Medial femoral cutaneous nerve(MFCN), a sensory branch of the femoral nerve, supplies the skin over the anteromedial aspect of the thigh and knee. Posterior femoral cutaneous nerve(PFCN), comprised of fibers originating from the anterior and posterior divisions of the first three sacral segments, supplies the skin over the posterior aspect of the thigh. Forty nerves of twenty healthy adults, ages from 20 to 58, were tested. The onset and peak latencies of MFCN were 2.3+/-0.2 ms and 2.9+/-0.2 ms respectively. The baseline to peak amplitude was 6.5+/-2.3 V. The onset and peak latencies of PFCN were 2.4+/-0.2 ms and 2.9+/-0.2 ms respectively. The baseline to peak amplitude was 7.1+/-1.7 V.
Adult ; Equipment and Supplies ; Femoral Nerve ; Humans ; Knee ; Skin ; Thigh

No abstract available.
Urinary Bladder

Trisomy 9 mosaicism syndrome is a rare chromosomal abnormality with a high incidence of natural abortion and perinatal death. This syndrome is characterized by intrauterine growth retardation, mental retardation, craniofacial dysmorphism including a prominent nasal bridge with a short root and a fish-shaped mouth with thin lips, skeletal abnormalities, congenital heart defects, and genital abnormalities. The incidence and severity of malformations depend on the percentage of trisomic cells in the different tissues. We report a neonate who had the characteristic features of trisomy 9 syndrome with dysmorphic features including micrognathia, microcephaly, a low-set and malformed ear, a prominent lip, and cardiac defect. No chromosomal abnormalities were detected on a routine peripheral blood chromosomal analysis; however, a chromosomal abnormality with trisomy 9 mosaicism (low-level mosaic type) was detected on genetic tests. This is thought to be due to the low proportion of trisomic cells, and for this reason, the patient in this case shows a better prognosis than four patients previously reported in Korea, they were all diagnosed by peripheral blood chromosome testing.

Trisomy 9 mosaicism syndrome is a rare chromosomal abnormality with a high incidence of natural abortion and perinatal death. This syndrome is characterized by intrauterine growth retardation, mental retardation, craniofacial dysmorphism including a prominent nasal bridge with a short root and a fish-shaped mouth with thin lips, skeletal abnormalities, congenital heart defects, and genital abnormalities. The incidence and severity of malformations depend on the percentage of trisomic cells in the different tissues. We report a neonate who had the characteristic features of trisomy 9 syndrome with dysmorphic features including micrognathia, microcephaly, a low-set and malformed ear, a prominent lip, and cardiac defect. No chromosomal abnormalities were detected on a routine peripheral blood chromosomal analysis; however, a chromosomal abnormality with trisomy 9 mosaicism (low-level mosaic type) was detected on genetic tests. This is thought to be due to the low proportion of trisomic cells, and for this reason, the patient in this case shows a better prognosis than four patients previously reported in Korea, they were all diagnosed by peripheral blood chromosome testing.

Despite therapeutic advance, the prevalence of ischemic heart disease continues to increase. Recently, cell transplantation of stem cell has been proposed as a strategy for cardiac repair following myocardial damage. However, low differentiation efficiency into cardiomyocyte and poor cell viability associated with transplantation have limited the reparative capacity of these cell. In this study, we engineered P19 embryonal carcinoma cells using plasmid vector to overexpress the transcription factor MEF2c, Nkx2.5 involved in cardiomyogenesis. We investigated 1) formation of intercellular junction of P19 in mono-culture and co-culture with cardiomyocyte for functional and structural synchronous contraction after transplantation, 2) differentiation into cardiomyocyte, 3) resistance to hypoxic condition. An P19 embryonal carcinoma cell line expressing GFP, MEF2c, Nkx2.5 was generated by gene transfection and clonal selection. Nkx2.5 overexpression induced connexin43 expression level decrease. Electron microscopy revealed myofibril organization and immunostaining with cTnT showed positive staining in P19-Nkx2.5, consistent with early stage cardiomyocyte. Connexin43 and N-cadherin was expressed between P19-MEF2c and cardiomyocyte, P19- Nkx2.5 and cardiomyocyte in co-culture. And beating rate of cardiomyocyte co-cultured with P19-Nkx2.5 increased much more than other group, even if P19-Nkx2.5 did not have synchronous contraction with cardiomyocyte. Additionally, P19-Nkx2.5 had a resistance against hypoxia. These result suggest that overexpression of Nkx2.5 induced differentiation of P19 into cardiomyocyte and would be electro-mechanical coupling with cardiomyocyte after transplantation. Futhermore, Nkx2.5 overexpression had protection potential to hypoxic injury. Therefore, P19 cell overexpressed Nkx2.5 would be promising cell source for further study of new therapy of myocardial disease and building up in vitro model.
Anoxia ; Cadherins ; Cardiomyopathies ; Cardiomyoplasty* ; Cell Survival ; Cell Transplantation ; Coculture Techniques ; Connexin 43 ; Embryonal Carcinoma Stem Cells ; Intercellular Junctions ; Microscopy, Electron ; Myocardial Ischemia ; Myocytes, Cardiac ; Myofibrils ; Plasmids ; Prevalence ; Stem Cells ; Transcription Factors* ; Transfection ; Transplants

