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Biomedical subjects

J H Xu

Publications and source records attributed to J H Xu.

At least 37 records · Page 2Linked to original sources
PubMed1996

The second web bilobed island flap for thumb reconstruction.

The second web bilobed island flap is described. The flap includes skin from the second web of the hand and the dorsum of the index and middle fingers. Usually the flap is based on the first and second dorsal metacarpal arteries, but it can be used with just the first dorsal metacarpal vessels in its pedicle. Sensation of the flap is provided by branches of the radial nerve. The flap has been successfully used to reconstruct 11 injured thumbs.

Adult↗
PubMed1996

[An animal model for screening of antiallergic and antipruritic drugs].

4-Aminopyridine(4-AP) 1 mg.kg-1 sc at the scruff induced a licking response in mice. Antiallergic and antipruritic drugs, such as diphenhydramine HCl(20 mg.kg-1 ip), doxepin(12.5 mg.kg-1 ig), prednisone(10 mg.kg-1 ig), dexamethasone(10 mg.kg-1 ip), fluocinolone (applied to the surface of skin), Pi Yan Ping(applied to the surface of skin), disodium cromoglicate(400 mg.kg-1 ip), ketotifen(1 mg.kg-1 ip), etc. markedly inhibited the licking response elicited by 4-AP. The calcium antagonist nifedipine(500 mg.kg-1 lg) and the potassium channel opener minoxidil(400 mg.kg-1 ig) produced the same inhibitory effect. H2-receptor antagonist cimetidine(200 mg.kg-1 ip) and ranitidine(150 mg.kg-1 ip) showed no effect. Morphine HCl(10 mg.kg-1 ip) and diazepam(0.02 mg.kg-1 ip) exhibited antagonistic effect on the licking response induced by 4-AP, but phenobarbital(25 mg.kg-1 ip), pentobarbital(15 mg.kg-1 ip) and aspirin(300 mg.kg-1 ig) did not. These results indicate that many antiallergic or antipruritic drugs inhibited the licking response induced by 4-AP. The method of licking response elicited by 4-AP has the merit of simplicity and convenience and may be used for screening antiallergic and antipruritic drugs.

4-Aminopyridine↗
PubMed1996

[Contragestational effects of dihydroartemisinin and artesunate].

In experiments carried out in mice, hamsters, guinea pigs and rabbits both dihydroartemisinin and artesunate showed contragestational effect. In mice and rabbits they caused embryo absorption whereas in hamsters and guinea pigs they induced abortion. The contragestational ED50 of dihydroartemisinin given sc on d 7 of pregnancy in mice and d 5 of pregnancy in hamsters were 32.8(27.7-38.9) mg.kg-1 and 6.1(5.6-6.7) mg.kg-1 respectively. The ED50 of this drug given im on d 18 of pregnancy in guinea pigs was 18.3(13.9-24.2) mg.kg-1. Dihydroartemisinin also showed mid-pregnancy terminating effect in hamsters. The contragestational ED50 of artesunate given sc on d 5 of pregnancy in hamsters and the ED50 of sodium artesunate given sc on d 5-8 of pregnancy in hamsters were 12.2(10.3-14.4) mg.kg-1 and 1.0(0.9-1.2) mg.kg-1 daily respectively. Results of light microscopic examination revealed that dihydroartemisinin was selectively toxic to embryo sac. At dose levels sufficient to induce embryo sac necrosis, dihydroartemisinin did not injure the uterus and ovary of the maternal animals. On the ground of the foregoing observations we consider that dihydroartemisinin, artesunate and their analogous drugs should not be used to treat malaria in pregnant women and there is the possibility to exploit intentional abortion agents from artemisinin derivatives.

Abortifacient Agents, Nonsteroidal↗
PubMed1995

Low-density lipoprotein binding affinity of arterial chondroitin sulfate proteoglycan variants modulates cholesteryl ester accumulation in macrophages.

