Biomedical subjects

H Zhao

Publications and source records attributed to H Zhao.

At least 325 records · Page 18Linked to original sources

PubMed1998

Salvage therapy after postoperative chemotherapy for primary brain tumors in infants and very young children.

BACKGROUND: A trend toward the use of prolonged postoperative chemotherapy, with radiotherapy deferred until relapse, has emerged for very young children with malignant brain tumors. This study was undertaken to determine the failure patterns among infants who receive such treatment and to evaluate their responses to first salvage therapy, particularly radiotherapy, after postoperative chemotherapy. METHODS: A retrospective cohort was assembled, which comprised all children younger than 36 months with biopsy-proven malignant brain tumors diagnosed during the years 1987-1993 at 3 pediatric oncology referral centers. Fifty-eight children were treated with postoperative chemotherapy without irradiation, 40 of whom experienced relapse of their malignancy. These patients' charts were reviewed for failure patterns. Thirty-five of these children received salvage therapy. Statistical and survival analysis with the Cox proportional hazards regression model was performed. RESULTS: Among the 40 children who experienced relapse, 30 of 31 (97%) with solitary disease at initial diagnosis relapsed at the primary site of disease. Thirty-seven of 39 infants (95%) developed relapse that included their primary site of disease. Sixty percent of relapses were asymptomatic and were detected by magnetic resonance imaging (MRI) surveillance rather than by clinical examination. Two-year progression free survival (PFS) after relapse for infants who received salvage therapy was 29% (standard error [SE] = 8%). For infants who received radiotherapy alone, the 2-year PFS was 21% (SE = 9%). PFS did not differ according to whether relapses were detected clinically or radiographically or treated by radiotherapy, chemotherapy, surgery, or multimodal therapy. CONCLUSIONS: Relapse of brain tumors in infants after prolonged postoperative chemotherapy is largely a problem of local disease control. Salvage is possible after prolonged postoperative chemotherapy, but it yields few instances of long term, progression free survival. No therapeutic modality is superior for salvage at relapse. A strategy of reserving radiotherapy for the salvage of infants whose brain tumors relapse during postoperative chemotherapy demonstrated only limited effectiveness.

Brain Neoplasms↗

PubMed1998

B-cell chronic lymphocytic leukemia cells express a functional inducible nitric oxide synthase displaying anti-apoptotic activity.

The expression of different isoforms of nitric oxide synthase (NOS) was investigated in B-cell chronic lymphocytic leukemia (B-CLL) to delineate a possible role for nitric oxide (NO) in the control of apoptosis of the tumoral cells. By reverse transcription-polymerase chain reaction (RT-PCR), all B-CLL cells were found to express spontaneously inducible NOS (iNOS) mRNA, whereas endothelial constitutive NOS (ecNOS) mRNA was undetectable. The iNOS protein was detected by immunofluorescence in the cytoplasm of permeabilized leukemic cells and identified by Western blotting, using different anti-iNOS antibodies, as a protein of 135 kD in B-CLL cytoplasmic extracts. B-CLL cell lysates also displayed basal NOS enzymatic activity, as measured by the conversion of 14C-labeled L-arginine into 14C-L-citrulline. Ligation of CD23, expressed on the vast majority of B-CLL cells, resulted in increased iNOS expression and activity. The NO released exerted an anti-apoptotic effect on B-CLL cells that was counteracted by NOS inhibitors and engagement of the APO-1/Fas pathway. Therefore, the existence of a functional iNOS in B-CLL cells will provide further insights into the mechanisms that control proliferation and apoptosis in these tumor cells.

Antigens, Neoplasm↗

PubMed1998

Identification of a consistent region of allelic loss on 1p32 in meningiomas: correlation with increased morbidity.

Meningioma is a common tumor of the central nervous system. Deletions of the short arm of chromosome 1 (1p) are the second most commonly observed chromosomal abnormality in these tumors. Here, we analyzed tumor and normal DNAs from 157 meningioma patients using PCR-based polymorphic loci. Loss of heterozygosity (LOH) for at least one informative marker on 1p was observed in 54 cases (34%), whereas LOH on 1q occurred in only 9 cases (8%). High-resolution deletion mapping defined a consensus region of deletion flanked distally by D1S2713 and proximally by D1S2134, which spans 1.5 cM within 1p32. LOH in this region has also been observed in several other malignancies, suggesting the presence of a tumor suppressor gene or genes that are important for several types of cancer. Statistical analysis revealed that 1p LOH was associated with chromosome 22 deletions and with abnormalities of the NF2 gene in meningioma. In addition, unlike other clinical and molecular characteristics, only 1p LOH was shown to be significantly associated with recurrence-free survival.

