• Title/Summary/Keyword: Cortical damage

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Anatomical and biochemical Changes of Corn Roots Infected with Pratylenchus vulnus (사과뿌리썩이선충의 침입과 기주의 해부학적 및 생화학적 변화에 관한 연구)

  • 한혜림;한상찬;김용균
    • Korean journal of applied entomology
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    • v.34 no.2
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    • pp.112-119
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    • 1995
  • Anatomical and biochemical changes of the corn root injured by the root lesion nematode, Pratylenchus vulnus, were examined to understand the interactions between the nematode and the crop which can be applied to a breeding program for nematode-resistant crop. The nematode and the crop which can be applied to be a breeding program for nematode-resistant crop. The nematode entered the cortex of corn root through its epidemis. They moved to other cortical cells by breaking their cell walls. They, finally, gathered around the endodermis of the roots and the bases of the root hairs. Parasitism of the nematode formed cavities within the root tissues where the females laid eggs. Major root damage by the nematode occurred in the cortical cells where must cell walls were broken and crushed to form empty spaces. These empty spaces in the base of the root resulted in this breakdown. Damage-induced biochemical changes of the corn roots were analysed by their total protein patterns and esterase activities in both control and nematode-infected roots. Denaturing gel did not show any significant difference in the banding patterns between them. Esterase patterns and activities, also, were not significantly different between the infected and the control roots.

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Neuroprotective and Antioxidant Effects of the Butanol Fraction Prepared from Opuntia ficus-indica var. saboten

  • Cho, Jung-Sook;Han, Chang-Kyun;Lee, Yong-Sup;Jin, Chang-Bae
    • Biomolecules & Therapeutics
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    • v.15 no.4
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    • pp.205-211
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    • 2007
  • The fruits and stems of Opuntia ficus-indica var. saboten have been reported to exhibit a variety of pharmacological actions, including antioxidant, analgesic, anti-inflammatory, and anti-ulcer effects. In the present study, we evaluated effects of the butanol fraction (SK OFB901) prepared from the 50% ethanol extract of the stems on various types of neuronal injuries induced by oxidative stress, excitotoxins, and amyloid ${\beta}\;(A_{\beta})$ in primary cultured rat cortical cells. Its antioxidant and radical scavenging activities were also evaluated by cell-free bioassays. We found that SK OFB901 strongly inhibited the oxidative neuronal damage induced by $H_2O_2$ or xanthine/xanthine oxidase. In addition, it exhibited marked inhibition of the excitotoxic neuronal damage induced by glutamate, N-methyl-D-aspartic acid, or kainate. Furthermore, the $A_{\beta(25-35)}$-induced neurotoxicity was also significantly attenuated by SK OFB901. It was found to inhibit lipid peroxidation initiated by $Fe^{2+}$ and L-ascorbic acid in rat brain homogenates and scavenge 1,1-diphenyl-2-picrylhydrazyl free radicals. These results indicate that the butanol fraction prepared from the stems of Opuntia ficus-indica var. saboten exerts potent antioxidant and neuroprotective effects through multiple mechanisms, implying its potential applications for the prevention or management of neurodegenerative disorders associated with oxidative stress, excitotoxicity, and $A{\beta}$.

Influence of Hippocampectomy and Adrenalectomy upon Gastric Ulceration in Rats (흰쥐의 위궤양 발생에 미치는 뇌해마 제거 및 부신 적출의 영향)