Background: Epinephrine (EPI) or norepinephrine (NOR) is widely used to treat cardiovascular collapse during lipid emulsion (LE) resuscitation for drug toxicity. However, the effect of LE on the vasoconstriction caused by EPI or NOR remains unknown. The purpose of this study was to examine the effect of an LE (Intralipid) on the vasoconstriction caused by EPI and NOR in isolated rat aorta. Methods: The effect of LE on the vasoconstriction caused by EPI or NOR in isolated rat aorta was examined. Additionally, the effect of LE on the calcium increase caused by EPI or NOR was investigated. The distribution constant (KD: lipid to aqueous phase) of EPI or NOR between a LE (1%) and an aqueous phase was determined. Results: LE (1 and 2%) did not significantly alter vasoconstriction caused by EPI or NOR in isolated endothelium-intact aorta. Moreover, the LE did not significantly alter the increased calcium level caused by EPI or NOR. The log KD of EPI in the LE (1%) was −0.71, −0.99, and −1.00 at 20, 50, and 100 mM ionic strength, respectively. The log KD of NOR in the LE (1%) was −1.22, −1.25, and −0.96 at 20, 50, and 100 mM ionic strength, respectively. Conclusions Taken together, the Intralipid emulsion did not alter vasoconstriction induced by EPI or NOR that seems to be due to the hydrophilicity of EPI or NOR, leading to sustained hemodynamic support produced by EPI or NOR used during LE resuscitation.

PURPOSE: To evaluate the prevalance of morphological variation of the kidney secondary to junctional parenchyma, as well as to analyze the ultrasonographic features of junctional parenchyma. MATERIALS AND METHODS: Two hundred and eighty two kidneys of 141 patient without clinical or radiologic evidence of renal disease were prospectively analysed using ultrasound. In all patients, ultrasonograms were obtained in sagittal, coronal and transaxial planes. The kidney was considered to have morphological variation if the ulrasonogram demonstrated junctional parenchymal defect or line ; those showing such variation were classified as one of three types :continuous, discontinuous, or junctional parenchymal line or defect without junctional parenchyma. The prevalance and ultrasonographic features of the kidneys were evaluated. RESULTS: Morphological variation was noted in 71 cases(25%). the continuous type accounted for 54% of these, the discontinuous type for 38%, and junctional parenchymal defect or line without junctional parenchyma for 8%. In all cases, junctional parenchyma was located approximately at the junction of the upper and middle third of the kidny, and had the same echogenecity as the renal cortex. CONCLUSION: An understanding of the morphological variation of the kidney resulting from junctional renal parenchyma would be helpful in differentiating pseudo tumor from true renal neoplasm.
Humans ; Kidney Neoplasms ; Kidney* ; Ultrasonography*

BACKGROUND: It is well known that propofol protects myocardium against myocardial ischemia/reperfusion injury in the rat heart model. The aim of this study was to investigate whether propofol provides a protective effect against a regional myocardial ischemia/reperfusion injury in an in vivo rat heart model after 48 h of reperfusion. METHODS: Rats were subjected to 25 min of left coronary artery occlusion followed by 48 h of reperfusion. The sham group received profopol without ischemic injury. The control group received normal saline with ischemia/reperfusion injury. The propofol group received profopol with ischemia/reperfusion injury. The intralipid group received intralipid with ischemia/reperfusion injury. A microcatheter was advanced into the left ventricle and the hemodynamic function was evaluated. The infarct size was determined by triphenyltetrazolium staining. The serum level of cardiac troponin-I (cTn-I) was determined by ELISA (enzyme-linked immunosorbent assay). RESULTS: Propofol demonstrated protective effects on hemodynamic function and infarct size reduction. In the propofol group, the +dP/dt(max) (P = 0.002) was significantly improved compared to the control group. The infarct size was 49.8% of the area at risk in the control group, and was reduced markedly by administration of propofol to 32.6% in the propofol group (P = 0.014). The ischemia/reperfusion-induced serum level of cTn-I was reduced by propofol infusion during the peri-ischemic period (P = 0.0001). CONCLUSIONS: Propofol, which infused at clinically relevant concentration during the peri-ischemic period, has delayed myocardial protective effect after regional myocardial ischemia/reperfusion injury in an in vivo rat heart model after 48 h of reperfusion.
Animals ; Coronary Vessels ; Emulsions ; Enzyme-Linked Immunosorbent Assay ; Heart ; Heart Ventricles ; Hemodynamics ; Myocardium ; Phospholipids ; Propofol ; Rats ; Reperfusion ; Salicylamides ; Soybean Oil ; Tetrazolium Salts ; Troponin I

