Search PubMed⌕ Search

Biomedical subjects

H Liu

Publications and source records attributed to H Liu.

At least 1,009 records · Page 56Linked to original sources

Recombinant human granulocyte colony-stimulating factor treatment improves macrophage suppression of granulocyte and macrophage growth after burn and burn wound infection.

Granulocyte and macrophage production after burn injury or burn wound infection is significantly reduced and further compromised by endotoxin (ET). Moreover, the macrophage seems to be the major source of this bone marrow suppression. We sought to determine if recombinant human granulocyte colony-stimulating factor (rhG-CSF), a hematopoietic growth factor that is capable of improving survival after experimental burn wound sepsis, altered postburn macrophage-mediated marrow suppression. Groups of male BDF1 mice (n = 6 to 10) receiving a 15% total body surface area burn +/- infection (B or B + I) with Pseudomonas aeruginosa were injected with 100 ng rhG-CSF twice daily. On day 3, peritoneal-elicited macrophages (5 x 10(6) cells/mL) from either rhG-CSF-treated or control (5% dextrose in water) mice were incubated +/- ET (300 ng/mL). The resultant macrophage supernatant was added to cultures of target marrow granulocyte-macrophage progenitor cells (GM-CFC) at a volume of 1:10. The GM-CFC growth as a percentage of cultures not containing macrophage supernatant were compared and reductions in the number of GM-CFC taken as an index of marrow suppression. Macrophages obtained from B and B + I animals reduced target GM-CFC growth, compared with macrophages from normal animals (B vs. normal animals p < 0.05). In addition, ET-stimulated macrophages induced further bone marrow suppression for all three groups (p < 0.01). Macrophages from granulocyte colony-stimulating factor-treated animals caused significantly less bone marrow suppression, compared with untreated animals for all groups (p < 0.05 to 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Suppression of haematopoiesis by IgG autoantibodies from patients with systemic lupus erythematosus (SLE).

The inhibiting activity of serum on haematopoiesis has been described in patients with SLE. To explore further the features of serum inhibitor, we first examined the suppression of granulocytic and erythroid colony formation in vitro by serum from patients with SLE using methylcellulose culture. The potent inhibiting activity was demonstrated in six of 20 patients. All of these six patients were associated with leukocytopenia and/or anaemia. Five of 10 sera from patients with active SLE suppressed the colony formation of both burst-forming units of erythrocyte (BFU-E) and colony-forming units of granulocyte/macrophage (CFU-GM), and one serum suppressed BFU-E only. IgG fraction isolated from sera with inhibiting activity suppressed colony formation without complement involvement. The elimination of monocytes and lymphocytes from target mononuclear cells did not affect the suppression by the IgG fractions. The suppressive effect was completely eliminated after incubation of the IgG fractions with progenitor-enriched mononuclear cells. Flow cytometric analysis showed these IgG bound to CD34+ haematopoietic progenitor cells, but not to CD33+ cells. These data suggest that (i) the inhibitor of colony formation in serum was observed in IgG fraction; (ii) its suppressive effect on colony formation was mediated by neither monocytes and lymphocytes nor complements; and (iii) IgG fraction could bind to primitive haematopoietic progenitor cells and suppress the growth of these cells. Thus, IgG autoantibodies to primitive haematopoietic progenitor cells are demonstrated to be present in the sera of a significant proportion of active SLE patients with anaemia and leukocytopenia and to suppress the progenitor cell growth.

Adolescent↗

A model for the evaluation of mandibular bone response to implant materials.

An in vivo animal (goat) mandibular bone model has been evaluated for the cortical and trabecular bone response to biomaterials with different elastic modulus and/or different surfaces. The effect of the elastic modulus on the bone formation was also studied. The difficulties encountered in orientation of the implants probably could have been surmounted if pre-operative radiographs had been available. It was also established that there is a large variance in the amount of trabecular and cortical bone in the mandible of the goat 'bone model'.

Aluminum Oxide↗

The effect of total blood exchange with PHP solution on cardiac xenotransplantation.