Alleles↗

PubMed1998

Absence of autophosphorylation site Y882 in the p185neu oncogene product correlates with a reduction of transforming potential.

Autophosphorylation of type I receptor tyrosine kinases (RTKs) comprises one step in the signaling events mediated by erbB receptors such as p185neu and EGFR. Previous analysis of p185neu has indicated that there are at least five tyrosine autophosphorylation sites, Y882, Y1028, Y1143, Y1226/7 and Y1253, of which Y882 might be important because of its location in the kinase activity domain. We have specifically analysed the effect of a Y882F (phenylalanine substituted for tyrosine at position 882) mutation in the enzymatic active domain. We also deleted the carboxyl terminal 122 amino acids which contained three other autophosphorylation sites (TAPstop) and combined mutants of that deletion with Y882F (Y882F/APstop). Both in vitro and in vivo transformation assays showed that substitution of tyrosine882 by phenylalanine significantly decreased the transforming potential of activated, oncogenic p185neu, although no significant difference in the total phosphotyrosine levels of the mutant proteins were observed. To analyse mitogenic signaling in response to ligand, the intracellular domains of p185neu and Y882F were fused with the extracellular domain of the EGF receptor. The proliferation of cells expressing these chimeric receptors was EGF-dependent, and cells expressing EGFR/Y882F chimeric receptors were less responsive to EGF stimulation than those expressing EGFR/neu receptors. In vitro kinase assays demonstrated that abolishing the autophosphorylation site Y882 diminished the enzymatic tyrosine kinase activity of p185neu. These studies, taken together with the phenotypic inhibition observed with cells expressing Y882F, suggest that the tyrosine882 residue may be important for p185neu-mediated transformation by affecting the enzymatic kinase function of the p185neu receptor.

Amino Acid Substitution↗

PubMed1998

Insulin receptor-mediated dissociation of Grb2 from Sos involves phosphorylation of Sos by kinase(s) other than extracellular signal-regulated kinase.

The Ras signaling pathway is rapidly activated and then down-regulated following stimulation of multiple cell-surface receptors including the insulin receptor (IR). Much recent attention has focused on elucidating the mechanism of Ras inactivation following IR engagement. Previous data suggest that IR-mediated serine/threonine phosphorylation of the Ras guanine nucleotide exchange factor Sos correlates with its decreased affinity for the adapter protein Grb2. This phosphorylation-induced disassembly of the Grb2.Sos complex is thought to be responsible, at least in part, for diminishing Ras activity in Chinese hamster ovary cells. In this report, we confirm the causal relationship between Sos phosphorylation and Grb2/Sos dissociation. We then examine several putative phosphorylation sites of Sos that could potentially regulate this event. Since a number of reports suggest that extracellular signal-regulated kinase (ERK) phosphorylates Sos, we generated a Sos mutant lacking all seven canonical phosphorylation sites for ERK. This mutant is a poor substrate of activated ERK in vitro and fails to undergo a change in its electrophoretic mobility following IR stimulation. It is, however, phosphorylated after IR stimulation when expressed in Chinese hamster ovary cells. Interestingly, the mutant protein still dissociates from Grb2 following insulin stimulation, suggesting that ERK is not the kinase responsible for regulating the stability of the Grb2.Sos complex.

Adaptor Proteins, Signal Transducing↗

PubMed1998

Structure of the catalytic domain of avian sarcoma virus integrase with a bound HIV-1 integrase-targeted inhibitor.

The x-ray structures of an inhibitor complex of the catalytic core domain of avian sarcoma virus integrase (ASV IN) were solved at 1.9- to 2.0-A resolution at two pH values, with and without Mn2+ cations. This inhibitor (Y-3), originally identified in a screen for inhibitors of the catalytic activity of HIV type 1 integrase (HIV-1 IN), was found in the present study to be active against ASV IN as well as HIV-1 IN. The Y-3 molecule is located in close proximity to the enzyme active site, interacts with the flexible loop, alters loop conformation, and affects the conformations of active site residues. As crystallized, a Y-3 molecule stacks against its symmetry-related mate. Preincubation of IN with metal cations does not prevent inhibition, and Y-3 binding does not prevent binding of divalent cations to IN. Three compounds chemically related to Y-3 also were investigated, but no binding was observed in the crystals. Our results identify the structural elements of the inhibitor that likely determine its binding properties.

