Biomedical subjects

H H Kim

Publications and source records attributed to H H Kim.

At least 37 records · Page 2Linked to original sources

PubMed2001

Proapoptotic effects of tau cleavage product generated by caspase-3.

Using an in vitro translation assay to screen a human brain cDNA library, we isolated the microtubule-associated protein Tau and determined it to be a caspase-3 substrate whose C-terminal cleavage occurred during neuronal apoptosis. DeltaTau, the 50-kDa cleavage product, was detected by Western blot in apoptotic cortical cells probed with anti-PHF-1 and anti-Tau-5 antibodies, but not anti-T-46 antibody which recognizes the C-terminus. Overexpression of DeltaTau in SK-N-BE2(C) cells significantly increased the incidence of cell death. Staurosporine-induced Tau cleavage was blocked by 20 microM z-Asp-Glu-Val-Asp-chloromethylketone, a caspase-3 inhibitor, and in vitro, Tau was selectively cleaved by caspase-3 or calpain, a calcium-activated protease, but not by caspases-1, -8, or -9. (D421E)-Tau, a mutant in which Asp421 was replaced with a Glu, was resistant to cleavage by caspase-3 and tended to suppress staurosporine-induced cell death more efficiently than did wild-type Tau in both transient and stable expression systems. Finally, the incidence of DeltaTau-induced cell death was augmented by expression of Abeta precursor protein (APP) or Swedish APP mutant. Taken together, these results suggest that the caspase-3 cleavage product of Tau may contribute to the progression of neuronal cell death in Alzheimer's disease.

Amyloid beta-Protein Precursor↗

PubMed2001

Blockade of the p38 mitogen-activated protein kinase pathway inhibits inducible nitric oxide synthase and interleukin-6 expression in MC3T3E-1 osteoblasts.

Treatment of MC3T3E-1 osteoblast cultures with combined interferon- gamma(IFN- gamma), lipopolysaccharide (LPS) and tumor necrosis factor- alpha(TNF- alpha) induces expressions of inducible nitric oxide synthase (iNOS) and interleukin-6 (IL-6), resulting in sustained releases of large amounts of nitric oxide and IL-6. However IFN- gamma, LPS and TNF- alpha individually induces non-detectable or small amounts of NO and IL-6 in MC3T3E-1 osteoblasts. The role of mitogen-activated protein kinase (MAPK) activation in the early intracellular signal transduction involved in iNOS and IL-6 transcription in the combined agents-stimulated osteoblasts has been investigated. The p38 MAPK pathway is specifically involved in the combined agents-induced NO and IL-6 release, since NO and IL-6 release in the presence of a specific inhibitor of p38 MAPK, 4-(4-fluorophenyl)-2-(4-metylsulfinylphenyl)-5-(4-pyridyl)imidazole (SB203580), are significantly diminished. In contrast, PD98059, a specific inhibitor of MEK1, had no effect on NO and IL-6 release. Northern blot analysis showed that the p38 MAPK pathway controlled iNOS and IL-6 transcription levels. These data suggest that p38 MAPK plays an important role in the secretion of NO and IL-6 in LPS/IFN- gamma or TNF- alpha /IFN- gamma -treated MC3T3E-1 osteoblasts.

Animals↗

PubMed2001

Optical peroxide biosensor using the electrically controlled-release technique.

An optical biosensor using an electrically controlled-release system was developed for the measurement of peroxide concentration. The electrically controlled-release system consisted of a current-supplying system and a polymer complex by hydrogen bonding between the carboxylic and oxazoline group. The polymer complex was formed below pH 5.0 and was degraded above pH 5.4. The local pH change near the surface of the polymer complex could be controlled by applying the electric current to release an enzyme reaction reagent, 4-hydroxyphenylacetic acid (HPA), in the polymer complex. The releasing rate of HPA was proportional to the electric current applied to the polymer complex. The model of the controlled-release system was proposed to predict the degradation velocity of the polymer complex, which is equivalent to the releasing rate of HPA. The released HPA and analyte, peroxide, flowed into the reactor with the immobilized enzyme and then reacted with the enzyme. The peroxide concentration was measured based on the fluorescence detection of enzyme reaction product, 6,6'-dihydroxy (1,1'-biphenyl) 3,3'-diacetic acid (DBDA). The proposed biosensor had the linear analytical range of 0.025 approximately 1.0 mM with a response time of 20 min, good repeatability, and reproducibility.