  • Kim, Myung-Suk;Ahn, Byung-Tae;Kim, Chul
    • The Korean Journal of Physiology
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    • v.10 no.2
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    • pp.39-45
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    • 1976
  • This study was conducted to see whether the hippocampectomy exerted facilitatory influence upon gastric ulceration in animals, and if so, whether the effect of hippocampectomy could be suppressed by adrenalectomy. 107 male rats were divided into 5 groups: rats that had over 90% of their hippocampal tissue removed through an opening on each side of the cerebral cortex(hippocampal group, N=21), rats that received bilateral adrenalectomy(adrenal group, N=29), rats that received adrenalectomy as well as hippocampectomy(hippocampo-adrenal group, N=10), rats that received damage to each side of the cortex over the hippocampus(cortical control group, N=20), and rats that had solely their head skin incised(normal control group, N=27). All rats were kept without restraint or food deprivation until on the 25th day after surgery, the stomach of each rat was inflated with 7ml of physiological saline and then removed under deep anesthesia. The mucosal surface was sketched under dissecting microscope, and enlarged photographs$(4{\times})$ were taken. The percentage of animals developing gastric ulcer in each animal group was calculated, the number of ulcer in each stomach was counted, and the total area of ulceration per stomach was measured on the Photograph with the aid of superimposed graph paper and expressed as permillage of total area of the glandular mucosa. Results obtained were as follows: 1. The percentage of animals developing gastric ulcer was significantly larger in the hippocampal group than they were in the hippocampo-adrenal, the adrenal, the cortical, and the normal control groups. 2. The mean number of ulcer per stomach was significantly larger in the hippocampal group than they were in the adrenal, the cortical control, and the normal control groups, while no significant difference existed between the hippocampal and the hippocampo-adrenal groups. 3. Total area of ulcer per stomach was significantly larger in the hippocampal group than they were in the cortical control and the normal control groups, but no significant differ-ence existed among the hippocampal, the adrenal, and the hippocampo·adrenal groups. 4. All measured values of the adrenal group were not significantly different from those of the hippocampo-adrenal, the cortical control, and the normal control groups. It is inferred from the above results that the hippocampus exerts an inhibitory influence upon gastric ulceration and that the hippocampal influence is mediated only partly through suppression of pituitary·adrenal activity.

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Methanol Extract of Paeonia Japonica Root Protects Cultured Rat Cortical Neurons Against Oxidative Damage Induced by Hydrogen Peroxide

  • Park, Min-Su;Ban, Ju-Yeon;Lee, Ju-Hyun;Song, Kyung-Sik;Seong, Yeon-Hee
    • Korean Journal of Medicinal Crop Science
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    • v.14 no.2
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    • pp.70-76
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    • 2006
  • Paeoniae radix has been widely used for its anti-allergic, anti-inflammatory and analgesic effects, and demonstrated to have anticonvulsant, memory enhancing and anxiolytic activities. The present study was performed to examine the protective effect of methanol extract of Paeoniae radix (PR) from Paeoniae Japonica Miyabe et Takeda (Paeoniaceae) on hydrogen peroxide $(H_2O_2)-induced$ neurotoxicity using cultured rat cerebral cortical neuron. $H_2O_2$ produced a concentration-dependent reduction of neuronal viability, PR, over a concentration range of 10 to $100\;{\mu}g/ml$ showed concentration-dependent decrease of the $H_2O_2$$(100\;{\mu}M)-induced$ neuronal cell death, as assessed by a 3-[4,5-dimethylthiazol-2-yl]-2,5-di-phenyl-tetrazolium bromide assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. PR $(100\;{\mu}g/ml$ inhibited $100\;{\mu}M$ $H_2O_2-induced$ elevation of the cytosolic $Ca^{2+}$ concentration $([Ca^{2+}]_c)$, which was measured by a fluorescent dye, flue-4 AM. PR $(50\;{\mu}g/ml$ inhibited glutamate release into medium induced by $100\;{\mu}M$ $H_2O_2$, which was measured by HPLC, and generation of reactive oxygen species (ROS). These results suggest that PR may mitigate the $H_2O_2-induced$ neurotoxiciy by interfering with the increase of $[Ca^{2+}]_c$, and then inhibiting glutamate release and generation of ROS in cultured neurons.

Eugenol Inhibits Excitotoxins-Induced Delayed Neurotoxicity, Oxidative Injury and Convulsion

  • Wie, Myung-Bok;Cheon, Byung-Hwa;Lee, Seon-Young;Son, Kun-Ho;Song, Dong-Keun;Shin, Tae-Kyun;Kim, Hyoung-Chun
    • Toxicological Research
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    • v.22 no.3
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    • pp.275-282
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    • 2006
  • In previous our studies, we have reported that eugenol derived from Eugenia caryophyllata(Myrtaceace) exhibits acute N-methyl-D-aspartate(NMDA)- and oxygen/glucose deprivation-induced neurotoxicity in primary cortical cultures and protects hippocampal neurons from global ischemia. In this study, we investigated whether the extracts and fractions of E. caryophyllata or eugenol shows the neuroprotective effects against delayed neuronal injury evoked by NMDA or ${\alpha}$-amino-3-hydroxy-5-methylisoxazole propionate(AMPA), and oxidative damage induced by arachidonic acid-, hydrogen peroxide-, $FeCl_2$/ascorbic acid-, and buthionine sulfoximine(BSO) in primary cortical cultures. We examined the neurotoxicity of eugenol itself in cultures and inhibitory effect of eugenol on NMDA- or kainate(KA)-induced convulsion in BALB/c mice. Each water, methanol extract and methanol fraction of E. caryophyllata was significantly attenuated NMDA-induced delayed neurotoxicity, respectively. Eugenol exhibited a significant inhibitory action against the convulsion evoked by NMDA and KA, and reduced delayed or brief neurotoxicity induced by NMDA, AMPA, and various oxidative injuries. These results suggest that eugenol derived from E. caryophyllata may contribute the neuroprotection against delayed-type excitotoxicity and excitotoxins-mediated convulsion through the amelioration of oxidative stress.

