Semivolatile organic pollutants in water, suspended solids, and surface sediments of the Huaihe River, Jiangsu Section, People's Republic of China.
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China↗
Biomedical subjects
L Jing
Publications and source records attributed to L Jing.
Aldehyde and monocyclic aromatic hydrocarbon mixing ratios at an urban site in Las Vegas, Nevada.
Oxidation of benzene, toluene, ethylbenzene, and xylenes (BTEX) in air, of significance due to, for example, the potential for O3 formation, is believed to be initiated by OH attack on the ring (addition) or on the alkyl side chain (H abstraction). A series of ring-breaking reactions follows, with major products predicted to be alpha-dicarbonyls, simple aldehydes, and organic acids. To test this prediction, ambient air mixing ratios of aldehydes (formaldehyde, acetaldehyde, benzaldehyde, glyoxal, and pyruvaldehyde), along with some supporting BTEX data, were measured at an urban site in Las Vegas, NV. Samples were collected on sorbents and determined by chromatographic methods; mixing ratios were compared to ambient levels of CO, O3, and NOx. A meteorological analysis (temperature, wind speed, and wind direction) was also included. Statistically significant relationships were noted among the BTEX hydrocarbons (HCs) and among the photochemically derived species (e.g., O3, NO2, and some of the aldehydes), although there was seasonal variation. The observations are consistent with a common primary source (i.e., vehicular exhaust or fuel evaporation) for the BTEX compounds and a common secondary source (e.g., OH attack) for glyoxal and pyruvaldehyde.
Air Pollutants↗
[The effectiveness of cyclosporin A in the treatment of autoimmune hemolytic anemia and Evans syndrome].
OBJECTIVE: To test the therapeutic effectiveness of cyclosporin A (CsA) in combination with corticosteroid in the treatment of autoimmune hemolytic anemia(AIHA) and Evans syndrome. METHODS: Forty-four cases of AIHA and Evans syndrome were treated with CsA in combination with a conventional regimen (prednisone + danazol) (18 cases) or conventional regimen alone(26 cases). RESULTS: The complete response rate of CsA group (88.9%) was higher than that of conventional regimen group (57.7%) (P < 0.05), and the relapse rate was lower (3.3% vs 70%) (P < 0.01). CONCLUSION: CsA in combination with conventional regimen can improve the complete response rate and reduce relapse of AIHA and Evans syndrome.
Adolescent↗
[Role of epithelial cell proliferation and apoptosis in human middle ear cholesteatoma].
OBJECTIVE: To determine the role of middle ear epithelial cell proliferation and apoptosis in the pathogenesis of human cholesteatoma. METHOD: 33 cholesteatoma, 25 auditory meatal skin of cholesteatoma and 10 normal human auditory meatal skin were detected by using immunohistochemistry analysis for cell proliferation with Ki 67, PCNA and PCNA antibody and TUNTEL methods for cell apoptosis. RESULT: PCNA expression and apoptosis cells exists different quantity in cholesteatoma, auditory metal skin of cholesteatoma and normal human auditory meatal skin and distributes in various cell layer. There were positive correlation between p53 and PCNA as well as negative correlation between p53 and apoptosis. CONCLUSION: The dyregulation of proliferation and apoptosis in keratinocyte is important in pathogenesis of cholesteatoma.
Adolescent↗
Frequency of SCA1, SCA2, SCA3/MJD, SCA6, SCA7, and DRPLA CAG trinucleotide repeat expansion in patients with hereditary spinocerebellar ataxia from Chinese kindreds.
