BACKGROUND: The lipids of the stratum corneum, which originate from polar lipid precursors provided by the cells of the stratum granulosum via the exocytosis of lamellar bodies, with cornified cell envelope form competent epidermal barrier structurally and functionally. The ontogeny of the epidermal barrier is not clearly defined because of difficulty of sampling and methodology which defines epidermal lipids. OBJECT: From ultrastructural observation of skin samples obtained from human fetuses and newborn on serial developmental timings, we tried to clarify the sequential development of epidermal barrier. METHODS: Skin samples were obtained from 13 human fetuses from EGA(estimated gestational age) 10 to 23wks and 2 newborns. Specimens were observed by fluorescent confocal microscopy with nile red to identify the distribution of epidermal lipids, by transmission electron microscope with lanthanum to investigate the functional permeability barrier, with RuO4 to observe the intercellular lipid bilayer and morphology of lamellar bodies, with ion capture cytochemistry to investigate the formation of epidermal calcium gradient. RESULT: In nile red stain, the amount of epidermal lipid increased during fetal period. At EGA 23wks, the lipid distribution revealed linear and continuous pattern. In lanthanum tracer study, the electron dense tracer permeated all the intercellular space of the epidermis up to periderm and subepidermal space until EGA 21wks. At EGA 23wks, the tracer permeated intercellular space of epidermis weakly. It might be predicted that incomplete epidermal barrier is present at this time. In RuO4 stain, precursor of lamellar body was observed at EGA 15wks, and intercellular lipid bilayer was observed at EGA 16wks. As gestation increases, there was a steady increase in epidermal lipid bilayers. In ion capture cytochemistry, epidermal calcium gradient was first observed in follicular epidermis at EGA 20wks, and in interfollicular epidermis at EGA 23wks. From these results, it is concluded that the basic structures of epidermal barrier are formed at EGA 23wks, but it is not complete, and epidermal barrier arises first from follicular epidermis.
Calcium ; Epidermis ; Exocytosis ; Extracellular Space ; Fetus* ; Histocytochemistry ; Humans* ; Infant, Newborn* ; Lanthanum ; Lipid Bilayers ; Microscopy, Confocal ; Permeability ; Pregnancy ; Skin

SO(4)(2-)/TiO(2)-La(2)O(3), a novel solid superacid, was prepared and its catalytic activities at different synthetic conditions are discussed with esterification of n-butanoic acid and n-butyl alcohol as probing reaction. The optimum conditions have also been found, mole ratio of n(La(3+)):n(Ti(4+)) is 1:34, the soaked consistency of H(2)SO(4) is 0.8 mol/L, the soaked time of H(2)SO(4) is 24 h, the calcining temperature is 480 degrees C, the calcining time is 3 h. Then it was applied in the catalytic synthesis of ten important ketals and acetals as catalyst and revealed high catalytic activity. Under these conditions on which the molar ratio of aldehyde/ketone to glycol is 1:1.5, the mass ratio of the catalyst used in the reactants is 0.5%, and the reaction time is 1.0 h, the yields of ketals and acetals can reach 41.4%-95.8%.
Acetylation ; Acids ; chemistry ; Catalysis ; Hydrogen-Ion Concentration ; Ketones ; chemistry ; Lanthanum ; chemistry ; Oxides ; chemistry ; Powders ; Sulfates ; chemistry ; Titanium ; chemistry

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

OBJECTIVETo evaluate the effect of lanthanum chloride on expressions of collagen protein and find a way to prevent and treat scar.

METHODSFour linear incisions were made on the dorsal skin of an adult, female Sprague-Dawley rat as an animal model. One was non-manipulated as a control; the second was injected with distilled water as a sham-control; the third was injected with 50 mmol/L of lanthanum chloride, and the fourth was injected with 50 micrograms neutralizing antibody of TGF-beta 1 as a positive control. All of the wound tissues were harvested and assayed with ABC method in 14 days and 28 days after the surgery.

RESULTSThe expressions of type I, III and IV of collagen protein in the third group significantly reduced in 14 and 28 days after the operation, compared with the control or sham-control group. Its values wen as similar as the fourth group.

