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PubMed2006

Influence of seat geometry and seating posture on NIC(max) long-term AIS 1 neck injury predictability.

OBJECTIVE: Validated injury criteria are essential when developing restraints for AIS 1 neck injuries, which should protect occupants in a variety of crash situations. Such criteria have been proposed and attempts have been made to validate or disprove these. However, no criterion has yet been fully validated. The objective of this study is to evaluate the influence of seat geometry and seating posture on the NIC(max) long-term AIS 1 neck injury predictability by making parameter analyses on reconstructed real-life rear-end crashes with known injury outcomes. METHODS: Mathematical models of the BioRID II and three car seats were used to reconstruct 79 rear-end crashes involving 110 occupants with known injury outcomes. Correlations between the NIC(max) values and the duration of AIS 1 neck injuries were evaluated for variations in seat geometry and seating posture. Sensitivities, specificities, positive predictive values, and negative predictive values were also calculated to evaluate the NIC(max) predictability. RESULTS: Correlations between the NIC(max) values and the duration of AIS 1 neck injuries were found and these relations were used to establish injury risk curves for variations in seat geometry and seating posture. Sensitivities, specificities, positive predictive values, and negative predictive values showed that the NIC(max) predicts long-term AIS 1 neck injuries also for variations in seat geometry and seating postures. CONCLUSION: The NIC(max) can be used to predict long-term AIS 1 neck injuries.

Accidents, Traffic↗

PubMed2005

Enamelin (Enam) is essential for amelogenesis: ENU-induced mouse mutants as models for different clinical subtypes of human amelogenesis imperfecta (AI).

Amelogenesis imperfecta (AI) is a group of commonly inherited defects of dental enamel formation, which exhibits marked genetic and clinical heterogeneity. The genetic basis of this heterogeneity is still poorly understood. Enamelin, the affected gene product in one form of AI (AIH2), is an extracellular matrix protein that is one of the components of enamel. We isolated three ENU-induced dominant mouse mutations, M100395, M100514 and M100521, which caused AI-like phenotypes in the incisors and molars of the affected individuals. Linkage analyses mapped each of the three mutations to a region of chromosome 5 that contained the genes encoding enamelin (Enam) and ameloblastin (Ambn). Sequence analysis revealed that each mutation was a single-base substitution in Enam. M100395 (Enam(Rgsc395)) and M100514 (Enam(Rgsc514)) were putative missense mutations that caused S to I and E to G substitutions at positions 55 and 57 of the translated protein, respectively. Enam(Rgsc395) and Enam(Rgsc514) heterozygotes showed severe breakage of the enamel surface, a phenotype that resembled local hypoplastic AI. The M100521 mutation (Enam(Rgsc521)) was a T to A substitution at the splicing donor site in intron 4. This mutation resulted in a frameshift that gave rise to a premature stop codon. The transcript of the Enam(Rgsc521) mutant allele was degraded, indicating that Enam(Rgsc521) is a loss-of-function mutation. Enam(Rgsc521) heterozygotes showed a hypomaturation-type AI phenotype in the incisors, possibly due to haploinsufficiency of Enam. Enam(Rgsc521) homozygotes showed complete loss of enamel on the incisors and the molars. Thus, we report here that the Enam gene is essential for amelogenesis, and that mice with different point mutations at Enam may provide good animal models to study the different clinical subtypes of AI.

Amelogenesis↗

PubMed2026

AI'm Here to Help: Enhancing Laboratory Genetic Counseling with Artificial Intelligence.

BACKGROUND: Artificial intelligence (AI) is transforming the fields of genetics and genetic counseling, enhancing both clinical and laboratory practices. The rise of AI technologies has drawn attention to their potential impact on genetic counseling, particularly in patient diagnosis and the counseling processes. CONTENT: In the laboratory, AI plays a critical role in improving communication between laboratory genetic counselors and healthcare providers by automating routine tasks and optimizing workflows. These advancements allow genetic counselors to dedicate more time to addressing complex inquiries, improving genetic test selection, and helping providers interpret genetic test results. As AI continues to integrate into laboratory genetic counseling practice, it presents both opportunities and challenges. At the time of submission, there is a large knowledge gap regarding AI and its application to laboratory genetic counseling, given the lack of published information on this topic. SUMMARY: This article summarizes existing literature, the history and current applications of AI in laboratory genetic counseling, examines its benefits and limitations, and explores future directions for its implementation in the field.

