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Y Yang

Publications and source records attributed to Y Yang.

At least 775 records · Page 43Linked to original sources

Involvement of the gapA- and epd (gapB)-encoded dehydrogenases in pyridoxal 5'-phosphate coenzyme biosynthesis in Escherichia coli K-12.

We show that epd (gapB) mutants lacking an erythrose 4-phosphate (E4P) dehydrogenase are impaired for growth on some media and contain less pyridoxal 5'-phosphate (PLP) and pyridoxamine 5'-phosphate (PMP) than their epd+ parent. In contrast to a previous report, we found that gapA epd double mutants lacking the glyceraldehyde 3-phosphate and E4P dehydrogenases are auxotrophic for pyridoxine. These results implicate the GapA and Epd dehydrogenases in de novo PLP and PMP coenzyme biosynthesis.

Aldehyde Oxidoreductases↗

Identification and function of the pdxY gene, which encodes a novel pyridoxal kinase involved in the salvage pathway of pyridoxal 5'-phosphate biosynthesis in Escherichia coli K-12.

pdrK encodes a pyridoxine (PN)/pyridoxal (PL)/pyridoxamine (PM) kinase thought to function in the salvage pathway of pyridoxal 5'-phosphate (PLP) coenzyme biosynthesis. The observation that pdxK null mutants still contain PL kinase activity led to the hypothesis that Escherichia coli K-12 contains at least one other B6-vitamer kinase. Here we support this hypothesis by identifying the pdxY gene (formally, open reading frame f287b) at 36.92 min, which encodes a novel PL kinase. PdxY was first identified by its homology to PdxK in searches of the complete E. coli genome. Minimal clones of pdxY+ overexpressed PL kinase specific activity about 10-fold. We inserted an omega cassette into pdxY and crossed the resulting pdxY::omegaKan(r) mutation into the bacterial chromosome of a pdrB mutant, in which de novo PLP biosynthesis is blocked. We then determined the growth characteristics and PL and PN kinase specific activities in extracts of pdxK and pdxY single and double mutants. Significantly, the requirement of the pdxB pdxK pdxY triple mutant for PLP was not satisfied by PL and PN, and the triple mutant had negligible PL and PN kinase specific activities. Our combined results suggest that the PL kinase PdxY and the PN/PL/PM kinase PdxK are the only physiologically important B6 vitamer kinases in E. coli and that their function is confined to the PLP salvage pathway. Last, we show that pdxY is located downstream from pdxH (encoding PNP/PMP oxidase) and essential tyrS (encoding aminoacyl-tRNA(Tyr) synthetase) in a multifunctional operon. pdxY is completely cotranscribed with tyrS, but about 92% of tyrS transcripts terminate at a putative Rho-factor-dependent attenuator located in the tyrS-pdxY intercistronic region.

Amino Acid Sequence↗

Transduction of dendritic cells by DNA viral vectors directs the immune response to transgene products in muscle fibers.

Immune responses to vector-corrected cells have limited the application of gene therapy for treatment of chronic disorders such as inherited deficiency states. We have found that recombinant adeno-associated virus (AAV) efficiently transduces muscle fibers in vivo without activation of cellular and humoral immunity to neoantigenic transgene products such as beta-galactosidase, which differs from the experience with recombinant adenovirus, where vibrant T-cell responses to the transgene product destroy the targeted muscle fibers. T cells activated following intramuscular administration of adenovirus expressing lacZ (AdlacZ) can destroy AAVlacZ-transduced muscle fibers, indicating a prior state of immunologic nonresponsiveness in the context of AAV gene therapy. Adoptive transfer of dendritic cells infected with AdlacZ leads to immune mediated elimination of AAVlacZ-transduced muscle fibers. AAVlacZ-transduced antigen-presenting cells fail to demonstrate beta-galactosidase activity and are unable to elicit transgene immunity in adoptive transfer experiments. These studies indicate that vector-mediated transduction of dendritic cells is necessary for cellular immune responses to muscle gene therapy, a step which AAV avoids, providing a useful biological niche for its use in gene therapy.

