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Biomedical subjects

Y Lin

Publications and source records attributed to Y Lin.

At least 217 records · Page 12Linked to original sources

Microsurgical treatment of Mooren's ulcer.

OBJECTIVE: To evaluate effect of microsurgery of lamellar keratoplasty (LKP) on Mooren's corneal ulcer. METHODS: The effect, postoperative astigmatism, postoperative vision, ulcer recurrence of postoperation, and surgical complications of two groups of consecutive Mooren's ulcer inpatients treated respectively by non-microsurgery of LKP and microsurgery of LKP were analyzed. RESULTS: There were significant differences of the effect, postoperative astigmatism, postoperative vision, ulcer recurrence of postoperation, and surgical complications between the two groups. The effect and postoperative vision of the microsurgery-treated group were better than those of the non-microsurgery-treated group. The postoperative astigmatism, ulcer recurrence of postoperation, and surgical complications of the microsurgery-treated group were less than those of the nonmicrosurgery-treated group. CONCLUSION: Microsurgery of LKP of Mooren's corneal ulcer can greatly improve the ulcer healing and postoperative vision, and reduce the surgical complication and the ulcer recurrence of postoperation.

Adolescent↗

[Otogenic hypertrophic cranial pachymeningitis associated with edema of the temporal lobe and organic mental disorder-case report].

OBJECTIVE: Hypertrophic cranial pachymeningitis(HCP) is a rare disease which might be misdiagnosed. One typical case of otogenic hypertrophic cranial pachymeningitis (HCP) associated with edema of the temporal lobe and organic mental disorder was reported. Literatures associated with HCP were reviewed for reference. METHODS: In July, 1997, a 26-year-old man was admitted for right-sided severe headache, dizziness, nausea, vomiting, facial and abducens nerve palsy. MRI and CT revealed inflammation in the temporal bone and locally thickened dura mater with obvious enhancement as a band in the petrous apex and nearby tentorium cerebellum. The patient then underwent operation including decompression of the facial nerve, labyrinthectomy, and eradication of the inflammatory cells in the mastoid and petrous portion. Postoperatively, the clinical signs disappeared except hearing loss. Seven months later, the patient suffered from mental disorder with interrupted excitement to hit and abuse the family members. He was then treated in a psychosis hospital but no improvement could be seen. On May 13, 1998, MRI and the enhanced MRI demonstrated diffuse thickened tentorium cerebellum and dura mater in the middle cranial fossa. The inferior portion of the temporal lobe was obvious edema. The internal carotid artery was partially occluded due to the thickened wall of cavernous sinus. RESULTS: Hence, the diagnosis of HCP associated with edema of temporal lobe and organic mental disorder was established. The patient was cured by high dosage of penicillin. CONCLUSION: MRI is an essential method for diagnosis of HCP. Antibiotic was an effective treatment.

Adult↗

[CT anatomic measurement of the optic canal and its clinical significance].

OBJECTIVE: To probe into the normal anatomy of the optic canal and its clinical significance. METHODS: The optic canals of 200 normal subjects were examined by thin layer CT scan in axial nd coronal positions. The distance and anatomic relationship with circumferentral structure were measured. RESULTS: In average: (1) The transverse diameter of the optic canal was (3.57 +/- 0.61) mm, the longitudinal diameter was (4.82 +/- 0.38) mm, the length of the inner wall was (12.62 +/- 2.59) mm, the length of the outer wall was (10.18 +/- 2.19) mm, and the length of the optic canal was (11.46 +/- 2.35) mm. The angle between optic canal and the middle line of the skull was 34.34 degrees +/- 6.48 degrees, the angle between optic canal and the intraorbital optic was 10.69 degrees +/- 6.48 degrees. The thickness of the inner wall was (0.68 +/- 0.46) mm. It showed no significant difference between the two sides of the optic canal in diameters(P > 0.05). (2) The optic canal, the superior orbital fissure and the inferior orbital fissure were respectively shown as track, crack and gorge type in CT axial pictures, while in the coronal pictures, they were respectively shown as butterfly eyes, horizontal fissure and vertical fissure type. (3) The relationship of the posterior ethmoid sinus and the optic canal was: anterocanal(42.00%), semicanal(27.5%), whole-canal(18.75%), sella turcica(9.75%) and circumcanal(2.00%). (4) The relationship of the position of the sphenoidal sinus and the optic canal was: I degree sphenoidal sinus(20%), II degree (63%) and III degree (17%). (5) The incidence of the bony defect of the inner optic canal wall was 25.5%. The range of the defect was (5.07 +/- 2.52) mm. CONCLUSION: It's a reliable way to show the relation of the optic canal and circumcanal by CT, and it is of important value in operation.

