ABSTRACT
BACKGROUND@#Accurate estimation of the glomerular filtration rate (GFR) and staging of chronic kidney disease (CKD) are important. Currently, there is no research on the differences in several estimated GFR equations for staging CKD in a large sample of centenarians. Thus, this study aimed to investigate the differences in CKD staging with the most commonly used equations and to analyze sources of discrepancy.@*METHODS@#A total of 966 centenarians were enrolled in this study from June 2014 to December 2016 in Hainan province, China. The GFR with the Modification of Diet in Renal Disease (MDRD), Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) and Berlin Initiative Study 1 (BIS1) equations were estimated. Agreement between these equations was investigated with the κ statistic and Bland-Altman plots. Sources of discrepancy were investigated by partial correlation analysis.@*RESULTS@#The κ values of the MDRD and CKD-EPI equations, MDRD and BIS1 equations, and CKD-EPI and BIS1 equations were 0.610, 0.253, and 0.381, respectively. Serum creatinine (Scr) explained 10.96%, 41.60% and 17.06% of the variability in these three comparisons, respectively. Serum uric acid (SUA) explained 3.65% and 5.43% of the variability in the first 2 comparisons, respectively. Gender was associated with significant differences in these 3 comparisons (P < 0.001).@*CONCLUSIONS@#The strengths of agreement between the MDRD and CKD-EPI equations were substantial, but those between the MDRD and BIS1 equations and the CKD-EPI and BIS1 equations were fair. The difference in CKD staging of the first 2 comparisons strongly depended on Scr, SUA and gender, and that of CKD-EPI and BIS1 equations strongly depended on Scr and gender. The incidence at various stages of CKD staging was quite different. Thus, a new equation that is more suitable for the elderly needs to be built in the future.
Subject(s)
Aged, 80 and over , Female , Humans , Male , Asian People , Creatinine , Blood , Cystatin C , Blood , Glomerular Filtration Rate , Physiology , Renal Insufficiency, Chronic , Blood , Uric Acid , BloodABSTRACT
BACKGROUND@#Growing industrialization of China exposes its labor population to the risk of musculoskeletal disorders (MSDs). This study aimed to investigate the prevalence and risk factors of MSDs in a modern industrial region of Beijing.@*METHODS@#A cross-sectional study included 1415 employees in six industrial companies was conducted between January 2018 and May 2018 in Fangshan district, Beijng, China. Nordic Musculoskeletal Questionnaire (NMQ) was used to collect the information about MSDs. Demographic factors, lifestyle factors, health and medical factors, and work-related factors were collected as independent variables. Descriptive statistics, the chi-squared (χ) test, and binary logistic regression analysis were used to analyze data.@*RESULTS@#Among 1415 participants, 498 reported MSDs. The regions involved were the neck (25.16%), shoulders (17.17%), and upper back (13.29%). There was a significant statistical difference between frontline industrial workers and other staff in the prevalence of self-reported symptoms involving the shoulders (χ = 4.33, P = 0.037), wrists and hands (χ = 8.90, P = 0.003), and ankles and feet (χ = 12.88, P < 0.001). Increased age (P = 0.005, OR = 1.63; P = 0.001, OR = 2.33), a high or a low salary (P < 0.001, OR = 0.49; P < 0.001, OR = 0.30), night-shift (P = 0.027, OR = 1.46), two-week-history of illness and treatment (P = 0.004, OR = 5.60; P = 0.013, OR = 4.19), concurrent chronic diseases (P = 0.001, OR = 3.45; P = 0.092, OR = 7.81), limited access to health information (P = 0.004, OR = 0.49), and negative attitude towards seeking healthcare (P = 0.010, OR = 1.77; P = 0.009, OR = 2.75) were associated with MSDs in frontline workers. Female gender (P < 0.001, OR = 2.30), high education (P = 0.001, OR = 1.96), no exercises (P = 0.027, OR = 0.59), night-shift (P = 0.017, OR = 1.98), concurrent chronic diseases (P = 0.002, OR = 3.73; P = 0.020, OR = 13.42), limited access to health information (P = 0.013, OR = 0.53), far distance to medical institution (P = 0.009, OR = 1.83), and negative propensity (P = 0.009, OR = 1.94; P = 0.014, OR = 2.74) were associated with MSDs in other staffs.@*CONCLUSIONS@#The prevalence of MSDs among industrial employees has changed. Frontline workers had different prevalence and risk factors for MSDs compared with other employees. Negative propensity to healthcare, limited ways to obtain health knowledge, and concomitant chronic diseases were associated with MSDs. Surprisingly, highly educated and high-income employees had a higher risk of MSDs.