Animals↗

Role of the NH2 terminus of the cloned renal K+ channel, ROMK1, in arachidonic acid-mediated inhibition.

We have previously demonstrated that the ROMK channel maintains the property of arachidonic acid (AA) sensitivity observed originally in the native ATP-sensitive K+ channel of the rat cortical collecting duct (16). We used the patch-clamp technique to extend these studies to other NH2-terminal splice variants of the ROMK channel family, ROMK2 and ROMK3, expressed in Xenopus oocytes to determine the mechanism by which AA inhibits channel activity. Although the conductance, channel open probability, and open/closed times of the three homologs were determined to be similar, addition of 5-10 microM AA caused only a moderate inhibition of ROMK2 (15 +/- 8%) and ROMK3 (13 +/- 9%) activity, indicating that differences in the NH2 termini of ROMK channels strongly influence the AA action. We consequently examined the effect of AA on a ROMK1 variant, R1ND37, in which the NH2 terminal amino acids 2-37 were deleted, and on a mutant ROMK1, R1S4A, in which the serine-4 residue was mutated to alanine. Like ROMK2 and ROMK3, AA had a diminished effect on these variants. Addition of 1 nM exogenous protein kinase C (PKC) inhibited ROMK1 but not the mutant, R1S4A. However, the effect of AA is not a result of stimulation of a membrane bound PKC, since PKC inhibitors, calphostin C and chelerythrine, failed to abolish the AA-induced inhibition. In contrast, application of 5 microM staurosporine, a nonspecific protein kinase inhibitor at high concentration, abolished the effect of AA. We conclude that phosphorylation of serine-4 residue in the NH2 terminus plays a key role in determination of AA effect on ROMK channels.

Alanine↗

pH-dependent modulation of the cloned renal K+ channel, ROMK.

pH is an important modulator of the low-conductance ATP-sensitive K+ channel of the distal nephron. To examine the mechanism of interaction of protons with the channel-forming protein, we expressed the cloned renal K channel, ROMK (Kir1.x), in Xenopus oocytes and examined the response to varied concentrations of protons both in the presence and in the absence of ATP. Initial experiments were performed on inside-out patches in the absence of ATP in Mg2+-free solution, which prevents channel rundown. A steep sigmoidal relationship was shown between bath pH and ROMK1 or ROMK2 channel function with intracellular acidification reducing channel activity. We calculated values for pK = 7.18 and 7.04 and Hill coefficients = 3.1 and 3.3, for ROMK1 and ROMK2, respectively. Intracellular acidification (pH 7.2) also increased the Mg-ATP binding affinity of ROMK2, resulting in a leftward shift of the relationship between ATP concentration and the reduction in channel activity. The K1/2 for Mg-ATP decreased from 2.4 mM at pH 7.4 to approximately 0.5 mM at pH 7.2. Mutation of lysine-61 to methionine in ROMK2, which abolishes pH sensitivity, modulated but did not eliminate the effect of pH on ATP inhibition of channel activity. We previously demonstrated that the putative phosphate loop in the carboxy terminus of ROMK2 is involved in ATP binding and channel inhibition [C. M. McNicholas, Y. Yang, G. Giebisch, and S. C. Hebert. Am. J. Physiol. 271 (Renal Fluid Electrolyte Physiol. 40): F275-F285, 1996]. Conceivably, therefore, protonation of the histidine residue within this region could alter net charge (i.e., positive shift) and increase affinity for the negatively charged nucleotide.

Acids↗

Ictal epileptiform activity in the CA3 region of hippocampal slices produced by pilocarpine.

