Lymphangiomas are congenital malformations of the lymphatic system. Cervicofacial lymphangioma represents 75% of all lymphangiomas. Surgical excision has been the treatment of choice, however the reported results have been unsatisfactory. Various sclerosants have been tried to treat lymphangiomas, with variable results and considerable side effects. Herein we report the results of treatment using intralesional picibanil for lymphangioma. Between January 1996 and January 1998, 16 patients with lymphangiomas, 10 boys and 6 girls, were treated with intralesional picibanil injections. All cases were treated as a primary therapy. Eight lymphagiomas were located in the neck, and 2 in the cheek, 2 in the parotid, 2 in the trunk, 1 in the oropharynx, 1 in the thigh. Dose and method of intralesional injection was similar to that reported by Ogita in 1987. Complete regression was observed in 10 cases and marked regression(> 75% size decrease) in 2 cases and moderate regression(75%-25% size decrease) in 2 cases and poor regression(< 25% size decrease) in 2 cases. No serious side effect was observed except fever lasting for 2-3 days. Intralesional injection of picibanil for lymphangiomas represents a safe, easy and effective way of treatment with high success rate. Picibanil injection can be used as a primary therapy for lymphangiomas.
Sun, Jing He;Joh, Chul W;Ahn, Young Hwan;Park, Chan Hee;Shim, Chull;Park, Kyung Bae;Cho, Kyung Gi
Journal of Korean Neurosurgical Society
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v.29
no.10
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pp.1309-1315
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2000
Objectives : We performed an in vivo experiment to investigate the effect of $^{166}Holmium$ and $^{166}Holmium$-chitosan complex($^{166}Ho$-CHICO) on the normal brain of rats and to determine the sublethal dose of $^{166}Ho$-CHICO. Materials and Methods : $^{166}Ho$ is a beta and gamma ray emitter. $^{166}Ho$-CHICO is a novel radio-pharmaceutical complex with chitosan to facilitate the transport of $^{166}Ho$ obtained from Korea Atomic Energy Research Center(Taejon, Korea). It is in acidic form and becomes gel state at alkaline pH. One hundred and seventy consecutive rats were divided into four groups : $^{166}Ho$ treated(n=50), $^{166}Ho$-CHICO treated(n=57), saline treated(n=5) and chitosan treated(n=5) groups. $^{166}Ho$ and $^{166}Ho$-CHICO were injected into the rat brain stereotactically with various doses of 0.1mCi/$20{\mu}l$, 0.2mCi/$20{\mu}l$, 0.3mCi/$20{\mu}l$, and 0.4mCi/$20{\mu}l$ using an automated microinjector. Nuclear imaging, histopathological and hematological studies were performed in 10 rats in each group at 1 day, 3days, 7 days, 1 month and 3 months after the injections. Results : An infiltration of inflammatory cells and necrotic changes were noted in $^{166}Ho$ treated group at 1 week after the injection. A wedge-shaped tissue defect due to necrosis, lined with infiltrated glial cells in $^{166}Ho$ treated group and a cystic defect lined with reactive astroglial cells in $^{166}Holmium$-CHICO treated group at 3 months after the injection were observed. $^{166}Ho$ alone without chitosan leaked out and caused necrotic lesion on the cerebral surface but $^{166}Holmium$-CHICO treated group did not show this feature. As the dose of $^{166}Ho$ increased, the mortality rates were also increased. The mortality rate of the $^{166}Holmium$-CHICO group was higher than the $^{166}Ho$ treated group at a dose of 0.4mCi/$20{\mu}l$/300g. There was no detectable radioactivity due to the leakage or extravasation from the injected site of the brain on the scintigraphy performed at 1 hour, 24 hours and 48 hours after the injection. There was also no detectable activity of $^{166}Holmium$-CHICO in other organs including spleen, liver and kidney. Conclusions : $^{166}Ho$-CHICO did not leak out to the critical cortical surface of the brain from the injection site and induced radiation changes of the parenchyma around the injection site without cortical damage. The sublethal dose of $^{166}Ho$-CHICO for the normal brain in rats was determined to be 0.2mCi/$20{\mu}l$/300g.