Prevention of hyperacute rejection is a difficult and unsolved problem in xenotransplantation. Natural antibodies and complement activation have been known to play an important role in the xenotransplantation between discordant species pairs. In the present study, total blood exchange (TBE) was performed with pyridoxalated-hemoglobin-polyoxyethylene conjugate (PHP) solution (Ajinomoto Co., Inc., Kawasaki, Japan) before cardiac xenotransplantation in order to remove the immunoglobulins and prolong xenograft survival time. Guinea pigs and rats were used as the discordant species combination for donor and recipient. Two groups were established: Group 1, untreated control (n = 8) and Group 2, TBT with PHP solution (n = 8). The exchange blood transfusion was carried out at the rate of 15-20 ml/h utilizing PHP solution using a blood pump. After the blood exchange was processed, hematocrit (Ht) levels dropped to 4 or 5%, and a cardiac xenotransplantation was performed within 24 h. The levels of serum IgA, IgM, and IgG were decreased to less than 25, 25, and 10% of the base line, respectively, after blood exchange. A mean xenograft survival time in Group 2 was prolonged to 472 +/- 74 min and to 10.4 +/- 1.8 min in Group 1 (p < 0.01). A titer of the anti-guinea pig lymphocytotoxic antibody in rat serum was decreased to almost nil. The data from this study suggest that total blood exchange with PHP solution may be useful in preoperative removal of xenograft antibodies in xenotransplantation.

Animals↗

Interactions of phenobarbital and phenytoin with carbamazepine and its metabolites' concentrations, concentration ratios, and level/dose ratios in epileptic children.

The effects of phenytoin (PHT) or phenobarbital (PB) comedication on the concentrations, concentration ratios, and level/dose ratios of carbamazepine (CBZ) and its metabolites were investigated. The hetero-induction effects of CBZ metabolism by PHT or PB were clearly demonstrated. Serum CBZ level/dose ratios in patients with CBZ polytherapy were decreased while CBZ-10,11-epoxide (CBZ-E) and trans-10,11-dihydroxy-10,11-dihydro-CBZ (CBZ-H) concentrations were increased as compared with those of patients receiving CBZ alone. The concentration ratios of CBZ-H/CBZ and CBZ-E/CBZ were also greater in patients receiving CBZ+PHT or CBZ+PB than in patients receiving CBZ alone. In addition, positive correlations between serum PHT concentration and CBZ-H/CBZ or CBZ-E/CBZ concentration ratios were observed. There were no significant differences in CBZ-H/CBZ-E concentration ratios, the free fractions of CBZ and its metabolites, and CBZ-E or CBZ-H level/dose ratios among the three groups of patients. Because this approach investigates the in vivo relation between the substrates and products of the enzymes involved in CBZ biotransformation, more detailed information about the drug interactions was obtained. The results suggest that the PHT has a potent induction effect on CBZ epoxidase, whereas PB is a moderate inducer.

Biotransformation↗

Influence of blood vessels on the measurement of hemoglobin oxygenation as determined by time-resolved reflectance spectroscopy.

We report the development of a heterogeneous resin-tube model to study the influence of blood vessels on the apparent absorption of the system, mu a(sys), using a time-resolved technique. The experimental results show that mu a(sys) depends on the absorption inside the tubes, mu a(tube), tube diameters, and tube-to-sample volume ratios. A mathematical expression relating mu a(sys) and mu a(tube) is derived based on the experimental results and is verified by time-resolved Monte Carlo simulations for heterogeneous models. This analytical formula predicts that the apparent absorption coefficient measured on a biological organ is a volume-weighted sum of the absorption coefficients of different absorbing components. We present some apparent absorption coefficients measured in vivo in animals and humans and discuss improved algorithms that calculate the hemoglobin saturation by including background-tissue absorption and blood vessel distribution.

Blood Vessels↗

Magnetic resonance imaging kappa-space segmentation using phase-encoding groups the accuracy of quantitative measurements of pulsatile flow.

The use of phase-encode grouping (PEG) allows acquisition of a complete cardiac cine in a single breath hold, eliminating respiratory artifacts and improving edge definition. One approach to quantitative magnetic resonance (MR) flow measurements in pulmonary, coronary, and renal arteries uses phase velocity mapping with a PEG, single breath-hold, cine technique. Phantom studies were designed to evaluate the accuracy of MR phase velocity mapping (MRV) with PEG in continuous and pulsatile flow measurements in small vessels. Experiments were performed on a 1.5-T MRI system and results were compared with those obtained by timed volume measurements and a transit-time ultrasound flowmeter. Flow velocity, pulsatile flow wave form, pulsing rate, and PEG size were varied. For continuous flow, MRV measured velocities correlated well with those calculated from timed volume measurements (r > 0.998) under mean spatial velocities ranging from 20-100 cm s-1. The temporal mean velocity difference between MRV and ultrasound flowmeter measurements was less than +/- 2.9 cms-1 under pulsatile flow conditions with PEG sizes of 5 or less, however, the mean velocity difference was > 7 cm s-1 for PEG sizes of 8 or more. Accurate MR velocity measurement with PEG in small vessels under conditions of pulsatile flow is possible if an appropriate PEG size is selected.