Pilocarpine, a muscarinic agonist, produces status epilepticus that is associated with the later development of chronic recurrent seizures. When applied to rat hippocampal slices, pilocarpine (10 microM) produced brief (<200 ms) epileptiform discharges that resembled interictal activity that occurs between seizures, as well as more prolonged synchronous neuronal activation that lasted seconds (3-20 s), and was comparable to ictal or seizures-like discharges. We assessed the factors that favored ictal patterns of activity and determined the biophysical properties of the ictal discharge. The probability of observing ictal discharges was increased when extracellular potassium ([K+]o) was increased from 5 to 7.5 mM. Raising [K+]o to 10 mM resulted in loss of ictal patterns and, in 20 of 34 slices, desynchronization of epileptiform activity. Making the artificial cerebrospinal fluid (ACSF) hyposmotic favored ictal discharges at 5 mM [K+]o, but shifted 7.5 mM [K+]o ACSF patterns to interictal discharges or desynchronized activity. Conversely, increasing osmolality suppressed ictal patterns. The pilocarpine-induced ictal discharges were blocked by atropine (1 microM, n = 5), a muscarinic antagonist, and pirenzepine (1 microM, n = 6), a selective M1 receptor antagonist. Kainate/alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid receptor blockade stopped all epileptiform activity (n = 8). The N-methyl--aspartate antagonist ,-2-amino-5-phosphonovaleric acid (100 microM, n = 34) did not change the pattern of epileptiform activity but significantly increased the rate of interictal discharges and prolonged the duration of ictal discharges. The ictal discharge was characterized intracellularly by a depolarization that was associated with action potential generation and persisted as a membrane oscillation of 4-10 Hz. The ictal oscillations reversed in polarity at -22.7 +/- 2.2 mV (n = 11) with current-clamp recordings and -20.9 +/- 3.1 mV (n = 7) with voltage-clamp recordings. The reversal potential of the ictal discharge in the presence of the gamma-aminobutyric acid-A blocker bicuculline (10 microM, n = 6) was -2.2 +/- 2.6 mV and was significantly different from that measured without bicuculline. Bicuculline added to 7.5 mM [K+]o and 10 microM pilocarpine did not cause epileptiform activity to change pattern but significantly increased the rate of interictal discharges and prolonged the ictal discharge duration. Both synaptic and nonsynaptic mechanisms are important for the generation of ictal patterns of epileptiform activity. Although the synchronous epileptiform activity produced by pilocarpine required fast glutamate-mediated synaptic transmission, the transition from an interictal to ictal pattern of activity depended on [K+]o and could be influenced by extracellular space.

2-Amino-5-phosphonovalerate↗

Prolonged asymptomatic dense deposit disease in Chinese. Report of 2 cases in Taiwan.

Dense deposit disease (DDD) is a less common form of membranoproliferative glomerulonephritis (MPGN). The disease occurs predominantly in children and young adults and the prognosis is variable. DDD varies considerably in incidence among different populations and has not been reported in Chinese. Herein we reported 2 cases of DDD in young Chinese girls in Taiwan. Although 1 case (case 2) had mild hypertension, both patients had asymptomatic proteinuria and ran a benign course of 8 and 14 years, respectively. The histological features of case 1 resembled membranous glomerulonephritis (MGN) on hematoxylin-eosin stain, but revealed DDD on periodic acid Schiff and chromotrope-2R silver methenamine stains. Whereas case 2 showed focal MPGN on light microscopy, she had a fine granular immunofluorescence pattern resembling MGN. Characteristic intramembranous dense deposits were demonstrated by electron microscopy in the basement membranes of the glomeruli, Bowman's capsules and the renal tubules. Both patients were followed closely, and had stable normal renal function 1 year after renal biopsy.

Adult↗

Diabetic nephropathy is associated with AGT polymorphism T235: results of a family-based study.