Proteoglycans are considered to facilitate lipid accumulation in the arterial wall, as part of the injury and repair process in atherogenesis. The present study determined (1) characteristics of arterial tissue chondroitin sulfate proteoglycan (CS-PG) monomers of versican type that vary in binding affinity to low-density lipoproteins (LDL), and (2) the ability of these variants to modulate LDL metabolism by macrophages. A large CS-PG devoid of dermatan sulfate (DS) was isolated and purified from bovine aorta intima-media under dissociative conditions. The proteoglycan was further subfractionated by LDL affinity chromatography into CS-PGI and CS-PGII variants, the former eluting at 0.1 M NaCl and the latter at 1.0 M NaCl. The core protein of both variants had a similar molecular mass (1.7 x 10(5). However, CS-PGII contained more glycosaminoglycan (GAG) chains (30 vs. 25) with higher average molecular mass (4.2 x 10(4) vs. 3.8 x 10(4)) than CS-PGI. Furthermore, CS-PGII contained a relatively higher proportion of CS6-sulfate to CS4-sulfate (65: 35 vs. 52: 48). Sulfate-to-hexosamine molar ratio of GAG measured approximately 1 in both variants. In terms of metabolism by macrophages, when compared to complex of LDL and CS-PGI, complex of LDL and CS-PGII produced consistent increase in degradation (10.3-fold vs. 8.4-fold over native LDL) and cell association (16.3-fold vs. 10.2-fold over native LDL) of the ligand, and stimulation of cholesteryl ester synthesis (8.4-fold vs. 6.4-fold over native LDL). CS-PGII was as potent as native CS/DS-PG aggregate, which is a complex made of proteoglycan monomers, hyaluronate, and link protein(s), in stimulating the above activities in macrophages. Thus, variations in LDL-binding affinity of CS-PG can potentially modulate the lipid accumulation in atherogenesis.

Amino Acids↗
PubMed1995

N-terminal sequence of a core protein from a biglycan isolated from bovine aorta.

A biglycan was isolated from bovine aorta intima media by 4M guanidine HCl extraction of the tissue; the material was fractionated and purified by using isopycnic ultracentrifugation and DEAE Sephacel ion-exchange chromatography. Core proteins, resulting from digestion of the proteoglycan preparation with chondroitinase ABC, were resolved by SDS-polyacrylamide gel electrophoresis into three bands. The apparent molecular weight of the fast migrating major protein band was 47 kDa and the other slow-moving minor protein bands were 90 and 105 kDa. These proteins were recognized by a monoclonal anti-proteoglycan deltaDi-6S (MAb 3-B-3/Cl). The amino acid composition of 47 kDa core protein revealed a high content of aspartic acid, glutamic acid and leucine, similar to those found for biglycans isolated from bovine cartilage, rat vascular smooth muscle cell culture and human bone. The N-terminal sequence of 47 kDa core protein was determined as Asp-Glu-Glu-Ala-X-Gly-Ala-Glu-Thr-Thr-X-Gly-Ile-Pro-Asp which is identical to the sequence of bovine articular cartilage biglycan. The proteoglycan had two glycosaminoglycan chains.

Animals↗
PubMed1995

[Influence of calcium concentration on 4-aminopyridine induced histamine release from isolated peritoneal mast cells].

4-Aminopyridine (4-AP) has been shown to induce histamine release from isolated peritoneal mast cells (PMC) in mice and rats. In the presence of extracellular calcium at normal level (0.9 mmol.L-1) histamine release induced by 4-AP (13.6 mmol.L-1) from mice PMC was 33.0% +/- 4.6%, while at low calcium concentration (0.5 mmol.L-1) and in calcium-free medium this parameter decreased to 25.5% +/- 4.2% and 16.3% +/- 3.7% respectively. Histamine release in response to 4-AP (10 mmol.L-1) from rat PMC was 39.1% +/- 6.7% (0.9 mmol.L-1 calcium), while at low calcium concentration (0.5 mmol.L-1) and in calcium-free medium this parameter decreased to 29.3% +/- 4.7% and 20.2% +/- 2.9% respectively. Results of statistical analysis indicate that 4-AP induced histamine release is related to Ca2+ concentration. When rat PMC were preincubated in calcium-free medium with EDTA 0.1 mmol.L-1 for 180 min 4-AP induced histamine release was 13.8% +/- 1.6%. This shows that 4-AP also elicited mobilization of endogenous calcium stores in mast cells. The mechanism of 4-AP induced histamine release was discussed.