Artifacts↗

The Vif protein of human and simian immunodeficiency viruses is packaged into virions and associates with viral core structures.

The vif gene of human and simian immunodeficiency viruses (HIV and SIV) encodes a late gene product that is essential for viral infectivity in natural target cells. Virions produced in the absence of Vif are abnormal in their ultrastructural morphology and are severely impaired in the ability to complete proviral DNA synthesis upon entry into new target cells. Because previous studies failed to detect Vif protein in virus particles, Vif is believed to influence virus infectivity indirectly, by affecting virion assembly, release, and/or maturation. In this report, we reexamined the possibility that Vif is a virion-associated protein. Utilizing high-titer Vif-specific antibodies, a sensitive immunoblot technique, and highly concentrated virus preparations, we detected a 23-kDa Vif-reactive protein in wild-type HIV type 1 (HIV-1) and a 27-kDa Vif-reactive protein in wild-type SIVSM virions. Neither protein was present in virions derived from vif-deficient HIV-1 and SIVSM proviral constructs. Vif protein content was similar among different strains of HIV-1 and was independent of the cell type (permissive or nonpermissive) used to produce the virus. To determine the subvirion localization of Vif, HIV-1 virions were treated with proteinase K or Triton X-100 to remove virion surface proteins and the viral membrane, respectively, purified through sucrose, and analyzed by immunoblot analysis. Vif protein content was not affected by the removal of external surface proteins or by the removal of the viral membrane and submembrane p17Gag matrix protein. Instead, Vif colocalized with viral core structures which sedimented at a density of 1.25 g/ml on linear sucrose gradients (enveloped HIV-1 particles sediment at a density of 1.17 g/ml). Finally, the amount of Vif protein packaged into virions was estimated to be on the order of 1 molecule of Vif for every 20 to 30 molecules of p24Gag, or between 60 and 100 molecules of Vif per particle. These results indicate that Vif represents an integral component of HIV and SIV particles and raise the possibility that it plays a direct role in early replication events.

Amino Acid Sequence↗

Targeting foreign proteins to human immunodeficiency virus particles via fusion with Vpr and Vpx.

The human immunodeficiency virus type 1 (HIV-1) and HIV-2 Vpr and Vpx proteins are packaged into virions through virus type-specific interactions with the Gag polyprotein precursor. To examine whether HIV-1 Vpr (Vpr1) and HIV-2 Vpx (Vpx2) could be used to target foreign proteins to the HIV particle, their open reading frames were fused in frame with genes encoding the bacterial staphylococcal nuclease (SN), an enzymatically inactive mutant of SN (SN*), and chloramphenicol acetyltransferase (CAT). Transient expression in a T7-based vaccinia virus system demonstrated the synthesis of appropriately sized Vpr1-SN/SN* and Vpx2-SN/SN* fusion proteins which, when coexpressed with their cognate p55Gag protein, were efficiently incorporated into virus-like particles. Packaging of the fusion proteins was dependent on virus type-specific determinants, as previously seen with wild-type Vpr and Vpx proteins. Particle-associated Vpr1-SN and Vpx2-SN fusion proteins were enzymatically active, as determined by in vitro digestion of lambda phage DNA. To determine whether functional Vpr1 and Vpx2 fusion proteins could be targeted to HIV particles, the gene fusions were cloned into an HIV-2 long terminal repeat/Rev response element-regulated expression vector and cotransfected with wild-type HIV-1 and HIV-2 proviruses. Western blot (immunoblot) analysis of sucrose gradient-purified virions revealed that both Vpr1 and Vpx2 fusion proteins were efficiently packaged regardless of whether SN, SN*, or CAT was used as the C-terminal fusion partner. Moreover, the fusion proteins remained enzymatically active and were packaged in the presence of wild-type Vpr and Vpx proteins. Interestingly, virions also contained smaller proteins that reacted with antibodies specific for the accessory proteins as well as SN and CAT fusion partners. Since similar proteins were absent from Gag-derived virus-like particles and from virions propagated in the presence of an HIV protease inhibitor, they must represent cleavage products produced by the viral protease. Taken together, these results demonstrate that Vpr and Vpx can be used to target functional proteins, including potentially deleterious enzymes, to the human or simian immunodeficiency virus particle. These properties may be exploitable for studies of HIV particle assembly and maturation and for the development of novel antiviral strategies.

