Summary Treatment of refractory cutaneous lupus is challenging. When conventional therapy, including hydroxychloroquine (HCQ), corticosteroids and immunosuppressants, has failed, the addition of quinacrine may be a promising option. We describe a case of refractory chronic cutaneous lupus erythematosus (CCLE) who responded well to quinacrine.
Quinacrine ; Lupus Erythematosus, Cutaneous

In this study seminal fluid samples were obtained from 20 normal adult males to know the percentage of the spermatozoa containing the fluorescent body (F-body), after staining the seminal fluid with 0.5% aqueous quinacrine HCI. In this study the preparations were observed with an AO fluorescent microscope. The following results were obtained. 1) In 20 men, the mean percentage of F-body containing spermatozoa was 31.3%. 2) There was no relationship between sperm density in semen analysis and F-body rate 3) There was no relationship between sperm motility in semen analysis and F-body rate. 4) In 5 men, methyl alcohol-acetic acid (3:1) preparations, as a fixation solution, showed better F-body rate than that of ethyl alcohol preparations. 5) In 4 men, the preparations which were fixed and stained within 2 hours after obtaining seminal fluid showed better F-body rate than that fixed and stained after 6 hours. 6) In 10 men, after low speed centrifuging of the seminal fluid, the deposit preparations, showed decreased mean percentage of F-body containing spermatozoa by 4.2%.
Adult ; Ethanol ; Humans* ; Male ; Quinacrine ; Semen Analysis ; Sperm Motility ; Spermatozoa*

OBJECTIVE: To identify cytogenetic diversity of Turner syndrome, and its correlation with clinical manifestation including fertility. METHOD: From 1986 to 1996, we reviewed medical records of 137 patients, cytogenetically and clinically diagnosed as Turner syndrome. Cytogenetic study was performed using peripheral lymphocytes with GTG banding. Marker chromosomes were re-evaluated by quinacrine staining. RESULTS: Overall incidence of mosaic pattern was 57.7% in Turner syndrome, showing 45,X line combined with structural anomalies of X chromosome(n=39), marker chromosome(n=22), numerical abnormalities of sex chromosome(n=6), and 46,XX(n=5). With comparison of clinical manifestation in 45,X/46,XX(n=5) and four most common pattern, 45,X(n=42), 45,X/46,X,i(Xq)(n=26), 45,X/46,X,+mar(n=22), 46,X,i(Xq)(n=9), there was no significant differences statistically, except short stature and diabetes. Incidence of short stature was significantly higher in 45,X or 46,X,i(Xq) than 45,X/46,XX(78.6%, 88.9%, 20.0%), and significant difference existed in incidence of diabetes between 45,X and 46,X,i(Xq)(0%, 22.2%). Sixteen patients had a history of marriage, but only one had a history of spontaneous conception and delivery with mosaic 45,X[2]/51,XXXXXXX[1]/46,XX[47]. CONCLUSION: The karyotypes of Turner syndrome was very variable, and about 60% had mosaicism. Patients with 45,X/46,XX had a significant lower incidence of short stature than in 45,X or 46,X,i(Xq), and 46,X,i(Xq) had a significant higher incidence of diabetes than in 45,X. We identified a woman with mosaic 45,X/51,XXXXXXX/46,XX was fertile.
Cytogenetics* ; Female ; Fertility ; Fertilization ; Humans ; Incidence ; Karyotype ; Lymphocytes ; Marriage ; Medical Records ; Mosaicism ; Quinacrine ; Turner Syndrome*