Humans↗

PubMed2006

Genetics of apolipoprotein B and apolipoprotein AI and premature coronary artery disease.

Increased low-density lipoprotein (LDL) and decreased high-density lipoprotein cholesterol (HDL-C) predict premature coronary artery disease, as do elevated levels of apolipoprotein B or reduced levels of apolipoprotein AI. Probands were studied of families with common genetic forms of dyslipidaemia to determine if apo B or apo AI define genetic groups and if apo B or apo AI levels relate to premature coronary artery disease risk. Elevated apo B was characteristic of familial hypercholesterolaemia, familial combined hyperlipidaemia (FCHL), and was seen in individuals with elevated Lp(a). Normal apo B levels were seen in familial hypertriglyceridaemia and in 'coronary artery disease with low-HDL cholesterol'. Apo AI levels tended to be low in FCHL and were decreased in 'coronary disease with low-HDL cholesterol'. In familial hypertriglyceraemia, even though HDL-C levels were low, normal apo AI and apo B levels were seen in the absence of premature coronary artery disease. Therefore, in genetic dyslipidaemias elevated apo B levels and reduced apo AI levels (or increased apo B/AI ratio) differ and predict premature coronary artery disease.

Apolipoprotein A-I↗

PubMed2001

Mapping stress-induced changes in autoinducer AI-2 production in chemostat-cultivated Escherichia coli K-12.

Numerous gram-negative bacteria employ a cell-to-cell signaling mechanism, termed quorum sensing, for controlling gene expression in response to population density. Recently, this phenomenon has been discovered in Escherichia coli, and while pathogenic E. coli utilize quorum sensing to regulate pathogenesis (i.e., expression of virulence genes), the role of quorum sensing in nonpathogenic E. coli is less clear, and in particular, there is no information regarding the role of quorum sensing during the overexpression of recombinant proteins. The production of autoinducer AI-2, a signaling molecule employed by E. coli for intercellular communication, was studied in E. coli W3110 chemostat cultures using a Vibrio harveyi AI-2 reporter assay (M. G. Surrette and B. L. Bassler, Proc. Natl. Acad. Sci. USA 95:7046-7050, 1998). Chemostat cultures enabled a study of AI-2 regulation through steady-state and transient responses to a variety of environmental stimuli. Results demonstrated that AI-2 levels increased with the steady-state culture growth rate. In addition, AI-2 increased following pulsed addition of glucose, Fe(III), NaCl, and dithiothreitol and decreased following aerobiosis, amino acid starvation, and isopropyl-beta-D-thiogalactopyranoside-induced expression of human interleukin-2 (hIL-2). In general, the AI-2 responses to several perturbations were indicative of a shift in metabolic activity or state of the cells induced by the individual stress. Because of our interest in the expression of heterologous proteins in E. coli, the transcription of four quorum-regulated genes and 20 stress genes was mapped during the transient response to induced expression of hIL-2. Significant regulatory overlap was revealed among several stress and starvation genes and known quorum-sensing genes.

Aerobiosis↗

PubMed1996

Apolipoprotein AI and apolipoprotein B containing particle analysis in normolipidemic hemodialyzed patients: evidence of free apolipoprotein E.

Whole plasma from 6 normolipidemic chronic renal failure (CRF) patients undergoing hemodialysis treatment was passed through the anti-apolipoprotein (Apo) AI immunosorbent column connected to the anti-Apo B immunoaffinity column. Apo AI and B containing particles were analyzed for lipid and Apo contents. The results were compared with findings obtained in age-matched normolipidemic healthy controls. Although plasma Apo AI and AII levels decreased in CRF patients, the concentrations of Apo CII, CIII, and E coeluted with Apo AI were similar to those of the controls. The slightly elevated plasma concentrations of Apo CII and CIII in the CRF patients studied were shown to be associated with Apo B containing particles. The nonretained fraction from both groups contains no Apo AI and no Apo B, but still contains lipids and other Apo such as Apo AII and Apo CII. The occurrence of approximately 29% of plasma Apo E in this fraction constitutes the main abnormality found in these patients (< 5% in controls). A two-phase electroimmunoassay shows that this Apo E did not correspond to the plasma E-AII complex. These findings show that the compositional alterations of Apo AI and Apo B containing particles in CRF patients were observed even in normolipidemic patients and suggest that the kidney may play a metabolic role in the removal of free forms of lipoprotein particles such as free Apo E.