Biosensing Techniques↗

PubMed2001

The p38 mitogen-activated protein kinase pathway regulates interleukin-6 synthesis in response to tumor necrosis factor in osteoblasts.

The induction of interleukin-6 (IL-6), using a proinflammatory cytokine (tumor necrosis factor-alpha), was studied in a human osteoblast cell line (MG-63) in relation to p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB transcription factor. When added to MG-63 cells, tumor necrosis factor-alpha (TNF-alpha) had a stimulatory effect on the production of IL-6, and this elevation was significantly reduced by SB203580, a specific p38 MAPK inhibitor. In addition, the stimulation of IL-6 release was also reduced by pyrrolidine dithiocarbamate (PDTC) or NF-kappaB SN50, which has been reported to be a potent NF-kappaB inhibitor. Both the NF-kappaB inhibitors in the presence of SB203580 had a more inhibitory effect on IL-6 release. In this study, TNF-alpha stimulated NF-kappaB binding affinity as well as p38 MAP kinase activation, leading to the release of IL-6. However, the specific inhibitor of p38 MAPK, SB203580, had no effect on TNF-alpha-induced NF-kappaB activation and both NF-kappaB inhibitors failed to reduce the p38 MAPK activation in the TNF-alpha-stimulated osteoblasts. In addition, inhibition of p38 MAPK partially, but significantly, impaired TNF-alpha-regulated release of osteocalcin, an important differentiation marker in osteoblasts. These results strongly suggest that both p38 MAPK and NF-kappaB are required in TNF-alpha-induced IL-6 synthesis and that these two TNF-alpha-activated pathways can be primarily dissociated. Furthermore, p38 MAPK may play a significant role in differentiation in MG-63 cells.

Antioxidants↗

PubMed2001

Cutaneous bronchogenic cyst of the abdominal wall.

We report a case of the unusual location of a cutaneous bronchogenic cyst on the abdominal wall. The patient was a 9-month-old boy who had presented with a 1.5 cm-sized polypoid mass, present since birth. Pathological examination of the excised mass revealed multiple small cystic structures surrounded by the fibroadipose tissue. The lining epithelium consisted of either pseudostratified ciliated columnar epithelium with goblet cells or a single layer of ciliated or non-ciliated cuboidal to columnar cells. The cystic walls contained a well-developed smooth muscle bundle, mucous glands and hyaline cartilage plate. This lesion was adherent to the peritoneum, but there was no direct communication with the abdominal cavity. Cutaneous bronchogenic cyst located in the abdominal wall has not been described in the English literature. The present case suggests a possible origin from a downward migration, from the sequestered bud of a tracheobronchial tree primordium along the midline of the body surface, during embryonic development.

Abdominal Muscles↗

PubMed2001

Molecular identification of Oxalobacter formigenes with the polymerase chain reaction in fresh or frozen fecal samples.

OBJECTIVE: To develop a simple and rapid polymerase chain reaction (PCR) method for detecting Oxalobacter formigenes (which degrades oxalate in the gut) in fecal specimens from healthy volunteers and patients with urolithiasis, and to determine whether O. formigenes can be detected in frozen or fresh fecal samples. MATERIALS AND METHODS: Whole bacterial DNA was isolated directly from fresh and frozen fecal samples obtained from 30 healthy volunteers free from urolithiasis and from fresh fecal samples obtained from 38 patients with urolithiasis. Genus-specific oligonucleotide sequences were designed, corresponding to homologous regions residing in the oxc gene that encodes for oxalyl-coenzyme A decarboxylase. A PCR-based assay was used on both fresh and frozen fecal samples, and the nucleotide sequences analysed to confirm oxc. RESULTS: A PCR product of 416 bp encoding the oxc gene was detected in 23 (77%) of 30 healthy volunteers free from urolithiasis and in 14 (37%) of 38 patients with urolithiasis. In healthy volunteers, the results of PCR for the fresh and the frozen samples were identical in each subject. The nucleotide sequence analysis showed that the sequence of the amplified product was compatible with that of oxc. CONCLUSION: O. formigenes can be identified easily and efficiently using this PCR-based detection system. The colonization rate of O. formigenes in patients with urolithiasis was significantly lower than that in healthy volunteers known to be free from urolithiasis. Furthermore, as the PCR-based assay results in the frozen fecal samples were identical to those from fresh samples in each subject, immediate processing of fecal samples may not be necessary to detect O. formigenes in the clinical setting.