Subject(s)
Adolescent , Adult , Female , Humans , Male , Middle Aged , Young Adult , Beijing , Epidemiology , China , Epidemiology , Cross-Sectional Studies , Musculoskeletal Diseases , Epidemiology , Occupational Diseases , Epidemiology , Occupational Injuries , Epidemiology , Risk Factors , Surveys and QuestionnairesABSTRACT
Abstract? AIM: To investigate changes of anterior chamber parameters after posterior chamber phakic implantable collamer lens ( ICL ) surgery and its correlation with intraocular pressure ( IOP) .?METHODS: This was a retrospective case series study. Seventy four eyes in 43 myopia patients were examined by Allegro Oculyzer anterior segment tomography to obtain the changes of anterior chamber volume ( ACV ) , anterior chamber angle ( ACA) , central anterior chamber depth ( ACD) and vault, meanwhile, to measure the IOP to analyze the correlation with anterior chamber parameters.?RESULTS: Compared with preoperative, ACV, ACA, ACD all decreased apparently ( P 0.05).?CONCLUSION:For patients underwent ICL, the anterior chamber parameters all decreased which included ACV, ACA, ACD, and had stabilized since early postoperative period. Correspondingly, IOP was stable and had not correlate with ACV, ACA, ACD and vault, however the long-term observation is still necessary.
ABSTRACT
<p><b>BACKGROUND</b>There are more than 300 genetic loci that have been found to be related to hereditary hearing impairment (HHI), including 92 causative genes for nonsyndromic hearing loss, among which 34 genes are related to autosomal dominant nonsyndromic HHI (ADNSHHI). Traditional linkage analysis and candidate gene sequencing are not effective at detecting the ADNSHHI, especially for the unconditional families that may have more than one pathogenic cause. This study identified two disease-causing genes TJP2 and GJB2 in a Chinese family with unconditional ADNSHHI.</p><p><b>METHODS</b>To decipher the genetic code of a Chinese family (family 686) with ADNSHHI, different gene screening techniques have been performed, including linkage analysis, candidate genes screening, high-throughput sequencing and Sanger sequencing. These techniques were done on samples obtained from this family over a period of 10 years.</p><p><b>RESULTS</b>We identified a pathogenic missense mutation, c. 2081G>A (p.G694E), in TJP2, a gene that plays a crucial role in apoptosis and age-related hearing loss (ARHL). The mutation was co-segregated in this pedigree in all, but not in the two patients who presented with different phenotypes from the other affected family members. In one of the two patients, we confirmed that the compound heterozygosity for p.Y136* and p.G45E in the GJB2 gene may account for the phenotype shown in this patient.</p><p><b>CONCLUSIONS</b>We identified the co-occurrence of two genetic causes in family 686. The possible disease-causing missense mutation of TJP2 in family 686 presents an opportunity for further investigation into ARHL. It is necessary to combine various genes screening methods, especially for some unconventional cases.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Asian People , Connexins , Genetics , Exome , Genetics , Genetic Linkage , Genetics , Haplotypes , Genetics , Hearing Loss, Sensorineural , Genetics , Mutation , Genetics , Pedigree , Zonula Occludens-2 Protein , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To gain a better understanding of gene expression changes in the brain following microwave exposure in mice. This study hopes to reveal mechanisms contributing to microwave-induced learning and memory dysfunction.</p><p><b>METHODS</b>Mice were exposed to whole body 2100 MHz microwaves with specific absorption rates (SARs) of 0.45 W/kg, 1.8 W/kg, and 3.6 W/kg for 1 hour daily for 8 weeks. Differentially expressing genes in the brains were screened using high-density oligonucleotide arrays, with genes showing more significant differences further confirmed by RT-PCR.</p><p><b>RESULTS</b>The gene chip results demonstrated that 41 genes (0.45 W/kg group), 29 genes (1.8 W/kg group), and 219 genes (3.6 W/kg group) were differentially expressed. GO analysis revealed that these differentially expressed genes were primarily involved in metabolic processes, cellular metabolic processes, regulation of biological processes, macromolecular metabolic processes, biosynthetic processes, cellular protein metabolic processes, transport, developmental processes, cellular component organization, etc. KEGG pathway analysis showed that these genes are mainly involved in pathways related to ribosome, Alzheimer's disease, Parkinson's disease, long-term potentiation, Huntington's disease, and Neurotrophin signaling. Construction of a protein interaction network identified several important regulatory genes including synbindin (sbdn), Crystallin (CryaB), PPP1CA, Ywhaq, Psap, Psmb1, Pcbp2, etc., which play important roles in the processes of learning and memorye.