Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Sparrows”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,099 records · Page 61Linked to original sources

Creeping patterns of human adults and infants.

The patterns of swing and support for the hands-and-feet or hands-and-knees gaits (creeping) of human adults and infants are compared based on data from a number of studies. Human infants show considerable variability in their creeping gait patterns, whereas adult patterns are less variable and fairly consistent after a few minutes of practice. Creeping on hands-and-knees appears to dictate a gait pattern characteristically different from creeping on hands-and-feet. The highly inefficient nature of adult creeping supports the view that our early hominid ancestors were poorly adapted to quadrupedal locomotion. Data obtained from high-speed film analysis of human creeping patterns show that the number of foot lengths per stride in creeping is about twice that for normal upright walking at the same speed. The support pattern of human creeping is different from that of nonhuman primates. These findings are discussed in the context of debate concerning the origin of the Laetoli hominid footprints and the knuckle-walking hypothesis.

Adult↗

Actin mutations are one cause of congenital fibre type disproportion.

We report three heterozygous missense mutations of the skeletal muscle alpha actin gene (ACTA1) in three unrelated cases of congenital fiber type disproportion (CFTD) from Japan and Australia. This represents the first genetic cause of CFTD to be identified and confirms that CFTD is genetically heterogeneous. The three mutations we have identified Leucine221Proline, Aspartate292Valine, and Proline332Serine are novel. They have not been found previously in any cases of nemaline, actin, intranuclear rod, or rod-core myopathy caused by mutations in ACTA1. It remains unclear why these mutations cause type 1 fiber hypotrophy but no nemaline bodies. The three mutations all lie on one face of the actin monomer on the surface swept by tropomyosin during muscle activity, which may suggest a common pathological mechanism. All three CFTD cases with ACTA1 mutations had severe congenital weakness and respiratory failure without ophthalmoplegia. There were no clinical features specific to CFTD cases with ACTA1 mutations, but the presence of normal eye movements in a severe CFTD patient may be an important clue for the presence of a mutation in ACTA1.

Actins↗

Effect of 'antiembolism' compression hosiery on leg blood volume.

Blood volume in the legs of healthy volunteers and the ability of graduated compression hosiery to reduce that volume were investigated with gamma scintigraphy. Changing posture from supine to upright, or pneumatic thigh cuffs inflated to either 20 or 40 mmHg with the subject supine, significantly increased leg blood volumes; the mean increase was: upright 126 ml, 20 mmHg cuff 44 ml, and 40 mmHg cuff 113 ml. A significant trend in reducing these volumes was noted in three brands of commercially available stockings, with the subject supine and without thigh cuffs (Page's L trend 132.5, P < 0.01) and when cuffs were applied at 20 mmHg (Page's L trend 128, P = 0.05). Few of the commercially available stockings delivered the 'standard' compression profile of 18 mmHg at the ankle, 14 mmHg at the calf and 8 mmHg at the upper thigh. The effects of other compression profiles were assessed, using custom-made stockings, and pneumatic cuffs inflated to 20 mmHg applied to the upper thighs to impede venous return. There was no consistent reduction of blood volume in the popliteal region, although decreases were seen in the upper and lower calf. The major determinant of performance was compression at the calf; the ankle to calf compression gradient was not important. Stockings with a profile of 16.8 mmHg at the ankle, 14.5 mmHg at the calf and 6.4 mmHg at the upper thigh performed best.

Adult↗

Absolute configurational determination of an all-trans-retinal dimer isolated from photoreceptor outer segments.