Adult↗

PubMed2001

New experiences with absolute ethanol sclerotherapy in the management of a complex form of congenital venous malformation.

BACKGROUND: Complex forms of congenital venous malformation have defied proper classification and confounded therapy. Through a newly designed multidisciplinary approach, these venous defects were properly diagnosed and classified according to the Hamburg classification. Absolute ethanol was adopted as a new scleroagent for this complex form of venous defects to improve overall treatment results with acceptable morbidity and recurrence rates. PATIENTS AND METHODS: Among 318 patients aged 2 months to 60 years (130 men: mean age, 24.6 years; 188 women: mean age, 24.5 years), 143 patients were confirmed as having venous defects predominantly (45%). We conducted diagnostic evaluation with magnetic resonance imaging, whole body blood pool scan, duplex scans, transarterial microalbumin lung scans, air plethysmography, bone x-ray film, and angiography. Thirty of 143 patients were indicated for the absolute ethanol sclerotherapy for the complex form of venous defects, and they completed 98 sessions of multistage therapy with direct puncture technique. Follow-up assessment (minimum, 6 months; average, 10.2 months) was made as early results after completion of therapy. RESULTS: The immediate success rate at the completion of treatment through 98 sessions on 30 patients was 92% (90/98). The reason for the failure of 8% (8/98 sessions) was mainly due to the lesion's inaccessibility to the nidus to deliver the alcohol safely. On follow-up assessment available on 28 of 30 patients, overall improvement of the lesions with good to fair response on clinical assessment was obtained in 27 (96%) of 28 patients. Similar good to fair responses were obtained on whole body blood pool scan assessment (14 [93%] of 15 patients) and also on magnetic resonance imaging assessment (12 [93%] of 13 patients). Various major to minor acute complications developed during the procedure in eight (26.7%) of 30 patients through 16 (16.3%) of 98 sessions of the therapy: ischemic bullae, tissue fibrosis, deep venous thrombosis, pulmonary embolism, peripheral nerve palsy, and temporary pulmonary hypertension. All 24 incidences of complication were successfully managed with full recovery except one case of permanent peroneal nerve palsy that was present during 18 months of follow-up. No single recurrence has been detected to date. CONCLUSION: Absolute ethanol sclerotherapy alone can deliver excellent results in complex forms of venous malformations with considerable but acceptable morbidity and may be able to reduce the morbidity involved with the conventional surgical therapy alone on complex forms of venous malformation. No recurrence or deterioration of the therapy results was observed during the follow-up period (average, 10.2 months) after the completion of multistaged therapy.

Adolescent↗

PubMed2001

Hypoxia induces apoptosis by caspase activation accompanying cytochrome C release from mitochondria in MC3T3E1 osteoblasts. p38 MAPK is related in hypoxia-induced apoptosis.

The aim of this study is to elucidate the possible mechanism of apoptosis in response to hypoxia in MC3T3E1 osteoblasts. MC3T3E1 osteoblasts under hypoxic conditions (2% oxygen) resulted in apoptosis in a time-dependent manner estimated by DNA fragmentation assay and nuclear morphologystained with fluorescent dye, Hoechst 33258. Pretreatment with Z-VAD-FMK, a pan-caspase inhibitor, or Z-DEVD-CHO, a specific caspase-3 inhibitor, completely suppressed the DNA ladder in response to hypoxia. An increase in caspase-3-like protease (DEVDase) activity was observed during apoptosis, but no caspase- activity (YVADase) was detected. To confirm what caspases are involved in apoptosis, western blot analysis was performed using anti-caspase-3 or -6 antibody. The 10-kDa protein, corresponding to the active products of caspase-3 and the 10-kDA protein of the active protein of caspase-6 were generated in hypoxia-challenged cells in which processing of the full length form of caspase-3 and -6 was evident. With a time course similar to this caspase-3 and -6 activation was evident, hypoxic stress caused the cleavage of lamin A, typical of caspase-6 activity. In addition, the stress elicited the release of cytochrome c into the cytosol during apoptosis. Furthermore, we have observed that pre-treatment with SB203580, a selective p38 MAP kinase (p38 MAPK) inhibitor, attenuated the hypoxia-induced apoptosis. The addition of SB203580 suppressed caspase-3 and -6-like protease activity by hypoxia up to 50%. In contrast, PD98059 had no effect on the hypoxia-induced apoptosis. To confirm the involvement of MAP kinase, JNK/SAPK, ERK, or p38 kinase assay was performed. Although p38 MAPK was activated in response to hypoxic treatment, the other MAP kinase -JNK/SAPK or ERK- was not or modestly activated. These results suggest that p38 MAPK positively regulates hypoxia-induced apoptosis in MC3T3E1 osteoblasts.

