Pharmacological inhibition of P2RX4 receptor as a potential therapeutic strategy to prevent intracranial aneurysm formation.

Intracranial aneurysms (IA) affect 1-5 % of the population and are a major cause of subarachnoid hemorrhage. Thus, preventing IA development and progression is crucial for public health. IA has been considered a non-physiological, high shear stress-induced chronic inflammatory disease affecting the bifurcation site of the intracranial arteries.

[Molecular Mechanisms Underlying Intracranial Aneurysm Rupture].

Intracranial aneurysms, a major cause of subarachnoid hemorrhage(SAH), pose a significant social burden due to their poor patient outcomes. Recent studies, including those using animal models, have shed light on a new disease concept: intracranial aneurysms as a chronic inflammatory disease. This process is triggered by abnormal hemodynamic forces and mediated by immune cells like macrophages and neutrophils.

JNK2-MMP-9 axis facilitates the progression of intracranial aneurysms.

Intracranial aneurysm (IA) can cause subarachnoid hemorrhage or some other hemorrhagic stroke after rupture. Because of the poor outcome in spite of the intensive medical care after the onset of hemorrhage, the development of a novel therapeutic strategy like medical therapy to prevent the progression of the disease becomes a social need. As the reduction of arterial stiffness due to the degeneration of the extracellular matrix via Matrix Metalloproteinases (MMPs) becomes one of the central machineries leading to the progression of IAs through a series of studies, factors regulating the expression or the activity of MMPs could be a therapeutic target.

The potential of disulfiram as a drug to improve the prognosis after the onset of subarachnoid hemorrhage.

Subarachnoid hemorrhage due to rupture of intracranial aneurysms has a poor outcome, making this disease being the social problem. Inflammation evoked by the increase in intracranial pressure and the clot in the subarachnoid space after the onset of SAH exacerbates neuronal death and vasospasm, resulting in the poor outcome and severe aftereffects. Here, FROUNT mediates CCR2 and CCR5 signaling as an intracellular molecule binding to these chemoattractant receptors which facilitate the migration of inflammatory cells, such as macrophages, in situ to trigger inflammation there.

C5a-C5AR1 axis as a potential trigger of the rupture of intracranial aneurysms.

Recent studies have indicated the involvement of neutrophil-mediated inflammatory responses in the process leading to intracranial aneurysm (IA) rupture. Receptors mediating neutrophil recruitment could thus be therapeutic targets of unruptured IAs. In this study, complement C5a receptor 1 (C5AR1) was picked up as a candidate that may cause neutrophil-dependent inflammation in IA lesions from comprehensive gene expression profile data acquired from rat and human samples.

[Inflammatory Responses in Hemorrhagic Stroke].

Inflammation is triggered by various intrinsic and extrinsic stimuli as a protective machinery to maintain homeostasis in the human body. Usually, it is magnified in intensity initially and regresses rapidly afterwards; this phenomenon is called acute inflammation. However, it occasionally lasts a long time; this phenomenon is called chronic inflammation.

True superficial temporal artery aneurysm: A case after extracranial-intracranial bypass surgery and a systematic review.

Background: Nontraumatic true superficial temporal artery aneurysm (STAA) is rare, and its characteristics and pathogenesis are unclear.

Methods: We report a case of STAA and performed a systematic review of PubMed, Scopus, and Web of Science using the keyword "superficial temporal artery aneurysm" to include studies on STAA reported through July 2022. We excluded studies on STAA associated with trauma, arterial dissection, infection, or vasculitis.

Symptomatic atherosclerotic plaque accompanied by carotid web.

Here, we describe a case of a 67-year-old man who was transferred to our hospital with complaints of sudden upper right limb weakness and ataxia. Scattered acute cerebral infarction was found in the watershed zone between the left anterior cerebral artery and the middle cerebral artery territories. A shelf-like structure at the origin of the left carotid artery and a vulnerable plaque distal to the lesion was found.

Intramural Hematoma in Vertebrobasilar Dolichoectasia-Related Stroke: A Retrospective Analysis of Six Consecutive Patients.