OBJECTIVE: To assess the frequency of SCA1 (spinocerebellar ataxia type 1), SCA2, SCA3/MJD (spinocerebellar ataxia type 3/Machado-Joseph disease), SCA6, SCA7, and DRPLA (dentatorubropallidoluysian atrophy) CAG trinucleotide repeat expansions [(CAG)n] among persons diagnosed with hereditary SCA from Chinese families. PATIENTS AND METHODS: Spinocerebellar ataxia type 1, SCA2, SCA3/MJD, SCA6, SCA7, and DRPLA (CAG)n mutation were detected with the polymerase chain reaction, highly denaturing polyacrylamide gel electrophoresis, and silver staining technique in 167 patients with autosomal dominant SCA from 85 Chinese families and 37 patients with sporadic SCA. RESULTS: Spinocerebellar ataxia type 1 (CAG)n mutation in 7 patients from 4 kindreds (4.70%) was expanded to 53 to 62 repeats. Spinocerebellar ataxia type 2 (CAG)n mutation in 12 patients from 5 kindreds (5.88%) was expanded to 42 to 47 repeats. Spinocerebellar ataxia type 3/Machado-Joseph disease (CAG)n mutation in 83 patients from 41 kindreds (48.23%) was expanded to 68 to 83 repeats. Sixty-five patients from 35 kindreds (41.19%) and 37 patients with sporadic SCA did not test positive for SCA1, SCA2, SCA3/MJD, SCA6, SCA7, or DRPLA. There was a predictable inverse relationship between the number of CAG repeats and the age at onset for SCA3/MJD and SCA2. Clinically, dementia and hyporeflexia were more frequent in patients with SCA2, while spasticity, hyperreflexia, and Babinski signs were more frequent in patients with SCA3/ MJD, and those might be helpful in clinical work to primarily distinguish patients with SCA3/MJD and SCA2 from others with different types of SCA. CONCLUSIONS: The frequency of SCA3/MJD is substantially higher than that of SCA1 and SCA2 in patients with autosomal dominant SCA from Chinese kindreds, who are non-Portuguese. Clinical expressions of the various types of SCAs overlap one another; therefore, for clinical study it is important to make a gene diagnosis and genetic classification for patients with SCA.
Adolescent↗
Characterization of monoclonal antibodies to glycodelin and recombinant glycodelin.
Glycodelin-A belongs to the lipocalin superfamily. Although it is associated with normal endometrial growth during the menstrual cycle, fertilization and normal pregnancy in humans, the molecular mechanism of its biological action has not been elucidated. To undertake studies to understand the functional relevance of any molecule, obtaining large quantities of the protein becomes essential. With the ultimate aim of purifying glycodelin either from its natural sources (human amniotic fluid) or the recombinant glycodelin from bacterial recombinant lysates, we raised monoclonal antibodies to this protein. As immunogens, recombinant glycodelin expressed in E. coli and Pichia pastoris as well as glycodelin from amniotic fluid were used. The monoclonal antibodies generated were characterized with respect to binding to both the native as well as the recombinant proteins using ELISA, immunoblotting, and immunohistochemistry.
Amniotic Fluid↗
Nitrotyrosine causes selective vascular endothelial dysfunction and DNA damage.
Vascular endothelial dysfunction is recognized as a contributor to a wide array of cardiovascular disease states, but the initiating events involved are incompletely defined. Elevated plasma levels of free 3-nitro-L-tyrosine (3NT, biomarker of peroxynitrite formation) have been measured in settings of endothelial dysfunction, but its pathologic significance is unknown. We tested the hypothesis that clinically demonstrated concentrations of 3NT can induce vascular and endothelial dysfunction in vitro. Further studies evaluated involvement of DNA fragmentation and/or apoptosis as a potential mechanism. Preincubation of rat thoracic aorta segments with 3NT (100, 250 microM) resulted in selective, concentration-dependent impairment of acetylcholine (ACH) maximal response, with no change in KCL, phenylephrine, nitroprusside, or ACH EC50 effects (ACH Emax, 53+/-2, 42+/-5, 31+/-2%; Control, 100 microM, 250 microM 3NT). Vascular segments treated with 3NT also demonstrated concentration-dependent DNA damage, assessed using DNA nick-end labeling techniques (TUNEL staining), compared with control (TUNEL-positive nuclei/linear mm: 5.4+/-1.2, 13.7+/-1.2, 16.9+/-3.2; Control, 100 microM, 250 microM 3NT), which was confined to the endothelial layer. Equimolar tyrosine had no significant effects. Frequency of positively stained nuclei was statistically correlated to extent of endothelial dysfunction (p < 0.01). Free 3NT is apparently more than a benign biomarker in vivo, and may contribute to vascular endothelial dysfunction through promotion of DNA damage and/or apoptosis.
