Histological and Nuclear Medical Comparison of Inflammation After Hemostasis with Non-Thermal Plasma and Thermal Coagulation

The objective of this study is to examine the invasiveness of hemostasis by non-thermal plasma (NTP) compared with hemostasis by thermal coagulation (TC). The inflammation recovery process after hemostasis by TC and NTP was compared by using histological methods and nuclear medical molecular imaging. The necrotic areas in the NTP group disappeared after 5 days, whereas they remained 15 days after hemostasis in the TC group. The accumulation of 2-deoxy-2-[F-18] fluoro-D-glucopyranose (F-18-FDG), which reflects the existence of inflammatory cells, was higher in the TC group than in the NTP group on day 15. Thus, this study indicates that hemostasis by NTP is less inflammatory than TC. This report is the first to evaluate inflammation that occurred after hemostasis with medical devices noninvasively

Psycholinguistic evidence for unaccusativity in an SOV language: A syntactic priming in comprehension

The unaccusative hypothesis (Perlmutter 1978) states that a theme subject of an unaccusative verb is originally an object, as schematized in (1a). In an unergative construction, in contrast, an agent subject originates in subject position, as shown in (1b). (1) a. Unaccusatives: NP1 [VP V t1] b. Unergatives: NP [VP V] The unaccusative hypothesis has been motivated on theoretical grounds (Borer and Grodzinsky 1986; Burzio 1986; Levin and Rappaport Hovav 1995) and further supported by psycholinguistic research (Friedmann et al. 2008; Momma et al. 2018). However, this hypothesis is hard to test in SOV (Subject Object Verb) languages like Japanese, because a surface word order does not provide sufficient information to determine the syntactic nature of the unaccusative subject. In other words, whether movement takes place or not, the surface word order is subject-verb. Hence, it remains less clear whether the subject of the unaccusative in Japanese is base-generated in subject position (Kishimoto 1996) (2a) or base-generated in object position and moves up to subject position (Miyagawa 1989; Takezawa 1991; Hasegawa 2007) (2b). (2) a. NP [VP V] b. NP1 [VP t1 V] The current study is aimed to test whether the unaccusative hypothesis holds in Japanese by conducting a sentence processing experiment

Impairment of endothelium-dependent vasodilator function of retinal blood vessels in adult rats with a history of retinopathy of prematurity

Retinopathy of prematurity (ROP) is a proliferative retinal vascular disease, initiated by delayed retinal vascular growth after premature birth. In the majority of cases, ROP resolves spontaneously; however, a history of ROP may increase the risk of long-term visual problems. In this study, we evaluated the endothelial function of retinal blood vessels in adult rats with a history of ROP. ROP was induced in rats by subcutaneous injection of a vascular endothelial growth factor receptor tyrosine kinase inhibitor (KRN633) on postnatal day (P) 7 and P8. On P56, vasodilator responses to acetylcholine, GSK1016790A (an activator of transient receptor potential vanilloid 4 channels), NOR3 (a nitric oxide [NO] donor), and salbutamol (a β2-adrenoceptor agonist) were assessed. Compared to age-matched controls, retinal vasodilator responses to acetylcholine and GSK1016790A were attenuated in P56 rats with a history of ROP. No attenuation of acetylcholine-induced retinal vasodilator response was observed under inhibition of NO synthase. Retinal vasodilator responses to NOR3 and salbutamol were unaffected. These results suggest that the production of and/or release of NO is impaired in retinal blood vessels in adult rats with a history of ROP. A history of ROP might increase the risk of impaired retinal circulation in adulthood

Metformin Protects against NMDA-Induced Retinal Injury through the MEK/ERK Signaling Pathway in Rats