</p><p><b>CONCLUSION</b>Long-term, low-level microwave exposure may inhibit learning and memory by affecting protein and energy metabolic processes and signaling pathways relating to neurological functions or diseases.</p>
Subject(s)
Animals , Mice , Computational Biology , Gene Expression , Radiation Effects , Learning , Memory , Microwaves , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
<p><b>BACKGROUND</b>Id3 plays a key role in the progression of breast cancer. Previously, four and a half LIM protein (FHL2) was identified as a repressor of Id family proteins by interacting with them. This study aimed to investigate the effects of FHL2 on the transcriptional regulation and oncogenic activities of Id3 in human breast cancer cells.</p><p><b>METHODS</b>Cell transfection was performed with SuperFect reagent. Stable transfectants that overexpressed Id3 were obtained by selection on G418. The level of Id3 protein was determined by Western blotting analysis. Dual luciferase assays were used to measure the effect of Id3 and FHL2 on E47-mediated transcriptional activity in MCF-7 human breast cancer cells. The MTT assay was used to measure cell proliferation. The transwell assay was used to measure the invasive capacity of MCF-7 cancer cells.</p><p><b>RESULTS</b>Id3 markedly repressed transcription mediated by the basic helix-loop-helix (bHLH) factor E47 in MCF-7 cells. This Id3-mediated repression was effectively antagonized by FHL2. Overexpression of Id3 markedly promoted the proliferation and invasive capacity of MCF-7 cells; however, these effects were significantly suppressed by the overexpression of FHL2.</p><p><b>CONCLUSIONS</b>FHL2 can inhibit the proliferation and invasive growth of human breast cancer cells by repressing the functional activity of Id3. The functional roles of FHL2-Id3 signaling in the development of human breast cancer need further research.</p>
Subject(s)
Humans , Blotting, Western , Breast Neoplasms , Genetics , Metabolism , Cell Line, Tumor , Cell Proliferation , Inhibitor of Differentiation Proteins , Genetics , Metabolism , LIM-Homeodomain Proteins , Genetics , Metabolism , MCF-7 Cells , Muscle Proteins , Genetics , Metabolism , Neoplasm Proteins , Genetics , Metabolism , Transcription Factor 3 , Genetics , Metabolism , Transcription Factors , Genetics , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate whether genomic copy number variants (CNVs), within metabotropic glutamate receptors 7 (GRM 7) gene are associated with schizophrenia.</p><p><b>METHODS</b>We examined CNVs in conserved region of GRM7 using real time quantitative PCR among 180 Chinese schizophrenia cases and 33 normal controls. Products of real time quantitative PCR were sequenced bilaterally.</p><p><b>RESULTS</b>Real time quantitative PCR found that a biallelic deletion existed at the 200 bps up-stream of exon 2 in a schizophrenia patient and a monoallelic deletion existed at this site in another 13 schizophrenia patients and a control subject. However, sequencing results showed a substitution of C to G at the 5bp up-stream of 3' end of reverse primer for real time PCR (GRM7-SV-1R). In addition, samples with this variant were exactly those having biallelic or monoallelic deletions, indicating that the results of the real time PCR were caused by the substitution variant at the 3' end of the primer rather than a bona fide genome deletion.</p><p><b>CONCLUSIONS</b>Real-time quantitative PCR combined with sequencing can avoid false positive deletions and therefore is effective in detecting CNVs. According to our results, CNVs in GRM 7 gene is not associated with schizophrenia in the Han Chinese population. However, some potential rare CNVs may still have such relationship, and require further study.</p>
Subject(s)
