Biomedical subjects

L Wang

Publications and source records attributed to L Wang.

At least 451 records · Page 25Linked to original sources

PubMed2001

Longitudinal ruptures of polyester knitted vascular prostheses.

AIM: The purpose of the study was the characterization of a type of rupture occurring on warp-knitted polyester vascular prostheses. MATERIALS AND METHODS: We studied 20 cases of warp-knitted polyester vascular prostheses that were explanted from humans that showed a longitudinal rupture as a part of a collaborative retrieval program. All the prostheses were immediately fixed in a 10% formaldehyde solution after their explantation in the operating room. The clinical data of these cases were recorded. The explants were photographed, washed to eliminate the surrounding tissues, and photographed again. The ruptures were characterized with macroscopic examination, optical stereomicroscopy, and scanning electron microscopy. RESULTS: The mean duration of implantation of the prostheses was 16.0 +/- 3.3 years (range, 9-20.7 years). The prostheses were Cooley Double Velour (n = 15) and Microvel Double Velour (n = 5). There were 16 aortobifemoral bypass grafts, 1 aorto-biiliac, 1 aorto-aortic, 1 iliofemoral, and 1 axillobifemoral. The longitudinal ruptures occurred on two specific parts of the prostheses: the guide line (6 cases) and the remeshing line (11 cases). In three cases both lines were affected. Scanning electron microscopy showed major degradation of the trilobar filaments of the velour and gradual ruptures of the flat filaments of the remeshing and guide lines. CONCLUSIONS: In this study, we have identified a specific mechanism of late (9-20 years) longitudinal rupture of knitted polyester prostheses consisting of degradation of the polyester filaments along the remeshing and guide lines that run the length of the graft.

Aorta, Abdominal↗

PubMed2001

Pigment epithelium derived factor as a neuroprotective agent against ischemic retinal injury.

PURPOSE: Pigment epithelium-derived factor (PEDF) is a protein shown to have neurotrophic activity. The purpose of this study was to determine whether PEDF is neuroprotective of retinal neurons that are exposed to transient ischemia-reperfusion. METHODS: Transient retinal ischemia was produced by increasing the intraocular pressure for 45 min in albino rats eyes. Immediately after reperfusion, PEDF was injected intravitreally into the experimental eyes. Injury was evaluated morphologically and by measuring the thickness of the inner retinal layers (IRL) and by counting the number of retinal ganglion cells (RGC) in epon embedded sections. RESULTS: Morphologic and morphometric analysis of the thickness of the IRL and the counting of RGC demonstrated that PEDF injected immediately after reperfusion protected the eyes partially but significantly from the ischemic injury. CONCLUSIONS: Intravitreal injection of PEDF even after the ischemia can ameliorate retinal injury. PEDF may be useful in preventing neuronal degeneration in the inner retina resulting from ischemia.

Animals↗

PubMed2001

Control of SV-40 transformed RCE cell proliferation by growth-factor-induced cell cycle progression.

PURPOSE: To determine in SV40-immortalized rabbit corneal epithelial cells (RCE), whether there is conservation of parent tissue serum growth-factor-stimulated cytokine receptor activation and downstream intracellular signaling events mediating control of cell cycle progression and differentiation. METHODS: Immunostaining and Western blot analysis were used to measure cytokeratin K3 and K12 expression with AE5 and AK12 antibodies. Karyotype analysis was performed based on comparison of the RCE chromosomal complement with its parent tissue. EGF receptor activation was evaluated based on immunochemistry and Western blot analyses of EGF receptor dimerization and phosphorylation. Functional status of EGF receptor was determined through measurements of EGF-induced stimulation of ERK-2 activity, which is a component of the mitogen-activated protein kinase cascade (MAPK). This was done by immunocomplex and kinase assay using anti-ERK antibodies and a specific substrate. EGF-induced increases in proliferation and cell cycle progression were determined based on measurements of [(3)H]-thymidine incorporation, G(2)-specific cyclin B1 expression and cell cycle mapping. RESULTS: From days 7 to 14, K12 expression increased based on marked rises in the levels of a 55 kD band. At day 14, a 64 kD band also appeared indicative of K3 expression. Karyotype analysis showed that there were no chromosomal losses due to SV-40 transformation. Upon exposure to EGF (5 ng/ml) for 1 min, EGF receptors were activated and formed clusters indicating that autophosphorylation and multimerization of the EGF receptor were occurred. In the presence of serum growth factors or EGF, ERK-2 kinase activity was markedly increased with a bell-shaped time-dependent activation pattern. Cell cycle progression was analyzed in G(1)/S boundary synchronized RCE cells. After releasing the cells into modified Supplemented Hormonal Epithelium Medium containing 10% serum and DMEM/F-12 medium, 80% of the cells had entered the S phase within 2 h. In addition, time dependent changes in [(3)H]-hymidine incorporation over 8 h confirmed RCE passage through the G(1)/S checkpoint. There were more RCE cells entered the G(2)/M phase of cell cycle in the 6-8 h interval after their release. Another indication of cell cycle progression into the G(2)/M phase was that at 8-10 h cyclin B(1) expression reached its maximal level. CONCLUSIONS: RCE in passage number 12-20 are a physiologically relevant model for studies on growth factor receptor mediated control of cell cycle progression and differentiation in its parent tissue as each of these phenomena were conserved: 1) EGF-induced EGF receptor activation; 2) EGF-activated ERK signaling; 3) expression of cornea-specific differentiation markers; 4) karyotype profile; and 5) cell cycle control and progression.