Amino Acid Sequence↗

Estradiol attenuates the antidiuretic action of vasopressin in ovariectomized rats.

To determine which ovarian hormone is involved in the sexually dimorphic antidiuretic action of vasopressin, the antidiuretic response to vasopressin was examined in sham-operated nonestrous female rats chronically treated with vehicle and in ovariectomized rats treated with vehicle, progesterone, estradiol, or the combination of estradiol and progesterone, respectively. Three-week-old female rats were sham operated or ovariectomized, and a slow-release hormone pellet was implanted at the 6th wk. The experiment was performed at the 10th to 12th wk in conscious, chronically instrumented rats hydrated with tap water (2% body wt). Infusion of vasopressin at rates of 10-1,000 pg.min-1.kg body wt-1 resulted in a dose-dependent antidiuretic response that was significantly enhanced in ovariectomized rats compared with the intact nonestrous females. Progesterone had no effect, whereas estradiol attenuated and restored the antidiuretic response to vasopressin to a level similar to that in intact nonestrous female rats. These results suggest that it is estrogen, but not progesterone, that reduces the antidiuretic response to vasopressin in the female rat.

Animals↗

Ischemic preconditioning stimulates sodium and proton transport in isolated rat hearts.

One or more brief periods of ischemia, termed preconditioning, dramatically limits infarct size and reduces intracellular acidosis during subsequent ischemia, potentially via enhanced sarcolemmal proton efflux mechanisms. To test the hypothesis that preconditioning increases the functional activity of sodium-dependent proton efflux pathways, isolated rat hearts were subjected to 30 min of global ischemia with or without preconditioning. Intracellular sodium (Nai) was assessed using 23Na magnetic resonance spectroscopy, and the activity of the Na-H exchanger and Na-K-2Cl cotransporter was measured by transiently exposing the hearts to an acid load (NH4Cl washout). Creatine kinase release was reduced by greater than 60% in the preconditioned hearts (P < 0.05) and was associated with improved functional recovery on reperfusion. Preconditioning increased Nai by 6.24 +/- 2.04 U, resulting in a significantly higher level of Nai before ischemia than in the control hearts. Nai increased significantly at the onset of ischemia (8.48 +/- 1.21 vs. 2.57 +/- 0.81 U, preconditioned vs. control hearts; P < 0.01). Preconditioning did not reduce Nai accumulation during ischemia, but the decline in Nai during the first 5 min of reperfusion was significantly greater in the preconditioned than in the control hearts (13.48 +/- 1.73 vs. 2.54 +/- 0.41 U; P < 0.001). Exposure of preconditioned hearts to ethylisopropylamiloride or bumetanide in the last reperfusion period limited in the increase in Nai during ischemia and reduced the beneficial effects of preconditioning. After the NH4Cl prepulse, preconditioned hearts acidified significantly more than control hearts and had significantly more rapid recovery of pH (preconditioned, delta pH = 0.35 +/- 0.04 U over 5 min; control, delta pH = 0.15 +/- 0.02 U over 5 min). This rapid pH recovery was not affected by inhibition of the Na-K-2Cl cotransporter but was abolished by inhibition of the Na-H exchanger. These results demonstrate that preconditioning alters the kinetics of Nai accumulation during global ischemia as well as proton transport after NH4Cl washout. These observations are consistent with stimulation of the Na-K-2Cl cotransporter and Na-H exchanger by preconditioning.

Ammonium Chloride↗

Sustained inhibition of intimal thickening. In vitro and in vivo effects of polymeric beta-cyclodextrin sulfate.