CONCLUSIONLanthanum chloride could inhibit the expressions of collagen protein, and it may be used to prevent and treat scars.

Animals ; Collagen ; biosynthesis ; drug effects ; Female ; Lanthanum ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Time Factors ; Wounds and Injuries ; metabolism

OBJECTIVETo probe the effects of long-term oral administration of lanthanum nitrate [La(NO(3))(3)] on morphological change in the liver, aftereffect of deposited La in the liver and their mechanism in rats.

METHODSYoung Wistar rats were divided into two groups, one fed with 0.1, 0.2, 2.0, 10.0 and 20.0 mg/kg of La(NO(3))(3) for six months and the other for the control. Changes in ratio of liver to body weight were observed after exposure to La(NO(3))(3) at varied doses for six months and one month after six-month exposure, as well as morphology of the liver in the rats with routine histochemistry and transmission electron microscopy (TEM) technique. Content of La in the liver was measured with inductively coupled plasma-mass spectrometry (ICP-MS).

RESULTSRatio of liver to body weight was significantly higher in the male rats exposed to 20.0 mg/kg of lanthanum for six months than that in the control group. Ratio of liver to body weight restored to normal in the rats exposed to 20.0 mg/kg of La one month after six-month exposure. Infiltration of inflammatory cells in the portal region of the liver, small amount of fat drops in hepatocytic cytoplasm, increased density of mitochondria stroma, lysosome containing highly-electronic-density bodies and dense granules, normal nucleus and slightly deformed nucleus of hepatocytes could be found in the rats exposed to 20.0 mg/kg. Areas of the liver deposited with glycogen after six-month exposure to 20.0 mg/kg of La accounted for (26.1 +/- 1.5)% and (4.1 +/- 1.4)%, respectively for male and female rats, significantly lower than those in the control group [(31.3 +/- 1.4)% and (39.4 +/- 0.9)%, respectively], with a statistical significance and very statistical significance, respectively. There was a little infiltration of inflammatory cells in the portal region of the liver one month after six-month exposure to 20.0 mg/kg of La, and amount of the dense bodies was lower in the rats exposed to La for six months. Liver contents of La in the rats of all experimental groups were lower one month after six-month exposure than those in the rats exposed for six months.

CONCLUSIONSExposure to a dose of 20.0 mg/kg La(NO(3))(3) for a long term could damage the liver structure to certain extent, but lanthanum deposited in the liver could be eliminated from the body gradually.

Administration, Oral ; Animals ; Female ; Lanthanum ; toxicity ; Liver ; drug effects ; metabolism ; pathology ; Male ; Organ Size ; Rats ; Rats, Wistar

The present study were designed to characterize the action mechanisms of acetylcholine (ACh) -induced endothelium-dependent relaxation in arteries precontracted with high K (70 mM). For this, we simultaneously measured both muscle tension and cytosolic free Ca2 concentration ([Ca2 ]i), using fura-2, in endothelium-intact, rabbit carotid arterial strips. In the artery with endothelium, high K increased both [Ca2 ]i and muscle tension whereas ACh (10microM) significantly relaxed the muscle and increased [Ca2 ]i. In the presence of NG-nitro-L-arginine (L-NAME, 0.1 mM), ACh increased [Ca2 ]i without relaxing the muscle. In the artery without endothelium, high K increased both [Ca2 ]i and muscle tension although ACh was ineffective. 4-DAMP (10 nM) or atropine (0.1microM) abolished ACh-induced increase in [Ca2 ]i and relaxation. The increase of [Ca2 ]i and vasorelaxation by ACh was siginificantly reduced by either 3microM gadolinium, 10microM lanthanum, or by 10microM SKF 96365. These results suggest that in rabbit carotid artery, ACh-evoked relaxation of 70 mM K -induced contractions appears to be mediated by the release of NO. ACh-evoked vasorelaxation is mediated via the M3 subtype, and activation of the M3 subtype is suggested to stimulate nonselective cation channels, leading to increase of [Ca2 ]i in endothelial cells.
Acetylcholine ; Arteries ; Atropine ; Carotid Arteries* ; Cytosol ; Endothelial Cells ; Endothelium ; Fura-2 ; Gadolinium ; Lanthanum ; Muscle Tonus ; Nitric Oxide ; Nitroarginine ; Relaxation* ; Vasodilation

