Kim, Jin Yeo;Park, Ji Eun;Jung, Min Jae;Kim, Jae Song;Kim, Soo Hyun;Son, Eun Sun
Journal of Korean Society of Health-System Pharmacists
/
v.35
no.4
/
pp.400-408
/
2018
Background : Palivizumab is an intravenous monoclonal antibody which is used in the prevention of respiratory syncytial virus (RSV) infection. It is currently recommended for infants who are at high-risk for RSV infections due to preterm birth or other medical conditions such as congenital heart disease. Palivizumab is a humanized monoclonal antibody directed against an epitope in the antigenic site A of the protein F of RSV particles. Palivizumab is given once a month via intramuscular (IM) injection throughout the duration of the RSV season. Since palivizumab is known to have preventive effects against RSV infection for children with older siblings, the insurance coverage for palivizumab was expanded in October 2016. Methods : The electronic medical records of children under 2 years old who have older siblings who visited or were admitted to the Severance Hospital from October 2015 to May 2016 and from October 2016 to May 2017 were reviewed retrospectively. The data were then divided into two groups depending on the pilivizumab administration. Results : A total of 67 patients were enrolled in this study. The effectiveness in the reduction of hospitalization was statistically significant (p=0.009). Palivizumab decreased respiratory symptoms such as cough, rhinorrhea, and fever in patients with older siblings (p 0.05). Conclusions : In this study, palivizumab administration was effective in preventing RSV infection in infants with older siblings. Expanding palivizumab-prophylaxis administration to infants with older siblings may be effective in the prevention of upper respiratory infections.
Lee, Ji Weon;Yoon, Yoonsun;Kim, Sang-Dae;Kim, Yun-Kyung
Pediatric Infection and Vaccine
/
v.29
no.1
/
pp.46-53
/
2022
It is challenging to treat ventriculitis with parenteral treatment alone in some cases because of the difficulty involved in maintaining an appropriate level of antibiotics in cerebrospinal fluid (CSF). We report two cases of ventriculitis who did not respond to intravenous (IV) antibiotics but were successfully treated with intraventricular antibiotics using IV agents. The first case was a four-month-old male patient with X-linked hydrocephalus. He showed ventriculitis due to Klebsiella pneumoniae not producing extended-spectrum β-lactamase and susceptible to third-generation cephalosporins and gentamicin, following ventriculoperitoneal (VP) shunt. His condition did not improve during the 47 days of treatment with IV cefotaxime and meropenem. We achieved improvement in clinical presentation and CSF profile after three times of intraventricular gentamicin injection. The patient was discharged from the hospital with antiepileptic drugs. The second case was a six-month-old female patient with a history of neonatal meningitis complicated with hydrocephalus at one month of age, VP shunt at two months of age, followed by a methicillin-resistant coagulase-negative staphylococci (CoNS) shunt infection with ventriculitis after the shunt operation. CoNS ventriculitis recurred four weeks later. We failed to treat intractable methicillin-resistant CoNS ventriculitis with IV vancomycin for ten days, and thus intraventricular antimicrobial treatment was considered. Five times of intraventricular vancomycin administration led to improvement in clinical parameters. There were only neurological sequelae of delayed language development but no other major complications. Patients in these two cases responded well to intraventricular antibiotics, with negative CSF culture results, and were successfully treated for ventriculitis without serious complications.
