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PubMed2001

4G/5G polymorphism of the plasminogen activator inhibitor-1 gene and insertion/deletion polymorphism of the tissue-type plasminogen activator gene in atherothrombotic stroke.

BACKGROUND AND PURPOSE: Decreased fibrinolytic capacity due to increased plasminogen activator inhibitor-1 (PAI-1) activity and decreased tissue-type plasminogen activator (t-PA) activity has been associated with hypertension or atherothrombotic disorders. The aims of this study were to observe associations of the genetic polymorphism for PAI-1 and t-PA with hypertension and atherothrombotic stroke, and to elucidate whether impaired fibrinolytic activity in atherothrombotic stroke was related to atherothrombosis per se or to other risk factors such as hypertension. METHODS: Patients with atherothrombotic stroke (n = 60), hypertension (n = 100), and control subjects (n = 100) were enrolled. We genotyped all subjects for 4G/5G polymorphism in the promoter region of the PAI-1 gene and the Alu-repeat insertion/deletion (I/D) polymorphism in intron h of the t-PA gene by polymerase chain reaction and endonuclease digestion. RESULTS: The frequency of the 4G/4G genotype of PAI-1 was significantly higher in the atherothrombotic stroke patients than the control subjects (41.7 versus 21%; p = 0.005), but not in the hypertensive subjects. There was a significant association between 4G/4G genotype of PAI-1 and atherothrombotic stroke (adjusted odds ratio = 3.11, 95% confidence interval 1.18-8.15), adjusting for age, sex, total cholesterol, low-density lipoprotein, triglyceride, and body mass index. However, the number of the I/I genotype of t-PA in the atherothrombotic stroke or hypertensive patients was virtually identical to the control subjects. CONCLUSION: Our results suggest that the 4G/4G genotype of the PAI-1 gene is significantly associated with an increased risk of atherothrombotic stroke. This finding also supports that impaired fibrinolytic activity in atherothrombotic stroke is related to atherothrombosis per se, but not to hypertension, one of the most important risk factors of atherothrombotic stroke.

Adult↗

PubMed1975

Chromosome polymorphism in a human newborn population. II. Potentials of polymorphic chromosome variants for characterizing the idiogram of an individual.

Replicate chromosome preparations of umbilical-cord-blood leukocytes from 376 neonates born at the Albert Einstein College Hospital, Bronx, New York, were stained with C-, Q-, and G-banding methods to determine the frequencies and distributions of the variable chromosome bands. The C-band variants of primarily chromosomes 1, 9, and 16, as well as those of the remaining C, E, and F-group chromosomes, and the brightly fluorescing Q-band variants of chromosomes 3 and 4 and all of the acrocentrics, including the Y, were similarly analyzed. Polymorphism of these chromosome regions was so extensive that the idiogram of each of the 376 newborns of this study had a unique variant pattern, even when only the C- or only the Q-band patterns were compared. The distribution of polymorphic Q-bands in the population sampled was consistent with the expectations of the Hardy-Weinberg law, with the exception of chromosomes 3 and 22, where some deficiency of individuals with "homozygous" Q-band patterns was found. The baseline data presented here reinforce the view that polymorphic chromosome characteristics are very useful markers for characterizing the karyotype of an individual, for pedigree studies, for prenatal chromosome analyses, for population studies, for attempts at gene localizations, and for identifying specific cells or their chromosomes in somatic cell genetic studies.

Chromosome Mapping↗

PubMed2006

Strand bias in complementary single-nucleotide polymorphisms of transcribed human sequences: evidence for functional effects of synonymous polymorphisms.