Avian Sarcoma Viruses↗

PubMed1998

Alpha 2-adrenergic receptor activation inhibits calcitonin gene-related peptide expression in cultured dorsal root ganglia neurons.

Calcitonin gene-related peptide (CGRP), a potent vasodilator, is produced in dorsal root ganglia (DRG) neurons which extend nerves peripherally to blood vessels and centrally to the spinal cord. We previously reported that neuronal CGRP expression is significantly reduced in the spontaneously hypertensive rat (SHR) which could contribute to the elevated BP. Other studies suggest that the enhanced activity of the sympathetic nervous system in the SHR may mediate, at least in part, this reduction in neuronal CGRP expression via activation of alpha 2-adrenoreceptors (alpha 2-AR) on DRG neurons. To test this hypothesis in vitro we employed primary cultures of adult rat DRG neurons. Neuronal cultures were initially exposed (24 h) to either the alpha 2-AR agonist UK 14,304 (10(-6) M) or vehicle; however, no changes in CGRP mRNA content or immunoreactive CGRP (iCGRP) release were observed. Using the rationale that in vivo DRG neurons receive a continuous supply of target tissue derived nerve growth factor (NGF), which stimulates CGRP synthesis, the cultured neurons were treated (24 h) with either vehicle, NGF (25 ng/ml) alone, or NGF plus UK. NGF treatment increased CGRP mRNA accumulation 5.5 +/- 0.9-fold (p < 0.001) and iCGRP release 2.9 +/- 0.4-fold (p < 0.001) over control levels. The stimulatory effects of NGF were markedly attenuated, but not abolished, by UK (NGF + UK vs. control, CGRP mRNA, 2.9 +/- 0.4-fold, p < 0.05; iCGRP, 1.7 +/- 0.2-fold, p < 0.05). These values were also significant (p < 0.05) when compared to NGF treatment alone. Experiments performed using the alpha 2-antagonist yohimbine confirmed that the effects of UK were mediated by the alpha 2-AR. These results, therefore, demonstrate that alpha 2-AR activation attenuates the stimulatory effects of NGF on CGRP expression in DRG neurons.

Adrenergic alpha-Agonists↗

PubMed1998

Random-priming in vitro recombination: an effective tool for directed evolution.

A simple and efficient method for in vitro mutagenesis and recombination of polynucleotide sequences is reported. The method involves priming template polynucleotide(s) with random-sequence primers and extending to generate a pool of short DNA fragments which contain a controllable level of point mutations. The fragments are reassembled during cycles of denaturation, annealing and further enzyme-catalyzed DNA polymerization to produce a library of full-length sequences. Screening or selecting the expressed gene products leads to new variants with improved functions, as demonstrated by the recombination of genes encoding different thermostable subtilisins in order to obtain enzymes more stable than either parent.

Bacillus subtilis↗

PubMed1998

Functional expression of a mammalian odorant receptor.

Candidate mammalian odorant receptors were first cloned some 6 years ago. The physiological function of these receptors in initiating transduction in olfactory receptor neurons remains to be established. Here, a recombinant adenovirus was used to drive expression of a particular receptor gene in an increased number of sensory neurons in the rat olfactory epithelium. Electrophysiological recording showed that increased expression of a single gene led to greater sensitivity to a small subset of odorants.

Adenoviridae↗

PubMed1998

Synaptic transmission deficits in Caenorhabditis elegans synaptobrevin mutants.