Animals↗

PubMed2001

Update on the molecular genetics of retinitis pigmentosa.

Retinitis pigmentosa (RP) is a heterogeneous group of retinal dystrophies characterized by photoreceptor cell degeneration. RP causes night blindness, a gradual loss of peripheral visual fields, and eventual loss of central vision. Advances in molecular genetics have provided new insights into the genes responsible and the pathogenic mechanisms of RP. The genetics of RP is complex, and the disease can be inherited in autosomal dominant, recessive, X-linked, or digenic modes. Twenty-six causative genes have been identified or cloned for RP, and an additional fourteen genes have been mapped, but not yet identified. Eight autosomal dominant forms are due to mutations in RHO on chromosome 3q21-24, RDS on 6p21.1-cen, RP1 on 8p11-21, RGR on 10q23, ROM1 on 11q13, NRL on 14q11.1-11.2, CRX on 19q13.3, and PRKCG on 19q13.4. Autosomal recessive genes include RPE65 on chromosome 1p31, ABCA4 on 1p21-13, CRB1 on 1q31-32.1, USH2A on 1q41, MERTK on 2q14.1, SAG on 2q37.1, RHO on 3q21-24, PDE6B on 4p16.3, CNGA1 on 4p14-q13, PDE6A on 5q31.2-34, TULP1 on 6p21.3, RGR on 10q, NR2E3 on 15q23, and RLBP1 on 15q26. For X-linked RP, two genes, RP2 and RP3 (RPGR), have been cloned. Moreover, heterozygous mutations in ROM1 on 11q13, in combination with heterozygous mutations in RDS on 6p21.1-cen, cause digenic RP (the two-locus mechanism). These exciting molecular discoveries have defined the genetic pathways underlying the pathogenesis of retinitis pigmentosa, and have raised the hope of genetic testing for RP and the development of new avenues for therapy.

Chromosome Mapping↗

PubMed2001

Novel rhodopsin mutation in a Chinese family with autosomal dominant retinitis pigmentosa.

PURPOSE: To identify mutations in the rhodopsin (RHO) gene in Chinese patients with autosomal dominant retinitis pigmentosa (ADRP) and to measure the prevalence rate of RHO mutations in Chinese ADRP cases. METHODS: Thirteen Chinese families with ADRP were clinically characterized. The complete coding region and intron splice sites of RHO were analyzed for mutations with single-strand conformation polymorphism (SSCP) analysis and direct genomic sequencing. RESULTS: One of the 13 Chinese families with ADRP was found to have a new, previously unidentified RHO mutation, a change from GAG to TAG at codon 341. The mutation (E341X) results in an in-frame stop codon, leading to the truncation of the rhodopsin protein. Mutation E341X was not detected in 100 normal control individuals. Patients carrying mutation E341X reported night blindness and showed optic atrophy, vessel attenuation, and a few bone spicule-like pigments in peripheral retina at the age of 23-25 years. At the age of 30 years, visual acuity was severely impaired, peripheral visual field was greatly constricted, rod and cone ERG was not detectable, and only a slight left cone response remained. CONCLUSIONS: We have identified a novel rhodopsin mutation (E341X) in a Chinese family with ADRP. The location and character of the mutation expand the spectrum of RHO mutations causing RP. Identification of a RHO mutation in one of the 13 ADRP families studied suggests that only 7.7% of the ADRP cases in a Chinese population were caused by RHO mutations, a ratio significantly lower than that from North America or Europe.