BACKGROUND: Complementary single-nucleotide polymorphisms (SNPs) may not be distributed equally between two DNA strands if the strands are functionally distinct, such as in transcribed genes. In introns, an excess of A<-->G over the complementary C<-->T substitutions had previously been found and attributed to transcription-coupled repair (TCR), demonstrating the valuable functional clues that can be obtained by studying such asymmetry. Here we studied asymmetry of human synonymous SNPs (sSNPs) in the fourfold degenerate (FFD) sites as compared to intronic SNPs (iSNPs). RESULTS: The identities of the ancestral bases and the direction of mutations were inferred from human-chimpanzee genomic alignment. After correction for background nucleotide composition, excess of A-->G over the complementary T-->C polymorphisms, which was observed previously and can be explained by TCR, was confirmed in FFD SNPs and iSNPs. However, when SNPs were separately examined according to whether they mapped to a CpG dinucleotide or not, an excess of C-->T over G-->A polymorphisms was found in non-CpG site FFD SNPs but was absent from iSNPs and CpG site FFD SNPs. CONCLUSION: The genome-wide discrepancy of human FFD SNPs provides novel evidence for widespread selective pressure due to functional effects of sSNPs. The similar asymmetry pattern of FFD SNPs and iSNPs that map to a CpG can be explained by transcription-coupled mechanisms, including TCR and transcription-coupled mutation. Because of the hypermutability of CpG sites, more CpG site FFD SNPs are relatively younger and have confronted less selection effect than non-CpG FFD SNPs, which can explain the asymmetric discrepancy of CpG site FFD SNPs vs. non-CpG site FFD SNPs.

Algorithms↗

PubMed2006

Negative association of endothelial nitric oxide gene polymorphism with hypertension in Turkish patients: effect of ecNOS polymorphism on left ventricular hypertrophy.

BACKGROUND: Endothelial nitric oxide synthase produces nitric oxide which is involved in many physiologic regulatory functions. Variable number of tandem repeats in intron 4 of endothelial nitric oxide synthase gene are reported to be associated with blood pressure regulation. Nitric oxide is involved in regulation of cardiomyocyte genes but it is not known If endothelial nitric oxide synthase 4 gene polymorphisms are related with left ventricular hypertrophy. We studied endothelial nitric oxide synthase 4a/b allele status in hypertensive and normotensive patients and echocardiographic parameters in a subgroup of hypertensive group. METHODS: We performed a case-control study involving 110 Turkish hypertensive patients and 87 controls. All subjects were genotyped for endothelial nitric oxide synthase 4a/b polymorphism. Echocardiographic measurements were obtained in 94 of the hypertensive patients. RESULTS: Endothelial nitric oxide synthase 4a/b genotype frequencies were 6.4%, 23.6%, 70% in hypertensives and 1.1%, 18.4%, 80.5% in controls for a/a, a/b, b/b, respectively. Left ventricular dimensions, mass and diastolic indices were not different across endothelial nitric oxide synthase 4 genotypes. Patients with 4a/a genotype had higher interventricular septal thickness than the other group; 14.83(1.6), 11.91(1.51), 12.21(1.56) for a/a, a/b, b/b, respectively and p = 0.0001. CONCLUSION: Endothelial nitric oxide synthase 4a/b gene polymorphism is not associated with hypertension in Turkish patients. 4a/a genotype was associated with higher interventricular septal thickness in hypertensive patients.

Case-Control Studies↗

PubMed2006

Frequency of CTLA-4 gene CT60 polymorphism may not be affected by vitamin D receptor gene Bsm I polymorphism or HLA DR9 in autoimmune-related type 1 diabetes in the Japanese.

One of the CTLA-4 SNPs, +6230G>A (CT60), has recently been reported to be related to susceptibility to type 1 diabetes and autoimmune thyroid disease. We have previously reported an association between acute-onset type 1 diabetes in Japanese and the Vitamin D receptor (VDR) gene Bsm I large B polymorphism, which is related to the Th1-type response. Moreover, we found a significant correlation between autoimmune-related type 1 diabetes with HLA DR9 and detection of GAD-reactive Th1 (T helper 1)-type cells. In the present article, we tried to clarify whether the frequency of one of the CTLA-4 SNPs, +6230G>A (CT60), is affected by the VDR gene Bsm I polymorphism or by HLA DR9 in Japanese type 1 diabetics. The frequency of the CT60 GG genotype did not appear to be affected by either the VDR gene Bsm I large B polymorphism or HLA DR9.