Many reports represent that angiotensin II (ANG II) caused a dose dependent biphasic effects on fluid transport in the proximal tubule. However, respective roles of different signaling pathways in mediating these effects remain unsettled. The aim of the present study was to examine signaling pathways at high doses of ANG II on the Na+ uptake of primary cultured rabbit renal proximal tubule cells(PTCs) in hormonally defined serum-free medium. High concentrations of ANG II (> 10(-9) M) inhibited Na+ uptake and increased (Ca2+)i level in the PTCs. However, low concentrations of (< 10(-11) ANG II) stimulated Na+ uptake and did not affect (Ca2+)i level. 8-(N, N-diethylamino)-octyl-3,3,5- trimethoxybenzoate (TMB-8), ethylene glycol-bis(beta-amino ethyl ether)-N,N,N', N'-tetra acetic acid (EGTA), and nifedifine partially blocked the inhibitory effects of ANG II on Na+ uptake. When ANG II and bradykinin (BK) were treated together, Na+ uptake was further reduced (88.47 +/- 1.98% of that of ANG II, 81.85 +/- 1.84% of that of BK). In addition, W-7 and KN-62 blocked the ANG II-induced inhibition of Na+ uptake. Arachidonic acid reduced Na+ uptake in a dose-dependent manner. When ANG II and arachidonic acid were treated together, inhibitory effects on Na+ uptake significantly exhibited greater reduction than that of each group, respectively. When PTCs were treated by mepacrine (10(-6) M) and AACOCF, (10-5 M) for 1 hr before the addition of 10(-9) M ANG II, the inhibitory effect of ANG II was reversed. In addition, econazole (10(-6) M) blocked ANG II-induced inhibition of Na+ uptake. In conclusion, the (Ca2+)i (calcium-calmodulin-dependent kinase) and phospholipase A2 (PLA2) metabolites are involved in the inhibitory effects of ANG II on Na+ uptake in the PTCs.
Acetic Acid ; Angiotensin II* ; Angiotensins* ; Arachidonic Acid ; Bradykinin ; Econazole ; Ion Transport* ; Kidney ; Negotiating ; Phospholipases A2 ; Quinacrine

The present study was designed to assess the roles of PLA2 activation and arachidonic acid (AA) metabolites in hypoxia-induced renal cell injury. Hypoxia increased LDH release in a dose-dependent manner in rabbit renal cortical slices, and this increase was significant after 20-min hypoxia. The hypoxia-induced LDH release was prevented by amino acids, glycine and alanine, and extracellular acidosis (pH 6.0). Buffering intracellular Ca2+ by a chelator, but not omission of Ca2+ in the medium produced a significant reduction in hypoxia-induced LDH release. The effect of hypoxia was blocked by PLA2 inhibitors, mepacrine, butacaine, and dibucaine. A similar effect was observed by a 85-kD cPLA2 inhibitor AACOCF3. AA increased hypoxia-induced LDH release, and albumin, a fatty acid absorbent, prevented the LDH release, suggesting that free fatty acids are involved in hypoxia-induced cell injury. These results suggest that PLA2 activation and its metabolic products play important roles in pathogenesis of hypoxia-induced cell injury in rabbit renal cortical slices.
Acidosis ; Alanine ; Amino Acids ; Anoxia ; Arachidonic Acid ; Dibucaine ; Fatty Acids, Nonesterified ; Glycine ; Phospholipases A2* ; Phospholipases* ; Quinacrine

The role of phospholipase A2 (PLA2) in tumor cell growth was investigated using SK-N-MC human neuroblastoma cells. 4-Bromophenacyl bromide (BPB) and mepacrine (Mep), known PLA2 inhibitors, suppressed growth of the tumor cells in a dose-dependent manner without a significant cytotoxicity. Melittin (Mel), a PLA2 activator, enhanced the cell growth in a concentration-dependent fashion. The growth-enhancing effects of Mel were significantly reversed by the co-treatment with PLA2 inhibitors. In addition, Mel induced intracellular Ca2+ release from internal stores like as did serum, a known intracellular Ca2+ agonist in the tumor cells. Intracellular Ca2+ release induced by these agonists was significantly blocked by PLA2 inhibitors at growth-inhibitory concentrations. Arachidonic acid (AA), a product of the PLA2-catalyzed reaction, induced cell growth enhancement and intracellular Ca2+ release. These effects of AA were significantly blocked by BAPTA/AM, an intracellular Ca2+ chelator. Taken together, these results suggest that the modulation of PLA2 activity may be one of the regulatory mechanisms of cell growth in human neuroblastoma cells. Intracellular Ca2+ may act as a key mediator in the PLA2-induced growth regulation.
Arachidonic Acid ; Cell Proliferation* ; Humans* ; Melitten ; Negotiating* ; Neuroblastoma* ; Phospholipases A2 ; Phospholipases* ; Quinacrine