Adult↗

PubMed2001

Novel deletion of the RPGR gene in a Chinese family with X-linked retinitis pigmentosa.

PURPOSE: To characterize a Chinese family with inherited retinitis pigmentosa (RP). METHODS: Linkage studies and haplotype analysis were used for gene mapping, and single-strand conformation polymorphism (SSCP) analysis and direct DNA sequence analysis were used for identifying the responsible mutation. RESULTS: Pedigree analysis suggests that RP in the Chinese family RP002 is inherited either as an autosomal recessive trait or as an X-linked trait. Linkage analysis of RP002 excluded all known autosomal recessive RP loci. Further analysis with 17 polymorphic markers covering the entire X chromosome localized the RP gene in RP002 between markers GATA175D03 and GATA144D04 on Xp11.4, a region where the RP3 gene (RPGR ) is found. Mutation analysis of the RPGR gene in RP002 revealed a novel 28-bp deletion in exon 7. This deletion resulted in an in-frame stop codon that eliminates the C-terminal two-thirds of the RPGR protein. The 28-bp deletion co-segregated with the disease in the family and was not present in 100 normal Chinese individuals. Female carriers of the deletion were affected with myopia and had ERG abnormalities and mild constriction of visual field. CONCLUSIONS: A novel 28-bp deletion in the RPGR gene identified in an X-linked Chinese RP family causes severe RP in male patients as well as myopia and ERG abnormalities in female carriers. The deletion represents the largest microdeletion identified in RPGR to date, and expands the spectrum of RPGR mutations causing XLRP.

Adolescent↗

PubMed2001

Transforming growth factor-alpha (TGF-alpha) is not needed for malignant transformation in experimental colitis.

BACKGROUND: Transforming growth factor-alpha (TGF-alpha) is a key mediator of colonic mucosal protection and/or repair mechanisms in orally induced acute dextran sodium sulphate (DSS) colitis. However, it also has been suggested that TGF-alpha may contribute to malignant transformation in the colon. The aim of the studies was to determine whether TGF-alpha is needed for malignant transformation in orally induced chronic DSS colitis using TGF-alpha deficient mice (wa-1) and Balb/c mice, a strain competent in TGF-alpha. METHODS: Chronic colitis was induced by oral administration of DSS (5%) for 7 days followed by drinking water for 10 days in wa-1 and Balb/c mice (n = 20, per group). In the two subsequent cycles (7 days DSS, 10 days water) 3% DSS-water was utilized due to a high mortality in the wa-1 group. Mucosal injury severity was assessed histologically and graded (three grades). A crypt damage score (CDS) reflecting all three grades of mucosal pathology was calculated. Mucosal dysplasia and cancerous lesions were noted. RESULTS: Seven per cent of the entire colonic mucosa was completely destroyed in wa-1 animals compared to 3% in Balb/c mice (P < 0.05). The CDS was 10.2 +/- 0.4 and 4.8 +/- 0.3 in wa-1 and Balb/c mice, respectively (P < 0.05). Fifteen incidences of mucosal dysplasia were found in the 10 surviving wa-1 animals and 31 incidences were found in 20 Balb/c animals. In both groups, one fully developed adenomatous cancerous lesion was present. CONCLUSIONS: The markedly increased severity of mucosal injury in chronic induced DSS colitis in TGF-alpha deficient wa-1 mice compared to Balb/c mice further substantiates that endogenous TGF-alpha is a pivotal mediator of protection and/or healing mechanisms in the colon. The appearance of dysplastic and cancerous lesions in TGF-alpha deficient animals suggests that TGF-alpha per se is not essential for malignant mucosal cell transformation in colitis.

Animals↗

PubMed2001

Gender difference in the relationships among hyperleptinemia, hyperinsulinemia, and hypertension.

Studies reveals that plasma leptin levels (LEP) in females are higher than those in males, and that LEP in hypertensive subjects are higher than those in BMI-matched normotensive subjects. To investigate the relationships among LEP, blood pressure (BP) and insulin sensitivity, we studied these relationships in 133 Japanese males and 263 females. LEP were positively correlated with BP, body mass index, body fat mass (FM) and homeostasis model assessment (HOMA). Regression analysis in which age and FM were adjusted showed LEP were associated with BP and HOMA. Even with adjustment by age, FM and HOMA, LEP were still positively correlated BP in males. LEP in insulin-resistant hypertensives was significantly higher than those in insulin-sensitive hypertensives, in insulin-sensitive normotensives and in insulin-resistant normotensives in males. However, in females, a significantly higher LEP was observed in insulin-resistant subjects than in insulin-sensitive subjects regardless of hypertension. These data suggest that it would be sexual difference in the relationships among hyperleptinemia, hyperinsulinemia and hypertension.