Female , Humans , Male , Asian People , Genetics , Case-Control Studies , DNA Copy Number Variations , Mutation , Receptors, Metabotropic Glutamate , Genetics , Schizophrenia , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To discuss and analyze the feasibility and strategy for perform the newborn gene screening in the process of newborn hearing screening in order to supply the defects or limitation in the hearing screening.</p><p><b>METHODS</b>Four hundreds and sixty newborn babies from December 2006 to April 2007 accepted the simultaneous hearing and gene screening. Otoacoustic emission (OAE) was used for the first step hearing screening and OAE combined with auto auditory brainstem response (AABR) detection for the second step screening. Newborn genetic disease screening cards were used for collecting the blood spot from the umbilical cord within the moment of newborn. The cards could be directly performed the polymerase chain reaction (PCR) for screening the mitochondrial 12SrRNA 1555G and GJB2 as well as SLC26A4 genes mutations. The restriction enzyme Alw26I was used to recognize the point mutation of 12SrRNA A1555G. The samples with the possible 12SrRNA A1555G mutation were then sequenced to verify. The PCR products from the GJB2 coding region and SLC26A4 IVS7-2A > G hot spot region were sequenced directly. The software of DNAStar was used to analysis the sequence.</p><p><b>RESULTS</b>The first step of hearing screening of 460 newborn babies showed " refer" on the left ear of nine babies and on the right ear of three babies. Seven showed "refer" on bilateral with the the total of babies 19. After 42 days, they accepted the second step for hearing screening. 16 of the 19 were showed "pass" with OAE and AABR. One baby showed "pass" on the left ear, "refer" on the right ear with the OAE detection but bilateral "pass" with AABR. Two babies failed to accept the re-examination. The newborn gene screening showed five of the 460 babies had the positive response on the A1555G restriction enzyme assay. Of the five babies, one was proved to be the 12SrRNA A1555G mutation and three were the C1556T mutations and one sequence was normal. For the SLC26A4 gene screening, five were the heterozygote of IVS7-2A > G mutation were found and one was carrier the polymorphism of IVS7-18T > G and another was IVS6-62_63insGT heterozygote carrier. For the GJB2 gene screening, eight were 235delC heterozygote carriers, four were G109A heterozygote carriers. All the gene screening found 23 newborn babies of the 460 harbored the changes in the three genes. Of those, one was the 12SrRNA A1555G. pathogenic mutation and 13 were pathogenic heterozygote carriers, nine were the polymorphisms. It was worth to pay more attentions that A1555G mutation was found in the baby whose hearing screening was "pass" in the hearing screening as well as the 13 heterozygote carrier for GJB2 and SLC26A4 gene.</p><p><b>CONCLUSIONS</b>It might be one of the powerful strategy for adding the concept of newborn gene screening into the hearing screening for the purpose of early diagnosis and discovery the prelingual or late-onset or the high risk as well as the pathogenic carriers. On the basis of the research progress, it was necessary to develop the national newborn gene screening into the process of newborn hearing screening.</p>
Subject(s)
Female , Humans , Infant, Newborn , Male , Connexins , Evoked Potentials, Auditory, Brain Stem , Hearing Disorders , Diagnosis , Genetics , Hearing Tests , Neonatal Screening , Point MutationABSTRACT
<p><b>OBJECTIVE</b>To investigate the prevalence of the mitochondrial DNA (mtDNA) A1555G mutation in nonsyndromic hearing impairment (NSHI) patients from Gansu province.</p><p><b>METHODS</b>Subjects included 802 students selected from five Deaf-Mute Schools in Gansu. DNA was extracted from peripheral blood of all patients. The mitochondrial DNA target fragments were amplified by polymerase chain reaction (PCR). The Mutations were detected by AIw26I digestion and sequence analysis.</p><p><b>RESULTS</b>The homoplasmic A1555G mutation was found in 67 individuals from 802 patients (8.4%). Fifteen of these 67 patients had family histories.</p><p><b>CONCLUSIONS</b>The mtDNA A1555G mutation had a higher incidence in Gansu population with nonsyndromic hearing impairment than other studies. The data not only gaven more evidences that the prevalence of mtDNA A1555G mutation in china was higher than that in Europe and America, but also gaven valuable information for gene diagnosis, genetic counseling and would improve the safety of aminoglycoside antibiotic therapy.</p>
Subject(s)