Apolipoprotein A-I↗

PubMed2006

The macrophage scavenger receptor SR-AI/II and lung defense against pneumococci and particles.

The class A macrophage scavenger receptor SR-AI/II is implicated as a pattern recognition receptor for innate immunity, but its functional role in lung defense has not been studied. We used mice genetically deficient in SR-AI/II and their wild-type C57BL/6 counterparts to investigate the contribution of this receptor to defense against pneumococcal infection and inhaled particles. SR-AI/II deficiency caused impaired phagocytosis of fluorescent bacteria in vivo, diminished clearance of live bacteria from the lungs, and substantially increased pneumonic inflammation. Survival studies also showed increased mortality in SR-AI/II-deficient mice with pneumococcal lung infection. Similarly, after challenge of the airways with TiO(2) particles, SR-AI/II-deficient mice showed increased proinflammatory cytokine levels in lung lavage fluid and a more pronounced neutrophilic inflammation. The data indicate that the lung macrophage class A scavenger receptor SR-AI/II contributes to innate defense against bacteria and inhaled particles.

Animals↗

PubMed1985

Processing of proapolipoprotein AI requires specific conformation.

Apolipoprotein AI of human high-density lipoproteins is secreted by hepatocytes as a proapolipoprotein with a N-terminal hexapeptide sequence (Arg-His-Phe-Trp-Gln-Gln-) which differs from the prosequence of rat apolipoprotein AI (Trp-Asp-Phe-Trp-Gln-Gln). The two proteins have in common the unusual cleavage site -Gln-Gln-Asp-Glu-. It is hydrolysed by a specific serum proteinase with the release of mature apo AI. We synthesized a model substrate for the study of the final processing of pro-apo AI by the serum proteinase. It is an undecapeptide embracing the human pro-hexapeptide sequence and the first five N-terminal residues of apo AI, covalently linked to a hydrophilic resin. The N-terminal arginine residue was 3H-labelled. [formula; see text] This sequence was not cleaved by human serum under the conditions under which rat serum processes the pro-form of apo AI secreted by rat hepatocytes. Pepsin and chymotrypsin fragmented the undecapeptide at sites characteristic for these proteinases. We conclude that the proteolytic cleavage at the specific site (-Gln-Gln-Asp-Glu-) requires the correct conformation in addition to the specific amino-acid sequence.

Amino Acid Sequence↗

PubMed1988

Expression of the human serum apolipoprotein AI and AII genes in Xenopus laevis oocytes. Lipid-associated secretion of gene products.

The two major apolipoproteins of plasma high-density lipoproteins (HDL) are apolipoprotein AI (apo AI) and AII (apo AII). The apo AI and the correctly oriented apo CIII genes separated by 2.6 kb were obtained by fusion of two human lambda-genomic clones. The apo AII gene was isolated as a 3 kb clone. These apolipoprotein genes have been injected independently and together into Xenopus laevis oocytes and their expression studied. Both apolipoprotein genes were transcribed and translated into their preproforms and processed in Xenopus laevis oocytes to their proforms. They were secreted into the medium associated with newly synthesized phospholipids and neutral lipids as particles floating in the high-density lipoprotein range between 1.12 and 1.21 g/ml. Secreted apo AI is associated mainly with newly synthesized phosphatidylethanolamine and little triglyceride, apo AII with phosphatidylethanolamine, lysophosphatidylethanolamine and neutral lipids. Simultaneous injection of the apo AI and apo AII genes led to the secretion of both apoproteins which separated into two bands during CsCl-density gradient centrifugation. The heavier particles were associated with proapo AI and AII, phosphatidylethanolamine (greater than 90%) and traces of lysophosphatidylethanolamine as lipid components. Proapo AII was immunoprecipitated from the less dense fraction and found to be mainly associated with lysophosphatidylethanolamine. Radiolabelled newly synthesized apolipoproteins in secreted particles were characterized by immunoprecipitation after delipidation of the secreted lipoprotein particles. The oocyte-system proved very suitable for studies of the expression of serum apolipoprotein genes, the assembly of the apolipoproteins with specific lipids to lipoprotein particles and their secretion.

