The primitive erythroblasts in 21 cases of embryonic hearts from 4 to 9 weeks of gestation were studied with a light microscope. The nuclear diameter, the motosis, and the loss of nuclei of the primitive erythoblasts were analyzed quantitatively. The results obtained were as follows. 1. At 4 weeks of gestation, the blood cells consisted of proerythroblasts, along with basophilic polychromatophilic primitive erythroblasts. The nuclear diameter ranged from 3.20 µm to 9.20 µm, but the main range was from 4.20 µm to 6.00 µm. It was revealed that 9.50% had diameter of more than 6 µm. 2. At the fist half of the 7 week gestation when hepatic hemopoiesis developed, the blood cells consisted of basophilic, polychromatophilic, and eosinophilic erythroblasts. Cells of more than 6 µm in nuclear diameter were about 1.10% and thereafter gradually disappeared. The range of the nuclear diameters was from 2.60 µm to 7.00 µm, while a range from 3.40 µm to 5.20 µm wqs the main. The proportion of cells less than 4 µm in nuclear diameter was 39.58% and thereafter rapidly increased. 3. From the second half of 7 weeks to 9 weeks of gestation, the erythrocytes originating from hepatic hemopoiesis increasingly replaced the circulating primitive erythroblasts, which became mature during this time. The erythrocytes showed 72.88% at 9 weeks of gestation. The proportions of cells less than 4 µm in nuclear diameter in the first and second haIves of 8 weeks and 9 weeks were 52.73%, 80.02%, and 89.09%, which represented the rapid destruction of nuclei. 4. Mitosis in the primitive erythroblasts occurred principally up to the early 6th weeks, and very weakly at 8 weeks. 5. As the crown-rump length increased, the average nuclear diameter decreased very significantly (P<0.01, y=-0.2811X + 0.3171). The results suggest that distrilbution of the nuclear diameter, the maturity, the rate of nuclear loss, and the mitotic figure offer credible data for estimating embryonic age.
Basophils ; Blood Cells ; Crown-Rump Length ; Embryonic Structures* ; Eosinophils ; Erythroblasts* ; Erythrocytes ; Heart ; Humans* ; Mitosis ; Pregnancy

No abstract available.
Asthma*

Authors analyzed the findings of nineteen cases of arthroscopic second-look operations after posterior cruciate ligament (PCL) reconstruction with autogenous bone-patellar tendon-bone (BPTB) and Trevira augmentation by two tunnel technique during the period from Nov, 1993 to Jan. l997 in fifty-one cases, along with the results of reconstruction in terms of clinica1 knee scoring, radiographichl and arthroscopic findings. The results were as follows; Age ranged fmm 20 to 53 years, the average being 32.3 years. Thirteen cases (68%) had associated knee injuries; five medial collateral ligament (MCL) injuries, four lateral collateral ligament (LCL) injuries, two associated injuries of MCL and medial meniscus, one both menisci and one associated injury of anterior cruciate ligament and MCL. The average period fmm PCL injury to reconstruction was 7 weeks (range, 1 to 52 wecks) and the mean period from PCL reconstruction to second-look operation was 20.3 months (range, 10 to 46 months). The average Miiller s knee score at the last follow-up was 86 paints. The radiographical results: The distance of posterior translation of the PCL reconstrueted knee compared with the normal sidc knee in posterior stress roentgenography was average 3.8mm (range, 0 to 1 1 mm). The position of the fernoral bone block on the plane of extended Blumansaats line, from the anterior end of the line, was average 32%. The level of proximal end of the tibial bone block according to the tibial tunnel orifice into the joint was mean negative 2.6 degrees position. The findings of arthroscopic second-look examination; In 9 cases (47%), the reconstructed ligamcnts were well covered with synovial tissue and looked like almost normal PCL. There were five cases (26%) of severe fragmentation, three cases (16%) of partial torn fibers of the grafted tendon. And one case showed the thinning of thc grafted tendon compared with the initial diameter at the time of reconstruction and one case showed overgrawth of the synovial membrane which suitounding the grafted tendon. All the Trevira which were augmented at the time of PCL reconstruction were ruptured. Twelve cases (63%) were stable, three cases (16%) were slightly lax and 4 cases (21%) showed laxity of the grafted tendon by the posterior drawer test and probing under arthroscopy, The isometricity which was checked at the time of PCL reconstruction was average 3.4mm. From the ahove results, PCL reconstruction with autogenous BPTB by the two tunnel technique seemed to be a valuable procedure, but there were some cases of unfavorable results. Authors think that a new graft fixation method is needed for resolving the problem mentioned above.
Anterior Cruciate Ligament ; Arthroscopy ; Collateral Ligaments ; Dronabinol ; Follow-Up Studies ; Joints ; Knee ; Knee Injuries ; Lateral Ligament, Ankle ; Menisci, Tibial ; Paint ; Posterior Cruciate Ligament* ; Radiography ; Synovial Membrane ; Tendons ; Transplants