Synaptobrevins are vesicle-associated proteins implicated in neurotransmitter release by both biochemical studies and perturbation experiments that use botulinum toxins. To test these models in vivo, we have isolated and characterized the first synaptobrevin mutants in metazoans and show that neurotransmission is severely disrupted in mutant animals. Mutants lacking snb-1 die just after completing embryogenesis. The dying animals retain some capability for movement, although they are extremely uncoordinated and incapable of feeding. We also have isolated and characterized several hypomorphic snb-1 mutants. Although fully viable, these mutants exhibit a variety of behavioral abnormalities that are consistent with a general defect in the efficacy of synaptic transmission. The viable mutants are resistant to the acetylcholinesterase inhibitor aldicarb, indicating that cholinergic transmission is impaired. Extracellular recordings from pharyngeal muscle also demonstrate severe defects in synaptic transmission in the mutants. The molecular lesions in the hypomorphic alleles reside on the hydrophobic face of a proposed amphipathic-helical region implicated biochemically in interacting with the t-SNAREs syntaxin and SNAP-25. Finally, we demonstrate that double mutants lacking both the v-SNAREs synaptotagmin and snb-1 are phenotypically similar to snb-1 mutants and less severe than syntaxin mutants. Our work demonstrates that synaptobrevin is essential for viability and is required for functional synaptic transmission. However, our analysis also suggests that transmitter release is not completely eliminated by removal of either one or both v-SNAREs.

Animals↗

PubMed1998

Differential effects of d, l-sotalol and d-sotalol on isoproterenol-increased delayed rectifier outward potassium current in guinea pig single ventricular myocytes.

The aim of this study was to compare the effects of d, l-sotalol and d-Sotalol on the delayed rectifier K+ outward current in the presence of isoproterenol at different concentrations. Time-dependent delayed rectifier K+ outward currents were measured in isolated guinea pig single myocytes using the whole-cell configuration of the patch-clamp technique. Currents were measured in response to 300 ms depolarizing pulses from a holding potential of -40 mV in three experimental protocols [control, isoproterenol (10(-9) mol/L-10(-6) mol/L), and isoproterenol (10(-9) mol/L-10(-6) mol/L) plus either d, l-Sotalol (10(-4) mol/L) or d-Sotalol (10(-4) mol/L)]. IK tail currents were measured upon repolarization to -40 mV. It was found that IK was significantly amplified in the presence of isoproterenol (10(-9) mol/L-10(-6) mol/L) plus d-Sotalol. At 10(-8) mol/L isoproterenol, IK was increased by 92.7% +/- 17.1% (P < 0.05) and 54.3% +/- 13.4% after d-Sotalol addition (P < 0.05). In contrast, d, l-Sotalol completely conteracted the increase of Ik by isoproterenol (< 10(-8) mol/L), and compared to control, IK was decreased by 35.6% +/- 8.1% at 10(-8) mol/L isoproterenol plus d, l-Sotalol (P < 0.05). It is concluded that the beta-adrenergic blocking property of d, l-Sotalol but not that of d-Sotalol maintains the delayed rectifier K+ outward current blockade in the presence of isoproterenol in guinea pig myocytes. This might contribute to a superior antiarrhythmic efficacy as compared to d-Sotalol.

Adrenergic beta-Agonists↗

PubMed1998

1H MR spectroscopy of the basal ganglia in childhood: a semiquantitative analysis.

Proton MR spectra of the basal ganglia were obtained from 28 patients, 24 male and 14 female, median age 16.3 months (5 weeks to 31 years). They included 17 patients with normal MRI of the basal ganglia without metabolic disturbance (control group) and 11 patients with various metabolic diseases: one case each of high serum sodium and high serum osmolarity, cobalamin C deficiency, Leigh disease, Galloway-Mowat syndrome, Pelizaeus-Merzbacher disease, hemolytic-uremic syndrome and Wilson disease and two cases of Alagille syndrome and methylmalonic acidemia with abnormal MRI of the basal ganglia or blood or urine analysis (abnormal group). The MR spectrum was measured by using STEAM. The MR-visible water content of the region of interest was obtained. Levels of myoinositol, choline, creatine and N-acetylaspartate were measured using a semiquantitative approach, with absolute reference calibration. In the control group, there was a gradual drop of water content over the first year of life; N-acetylaspartate, creatine and myoinositol levels showed no significant change with age, in contrast to the occipital, parietal and cerebellar regions. Choline showed a gradual decrease for the first 2 years of life and then remained fairly constant. In the abnormal group the water content was not significantly different. N-Acetylaspartate was decreased in patients with high serum sodium and high serum osmolarity, cobalamin C deficiency, Leigh disease and one case of methylmalonic acidemia. Decreased creatine was also found in Leigh disease, and decreased choline in Galloway-Mowat syndrome and Wilson disease. Myoinositol was elevated in the patient with abnormally high serum sodium, and decreased in the hemolytic-uremic syndrome.

Adolescent↗

PubMed1998

A global survey of haplotype frequencies and linkage disequilibrium at the DRD2 locus.