3T3 Cells↗

PubMed2001

Cyclic-AMP inhibits nitric oxide-induced apoptosis in human osteoblast: the regulation of caspase-3, -6, -9 and the release of cytochrome c in nitric oxide-induced apoptosis by cAMP.

Nitric oxide (NO) induces apoptotic cell death and cAMP has a significantly protective effect on NO-induced cytotoxicity in human osteoblasts, MG-63 cells. Treatment with S-nitroso-N-acetylpenicillamine (SNAP) (0.6 mM) resulted in genomic DNA fragmentation, characteristic of apoptosis. However, concomitant incubation of the cells with either DBcAMP or forskolin markedly inhibited SNAP-induced apoptosis in a dose-dependent manner. Furthermore, pretreatment of MG-63 cells with H-89 or KT5720, which is known to inhibit cAMP-dependent protein kinase (PKA), abolished the protective effect of DBcAMP and forskolin on SNAP-induced apoptosis. In this study, we explored the involvement of caspases in the regulatory mechanism of SNAP-induced apoptosis by cAMP. Our data show that DBcAMP or forskolin blocked SNAP-induced caspase-3-like cysteine protease activation and that H-89, a PKA inhibitor, reversed the cAMP-induced regulatory effect of caspase-3 like protease. Consistent with the results, cAMP inhibited the proteolytic cleavage of caspase-3, -6, -9 and cytochrome c release to cytoplasm. The inhibition of caspase-3 activation did not block SNAP-induced cytochrome c release to cytoplasm, suggesting that caspase-3 activation may occur downstream of cytochrome c release. In summary, these findings show that the exposure of MG-63 cells to cAMP analogs renders them more resistant to NO-induced damage and suggests the presence of regulatory mechanisms of the cell death pathway by cAMP in which caspase-3, -6, and -9 and cytochrome c release serves to mediate NO-induced apoptosis.

Apoptosis↗

PubMed2001

CT differentiation of pneumonic-type bronchioloalveolar cell carcinoma and infectious pneumonia.

The objective was to analyse the potential of CT to distinguish pneumonic-type bronchioloalveolar cell carcinoma (BAC) from infectious pneumonia. The study consisted of 21 patients with pathologically proven BAC and 30 patients with infectious pneumonia. Both groups of patients had patchy or diffuse consolidation of more than half the area of a lobe or lobes on CT. CT findings in these two groups were compared with regard to morphological appearance, including CT angiogram, air bronchogram, mucous bronchogram, contrast enhancement pattern, pseudocavitation, cavity with air-fluid level, location, satellite lesion, ground-glass opacity and bulging of the interlobar fissure. Air-filled bronchi were morphologically analysed as dilatation, stretching, sweeping, widening of the branching angle, squeezing and crowding. Lymphadenopathy and pleural effusion were also analysed. CT findings favouring the diagnosis of BAC included an air-filled bronchus within the consolidation with stretching, squeezing, sweeping, widening of the branching angle and bulging of the interlobar fissure (p<0.05). It is concluded that CT may be helpful in differentiating pneumonic-type BAC from infectious pneumonia if the air-filled bronchus within the consolidation shows stretching, squeezing, widening of the branching angle or bulging of the interlobar fissure.

Adenocarcinoma, Bronchiolo-Alveolar↗

PubMed2001

The value of cystoscopy as an initial diagnostic modality for asymptomatic microscopic hematuria.