Acetylcholine↗
[A case of LGMD2A identified with both western blot analysis and immunostaining of calpain 3 in biopsied muscle].
A 45-year-old housewife had proximal dominant limb muscle weakness from around 25 years of age. Her parents were cousins. None of family members was affected. Progressive muscle weakness and atrophy were prominent at the posterior compartments of legs and trunk. Serum CK was moderately elevated. Muscle pathology revealed variation in fiber size, moderate increase in numbers of internal nuclei and abundant lobulated fibers. On immunostaining using by monoclonal antibody against human calpain 3 (NCL-CALP-2 C4; Novocastra) to the biopsied muscle, calpain 3 was completely absent in the sarcoplasm, while granular debris and in part positive striation were noted in control muscle. By Western blot analysis, a band corresponding to 94 kDa of calpain 3 was not detected. A genetic analysis of calpain 3 revealed homozygous C-565-G mutation (Leu189Val). From the present study. Western blot analysis and immunostaining by using calpain 3 antibody were suggested to be useful to diagnose LGMD2A in LGMD patients.
Biomarkers↗
Depolarization of membrane potential and the smooth muscle contraction by isothiocyanatobenzyl imidazoline in guinea-pig stomach circular muscle.
Isothiocyanatobenzyl imidazoline (IBI) produces characteristic slowly developing contraction of many smooth muscle preparations including the circular smooth muscle of the guinea-pig stomach. Changes in the membrane potential were recorded intracellularly, and the muscle contraction induced by IBI was investigated. IBI at 100 micromol/l slowly produced a sustained depolarization of the membrane with a maximum change of approximately 15 mV. This depolarization could not be blocked by 1-hyoscyamine, 100 nmol/l. An imidazoline analogue, oxymetazoline at 1 micromol/l, did not change the resting membrane potential as observed after IBI. Significant membrane depolarization after IBI still occurred in Ca2+-free medium. During IBI-induced depolarization, sudden reduction of Na+ to 30 mmol/l in the medium reduced the depolarization slightly. IBI-induced depolarization was additive with that produced by 20 mmol/l K+ in the medium. In the presence of tetraethylammonium chloride or levcromakalim or nifedipine, IBI continued to depolarize the membrane although functional pharmacological experiments showed that the contractile effects of IBI were significantly inhibited by 30 micromol/l levcromakalim and abolished by 100 nmol/l nifedipine. At 100 micromol/l phentolamine (reported by others as an inhibitor of ATP-sensitive potassium channels) completely blocked IBI-induced contraction. Phentolamine (30 micromol/l) blocked the contractile effects of IBI by 50%. On the other hand, S(-)-Bay K 8644, a voltage-dependent calcium channel activator, was additive with the contractile response of IBI. These results indicated that IBI produced membrane depolarization and contraction of the guinea-pig stomach circular muscle, by a mechanism not involving muscarinic receptors or alpha-adrenoceptors. Even though levcromakalim, an ATP-sensitive potassium channel opener, could not inhibit IBI-induced depolarization, the ATP-sensitive potassium channel and the voltage-dependent calcium channel may be intrinsically linked with the action of IBI.
Animals↗
Macrophage inflammatory protein 1 alpha expression by synovial fluid neutrophils in rheumatoid arthritis.