An all-trans-retinal (ATR) dimer (1) isolated from photoreceptor outer segments was found to have a stereogenic center at C13' flanked by tetraene (295 nm) and hexaenal (438 nm) chromophores. Analytical chiral HPLC (Chiralcel OD) revealed that the isolated retinoid had formed in 13% enantiomeric excess. Using a combination of (1)H-(1)H NOESY constraints, molecular modeling, and CD exciton coupling analysis, it was determined that the favored enantiomer was 13'(R). Three low-energy conformers of the 13'(S) model were found with MMFF/DFT and were used to calculate the CD spectrum of the ATR dimer (DeVoe method). The Boltzmann weighted spectrum was found to exhibit a positive exciton couplet, in excellent agreement with the experimental spectrum for the first eluted enantiomer. This further suggested that despite the large energy difference between the two interacting chromophores, the dominant source of optical activity in the CD spectrum is the nondegenerate exciton mechanism.

Computational Biology↗

Contractility of single human dermal myofibroblasts and fibroblasts.

Human dermal myofibroblasts, characterised by the expression of alpha-smooth muscle actin, are part of the granulation tissue and implicated in the generation of contractile forces during normal wound healing and pathological contractures. We have compared the contractile properties of single human dermal fibroblasts and human dermal myofibroblasts by culturing them on flexible silicone elastomers. The flexibility of the silicone substratum permits the contractile forces exerted by the cells to be measured [Fray et al., 1998: Tissue Eng. 4:273-283], without changing their expression of alpha-smooth muscle actin. The mean contractile force produced by myofibroblasts (2.2 microN per cell) was not significantly different from that generated by fibroblasts (2.0 microN per cell) when cultured on a substrata with a low elastomer stiffness. Forces produced by fibroblasts were unaffected by increases in elastomer stiffness, but forces measured for myofibroblasts increased to a mean value of 4.1 microN/cell. This was associated with a higher proportion of myofibroblasts being able to produce wrinkles on elastomers of high stiffness compared to fibroblasts. We discuss the force measurements at the single cell level, for both fibroblast and myofibroblasts, in relation to the proposed role of myofibroblasts in wound healing and pathological contractures.

Adult↗

Enumeration of CD34+ cells in cord blood: a variation on a single-platform flow cytometric method based on the ISHAGE gating strategy.

Single-platform flow cytometric absolute cell counting protocols provide increased robustness for CD34+ cell enumeration by limiting potential sources of imprecision. However, samples with any cellular fragmentation or debris, such as cord blood samples, provide challenges for these assays. We describe a simple, robust absolute CD34+ cell counting protocol, suitable for cord blood, using TRUCOUNT absolute count tubes (BD Biosciences, San Jose, CA) and a modified ISHAGE (International Society for Hematotherapy and Graft Engineering) gating strategy. An advantage of TRUCOUNT tubes is that each tube is supplied with a known number of lyophilized fluorescent beads. The method includes no-wash fixative-free ammonium chloride red blood cell lysis and the viability dye, 7-amino actinomycin D, to exclude dead cells. The threshold was set on CD45 expression in the FL1 channel and an exclusion gate in the forward scatter channel reduced debris. No manual adjustment of the gating regions was required, even for samples in less than optimal condition. Comparison of the TRUCOUNT-ISHAGE protocol with the original dual-platform ISHAGE assay (n = 30) and the single-platform ISHAGE protocol using Flow-Count Fluorospheres (Beckman Coulter, Fullerton, CA; n = 22) showed high correlation (R(2) = 0.949 and 0.989, respectively) and no significant difference or bias for samples ranging from 22 to 600 CD34+ cells per microliter. Results are presented that demonstrate the detrimental effect of a fixative-containing lysis reagent when used in a lyse-and-wash procedure. The TRUCOUNT-ISHAGE protocol combines the attributes of TRUCOUNT tubes and the ISHAGE gating strategy to provide a single-platform protocol capable of achieving readily standardization of CD34+ cell enumeration.

Antigens, CD34↗

Salivary monomorphic adenomas of dermal analogue type: report of two cases.

