No abstract available.

No Abstract available.

No abstract available.

PURPOSE: This study was aimed to elucidate the effect of hyperthermia on neuronal nitric oxide synthase(nNOS) expression in both cerebral hemispheres after left common carotid artery occlusion in gerbils. METHODS: Using Mongolian gerbils, cerebral ischemia was produced by occluding carotid artery for 1-4 hours. Rectal temperature was maintained at 36degrees C for normothermia and 40degrees C for hyperthermia by heating pad. Western blot and RT-PCR was used to examine the nNOS and the mRNA expression. Neuronal damages were observed by histological study. RESULTS: After cerebral ischemia, mRNA of nNOS was expressed more abundantly in ischemic hemisphere than control in both normothermia and hyperthermia. Hyperthermia reduced nNOS protein expression markedly. In pathological study, neurons of hippocampal region were degenerated by ischemia. Hyperthermia by itself induced neuronal degeneration in both control and ischemic region. In immunohistochemistry of brain, there was no significant difference of nNOS expression between normothermia and hyperthermia. CONCLUSION: These findings suggest that increase in body temperature might enhance nNOS mRNA expression but reduce nNOS protein, and that hyperthermia aggravates neuronal damage by ischemia, independent of nNOS gene expression.
Blotting, Western ; Body Temperature ; Brain ; Brain Ischemia* ; Carotid Arteries ; Carotid Artery, Common ; Cerebrum ; Fever* ; Gene Expression ; Gerbillinae* ; Heating ; Hot Temperature ; Immunohistochemistry ; Ischemia ; Neurons* ; Nitric Oxide ; Nitric Oxide Synthase Type I* ; RNA, Messenger

The rabbit cornea was studied in vitro in modified Ussing chambers to determine the effects of ion transport inhibitors and hydrogen peroxide(H2O2) on ion transport through the cornea by measuring the bioelectric properties. Apical(tear side, T side) addition of furosemide, bumetanide and SITS were ineffective on resting Isc(short circuit current). Apical addition of 1.0mM amiloride(Na+/H+ antiport inhibitor) and NPAA(Cl- channel blocker) markedly reduced the resting Isc, but basolateral(stromal side, S side) addition of amiloride was ineffective. The site of action of these agents was the apical membrane. H2O2, an oxygen free radical, markedly increased the lsc when was added to the T side, but S side addition of the H2O2 was ineffective. To determine the degree of cellular catalase participation in protection against H2O2 induced injury the cornea was pretreated with ATAZ for 30 min prior to H2O2 action. The increase of lsc by H2O2 was markedly potentiated after pretreatment with ATAZ on T side compared to that of S side addition. This result indicates that the corneal endothelial H2O2 may be largely degraded by catalase. When H2O2 was added to the T side, Isc was raised by increased ion transport. All ion transport inhibitors that were used inhibited the H2O2 effect on Isc. Moreover, amiloride and NPAA markedly inhibited induced lsc by H2O2. These results suggest that H2O2 stimulates the corneal epithelial ion transport and that its site of action is apical membrane Na+/H+ antiport system and CI- channel system.
4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid ; Amiloride ; Bumetanide ; Catalase ; Cornea ; Furosemide ; Hydrogen Peroxide* ; Hydrogen* ; Ion Transport ; Membranes ; Oxygen

BACKGROUND AND OBJECTIVES: The aim of this study was to determine the effect of ethanol on the regulation of vascular tone. MATERIAL AND METHODS: Using rat aorta ring, isometric contraction and 45Ca uptake were measured. Phorbol 12,13-dibutyrate (PDBu), phenylephrine, KCl were used for the regulation of smooth muscle tone. RESULTS: Ethanol induced transient contraction in rat aorta ring by dose-dependent manner. Ethanol suppressed the dose dependent contractile responses of vascular strip by phenylephrine, KCl and PDBu. Endothelium-dependent relaxation by acetylcholine was inhibited by ethanol. Ethanol depressed 45Ca uptake by high KCl but not by phenylephrine or PDBu in rat aorta. n-butanol selectively suppressed tonic contraction by high KCl, but t-butanol did not at the same concentration of butanol in rat aorta. PDBu-induced contraction was selectively suppressed by n-butanol but not by t-butanol. CONCLUSIONS: These findings suggest that the action of ethanol on phospholipase D is involved in the decreased response of rat aorta strip by vasoconstrictors.
1-Butanol ; Acetylcholine ; Animals ; Aorta* ; Ethanol* ; Isometric Contraction ; Muscle, Smooth* ; Phenylephrine ; Phorbol 12,13-Dibutyrate ; Phospholipase D ; Protein Kinase C ; Rats* ; Relaxation ; tert-Butyl Alcohol ; Vasoconstrictor Agents