A four-site haplotype system at the dopamine D2 receptor locus (DRD2) has been studied in a global sample of 28 distinct populations. The haplotype system spans about 25 kb, encompassing the coding region of the gene. The four individual markers include three TaqI restriction site polymorphisms (RSPs) -- TaqI "A", "B", and "D" sites -- and one dinucleotide short tandem repeat polymorphism (STRP). All four of the marker systems are polymorphic in all regions of the world and in most individual populations. The haplotype system shows the highest average heterozygosity in Africa, a slightly lower average heterozygosity in Europe, and the lowest average heterozygosities in East Asia and the Americas. Across all populations, 20 of the 48 possible haplotypes reached a frequency of at least 5% in at least one population sample. However, no single population had more than six haplotypes reaching that frequency. In general, African populations had more haplotypes present in each population and more haplotypes occurring at a frequency of at least 5% in that population. Permutation tests for significance of overall disequilibrium (all sites considered simultaneously) were highly significant (P<0.001) in all 28 populations. Except for three African samples, the pairwise disequilibrium between the outermost RSP markers, TaqI "B" and "A", was highly significant with D' values greater than 0.8; in two of those exceptions the RSP marker was not polymorphic. Except for those same two African populations, the 16-repeat allele at the STRP also showed highly significant disequilibrium with the TaqI "B" site in all populations, with D' values usually greater than 0.7. Only four haplotypes account for more than 70% of all chromosomes in virtually all non-African populations, and two of those haplotypes account for more than 70% of all chromosomes in most East Asian and Amerindian populations. A new measure of the amount of overall disequilibrium shows least disequilibrium in African populations, somewhat more in European populations, and the greatest amount in East Asian and Amerindian populations. This pattern seems best explained by random genetic drift with low levels of recombination, a low mutation rate at the STRP, and essentially no recurrent mutation at the RSP sites, all in conjunction with an "Out of Africa" model for recent human evolution.

Alleles↗

PubMed1998

Periodic limb movement in sleep in children with Williams syndrome.

OBJECTIVE: Williams syndrome (WS) is associated with neurobehavioral abnormalities that include irritability and attention-deficit/hyperactivity disorder. Parents often report children having difficulties initiating and maintaining sleep because of restlessness and arousals. Therefore we evaluated a group of children with WS for the presence of a movement arousal sleep disorder. METHODS: Twenty-eight families of children with WS participated in a telephone survey aimed to screen for a movement arousal disorder. Of the 16 children identified as having such a disorder, 7 (mean age, 3.9 +/- 2.2 years) underwent polysomnography. Their studies were compared with those of 10 matched control subjects (mean age, 5.3 +/- 2.0 years). RESULTS: The 7 subjects with WS who were screened by the survey had sleep latency, total sleep time, arousals, and awakenings that were similar to those of control subjects. However, they presented with a disorder of periodic limb movement in sleep (PLMS). The PLMS index in the subjects with WS was 14.9 +/- 6.2 versus 2.8 +/- 1.9 in control subjects (P < .0001). In addition, arousal and awakening in subjects with WS were strongly associated with PLMS. Moreover, children with WS spend more time awake during sleep periods than control subjects (10.0% +/- 7.0% vs 4.4% +/- 4.7%; P < .05). Five children were treated with clonazepam, and in 4 a significant clinical response was noted. CONCLUSION: We report an association between WS and PLMS. Clonazepam may reduce the clinical symptoms of PLMS in some of these children.

Anticonvulsants↗

PubMed1998

Short interpregnancy interval and the risk of disabling cerebral palsy in a low birth weight population.

OBJECTIVE: The objective of this study was to investigate the relation of short interpregnancy interval and cerebral palsy (CP) in a low birth weight population in whom neonatal brain injury was systematically ascertained in the newborn period. STUDY DESIGN: We used data from a prospective cohort study of 1105 infants born < or = 2000 gm, designed to study the cause and consequences of neonatal brain injury. Of the 777 children with data on brain injury and CP, 382 were born to multiparous women, and 375 had information available to calculate interpregnancy interval, defined as the number of days from the end of the last pregnancy to conception of the index pregnancy. RESULTS: In the presence of the strong explanatory power of neonatal brain injury, short interpregnancy interval maintains an independent risk for disabling CP. CONCLUSION: In this cohort of low birth weight infants, short interpregnancy interval appears to represent a significant risk for the development of disabling CP.