Diabetic nephropathy is a serious and frequent complication of insulin-dependent diabetes mellitus (IDDM) that has a strong genetic component. Several case-control studies have reported conflicting results with regard to the role of angiotensinogen gene polymorphisms, specifically the M235T T allele, in the development of diabetic nephropathy. The primary limitation of the case-control approach is that bias may be introduced by unrecognized differences in the populations selected for cases and control subjects. In contrast, family-based approaches, such as the transmission/disequilibrium test, assess whether a particular variant, or allele, is transmitted preferentially from a parent having a single copy of that allele. Thus each family provides its own control, thereby eliminating spurious results caused by mismatched population samples. To take advantage of this study design for further investigation of M235T, we collected from the Joslin Diabetes Center in Boston 148 IDDM patients with diabetic nephropathy, 62 nephropathy-free patients with long-duration IDDM, and, very importantly, parents of all these individuals. We found that among males (but not females) the T allele of the M235T polymorphism was transmitted preferentially to those with nephropathy compared with IDDM patients without nephropathy (P=.05). Moreover, the T allele was transmitted preferentially to patients with the most severe manifestation of nephropathy, end-stage renal disease (P=.04). In conclusion, results obtained in our family-based study support a role of the angiotensinogen gene M235T polymorphism, and specifically the T allele, in the development of diabetic nephropathy in IDDM.

Adolescent↗

Comparison of valproate and phenobarbital treatment after status epilepticus in rats.

OBJECTIVE: To investigate the long-term effects of two widely used antiepileptic medications, valproate and phenobarbital, on learning and behavior in the kainic acid (KA) model of epilepsy. BACKGROUND: Prior clinical and animal studies have demonstrated that phenobarbital administered during development may result in subsequent cognitive impairment. It is unclear whether these adverse effects of phenobarbital extend to other antiepileptic drugs. METHODS: A convulsant dose of KA was administered to rats on postnatal day (P) 35. From P36-75 rats received daily injections of phenobarbital (PH), valproate (VPA), or saline and spontaneous seizure frequency was monitored with video recordings. After tapering of the drugs, the rats were tested in the water maze (a measure of visuospatial memory) and handling test (a measure of emotionality). Brains were then analyzed for histologic lesions. RESULTS: KA caused status epilepticus in all the rats. In the PH- and saline-treated groups, there was impaired learning in the water maze, increased emotionality, recurrent seizures, and histologic lesions in the hippocampal areas CA3, CA1, and dentate hilus. However, VPA-treated rats had no spontaneous seizures, abnormalities in handling, or deficits in visuospatial learning, and had fewer histologic lesions than animals receiving KA alone. CONCLUSIONS: The long-term consequences of AED treatment during development are related to the drug used. VPA treatment after KA-induced status epilepticus prevents many of the neurologic sequelae typically seen after KA.

Animals↗

Role of laminin polymerization at the epithelial mesenchymal interface in bronchial myogenesis.

Undifferentiated mesenchymal cells were isolated from mouse embryonic lungs and plated at subconfluent and confluent densities. During the first 5 hours in culture, all the cells were negative for smooth muscle markers. After 24 hours in culture, the mesenchymal cells that spread synthesized smooth muscle alpha-actin, muscle myosin, desmin and SM22 in levels comparable to those of mature smooth muscle. The cells that did not spread remained negative for smooth muscle markers. SM differentiation was independent of cell-cell contact or proliferation. In additional studies, undifferentiated lung mesenchymal cells were cocultured with lung embryonic epithelial cells at high density. The epithelial cells aggregated into cysts surrounded by mesenchymal cells and a basement membrane was formed between the two cell types. In these cocultures, the mesenchymal cells in contact with the basement membrane spread and differentiated into smooth muscle. The rest of the mesenchymal cells remained round and negative for smooth muscle markers. Inhibition of laminin polymerization by an antibody to the globular regions of laminin beta1/gamma1 chains blocked basement membrane assembly, mesenchymal cell spreading and smooth muscle differentiation. These studies indicated that lung embryonic mesenchymal cells have the potential to differentiate into smooth muscle and the process is triggered by their spreading along the airway basement membrane.