Two cases of monomorphic adenoma, dermal analogue type, are presented illustrating fine-needle aspiration cytology and subsequent histopathology. Aspiration findings were similar in both cases, demonstrating aggregates of mildly disorganised small regular epithelial cells bordered by a thick rim of basement membrane material. In the first case seen, there was a prominent lymphoid component which gave rise to the false suspicion that the lesion was lymphoepithelial in nature. The cytological features of this tumour are characteristic, however, and their recognition is important to enable distinction from malignancy (e.g., adenoid cystic carcinoma), other benign neoplasms (e.g., plemorphic adenoma), and non-neoplastic conditions.

Adenoma↗

Spatial and temporal distribution of nerves, ganglia, and smooth muscle during the early pseudoglandular stage of fetal mouse lung development.

Neural tissue and smooth muscle appear early in the developing fetal lung, but little is known of their origin and subsequent distribution. To investigate the spatial and temporal distribution of nerves, ganglia, and airway smooth muscle during the early pseudoglandular stage, fetal mouse lungs at embryonic days (E) 11 to 14 were immunostained as whole-mounts and imaged by confocal microscopy. At E11, the primordial lung consisted of the future trachea and two budding epithelial tubules that were covered in smooth muscle to the base of the growing buds. The vagus and processes entering the lung were positive for the neural markers PGP 9.5 (protein gene product 9.5) and synapsin but no neurons were stained at this stage. An antibody to p75NTR revealed neural crest cells on the future trachea as well as in the vagus and in processes extending from the vagus to the lung. This finding indicates that even though neuronal precursors are already present at this stage, they are still migrating into the lung. By E12, neural tissue was abundant in the proximal part of the lung and nerves followed the smooth muscle-covered tubules to the base of the growing buds. At E13 and E14, a neural network of interconnected ganglia, innervated by the vagus, covered the trachea. The postganglionic nerves mainly followed the smooth muscle-covered tubules, but some extended out into the mesenchyme beyond the epithelial buds. Furthermore, we show in a model of cultured lung explants that neural tissue and smooth muscle persist and continue to grow and differentiate in vitro. By using fluorescent markers and confocal microscopy, we present the developing lung as a dynamic structure with smooth muscle and neural tissue in a prime position to influence growth and development.

Actins↗

The MLC1v gene provides a transgenic marker of myocardium formation within developing chambers of the Xenopus heart.

Many details of cardiac chamber morphogenesis could be revealed if muscle fiber development could be visualized directly within the hearts of living vertebrate embryos. To achieve this end, we have used the active promoter of the MLC1v gene to drive expression of green fluorescent protein (GFP) in the developing tadpole heart. By using a line of Xenopus laevis frogs transgenic for the MLC1v-EGFP reporter, we have observed regionalized patterns of muscle formation within the ventricular chamber and maturation of the atrial chambers, from the onset of chamber formation through to the adult frog. In f1 generation MLC1v-EGFP animals, promoter activity is first detected within the looping heart tube and delineates the forming ventricular chamber and proximal outflow tract throughout their development. The 8-kb MLC1v promoter faithfully reproduces the embryonic expression of the endogenous MLC1v mRNA. At later larval stages, weak patches of EGFP fluorescence are found on the atrial side of the atrioventricular boundary. Subsequently, an extensive lattice of MLC1v-expressing fibers extend across the mature atrial chambers of adult frog hearts and the transgene reveals the differing arrangement of muscle fibers in chamber versus outflow myocardium. The complete activity of the promoter resides within the proximal 4.5 kb of the MLC1v DNA fragment, whereas key elements regulating chamber-specific expression are present in the proximal-most 1.5 kb. Finally, we demonstrate how cardiac and craniofacial muscle expression of the MLC1v promoter can be used to diagnose mutant phenotypes in living embryos, using the injection of RNA encoding a Tbx1-engrailed repressor-fusion protein as an example.

Animals↗

Generation of conditional Cited2 null alleles.