The present study was undertaken to confirm whether melittin, a major constituent of whole bee venom (WBV), had the ability to produce the same nociceptive responses as those induced by WBV. In the behavioral experiment, changes in mechanical threshold, flinching behaviors and paw thickness (edema) were measured after intraplantar (i.pl.) injection of WBV (0.1 mg & 0.3 mg/paw) and melittin (0.05 mg & 0.15 mg/paw), and intrathecal (i.t.) injection of melittin $(6{\mu}g)$. Also studied were the effects of i.p. (2 mg & 4 mg/kg), i.t. $(0.2{\mu}g\;&\;0.4{\mu}g)$ or i.pl. (0.3 mg) administration of morphine on melittin-induced pain responses. I.pl. injection of melittin at half the dosage of WBV strongly reduced mechanical threshold, and increased flinchings and paw thickness to a similar extent as those induced by WBV. Melittin- and WBV-induced flinchings and changes in mechanical threshold were dose- dependent and had a rapid onset. Paw thickness increased maximally about 1 hr after melittin and WBV treatment. Time-courses of nociceptive responses induced by melittin and WBV were very similar. Melittin-induced decreases in mechanical threshold and flinchings were suppressed by i.p., i.t. or i.pl. injection of morphine. I.t. administration of melittin $(6{\mu}g)$ reduced mechanical threshold of peripheral receptive field and induced flinching behaviors, but did not cause any increase in paw thickness. In the electrophysiological study, i.pl. injection of melittin increased discharge rates of dorsal horn neurons only with C fiber inputs from the peripheral receptive field, which were almost completely blocked by topical application of lidocaine to the sciatic nerve. These findings suggest that pain behaviors induced by WBV are mediated by melittin-induced activation of C afferent fiber, that the melittin-induced pain model is a very useful model for the study of pain, and that melittin-induced nociceptive responses are sensitive to the widely used analgesics, morphine.
Pharmacokinetics of a new capsaicin analog, DA-5018 were evaluated after a subcutaneous injection or topical application of $[^{14}C]$--labelled or unlabelled DA-5018 to rats and rabbits. After subcutaneous injection of $_{14}$c-labelled or unlabelled DA-5018, 0.5 mg/kg (equivalent to DA-5018) to rats, the plasma total activity peaked at 2 hr with the terminal half life of 5.34 hr, however, unlabelled-DA-5018 peaked at 1 hr with the terminal half life of 1.26 hr. Moreover, the AUC (0.726 versus 0.2337g hr/ml) and MRT (7.82 versus 3.55 hr) increased significantly based on total radioactivity compared with intact DA-5018. Above data indicated that DA-5018 is extensively metabolized in rats and the terminal half- life of the metabolite(5) had a longer half-life than that of DA-5018. The cumulative percentages of biliary excretion of dose after subcutaneous injection of $[^{14}C]$DA-5018 was 40.2%, however, the value was only 2.14% when unlabelled DA-5018 was injected. After topical application of 0.1% or 0.3% $_{14}$C-labelled or unlabelled DA-5018 cream, 500 mg/kg to rats, the plasma and tissue concentrations except applied skin were under the detection limit. After consecutive 7 days topical application of unlabelled DA-5018, 0.1% and 0.3% cream to rats, the plasma concentrations were also under the detection limit. But the urinary excretion of DA-5018 was significantly increased by repeated topical administration. After topical application of unlabelled DA-5018, 0.1% and 0.3% cream to rabbits, the plasma and urine concentrations were under the detection limit. Above data indicated that the skin permeation of DA-5018 was lower and the metabolism of DA-5018 was higher in rabbits than that in rats.