It is well known that nitric oxide (NO) mediates smooth muscle relaxation via an increase in cyclic GMP (cGMP) 1evels. Acetylcholine (ACh) and nitroprusside (SNP) are known to mediate relaxation of cavernous smooth muscle via increasing the levels of NO. In recent years, the role of K+ channels in the hyperpolarization induced by nitrates and ACh in smooth muscle have been investigated. In this study, we attempted to characterize the role of K+ channel in rabbit cavernous smooth muscle relaxation by ACh and SNP under organ bath. Changes in isometric tension of corporal strips were monitored. The results were as follows; 1. The relaxant effects of ACh and SNP on contracted smooth muscle induced by 80 mM K' were less than those by phenylephrine. The ACh-induced relaxation was almost abolished in rabbit cavernous smooth muscle which endothelium was denuded, but the that of SNP was not affected by removal of endothelium. 2. Ng-nitro-L-arginine(L-NOARG) (3x0.00001M) and methylene blue (3x0.00001M) significantly inhibited the relaxant effect of ACh in cavernous smooth muscle, but that of SNP was not influenced by these drugs. The inhibition of L-NOARG on the relaxant effect of Ach was reversed by the addition of L-arginine(3x0.0001M). 3. Charybdotoxin (ChTx, 0.0000001M), significantly inhibited the relaxant effects of ACh,SNP and 8-Br-cGMP, but glibenclamide (0.00001M) and apamin (0.00001M) did not influence those of ACh and SNP 4. ACh (0.0001M} and SNP (0.0001M) increased the tissue content of cGMP The effect of ACh on the tissue content of cGMP was significantly affected by L-NOARG (3x0.00001M) and methylene blue (3x0.0000lM), but that of SNP was not influenced by these drugs. ChTx (0.000000lM) did not attenuate the accumulation of cGMP induced by ACh and SNP. Above results suggest that the relaxing effect of Ach and SNP on the isolated rabbit cavernous smooth muscle is associated with an increase in the tissue content of cGMP. Furthermore, ChTx sensitive-K+ channel-mediated hyperpolarization by increased cGMP may play a part in the relaxation of rabbit cavernous smooth muscle by ACh and SNP
Acetylcholine* ; Apamin ; Baths ; Charybdotoxin ; Cyclic GMP ; Endothelium ; Glyburide ; Methylene Blue ; Muscle, Smooth* ; Nitrates ; Nitric Oxide ; Nitroprusside* ; Phenylephrine ; Relaxation*

K+ -selective ion channels were studied in excised inside-out membrane patches from human osteoblast-like cells(G292). There classes of K+ channels were present and could be distinguished on the basis of conductance. Conductances were 270+/-27 pS, 113+/-12 pS, 48+/-8 pS according to their approximate conductances in symmetrical 140 mM KCI saline at holding potential of -80 mV. It was found that the small conductance (48 pS) K+ channel activation was dependent on membrane voltage. In current-voltage relationship, small conductance K+ channel showed outward rectification, and it was activated by the positive potential inside the membrane. In recordings, single channel currents were activayed by a negative pressure outside the membrane. The membrane pressure increased P(open) of the K+ channel in a pressure-dependent manner. In the excised-patch clamp recordings, G292 osteoblast-like cells have been shown to contain three types of K+ channels. Only the small conductance (48 pS) K+ channel is sensitive to the membrane stretch. These findings suggest that a hyperpolarzing current, mediated in part by this channel, may be associated with early events during the mechanical loading of the osteoblast. In G292 osteoblast-like cells, K+ channel is sensitive to membrane tension, and may represent a unique adaptation of the bone cell membrane to mechanical stress.
Cell Membrane ; Humans ; Ion Channels ; Membranes ; Osteoblasts ; Stress, Mechanical

Neurofibromatosis, or von Recklinghausen's disease, is a hereditary, harmartomatous disorder that primarilyinvolves neuroectoderm and mesoderm. The estimated incidence is 1 in 2,500 to 3,000 births. The clinical featuresare skin manifestations such as cafe-au-lait spots, skeletal manifestations primarily in volving vertebrae,central and peripheral nervous manifestations, and other associated abnormalities with increased risk ofmalignancy. The authors analysed the radiologic findings of 18 cases of patients with neurofibromatosis whovisited Pusan Kosin Medical Center and Taegu Dongsan Medical Center during the last five years. All were proven bysurgery, biopsy and other diagnostic criteria. The results obtained were as follows: 1. The male ot female ratiowas 11:7 and the age ranged from 11 months to 51 years. 2. All the cases fulfilled the diagnotic criteria of Croweand associates. 3. Bone manifestations were present in 44% of the cases. The other radiologic findings wereintrathoracic meningocele, bilateral acoustic neurinomas, mediastinal or chest wall mass shadows, and peripheralsoft tissue masses. 4. One of the soft tissue masses was proved to be malignant.
Biopsy ; Busan ; Cafe-au-Lait Spots ; Daegu ; Female ; Humans ; Incidence ; Male ; Meningocele ; Mesoderm ; Neural Plate ; Neurofibromatoses ; Neurofibromatosis 1 ; Neurofibromatosis 2 ; Parturition ; Skin Manifestations ; Thoracic Wall

We previously reported that nidogen is an extracellular matrix protein regulating Schwann cell proliferation and migration. Since Schwann cells play a critical role in peripheral nerve regeneration, nidogen may play a role in it via regulation of Schwann cells. Here, we demonstrate direct evidence that nidogen induces elongation of regenerative axon growth of adult sensory neurons, and that the effect is Schwann cell dependent. Continuous infusion of recombinant ectodomain of tumor endothelial marker 7, which specifically blocks nidogen function in Schwann cells, suppressed regenerative neurite growth in a sciatic nerve axotomy model. Taken together, it is likely that nidogen is required for proper regeneration of peripheral nerves after injury.
Animals ; Axotomy ; Cell Movement ; Cell Proliferation ; Male ; Membrane Glycoproteins/*physiology ; Membrane Proteins/pharmacology ; *Nerve Regeneration ; Nerve Tissue Proteins/pharmacology ; Neurites/drug effects/*physiology/ultrastructure ; Rats ; Rats, Sprague-Dawley ; Recombinant Proteins/pharmacology ; Schwann Cells/cytology/*physiology ; Sensory Receptor Cells/*physiology