4-Aminopyridine↗
PubMed1995

Primary structure of bovine aorta biglycan core protein deduced from cloned CDNA.

Two overlapping cDNA clones for core protein of a biglycan of bovine aorta were isolated from a pSPORT bovine aorta tissue cDNA library. The 2043-bp cDNA contains a 114-bp 5' untranslated region, a 1224-bp cDNA open reading frame and a 705-bp 3' untranslated region. The encoded core preproprotein contains a prepeptide (residues no. -37 to -19) and a propeptide (residues no. -18 to -1), with 369 amino acid residues corresponding to a molecular mass of 41.6 kDa. The deduced amino acid sequence revealed a striking homology to rat vascular smooth muscle cell, human bone and bovine articular cartilage biglycans from cell culture.

Amino Acid Sequence↗
PubMed1995

[Potassium channel openers antagonize 4-aminopyridine induced histamine release from rat peritoneal mast cells].

4-Aminopyridine (4-AP) was shown to promote histamine release from isolated rat peritoneal mast cells (PMC) in a dose-dependent manner. Potassium channel openers, minoxidil (Min) 200 mg.kg-1 ig, diazoxide (Dia) 500 mumol.L-1 in vitro and calcium antagonist nifedipine (Nif) 125 mg.kg-1 ig were found to inhibit 4-AP induced histamine release from rat PMC. Electron microscopy revealed that 4-AP caused partial degranulation of PMC and extrusion of granules and Min 200 mg.kg-1 ig retarded this phenomenon. These results provide evidence that potassium channels are present in rat mast cell membrane and indicate that the mechanism of histamine release by 4-AP may be related to its potassium channel blocking effect. As a result of this effect, the calcium channels open and Ca2+ influx to the mast cells increases, thus eliciting histamine release. Potassium channel openers seemed to be a new group of inhibitors of histamine release from mast cells.

4-Aminopyridine↗
PubMed1994

[4-Aminopyridine induced histamine release and its antagonism by certain drugs].

4-Aminopyridine (4-AP), a known potassium channel blocker, was shown to induce histamine release from mast cells in mice. After ip 4-AP 5 mg.kg-1 the histamine content increased in blood, but decreased in the lung tissue. Calcium antagonists nifedipine (NIF) 500 mg.kg-1 ig, TMB-8 300 mumol.L-1 in vitro and potassium channel opener minoxidil (MIN) 100 mg.kg-1 inhibited the histamine release induced by 4-AP from mouse peritoneal mast cells (PMC). These results provide evidence that potassium channels are present in mouse mast cell membranes and indicate that the mechanism of histamine release by 4-AP may be related to the potassium channel blocking effect. As the result of this effect, the calcium channels open and the Ca2+ influx to the mast cells increases, thus eliciting histamine release.

4-Aminopyridine↗
PubMed1994

[4-Aminopyridine-induced licking response and histamine liberation in mice].

4-Aminopyridine (4-AP) 1 mg.kg-1 sc at the scruff induced a licking response in mice. H1 receptor blockaders, such as diphenhydramine HCl (1, 10 mg.kg-1, sc at the scruff or 40 mg.kg-1, i.p.), chlorphenamine maleate (20 mg.kg-1, i.p.), and astemizole (2 mg.kg-1, i.g.), inhibited the licking response caused by 4-AP. Repeated injections of 4-AP (1 mg.kg-1) reduced the times of lick and the histamine content in the skin of injected site. 4-AP also promoted histamine release from incubated mouse peritoneal mast cells (PMC) in a dose-dependent manner. The results indicate that the licking response may originate from the histamine liberation of mast cells.

4-Aminopyridine↗
PubMed1994

Using complexity measure to characterize information transmission of human brain cortex.

The information transmission among various parts of the cortex are computed with the theory of mutual information from the data of the electroencephalogram (EEG) time series of normal human subjects. The intensities of these transmissions are characterized by the "complexity" measures. These measures have revealed to be sensitively related to the functional conditions of human beings.