Background: Sympathectomy relieves pain in sympathectically maintained pain, and subcutaneous injection of norepinephrine(NE) can rekindle mechanical allodynia. However, the mechanism of rekindling is not clear. The purpose of this study is to investigate which subtype of $\alpha$-adrenoceptor is involved in NE-induced rekindling of mechanical allodynia in sympathectomized neuropathic rats. Methods: Neuropathic injury was produced by tightly ligating the left L5 and L6 spinal nerves of 36 male Sprague-Dawley rats and bilateral lumbar sympathectomy was done at two weeks postoperatively. Starting at 7 days after sympathectomy, rekindling of mechanical allodynia was induced by NE and clonidine injected into the left paw, which was reversed by pretreatment of phentolamine and idazoxan. Mechanical allocynia was quantified by measuring the frequency of foot lifts to two von Frey filaments applied to the paw. Results: All tested rats displayed well-developed signs of mechanical allodynia at the left paw that were abolished by a bilateral lumbar sympathectomy. Subcutaneous (s.c.) injection of NE (0.05 ${\mu}g$) into the affected paw of sympathectomized neuropathic rats rekindled previous mechanical allodynia. These effects could be mimicked by an ${\alpha}_2$-receptor agonist clonidine, but not by an ${\alpha}_1$-receptor agonist phenylephrine. The NE-induced rekindling of mechanical allodynia was significantly reduced by prior s.c. injection of a mixed $\alpha$-receptor antagonist phentolamine (20${\mu}g$) and ${\alpha}_2$-receptor antagonist idazoxan(20${\mu}g$), but not by a ${\alpha}_1$-receptor antagonist terazosin (20${\mu}g$). The pretreatment of idazoxan produced dose-related inhibition of NE-induced rekindling of mechanical allodynia. The rekindling induced by ${\alpha}_2$-receptor agonist clonidine (5${\mu}g$) was also reversed by prior s.c. injection of ${\alpha}_2$-receptor antagonist idazoxan (20${\mu}g$). Conclusion: Subcutaneous injection of NE into the paw of sympathectomized neuropathic rats rekindles mechanical allodynia, which is reversed by an ${\alpha}_2$-, but not by an ${\alpha}_1$-receptor antagonist. Therefore, rekindling of mechanical allodynia in sympathectomized neuropathic rats is mediated by ${\alpha}_2$-adrenoceptor.
The growth and survival rate of larvae and juveniles from female rockfish (Sebastes schlegeli) broodstock in vitellogenesis by injection of 3,5,3'-triiodo-L-thyronine $T_3$ with a dose of 20 mg/kg fish wt. were examined for 30 days and compared with sham-control fish injected dime-thyl sulfoxide and control fish. Larvae were fed with rotifers for first 5 days after parturition, rotifers and Artemia nauplii for next 10 days. And then, they were fed with Artemia nauplii and commercial diet. Growth of larvae and juveniles from maternal $T_3$injection was significantly faster than that of two controls, nevertheless, the condition factor was lower than that of controls. The whole body proximate analyses indicated that there were significant effects of $T_3$ injection on protein and lipid, but no significant on moisture and ash contents. Survival rate of the fish from maternal $T_3$injection was significantly higher than that of fish from the two controls. These results indicate that thyroid hormone supplements appear to confer a distinct advantage to larval and juvenile rockfish in early, fragile development stage.
Kim, Tae-Ho;Lee, Nam-Sil;Choi, Hye-Sung;Jung, Sung-Hee;Han, Hyun-Ja
Korean Journal of Fisheries and Aquatic Sciences
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v.53
no.4
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pp.628-636
/
2020
Streptococcosis in the olive flounder Paralichthys olivaceus can be caused by Streptococcus parauberis. We compared three routes of administration for experimental injections of the S. parauberis 19FBSPa0003 strain in the olive flounder. Pathological changes were observed during the experimental infection. Inflammation of the serous membrane in the liver, intestine, spleen and heart was the major pathological change found in the infected olive flounder. No mortality was observed in fish that received intraperitoneal (IP) injection at less than 1×104 colony-forming unit (CFU)/fish. The lethal dose 50 for olive flounder, given an intravenous (IV) injection, was 7.94×104 CFU/fish. Fish with a higher concentration of IV injected S. parauberis (1×108 CFU/fish) died within a maximum of two days. However, serious necrosis and bacterial proliferation in ellipsoidal cells of the spleen and heart tissues were found in moribund or dead fish, 1-2 days after IV injection. Similar histopathological signs were observed in olive flounder inoculated by subcutaneous (SC) infected and naturally infected. In addition, SC was also strongly associated with bacteria concentration and cumulative mortality rate. Based on these results, SC is the recommended method for artificial infection by S. parauberis in the olive flounder.
