No abstract available.
Bone Marrow* ; Histiocytes* ; Niemann-Pick Diseases*

Idiopathic myelofibrosis (IMF), which is characterized by marrow fibrosis, leukoerythroblastic anemia, teardrop poikilocytosis and splenomegaly due to extrumedullary hematopoiesis, has known to have no form of therapy. On the ground of the possibility of reversing collagen deposion in IMF using 1, 25dihydroxycholecalciferol [1, 25(OH)2D3], we report here our observations of 5 patients (M:F=1:4) with IMF before and after treatment with 0.5 microgram/day of alfacalcidol, precursor of 1, 25(OH)2D3. In 3 fo 5 patients the hemoglobin rose and in 4 of 5 the platelet count increased. Follow-up marrow examination revealed that marrow trephine reticulin fibrosis decreased according as the amelioration of clinical and laboratory findings. But these did not persist except one patient in spite of the sustained use of alfacalcidol. Our results suggest that alfacalcidol may have a therapeutic role in some patients with IMF. More extensive studies will be clarify the action of alfacalcidol in IMF.
Anemia, Myelophthisic ; Bone Marrow ; Child* ; Collagen ; Fibrosis ; Follow-Up Studies ; Hematopoiesis ; Humans ; Platelet Count ; Primary Myelofibrosis* ; Reticulin ; Splenomegaly

No abstract available.
Mycobacterium bovis* ; Prostatitis*

Congenital absence of the gallbladder is a rare anomaly and an interesting subject. The overall incidence of gallbladder agenesis is said to approximately 0.035% to 0.065%. It is extremely difficult to make the correct diagnosis of gallbladder agenesis preoperatively in symptomatic patients because its clinical and radiological features are like those of cholecystitis, cholelithiasis, or choledocholithiasis in patients with anatomically normal biliary tracts. Gallbladder agenesis is suspected when the surgeon or the pathologist has failed to identify the gallbladder in its usual position but ectopic location or necrosis of the gallbladder from any causes should be ruled out. Recently, two cases of gallbladder agenesis were encountered in adult patients. We summarize our experience and give a brief review of the literature.
Adult ; Biliary Tract ; Cholecystitis ; Choledocholithiasis ; Cholelithiasis ; Diagnosis ; Gallbladder* ; Humans ; Incidence ; Necrosis

PURPOSE: Tethered cord syndrome(TCS) is defined as low position of the conus medullaris by the abnormally fixed spinal cord with progressive neurologic deficit MATERIALS AND METHODS: To evaluate the findings of TCS at MRI and its diagnostic value, we performed a retrospective analysis of MRI of 30 patients with emphasis on clinical manifestation, level of conus medullaris, cause of tethering, and associated findings. RESULTS: Clinical presentation included back mass(26 cases), neurogenic bladder(5 cases), urinary incontinence(5 cases), progressive constipation(2 cases), skin dimpling(1 case), gait disturbance(1 case) and club foot (1 case). Neurologic deficit was developed in 11 cases(40% and mean age of these patients at the time of diagnosis was 8.6 years. The most common cause of tethering was lipoma(63%). The tips of conus medullaris were below the level of the second lumbar spine in all patients. The causes of tethering were lipomatous component(spinal lipoma and lipomyelomenigocele) in 67% myelomeningocele in 20%, presacral mass in 7%, thickened filum terminale in 3% and postoperative change in 3%. Associated anomalies included syringomyelia(20%) and hydrocephalus was associated in 3 out of 5 patients who underwent brain MRI. CONCLUSION: MRI clearly delineated the location of conus, tethering of the filum terminale with their causes and associated abnormalities. MRI examination is a very useful diagnostic tool for the early evaluation of TCS and the postoperative follow up.
Brain ; Cauda Equina ; Conus Snail ; Diagnosis ; Follow-Up Studies ; Foot ; Gait ; Humans ; Hydrocephalus ; Lipoma ; Magnetic Resonance Imaging ; Meningomyelocele ; Neural Tube Defects* ; Neurologic Manifestations ; Retrospective Studies ; Skin ; Spinal Cord ; Spine

No abstract available.