Cited2 is a transcriptional co-factor that is widely expressed in both embryonic and extraembryonic cells during early development. It is essential for embryonic development with Cited2 null embryos showing abnormal development of organs including heart, neural tube, adrenal glands, and placenta (both in trophoblast derivatives and invading fetal vasculature), as well as having defects in the establishment of the left-right body axis. We report the generation of two conditional null alleles allowing Cre-recombinase-mediated somatic cell gene inactivation. Mice heterozygous or homozygous for these alleles are viable and fertile. Crossing conditional mutants with CMV-Cre transgenic mice produces an embryonic-lethal phenotype in the offspring indistinguishable from germline null mutants. We also demonstrate that conditional deletion results in lacZ expression under the control of the Cited2 promoter. These alleles are therefore useful genetic tools for dissecting the functions of Cited2 in the formation of different organs and patterning of the developing embryo. genesis

Alleles↗

Tissue-specific and allelic expression of the complement regulator CD46 is controlled by alternative splicing.

CD46 (membrane cofactor protein) is a human cell surface glycoprotein with cofactor activity for factor I-mediated cleavage of complement components C3b and C4b. The CD46 protein from normal lymphocytes resolves on sodium dodecyl sulfate-polyacrylamide gel electrophoresis as two major bands of 66 and 56 kDa. CD46 cDNA encodes four extracellular short consensus repeat domains, a Ser/Thr/Pro (STP)-rich region, a transmembrane region and a cytoplasmic tail. We now show that exquisite control of mRNA splicing is responsible for the heterogeneous expression of CD46 isoforms. Differential splicing of 5 exons generates at least 14 CD46 mRNA variants whose expression is stringently regulated by allelic, tissue-specific and malignancy-related factors, as: (a) leukemic cells and Epstein-Barr virus-transformed B cells preferentially incorporate the first of three STP exons (exon 7) into mRNA, and produce a larger CD46 isoform of 74 kDa, (b) an allelic difference in the proportion of 66- and 56-kDa CD46 isoforms on lymphocytes corresponds to the preferential inclusion or exclusion of the second STP exon (exon 8), (c) the third STP exon (exon 9) is specifically deleted in some placentae, (d) spermatozoa delete both exons 12 and 13, encoding a shorter transmembrane region and a unique cytoplasmic tail and (e) all tissues tested differentially splice exon 13, resulting in two alternative cytoplasmic tails. The distribution of the 14 alternatively spliced RNA transcripts correlated with the presence of protein isoforms of the predicted size, indicating that alternative splicing leads to heterogeneity of CD46 glycoproteins.

Alleles↗

Induction of anti-HIV neutralizing antibodies by synthetic peptides.

Two synthetic peptides containing amino acid sequences analogous to the envelope glycoprotein of human T-lymphotropic virus (HTLV) type III (HTLV-III) and lymphadenopathy associated virus (LAV) were produced and used to immunize rabbits. The subsequent rabbit antisera neutralized HTLV-III infectivity in vitro. The two synthetic peptides corresponded to regions associated with the gp120 or gp41 subunits respectively, of human immunodeficiency virus (HIV). This data indicates that at least two neutralizing epitopes are present on the envelope glycoprotein of HIV and these epitopes are associated with two distinct virus envelope glycoproteins. Antisera generated against these peptides neutralized infectivity of two different isolates of HTLV-III. The data is discussed in terms of possible strategy for developing an effective vaccine against the etiologic agents of acquired immune deficiency syndrome (AIDS).

Amino Acid Sequence↗

Localization of drug release sites from an oral sustained-release formulation of 5-ASA (Pentasa) in the gastrointestinal tract using gamma scintigraphy.