Moutan Cortex Extract Inhibits Amyloid ${\beta}$ Protein (25-35)-induced Neurotoxicity in Cultured Rat Cortical Neurons (Amyloid ${\beta}$ 2 Protein (25-35) 유도 배양신경세포 독성에 대한 목단피의 억제효과)

  • Kim, Joo-Youn;Ju, Hyun-Soo;Ban, Ju-Yeon;Song, Kyung-Sik;Seong, Yeon-Hee
    • Korean Journal of Medicinal Crop Science
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    • v.16 no.6
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    • pp.409-415
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    • 2008
  • Moutan cortex, the root bark of Paeonia suffruticosa Andrews (Paeoniaceae), has pharmacological effects such as anti-inflammatory, antiallergic, analgesic and antioxidant activities. We investigated a methanol extract of Moutan cortex for neuroprotective effects on neurotoxicity induced by amyloid ${\beta}$ protein ($A{\beta}$) (25-35) in cultured rat cortical neurons. Exposure of cultured cortical neurons to $10\;{\mu}M\;A{\beta}$ (25-35) for 24 h induced neuronal apoptotic death. Moutan cortex inhibited $10\;{\mu}M\;A{\beta}$ (25-35)-induced neuronal cell death at 30 and $50\;{\mu}g/m{\ell}$, which was measured by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. Moutan cortex inhibited $10\;{\mu}M\;A{\beta}$ (25-35)-induced elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), and generation of reactive oxygen species (ROS) which were measured by fluorescent dyes. Moutan cortex also inhibited glutamate release into medium induced by $10\;{\mu}M\;A{\beta}$ (25-35), which was measured by HPLC. These results suggest that Moutan cortex prevents $A{\beta}$ (25-35)-induced neuronal cell damage by interfering with the increase of $[Ca^{2+}]_i$, and then inhibiting glutamate release and ROS generation. Moutan cortex may have a therapeutic role in preventing the progression of Alzheimer's disease.

Cortical Deafness Due to Ischaemic Strokes in Both Temporal Lobes

  • Lachowska, Magdalena;Pastuszka, Agnieszka;Sokolowski, Jacek;Szczudlik, Piotr;Niemczyk, Kazimierz
    • Journal of Audiology & Otology
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    • v.25 no.3
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    • pp.163-170
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    • 2021
  • Cortical deafness is a clinical rarity whereby a patient is unresponsive to all types of sounds despite the preserved integrity of the peripheral hearing organs. In this study, we present a patient who suddenly lost his hearing following ischaemic infarcts in both temporal lobes with no other neurological deficits. The CT confirmed damage to the primary auditory cortex (Heschl's gyrus) of both hemispheres. Initially, the patient was unresponsive to all sounds, however, he regained some of the auditory abilities during 10 months follow up. Pure tone threshold improvement from complete deafness to the level of moderate hearing loss in the right ear and severe in the left was observed in pure tone audiometry. Otoacoustic emissions, auditory brainstem responses, and acoustic reflex findings showed normal results. The middle and late latency potential results confirmed objectively the improvement of the patient's hearing, however, after 10 months still, they were somewhat compromised on both sides. In speech audiometry, there was no comprehension of spoken words neither at 3 nor at 10 months. The absent mismatch negativity confirmed above mentioned comprehension deficit. The extensive auditory electrophysiological testing presented in this study contributes to the understanding of the neural and functional changes in cortical deafness. It presents the evolution of changes after ischaemic cerebrovascular event expressed as auditory evoked potentials starting from short through middle and long latency and ending with event-related potentials and supported by neuroimaging.