Intimal thickening after vascular injury may be modulated in part by heparin binding growth factors. We hypothesized that placement of a therapeutic polymer in the periadventitial space capable of tightly binding growth factors might alter the vascular response to injury. We first demonstrated that incubation of rat aortic smooth muscle cells with an insoluble, sulfated polymer of beta-cyclodextrin (P-CDS) was associated with a dose-dependent inhibition of proliferation induced by fetal calf serum, fibroblast growth factor-2 (FGF-2), platelet-derived growth factor BB, or epidermal growth factor. Preincubation studies of P-CDS with FGF-2 revealed a very rapid removal of mitogenic activity. Using radiolabeled FGF-2 (0.25 microg/ml), we observed a very rapid association rate (0.34 +/- 0.07 min-1, n=4) and a very slow dissociation rate (3.3 +/- 0.2 X 10(-7) min-1) at 37 degrees C, suggesting a high affinity interaction. Using both Transwell and linear under-agarose assays, we demonstrated a significant inhibition of random migration (chemokinesis) by P-CDS. Unsulfated polymeric beta-cyclodextrin (P-CD) had little if any of these effects, suggesting that the high negative charge density of P-CDS was important for the effects. Finally, rats undergoing carotid artery balloon injury were randomized to treatment with periadventitial P-CDS or no treatment, and were killed at 4 (n=20), 14 (n=59), and 88 d (n=14). Morphometric analysis demonstrated significant and sustained inhibition of intimal thickening in P-CDS-treated rats at 14 (P < 0.01) and 88 d (P < 0.05) using absolute intimal area or intima/media area ratios. No inhibition was seen in a group of rats treated with P-CD. In P-CDS-treated rats, bromodeoxyuridine labeling studies revealed fewer labeled smooth muscle cells in the intima at 14 d (P=0.01), while staining with Evans blue revealed enhanced late endothelial cell regrowth. Thus, periadventitially applied sulfated beta-cyclodextrin polymer, which can tightly bind heparin binding growth factors, inhibits intimal thickening in vivo in a sustained fashion without using an additional delivery system. These studies suggest that cellular processes mediated by heparin binding growth factors may be modulated by P-CDS.

Angioplasty, Balloon↗

Co-injection of wheat germ agglutinin-HRP and choleragenoid-HRP into the sciatic nerve of the rat blocks transganglionic transport.

We report on the surprising loss of transganglionic and retrograde labeling in the spinal cord of the rat after co-injection of the tracers wheat germ agglutinin-HRP (WGA-HRP) and choleragenoid toxin-HRP (CTB-HRP) into the sciatic nerve. Injection of WGA-HRP alone produced a pattern of transganglionic label consistent with transport by small-diameter primary afferent fibers. Small cell bodies were labeled in the ipsilateral dorsal root ganglion (DRG) and there was dense terminal labeling in the superficial dorsal horn of the lumbar spinal cord. Injection of CTB-HRP alone produced a pattern of transganglionic labeling consistent with transport by large-diameter primary afferent fibers. Large cell bodies were labeled in the DRG and there was dense terminal labeling in the nucleus proprius (Laminae III-V) in the spinal cord. CTB-HRP also produced extensive retrograde labeling of ventral horn motor neurons. When the two tracers were co-injected, we found few labeled cells in the ipsilateral DRG and there was almost complete loss of transganglionic terminal labeling in the lumbar spinal cord. Retrograde labeling of motor neurons was also significantly reduced. Even when one of the tracers (e.g., WGA-HRP) was injected 24 hr after and up to 10 mm proximal to the site of the first tracer (e.g., CTB-HRP), an inhibitory interaction was detected. The labeling pattern was always characteristic of the first tracer injected.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Limb reduction defects after prenatal inhibition of nitric oxide synthase in rats.

To determine the influence of nitric oxide (NO) on vascular tone during fetal development, timed pregnant rats received the NO synthase inhibitor NG-nitro-L-arginine methyl ester for consecutive 4, 7, or 14 d before parturition (postorganogenesis). Offspring demonstrated limb reduction defects (incidence, 53%) involving either or both hindlimbs, whereas forelimbs were uniformly spared. Defects were dose-dependent but independent of the duration of administration occurring with equal frequency in 4-, 7-, and 14-d treatment groups. Histologic analysis revealed features characteristic of vascular disruption with hemorrhagic necrosis and loss of structure. The defects were prevented by concurrent maternal administration of L-arginine or the NO donors S-nitroso-N-acetyl-penicillamine and sodium nitroprusside. Defects were not seen after prenatal treatment with aminoguanidine. To study basal and agonist-mediated NO release, newborn femoral and brachial arteries were cannulated with a glass micropipette under constant pressure, and changes in intraluminal diameter (micrometers) were measured in response to acetylcholine and the NO synthase inhibitor N omega-nitro-L-arginine. Newborn femoral and brachial vessels demonstrated a dramatic (59%) decrease in resting diameter compared with adult vessels (16%). These findings suggest that basal NO release is upregulated during fetal development concurrent with the processes that increase maternal NO release. The data also suggest that up-regulation of NO release occurs throughout the fetal systemic circulation and is not restricted to hindlimbs. This is the first study to demonstrate inhibition of NO release in the pathogenesis of limb reduction defects.