For the patients who visit outpatient clinics due to asymptomatic microscopic hematuria, cystoscopy has been looked upon as rather invasive compared to other diagnostic methods. We tried to elucidate the actual diagnostic value of cystoscopy in the initial evaluation of asymptomatic microscopic hematuria. We reviewed the results of cystoscopic examinations in 213 patients who visited our hospital due to asymptomatic microscopic hematuria. No definite lesion that could explain the microscopic hematuria was detected by means of IVP, urine cytology, and other nephrologic evaluations for all the patients. Among the abnormal cystoscopic findings in 55 patients, the lesions suspected to be directly related to microscopic hematuria were classified as 'significant lesions' (31 patients, 17.6%) which include entities such as bladder cancer (1.31%). 27 of 31 patients with significant lesions (85.2%) were over 50 yr old, and furthermore, 3 patients who were diagnosed as bladder tumor by cystoscopy were over 60 yr. Cystoscopy should be utilized as initial diagnostic modality in older patients with asymptomatic microscopic hematuria to rule out any possibility of bladder cancer occurrence. Further studies are needed to justify implementation of cystoscopy as an initial diagnostic modality in younger patients with asymptomatic microscopic hematuria.

Cystoscopy↗

PubMed2001

Antiangiogenic effect of KR31372 in rat sponge implant model.

A rat sponge implant model was used to examine the antiangiogenic effect of KR31372. Topical administration of angiotensin II (AII, 100 ng, daily) into the sponges enhanced the basal sponge-induced neovascularization, leading to higher clearance of (99m)Tc, increased retention of dye in the vessels, and increased numbers of blood vessels. These AII-induced changes were significantly suppressed by oral administration of KR31372 (1 mg/kg for 7 days). Angiogenic effect of recombinant human VEGF(165) (200 ng) was modestly higher than that of AII, which was also significantly inhibited by KR31372. KR31372-mediated suppression of (99m)Tc clearance was reversed by glibenclamide. Levcromakalim showed a modestly suppressive effect on the AII-induced angiogenesis. In conclusion, KR31372 exerted a strong inhibitory effect on the sponge-induced neovascularization, in part, through mediation of glibenclamide-sensitive K(+) channel activation. It is suggested that it may have therapeutic potential in the treatment of angiogenic disorders.

Angiogenesis Inhibitors↗

PubMed2001

Caspase-mediated cleavage of TRAF3 in FasL-stimulated Jurkat-T cells.

The tumor necrosis factor receptor (TNFR)-associated factor (TRAF) proteins play a central role in the early steps of signal transduction by TNFR superfamily proteins, which induce various cellular responses, including apoptosis. Influences of TRAF proteins on the regulation of cell death and physical interactions between TRAFs and caspases have been reported. In this study, we demonstrate that TRAF3 is proteolyzed during cell death in a caspase-dependent manner. TRAF3 was found to be cleaved by incubation with caspase3 in vitro and by Fas- or CD3-triggering in Jurkat-T cells. The Fas- or CD3-induced cleavage of TRAF3 was blocked by caspase inhibitors and by introduction of alanine substitutions for D347 and D367 residues. Furthermore, the amino-terminal fragment of TRAF3 showed a different intracellular localization from the full-length TRAF3 with preferential distribution to particulate fractions and the nucleus. These findings suggest that TRAF3 may be regulated by caspases during apoptosis of T cells.

Amino Acid Chloromethyl Ketones↗

PubMed2001

False-positive growth of Mycobacterium tuberculosis attributable to laboratory contamination confirmed by restriction fragment length polymorphism analysis.

SETTING: Despite the high prevalence of tuberculosis in Korea, false-positive cultures have not yet been reported. At Pusan National University Hospital, in which positive mycobacterial culture specimens were 2.8 daily on average, 12 specimens from 10 patients requested on the same day were positive for Mycobacterium tuberculosis. OBJECTIVE: To identify an episode of laboratory cross-contamination in a tertiary care hospital. DESIGN: All isolates were analyzed by restriction fragment length polymorphism, and patients' medical records were reviewed. RESULTS: All isolates from 10 patients with supposed cross-contamination were identical. Anti-tuberculosis drugs were administered to two patients unnecessarily, resulting in adverse drug reactions in one patient. In one patient who had known tuberculous empyema, the medication course was probably lengthened unnecessarily. CONCLUSIONS: An episode of laboratory cross-contamination in mycobacterial cultures occurred, possibly due to droplets splashed from a sample in a centrifuge tube. Consequently, the aerosol soiled the tip of the dispenser and contaminated the following specimens sequentially. This episode of laboratory cross-contamination resulted in some modifications in our methods of specimen processing and interpretation of the results.

Adult↗

PubMed2000

Activation of c-jun N-terminal kinase by 4-1BB (CD137), a T cell co-stimulatory molecule.