Cortical Deafness Due to Ischaemic Strokes in Both Temporal Lobes

  • Lachowska, Magdalena;Pastuszka, Agnieszka;Sokolowski, Jacek;Szczudlik, Piotr;Niemczyk, Kazimierz
    • Korean Journal of Audiology
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    • v.25 no.3
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    • pp.163-170
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    • 2021
  • Cortical deafness is a clinical rarity whereby a patient is unresponsive to all types of sounds despite the preserved integrity of the peripheral hearing organs. In this study, we present a patient who suddenly lost his hearing following ischaemic infarcts in both temporal lobes with no other neurological deficits. The CT confirmed damage to the primary auditory cortex (Heschl's gyrus) of both hemispheres. Initially, the patient was unresponsive to all sounds, however, he regained some of the auditory abilities during 10 months follow up. Pure tone threshold improvement from complete deafness to the level of moderate hearing loss in the right ear and severe in the left was observed in pure tone audiometry. Otoacoustic emissions, auditory brainstem responses, and acoustic reflex findings showed normal results. The middle and late latency potential results confirmed objectively the improvement of the patient's hearing, however, after 10 months still, they were somewhat compromised on both sides. In speech audiometry, there was no comprehension of spoken words neither at 3 nor at 10 months. The absent mismatch negativity confirmed above mentioned comprehension deficit. The extensive auditory electrophysiological testing presented in this study contributes to the understanding of the neural and functional changes in cortical deafness. It presents the evolution of changes after ischaemic cerebrovascular event expressed as auditory evoked potentials starting from short through middle and long latency and ending with event-related potentials and supported by neuroimaging.

Predictive Markers for Screening Renal Damage in Children with Urinary Tract infections and Vesicoureteral Reflux

  • Lee, Hyeonju;Choi, Jae Hong;Kang, Dong-Hyeok;Kim, Seunghyo;Kang, Ki-Soo;Han, Kyoung Hee
    • Childhood Kidney Diseases
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    • v.24 no.1
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    • pp.27-35
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    • 2020
  • Purpose: Urinary tract infections (UTIs) are the most common and serious bacterial infections in children. Therefore, early diagnosis of vesicoureteral reflux (VUR) for treatment planning and the identification of noninvasive markers that can predict renal injury are important in patients with UTIs. We analyzed the clinical features of pediatric UTIs commonly encountered by general practitioners and reinterpreted the blood tests and imaging findings to identify the important clinical predictive markers of VUR in order to selectively perform VCUG. Methods: This retrospective study was performed among 183 children diagnosed with a UTI or acute pyelonephritis. Results: The most significant predictor of high grade and bilateral VUR identified using area under the curve analyses was hydronephrosis on kidney ultrasound images with renal cortical defects on dimercaptosuccinic acid (DMSA) kidney scan simultaneously, followed by hydronephrosis only on kidney ultrasound. Conclusion: The presence of hydronephrosis on kidney ultrasound images or cortical defects or asymmetric kidneys on the DMSA kidney scans can be predictive markers of VUR, reducing the need for VCUG. Our study can thus help minimize the exposure to radiation among patients through selective VCUG.

Neuroprotective Effect of Taurine against Oxidative Stress-Induced Damages in Neuronal Cells

  • Yeon, Jeong-Ah;Kim, Sung-Jin
    • Biomolecules & Therapeutics
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    • v.18 no.1
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    • pp.24-31
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    • 2010
  • Taurine, 2-aminoethanesulfonic acid, is an abundant free amino acid present in brain cells and exerts many important biological functions such as anti-convulsant, modulation of neuronal excitability, regulation of learning and memory, anti-aggressiveness and anti-alcoholic effects. In the present study, we investigated to explore whether taurine has any protective actions against oxidative stress-induced damages in neuronal cells. ERK I/II regulates signaling pathways involved in nitric oxide (NO) and reactive oxygen species (ROS) production and plays a role in the regulation of cell growth, and apoptosis. We have found that taurine significantly inhibited AMPA induced cortical depolarization in the Grease Gap assays using rat cortical slices. Taurine also inhibited AMPA-induced neuronal cell damage in MTT assays in the differentiated SH-SY5Y cells. When the neuronal cells were treated with $H_2O_2$, levels of NO were increased; however, taurine pretreatment decreased the NO production induced by $H_2O_2$ to approximately normal levels. Interestingly, taurine treatment stimulated ERK I/II activity in the presence of AMPA or $H_2O_2$, suggesting the potential role of ERK I/II in the neuroprotection of taurine. Taken together, taurine has significant neuroprotective actions against AMPA or $H_2O_2$ induced damages in neuronal cells, possibly via activation of ERK I/II.