Adult↗

PubMed2004

Effect of polymorphic colour vision for fruit detection in the spider monkey Ateles geoffroyi, and its implications for the maintenance of polymorphic colour vision in platyrrhine monkeys.

Most platyrrhine monkeys have an X-linked tri-allelic polymorphism for medium and long wavelength (M/L) sensitive cone photopigments. These pigments' sensitivity maxima (lambdamax) range from 535 to 562 nm. All animals also have an autosomally coded short-wavelength-sensitive (S) cone pigment. In populations with three M/L alleles there are six different colour vision phenotypes. Heterozygous females have trichromatic colour vision, while males and homozygous females are dichromats. The selective basis for this polymorphism is not understood, but is probably affected by the costs and benefits of trichromatic compared to dichromatic colour vision. For example, it has been suggested that trichromats are better equipped than dichromats to detect fruit against a leaf background. To investigate this possibility, we modeled fruit detection by various colour vision phenotypes present in the frugivorous spider monkey, Ateles geoffroyi. Our study population is thought to have three M/L alleles with cone pigment lambdamax values close to 535, 550 and 562 nm. The model predicted that all trichromat phenotypes had an advantage over dichromats, and the 535/562 nm phenotype was best; however, the model predicted that dichromats could detect all of the fruit species consumed by spider monkeys. We conclude that the heterozygote advantage experienced by females may be the most plausible explanation for the maintenance of this polymorphism in A. geoffroyi. Nevertheless, more studies need to evaluate social foraging behaviour and the performance of different phenotypes of other New World monkeys to determine if this is a global explanation for this phenomena or more specific to A. geofforyi.

Alleles↗

PubMed2006

The PPARG Pro12Ala polymorphism is associated with a decreased risk of developing hyperglycemia over 6 years and combines with the effect of the APM1 G-11391A single nucleotide polymorphism: the Data From an Epidemiological Study on the Insulin Resistance Syndrome (DESIR) study.

Although cross-sectional studies have associated the Pro12Ala polymorphism of PPARG with type 2 diabetes, prospective studies offer more opportunities to investigate genetic variants. Associations between PPARG polymorphisms with insulin resistance parameters and with the 6-year incidence of impaired fasting glucose or type 2 diabetes were tested in 3,914 French Caucasians from the DESIR (Data From an Epidemiological Study on the Insulin Resistance Syndrome) cohort. In subjects normoglycemic at baseline (n = 3,498), the 6-year risk of hyperglycemia was lower in PPARG Ala carriers (odds ratio [OR] vs. ProPro = 0.66 [95% CI 0.44-0.99], P = 0.046 adjusted for sex, age, and BMI). Similar results were found with the PPARG C1431T single nucleotide polymorphism (SNP; adjusted OR = 0.65 [0.44-0.96], P = 0.036). Both alleles are in strong linkage disequilibrium (D' = 0.669, P < 0.001). The baseline mean fasting insulin and homeostasis model assessment of insulin resistance (HOMA-IR) were lower in Ala carriers compared with ProPro homozygotes (P = 0.001 for both), with smaller increases in mean insulin and HOMA-IR during follow-up (P = 0.007 and 0.018, respectively). No association with insulin levels or HOMA-IR was found with C1431T. In this cohort, the APM1 G-11391A SNP is associated with the development of hyperglycemia. The combined effects of PPARG Pro12Ala and APM1 G-11391A SNPs showed no interaction on the risk of 6-year hyperglycemia. The PPARG Ala allele showed a relatively high protective effect in developing hyperglycemia and hyperinsulinemia during a 6-year period. Cumulative rather than synergistic effects of PPARG Pro12Ala and APM1 SNPs on diabetes risk are suggested.

Adiponectin↗

PubMed2005

Effect of hepatic lipase -514C->T polymorphism and its interactions with apolipoprotein C3 -482C->T and apolipoprotein E exon 4 polymorphisms on the risk of nephropathy in chinese type 2 diabetic patients.