BACKGROUND: Ulinastatin has anti-inflammatory properties and protects organs from ischemia/reperfusion-induced injury. The aim of this study was to investigate whether ulinastatin provides a protective effect on a regional myocardial ischemia/reperfusion injury in an in vivo rat heart model and to determine whether the anti-inflammatory response is related to its myocardial protective effect. METHODS: Rats were randomized to two groups. One group is received ulinastatin (50,000 U/kg or 100,000 U/kg) diluted in normal saline and the other group is received normal saline, which was administered intraperitoneally 30 min before the ischemic insult. Reperfusion after 30 min of ischemia of the left coronary artery territory was applied. Hemodynamic measurements were recorded serially during 6 h after reperfusion. After the 6 h reperfusion, myocardial infarct size, cardiac enzymes, myeloperoxidase activity, and inflammatory cytokine levels were compared between the ulinastatin treated and untreated groups. RESULTS: Ulinastatin improved cardiac function and reduced infarct size after regional ischemia/reperfusion injury. Ulinastatin significantly attenuated tumor necrosis factor-alpha expression and reduced myeloperoxidase activity. CONCLUSIONS: Ulinastatin showed a myocardial protective effect after regional ischemia/reperfusion injury in an in vivo rat heart model. This protective effect of ulinastatin might be related in part to ulinastatin's ability to inhibit myeloperoxidase activity and decrease expression of tumor necrosis factor-alpha.
Animals ; Coronary Vessels ; Glycoproteins ; Heart ; Hemodynamics ; Inflammation ; Ischemia ; Myocardial Reperfusion ; Myocardium ; Peroxidase ; Rats ; Reperfusion ; Tumor Necrosis Factor-alpha

PURPOSE: Fentanyl was reported to inhibit the alpha1-adrenoceptor agonist-induced contraction. The goal of this in vitro study was to identify the alpha1-adrenoceptor subtype primarily involved in the fentanyl-induced attenuation of phenylephrine-induced contraction in isolated endothelium-denuded rat aorta. MATERIALS AND METHODS: Aortic rings were suspended in order to record isometric tension. Concentration-response curves for phenylephrine (10-9 to 10-5 M) were generated in the presence or absence of one of the following drugs: fentanyl (3x10-7, 10-6, 3x10-6 M), 5-methylurapidil (3x10-8, 10-7, 3x10-7 M), chloroethylclonidine (10-5 M) and BMY 7378 (3x10-9, 10-8, 3x10-8 M). Phenylephrine concentration-response curves were generated in the presence or absence of fentanyl in rings pretreated with either 3x10-9 M prazosin, 10-9 M 5-methylurapidil or 3x10-9 M BMY 7378. RESULTS: Fentanyl (10-6, 3x10-6 M) attenuated phenylephrine-induced contraction in the rat aorta. 5-Methylurapidil and BMY 7378 produced a parallel rightward shift in the phenylephrine concentration-response curve. The pA2 values for 5-methylurapidil and BMY 7378 were estimated to be 7.71 +/- 0.15 and 8.99 +/- 0.24, respectively. Fentanyl (10-6 M) attenuated phenylephrine-induced contraction in rings pretreated with 10-9 M 5-methylurapidil, but did not alter the rings when pretreated with 3x10-9 M BMY 7378. Pretreatment of the rings with chloroethylclonidine showed a 72.9 +/- 2.3% reduction in phenylephrine-induced maximal contraction. CONCLUSION: The results suggest that fentanyl attenuates phenylephrine-induced contraction by inhibiting the pathway involved in the alpha1D-adrenoceptor-mediated contraction of the rat aorta.
Adrenergic alpha-Agonists/*pharmacology ; Adrenergic alpha-Antagonists/*pharmacology ; Animals ; Aorta/*drug effects ; Clonidine/analogs & derivatives/pharmacology ; Fentanyl/*pharmacology ; Male ; Phenylephrine/*pharmacology ; Piperazines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Vasoconstriction/*drug effects