Adult↗

PubMed2001

Formulation and pharmacokinetic studies of acyclovir controlled-release capsules.

Acyclovir controlled-release capsules (CRCs) were prepared by a three-step process: (1) melt granulation of acclovir; (2) coating of granules with ethyl-cellulose, (3) incorporation of coated granules into hard gelatin capsules. In vitro release experiments showed that the main factors affecting the release rate were the mean particle size of the actylovir raw material and the amount of coating material applied. Release of acyclovir from the capsules was in accordance with the Higuchi equation. Pharmacokinetic studies in dogs after oral administration of acyclovir controlled-release capsules showed that the formulation was successful in providing slow release of aciclovir and was superior to a commercially available controlled-release formulation.

Acyclovir↗

PubMed2001

Anti-HBc IgG subclasses in different populations by comparing a variety of ELISA plates.

The number of IgG subclasses for hepatitis B virus (HBV) core antigen (anti-HBc), demonstrated for HBV-infected individuals, was measured by enzyme-linked immunosorbent assay (ELISA). Four commercially available hepatitis B core antigen (HBcAg) plates and one prepared plate were tested for ELISA sensitivity by the detection of 14 serum samples drawn from HBV chronic carriers, cured patients, vaccinees, and non-infected individuals. Differences in optical density (OD) values were obtained by comparing data gathered from the five plate types, suggesting that different plates may have different binding capabilities for each anti-HBc IgG subclass and, thus, contribute to the different ELISA sensitivities. Of these plates, the GB plate showed the most obvious absorbance changes for anti-HBc subclasses in different populations. These data also indicated different patterns for IgG-specific subclasses for various populations. For HBsAg+ carriers, the OD for IgG1 was greater than for IgG3. By contrast, the OD for IgG3 was higher than that for IgG1 in those subjects who were negative for HBsAg.

Adult↗

PubMed2001

Effects of nitric oxide synthesis inhibition on FK506-induced nephrotoxicity in rats.

This study was designed to evaluate the role of nitric oxide (NO) in FK506-induced nephrotoxicity by administering an inhibitor of NO synthesis, N omega-nitro-L-arginine methyl ester (L-NAME) to rats treated with FK506. After one week of treatment with FK506 (3.2 mg/kg/day, intramuscularly) and/or L-NAME (5 mg/100 mL of L-NAME in the drinking water), the arterial pressure, urinary NOx, and parameters for renal function were measured, and histological analysis of the kidney was made. In the L-NAME without FK506 group, L-NAME administration effectively inhibited urinary NOx excretion and increased mean arterial pressure (MAP) without any change in renal function. In the FK506 without L-NAME group, FK506 treatment showed increase in urinary NOx excretion and mild renal dysfunction. In the FK506 with L-NAME group, urinary NOx excretion was decreased by L-NAME administration and renal function was significantly worsened than FK506 without L-NAME group. The plasma creatinine, BUN and urinary N-acetyl-beta-D-glucosaminidase increased 2-, 3-, and 3-fold, respectively and the creatinine clearance was reduced by 50% as compared with that in the FK506 without L-NAME group. Histological analysis revealed severe interstitial fibrosis and tubular atrophy in the FK506 + L-NAME treatment group. Thus, results suggest that NO synthesis is enhanced in the kidney during FK506-induced nephrotoxicity and that NO synthesis inhibition aggravates FK506-induced nephrotoxicity. NO may play a protective role attributable to the balance of vasoactive substances in FK506-induced nephrotoxicity.

Animals↗

PubMed2001

Pneumatic lithotripsy versus laser lithotripsy in the endoscopic treatment of ureteral calculi.