OBJECTIVE: Triglyceride-rich lipoprotein particles may promote the progression of diabetic nephropathy. Patients with diabetic nephropathy have increased plasma triglycerides and reduced activity of hepatic lipase (HL), which hydrolyzes triglycerides. We hypothesized that the HL -514C-->T polymorphism, which reduces HL expression, and its interactions with polymorphisms in apolipoprotein (apo) E and apoC3 increase the risk of diabetic nephropathy. RESEARCH DESIGN AND METHODS: In a case-control study involving 374 Chinese type 2 diabetic patients with and 392 without diabetic nephropathy, we genotyped the HL -514C-->T, apoE exon 4, and apoC3 -482C-->T polymorphisms. RESULTS: HL -514T-containing genotypes (T+) were associated with diabetic nephropathy (OR = 1.7, P = 0.0009). Adjustment by multiple logistic regression for hypertension, triglycerides, sex, non-HDL cholesterol, BMI, smoking, and alcohol intake did not diminish the association (OR = 1.8, P = 0.003). The association between HL T+ genotypes and diabetic nephropathy appeared stronger in diabetic patients with apoC3 -482 non-TT genotypes (OR = 1.9, P = 0.003) or apoE epsilon2 or epsilon4 alleles (OR = 2.2, P = 0.005). Subjects with HL TT exhibited trends toward increased triglyceride and non-HDL cholesterol levels compared with CC carriers. CONCLUSIONS: HL T+ genotypes might increase the risk of developing diabetic nephropathy by slowing clearance of triglyceride-rich remnant lipoproteins. In concert with other risk factors (e.g., hyperglycemia), lipid abnormalities may damage the kidneys and endothelium, where reduced binding sites for lipases may precipitate a vicious cycle of dyslipidemia, proteinuria, and nephropathy.

Apolipoprotein C-III↗

PubMed2007

Development of a single nucleotide polymorphism genotyping microarray platform for the identification of bovine milk protein genetic polymorphisms.

The objective of this study was to develop and validate a fast method for typing the main mutations of bovine milk protein genes by using microarray technology. An approach based on the ligation detection reaction (LDR) and a universal array (UA) was used. Polymorphisms in both the coding and noncoding sequences of alpha(S1)-casein, beta-casein, kappa-casein, and beta-lactoglobulin genes were considered because of their well-known effects on milk composition and cheese production. A total of 22 polymorphic sites, corresponding to 21 different variants, were included in the diagnostic microarray. First, a multiplex PCR was developed to amplify all the DNA target sequences simultaneously. Second, the LDR-UA assay was implemented. The method was validated by analyzing 100 Italian Friesian DNA samples, which were also genotyped by conventional methods both at the protein level by means of milk isoelectrofocusing and at the molecular level using PCR-RFLP and PCR-single strand conformation polymorphism techniques. The genotypes obtained using the LDR-UA approach were in full agreement with those obtained by the conventional analyses. An important result of the LDR-UA assay was a more accurate genotyping of the different milk protein alleles than was found with conventional typing methods. At the kappa-casein gene, in fact, 4 samples were heterozygous (3 reference samples and 1 validation sample) for an allele coding for Thr(136) and Ala(148). This variant, which can be considered as the wild type of the genus Bos, is not usually identifiable by the conventional typing methods used. The multiplex PCR-LDR-UA approach developed provides for an accurate, inexpensive, and high-throughput assay that does not exhibit false positive or false negative signals, thus making it highly suitable for animal genotyping.

Animals↗

PubMed1997

The angiotensin converting enzyme genetic polymorphism in acute coronary syndrome--ACE polymorphism as a risk factor of acute coronary syndrome.