Adolescent , Child , Child, Preschool , Female , Humans , Male , Young Adult , Asian People , Genetics , DNA, Mitochondrial , Genetics , Deafness , Genetics , MutationABSTRACT
<p><b>OBJECTIVE</b>To investigate EGFR gene mutations in non-small cell lung cancers (NSCLCs) and their correlation with clinicopathologic features and clinical characteristics in Chinese NSCLC patients.</p><p><b>METHODS</b>To analyse EGFR mutations of exons 19 and 21 in NSCLCs by PCR amplification and sequencing.</p><p><b>RESULTS</b>Somatic mutations in TK domain of EGFR were found in 13 cases (17.3%), the majority of mutations were in-frame exon 19 (9.3%) and 6 cases missense mutation in exon 21 (8.0%). The mutation rate was significantly higher in adenocarcinoma (12/31, 38.7%), than in bronchioloalveolar cancer (1/10, 10. 0%), adeno-squamous carcinoma (0/5), pulmonary blastoma (0/2), large cell carcinoma (0/1) and squamous cell carcinoma (0/26). Moreover, mutations were more frequently observed in females (30.0%) than in males (8.9%), and significantly higher in non-smokers (28.2%) than in smokers (5.6%).</p><p><b>CONCLUSION</b>EGFR gene mutation is significantly higher related to adenocarcinomas, females and never-smokers. The results may suggest that a lager portion of adenocarcinomas in Chinese patients, females and non-smokers could be associated with favorable response to gefinib.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Adenocarcinoma , Drug Therapy , Genetics , Antineoplastic Agents , Therapeutic Uses , Base Sequence , Carcinoma, Non-Small-Cell Lung , Drug Therapy , Genetics , DNA Mutational Analysis , Exons , Genetics , Gene Frequency , Lung Neoplasms , Drug Therapy , Genetics , Mutation , Point Mutation , Protein Kinase Inhibitors , Therapeutic Uses , Quinazolines , Therapeutic Uses , ErbB Receptors , Genetics , Sequence Deletion , Sex Factors , Smoking , Treatment OutcomeABSTRACT
<p><b>OBJECTIVE</b>To map the gene locus in a Chinese pedigree with autosomal dominant nonsyndromic hearing loss.</p><p><b>METHODS</b>A genome wide screening was performed with 394 microsatellite markers distributed with an average spacing of 10 cM (ABI Prism Linkage Mapping Set 2, Applied Biosystems, Foster City, CA, U.S.A.).</p><p><b>RESULTS</b>Affected family members showed a bilateral, symmetrical, progressive neurosensory deafness. Significant linkage was found to marker D1 S937 (maximum two point LOD score of 5. 71 at theta = 0.05) on chromosome 11q. The position of the novel deafness locus, DFNA11, was delimited by analysis of the recombinant haplotypes (D11S165-D11S1874). This analysis placed DFNA11 between the proximal marker D11S1314 and the distal marker D11S898, which define a critical interval of 25.34 cM.</p><p><b>CONCLUSIONS</b>Mapping of the DFNA11 locus further confirms the great genetic heterogeneity underlying the autosomal dominant forms of hereditary deafness. Reports of more families with hearing impairment linked to this locus should contribute to the identification of the responsible gene, providing insights into the auditory function and the molecular pathophysiology of age related hearing loss.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Chromosome Mapping , Deafness , Genetics , Genes, Dominant , Haplotypes , Microsatellite Repeats , Myosins , Genetics , PedigreeABSTRACT
The study was aimed to investigate the expression of VEGF mRNA and VEGF protein in HL-60 cells treated with diallyl disulfide (DADS), and to explore the antileukemic mechanism of DADS in respect of VEGF production. Semi-quantitative RT-PCR and ELISA were used to detect the expression of VEGF mRNA and secretion of VEGF protein in HL-60 cell lines treated by DADS respectively. The results showed that the expression of VEGF mRNA and secretion of VEGF protein were found in HL-60 cells. The expression of VEGF mRNA and secretion of VEGF protein in HL-60 cells could be down regulated by treatment with 0.625, 1.25, and 2.5 microg/mL DADS for 48 and 72 hours and the effects had a dose dependent relationship (r > 0.9, P < 0.01). The differences between DADS treated HL-60 cell groups and the control group were statistically significant (P < 0.01), there were also statistically significant differences among three DADS-treated HL-60 cell groups (P < 0.05). It is concluded that DADS effectively inhibits the proliferation of human leukemia cell line HL-60 cells; DADS exerts its antileukemic effects by reduction of the expression of VEGF mRNA and VEGF protein secretion.