PURPOSE: To compare the efficacy, safety, and features of pneumatic lithotripsy (PL) with those of laser lithotripsy (LL) and present our clinical experience in the endoscopic management of ureteral calculi. PATIENTS AND METHODS: From August 1994 to February 2000, 285 consecutive patients underwent endoscopic lithotripsy with either the Swiss Lithoclast pneumatic lithotripter (145 patients) or the Ho:YAG laser lithotripter (140 patients) for the treatment of ureteral calculi. RESULTS: In one single session, the overall successful stone fragmentation rate of LL was higher than that of PL (95.7% v 69.7%; P < 0.01). The average time to stone-free status was shorter for LL than for PL (18 days v 31 days; P < 0.01). No major complications were observed in LL, while five ureteral perforations were encountered in PL. CONCLUSIONS: Laser lithotripsy has advantages over PL in high efficiency of stone fragmentation and a low complication rate. Laser lithotripsy is a powerful, effective, and safe treatment modality for ureteral calculi.

Adolescent↗

PubMed2001

Intraarterial administration of marrow stromal cells in a rat model of traumatic brain injury.

To test the efficacy of various delivery routes of stem cells to treat cerebral injury, we investigated the parenchymal distribution of marrow stromal cells (MSCs) injected into the internal carotid artery (ICA) of the adult rat after traumatic brain injury (TBI). Bromodeoxyuridine (BrdU)-labeled MSCs were injected via the ipsilateral ICA at 24 h after TBI. Using histology and immunohistochemistry, the distribution of implanted MSCs was analyzed at 7 days after transplantation. Four groups (n = 4/group) were studied: group 1, animals transplanted with MSCs cultured with NGF and BDNF at 24 h after TBI; group 2, animals transplanted with MSCs cultured without NGF and BDNF; group 3, animals injected with a placebo, phosphate buffered saline into the ICA at 24 h after TBI; and group 4, rats subjected to TBI only. In groups 1 and 2, BrdU-positive cells were localized to the boundary zone of the lesion, corpus callosum and cortex of the ipsilateral hemisphere. The number of BrdU-positive cells was significantly higher in the ipsilateral hemisphere than in the contralateral hemisphere. More MSCs infused intraarterially engrafted in group 1 (18.9%) than in group 2 (14.4%, p < 0.05). Using double staining, BrdU-positive cells expressed MAP-2, NeuN, and GFAP in both groups 1 and 2, with this expression being greater in group 1 and the difference between two groups reaching statistical significance in case of MAP-2. Our data suggest that intraarterial transplantation of MSCs is a viable route for the intracerebral administration of MSCs for the treatment of TBI, since MSCs infused intraarterially after TBI survive and migrate into the brain. Some implanted MSCs express proteins specific to neurons and astrocytes. The addition of NGF and BDNF promote migration of MSCs into the brain and subsequent expression of neuronal protein MAP-2.

Animals↗

PubMed2001

Identification of new sites of binding and activation of the murine alpha1(I) collagen promoter by CCAAT/enhancer binding protein beta.

The CCAAT/enhancer binding protein beta (C/EBPbeta) was previously shown to bind to the alpha(1)(I) collagen promoter at -365 to -335 (site 1) and to activate it. Acetaldehyde also activates the promoter, and this effect is mediated by an increase in stellate-cell C/EBPbeta protein and C/EBPbeta binding. The present study identified two additional distal sites (sites 2 and 3) of binding of C/EBPbeta, in the nuclear extracts of stellate cells, at -399 to -370 and -623 to -592 in the alpha(1)(I) collagen promoter. The C/EBPbeta protein activates the promoter at all three sites. Acetaldehyde increases C/EBPbeta binding to all three sites. Activation by acetaldehyde is abrogated in the transfected promoter mutated at either site 1 or site 3 but is not affected by mutation at site 2. Binding of the 20-kDa C/EBPbeta isoform (p20C/EBPbeta), which is eliminated by mutation at the distal site 3 of C/EBP binding, is necessary for the activation by acetaldehyde of the alpha(1)(I) collagen promoter.

Animals↗

PubMed2001

Perfect phylogenetic networks with recombination.

The perfect phylogeny problem is a classical problem in evolutionary tree construction. In this paper, we propose a new model called phylogenetic network with recombination that takes recombination events into account. We show that the problem of finding a perfect phylogenetic network with the minimum number of recombination events is NP-hard; we also present an efficient polynomial time algorithm for an interesting restricted version of the problem.

Algorithms↗

PubMed2001

Rapid intermittent movement of axonal neurofilaments observed by fluorescence photobleaching.