Adult↗
PubMed1994

[Roentgenological and pathological findings in 22 cases of secondary fungus ball of pulmonary aspergillosis].

Twenty-two cases of secondary fungus ball of pulmonary aspergillosis defined by operation were reported. All cases were referred with incorrectly diagnosis to the authors and only 45.3% were correctly diagnosed before operation. The roentgenological and pathological findings were studied. The results show that not familiar with non-typical appearance is the most common cause for incorrect diagnosis.

Adult↗
PubMed1993

Injury to the arterial wall of rabbits produces proteoglycan variants with enhanced low-density lipoprotein-binding property.

The effect of arterial injury on proteoglycans (PG) and their ability to bind low-density lipoprotein (LDL) were studied in rabbits 12 weeks after balloon injury. Following biosynthetic labeling in an organ culture system, PG were isolated under dissociative conditions from deendothelialized areas (DEA), reendothelialized areas (REA), and uninjured areas (control) of the aortic tissue. DEA and REA tissues yielded 42-52% more PG and incorporated 39-67% more 35S-label into proteoglycans than control tissues. Ion-exchange chromatography of PG from DEA and REA tissues yielded PG-I, PG-II, and PG-III, while from control tissue only PG-I and PG-II. PG-II formed major portion (74-84%) of the isolated PG in all three tissue types. PGI preparations comprised entirely of heparan sulfate (HS)-PG of similar hydrodynamic size (Kav = 0.45-0.47). PG-II from DEA and REA tissues consisted of PGII-A (Kav = 0.02-0.04) and PGII-B (Kav = 0.32), while PG-II from control tissue contained only PGII-B with relatively smaller hydrodynamic size (Kav = 0.40). PGII-A preparations contained predominantly chondroitin sulfate (CS)-PG with no dermatan sulfate (DS); whereas PGII-B consisted mainly of CS/DS-PG, with relatively high proportion of DS in DEA and REA tissues vs. control tissue (50-54% vs. 43%). Further, the glycosaminoglycan chains of CS/DS-PG from DEA and REA tissues were 1.7-fold longer than those from control tissue. PG-III contained about 80% CS/DS-PG and 20% HS-PG; CS/DS-PG was similar to those found in PGII-B from DEA and REA tissues. HS-PG from PG-II and PG-III, unlike those from PG-I, was enriched with N-sulfated residues. PGI from all the three tissue types bound poorly to LDL. On the other hand, PGII-A, PGII-B, and PG-III from DEA and REA tissues showed enhanced ability to bind LDL, in that order. For example, the LDL-binding ability of PGII-B from DEA and REA was 2.9- to 3.1-fold above that from control tissue. Thus, arterial injury with or without regenerated endothelium produces proteoglycan variants with altered characteristics and enhanced LDL-binding ability.

Animals↗
PubMed1993

Sound direction influences the frequency-tuning characteristics of neurons in the frog inferior colliculus.