Purpose: The purpose of this study was to understand the effects of infection control fatigue and social support on burnout among nurses during the Coronavirus Disease 2019 (COVID-19) pandemic. Methods: This study is a descriptive survey study designed to confirm the effects of nurses' infection control fatigue and social support on burnout among nurses during the COVID-19 pandemic. The collected data were analyzed using frequency, percentage, mean, standard devia analyzed using frequency, percentage, mean, standard deviation, independent t-test, One-way ANOVA, Scheffé test, Pearson’s correlation coefficient, and stepwise multiple regression analysis using SPSS Statistics 26.0. Results: An analysis of the correlations between fatigue from infection control, social support, and burnout showed a positive correlation between burnout and fatigue from infection control (r=.39, p<.001), and a negative correlation between burnout and social support (r=-.29, p<.001). Conflict and lack of support due to uncertain circumstances (β=.51, p<.001), support from supervisor's (β=-.22, p<.001), and experience of infection management education during the previous 1year (β=-.15, p=.007) were identified as the factors that influenced burnout among nurses, and explained 39.0% of the variance in burnout. Conclusion The results of this study demonstrate that fatigue from infection control and social support influence burnout levels among nurses, which suggests the need to establish a new kind of work culture. Additionally, the findings call for the development and implementation of interventional programs that can reduce fatigue from infection control and increase social support for nurses.

BACKGROUND: The present study was attempted to compare enalapril, an angiotensin-converting enzyme inhibitor with losartan an angiotensin II (Ang II) receptor blocker in the inhibitory effects on the secretion of catecholamines (CA) from the perfused model of the rat adrenal gland. METHODS: The adrenal gland was isolated and perfused with Krebs-bicarbonate. CA was measured directly by using the fluorospectrophotometer. RESULTS: Both enalapril and losartan during perfusion into an adrenal vein for 90 minutes inhibited the CA release evoked by acetylcholine (ACh), 1.1-dimethyl-4-phenyl piperazinium (DMPP, a selective Nn agonist), high K+ (a direct membrane-depolarizer), 3-(m-chloro-phenyl-carbamoyl-oxy-2-butynyl-trimethyl ammonium (McN-A-343, a selective M1 agonist), and Ang II in a time-dependent manner. Also, in the presence of enalapril or losartan, the CA release evoked by veratridine (an activator of voltage-dependent Na+ channels), 6-dimethyl-3-nitro-4-(2-trifluoromethyl-phenyl)-pyridine-5-carboxylate (BAY-K-8644, an L-type Ca2+ channel activator), and cyclopiazonic acid (a cytoplasmic Ca2+-ATPase inhibitor) were significantly reduced. Based on the same concentration of enalapril and losartan, for the CA release evoked by ACh, high K+, DMPP, McN-A-343, Ang II, veratridine, BAY-K-8644, and cyclopiazonic acid, the following rank order of inhibitory potency was obtained: losartan > enalapril. In the simultaneous presence of enalapril and losartan, ACh-evoked CA secretion was more strongly inhibited compared with that of enalapril- or losartan-treated alone. CONCLUSIONS: Collectively, these results demonstrate that both enalapril and losartan inhibit the CA secretion evoked by activation of both cholinergic and Ang II type-1 receptors stimulation in the perfused rat adrenal medulla. When these two drugs were used in combination, their effects were enhanced, which may also be of clinical benefit. Based on concentration used in this study, the inhibitory effect of losartan on the CA secretion seems to be more potent than that of enalapril.
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride ; 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester ; Acetylcholine ; Adrenal Glands ; Adrenal Medulla ; Ammonium Compounds ; Angiotensin II ; Animals ; Catecholamines ; Cytoplasm ; Dimethylphenylpiperazinium Iodide ; Enalapril* ; Losartan* ; Perfusion ; Rats ; Veins ; Veratridine