Release of 5-ASA from a sustained release formulation (Pentasa, Ferring A/S, Copenhagen, Denmark) was monitored with plasma sampling for up to 24 hours in nine volunteers under both fasted and fed conditions. Drug absorption was correlated with location of the sustained-release microgranules in the gastrointestinal tract by gamma scintigraphy. Disintegration of the labeled tablet preparation occurred in the stomach within 20 minutes and acetylated 5-ASA was detectable in the plasma less than 60 minutes after ingestion. No significant differences were detected in either transit times through the small intestine, peak plasma acetylated 5-ASA concentration or lag time to absorption between fasted and fed individuals. Peak plasma concentration of acetylated 5-ASA usually occurred when the microgranules were present in the small intestine or ascending colon. The pharmacoscintigraphic study confirmed that 5-ASA release from the formulation occurred throughout the gastrointestinal tract, and that food effects on the in vivo behavior of the preparation were minimal.

Administration, Oral↗

2,3,7,8-Tetrachlorodibenzo-p-dioxin induced alterations of pyruvate carboxylase levels and lactate dehydrogenase isozyme shifts in C57BL/6J male mice.

A dose-dependent reduction of hepatic pyruvate carboxylase levels and activity occurs in C57BL/6J male mice given 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) i.p. in a corn oil carrier. The dose range was from 1 to 75 micrograms/kg body weight and the analysis was done 8 days postinjection. At the maximum TCDD level investigated, we found a 10-fold reduction in pyruvate carboxylase activity. Furthermore, TCDD at a dose of 1 microgram/kg body weight blocks corn oil induction of an increase in the amount of pyruvate carboxylase in liver protein extracts. At doses beyond those required to initiate a reduction in pyruvate carboxylase, lactate dehydrogenase isozyme patterns shift. This is accompanied by an increase in blood lactic acid levels. We propose that TCDD-mediated reduction in pyruvate carboxylase and lactate dehydrogenase isozyme shifts may represent a major component in TCDD toxicity.

Animals↗

Ah receptor involvement in mediation of pyruvate carboxylase levels and activity in mice given 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The arylhydrocarbon receptor (AhR) plays a central role in mediating 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxicity in animals. The investigations described here provide evidence that support a role for the AhR in TCDD-mediated pyruvate carboxylase (PC) level/activity reductions in mice. Pyruvate carboxylase plays a pivotal role in gluconeogenesis and in supplying carbon units for the citric acid cycle. Delivered ip in a corn oil carrier, TCDD suppresses PC activity/amount at doses as low as 1 microgram/kg in responsive C57BL/6J(Ahb/b) mice. Corn oil alone injected ip into mice at 4 mL/kg appears to be an inducer that increases the amount and activity of PC. However, TCDD suppresses this induction. In the Ahb/b mouse, PC levels and activity are reduced to 10% of control values at a dose of 75 micrograms/kg. A time-course experiment shows that the PC reductions are apparent within 16 hours post-TCDD exposure. Here we report investigations on the PC/TCDD response using a congenic C57BL/6J(Ahd/d) mouse strain having an AhR with a low affinity for TCDD. If the PC/TCDD response is AhR mediated, the congenic mouse strain (Ahd/d) would require much higher doses of TCDD to suppress PC. In the Ahd/d mice, we observe that an approximately 60-fold increase in TCDD dose is necessary to produce a PC/TCDD effect. We also find that in Ahd/d mice, corn oil does not induce an increase in PC activity/amounts, as reported for Ahb/b mice.

Animals↗

Control of nitric oxide production by endogenous TGF-beta1 and systemic nitric oxide in retinal pigment epithelial cells and peritoneal macrophages.