The deletion polymorphism of angiotensin converting enzyme (ACE) genotype has been reported as an independent risk factor for the development of myocardial infarction (MI). However there are conflicting data showing no relationship between the ACE genotype and coronary artery disease. The present study was performed to investigate the correlation between ACE genetic polymorphism and acute coronary syndrome by comparing the distribution of ACE genotypes and ACE activities in patients with acute MI and unstable angina with those in control group. The frequency of genotype DD was significantly higher in patients with acute coronary syndrome than in controls. Logistic regression analysis showed that ACE polymorphism affected the development of acute coronary syndrome in recessive pattern of D allele. When we divided the patients into MI and unstable angina groups, the frequencies of genotype DD and D allele were significantly higher in unstable angina group than in MI or control groups. In the patients with MI, the frequency of D allele was significantly higher in patients without previous angina than in those with previous angina. There was no significant difference in ACE genotype or allelic frequency according to the severity of coronary lesions. The ACE genotype was associated with marked differences of ACE activity, but there was no difference between the patient and control groups for each genotype. In conclusion, the genotype DD of ACE gene associated with acute coronary syndrome, but not with the severity of coronary artery lesion. These results showed that the genotype DD of ACE gene might be associated with acute coronary syndrome by another mechanism rather than the coronary atherosclerosis.

Acute Disease↗

PubMed2005

Leukotriene-related gene polymorphisms in patients with aspirin-intolerant urticaria and aspirin-intolerant asthma: differing contributions of ALOX5 polymorphism in Korean population.

The pathogenesis of aspirin (acetylsalicylic acid, ASA)-intolerant urticaria (AIU) is still poorly understood but it has recently been suggested that it is associated with the overproduction of leukotriene (LT). This is supported by evidence that cyclooxygenase 2 inhibitor is given safely to patients with AIU. The present study was designed to investigate the role of genetic polymorphism of LT related genes in the pathogenesis of AIU via a case-control study. We screened single nucleotide polymorphisms (SNPs) in genes encoding enzymes involved in leukotriene synthesis in the Korean population with AIU (n = 101), ASA-intolerant asthma (AIA, n = 95) and normal healthy controls (n = 123). Genotype was determined by primer extension reactions using the SNapShot ddNTP primer extension kit. Among 8 SNPs of four LT related genes, the polymorphism of ALOX5 at positions of -1708 G > A showed significant difference in genotype frequency between AIU and AIA (p = 0.01). Furthermore, there were significant differences observed in the frequencies of two ALOX5 haplotypes between the AIU group and AIA group (p < 0.05). However, there were no differences in allele, genotype, or haplotype frequencies of ALOX5 between the AIU group and the normal control group. These results suggested that ALOX5 has a differing contribution in two major clinical pathogenesis related to ASA-sensitivity.

5-Lipoxygenase-Activating Proteins↗

PubMed2003

Apolipoprotein E and apolipoprotein CI polymorphisms in the Czech population: almost complete linkage disequilibrium of the less frequent alleles of both polymorphisms.

Apolipoproteins E and CI are the predominant components of triglyceride-rich lipoproteins. The genes are located in one gene cluster and both are polymorphic. Three allelic (epsilon2, epsilon3 and epsilon4) polymorphisms of the APOE gene influence plasma cholesterol levels. The distribution of these alleles differ between ethnic groups. PCR genotyping was used to determine the APOE and APOCI allele incidence in a representative group of 653 probands (302 men and 351 women) of Czech origin. The observed relative frequencies for the epsilon2, epsilon3 and epsilon4 alleles were 7.1 %, 82.0 % and 10.9 %, respectively, and are similar to other middle European populations. APO epsilon4 carriers have the highest and APO epsilon2 carriers the lowest levels of plasma total cholesterol (p<0.0001) and LDL cholesterol (p<0.0001). The frequency of the insertion (I) allele (HpaI restriction site present) of the APOCI polymorphism was 18.5 %. APOCI I/I homozygotes have the highest level of triglycerides (p<0.003). An almost complete linkage disequilibrium of the insertion allele of APOCI with the APOE alleles epsilon2 and epsilon4 has been detected and suggests that the deletion in the APOCI gene probably follows the deriving of all three APOE alleles on the APO epsilon3 allele background.