Observations on naturally occurring gaps in the axonal neurofilament array of cultured neurons have demonstrated that neurofilament polymers move along axons in a rapid, intermittent, and highly asynchronous manner. In contrast, studies on axonal neurofilaments using laser photobleaching have not detected movement. Here, we describe a modified photobleaching strategy that does permit the direct observation of neurofilament movement. Axons of cultured neurons expressing GFP-tagged neurofilament protein were bleached by excitation with the mercury arc lamp of a conventional epifluorescence microscope for 12-60 s. The length of the bleached region ranged from 10 to 60 microm. By bleaching thin axons, which have relatively few neurofilaments, we were able to reduce the fluorescent intensity enough to allow the detection of neurofilaments that moved in from the surrounding unbleached regions. Time-lapse imaging at short intervals revealed rapid, intermittent, and highly asynchronous movement of fluorescent filaments through the bleached regions at peak rates of up to 2.8 microm/s. The kinetics of movement were very similar to our previous observations on neurofilaments moving through naturally occurring gaps, which indicates that the movement was not impaired by the photobleaching process. These results demonstrate that fluorescence photobleaching can be used to study the slow axonal transport of cytoskeletal polymers, but only if the experimental strategy is designed to ensure that rapid asynchronous movements can be detected. This may explain the failure of previous photobleaching studies to reveal the movement of neurofilament proteins and other cytoskeletal proteins in axons.

Animals↗

PubMed2001

Pharmaceutical cost-containment policy: experiences in Shanghai, China.

BACKGROUND: In the decade after 1983, the annual growth rate of drug expenditure was about four times as high as that of per capita gross domestic product (GDP) in Shanghai. In 1993 and 1994, a drug list policy and hospital revenue capping policy were introduced in Shanghai to contain drug expenditure. We studied the impact of these two policies, as a model for similar policies in other parts of China and elsewhere. METHODS: Quarterly drug expenditure data were collected from 1992 to 1996 and more detailed drug expenditure flow was obtained at seven selected hospitals. Twelve focus group discussions were organized to obtain opinions from all stakeholders. RESULTS: The research findings showed a dramatic and continuing decline in the growth rates of total medical and drug expenditures after the implementation of the two policies. The proportion of total medical expenditure attributable to drugs declined from 67% in 1992 to 51% in 1996. The annual growth rate of drug expenditure per ambulatory visit and per bed-day was reduced as well. Drug revenue as a proportion of total hospital revenue declined gradually in all seven hospitals. The two policies did not alter the equity of drug utilization between the insured and non-insured. The government, insurance authority and state-owned drug enterprises all favoured the new policies, while hospital administrators, professionals, joint venture and foreign manufacturers wished for the reimbursement mechanisms to be improved, for retention of their freedom of choice, and for the drug list to be further expanded. CONCLUSIONS: The drug list and capping policies in Shanghai appear to have achieved their objectives of containing the escalation of drug expenditure and improving the rational use of drugs without loss of equity. The underlying causes of the escalation of drug expenditure in China need to be further elucidated.

Ambulatory Care↗

PubMed2001

Previous pulmonary diseases and risk of lung cancer in Gansu Province, China.

BACKGROUND: Although active smoking is well established as the main cause of lung cancer, there is accumulating evidence that history of prior lung diseases may be an independent risk factor for lung cancer. METHODS: A population-based case-control study in Gansu Province, China identified 886 lung cancer cases (656 male, 230 female) diagnosed between January 1994 and April 1998. A standardized interview collected information on a variety of potential risk factors including a history of physician-diagnosed non-malignant lung diseases (pulmonary tuberculosis, chronic bronchitis/emphysema, asthma, pneumonia), age and year in which each condition was first diagnosed, and any therapy or hospitalization received. RESULTS: Pulmonary tuberculosis (odds ratio [OR] = 2.1, 95% CI : 1.4-3.1) and chronic bronchitis/emphysema (OR = 1.4, 95% CI : 1.1-1.8) were associated with increased risk of lung cancer, after adjustment for active smoking and socioeconomic status. The OR for asthma (OR = 1.4, 95% CI : 0.9-2.1) and pneumonia (OR = 1.5, 95% CI : 1.0-2.3) were also elevated. The risk of lung cancer remained significant for pulmonary tuberculosis and chronic bronchitis/emphysema when analysis was limited to the pathologically confirmed cases and self-responders. CONCLUSIONS: This study provides additional evidence that previous pulmonary tuberculosis and chronic bronchitis/emphysema are causally related to lung cancer, although the precise mechanism is still unclear. The results for asthma and pneumonia, while suggestive of a positive association, did not reach the traditional level of statistical significance and should be interpreted with caution.

Adult↗