Animals↗

Evidence that preaxial polydactyly in the Doublefoot mutant is due to ectopic Indian Hedgehog signaling.

Patterning of the vertebrate limb along the anterior-posterior axis is controlled by the zone of polarizing activity (ZPA) located at the posterior limb margin. One of the vertebrate Hh family members, Shh, has been shown to be able to mediate the function of the ZPA. Several naturally occurring mouse mutations with the phenotype of preaxial polydactyly exhibit ectopic Shh expression at the anterior limb margin. In this study, we report the molecular characterization of a spontaneous mouse mutation, Doublefoot (Dbf). Dbf is a dominant mutation which maps to chromosome 1. Heterozygous and homozygous embryos display a severe polydactyly with 6 to 8 digits on each limb. We show here that Shh is expressed normally in Dbf mutants. In contrast, a second Hh family member, Indian hedgehog (Ihh) which maps close to Dbf, is ectopically expressed in the distal limb bud. Ectopic Ihh expression in the distal and anterior limb bud results in the ectopic activation of several genes associated with anterior-posterior and proximal-distal patterning (Fgf4, Hoxd13, Bmp2). In addition, specific components in the Hedgehog pathway are either ectopically activated (Ptc, Ptc-2, Gli1) or repressed (Gli2). We propose that misexpression of Ihh, and not a novel Smoothened ligand as recently suggested (Hayes et al., 1998), is responsible for the Dbf phenotype. We consider that Ihh has a similar activity to Shh when expressed in the early Shh-responsive limb bud. To determine whether Dbf maps to the Ihh locus, which is also on chromosome 1, we performed an interspecific backcross. These results demonstrate that Dbf and Ihh are genetically separated by approximately 1.3 centimorgans, suggesting that Dbf mutation may cause an exceptionally long-range disruption of Ihh regulation. Although this leads to ectopic activation of Ihh, normal expression of Ihh in the cartilaginous elements is retained.

Animals↗

Lack of synergy by mixtures of weakly estrogenic hydroxylated polychlorinated biphenyls and pesticides.

We examined the estrogenicity of binary mixtures of the hydroxylated polychlorinated biphenyls (OHPCBs) 2,4,6-trichloro-4'-biphenylol (2,4,6-TCB-4'-OH) and 2,3,4,5-tetrachloro-4'-biphenylol and the pesticides endosulfan and dieldrin. The OHPCBs and pesticides were tested in both the MCF-7 focus assay and a competitive estrogen-receptor binding assay. Although the individual OHPCBs were estrogenic in both assays, there was no synergy when they were combined at various concentrations as equimolar mixtures. Of the pesticides, only endosulfan was estrogenic. Its weak estrogenicity was seen only in the MCF-7 focus assay at the highest concentration tested--10 microM. There was no synergy of the equimolar mixture of pesticides. To determine whether OHPCBs might respond synergistically when combined with the natural estrogen 17-beta-estradiol (E2), we tested various concentrations of 2,4,6-TCB-4'-OH in the MCF-7 focus assay in combination with physiologically relevant concentrations of E2. There was no synergy between 2,4,6-TCB-4'-OH and E2. Pretreatment for 3 or 7 days with 2,4,6-TCB-4'-OH had no effect on subsequent foci induced by a concentration of 2,4,6-TCB-4'-OH and E2. Although our results showing no synergy between the pesticides or the OHPCBs are in contrast to a recent report that binary mixtures of these same compounds produce synergistic responses in estrogen-sensitive assays, they are in agreement with the results from other assays showing a lack of synergy. Considering all results, it appears that synergy of these weakly estrogenic compounds acting through the estrogen receptor is unlikely.

Adenocarcinoma↗

Elevated level of cyclin D1 in mos-transformed cells.