Animals↗

PubMed1999

Hormonal regulation of apolipoprotein AI.

Apolipoprotein AI (apo AI) is the major protein component of the serum high-density lipoprotein (HDL) particles. The antiatherogenic properties of apo AI alone or as part of HDL and their inverse correlation with the incidence of coronary heart disease underlie the clinical importance of the protein. A detailed understanding of the mechanisms by which apo AI is regulated will help us develop new and better ways to manipulate expression of the protein. Although there are many factors that influence apo AI expression, endogenous hormones are attractive because simple changes in abundance of these compounds will alter gene activity. Hormones belonging to the thyroid/steroid family that influence activity of the gene include thyroid hormone, glucocorticoids, gender-specific steroids and retinoic acid. Whereas thyroid, glucocorticoid and estradiol enhance activity of the gene, retinoic acid and androgens decrease it. The mechanisms that mediate the effects of the hormones include direct effects of the ligand and nuclear receptor complex on gene activity. However, indirect means involving the participation of transcription factors other than the hormone receptors are also possible. In summary, members of the same hormone family may have different mechanisms that mediate their activities on apo AI gene activity.

Animals↗

PubMed1997

The effect of T'ai Chi Chuan training on balance, kinesthetic sense, and strength.

The purpose of this study was to assess the effect of T' ai Chi Chuan training on lateral stability, kinesthetic sense, and strength of voluntary knee extension. Subjects consisted of 24 naive volunteers (12 men and 12 women) between the ages of 20 and 45 years. Pre- and 12-week posttests included lateral body stability, kinesthetic sense in the glenohumeral joint for 30 degrees, 45 degrees, and 60 degrees, and strength of knee extension. After pretest data collection, 12 subjects performed T'ai Chi Chuan three times per week for 12 weeks, learning 108 forms of T'ai Chi Chuan. A 2 x 2 analysis of variance was used to estimate significance of group differences on all of the dependent variables. Significant group differences were found in lateral body stability, kinesthetic sense at 60 degrees, and strength of the dominant knee extensor. No significant differences between the T'ai Chi and the control group were found for kinesthetic sense at 30 degrees and 45 degrees rotation of the glenohumeral joint. Film analysis indicated that the two lesser angles were not as common in the T'ai Chi training as the greater angle (60 degrees) and thus may be less practiced. It appears that T'ai Chi Chuan presents a low-stress method to enhance stability, selected kinesthetic sense, and strength of knee extension.

Adult↗

PubMed1998

[The effect of expressed human apolipoprotein AI on plasma high density lipoprotein level in transgenic mice].

OBJECTIVE: To study the regulation of human apolipoprotein AI(h-apo AI) gene expression and its role in high density lipoprotein (HDL) metabolism. METHODS: Transgenic C57BL/6 mice established in this laboratory with human apoAI gene containing mouse metallothionein-I(MT-I) promoter were used for investigation. RESULTS: Southern blot identified the presence of 4-15 copies of h-apo AI gene in the transgenic mice. Northern blot showed that human apo AI mRNA was expressed mainly in the liver and kidneys, and the high level of h-apo AI mRNA was obtained in liver, kidneys and small intestine after Zinc(Zn) induction. Total Plasma apoAI Level in transgenic mice was significantly increased than that in the controls, and a high h-apoAI level was detected in the transgenic mice (46% increased after Zn induction). Additionally, total and HDL cholesterol levels were noticed to be highly increased to 47% before and 103% after Zn induction in the transgenic mice comparing to that of the controls. The plasma HDL and h-apoAI levels were significantly correlated (r = 0.85, P < 0.01) in the transgenic mice. CONCLUSION: Apo AI has a profound effect on regulating HDL levels in the transgenic mice. This animal model is considered appropriate for studying the effect of apoAI on lipid metabolism and the mechanism combating atherogenesis.

Animals↗

PubMed1990

Tissue-specific methylation patterns and expression of the human apolipoprotein AI gene.