Adolescent↗

[The study about the characteristics of upper airway in obstructive sleep apnea syndrome].

OBJECTIVE: To investigate the upper airway (UA) characteristics of the patient's with obstructive sleep apnea syndrome (OSAS) and analyses the value of computer assisting fiberoptic pharyngoscopy with müller's maneuver (CFPMM) in topodiagnosis of OSAS. METHODS: The pharyngxes of 30 cases with OSAS and 30 controls were examined by CFPMM. The cross-section area at velo- and tongue-pharyngeal, pharyngeal collapsibility, sites of UA obstructive and their anatomical factors were measured and calculated and the correlation between the anatomical abnormalities of UA and outcomes of polysomnography (PSG) were analysed. RESULTS: 1. CFPMM can accurately measure and calculate the cross-section area of the upper airway. 2. mean areas of velopharyngeal and tongue-pharyngeal were significantly less than those in control subjects (all P < 0.05). OSAS patient's also showed relatively much larger collapsibility at sach site of the UA than controls. 3. At müller's maneuver, all the areas of OSAS patient's were below 40 mm2 and 60% cases appeared complete occlusion in pharyngeal. 4. All patient's had obstruction at velopharymx and airway collapses at multiple sites in 40% of cases. 5. At velopharyngeal the anatomical factors causing obstruction mainly were posterior displacement of soft palate, thicken and collapse of the pharyngeal wall. Besides the redundant lymph tissue at tongue base and posterior displacement of the tongue base, enlarged inferior pole of tonsil and collapse of pharyngeal wall played an important role at tongue-pharyngeal obstruction. 6. Diminished pharyngeal apertures and collapsibility were associated with increased rates of apnea and hypopnea index (P < 0.05). CONCLUSION: 1. CFPMM is able to measure and calculate UA's cross-section area and collapsibility, determine the site of obstruction, and helping the treatment. 2. Complete occlusion of UA at müller's maneuver is the criterion to determine site of UA obstruction in OSAS patient's during waking hours. 3. The anatomical abnormalities of UA of patients is reflects the severity of the OSAS.

Adult↗

[Value of preservation of uvula in uvulopalatopharyngoplasty].

OBJECTIVE: To explore the effect of the modified Uvulopalatopharyngoplasty (UPPP) where uvula is preserved in the operation, and whether the postoperative complications are diminished. METHODS: Thirty consecutive patients with the obstructive sleep apnea syndrome (29 men, 1 woman) were analyzed by questionnaire, polysomnography and oral cavity measurement before and 6 months after uvulopalatopharyngoplasty to assess the surgical outcome and value of preservation of uvula in the operation. RESULTS: Eighty-seven percent of patients reported improvement of snoring and daytime sleepiness. Fifty-three percent of patients showed a decrease of at least 50% in the apnea and hypopnea indices. Among the mild and moderate obstructive sleep apnea (AHI < 50), 73.3% of them showed a decrease of at least 50% in the AHI. No velopalatal insufficiency occurred. The result of oral cavity measurement showed that the uvula, which was preserved completely during the operation, began to contract 2 weeks after the operation. Three to six month after operation, uvula contracted to the normal length and the anatomical shape of the pharyngeal cavity became normal. CONCLUSIONS: The results of the uvula preserving UPPP indicate that this approach not only improves the effect of the UPPP, but also avoids the postoperative complications. The uvula that preserved completely during the operation will contract to the normal length progressively.