Metformin, an anti-hyperglycemic drug of the biguanide class, exerts positive effects in several non-diabetes-related diseases. In this study, we aimed to examine the protective effects of metformin against N-methyl-D-aspartic acid (NMDA)-induced excitotoxic retinal damage in rats and determine the mechanisms of its protective effects. Male Sprague–Dawley rats (7 to 9 weeks old) were used in this study. Following intravitreal injection of NMDA (200 nmol/eye), the number of neuronal cells in the ganglion cell layer and parvalbumin-positive amacrine cells decreased, whereas the number of CD45-positive leukocytes and Iba1-positive microglia increased. Metformin attenuated these NMDA-induced responses. The neuroprotective effect of metformin was abolished by compound C, an inhibitor of AMP-activated protein kinase (AMPK). The AMPK activator, AICAR, exerted a neuroprotective effect in NMDA-induced retinal injury. The MEK1/2 inhibitor, U0126, reduced the neuroprotective effect of metformin. These results suggest that metformin protects against NMDA-induced retinal neurotoxicity through activation of the AMPK and MEK/extracellular signal-regulated kinase (ERK) signaling pathways. This neuroprotective effect could be partially attributable to the inhibitory effects on inflammatory responses

Role of Neuron–Glia Signaling in Regulation of Retinal Vascular Tone in Rats

The interactions between neuronal, glial, and vascular cells play a key role in regulating blood flow in the retina. In the present study, we examined the role of the interactions between neuronal and glial cells in regulating the retinal vascular tone in rats upon stimulation of retinal neuronal cells by intravitreal injection of N-methyl-d-aspartic acid (NMDA). The retinal vascular response was assessed by measuring the diameter of the retinal arterioles in the in vivo fundus images. Intravitreal injection of NMDA produced retinal vasodilation that was significantly diminished following the pharmacological inhibition of nitric oxide (NO) synthase (nNOS), loss of inner retinal neurons, or intravitreal injection of glial toxins. Immunohistochemistry revealed the expression of nNOS in ganglion and calretinin-positive amacrine cells. Moreover, glial toxins significantly prevented the retinal vasodilator response induced by intravitreal injection of NOR3, an NO donor. Mechanistic analysis revealed that NO enhanced the production of vasodilatory prostanoids and epoxyeicosatrienoic acids in glial cells in a ryanodine receptor type 1-dependent manner, subsequently inducing the retinal vasodilator response. These results suggest that the NO released from stimulated neuronal cells acts as a key messenger in neuron–glia signaling, thereby causing neuronal activity-dependent and glial cell-mediated vasodilation in the retina

Pharmaceutical stability of colloidal saccharated iron oxide injection in normal saline

Abstract Background Colloidal saccharated iron oxide injection is used for the treatment of iron deficiency anemia in patients with a poor oral intake. Because of the poor stability of the colloid particle, there have been concerns regarding its compatibility with various injections in clinical practice. To assess the stability of colloidal saccharated iron oxide in normal saline as a diluent, pharmaceutical stability analyses were conducted using various concentrations of glucose and sodium chloride (NaCl). Methods Colloidal saccharated iron oxide injection was diluted in three different diluents (5% glucose solution, normal saline, and 10% NaCl solution), and its appearance, colloid particle diameter, and pH were assessed. Free iron ions, which cause adverse effects, such as nausea and vomiting, were separated from the colloid particle using a dialysis membrane for 24 h, and their concentration was determined. Results No difference in the appearance, colloid diameter, and free iron ion fraction was observed after dilution in 5% glucose solution and normal saline. Conversely, an increased colloid aggregation and iron ion release were observed after dilution in 10% NaCl solution. Although iron colloid is unstable in acidic conditions (pH 4.0–6.0), normal diluents such as 5% glucose and normal saline did not cause colloid destabilization by pH change (pH > 8.0). Conclusion Normal saline may be used as a diluent of colloidal saccharated iron oxide injection as well as glucose solution, which is recommended by the pharmaceutical company. Therefore, normal saline can be used as a diluent of colloidal saccharated iron oxide injection in patients with an underlying disease, such as diabetes mellitus, who are difficult to use glucose solution as a diluent