OBJECTIVE: To determine the contribution made by synovial fluid (SF) neutrophils to the augmented expression of macrophage inflammatory protein 1 alpha (MIP-1alpha) in rheumatoid arthritis (RA). METHODS: Neutrophils were isolated from samples of SF from RA patients and peripheral blood (PB) samples from RA patients and healthy controls. Cell associated MIP-1alpha was visualised immunohistochemically, and cell associated MIP-1alpha as well as MIP-1alpha secreted into the SF was assayed by ELISA. Steady state expression of MIP-1alpha mRNA was assessed by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: Freshly isolated SF neutrophils contained significantly higher concentrations of both MIP-1alpha protein and its transcript than PB neutrophils from either RA patients or healthy controls; incubation in the absence or presence of tumour necrosis factor alpha for 24 hours resulted in a significant increase in MIP-1alpha secretion by RA SF neutrophils compared with neutrophils obtained from either normal PB or RA PB; and expression of MIP-1alpha by SF neutrophils was well correlated with both RA disease activity and SF mononuclear cell (MNC) counts. CONCLUSION: Expression and secretion of MIP-1alpha by SF neutrophils may be indicative of local and systemic inflammation in RA. Moreover, this C-C chemokine may contribute to the recruitment of MNCs from the bloodstream into synovial joints and tissues.
Adult↗
Vascular peroxynitrite formation during organic nitrate tolerance.
Nitroglycerin (NTG) is an important cardiovascular agent, but tolerance during continuous administration limits its clinical utility. Increased vascular superoxide production may mediate nitrate tolerance via a reduction in nitric oxide availability. Because superoxide anion and nitric oxide react avidly to form peroxynitrite, an aggressive cellular toxicant that nitrates protein tyrosine residues, we tested the hypotheses that protein nitration, indicative of peroxynitrite formation, occurs during vascular tolerance, and that protein nitration participates in tolerance development. Preincubation of rat thoracic aorta segments with NTG (22 microM, EC(95) for 30 min) caused a significant shift in NTG relaxation response (EC(50); 6.7 +/- 1.7 versus 0.50 +/- 0.13 microM, NTG versus vehicle, p <.05). After functional evaluations, tissues were fixed in formalin for immunohistochemistry and digital image analysis. NTG-induced vascular tolerance was associated with increased immunoprevalence of 3-nitrotyrosine (3NT, stable biomarker of protein nitration; 11.41 +/- 2.48 versus 0.04 +/- 0.02% positive pixels, NTG versus vehicle, p < .05). Staining was observed throughout vascular smooth muscle layers. Addition of 500 microM free tyrosine to the preincubation medium did not alter tolerance development (NTG EC(50) 6.5 +/- 3.0 microM) but abolished 3NT immunoprevalence (0.16 +/- 0.10%). No significant relationship between NTG potency and 3NT immunoprevalence was observed. These data support the hypothesis that protein nitration occurs during nitrate vascular tolerance, however, it apparently does not mediate this phenomenon.
Animals↗
Stabilization and reactivation of the p53 tumor suppressor protein in nontumorigenic revertants of HeLa cervical cancer cells.
We demonstrated previously that loss of in vitro transformation and in vivo tumorigenicity in two independent revertant clones of HeLa cells (designated HA and HF) resulted from dominant-acting genetic changes. Analysis of the p53 tumor suppressor gene revealed stabilization and at least partial restoration of wild-type p53 transactivation properties pathways in both revertants of HPV-induced cell transformation. The half-lives of the p53 protein and both of the HA and HF clones were increased approximately 4 fold compared with the parental HeLa cells (16, 17, and 4 min, respectively). The levels of E6 viral protein expression were similar in the three cell lines, whereas the levels of the ubiquitin ligase protein, E6 associated protein (E6-AP), were elevated in the revertants. Western blot analysis of immunoaffinity-purified p53 demonstrated that stabilization of p53 in the revertants was correlated with a reduction in the in vivo formation of complexes involving the E6 oncoprotein and p53. Stabilization of p53 function in the revertants did not result from mutations in either the p53 or E6-AP genes. Despite the observed stabilization and restoration of p53 transactivation function in the revertants, exposure of the revertants to DNA-damaging agents did not result in elevated levels of p21(waf-1) protein and failed to induce growth arrest in the G1 phase of the cell cycle. However, p53-independent induction of p21(waf-1) protein also failed to induce the G1 phase of the cell cycle. Thus, restoration of wild-type p53 transactivation activity in the HA and HF revertants is insufficient to induce G1 arrest and reversion from HPV-induced cell transformation in our model system.