Adult↗

Polymorphism of angiotensin-converting enzyme gene and genetic susceptibility to asthma with familial aggregation.

OBJECTIVE: Angiotensin-converting enzyme (ACE) plays a key role in the metabolism of angiotensin II (AT II) and inactivation of bradykinins and tachykinins, which are potent bronchialconstrictors and mediators of inflammation asthma, and ACE is heavily expressed in the lungs. An insertion-deletion (D/I) polymorphism of ACE gene has been shown to be associated with levels of ACE. We investigate whether the polymorphism of ACE gene is associated with asthma and bronchial responsiveness. METHODS: A case-control study was carried out in 50 asthmatics, 7 families with at least 2 asthmatic individuals, and 50 healthy subjects. The insertion/deletion (I/D) polymorphism of ACE gene was amplified by polymerase chain reaction (PCR). Methacholine brocho-provocation and pulmonary function tests were performed in all asthmatics. RESULTS. There was an higher gene frequency of DD genotype of ACE gene in asthmatic subjects and families individuals compared with healthy subjects (46%, 53% vs 16%, P<0.05; odd ratio 4.98). An- higher prevalence of DD genotype of ACE was in patients with bronchial hyperresposiveness (BHR) (67% vs 33%, P<0.05; odd ratio 3.8). Accordingly, the mean values of FEV1% and FEV1/FVC were higher in asthmatics carrying non-DD alleles than patients with DD genotype (73.78% vs 56.56%, P<0.05, 79.19% vs 69.29%, P<0.05, respectively). CONCLUSION: These results suggested that DD allele of ACE genotype was significantly involved in genetic susceptibility to asthma. DD genotype of ACE might be a risk factor for the degree of airway obstruction, it could also be implicated in pathogenesis of bronchial hyperresponsiveness.

Adolescent↗

[Change of angiotensin system activity and the effects of corticosteroid on it in asthmatic guinea pigs].

OBJECTIVE: To investigate the role of angiotensin system(ATs) and effect of corticosteroid on ATs activity at the onset of asthma. METHODS: After establishing asthmatic model of guinea pig by intraperitoneal injection with ovalbumin to sensitize and inhalation with the same sensitizer 3 weeks later to induce asthma attack, the levels of angiotensin(AT) I and AT II and the activity of angiotensin converting enzyme(ACE) were measured respectively in extractive fluid of chopped lung tissue, bronchial alveolar lavage fluid (BALF) and plasma (ACE activity in serum) in three groups of experimental guinea pigs including asthmatic group, control group and corticosteroid group. RESULTS: In the chopped lung tissue and BALF, the AT I, AT II levels and the ACE activity in the asthmatic group were significantly higher than that in the control group(P < 0.01), however, they did not differ significantly each other in plasma in three groups(P > 0.05). In corticosteroid group, the levels of AT I, AT II and ACE activity were significantly decreased in the BALF compared with that in the asthmatic group(P < 0.01). CONCLUSION: The results suggest that the lung tissue may have a local angiotensin system that may be activated and play a role in asthma attack, and the inhibition of ATs activity may be one of the mechanisms in the effects of inhaled corticosteroid on prevention and control of asthma.

Adrenal Cortex Hormones↗

[Expression of inducible nitric oxide synthase in asthmatic rat lung].

OBJECTIVE: In order to study the role of nitric oxide (NO) during the airway inflammation of asthmatic rat, we investigated expression of inducible nitric oxide synthase (iNOS) in the lung tissue of asthmatic rats. METHODS: Animal model of asthmatic Wistar rats was developed by being sensitized and challenged with ovalbumin. Activities of iNOS were measured by using SP immunohistochemical method. RESULTS: In asthmatic rat group (n = 10), lung tissue showed stronger immunostaining (90%) for iNOS than control group (20%) (P < 0.001). Immunostaining was mainly present in the bronchial epithelium, alveolar epithelium, bronchial smooth muscle, vascular endothelial and smooth muscle cells and inflammatory cells such as macrophages and neutrophils. In glucocorticoid treated group (n = 10), there was down regulation of iNOS immunoreactivity (30% positive) compared with control asthmatic rat group (20%). CONCLUSIONS: The increased expression of iNOS in asthmatic rat lung tissue showed NO playing a critical role in asthmatic inflammation, otherwise expression of iNOS was inhibited by glucocorticoid.