Authors performed angio-CT(portal &/or arterial CT) in 35 patients with various hepatic masses. We obtained portal CT in 32 and arterial CT in 13 patients. The contrast material was injected into superior mesenteric artery for portal CT and into hepatic artery for arterial CT after transfemoral cathetrization of these arteries. We concluded that portal CT was superior to other imaging modalities highly sensitive in detecting hepatic masses, especially, early hepatocellular carcinomas, daughter nodules, and subclinical metastatic hepatic malignancy, With this method, detection rate of early hepatocelluar carcinomas improved 62% in number of patients and 90% in number of masses. Detection rate of subclinical hepatic metastases improve 60% each in number of patients and in number of masses. It was also useful for the detection of portal vein invasion. Arterial CT was useful in differential of masses and in defining the characteristics of entire or part of the masses because this method revealed hemodynamic patterns more definitely.
Arteries ; Carcinoma, Hepatocellular ; Hemodynamics ; Hepatic Artery ; Humans ; Mesenteric Artery, Superior ; Methods ; Neoplasm Metastasis ; Nuclear Family ; Portal Vein

The present study was intended to examine the effect of sodium vanadate on contractility of vascular smooth muscle. Aortic ring preparations were made from the rabbit thoracic aorta and endothelial cells were removed from the ring. The contractility of the aortic ring was measured under various conditions. The results were summarized as follows; 1) Sodium vanadate induced contraction of vascular smooth muscle in a dose-dependent fashion. 2) The contractile effects were not blocked by treatments with adrenergic blocking agent(phentolamine) and indomethacin, indicating the direct action of the drug on vascular smooth muscle. 3) In the presence of ouabain, Na(+)-K(+)-ATPase inhibitor, sodium vanadate still increased the contractility of vascular smooth muscle. 4) Treatment with 4.4'-diisothiocyanostilbene-2.2'-disulfonic acid(DIDS) blocked completely the contractile effects of sodium vanadate. 5) In the presence of verapamil, lanthanum and ryanodine, the contractility of the vascular smooth muscle by sodium vanadate was decreased. From the above results. it was suggested that sodium vanadate acts directly on vascular smooth muscle and causes contraction. It was probably due to inhibition of Ca(++)-ATPase in plasma membrane as well as increasing the release of Ca(++) from sarcoplasmic reticulum and Ca(++) influx across the plasma membrane, but not inhibition of Na(+)-K(+)-ATPase.
Aorta, Thoracic ; Cell Membrane ; Endothelial Cells ; Indomethacin ; Lanthanum ; Muscle, Smooth, Vascular* ; Ouabain ; Ryanodine ; Sarcoplasmic Reticulum ; Sodium* ; Vanadates* ; Verapamil