Wnk kinase maintains cell volume, regulating various transporters such as sodium-chloride cotransporter, potassium-chloride cotransporter, and sodium-potassium-chloride cotransporter 1 (NKCC1) through the phosphorylation of oxidative stress responsive kinase 1 (OSR1) and STE20/SPS1-related proline/alanine-rich kinase (SPAK). However, the activating mechanism of Wnk kinase in specific tissues and specific conditions is broadly unclear. In the present study, we used a human salivary gland (HSG) cell line as a model and showed that Ca2+ may have a role in regulating Wnk kinase in the HSG cell line. Through this study, we found that the HSG cell line expressed molecules participating in the WNK-OSR1-NKCC pathway, such as Wnk1, Wnk4, OSR1, SPAK, and NKCC1. The HSG cell line showed an intracellular Ca2+ concentration ([Ca2+]i) increase in response to hypotonic stimulation, and the response was synchronized with the phosphorylation of OSR1. Interestingly, when we inhibited the hypotonically induced [Ca2+]i increase with nonspecific Ca2+ channel blockers such as 2-aminoethoxydiphenyl borate, gadolinium, and lanthanum, the phosphorylated OSR1 level was also diminished. Moreover, a cyclopiazonic acid-induced passive [Ca2+]i elevation was evoked by the phosphorylation of OSR1, and the amount of phosphorylated OSR1 decreased when the cells were treated with BAPTA, a Ca2+ chelator. Finally, through that process, NKCC1 activity also decreased to maintain the cell volume in the HSG cell line. These results indicate that Ca2+ may regulate the WNK-OSR1 pathway and NKCC1 activity in the HSG cell line. This is the first demonstration that indicates upstream Ca2+ regulation of the WNK-OSR1 pathway in intact cells.
Cell Line* ; Cell Size ; Gadolinium ; Humans ; Lanthanum ; Oxidative Stress ; Phosphorylation ; Phosphotransferases ; Salivary Glands* ; Sodium Chloride Symporters ; Sodium-Potassium-Chloride Symporters

PURPOSE: Hyperphosphatemia and renal osteodystrophy increase the mortality and morbidity in chronic kidney disease. We compared the effects of lanthanum carbonate (LC) and calcium carbonate (CC) on phosphate homeostasis and bone bio-markers in hemodialysis patients. METHODS: The Korean dialysis patients with serum phosphorus more than 5.6 mg/dL were randomized to LC (n=12) or CC (n=11). Serum calcium, phosphorus, intact PTH, bone alkaline phosphatase, and osteocalcin were checked at regular intervals for 6 months. RESULTS: The reduction of serum phosphorus and calcium x phosphorus product at 24-week (wk) from baseline values was similar in LC and CC groups (Phosphorus: baseline, 7.28+/-1.04 mg/dL vs 7.41+/- 1.39 mg/dL, p=NS; at 24-wk, 5.39+/-1.85 mg/dL vs 5.67+/-1.43 mg/dL, p=NS) (Calcium x phosphorus product: baseline, 64.5+/-11.1 mg2/dL2 vs 61.3+/-11.9 mg2/dL2, p=NS; at 24-wk, 47.9+/-14.5 mg2/dL2 vs 51.8+/-14.0 mg2/dL2, p=NS). Despite higher baseline serum calcium levels in LC group, the changes of serum calcium from the baseline at 24-wk were significantly higher in CC group (LC vs CC; 0.23+/-0.38 mg/dL vs 0.94+/-0.87 mg/dL, p<0.05). Bone bio-markers, including iPTH, bone ALP, and osteocalcin, were comparable in 2 groups. However, significant gastrointestinal side effects leading to discontinuing the study were predominantly observed in LC (LC vs CC; n=5/12 vs n=0/11). CONCLUSION: Compared to calcium carbonate, lanthanum carbonate has similar efficacy to reduce serum phosphorus level, but less tendency to increase serum calcium level. However, the high incidence of gastrointestinal side effects in lanthanum carbonate needs further investigation in its correlation to Korean.
Alkaline Phosphatase ; Calcium ; Calcium Carbonate ; Carbon ; Dialysis ; Homeostasis ; Humans ; Hyperphosphatemia ; Incidence ; Lanthanum ; Osteocalcin ; Phosphorus ; Renal Dialysis ; Renal Insufficiency, Chronic ; Renal Osteodystrophy