Animals↗

The bi-directional regulation of filamin on the ATPase activity of smooth muscle myosin.

OBJECTIVE: The aim of this study is to investigate the functional relationship between filamin, a known actin binding protein, and myosin and the effects of filamin on the interaction between myosin and actin. METHODS: Ultra-centrifugation method was used to investigate the binding of filamin to both phosphorylated and unphosphorylated myosins. Mg-ATPase activities of both phosphorylated and unphosphorylated myosins in the presence and absence of actin were measured to observe the effects resulted from filamin-actin and filamin-myosin interactions. RESULTS: It was found that filamin is also a myosin binding protein. Filamin inhibited the actin activated Mg-ATPase activity of phosphorylated myosin and stimulated Mg-ATPase of phosphorylated myosin in the absence of actin; in addition, filamin stimulated Mg-ATPase activity of unphosphorylated myosin in both the presence or absence of actin. CONCLUSION: The result suggest that the effects of filamin on the myosin Mg-ATPase activities are bi-directional, i.e., stimulatory via binding to myosin and inhibitory via binding to actin.

Actins↗

[Photochemistry study on novel water soluble thioxanthone photoinitiators].

The photochemistry of nine water soluble thioxanthone photoinitiators was examined by UV absorption, fluorescence, phosphorescence and ESR techniques. Maximal absorption, extinction coefficients, fluorescence and phosphorescence quantum yields, ESR intensity were determined. The solvent effects on absorption and fluorescence as well as the relationship between structure and photochemical activities were discussed.

Electron Spin Resonance Spectroscopy↗

Predominant expression of the mitochondrial dicarboxylate carrier in white adipose tissue.

We report the identification of a novel mouse protein closely related to the family of mitochondrial uncoupling proteins and the oxoglutarate carrier. The cDNA encodes a protein of 287 amino acids that shares all the hallmark features of the mitochondrial transporter superfamily, including six predicted transmembrane domains. It is nearly identical to the sequence recently reported for the rat mitochondrial dicarboxylate carrier (DIC). We find that murine DIC (mDIC) is expressed at very high levels in mitochondria of white adipocytes and is strongly induced in the course of 3T3-L1 adipogenesis. To determine the consequences of the presence of mDIC on the mitochondrial membrane potential, we transiently expressed mDIC in 293-T cells. Overexpression of mDIC leads to significant mitochondrial hyperpolarization. In addition, exposure to cold down-regulates mDIC levels in vivo. In contrast, free fatty acids lead to an up-regulation of mDIC protein in 3T3-L1 adipocytes. This is the first report demonstrating preferential expression in white adipose tissue of any mitochondrial transporter. However, it remains to be determined which metabolic pathways most critically depend on high level expression of mDIC in the adipocyte.

3T3 Cells↗

T cell-derived IL-10 promotes lung cancer growth by suppressing both T cell and APC function.

We have found previously that human lung cancers potently induce T lymphocyte IL-10 production in vitro. To assess the impact of enhanced T cell-derived IL-10 on antitumor immunity in vivo, we utilized transgenic mice expressing IL-10 under the control of the IL-2 promoter. We have shown previously that Lewis lung carcinoma cells (3LL) have more aggressive growth potential in IL-10 transgenic mice compared with control littermates. In this study, we show that transfer of T cells from IL-10 transgenic mice to control littermates transferred the IL-10 immunosuppressive effect and led to enhanced 3LL tumor growth. In addition to changes in T cell-mediated immunity, professional APC from IL-10 transgenic mice were found to have significantly suppressed capacity to induce MHC alloreactivity, CTL responses, and IL-12 production. Tumor Ag-pulsed dendritic cells from IL-10 transgenic mice also failed to generate antitumor reactivity. These results suggest that increased levels of T cell-derived IL-10 severely impair antitumor immunity in vivo, due to defects in both T cell and APC function.