No abstract available.
Hemorrhagic Fever with Renal Syndrome* ; Pregnancy*

Caffeine has been known to induce the contraction of rabbit aortic ring resulting from Ca2+ release from the intracellular stores. But in contrast, contraction of aortic ring induced by depolarizing agents or agonist was reported to be suppressed by caffeine. The present study was intended to examine the effect of caffeine on Ca2+ movement across the plasma membrane and actomyosin ATPase activity of vascular smooth muscle to elucidate the modes of action of caffeine on the vascular smooth muscle. Aortic ring preparation were made from the rabbit thoracic aorta and the endothelial cells were removed from the ring by gentle rubbing. The contractilty of the aortic ring was measured under varying conditions, and Ca2+ influx across the membranes of the aortic ring was measured with Ca2+ sensitive electrode with and without caffeine and the effect of caffeine on actomyosin ATPase activity were measured by modified Hartshrone's method. 45Ca wash out curves with and without caffeine were studied by Richard's method. The results were summarized as follows: 1) Caffeine inhibited the contractilty induced by norepinephrine. high K+, and histamine. but caffeine alone induced a transient contraction of vascular smooth muscle. The caffeine induced contraction was demonstrable even in the absence of external Ca2+. 2) Caffeine increased 45Ca efflux from vascular smooth muscle. 3) In the presence of propranolol, the inhibitory effect of caffeine on epinephrine induced contraction still persisted. 4) Caffeine decreased norepinephrine induced Ca2+ influx through the plasma membranes of aortic ring. 5) Caffeine decreased the actomyosin ATPase activity of vascular smooth muscle. From the above results, it is suggested that caffeine induces the contraction of vascular smooth muscle by release of Ca2+ from intracellular Ca2+ stone, but inhibits drug-induced contraction by decrease of Ca2+ influx across the plasma membranes and a decreased Ca2+ sensitivity of contractile protein in vascular smooth muscle.
Actomyosin* ; Aorta, Thoracic ; Caffeine* ; Cell Membrane ; Electrodes ; Endothelial Cells ; Epinephrine ; Histamine ; Membranes ; Muscle, Smooth, Vascular* ; Myosins* ; Norepinephrine ; Propranolol

No abstract available.

Various anatomical defects have been described in the surviving co-twin who had stillborn, macerated monozygotic co-twin with disseminated intravascular coagulation. The suggested mechanism was the transfer of emboli or thromboplastic materials of dead fetus to co-twin through placental vascular anastomoses. Multicystic encephalomalacia is the condition defined anatomically by the presence of multiple cavities in the great part of both cerebral hemispheres. The most common pathogenesis is circulatory disturbance caused by neonatal asphyxia during the perinatal period. We experienced two cases of monozygotic twin with deceased co-twin at 26 weeks, 33 weeks of gestation and confirmed the diffuse multicystic encephalomalacia by cranial ultrasonography and MRI in a surviving co-twin. Only one patient has been followed who showed spastic cerebral palsy and severe mental retardation. We report two cases of multicystic encephalomalacia in a surviring co-twin with a intrauterine fetal death and its related literatures.
Asphyxia ; Cerebral Palsy ; Cerebrum ; Disseminated Intravascular Coagulation ; Encephalomalacia* ; Fetal Death* ; Fetus ; Humans ; Intellectual Disability ; Magnetic Resonance Imaging ; Pregnancy ; Pregnancy, Twin ; Twins, Monozygotic ; Ultrasonography

BACKGROUND: Impairment of relaxing response and augmentation of contractile response to vasoactive substances have been reported in atherosclerotic arteries. These alterations in vascular reactivity are considered as an underlying mechanism for the development of acute vasospasm in atherosclerotic coronary artery. Recently, it has been reported that lysophophatidylcholine (LPC), an oxidative metabolite of low density lipoprotein causes this functional abnormality. However, the precise mechanism of LPC induced change of vascular reactivity is still uncertain. METHOD: In this study, to elucidate the underlying mechanisms of abnormal vascular reactivity in atherosclerotic coronary artery, we examined the effect of LPC on whole cell K+current using patch clamping technique in rabbit coronary smooth muscle cells. RESULTS: Application of LPC(1microM) showed dual effect on whole cell outward current which depends on the magnitude of test potentials. At relatively high depolarizing test potentials (> 10 mV), LPC increased amplitude of outward current which was blocked by Gd3+ not by iberiotoxin (100 nM) and TEA (1 mM). Reversal potential of this Gd3+sensitive, LPC-induced current was -9.7 +/- 0.6 mV. At less depolarizing test potentials (< 10 mV), LPC decreased whole cell K+currents in a dose dependent manner (from 0.01 to 10 microM) in the range of -30 mV to +0 mV. Half maximal inhibition of K+current was 1.509 microM at 0 mV test potential (n =5). Depolarizing holding potential (0 mV) prevented this LPC-induced inhibition of K+current. Steady state activation and inactivation parameters of K+current were significantly shifted to the positive direction by application of LPC (p < 0.01, n =8). Pretreatment of staurosporine (100 nM), a blocker of protein kinase C partially blocked LPC-induced decrease of K+currents. CONCLUSION: LPC-induced inhibition of voltage dependent K+current may explain abnormal vascular reactivity in atherosclerotic coronary artery.
Arteries ; Constriction ; Coronary Vessels ; Lipoproteins ; Lysophosphatidylcholines* ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Protein Kinase C ; Staurosporine ; Tea