Subject(s)
Humans , Allyl Compounds , Pharmacology , Antineoplastic Agents , Pharmacology , Cell Proliferation , Disulfides , Pharmacology , HL-60 Cells , RNA, Messenger , Genetics , Vascular Endothelial Growth Factor A , GeneticsABSTRACT
<p><b>BACKGROUND</b>Ageing is associated with increased incidence of dyslipidemia. To investigate potential molecular mechanisms, the effects of age and fibrate administration on peroxisome proliferator-activated receptor alpha (PPARalpha) expression in livers of young and old rats were studied.</p><p><b>METHODS</b>A total of 16 young (2-month-old) and 16 old rats (24-month-old) were randomly assigned to a control group and fenofibrate group (fenofibrate in a total therapeutic dosage of 0.5% in ratio to each treated rat weight in 14 days). RT-PCR was applied to evaluate hepatic mRNA expression of PPARalpha and its target genes. Western blotting was used to determine PPARalpha protein level in liver tissue.</p><p><b>RESULTS</b>When compared with 2-month-old rats, the liver tissue from 24-month-old rats showed reduced expression of PPARalpha mRNA (52%, P < 0.05) and protein (109%, P < 0.01). Consequently, the mRNA levels of PPAR target genes, LPL, ACO, ACS and CPT-1 were markedly lowered by 19%, 8%, 13% and 9% respectively, and apoCIII increased by 24% in livers from 24-month-old rats, compared with values obtained from 2-month-old rats (P < 0.05). Fenofibrate therapy significantly lowered plasma triglyceride and total cholesterol levels in old rats, accompanied with improvement in hepatic expression of genes, including LPL, ACO, ACS, CPT-1 and apoCIII, but no change was found in PPARalpha expression in livers from either 24-month or 2-month-old rats.</p><p><b>CONCLUSIONS</b>The decrease in the hepatic PPARalpha expression is probably directly related to the lipid metabolic disturbances observed in old animals. The beneficial effects of fenofibrate administration in old rats suggests that fibrates may be useful for treating lipid disturbances in old people.</p>
Subject(s)
Animals , Male , Rats , Aging , Metabolism , Fenofibrate , Pharmacology , Therapeutic Uses , Hyperlipidemias , Drug Therapy , Lipids , Blood , Liver , Metabolism , PPAR alpha , Genetics , Rats, Sprague-DawleyABSTRACT
<p><b>BACKGROUND</b>The role of the G alpha q/11-mediated signal transduction pathway in angiotensin II (AngII) induced cardiac hypertrophy remains unclear. This study was to investigate the role of the G alpha q/11 signal transduction pathway in the development of cardiac hypertrophy in 2K1C hypertensive rats and in cultured neonatal rat ventricular myocytes (NRVMs) and to elucidate the effects of the pathway on AngII induced cardiac hypertrophy.</p><p><b>METHODS</b>Renal hypertension was induced in 2K1C hypertensive rats by placing a silver clip around the left renal artery. At 8 weeks after operation, the systolic blood pressure, the ratio of left ventricular weight to body weight (LV/BW), and the concentration of AngII in the heart were measured. The protein levels of G alpha q/11 and extracellular signal-regulated kinase 1/2 (ERK1/2) were assayed by Western blot analysis, and the activity of phospholipase C (PLC) in the myocardium was detected using [(3)H]-PIP2 as a substrate. Changes in [(3)H]-leucine incorporation and in the protein levels of the signal molecules G alpha q/11, PLC beta 3, and ERK1/2 were measured after NRVMs were stimulated with 10(-7) mol/L AngII.</p><p><b>RESULTS</b>The protein levels of G alpha q/11 and ERK1/2 in the hearts of 2K1C rats increased by 35.8% and 31.9%, respectively, compared with the sham group. The PLC activity in the 2K1C group was also significantly increased (P < 0.05). The levels of G alpha q/11, PLC beta 3, and ERK1/2 increased significantly after NRVMs were stimulated by AngII. The upregulation of G alpha q/11, PLC beta 3 and ERK1/2 in NRVMs occurred prior to [(3)H]-leucine incorporation increases, and could be inhibited with losartan.</p><p><b>CONCLUSION</b>AngII can initiate cardiac hypertrophy and upregulate signal molecules in the G alpha q/11-mediated signal transduction pathway, such as G alpha q/11, PLC beta 3 and ERK1/2, at both tissue and cellular levels.</p>