysfunction

당뇨병성-발기부전-환자의-해면체-조직-단일세포-전사체-분석을-통해-밝혀낸-주요-혈관주위세포의-역할


당뇨병성 발기부전 환자의 해면체 조직 단일세포 전사체 분석을 통해 밝혀낸 주요 혈관주위세포의 역할



허혈성 질환에서 내피세포 이식을 위해 중간엽 줄기세포가 내피세포에 미토콘드리아를 전달하고, 이를 통해 내피세포의 생존과 기능이 향상된다.


Under stressful conditions, mesenchymal stromal cells transfer mitochondria to endothelial cells through tunnelling nanotubes, and artificially transplanting mitochondria into endothelial cells improves the ability of these cells to engraft and to revascularize ischaemic tissues.

Mitochondrial transfer mediates endothelial cell engraftment through mitophagy - Nature

허혈성-질환에서-내피세포-이식을-위한-미토콘드리아-전달-메커니즘


허혈성 질환에서 내피세포 이식을 위한 미토콘드리아 전달 메커니즘



BioBERT를 활용하여 유전체 문헌에서 유전자와 질병 간 연관성을 추출하고, 이를 지식 그래프로 구축하였다.


유전체-유전자-질병-연관성-추출을-통한-생의학-문헌-지식-그래프-구축


유전체 유전자-질병 연관성 추출을 통한 생의학 문헌 지식 그래프 구축