Kim, Bum-Seok;Cho, Jae-Woo;Kwon, Hyuk-Nyun;Blank, Ivar;Borisova, Irina;Ejaz, Sohail;Chekarova, Irina;Kwon, Jung-Kee;Lim, Chae-Woong
Toxicological Research
/
v.22
no.4
/
pp.375-380
/
2006
Microcystin-LR (MC-LR) is a cyanobacterial hepatotoxin mainly produced by Microcystis aeruginosa. The current study examined the effects of a single intraperitoneal dose of MC-LR in rats. Female Sprague-Dawley rats were intraperitoneally injected with MC-LR ($100{\mu}g/kg$ body weight) and they were sacrificed at 0, 20, 40, 80, 160 min, or 12 h after injection. Clinically, animals showed lethargy and had ruffled hair beginning at 40 min post injection. In the gross findings, liver was enlarged and its color was changed into dark red beginning at 40 min post injection. Microscopically, dissociation of centrilobular hepatocytes and hemorrhage was observed in the hepatic central legions and such pathological changes were then extended to the portal regions of liver by time course manner. Interestingly at 80 min after MC-LR injection, the entrapped eosinophilic materials that may be necrotic fragments of dissociated hepatocytes were found in the capillaries of lung and renal glomerulus. Ultrastructurally, microvilli of the hepatocytes were disrupted or lost at all time points. Furthermore, the Disse space and gap junctions were widened beginning at 40 min post injection. These results suggest that liver is the major target organ of MC-LR and isolated hepatocytes by the effects of such hepatotoxin may secondarily reduce the physiological function of lung and kidney.
Bleomycin and cyclophosphamide are widely used and effective anti-cancer agents for treatment of various forms of cancer. Bleomycin has no myelotoxicity, but because of potential risk of pulmonary complications including interstitial pneumonitis and idiopathic interstitial pulmonary fibrosis, it has been limited in use. Some investigator has also suggested that cyclophosphamide can induce pulmonary toxicity like bleomycin. Recently, The combination chemotherapy including bleomycin and cyclophosphamide has been adopted effectively in some types of cancer. But there are no available literatures for synergistic effect of pulmonary toxicity in combination chemotherapy including these two drugs. We tried this study to observe synergism of pulmonary toxicity using these two drugs in rats. The animals were divided into five groups: group 1 received intra-peritoneal injection of saline, group 2-a received only bleomycin 0.1 mg [0.4 mg/kg] by intra-peritoneal injection twice a week, group 2-b received only bleomycin 0.5 mg [2 mg/kg] by intra-peritoneal injection twice a week, group 3-a received bleomycin 0.1 mg [0.4 mg/kg] twice a week +cyclophosphamide 5 mg [20 mg/kg] two weeks interval by intra-peritoneal injection, group 3-b received bleomycin 0.5 mg [2 mg/kg] twice a week + cyclophosphamide 5 mg[20 mg/kg] two weeks interval by intra-peritoneal injection. The animals were sacrificed at 2 and 4 weeks later. Lung tissues were obtained and observed by light microscope. The results are as follows: 1. The pathologic findings of group 1 were normal without change. 2. There was no difference between group 2-a and group 3-a at 2 weeks later, group 3-a, however, revealed more severe change in lung tissue at 4 weeks later compared with group 2-a. 3. In group 3-b there was more severe pulmonary injury compared with group 2-b at 2 and 4 weeks later. We conclude that the combined administration of bleomycin and cyclophosphamide induce more severe pulmonary toxic effect than bleomycin administration alone and the combination chemotherapy including these two drugs will be require special attention to selection of the dose of each drug.
This study was designed to investigate the effect of dietary vitamin E on the lipid peroxidation by dietary iron-injected to male rats. Sprague-Dawely strain male rats were divided into three experimental groups, namely control, iron injected and iron-vitamin E injected groups. The control group was fed with normal diet; the iron injected group was given normal diet and while injected intraperitoneally 30mg of ferric hydroxide/100g of body weight 20 times every 3 days. The iron-vitamin E injected group was intraperitoneally administered 30mg of ferric hydroxide/100g of body weight 20 times every 3 days and vitamin E every day with the dose of 5IU(5mg)/100g body weight. All experimental groups were maintained for 60 days with feeding on the respective ratio. The results obtained from this experiment were summarized as following: 1. The net weight gain was significantly decreased by the iron injection, but much increased by the vitamin E injection. 2. The contents of unsaturated fatty acid in phospholipid in liver, kidney, muscle and serum were decreased by the iron injection, but increased by the vitamin E injection. 3. The increment of malondialdehyde contents was induced by the iron overloading, but significantly decreased by the vitamin E injection. Therefore, it is suggested that dietary iron administration to male rats facilitates the lipid peroxidation in vivo and vitamin E has the inhibiting effect on lipip peroxidation process by iron.
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