Both in vivo and in vitro experiments demonstrate that transforming growth factor-beta1 (TGF-beta1) suppresses expression of the inducible form of nitric oxide synthase (iNOS). In this study, we examined the effects of exogenous and endogenous TGF-beta1 on retinal pigment epithelial (RPE) cells and resident peritoneal macrophages ex vivo using cells from TGF-beta1 null (TGF-beta1-/-) mice or age-matched wild-type (TGF-beta1+/+) or heterozygous (TGF-beta1+/-) littermates. RPE cells from both TGF-beta1-/- mice and TGF-beta1+/+ littermates produced NO and were immunocytochemically positive for iNOS protein only following treatment with interferon-gamma (IFN-gamma) and bacterial lipopolysaccharide (LPS); however, RPE cells from TGF-beta1-/- mice produced 40% more NO than cells from TGF-beta1+/+ mice. In contrast, resident peritoneal macrophages from both TGF-beta1+/+ and TGF-beta1-/- mice expressed iNOS protein without stimulation and in the absence of detectable production of NO. The expression of iNOS was increased by treatment with IFN-gamma, resulting in detectable levels of NO. Macrophages from TGF-beta1+/+ mice appeared to produce NO in a manner inversely proportional to the serum content of NO2- and NO3- of the mice from which the cells were obtained; no such correlation existed in TGF-beta1+/- or TGF-beta1-/- mice. Treatment of RPE cells or macrophages from both TGF-beta1+/+ and TGF-beta1-/- mice with exogenous TGF-beta1 decreased both iNOS protein and NO production. These findings demonstrate a novel role of endogenous TGF-beta1 in coupling systemic NO production to the production of NO by macrophages, and demonstrate that endogenous and exogenous TGF-beta1 can act differently to suppress NO production.

Animals↗

Tolerance of MRI vs. SPECT myocardial perfusion studies--a patient survey.

PURPOSE: To compare patients' perceived satisfaction and tolerance of magnetic resonance imaging (MRI) and single photon emission computed tomography (SPECT) myocardial perfusion imaging. MATERIALS AND METHODS: A questionnaire was sent retrospectively to 41 patients who had undergone both SPECT and MRI myocardial perfusion scans at our institution. The questionnaire assessed SPECT and MRI separately, and in a separate section compared the tests directly. The answers were scored and analyzed for statistical significance by the use of Wilcoxon signed-ranks and chi2 tests. RESULTS: Thirty-five completed questionnaires were returned. In a direct comparison, 12 patients (34%) preferred MRI overall, nine (26%) preferred SPECT, and 14 (40%) expressed no preference. The ratings for the overall comfort of the scans were similar, with a score of 5.8 for SPECT and 5.7 for MRI (on a scale of 1-10). More patients stated a preference for MRI on scan comfort, duration, and safety (no statistical significance), but it was less well rated than SPECT for space on the scanner (P = 0.008). Three patients (9%) stated that they would not have an MRI scan again, while two patients (6%) said they would not repeat a SPECT scan. CONCLUSION: MRI myocardial perfusion imaging represents an acceptable alternative to SPECT with respect to patient tolerance and satisfaction.

Aged↗

Antibodies to gangliosides inhibit goldfish optic nerve regeneration in vivo.

Intraocular injection of antiserum to mixed ganglioside or to GM1 inhibited the regeneration of goldfish optic axons following an optic nerve crush. For example, injections of antiserum on 5 consecutive days beginning the day before the crush resulted in a decrease of about 40% in the axonal outgrowth distance measured at 10 days after the crush. The inhibition was observed even when the treatment was begun a few days after the lesion, and greater degrees of inhibition were observed when the treatment was given later in regeneration. This indicates that the antiganglioside serum interfered with axonal elongation more than with the initial sprout formation. The antiganglioside treatment did not impair the enlargement of the cell bodies and nucleoli that accompanies regeneration, nor did it affect fast axonal transport of protein, glycoprotein, or glycolipid in regenerating nerves. Thus inhibition of outgrowth by antiganglioside treatment was not mediated by a gross change in the metabolism of the regenerating neurons. Treatment of normal neurons with the antiserum produced a 20-30% increase in the amount of 3H-glucosamine-labeled glycoproteins and glycolipids conveyed by fast axonal transport. These results suggest that membrane gangliosides may normally influence the supply of axonally transported glycosylated macromolecules. However, the effect of antiganglioside on axonal transport of glycosylated molecules and on axonal outgrowth are not necessarily related to each other.

Animals↗