Lopez-Canales, Oscar Alberto;Pavon, Natalia;Ubaldo-Reyes, Laura Matilde;Juarez-Oropeza, Marco Antonio;Torres-Duran, Patricia Victoria;Regla, Ignacio;Paredes-Carbajal, Maria Cristina
The Korean Journal of Physiology and Pharmacology
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v.26
no.2
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pp.77-86
/
2022
The effect of PHAR-DBH-Me, a cannabinoid receptor agonist, on different cardiovascular responses in adult male rats was analyzed. The blood pressure was measured directly and indirectly. The coronary flow was measured by Langendorff preparation, and vasomotor responses induced by PHAR-DBH-Me in aortic rings precontracted with phenylephrine (PHEN) were analyzed. The intravenous injection of the compound PHAR-DBH-Me (0.018-185 ㎍/kg) resulted in decreased blood pressure; maximum effect was observed at the dose of 1,850 ㎍/kg. A concentrationdependent increase in the coronary flow was observed in a Langendorff preparation. In the aortic rings, with and without endothelium, pre-contracted with PHEN (10-6 M), the addition of PHAR-DBH-Me to the superfusion solution (10-12-10-5 M), produced a vasodilator response, which depends on the concentration and presence of the endothelium. L-NAME inhibited these effects. Addition of CB1 receptor antagonist (AM 251) did not modify the response, while CB2 receptor antagonist (AM630) decreased the potency of relaxation elicited by PHAR-DBH-Me. Indomethacin shifted the curve concentration-response to the left and produced an increase in the magnitude of the maximum endothelium dependent response to this compound. The maximum effect of PHAR-DBH-Me was observed with the concentration of 10-5 M. These results show that PHAR-DBH-Me has a concentration-dependent and endothelium-dependent vasodilator effect through CB2 receptor. This vasodilation is probably mediated by the synthesis/release of NO. On the other hand, it is suggested that PHAR-DBH-Me also induces the release of a vasoconstrictor prostanoid.
Kim, Min Jung;Lee, Sang-Yeol;Lee, Hui Joong;Lee, Taekwan;Chang, Yongmin
Journal of Biomedical Engineering Research
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v.43
no.4
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pp.193-198
/
2022
Contrast enhanced magnetic resonance imaging using gadolinium-based contrast agent (GBCA) is a very useful in vivo technique to visualize the inner ear pathology including endolymphatic hydrops. Although systemic intravenous (IV) administration can visualize the perilymph space, the visualization was possible by indirect passage of contrast agent through blood-perilymph barrier. All animal experimental procedures were performed under anesthesia with 5% isoflurane. Lipopolysaccharide (LPS) was instilled into the left tympanic cavity through the tympanic membrane using a sterile 27gauge needle to induce hydrops model. Tucker-Davis Technologies system was used to measure Auditory Brainstem Responses (ABRs). For intracerebroven-tricular (ICV) administration, 25 µmol of GADOVIST (Bayer, Berlin, Germany) was used and diluted GADOVIST injection was 10 µl. MR imaging was acquired with a 9.4 Tesla MRI scanner. Transmit-receive volume coil with 40 mm inner diameter and 75 mm out diameter was used. ICV administration well demonstrated the strong enhancement along the cerebrospinal fluid (CSF) microcirculation pathway including CSF fluid in the subarachnoid space and CSF space of the inner ear structures. On the other hand, IV administration showed no contrast enhancement along the CSF microcirculation pathway and showed weak enhancement in the inner ear structures. In case of rat hydrops model, ICV administration showed that the reduced contrast enhancement in the perilymph space of the hydrops induced inner ear compared to the contrast enhancement in the perilymph space of the normal inner ear. New systemic ICV administration method provide contrast enhancement of GBCA in the inner ear through CSF microcirculation pathway.
The β subunits of high voltage-gated calcium channels (HGCCs) are essential for optimal channel functions such as channel gating, activation-inactivation kinetics, and trafficking to the membrane. In this study, we report for the first time the potent blood pressure-reducing effects of peptide fragments derived from the β subunits in anesthetized and non-anesthetized rats. Intravenous administration of 16-mer peptide fragments derived from the interacting regions of the β1 [cacb1(344-359)], β2 [cacb2(392-407)], β3 [cacb3(292-307)], and β4 [cacb4(333-348)] subunits with the main α-subunit of HGCC decreased arterial blood pressure in a dose-dependent manner for 5-8 min in anesthetized rats. In contrast, the peptides had no effect on the peak amplitudes of voltage-activated Ca2+ current upon their intracellular application into the acutely isolated trigeminal ganglion neurons. Further, a single mutated peptide of cacb1(344-359)-cacb1(344-359)K357R-showed consistent and potent effects and was crippled by a two-amino acid-truncation at the N-terminal or C-terminal end. By conjugating palmitic acid with the second amino acid (lysine) of cacb1(344-359)K357R (named K2-palm), we extended the blood pressure reduction to several hours without losing potency. This prolonged effect on the arterial blood pressure was also observed in non-anesthetized rats. On the other hand, the intrathecal administration of acetylated and amidated cacb1(344-359)K357R peptide did not change acute nociceptive responses induced by the intradermal formalin injection in the plantar surface of rat hindpaw. Overall, these findings will be useful for developing antihypertensives.