Adoptive Transfer↗

Cleavage of the death domain kinase RIP by caspase-8 prompts TNF-induced apoptosis.

Although the molecular mechanisms of TNF signaling have been largely elucidated, the principle that regulates the balance of life and death is still unknown. We report here that the death domain kinase RIP, a key component of the TNF signaling complex, was cleaved by Caspase-8 in TNF-induced apoptosis. The cleavage site was mapped to the aspartic acid at position 324 of RIP. We demonstrated that the cleavage of RIP resulted in the blockage of TNF-induced NF-kappaB activation. RIPc, one of the cleavage products, enhanced interaction between TRADD and FADD/MORT1 and increased cells' sensitivity to TNF. Most importantly, the Caspase-8 resistant RIP mutants protected cells against TNF-induced apopotosis. These results suggest that cleavage of RIP is an important process in TNF-induced apoptosis. Further more, RIP cleavage was also detected in other death receptor-mediated apoptosis. Therefore, our study provides a potential mechanism to convert cells from life to death in death receptor-mediated apoptosis.

Adaptor Proteins, Signal Transducing↗

Response tuning in bacterial chemotaxis.

Chemotaxis of enteric bacteria in spatial gradients toward a source of chemoattractant is accomplished by increases in the length of swimming runs up the gradient. Biochemical components of the intracellular signal pathway have been identified, but mechanisms for achieving the high response sensitivity remain unknown. Binding of attractant ligand to its receptor inactivates a receptor-associated histidine kinase, CheA, which phosphorylates the signal protein CheY. The reduction in phospho-CheY, CheY-P, levels prolongs swimming runs. Here, the stimulus-response relation has been determined by measurement of excitation responses mediated by the Tar receptor to defined concentration jumps of the attractant, aspartate, administered within milliseconds by photolysis of a photolabile precursor. The bacteria responded to <1% changes in Tar occupancy when adapted to aspartate over concentrations spanning three orders of magnitude. Response amplitudes increased approximately logarithmically with stimulus strength, extending responsiveness over a greater stimulus range. The extent and form of this relation indicates that, in contrast to mechanisms for adaptive recovery, excitation signal generation involves amplification based on cooperative interactions. These interactions could entail inactivation of multiple receptor-CheA signaling complexes and/or simultaneous activation of CheY-P dephosphorylation.

Adaptation, Physiological↗

Chimeric analysis of a neuronal nicotinic acetylcholine receptor reveals amino acids conferring sensitivity to alpha-bungarotoxin.

We have investigated the molecular determinants responsible for alpha-bungarotoxin (alphaBgtx) binding to nicotinic acetylcholine receptors through chimeric analysis of two homologous alpha subunits, one highly sensitive to alphaBgtx block (alpha1) and the other, alphaBgtx-insensitive (alpha3). By replacing rat alpha3 residues 184-191 with the corresponding region from the Torpedo alpha1 subunit, we introduced a cluster of five alpha1 residues (Trp-184, Trp-187, Val-188, Tyr-189, and Thr-191) into the alpha3 subunit. Functional activity and alphaBgtx sensitivity were assessed following co-expression in Xenopus oocytes of the chimeric alpha3 subunit (alpha3/alpha1[5]) with either rat beta2 or beta4 subunits. Agonist-evoked responses of alpha3/alpha1[5]-containing receptors were blocked by alphaBgtx with nanomolar affinity (IC(50) values: 41 nM for alpha3/alpha1[5]beta2 and 19 nM for alpha3/alpha1[5]beta4). Furthermore, receptors containing the single point mutation alpha3K189Y acquire significant sensitivity to alphaBgtx block (IC(50) values: 186 nM for alpha3K189Ybeta2 and 179 nM for alpha3K189Ybeta4). Another alpha3 chimeric subunit, alpha3/alpha7[6], similar to alpha3/alpha1[5] but incorporating the corresponding residues from the alphaBgtx-sensitive alpha7 subunit, also conferred potent alphaBgtx sensitivity to chimeric receptors when co-expressed with the beta4 subunit (IC(50) value = 31 nM). Our findings demonstrate that the residues between positions 184 and 191 of the alphaBgtx-sensitive subunits alpha1 and alpha7 play a critical functional role in the interaction of alphaBgtx with nicotinic acetylcholine receptors sensitive to this toxin.

