scholarly journals Cerebrovascular Injuries Induce Lymphatic Invasion into Brain Parenchyma to Guide Vascular Regeneration in Zebrafish

2019 ◽  
Vol 49 (5) ◽  
pp. 697-710.e5 ◽  
Author(s):  
Jingying Chen ◽  
Jianbo He ◽  
Rui Ni ◽  
Qifen Yang ◽  
Yaoguang Zhang ◽  
...  
Keyword(s):  
Lymphatic Invasion ◽  
Brain Parenchyma ◽  
Vascular Regeneration

scholarly journals Cerebrovascular Injuries Induce Lymphatic Invasion into Brain Parenchyma to Guide Vascular Regeneration in Zebrafish

2018 ◽  
Author(s):  
Jingying Chen ◽  
Jianbo He ◽  
Qifen Yang ◽  
Yaoguang Zhang ◽  
Lingfei Luo
Keyword(s):  
Blood Vessels ◽  
Brain Edema ◽  
Interstitial Fluid ◽  
Molecular Mechanisms ◽  
Lymphatic Vessels ◽  
Lymphatic Invasion ◽  
Brain Parenchyma ◽  
Genetic Ablation ◽  
Vascular Regeneration ◽  
Promising Therapeutic Approach

SUMMARYDamage to regional cerebrovascular network and neuronal tissues occurs during acute cerebrovascular diseases, such as ischemic stroke. The promotion of vascular regeneration is the most promising therapeutic approach. To understand cellular and molecular mechanisms underlying brain vascular regeneration, we developed two zebrafish cerebrovascular injury models using genetic ablation and photochemical thrombosis. Although brain parenchyma is physiologically devoid of lymphatic vasculature, we found that cerebrovascular injuries induce rapid ingrowth of meningeal lymphatics into the injured parenchyma. The ingrown lymphatics on one hand become lumenized drain interstitial fluid to resolve brain edema, on the other hand act as “growing tracks” for nascent blood vessels. The ingrown lymphatic vessels undergo apoptosis and clearance after cerebrovascular regeneration. This study reveals a pathological function of meningeal lymphatics, through previously unexpected ingrowth into brain parenchyma and a newly identified lymphatic function as vascular “growing tracks”.HIGHLIGHTSCerebrovascular injuries induce lymphatic ingrowth into the injured brain parenchyma The ingrown lymphatics drain interstitial fluid to resolve brain edema Nascent blood vessels use the ingrown lymphatic vessels as “growing tracks” The ingrown lymphatic vessels undergo apoptosis after vascular regeneration completes

Transcranial Sonography (TCS) of Brain Parenchyma in Corticobasal Degeneration

2004 ◽  
Vol 35 (03) ◽  
Author(s):  
L Niehaus ◽  
D Gruber ◽  
R Hertel ◽  
G Ebersbach ◽  
M Eckert ◽  
...  
Keyword(s):  
Corticobasal Degeneration ◽  
Brain Parenchyma ◽  
Transcranial Sonography

TRIM44 promotes cell proliferation and migration by inhibiting FRK in renal cell carcinoma

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Lymphatic Invasion ◽  
Cancer Specific Survival ◽  
Candidate Target ◽  
Candidate Target Gene ◽  
And Migration

TRIM44 has oncogenic roles in various cancers. However, TRIM44 expression andits function in renal cell carcinoma (RCC) are still unknown. Here in this study, weinvestigated the clinical significance of TRIM44 and its biological function in RCC.TRIM44 overexpression was significantly associated with clinical M stage, histologictype (clear cell) and presence of lymphatic invasion (P = .047, P = .005, and P = .028,respectively). Moreover, TRIM44 overexpression was significantly associated withpoor prognosis in terms of cancer-specific survival (P = .019). Gain-of-function andloss-of-function studies using TRIM44 and siTRIM44 transfection showed thatTRIM44 promotes cell proliferation and cell migration in two RCC cell lines, Caki1and 769P. To further investigate the role of TRIM44 in RCC, we performed integratedmicroarray analysis in Caki1 and 769P cells and explored the data in the Oncominedatabase. Interestingly, FRK was identified as a promising candidate target gene ofTRIM44, which was downregulated in RCC compared with normal renal tissues. Wefound that cell proliferation was inhibited by TRIM44 knockdown and then recoveredby siFRK treatment. Taken together, the present study revealed the associationbetween high expression of TRIM44 and poor prognosis in