Cell Division↗
[Fluid therapy for acute brain edema in children].
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Brain Edema↗
[Determination of oridonin in Rabdosia rubescens by TLC-scanning method].
We have determingd the content of oridonin in Rabdosia rubescens Hemsl by TLC-scenning method. This method is proved to be simple, fast, precise and sensitive, and the result is stable, repetition property is good. Its rate of recovery is as high as 98.03 percent.
Antineoplastic Agents↗
[Clinico-pathological significance of the immunostaining of myosin heavy chain isoforms in pathological human skeletal muscle].
Expression of the four myosin heavy chain isoforms (fast-twitch, slow-twitch, neonatal and embryonal isoforms) was immunohistochemically observed in 500 biopsied limb muscles of neuromuscular disorders. Fast-twitch isoform was expressed in type 2A, 2B and pathologic 2C fibers. Slow-twitch isoform was expressed in type 1 and 2C fibers. Embryonic isoform was expressed in regenerating type 2C fibers of active myopathies such as Duchenne dystrophy and polymyositis. Expression of neonatal isoform, which was longer positive than that of embryonic isoform, was noted in regenerating fibers, denervated fibers and highly atrophic fibers in chronic myopathies of limb-girdle dystrophy and myotonic dystrophy. In conclusion, the immunostaining of MHC isoforms are useful to make a clinico-pathological diagnosis to determine the stages in evolution of regeneration or degeneration of pathologic muscle fiber per se.
Humans↗
The possible role of nitric oxide in relaxations and excitatory neuroeffector transmission in the cat airway.
1. To study the possible role of nitric oxide (NO free radical; NO) or NO-containing compounds in the non-adrenergic, non-cholinergic (NANC) relaxations, we observed the effects of carboxy-2-phenyl-4, 4, 5, 5-tetramethyl-imidazoline-1-oxyl-3-oxide (C-PTIO; a newly synthesized NO scavenger) on NANC relaxations in the cat airway. In addition, we also observed the effects of C-PTIO on excitatory junction potentials (EJPs), since NO has a prejunctional action on transmitter release. 2. Nitrosocystine (Cys-NO) (10(-7)-10(-3) M) dose-dependently relaxed the bronchial tissue in the presence of 5-HT, atropine and guanethidine and C-PTIO (10(-4) M) shifted the concentration-response curve of the Cys-NO to the right. 3. Electrical field stimulation (EFS) evoked biphasic NANC relaxations in the small bronchi of the cat. In general, C-PTIO suppressed non-selectively both the first and second components of the NANC relaxations to a similar extent. However, in some bronchial preparations C-PTIO (10(-4) M) selectively suppressed the first component of the NANC relaxation to approximately 50% of the initial value, enhancing the amplitude of the second component of the NANC relaxations. 4. After pretreatment of the bronchial tissues with alpha-chymotrypsin (1 unit ml-1) for 30 min in order to inhibit any response to peptides, EFS evoked monophasic NANC relaxation. C-PTIO (10(-5) - 10(-4) M) dose-dependently suppressed, and at a concentration of 10(-4) M almost halved, the amplitude of NANC relaxation. Additional application of L-NAME further reduced the C-PTIO-resistant NANC relaxation to 20-30% of the initial value. 5. C-PTIO (10(-4) M) enhanced the EJP amplitude evoked by single EFS in the trachea but not in the bronchi. However, C-PTIO enhanced the summation of the EJPs to repeated stimulation to a similar extent in the tracheal and bronchial tissues. Simultaneous application of C-PTIO and L-NAME did not further enhance the summation. 6. These results indicate that NO. and NO-containing compounds are involved in the L-NAME-sensitive NANC relaxation in the cat airway, and that only NO. has a prejunctional action which inhibits excitatory neuroeffector transmission.