To better understand the tissue-specific expression of the human apolipoprotein (apo)AI gene, we performed a detailed analysis of the pattern of methylation of the gene in various human adult and embryonic tissues and in tissues of transgenic mice harboring the human apo-AI gene. In addition, the gene was analyzed also in liver and intestine-derived human cell lines (HepG2 and Caco2, respectively). Using methyl-sensitive restriction enzymes (HpaII, HhaI, and SmaI) and the appropriate radioactive probes, we were able to determine separately the status of methylation of the 5'-end, the body of the gene, and 3'-end flanking sequences. The apo-AI gene in tissues that express the gene was undermethylated at the 5'-end. However, the 5'-end of the gene in sperm and in all adult tissues that do not express the gene was heavily methylated. The body of the gene which contains a CpG island and the 3'-end flanking sequences were, in general, hypomethylated except for specific sites that showed partial methylation. In contrast, while the gene showed tissue-specific expression already in a 12-week-old embryo, the 5'-end was invariably hypomethylated in all tissues of the embryo. A human apo-AI transgene has recently been shown to be active exclusively in the liver, while the endogenous gene is expressed in both liver and intestine (6). We show here that the 5'-end of the apo-AI transgene was methylated in all tissues of the mouse (including intestine) except liver. The results presented here demonstrate a clear correlation between hypomethylation of the 5'-end and activity of the apo-AI gene. However, the observed methylation pattern of the gene in embryonic tissues suggests that tissue-specific expression precedes formation of the tissue-specific methylation pattern.

Animals↗

PubMed1990

The projection from medial geniculate to field AI in cat: organization in the isofrequency dimension.

The topography of the anatomical projection from isofrequency contours (IFCs) in auditory thalamus to IFCs in primary auditory cortex (field AI) was investigated in the cat. In each experiment, a best-frequency map of AI was obtained with electrophysiological recording techniques. Then, different retrogradely transported tracers (HRP, fluorescent dyes) were introduced into AI. In some experiments, different parts (e.g., dorsal, central, and ventral) of a previously mapped IFC were injected, each part with a different tracer. In other experiments, 2 or 3 rows of tracer injections were made at different dorsoventral levels of AI, over a large frequency range (5-38 kHz); each injection row was oriented orthogonal to the IFCs and contained a different tracer. The main mass of the labeled thalamic cells was found in the ventral nucleus of the medial geniculate body (MGv). The MGv cells projecting to a limited sector (1-2 mm in length in most experiments) of an IFC in AI form one or several densely packed neuron clusters of variable shape. The cells labeled by a given tracer are largely separated in space from cells labeled by a different tracer. Thus, different sectors of a cortical IFC receive input from different portions of the corresponding thalamic IFC. As a general rule, cells labeled from dorsal (ventral) injections are centered rostrally (caudally) in the part of MGv innervating AI. However, the topographic details are variable between individuals, and the rostrocaudal gradient is complicated by numerous irregularities and gradients. Previous studies of the auditory thalamocortical projection in the cat have not recognized the topographic order in the isofrequency dimension. Instead, it was believed that different sectors of a cortical IFC were innervated by coincident thalamic populations.

Animals↗

PubMed1996

Serum Lp AI lipoprotein particles and other antiatherogenic lipid parameters in normolipidaemic obese subjects.

The android pattern of body fat distribution has been shown to increase the risk of metabolic and coronary heart disease. Protective lipid markers against cardiovascular disease were studied in 98 obese normolipidaemic, non diabetic, non-smoker subjects over 18 years of age according to regional distribution of adipose tissue as estimated by the waist ship ratio (WHR) and overall obesity as estimated by the body mass index (BMI). WHR was inversely correlated with Lp AI (r = 0.46) and HDL-cholesterol (r = 0.37). BMI was not correlated with protective lipid parameters but only with triglycerides. After adjustment, Lp AI was lower in men and in upper body obese women (p < 0.05). Lp AI is a better indicator of body fat distribution than HDL-cholesterol or apo AI, and its variations appear to be indirectly related to gender, menopause, and age, thereby influencing body fat distribution (the main factor accounting for Lp AI variation). Lp AI was inversely correlated with WHR in gluteal-femoral obese women but not in abdominally obese women or men, possibly because of a threshold effect.

Adult↗

PubMed1994

Morphology and spatial distribution of GABAergic neurons in cat primary auditory cortex (AI).