It has been widely accepted that T cell activation requires two signals; one from the binding of the antigen/major histocompatibility complex to the T-cell receptor (TCR)/CD3 complex and the other from the interaction between a surface molecule on antigen presenting cells and its receptor on T cells. The second signal is considered as co-stimulatory and the B7/CD28 pair has been well studied as a prototype. Recently 4-1BB (CD137) has been characterized as another co-stimulatory molecule for T cell activation. However, unlike the CD28/B7 pair, 4-1BB and its ligand 4-1BBL constitute a member of the tumor necrosis factor (TNF) receptor/TNF pair superfamily. The signaling mechanism of 4-1BB has not been revealed in detail. To investigate whether 4-1BB takes the signaling pathways analogous to those for TNF receptors, we generated polyclonal antibodies against human 4-1BB and 4-1BBL and established stable transfectants of the receptor and the ligand with a high level of cell surface expression. Over-expression of h4-1BB was found to result in the activation of c-Jun N-terminal kinase (JNK) in the human embryonic kidney cell line 293. In T cells, it has been previously demonstrated that JNK activation requires dual signals such as the ligation of TCR/CD3 complex plus CD28 co-stimulation or PMA plus ionomycin. The JNK activation by 4-1BB in Jurkat T cells was also found to require stimulation of the TCR/CD3 complex, consistent with the notion that 4-1BB functions as a co-stimulatory molecule for T cell activation.

4-1BB Ligand↗

PubMed2000

Hepatic expression, synthesis and secretion of a novel fibrinogen/angiopoietin-related protein that prevents endothelial-cell apoptosis.

Using degenerate PCR we isolated a cDNA encoding a novel 406- and 410-amino acid protein from human and mouse embryonic cDNAs and have designated it 'hepatic fibrinogen/angiopoietin-related protein' (HFARP). The N-terminal and C-terminal portions of HFARP contain the characteristic coiled-coil domains and fibrinogen-like domains that are conserved in angiopoietins. In human and mouse tissues, HFARP mRNA is specifically expressed in the liver. HFARP mRNA and protein are mainly present in the hepatocytes. HFARP has a highly hydrophobic region at the N-terminus that is typical of a secretory signal sequence and one consensus glycosylation site. Recombinant HFARP expressed in COS-7 cells is secreted and glycosylated. HFARP protein is present not only in the hepatocytes, but also in the circulating blood. Recombinant HFARP acts as an apoptosis survival factor for vascular endothelial cells, but does not bind to Tie1 or Tie2 (endothelial-cell tyrosine kinase receptors). These results suggest that HFARP may exert a protective function on endothelial cells through an endocrine action.

Amino Acid Sequence↗

PubMed2000

Anticancer activity of hydrophobic peptides from soy proteins.

An anticancer peptide from soy protein was purified and isolated. Defatted soy protein was hydrolyzed with thermoase and hydrophobic peptides were extracted with ethanol. The peptide extract was fractionated by XAD-2 hydrophobic, gel filtration chromatography, and different C18 HPLCs. Anticancer activity of each fraction was assayed by measuring in vitro cytotoxicity on P388D1, a mouse monocyte macrophage cell line. IC50 value of a peptide fraction from Sephadex G-25 chromatography was 0.16 mg/ml. This peptide fraction at 1 mg/ml significantly affected cell cycle progression by arresting P388D1 at G2/M phases. Finally purified peptide from analytical C18 HPLC was nonapeptide of which molecular weight was 1157 Da and the sequence was X-Met-Leu-Pro-Ser-Tye-Ser-Pro-Tyr.

Amino Acid Sequence↗

PubMed2000

Diarylheptanoids from the leaves of Alnus hirsuta Turcz.

Diarylheptanoids, (5S)-1,7-bis-(3,4-dihydroxyphenyl)-5-hydroxyheptane-3-one (1, hirsutanonol), (5S)-1,7-bis-(3,4-dihydroxyphenyl)-heptane-3-one-5-O-beta-D-xylopyranosi de (2, oregonin), (5R)-1,7-bis-(3,4-dihydroxyphenyl)-heptane-5-O-beta-D-xylopyranoside (3), and (5R)-1,7-bis-(3,4-dihydroxyphenyl)-heptane-5-O-beta-D-glucopyranoside (4) were isolated from the leaves of Alnus hirsuta Turcz. The structures of these compounds were identified based on the spectral and physicochemical data.

Korea↗