Nicotine suppresses central post-stroke pain via facilitation of descending noradrenergic neuron through activation of orexinergic neuron.

Central post-stroke pain (CPSP) is a type of central neuropathic pain, whose underlying mechanisms remain unknown. We previously reported that bilateral carotid artery occlusion (BCAO)-induced CPSP model mice showed mechanical hypersensitivity and decreased mRNA levels of preproorexin, an orexin precursor, in the hypothalamus. Recently, nicotine was shown to regulate the neuronal activity of orexin in the lateral hypothalamus (LH) and suppress inflammatory and neuropathic pain.

Involvement of descending pain control system regulated by orexin receptor signaling in the induction of central post-stroke pain in mice.

Central post-stroke pain (CPSP) is a type of neuropathic pain for which the mechanism and relevant drug pathways remain unknown. Recently, it was reported that intracerebroventricular (ICV) administration of orexin-A suppresses pain and ischemia. In this study, we tested the role of orexin-A in CPSP induction in mice.

The Involvement of DDAH1 in the Activation of Spinal NOS Signaling in Early Stage of Mechanical Allodynia Induced by Exposure to Ischemic Stress in Mice.

The pathophysiological mechanism of central post-stroke pain (CPSP) is complicated and not well understood. Recently, it has been reported that an increase in the levels of spinal nitric oxide synthetase (NOS) occurs in cerebral ischemia, and spinal NOS is involved in the development of neuropathic pain. The aim of this study was to elucidate the mechanism of spinal NOS signaling in the development of CPSP.

Evidence of a role for spinal HMGB1 in ischemic stress-induced mechanical allodynia in mice.

We have previously showed that spinal high-mobility group box-1 (HMGB1) plays an important role in the induction of central post-stroke pain (CPSP). It has been reported that HMGB1 exacerbates inflammation and pain via TLR4 or RAGE. Furthermore, the relationship between glial cells, such as microglia and astrocytes, involved in pain exacerbation and HMGB1 has also attracted attention.

RETRACTED: Cerebral ischemia-induced elevation of hepatic inflammatory factors accompanied by glucose intolerance suppresses hypothalamic orexin-A-mediated vagus nerve activation.

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RETRACTED: Possible involvement of the HMGB1/RAGE signaling mechanism in the induction of central post-stroke pain induced by acute global cerebral ischemia.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal).

Unique action mechanisms of tramadol in global cerebral ischemia-induced mechanical allodynia.

Central poststroke pain is associated with specific somatosensory abnormalities, such as neuropathic pain syndrome. Although central poststroke pain is a serious condition, details pertaining to underlying mechanisms are not well established, making current standard treatments only partially effective. Here, we assessed the effects of tramadol, an analgesic drug mediated by opioid receptors, using a mouse model of global cerebral ischemia.

Effects of Adjuvant Analgesics on Cerebral Ischemia-Induced Mechanical Allodynia.

Central post-stroke pain (CPSP), a potential sequela of stroke, is classified as neuropathic pain. Although we recently established a CPSP-like model in mice, the effects of adjuvant analgesics as therapeutic drugs for neuropathic pain in this model are unknown. Hence, the aim of the present study was to assess the usefulness of our model by evaluating the effects of adjuvant analgesics used for treating neuropathic pain in this mouse model of CPSP.

Proteomic Profiling in the Spinal Cord and Sciatic Nerve in a Global Cerebral Ischemia-Induced Mechanical Allodynia Mouse Model.

Central post-stroke pain (CPSP) is one of the complications of cerebral ischemia and neuropathic pain syndrome. At present, there are few studies of pain in regions such as the spinal cord or sciatic nerve in cerebral ischemic animal models. To identify proteomic changes in the spinal cord and sciatic nerve in global cerebral ischemic model mice, in the present study we performed an investigation using proteomic methods.

Involvement of GPR40, a long-chain free fatty acid receptor, in the production of central post-stroke pain after global cerebral ischemia.

Central post-stroke pain (CPSP), one of the complications of cerebral ischemia and neuropathic pain syndrome, is associated with specific somatosensory abnormalities. Although CPSP is a serious problem, detailed underlying mechanisms and standard treatments for CPSP are not well established. In this study, we assessed the role of GPR40, a long-chain fatty acid receptor, showing anti-nociceptive effects, in CPSP.

SLC39A9 (ZIP9) regulates zinc homeostasis in the secretory pathway: characterization of the ZIP subfamily I protein in vertebrate cells.

The SLC39A family of zinc transporters can be divided into four subfamilies (I, II, LIV-1, and gufA) in vertebrates, but studies of their functions have been restricted exclusively to members of subfamilies II and LIV-1. In this study, we characterized SLC39A9 (ZIP9), the only member of subfamily I in vertebrates. Confocal microscopy demonstrated that transiently expressed, HA-tagged human ZIP9 (hZIP9-HA) was localized to the trans-Golgi network regardless of zinc status.

Pulmonary endarteritis and subsequent pulmonary embolism associated with clinically silent patent ductus arteriosus.

A 49-year-old man without heart murmur was admitted with fever because of bacteremia following a tooth extraction. Antibiotics rapidly alleviated the fever; however, a small nodule in the pulmonary artery was identified on computed tomography (CT). When the patient experienced chest discomfort with fever, CT demonstrated the absence of the nodule and the appearance of an abnormal lung opacity, and echocardiography showed turbulent retrograde flow in the pulmonary artery.

Infective endocarditis and acute purulent pericarditis in a patient with hyperglycemia.

A diabetic patient was admitted to our hospital for infective endocarditis with acute purulent pericarditis and diabetic ketoacidosis. Echocardiography revealed attachment of vegetation to the chordae tendineae in the left ventricle and pericaridial effusion. The vegetation was enlarged and pendulated for a few days despite maximal antimicrobial therapy.

Zinc transporters, ZnT5 and ZnT7, are required for the activation of alkaline phosphatases, zinc-requiring enzymes that are glycosylphosphatidylinositol-anchored to the cytoplasmic membrane.

Numerous proteins are properly folded by binding with zinc during their itinerary in the biosynthetic-secretory pathway. Several transporters have been implicated in the zinc entry into secretory compartments from cytosol, but their precise roles are poorly understood. We report here that two zinc transporters (ZnT5 and ZnT7) localized in the secretory apparatus are responsible for loading zinc to alkaline phosphatases (ALPs) that are glycosylphosphatidylinositol-anchored membrane proteins exposed to the extracellular site.

Long-term effects of quinapril with high affinity for tissue angiotensin-converting enzyme after coronary intervention in Japanese.

Background: Angiotensin-converting enzyme inhibitors have been shown experimentally to prevent restenosis after balloon injury. We previously reported that quinapril reduced the 6-month restenosis (percent diameter stenosis >or=50%) rate after percutaneous coronary intervention (PCI). However, it was not established whether this favorable outcome was maintained for longer periods.