Kim, Sueun;Ok, Jong Sun;Choi, Jin Yi;Choi, Heejung
The Journal of Korean Academic Society of Nursing Education
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v.29
no.4
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pp.381-394
/
2023
Purpose: This study aimed to develop an intentional rounding protocol to enhance the clinical competence of nursing students. Methods: An intentional rounding protocol for nursing students' clinical practice was developed following the ADDIE (Analysis, Design, Development, Implementation, and Evaluation) model. A convenient sampling method was used to select 23 junior year university nursing students during their clinical practice in adult nursing. The program evaluation included a quantitative assessment (communication and relationship efficacy, empathy, and patient safety competency) and focus group interviews. Results: The intentional rounding protocol focused on the 4Ps (pain, position, potty, and possessions) and encompassed aspects such as level of consciousness, pain management, personal care needs, intravenous injection, oxygen administration, nasogastric/nasoenteric tube care, maintenance of urine collection bags, and the identification of environmental fall risks. Nursing students performed intentional rounding at least twice a day. Following the implementation of this protocol, nursing students demonstrated a significant improvement in communication and interpersonal efficacy. The focus group interviews revealed four main themes: growth of human relationships, acquiring knowledge in and about the clinical field, becoming a nurse, and barriers in reality. Conclusion: The intentional rounding protocol has the potential to enhance nursing students' communication and interpersonal skills during clinical practice and to provide them with positive experiences in nursing clinical education. Therefore, it is recommended that this protocol be incorporated into nursing clinical practice education.
Dexmedetomidine displays multiple mechanisms of neuroprotection in ameliorating ischemic brain injury. In this study, we explored the beneficial effects of dexmedetomidine on blood-brain barrier (BBB) integrity and neuroinflammation in cerebral ischemia/reperfusion injury. Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 1.5 h and reperfusion for 24 h to establish a rat model of cerebral ischemia/reperfusion injury. Dexmedetomidine (9 ㎍/kg) was administered to rats 30 min after MCAO through intravenous injection, and SB203580 (a p38 MAPK inhibitor, 200 ㎍/kg) was injected intraperitoneally 30 min before MCAO. Brain damages were evaluated by 2,3,5-triphenyltetrazolium chloride staining, hematoxylin-eosin staining, Nissl staining, and brain water content assessment. BBB permeability was examined by Evans blue staining. Expression levels of claudin-5, zonula occludens-1, occludin, and matrix metalloproteinase-9 (MMP-9) as well as M1/M2 phenotypes-associated markers were assessed using immunofluorescence, RT-qPCR, Western blotting, and gelatin zymography. Enzyme-linked immunosorbent assay was used to examine inflammatory cytokine levels. We found that dexmedetomidine or SB203580 attenuated infarct volume, brain edema, BBB permeability, and neuroinflammation, and promoted M2 microglial polarization after cerebral ischemia/reperfusion injury. Increased MMP-9 activity by ischemia/reperfusion injury was inhibited by dexmedetomidine or SB203580. Dexmedetomidine inhibited the activation of the ERK, JNK, and p38 MAPK pathways. Moreover, activation of JNK or p38 MAPK reversed the protective effects of dexmedetomidine against ischemic brain injury. Overall, dexmedetomidine ameliorated brain injury by alleviating BBB permeability and promoting M2 polarization in experimental cerebral ischemia/reperfusion injury model by inhibiting the activation of JNK and p38 MAPK pathways.
In this experiment, we investigated 82 patients who suffered adverse reactions due to contrast medium. We selected the subjects out of 21,178 people who had an intravenous injection of contrast medium to undergo MDCT examination at one university hospital in Busan in 2007. As a result, the largest groups of the patients were as follows. 52.4% of the patients were male when classify by gender; 28.0% of the patients were 50's by age; 45% of the patients got when it was spring(April and March); 75.6% of the patients had a side effects when the speed of injection is 2.5mL/sec; 58.5% of the patients were suffered when the volume of injected contrast medium is over 130mL. Urticaria was the main symptom of side effect as 26.8%. And the main treatment for the effect was alleviating the symptoms before making patients to return home. Thus, practical preventive measures are needed as follows : use the OCS system to observe warning signs at risky patients, secure warming spaces for patients to cope with season changing, prepare enough emergency kits for the patients in danger, and establish CPR call systems, explain the risk of contrast medium and get agree about using contrast medium.