Animals↗
[Immunostaining of anti-Bcl-2 antibody in diseased human muscles].
Immunostaining of Bcl-2 protein which represses apoptosis was performed on 178 biopsied human pathologic muscles and 10 control muscles by the ABC method using two monoclonal anti-Bcl-2 antibodies. Bcl-2 in control muscles was positive mainly in nuclear membrane and cytoplasm in type 2 fibers (especially type 2B fibers), and negative in type 1 fibers. In myopathies, it was not expressed in type 2C (regenerating) fibers, and its expression in atrophic fibers such as forming pyknotic nuclear clumps was strong. In inflammatory myopathies, expression was observed in infiltrating lymphocytes, and especially in dermatomyositis in atrophic fibers facing perimysium. In mitochondrial myopathies, the positivity was observed only in type 2 ragged-red fibers. In muscles of neurogenic disorders, both small angulated fibers and atrophic grouped fibers were strongly positive. Western blot analysis using anti-Bcl-2 antibody showed a single band at 26 kDa in control and diseased skeletal muscles. Compared to immunostaining of Fas antigen in serial sections, both Bcl-2 and Fas were expressed in same atrophic fibers in distal myopathy with rimmed vacuoles. In myotonic dystrophy, they were often expressed in type 2 fibers containing internal nucleus. In carriers of Duchenne dystrophy, Fas-positive but Bcl-2 negative fibers were observed in same dystrophin-negative fibers. In conclusion, expression of Bcl-2 in skeletal muscles might suggest that Bcl-2 plays a role on surviving muscle fibers.
Apoptosis↗
Regional difference in the distribution of L-NAME-sensitive and -insensitive NANC relaxations in cat airway.
1. To investigate the distribution profile of functional inhibitory non-adrenergic non-cholinergic (i-NANC) nerves and the contribution of NO to the NANC relaxation in the cat, we studied the effects of N omega-nitro-L-arginine methyl ester (L-NAME) on NANC relaxation elicited by electrical field stimulation (EFS) in the trachea, bronchus and bronchiole. 2. EFS applied to the tracheal smooth muscle during contraction induced by 5-HT (10(-5) M) in the presence of atropine (10(-6) M) and guanethidine (10(-6) M) elicited a monophasic NANC relaxation. By contrast, NANC relaxation elicited in the peripheral airway was biphasic, comprising an initial fast followed by a second slow component and L-NAME (10(-5) M) selectively abolished the first component without affecting the second one. In the trachea, L-NAME (10(-5) M) completely suppressed the monophasic NANC relaxation when single or short repetitive stimuli (< 5) with 1 ms pulse duration were applied. However, at higher repetitive stimuli (> 10) with 1 or 4 ms pulse duration, suppression of NANC relaxation was incomplete. 3. In the small bronchi obtained from L-NAME-pretreated cats, EFS applied during contraction induced by 5-HT (10(-5) M) elicited only the slow component of NANC relaxation which is sensitive to tetrodotoxin. 4. In the peripheral airway, a newly synthesized VIP antagonist (10(-6) M) or alpha-chymotrypsin (1 U ml-1) considerably attenuated the amplitude of L-NAME-insensitive relaxation. 5. Single or repetitive EFS consistently evoked excitatory junction potentials (EJPs) in the central and peripheral airways. When tissues were exposed to atropine (10(-6) M) and guanethidine (10(-6) M), single or repetitive EFS did not alter the resting membrane potential. 6. These results indicate that at least two neurotransmitters, possibly NO or NO-containing compounds and VIP, are involved in i-NANC neurotransmission and the distribution profile of the two components differs in the central and peripheral airway of the cat.
Animals↗