Radiotherapy for Brain Tumors: Current Practice and Future Directions

2020 ◽  
Vol 16 (3) ◽  
pp. 182-195
Author(s):  
Sarah Baker ◽  
Natalie Logie ◽  
Kim Paulson ◽  
Adele Duimering ◽  
Albert Murtha
Keyword(s):  
Brain Tumors ◽  
Treatment Strategies ◽  
Brain Parenchyma ◽  
Benign Tumors ◽  
Tumor Control ◽  
Normal Brain ◽  
Neurocognitive Deficits ◽  
Close Proximity ◽  
Recent Developments ◽  
High Level

Radiotherapy is an important component of the treatment for primary and metastatic brain tumors. Due to the close proximity of critical structures and normal brain parenchyma, Central Nervous System (CNS) radiotherapy is associated with adverse effects such as neurocognitive deficits, which must be weighed against the benefit of improved tumor control. Advanced radiotherapy technology may help to mitigate toxicity risks, although there is a paucity of high-level evidence to support its use. Recent advances have been made in the treatment for gliomas, meningiomas, benign tumors, and metastases, although outcomes remain poor for many high grade tumors. This review highlights recent developments in CNS radiotherapy, discusses common treatment toxicities, critically reviews advanced radiotherapy technologies, and highlights promising treatment strategies to improve clinical outcomes in the future.

A Case of Neurosarcoidosis Mimicking Brain Tumor

2020 ◽  
Vol 16 ◽  
Author(s):  
Lutfullah Sari ◽  
Abdusselim Adil Peker ◽  
Dilek Hacer Cesme ◽  
Alpay Alkan
Keyword(s):  
Brain Tumor ◽  
Contrast Enhancement ◽  
Clinical Laboratory ◽  
Vasogenic Edema ◽  
Pulmonary Sarcoidosis ◽  
Brain Parenchyma ◽  
The Body ◽  
Oligoclonal Bands ◽  
Flair Sequence ◽  
History Of

Background: Neurosarcoidosis manifests symptomatically in 5% of patients with sarcoidosis and diagnosis can be challenging if not clinically suspected. Cerebral mass-like presentation of neurosarcoidosis rarely reported in the literature. We presented a woman with neurosarcoidosis who had a cerebral mass-like lesion which completely disappeared after medical treatment. Discussion: A 37-year-old woman with history of pulmonary sarcoidosis referred to the emergency service of our hospital with a one-month history of progressive dizziness, nausea and seeing flashing lights. At neurologic examination, numbness and weakness on the left side of the body, deviation of uvula toward the right side was seen. Cranial MRI demonstrated a 2.5x2 cm in size mass lesion which hypointense on T1 WI, heterogeneous hyperintense on T2 and FLAIR sequence with peripheral vasogenic edema and heterogeneous, irregular contrast enhancement simulating brain tumor. Also, leptomeningeal and nodular contrast enhancement was seen on brainstem, cerebellar vermis, perimesencephalic cistern and left frontal, bilateral parietooccipital sulcus. In laboratory tests; The level of serum angiotensin-converting enzyme (ACE) was 53 IU/mL (N:8-52 IU/mL) and cerebrospinal fluid (CSF) ACE was 23 IU/mL (N:0-2.6 IU/mL). CSF cytology analysis was normal. Pattern 2 oligoclonal bands were present. With these clinical, laboratory and radiological findings, cerebral involvement of sarcoidosis was suspected. Biopsy was not performed due to the high risk of morbidity caused by the deep location of the lesion.Patient was treated with methylprednisolone and Azathioprine for a month.On post-treatment control imaging; lesion disappeared completely without residual leptomeningeal and nodular contrast enhancement.Also, neurologic symptoms were decreased remarkably. Conclusion: Multi-system inflammatory disorders like sarcoidosis, can present with mass-like lesion in the brain parenchyma. While early diagnosis is important to prevent unnecessary interventions like biopsy and surgery, it is crucial to initiate the necessary treatment with the aim of recovery without sequelae. Radiological and clinical follow-up are fundamental in differential diagnosis.

scholarly journals Author Correction: In vivo transduction of ETV2 improves cardiac function and induces vascular regeneration following myocardial infarction

2019 ◽  
Vol 51 (9) ◽  
pp. 1-1 ◽  
Author(s):  
Sunghun Lee ◽  
Dong Hun Lee ◽  
Bong-Woo Park ◽  
Ri Youn Kim ◽  
Anh Duc Hoang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Vascular Regeneration
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