Acetylcholine↗

Recurrent Guillain-Barré syndrome in Japan.

The clinical profiles of 11 Japanese patients with recurrent episodes of Guillain-Barré syndrome (GBS), including 3 of our cases out of a total of 76 patients (48 males and 28 females), are reviewed. The recurrence rate was estimated as 4%. Among the 11 Japanese patients, 10 were male. Various viral infections had been confirmed in 1 case. No patients showed recurrent ophthalmoplegia. Sensory involvement varied from one episode to the next. These findings suggest the changing distribution of the demyelinating lesions and possibly a different reaction to the unknown pathogens in the recurrence of GBS.

Adolescent↗

[Xin'an Dispensaries and its role in medicine in the Ming-Qing dynasties].

The Xin'an Dispensaries were set up in the Song dynasty, completed in the Ming dynasty and reached its peak of development at the end of the Qing dynasty. The representative ones of the dispensaries include Lu's Baohetang of the Song dynasty, Xu's Baoyuantang, Zhengtian dispensary, and Baoyutang of the Ming dynasty, Hu Xian Chun, Zhongdetang of the Qing dynasty. All these dispensaries were mostly run by the physicians themselves in the Ming dynasty, while they were run by Anhui businessmen in the Qing dynasty. As a union embodying health care, production and trading of traditional handicraft, not a few of them had become famous pharmaceutical factories today, such as Hu Qing Yu Tang, Jianmin Pharmaceutical Factory of Wuhan. Rich experience on production and management were accumulated, alongside achievements on prescription, drug processing, storage, collection and ready-made drug manufacturing.

China↗

[The role of Epstein-Barr virus infection and infective copy number in pulmonary carcinogenesis].

To study the possible role of EBV in pulmonary carcinogenesis, surgically resected and paraffin-embedded pulmonary carcinoma specimens from 87 cases in which each specimen contained separable carcinoma tissue and normal lung tissue (twin pair) were collected to detect EBV infection and infective copy number by polymerase chain reaction (PCR) and dot blot hybridization. Of the 87 cases (174 samples), EBV genomic DNA sequences were positive in 52 (59.8%) carcinoma tissue samples and 39 (44.8%) normal tissue samples by PCR. There were no significant differences in positive rates between the two tissues. By dot blot hybridization, a significant difference was found between carcinoma (43.7%) and normal lung (8.0%) tissues. The results suggest that EBV infection may be common in both normal and carcinoma tissues, but carcinoma tissue contains higher EBV infective copy number than normal tissue. Infective copy number of EBV rather than simple EBV infection may play an important role in pulmonary carcinogenesis.

Adult↗

Clinical studies of primary angle closure glaucoma.

The ocular anatomic features, pupil-blocking force, status of angle synechia closure and positivity of provocative tests were compared between the primary chronic angle closure glaucoma (PCACG) and primary acute angle closure glaucoma (PAACG) by ultrasonic biometry, computerized image processing technique of the anterior ocular segment, gonioscopy and provocative tests. The studies showed that the anterior chamber depth of PAACG was shallower than that of PCACG, the pupil-blocking force of PAACG was stronger than that of PCACG, the status of angle synechia closure of PCACG was mainly creeping synechia closure and the positivity of mydriasis test after iridectomy was much higher (37.93%) in PCACG than that (11.43%) in PAACG. These facts suggested that the mechanisms of the angle closure of more than half of PCACG cases be multiple, besides the mechanism of pupillary block. Therefore, the authors emphasize that the pupillary block must be eliminated as well as the other mechanisms for the treatment of PCACG. The criteria of diagnosis and principles of management of PCACG were proposed.

Adult↗