Mos is a germ cell-specific serine/threonine protein kinase that plays an important role during meiotic divisions of oocytes. Upon expression in somatic cells, Mos causes cell cycle perturbations leading to neoplastic transformation. Mos activates the MAP kinase pathway in both oocytes and transformed somatic cells. To determine the mechanism of cell cycle perturbation in mos-transformed cells, we examined the status of some key regulators of G1 phase. We provide evidence that Mos causes an elevation in the level of cyclin D1 in NIH/3T3 cells. As expected from the increased cyclin D1 level, mos transformation of NIH/3T3 cells caused an increase in the protein kinase activities of cyclin D1-Cdk4 and cyclin E-Cdk2 and induced hyperphosphorylation of the retinoblastoma protein. Of importance, the level of cyclin D1 was also elevated in eye lens of the c-mos-transgenic mice compared to normal mice. Our results indicate that the mechanism of cellular transformation by Mos involves an elevation in the level of cyclin D1 in somatic cells.

3T3 Cells↗

Protective immunity in mice elicited by living infective third-stage hookworm larvae (Shanghai strain of Ancylostoma caninum).

OBJECTIVE: To elucidate the mechanisms of protective immunity in mice elicited by living hookworm (Ancylostoma caninum third-stage infective larvae (L3). METHODS: The number of migrating infective larvae recovered from the lungs was used as an endpoint for vaccine immunity. The timing of maximal L3 lung entry was determined by counting the number of lung larvae at several time points after infection with 500 or 1000 L3. Mice were immunized either orally or subcutaneously with 500 L3, followed by two boosts of L3 once every two weeks. The immunized mice were challenged orally with 500 L3 one week after the final boost. To evaluate the protective immunity, the number of L3 recovered from the lungs of the immunized mice during the time of maximal larval entry was compared with that of controls. Host immunity was also evaluated by comparing circulating anti-L3 antibodies between immunized and controlled mice, using both enzyme immunoassays and immunoblotting techniques, and by lung histopathology. RESULTS: The peak time of larval entry into the lungs occurred 48 hours after infection. Mice immunized either orally or subcutaneously with L3 exhibited a marked reduction (90.2% and 86.2% respectively) in the number of recovered lung larvae in comparison to controls (P < 0.01). The protection might be associated with circulating anti-L3 antibodies, including antibodies directed against 132-200 kDa L3 antigens, as well as three major antigens ranging from 28 to 51 kDa. Larvae migrating through the lungs of vaccinated mice showed cuticular damages accompanied with host-inflammatory cell invasion. CONCLUSIONS: Immunization with living L3 protects mice against lung invasion after challenged with hookworm infection. Vaccine immunity is associated with circulating antibodies against L3 antigens and lung inflammatory responses. The mouse model is potentially useful for developing a hookworm vaccine.

Ancylostoma↗

[Study on health status of 3,333 old people in Chengdu City, Sichuan Province].

In order to study the health status of 3,333 old people (over 60) in Chengdu city, a survey was carried out from May 1996 to Nov. 1996. Results revealed that 79.4% of old people had a history of chronic diseases. The first ten common chronic diseases were stated as follows: rheumatic arthritis, hypertension, benign prostatic hypertrophy, chronic bronchitis, cataract, chronic gastritis, osteoarthrosis, asthma and diabetes mellitus. There were significant differences of body weight index, vision and auditus disorder among old people according to their age (P < 0.01). As ageing grows, old people's physical condition and daily-life-capacity decline. In order to improve the quality of life among the aged, following aspects as popularizing health education on self care, strengthening programs on prevention and care of chronic diseases, expanding the medical and nursing services in community and easier access to hospitalization etc should be promoted.

Aged↗

Beneficial effects of early coronary reperfusion on left ventricular remodeling and systolic function in patients with acute myocardial infarction.