Amino Acid Sequence↗

Accommodated xenografts survive in the presence of anti-donor antibodies and complement that precipitate rejection of naive xenografts.

Hamster hearts transplanted into transiently complement-depleted and continuously cyclosporin A (CyA)-immunosuppressed rats survive long-term despite deposition of anti-donor IgM Abs and complement on the graft vascular endothelium. This phenomenon is referred to as "accommodation." The hypothesis tested here is that accommodated xenografts are resistant to IgM Abs and complement that could result in rejection of naive xenografts. After first hamster hearts had been surviving in cobra venom factor (CVF) + CyA-treated rats for 10 days, a time when the anti-donor IgM Ab level was maximal and complement activity had returned to approximately 50% of pretreatment levels, naive hamster hearts or hamster hearts that had been accommodating in another rat for 14 days were transplanted into those rats carrying the surviving first graft. The naive hearts were all hyperacutely rejected. In contrast, a majority of regrafted accommodating hearts survived long-term. There was widespread Ab and activated complement deposition on the vascular endothelium of accommodating first hearts, second accommodating hearts, and rejected second naive hearts. However, only the rejected naive hearts showed extensive endothelial cell damage, myocardial necrosis, fibrin deposition, and other signs of inflammation. Accommodating first and second hearts but not rejected second naive hearts expressed high levels of the protective genes A20, heme oxygenase-1 (HO-1), bcl-2, and bcl-xL. These data demonstrate that accommodated xenografts become resistant to effects of anti-donor IgM Abs and complement that normally mediate rejection of xenografts. We hypothesize that this resistance involves expression by accommodated xenografts of protective genes.

Adoptive Transfer↗

Camouflaging endothelial cells: does it prolong graft survival?

Camouflaging antigens on the surface of cells seems an appealing way to prevent activation of the immune system. We explored the possibility of preventing hyperacute rejection by chemically camouflaging endothelial cells (EC). In vitro as well as in vivo experiments were performed. First, the ability of mPEG coating to prevent antibody-antigen interactions was evaluated. Second, we tested the degree to which mPEG coating prevents activation of EC by stimuli such as TNF-alpha and LPS. Third, in vivo experiments were performed to test the ability of mPEG coating to prolong xenograft survival. We demonstrate that binding of several antibodies to EC or serum proteins can be inhibited by mPEG. Furthermore, binding of TNF-alpha as well as LPS to EC is blocked since mPEG treatment of EC inhibits the subsequent up-regulation of E-selectin by these stimuli. However, in vivo experiments revealed that currently this method alone is not sufficient to prevent hyperacute rejection.

Animals↗

Identification of four novel ADAMs with potential roles in spermatogenesis and fertilization.

The ADAM (A Disintegrin And Metalloprotease) family is known to have important roles in various developmental systems, e.g., myogenesis and neurogenesis. In this study, we searched for ADAMs that may function in spermatogenesis or fertilization, and have cloned and sequenced four new mouse ADAM cDNAs: ADAM 24, ADAM 25, ADAM 26 and ADAM 27. The deduced amino acid sequences show that all four contain the complete domain organization common to ADAM family members. Messenger RNA for each of the four ADAMs was found only in the testis. The conserved zinc-dependent metalloprotease active site HEXGHXXGXXHD was found in the metalloprotease domain of three of the novel ADAMs, suggesting that they are testis-specific proteases, to which we give the alternative names: testase 1, ADAM 24; testase 2, ADAM 25; and testase 3, ADAM 26. Using RNA extracted from testes of pre-pubertal males of increasing age (8-40days), we found that adult levels of transcription, assessed in Northern blots, are reached by day 20 (ADAM 27), day 25 (ADAMs 24 and 25) and in the range day 25-50 (ADAM 26). These results suggest that each ADAM is transcribed in spermatogenic cells in a regulated pattern at a specific developmental stage.

ADAM Proteins↗