1. We investigated the influence of sound direction on the frequency-tuning characteristics of neurons in the frog inferior colliculus, the torus semicircularis. For each neuron, we used tone bursts to determine the frequency-threshold curves (FTCs) for three to seven loudspeaker azimuths. The loudspeaker was mounted on a rotatable arc and could be swung through the frontal field between positions opposite the ear that was contralateral to the recording site (C90 degrees) and the ear that was ipsilateral to the recording site (I90 degrees). 2. Frequency-tuning data from 83 units showed that the characteristic frequency (CF) shift through a 180 degrees change in loudspeaker azimuth was typically small, i.e., 85% of neurons showed maximum absolute changes in CF that were < 0.4 octaves. Paired comparisons of CFs for each neuron when the loudspeaker was located at C90 degrees, and the frontal midline position (0 degree) revealed no significant differences (P > 0.2) between azimuths. The magnitude of CF shift between different sound directions showed no systematic pattern. 3. In contrast to the CF, midbrain neurons showed distinct changes in the minimum threshold (MT) at CF across 180 degrees of azimuth. The maximum absolute change in MT ranged from 0 to 38 dB, with a mean of 10.9 dB. A pair-wise comparison of MTs, for each neuron, derived with the speakers at C90 degrees, 0 degree, and I90 degrees, revealed that the MT typically increased when the loudspeaker was rotated toward I90 degrees (P < 0.0001). 4. The most prominent effect of rotating the loudspeaker from C90 degrees to I90 degrees was a narrowing of the FTC. Sharpness of tuning in simple V-shaped FTCs was most directly shown by changes in the Q factors at 10, 20, and 30 dB above MT as a function of sound direction. A pair-wise comparison for individual neurons showed that all Q factors were significantly larger (sharper tuning) for I90 degrees compared with C90 degrees (P < 0.02). The Q20dB values were also significantly larger for I90 degrees compared with 0 degree (P < 0.05). For the majority of units, the maximum Q10dB and Q20 dB values were displayed when the loudspeaker was positioned at I90 degrees; however, the maximum Q30dB was distributed nearly equally for the three azimuths. These results suggest that a change in sound direction has the most robust effect on tuning properties of the FTCs nearest the MT.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗
PubMed1993

Lipoprotein-proteoglycan complexes induce continued cholesteryl ester accumulation in foam cells from rabbit atherosclerotic lesions.

We studied the metabolism of lipoprotein-proteoglycan complexes by macrophage-derived foam cells. Foam cells were isolated from atherosclerotic rabbit aortas. ApoB-lipoprotein-proteoglycan complex was isolated from human aorta fibrous plaque lesions and LDL-proteoglycan complex was formed in vitro. Both in vitro and in vivo complexes stimulated cholesteryl ester synthesis in foam cells by a dose-dependent, saturable process that resulted in the intracellular accumulation of cholesteryl ester. Stimulation of cholesteryl ester synthesis was linear with time over a 32-h period. Polyinosinic acid inhibited the stimulation of cholesteryl ester synthesis by the complexes by 32-37%, whereas cytochalasin D only produced a 6-16% inhibition. Foam cells degraded 125I-LDL-proteoglycan complex and 125I-acetyl LDL in a saturable, dose-dependent manner. Excess unlabeled acetyl-LDL inhibited the degradation of 125I-LDL-proteoglycan complex by 52%, while LDL had no effect. Similarly, excess unlabeled complex suppressed the degradation of 125I-acetyl-LDL by 48%. Foam cells degraded 125I-methyl-LDL-proteoglycan complex to the same extent as 125I-LDL-proteoglycan complex. These results show that foam cells from atherosclerotic lesions metabolize lipoprotein-proteoglycan complexes predominantly via receptor-mediated endocytosis and consequently continue to accumulate intracellular cholesteryl ester.

Animals↗
PubMed1993

[Intracerebral-ventricular injection of 4-aminopyridine induced convulsion in rabbits].

Intracerebral-ventricular (icv) injection of 4-aminopyridine (4-AP) 8 micrograms to rabbits generated convulsions and epileptic discharges in electrocorticogram (ECoG). With 40 rabbits, the occurrence of convulsion at this dose level was 100%. The results from five rabbits showed that seizures may break out repeatedly at intervals of 1-5 min and such state may last about 1.5 h. Antiepileptic drugs, such as phenytoin sodium, phenobarbital sodium and diazepam, were found to effectively control the seizures provoked by icv 4-AP. Sodium valproate was less effective than the foregoing drugs. The icv 4-AP-induced convulsion appeared to have some merits as compared with the old epilepsy models, such as those induced by electric stimulation, cardiazol, or icv ferrous sulfate. We feel that it may be recommended as a model for the preliminary screening of antiepileptic drugs. The seizures provoked by icv 4-AP were shown to be antagonized by scopolamine, haloperidol, phentolamine, or propranolol, but potentiated by l-dopa. It is now recognized that 4-AP can enhance the release of ACh, DA, and NE in the central nervous system. The present results suggest that the convulsion elicited by 4-AP seems to be related to the disturbance of synaptic transmission in the brain.

4-Aminopyridine↗