The present study was undertaken to examine the role of phospholipase A2 (PLA2) in oxidant-induced inhibition of phosphate transport in primary cultured rabbit renal proximal tubule cells. Uptakes of phosphate and glucose were dose-dependently inhibited by an oxidant t-butylhydroperoxide (tBHP), and the significant inhibition appeared at 0.025 mM of tBHP, whereas tBHP-induced alterations in lipid peroxidation and cell viability were seen at 0.5 mM. tBHP stimulated arachidonic acid (AA) release in a dose-dependent fashion. A PLA2 inhibitor mepacrine prevented tBHP-induced AA release, but it did not alter the inhibition of phosphate uptake and the decrease in cell viability induced by tBHP. tBHP-induced inhibition of phosphate transport was not affected by a PKC inhibitor, staurosporine. tBHP at 0.1 mM did not produce the inhibition of Na+-K+-ATPase activity in microsomal fraction, although it significantly inhibited at 1.0 mM. These results suggest that tBHP can inhibit phosphate uptake through a mechanism independent of PLA2 activation, irreversible cell injury, and lipid peroxidation in primary cultured rabbit renal proximal tubular cells.
Arachidonic Acid ; Cell Survival ; Glucose ; Lipid Peroxidation ; Phospholipases A2* ; Phospholipases* ; Quinacrine ; Staurosporine ; tert-Butylhydroperoxide

BACKGROUND: The underlying pathogenesis of fat embolism-induced acute lung injury (ALI) has not been elucidated. In the present study, the pathogenesis of fat embolism-induced ALI was probed in association with neutrophilic oxidative stress in oleic acid (OA)-induced ALI of S-D rats. METHODS: OA was injected intravenously to provoke ALI in experimental rats. Five hours later, indices of ALI were measured to confirm the role of the neutrophilic respiratory burst. The effect of an inhibition of phospholipase A2 (PLA2) was also evaluated. RESULTS: The accumulation of neutrophils in the lung due to OA caused increased neutrophilic oxidative stress in lung, which was ameliorated by mepacrine. What were the results from inhibition of PLA2. CONCLUSION: Excess neutrophilic oxidative stress contributes to OA-induced ALI, which is lessened by the inhibition of PLA2.
Acute Lung Injury ; Animals ; Embolism, Fat ; Lung ; Neutrophils ; Oleic Acid ; Oxidative Stress ; Phospholipases A2 ; Quinacrine ; Rats ; Respiratory Burst

*Asia, Southeastern ; *Chloroguanide ; *Chloroquine ; *Drug Resistance, Microbial ; *Drug Therapy ; *Malaria ; *Plasmodium falciparum ; *Pyrimethamine ; *Quinacrine ; *Quinine ; *Statistics ; *Adolescent ; *Child

Serum ferritin levels are increased in subjects at-risk for or with acute lung injury (ALI), and there are observations to suggest that increases in serum ferritin levels may help predict the development of ALI in at-risk individuals. To deepen our understanding of increases of serum ferritin and their relationship to the development of ALI, we measured serum ferritin levels before and after intestinal ischemia/reperfusion (I/R) injury in rats, and found that serum ferritin levels increased significantly following I/R. Increases in serum and lavage ferritin levels paralleled increases in lung inflammation (lavage leukocyte numbers and tissue myeloperoxidase activities) and lung leak (lavage protein levels). In contrast, pre-treatment of rats with mepacrine (60 mg/kg, i.p.), a phospholipase A2 inhibitor, attenuated not only I/R-induced serum and lavage ferritin increases, but also the development of ALI. These findings indicate that, besides of human subjects with ALI, serum ferritin levels increase early on also in an animal model of ALI. Therefore, serum and lavage ferritin can be a candidate for early biomarker of ALI.
Acute Lung Injury* ; Animals ; Ferritins* ; Humans ; Leukocyte Count ; Lung ; Models, Animal ; Peroxidase ; Phospholipases A2 ; Pneumonia ; Quinacrine ; Rats ; Therapeutic Irrigation