This is a survey of the distribution, form, and proportion of neurons immunoreactive for gamma-aminobutyric acid (GABA) or glutamic acid decarboxylase (GAD) in cat primary auditory cortex (AI). The cells were studied in adult animals and were classified with respect to their somatic size, shape, and laminar location, and with regard to the origins and branching pattern of their dendrites. These attributes were used to relate each of the GAD-positive neuronal types to their counterparts in Golgi preparations. Each layer had a particular set of GABAergic cell types that is unique to it. There were 10 different GABAergic cell types in AI. Some were specific to one layer, such as the horizontal cells in layer I or the extraverted multipolar cells in layer II, while other types, such as the small and medium-sized multipolar cells, were found in every layer. The number and proportion of GABAergic cells were determined by using postembedding immunocytochemistry. The proportion of GABAergic neurons was 24.6%. This was slightly higher than the values reported elsewhere in the neocortex. The laminar differences in density and proportion of GABAergic and non-GABAergic neurons were also comparable (though somewhat higher) to those found in other cortical areas: thus, 94% of layer I cells were GABAergic, while the values in other layers ranged from 27% (layer V) to 16% (layer VI). Layer VI had the most heterogeneous population of GABAergic neurons. The proportion of these cells across different regions within AI was studied. Since some receptive field properties such as sharpness of tuning and aurality are distributed non-uniformly across AI, these might be reflected by regional differences across the cerebral cortex. There were significantly more GABAergic somata in layers III and IV in the central part of AI, along the dorsoventral axis, where physiological studies report that the neurons are tuned most sharply (Schreiner and Mendelson [1990] J. Neurophysiol. 64:1442-1459). Thus, there may be a structural basis for certain aspects of local inhibitory neuronal organization.

Animals↗

PubMed1988

Genetic factors influencing apolipoprotein AI and AII levels in a kindred with premature coronary heart disease.

A single 51-member kindred, ascertained on the basis of a normotriglyceridemic proband with depressed high-density lipoprotein cholesterol (HDL-C) and myocardial infarctions at ages 40 and 42, was studied with respect to quantitative variation in HDL-C and apolipoprotein (apo) AI and AII levels. The results of bivariate segregation analysis suggest that the etiology of depressed HDL-C involves one or possibly two major loci: one has a pleiotropic effect on apo AI and apo AII levels and, possibly another one that affects apo AI levels. Both the major loci were characterized as having a dominant allele leading to depression of the respective trait(s). In addition, analysis of the cosegregation of HDL-C and apo AI levels gave evidence of residual nonfamilial factors common to both traits, leading to a positive covariance between them. This could reflect the role of apo AI in the transformation of nascent HDL-C particles into mature ones via its cofactor activity to lecithin cholesterol acyltransferase. The proposed two-locus model represents one possible etiology for the heterogeneous disorder of hypoalphalipoproteinemia. This analysis of a single pedigree does not completely define the genetic mechanism, but it does illustrate a useful new analytic approach.

Apolipoprotein A-I↗

PubMedDate not supplied

Apolipoprotein AI and alcoholic liver disease.

A prospective study of apolipoprotein AI has been undertaken in 581 alcoholic patients and in 100 controls in order to describe the changes of apolipoprotein AI according to the different stages of the alcoholic liver disease, to correlate the changes to serum liver tests and to estimate its diagnosis and prognostic value. Results showed that apolipoprotein AI concentration is highly related to the degree of liver injury, reaching a maximum in patients with steatosis (229 +/- 90 mg per dl), beginning to decrease in patients with fibrosis (188 +/- 88 mg per dl) and reaching a minimum in patients with severe cirrhosis (91 +/- 46 mg per dl). Apolipoprotein AI had an independent and discriminative value for the diagnosis of fibrosis (p less than 0.001) vs. steatosis and for the diagnosis of cirrhotic vs. noncirrhotic fibrosis (p less than 0.001) or vs. acute alcoholic hepatitis without cirrhosis (p less than 0.001). Cirrhotic patients with apolipoprotein AI less than 100 mg per dl had a lower survival rate at 1 year (62 +/- 7%) than patients with greater value (80 +/- 6%; p less than 0.05), but this prognostic value disappeared in multivariate analysis when other known prognostic factors were taken into account.

Adult↗