Apolipoprotein C-I↗

PubMed2004

Polymorphism of N-acetyltransferase 2 (NAT2) gene polymorphism in shanghai population: occupational and non-occupational bladder cancer patient groups.

OBJECTIVE: Arylamine N-acetyltransferases (NATs) are involved in the detoxification of aromatic amines and hydrazine. In order to explore the possible association of NAT2 polymorphism with bladder cancer risk in benzidine exposed or non-exposed Chinese individuals, healthy subjects, subjects with bladder cancer of a former benzidine exposed cohort in Shanghai dyestuff industry and a group of bladder cancer patients without known occupational exposure to aromatic amines were genotyped for NAT2 gene polymorphism. METHODS: NAT2 genotyping was performed with a set of RFLP procedures at seven major polymorphic loci of gene coding area: G191A, C282T, T341C, C481T, G590A, A803G and G857A. RESULTS: The wild allele NAT2 *4 was the most prevalent allele (59%) in healthy individuals. The alleles NAT2*6A and NAT2*7B were also frequently observed (21% and 17%, respectively). In contrast to Caucasians, the percentage of slow acetylators was lower (12% in Chinese vs. 58% in Caucasians, P < 0.001). No relevant differences were observed for homogenous rapid, heterogeneous rapid/slow and homogeneous slow acetylation genotypes between the healthy subjects and both groups of bladder cancer patients. CONCLUSION: The present work did not support the association of slow acetylating genotypes of NAT2 gene with elevated risk of bladder cancer in Chinese whereas it was documented as an important genetically determined risk factor in Caucasians. Different mechanisms might play a role in individual susceptibility to bladder cancer related with aromatic amine exposure in various races or ethnic groups.

Arylamine N-Acetyltransferase↗

PubMedDate not supplied

Relation of the CD36 gene A52C polymorphism to the risk of colorectal cancer among Japanese, with reference to with the aldehyde dehydrogenase 2 gene Glu487Lys polymorphism and drinking habit.

High consumption of white meat (or saturated fatty acids) and alcohol has been demonstrated to have a tendency to increase the risk of colorectal cancer, according to the level of malondialdehyde-deoxyguanosine adducts derived from lipid per-oxidation in the colorectal mucosa. CD36 plays important roles as a long-chain fatty acid translocase and oxidized low-density lipoprotein (LDL) scavenger, while alcohol is metabolized by aldehyde dehydrogenase 2 (ALDH2) and decreases transiently metabolism of dietary fat and serum lipids. To examine associations between the risk of colorectal cancer and the CD36 gene A52C polymorphism according to the ALDH2 gene Glu487Lys polymorphism and drinking habit, a hospital-based case-control study was conducted with 128 colorectal cancer cases and 238 cancer-free controls. Odds ratios (ORs) for the C/C genotype relative to the A/A genotype were 1.70 [95% confidence interval (CI), 0.76-4.11] and 4.24 (95% CI, 1.42-22.66) for men and women, respectively, with the low-activity (Glu/Lys + Lys/Lys) ALDH2 genotype. The high-activity (Glu/Glu) genotype for men and women had no associations. On the other hand, the OR for the C/C genotype with high frequency of drinking habit relative to the A/A genotype with low frequency of drinking habit among men was 3.63 (95% CI, 1.29-13.15). The number of women with a high frequency drinking habit was too small for any corresponding analyses. Our findings suggest a significant interaction between alcohol consumption and the CD36 gene A52C polymorphism related to the metabolism of long-chain fatty acids and oxidized LDL in the etiology of colorectal cancer.

Adult↗

PubMed2006

Association of phosphodiesterase 4D gene polymorphisms with chronic obstructive pulmonary disease: relationship to interleukin 13 gene polymorphism.