PURPOSE: Although the purpose of the blood-testis barrier (BTB) is to protect germ cells from harmful influences, it also impedes the delivery of chemotherapeutic agents to the testis. This study was undertaken to determine whether a triolein emulsion could transiently alter the permeability of the BTB in cats. MATERIALS AND METHODS: An emulsion of 0.05ml triolein in 20ml of saline or just 20ml of normal saline, as the control, were infused into the testicular arteries in 18 and 15 cats, respectively (embolic and control group). Pre- and post-contrast magnetic resonance images (MRIs) were obtained 30 minutes and 2 hours after embolization. Qualitative and quantitative analyses of the MRIs were performed via the presence and degree of contrast enhancement and the contrast enhancement ratios (CERs), respectively. An electron microscopy (EM) study was subsequently performed, using a lanthanum tracer, to correlate with the MRI results. RESULTS: Contrast enhancement of the testis was observed in both groups and at both time points, but was more prominent in the embolic group. The CERs in the embolic group were significantly higher than those in the control group (p=0.0001). In each group, the CERs at 2 hours were significantly lower than those at 30 minutes (p=0.006). In the EM study, the entry of lanthanum was markedly increased at 30 mins, but recovered at 2 hours after embolization compared to the control. CONCLUSIONS: Intra-arterial infusion of triolein emulsion transiently increased the permeability of the BTB. This result may be useful in future studies for a chemotherapy delivery system to the testis.
Animals ; Arteries ; Blood-Testis Barrier* ; Cats ; Drug Therapy ; Emulsions ; Fats ; Germ Cells ; Infusions, Intra-Arterial ; Lanthanum ; Magnetic Resonance Imaging ; Microscopy, Electron ; Permeability ; Testis ; Triolein*

The author studied the functional derangement of blood-retinal barrier induced by destruction of the pigment epithelial cells of the retina. Sodium iodate, which was well known to exert a selectively destructive action to the retinal pigment epithelial cells, was injected to the rabbits intravenously(60mg/kg of body weight). Eyes were enucleated 2 days and 4 days after sodium iodate injection and examined by electron microscope. Some of the tissue were fixed in colloid lanthanum, to investigate the changes of the permeability of plasma membrane in accordance with cellular damages induced by sodium iodate. The permeability of the blood-retinal barrier was also studied after intravenous(200mg/kg) or intraocular(4 microgram/20ml of saline) injection of horseradish peroxidase(HRP). The results obtained were summarized as the following: Sodium iodate induced patchy areas of loss of pigment epithelial cells after 2 days, which were more widespread and severe after 4 days with regenerative activities. Loss of outer segment and mitochondrial swelling of the inner segment of visual cells were also noted after 4 days. Colloidal lanthanum penetrated into the mitochondria of pigment epithelial cells at 2 days after sodium iodate injection, which was extended to the mitochondria of inner segment of visual cells after 4 days. Intraocularly injected HRP appeared from the internal limiting membrane to Bruch's membrane after 2 days. Intravenously injected HRP appeared from the Bruch's membrane to ganglion cell layer after 2 days, which were extended to the vitreal cavity. The results suggested that the damage of the pigment epithelial cells induced by sodium iodate destroy blood-retinal barrier. HRP exudation is more extensive in direction of retina to choroid than choroid to retina.
Armoracia ; Blood-Retinal Barrier* ; Bruch Membrane ; Cell Membrane ; Choroid ; Colloids ; Epithelial Cells ; Ganglion Cysts ; Lanthanum ; Membranes ; Mitochondria ; Mitochondrial Swelling ; Permeability ; Rabbits ; Retina ; Retinal Pigment Epithelium* ; Retinaldehyde* ; Sodium