OBJECTIVE: To evaluate the beneficial effects of early coronary reperfusion on left ventricular remodeling (LVRM) and systolic function in patients with acute myocardial infarction (AMI). METHODS: Eighty-one patients with first AMI in the convalescent stage and having undergone left ventriculography (LVG) and coronary arteriography (CAG) were divided into four groups: the anterolateral wall (ALW) myocardial infarction (MI) non-reperfusion (n = 20) and reperfusion (n = 21), and inferoposterial wall (IPW) MI non-reperfusion (n = 20) and reperfusion (n = 20), according to infarct location and early treatment with or without successful coronary reperfusion therapy within 6 hours after onset of symptoms. By LVG, the parameters of LVRM and systolic function in the four MI groups were analyzed and compared with those in normal group (n = 25) and between the two reperfusion and non-reperfusion MI groups. RESULTS: In both ALW and IPW MI non-reperfusion groups, the left ventricular (LV) end-diastolic volume (EDV), circumference (EDC), short-axis dimension (EDD), short to long axis ratio (ED-D/L), sphericity index (ED-SI) and end-systolic volume (ESV) were all significantly increased (P < 0.01-0.001), while LV ejection fractions (LVEF) were significantly decreased (both P < 0.001) when compared with those of normal group; and the increase in ESV and decrease in LVEF were both significantly greater in ALW than in IPW MI groups (both P < 0.01). In both ALW and IPW MI reperfusion groups, however, the EDV, EDD, ESV, as well as the extent and severity of regional wall motion abnormality (RW-MA) were significantly smaller (P < 0.05-0.001), while LVEF were significantly higher (P < 0.01-0.001) when compared with those in the two non-reperfusion MI groups respectively. There were no longer significant differences in LVEF and ESV between ALW and IPW MI groups (both P > 0.05). The EDC in IPW MI reperfusion group and the ED-D/L and ED-SI in ALW MI reperfusion group were also significantly reduced compared with those in the two non-reperfusion MI groups respectively (P < 0.05-0.001). All the above parameters in the two reperfusion MI group were decreased to the normal in comparison with normal group except ESV and LVEF, and ED-D/L and ED-SI in IPW MI group. CONCLUSION: It was indicated that in both ALW and IPW MI non-reperfusion groups, LVRM had occurred in convalescent stage of AMI with an increase in EDV and EDC, spherical change in LV shape, and accompanying reduction in LV systolic function; and early coronary reperfusion in AMI could reduce the extent and severity of RWMA, prevent from LV enlargement and remodeling, and preserve or improve LV systolic function with more prominence in ALW MI.

Convalescence↗

[Dynamic analysis of incidence of silicosis in uranium miners].

OBJECTIVE: To understand the laws and characteristics of incidence of silicosis and to evaluate the effectiveness of prevention and treatment measures for it in uranium miners. METHODS: An epidemiological study was carried out in three uranium mines and two geological prospecting teams for uranium mines. RESULTS: Exposure to dust in all patients with silicosis initiated in 1950s to 1960s. Dust concentration and detection rate of silicosis have been decreasing, the length of employment in uranium mines and age at occurrence of the disease, interval between lower and upper stages of the disease, its duration and age at their death all have showed an increasing trend since the founding of the mines and geological prospecting teams more than thirty years ago. Those with delayed occurrence of the disease accounting for 20.31% of the total cases. The length of employment in the cases exposed to uranium dust averaged 7.47 years, and the age at occurrence averaged 36.74 years, less than in those exposed to mixed non-uranium dust. CONCLUSION: Effectiveness of comprehensive prevention and treatment measures for silicosis in uranium mines is significant. The average length of employment and age of the occurrence of the silicosis in those exposed only to uranium dust showed and younger.

Adult↗

[Fibronectin mRNA expression in hypertrophic scars].

OBJECTIVE: This study was to compare the content of fibronectin messenger RNA in the normal skin and hypertrophic scars. METHODS: The mRNA levels of fibronectin were measured by quantitative RT-PCR. RESULT: The study revealed that in vivo, the content of fibronectin messenger RNA was higher in hypertrophic scars than in normal skin. CONCLUSION: It indicates that altered regulation of extracellular matrix components is an important factor for abnormal human wound healing.

Adolescent↗