Activation of the cyclic AMP (cAMP) signaling pathway leads to the suppression of inflammation in the airways and relaxation of airway smooth muscle. Intracellular cAMP levels are determined by a balance between the activities of adenylate cyclase and phosphodiesterases. We hypothesized that polymorphisms of the phosphodiesterase 4D (PDE4D) gene activate its protein function which leads to the downregulation of cAMP, resulting in the development of chronic obstructive pulmonary disease (COPD). A case-control study was performed using Japanese (96 COPD patients and 61 controls) and Egyptians (106 COPD patients and 72 controls) to investigate the association between the polymorphisms of the PDE4D gene and the development of COPD. Genotyping of all subjects for SNP7 (dbSNP ID, rs10075508), SNP13 (rs829259) and SNP15 (rs702531) in exon 15 of the PDE4D gene was conducted. Furthermore, the distributions of haplotypes consisting of PDE4D polymorphisms and those of interleukin (IL) 4, IL13 and beta2 adrenoceptor were analyzed. The distribution of SNP13 allele frequencies of the PDE4D gene was significantly different between the COPD and control groups in the Japanese population (p = 0.041). In haplotype analysis, haplotypes composed of PDE4D SNP7 and IL13 +2044 G/A in the Japanese population showed significant difference between the patients and controls (pcorr = 0.00048). Thus, SNP13 and haplotypes, SNP7 G/A and IL13 +2044 G/A, may be useful for predicting COPD susceptibility.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1979

[Physiological polymorphism of a grass frog population. III. The effect of the season on the phenotypic manifestation of frog polymorphism by the level of muscle tissue thermostability].

A study was made of the phenotypical manifestation of physiological polymorphism of the population of the grass frog by the heat resistance level of m. interphalangealis in different seasons. In autumn (starting from the 2nd half of October), throughout winter, and in summer the polymorphism of frogs is well expressed, whereas in spring (during the reproduction period) and in the first half of October (during the migration of animals to the places of hibernation) the polymorphism appears to be hidden. The latter phenomenon is due to differences in the pattern of individual seasonal changes in the heart resistance of muscles in individuals of different groups.

Animals↗

PubMed1988

A novel guinea pig macrophage-specific polymorphic molecule. II. Biochemical analysis of the polymorphism.

We have identified a macrophage-specific molecule, termed gp98, which has a m.w. of 98,000, is encoded by a gene not linked to the guinea pig lymphocyte antigen complex, is highly immunogenic, and displays a serologic polymorphism among several inbred guinea pig strains. The gp98 molecule was biochemically analyzed to identify a basis for the serologically detected polymorphism. The molecule was demonstrated to be a glycoprotein containing N-linked oligosaccharides. The strain 2 serologic variant, gp98-2, migrated with an apparent m.w. approximately 2500 more than did the strain 13 variant gp98-13. This differential migration was observed in a (strain 2 X strain 13) F1 animal, and persisted after neuraminidase and endoglycosidase F treatment, and after reduction. Trypsin and endoproteinase Lys-C digestion localized the biochemical basis of the polymorphism to the peptide portion of the molecule. Biochemical analysis of the gp98 molecules from five different inbred strains indicated that only two biochemical variants correlating with the serologic variants existed among the five strains.

Animals↗

PubMed1994

Mitochondrial DNA polymorphism in natural populations of Drosophila albomicans (I)--Remarkable mtDNA polymorphism in the population of D. albomicans.

The technique of mtDNA restriction fragments length polymorphism (RFLP) was used to survey the population structure of D. albomicans. Remarkable mtDNA polymorphism has been observed in D. albomicans populations. A total of 34 nucleomorphs were detected from 82 isofemale lines assayed by only 8 restriction enzymes. The cause and the effect of this phenomenon were discussed. As a result, it is suggested that a mechanism which maintains mtDNA diversity exists in this fly, and that the high intra-populational polymorphism could numerically conceal the extent of differentiation between populations. In addition, on the base of restriction maps, it was found that the mtDNA molecule of D. albomicans might be impacted by the selection pressure during its evolution process both on the nucleotide composition and on the functional regions.

Animals↗