Birth Intervals↗

PubMed1998

Structure of a snake venom phospholipase A2 modified by p-bromo-phenacyl-bromide.

The crystal structure of acidic phospholipase A2 (APLA2) from Agkistrodon halys pallas covalently modified by p-bromo-phenacyl-bromide (pBPB) was determined to a resolution of 2.0 A by an isomorphous difference Fourier method with the native APLA2 structure as an initial model and refined to a crystallographic R factor of 15.3%. The modified APLA2 structure is remarkably similar to that of the native one. Least-squares superposition of C alpha atoms of native and modified APLA2 results in a root-mean-square coordinate deviation of 0.243 A. The p-bromo-phenacyl group near the active site occupies a position similar to that in pBPB modified bovine pancreatic PLA2. The inhibitor covalently bound to the NDI atom of His48 fits well in the hydrophobic channel, forming extensive hydrophobic interactions with the surrounding residues, especially with the side chains of Phe5 and Cys45 and the main chain of Gly30. However, the inhibitor does not change the conformation of these residues except that Trp31 at the entrance of the hydrophobic channel moves slightly toward the inhibitor. Compared with native APLA2, the Ca2+-binding loop shows a little conformational change and a cation, probably Na+, occupies in the position of Ca2+. The binding of pBPB to APLA2 induce no other significant conformational changes in the enzyme molecule elsewhere.

Acetophenones↗

PubMed1998

Parafusin is a membrane and vesicle associated protein that cycles at exocytosis.

In the unicellular eukaryote Paramecium tetraurelia, stimulation of exocytosis leads to Ca2+ activation of an alpha Glc-1-phosphodiesterase that dephosphoglucosylates the phosphoglycoprotein parafusin (PFUS). This process fails in exo mutant nd9 and also in the absence of Ca2+ influx upon stimulation suggesting that PFUS dephosphoglucosylation may be causally related to exocytosis. To further corroborate the hypothesis that PFUS is involved in the molecular events in exocytosis, we used laser confocal scanning microscopy and a PFUS specific peptide antibody to perform localization studies of PFUS in wild type (wt) and mutant Paramecium. In unstimulated wt cells, PFUS was associated both with the exocytic site of the cell membrane and with the membrane of the dense core secretory vesicles. Localization at these two sites was shown to be independent of each other since the exocytosis mutant (exo-) tam8, in which docking of its vesicles is blocked, still showed cell membrane staining. Immunofluorescence and immunoblotting of isolated intact secretory vesicles also revealed PFUS association. Upon stimulation of exocytosis, PFUS dissociated from both the dense core secretory vesicles and the cell membrane in a Ca(2+)-dependent manner. During recovery of exocytic capacity, PFUS reassociated with the newly formed secretory vesicles in the cytoplasm prior to their docking at the exocytic sites. Immunoblot analysis of PFUS during this time showed no changes in levels of the protein. Stimulation of exocytosis in wt in Mg2+ buffer or in the exo- temperature sensitive mutant (nd9) at the non-permissive temperature did not lead to dissociation of the PFUS. We conclude that PFUS is a novel critical component whose cycling probably participates in the molecular exocytic fusion machinery in these cells.

Animals↗

PubMed1998

Raman spectroscopic study of microcosmic and photosensitive damage on the liposomes of the mixed phospholipids sensitized by hypocrellin and its derivatives.

Using Raman spectroscopy, we studied and compared the characteristics of microcosmic and photosensitive damage of the liposomes of mixed DPPE and DPPC sensitized by hypocrellin and its derivatives at the molecular level. After photosensitive damage, the structure of the liposomes of mixed phospholipids changed considerably. The trans conformation decreased and gauche conformation increased. The longitudinal order parameter in chains and the lateral order parameter between chains decreased clearly. The results suggested that the hydrocarbon chains of DPPE and DPPC were broken after the photodamage sensitized by hypocrellin B (HB) and 5-Br-hypocrellin B (5-Br-HB). Photosensitive damage on the liposomes sensitized by 5-Br-HB is stronger than that by hypocrellin A (HA) and HB, that is, 5-Br-HB > HB > HA. The results elucidated the sites of interaction or binding to HA, HB and 5-Br-HB in the liposomes and these changed with the use of drugs.

1,2-Dipalmitoylphosphatidylcholine↗