Magnesium ion ($Mg^{2+}$) is a vasodilator, but little is known about its mechanism of action on vascular system. In vitro, extracellular magnesium sulfate ($MgSO_4$) produced relaxation in phenylephrine (PE) or high KCl-precontracted isolated rat thorocic aorta with (+E) or without (-E) endothelium in a concentration-dependent manner. The $MgSO_4$-induced relaxations were not affected by removal of the endothelium. Pretreatment of +E or -E aortic rings with nitric oxide synthase (NOS) inhibitors ($20{\mu}M$ L-NNA, $100{\mu}M$ L-NAME, $1{\mu}M$ dexamethasone and $400{\mu}M$ aminoguanidine), cyclooxygenase inhibitor ($10{\mu}M$ indomethacin), guanylate cyclase inhibitors ($10{\mu}M$ ODQ and $30{\mu}M$ methylene blue) and $Ca^{2+}$ transport blocker ($10{\mu}M$ ryanodine) did not affect the relaxant effects of $MgSO_4$. $Ca^{2+}$ channel blockers ($0.3{\mu}M$ nifedipine and $0.5{\mu}M$ veropamil) completely decreased the relaxant effects of $MgSO_4$ in +E and -E aortic rings. However, in $Ca^{2+}$-free medium, $MgSO_4$-induced vasorelaxation was potentiated and this response was inhibited by nifedipine. Protein kinase C (PKC) inhibitors ($1.0{\mu}M$ staurosporine, $0.5{\mu}M$ tamoxifen and $0.1{\mu}M$ H7) or PLC inhibitor ($100{\mu}M$ NCDC) markedly decreased the relaxant effects of $MgSO_4$ in +E and -E aortic rings. In vivo, infusion of $MgSO_4$ elicited significant decreases in arterial blood pressure. After intravenous injection of nifedipine ($150{\mu}g/kg$) and NCDC (3 mg/kg), infusion of $MgSO_4$ inhibited the $MgSO_4$-lowered blood pressure markedly. However, after introvenous injection of saponin (15 mg/kg), L-NNA (3 mg/kg), L-NAME (5 mg/kg), indomethacin (2 mg/kg), methylene blue (15 mg/kg) and aminoguanidine (10 mg/kg) failed to inhibit it. These results suggest that endothelial NQ-cGMP or prostaglandin pathway is not involved in vasorelaxant or hypotensive action of $Mg^{2+}$ and that these effects are due to the inhibitory action of $Mg^{2+}$ on the $Ca^{2+}$ channel or PLC-PKC pathway, and are due to the competitive influx of $Mg^{2+}$ and $Ca^{2+}$ through the $Ca^{2+}$ channel.
Conflicting data have been reported on the effect of nicotine on gastric mucosal damage. To elucidate the effect of chronic intermittent nicotine on gastric mucosal damage, intragastric nicotine (5 mg/kg, 10 mg/kg) was administered twice per day for 9 days. Gastric mucosal damage was created by s.c. injection of a large dose (1.2 mg/kg) of pentagastrin followed by pylorus ligation for 6 hours. Nicotine treated rats showed reduced gastric mucosal damage about 50% of the control. To examine the mechanism of the protective effect of nicotine, gastric perfusion experiments were done. Basal acid secretion was not affected by intragastric or intravenous nicotine. However, pentagastrin-stimulated acid secretion markedly inhibited by a bolus injection of nicotine, and this response was dose-related. These data indicates that chronic intermittent administration of nicotine protects gastric mucosa against gastrin-induced gastric mucosal damage, and nicotine-induced inhibition of gastrin-stimulated acid secretion has an important role for the protective effect of nicotine. Considering reports concerning nicotine's aggravating effect on the gastric mucosal damage, it is suggested that the methods of administration of nicotine may be an important decisive factor of the divergent action of nicotine on the gastric mucosa.
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