The aim of this study was to determine whether fimasartan, a newly developed AT1 receptor blocker, can affect the CA release in the isolated perfused model of the adrenal medulla of spontaneously hypertensive rats (SHRs). Fimasartan (5~50 microM) perfused into an adrenal vein for 90 min produced dose- and time-dependently inhibited the CA secretory responses evoked by ACh (5.32 mM), high K+ (56 mM, a direct membrane depolarizer), DMPP (100 microM) and McN-A-343 (100 microM). Fimasartan failed to affect basal CA output. Furthermore, in adrenal glands loaded with fimasartan (15 microM), the CA secretory responses evoked by Bay-K-8644 (10 microM, an activator of L-type Ca2+ channels), cyclopiazonic acid (10 microM, an inhibitor of cytoplasmic Ca(2+)-ATPase), and veratridine (100 microM, an activator of Na+ channels) as well as by angiotensin II (Ang II, 100 nM), were markedly inhibited. In simultaneous presence of fimasartan (15 microM) and L-NAME (30 microM, an inhibitor of NO synthase), the CA secretory responses evoked by ACh, high K+, DMPP, Ang II, Bay-K-8644, and veratridine was not affected in comparison of data obtained from treatment with fimasartan (15 microM) alone. Also there was no difference in NO release between before and after treatment with fimasartan (15 microM). Collectively, these experimental results suggest that fimasartan inhibits the CA secretion evoked by Ang II, and cholinergic stimulation (both nicotininc and muscarinic receptors) as well as by membrane depolarization from the rat adrenal medulla. It seems that this inhibitory effect of fimasartan may be mediated by blocking the influx of both Na+ and Ca2+ through their ion channels into the rat adrenomedullary chromaffin cells as well as by inhibiting the Ca2+ release from the cytoplasmic calcium store, which is relevant to AT1 receptor blockade without NO release.
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride ; 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester ; Adrenal Glands ; Adrenal Medulla ; Angiotensin II ; Animals ; Biphenyl Compounds ; Calcium ; Chromaffin Cells ; Cytoplasm ; Dimethylphenylpiperazinium Iodide ; Indoles ; Ion Channels ; Membranes ; NG-Nitroarginine Methyl Ester ; Pyrimidines ; Rats ; Rats, Inbred SHR ; Tetrazoles ; Veins ; Veratridine

The aim of the present study was to investigate whether ginsenoside-Rb2 (Rb2) can affect the secretion of catecholamines (CA) in the perfused model of the rat adrenal medulla. Rb2 (3~30 microM), perfused into an adrenal vein for 90 min, inhibited ACh (5.32 mM)-evoked CA secretory response in a dose- and time-dependent fashion. Rb2 (10 microM) also time-dependently inhibited the CA secretion evoked by DMPP (100 microM, a selective neuronal nicotinic receptor agonist) and high K+ (56 mM, a direct membrane depolarizer). Rb2 itself did not affect basal CA secretion (data not shown). Also, in the presence of Rb2 (50 microg/mL), the secretory responses of CA evoked by veratridine (a selective Na+ channel activator (50 microM), Bay-K-8644 (an L-type dihydropyridine Ca2+ channel activator, 10 microM), and cyclopiazonic acid (a cytoplasmic Ca2+-ATPase inhibitor, 10 microM) were significantly reduced, respectively. Interestingly, in the simultaneous presence of Rb2 (10 microM) and L-NAME (an inhibitor of NO synthase, 30 microM), the inhibitory responses of Rb2 on ACh-evoked CA secretory response was considerably recovered to the extent of the corresponding control secretion compared with the inhibitory effect of Rb2-treatment alone. Practically, the level of NO released from adrenal medulla after the treatment of Rb2 (10 microM) was greatly elevated compared to the corresponding basal released level. Collectively, these results demonstrate that Rb2 inhibits the CA secretory responses evoked by nicotinic stimulation as well as by direct membrane-depolarization from the isolated perfused rat adrenal medulla. It seems that this inhibitory effect of Rb2 is mediated by inhibiting both the influx of Ca2+ and Na+ into the adrenomedullary chromaffin cells and also by suppressing the release of Ca2+ from the cytoplasmic calcium store, at least partly through the increased NO production due to the activation of nitric oxide synthase, which is relevant to neuronal nicotinic receptor blockade.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester ; Adrenal Medulla ; Animals ; Calcium ; Catecholamines ; Chromaffin Cells ; Cytoplasm ; Dimethylphenylpiperazinium Iodide ; Membranes ; Neurons ; NG-Nitroarginine Methyl Ester ; Nitric Oxide Synthase ; Rats ; Receptors, Nicotinic ; Veins ; Veratridine