Background: The pathophysiology underlying vertebrobasilar dolichoectasia (VBD) is largely unknown. However, a few reports have demonstrated that acute intramural hematoma (IMH) in VBD is associated with stroke. We aimed to investigate the clinical and radiological features of IMH in VBD and the role of IMH in predicting rupture and patient outcomes.

3D Turbo Spin-echo MRI-based Mechanical Thrombectomy at Middle Cerebral Artery Bifurcations.

We describe three cases with acute middle cerebral artery (MCA) occlusion. From the pre-operative MRI, including three-dimensional turbo spin-echo sequences using T1WI and T2WI, we assessed both thrombus configuration and arterial anatomy at the MCA bifurcations. For efficient endovascular thrombectomy, we identified the applied MCA segment 2 (M2) branch, in which the main thrombus was buried.

A convexity meningioma presenting with an acute subdural hematoma.

Background: Meningiomas presenting with acute subdural hematomas are extremely rare. To the best of our knowledge, only 45 cases have been reported to date. We report on a case of a meningioma mimicking an acute subdural hematoma as well as a thorough literature review.

Cisplatin and ultra-violet-C synergistically down-regulate receptor tyrosine kinases in human colorectal cancer cells.

Background: Platinum-containing anti-cancer drugs such as cisplatin are widely used for patients with various types of cancers, however, resistance to cisplatin is observed in some cases. Whereas we have recently reported that high dose UV-C (200 J/m²) induces colorectal cancer cell proliferation by desensitization of EGFR, which leads oncogenic signaling in these cells, in this study we investigated the combination effect of low dose cisplatin (10 μM) and low dose UV-C (10 J/m²) on cell growth and apoptosis in several human colorectal cancer cells, SW480, DLD-1, HT29 and HCT116.

Results: The combination inhibited cell cycle and colony formation, while either cisplatin or UV-C alone had little effect.

UVC irradiation suppresses platelet-derived growth factor-BB-induced migration in human pancreatic cancer cells.

We have recently reported that short wavelength ultraviolet-C (UVC) irradiation inhibits cell growth and induces apoptosis in human pancreatic cancer cells. In this study, we investigated the effect of UVC on platelet-derived growth factor (PDGF)-BB-induced migration in pancreatic cancer cells, AsPC1 and BxPC3. In cell migration assays using a Boyden chamber Transwell, PDGF-BB exerted a maximum effect on migration of these cells at a dose of 70 ng/ml after 36 h of treatment.

Phosphorylation status of heat shock protein 27 plays a key role in gemcitabine-induced apoptosis of pancreatic cancer cells.

Gemcitabine, an antitumor drug, is currently considered to be the standard of care for the treatment of advanced pancreatic cancer, but the clinical outcome is still not satisfactory. Although heat shock protein (HSP) 27 is implicated in the resistance to chemotherapy in several types of cancers, the precise role of phosphorylated HSP27 in cancer cells remains to be clarified. In this study, we investigated the relationship between the effect of gemcitabine and the phosphorylation status of HSP27 in pancreatic cancer cells, Panc1 and KP3.

Ultraviolet enhances the sensitivity of pancreatic cancer cells to gemcitabine by activation of 5' AMP-activated protein kinase.

Although gemcitabine is recognized as the standard drug for the treatment of advanced pancreatic cancer, the clinical outcome is not satisfactory. We recently reported that relatively high dose ultraviolet-C (UV-C; 200J) inhibits cell growth by desensitization of epidermal growth factor receptor (EGFR) in human pancreatic cancer cells. In the present study, we investigated the combination effects of low dose UV-C (10J) and gemcitabine on apoptosis and cell growth in these cells.

Ultraviolet irradiation can induce evasion of colon cancer cells from stimulation of epidermal growth factor.

Receptor down-regulation is the most prominent regulatory system of EGF receptor (EGFR) signal attenuation and a critical target for therapy against colon cancer, which is highly dependent on the function of the EGFR. In this study, we investigated the effect of ultraviolet-C (UV-C) on down-regulation of EGFR in human colon cancer cells (SW480, HT29, and DLD-1). UV-C caused inhibition of cell survival and proliferation, concurrently inducing the decrease in cell surface EGFR and subsequently its degradation.