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X Zhao

Publications and source records attributed to X Zhao.

At least 145 records · Page 8Linked to original sources
PubMed2001

Computing the relative gas-phase populations of C60 and C70: beyond the traditional delta H(fo),298 scale.

Computations and experiments have shown that the relative heat of formation (i.e., the heat of formation per carbon atom) of C70 is lower than of C60. Moreover, various computations suggest that this is actually a general trend among fullerene cages. The relationship is particularly important for gas-phase fullerenes. Experiments have shown that C60 is typically more populated than C70 when produced in high-temperature gas-phase synthesis. It is not immediately obvious how to reconcile those two terms, or whether the relative heats of formation and the relative populations are in conflict or in agreement. This article deals with this problem, treating it as a general task of relative stabilities of gas-phase clusters of different dimensions (i.e., nonisomeric clusters) under different types of thermodynamic equilibria. The results are then applied to C60 and C70 and point out that the conventional standard pressure of 1 atm is considerably different from actual fullerene-synthesis conditions. Apparently, we should expect considerably lower cluster pressures in carbon-arc synthesis. At 1 atm, C70 is more populated than C60, but at the conditions of a saturated carbon vapor the stability order is reversed in favor of C60 so that an agreement with experiment is obtained already within the thermodynamic treatment. The pressure effects are modeled using the MNDO, AM1, PM3, and SAM1 quantum-chemical semi-empirical methods as well as the available experimental data. The computations consistently show that, if the pressure effects are considered, C60 becomes more populated than C70. Relationships of the thermodynamic treatment to more sophisticated but impractical kinetic analysis are also discussed.

Carbon↗
PubMed2001

A positioned nucleosome on the human U6 promoter allows recruitment of SNAPc by the Oct-1 POU domain.

The human snRNA promoters contain a proximal sequence element (PSE) required for basal transcription and a distal sequence element (DSE) required for activated transcription. The PSE recruits the multisubunit factor SNAPc, whereas the DSE recruits Oct-1. Oct-1 and SNAPc bind cooperatively to DNA when their respective binding sites are moved into proximity through a mechanism that involves a defined protein-protein contact. Here, we show that on the natural U6 promoter, cooperative binding of Oct-1 and SNAPc is mediated by a positioned nucleosome that resides between the DSE and the PSE. This cooperative binding requires the same protein-protein contact as cooperative binding to closely spaced sites on naked DNA and mediates transcription activation.

Allosteric Site↗
PubMed2001

Overexpressing eukaryotic translation initiation factor 4E stimulates bovine mammary epithelial cell proliferation.

BACKGROUND AND AIMS: The eukaryotic translation initiation factor 4E regulates the proliferation of many cell types. In the present study, the effect of its overexpression on the growth of an immortalized bovine mammary epithelial cell line, MAC-T, has been investigated. Since involvement of cyclin D1 in growth regulation of other cell types has been suggested previously, the differences in cyclin D1 expression among the 4E-overexpressing and parental cells were also investigated. METHODS: The cDNA of mouse eukaryotic translation initiation factor 4E coding region (either wild-type or mutant, where Trp-56 was mutated to Ala) was transfected into MAC-T cells, and its protein expression was detected by Western blot analysis. Growth rates and saturation densities were calculated based on the cell counting data at desired time points. KEY RESULTS: The cells overexpressing wild-type 4E displayed higher growth rates and saturation densities compared to the parental cells (P<0.05), whereas cells expressing mutant 4E showed lower growth rates and saturation densities than the parental controls (P<0.05). The amounts of cyclin D1 mRNA and protein were higher in the wild-type transfectants than in the parental controls, whereas the mutant transfectants contained lower amounts of cyclin D1 mRNA and protein compared to the parental cells. CONCLUSION: Our results suggest that overexpression of eukaryotic translation initiation factor 4E leads to increased cyclin D1 expression at the transcriptional level, which consequently stimulates the proliferation of MAC-T cells.

Animals↗
PubMed2001

Mutations in a newly identified GTPase gene cause autosomal dominant hereditary spastic paraplegia.

The hereditary spastic paraplegias (HSPs; Strümpell-Lorrain syndrome, MIM number 18260) are a diverse class of disorders characterized by insidiously progressive lower-extremity spastic weakness (reviewed in refs. 1-3). Eight autosomal dominant HSP (ADHSP) loci have been identified, the most frequent of which is that linked to the SPG4 locus on chromosome 2p22 (found in approximately 42%), followed by that linked to the SPG3A locus on chromosome 14q11-q21 (in approximately 9%). Only SPG4 has been identified as a causative gene in ADHSP. Its protein (spastin) is predicted to participate in the assembly or function of nuclear protein complexes. Here we report the identification of mutations in a newly identified GTPase gene, SPG3A, in ADHSP affected individuals.

Amino Acid Sequence↗
PubMed2001

Escherichia coli induces apoptosis and proliferation of mammary cells.

Mammary cell apoptosis and proliferation were assessed after injection of Escherichia coli into the left mammary quarters of six cows. Bacteriological analysis of foremilk samples revealed coliform infection in the injected quarters of four cows. Milk somatic cell counts increased in these quarters and peaked at 24 h after bacterial injection. Body temperature also increased, peaking at 12 h postinjection. The number of apoptotic cells was significantly higher in the mastitic tissue than in the uninfected control. Expression of Bax and interleukin-1beta converting enzyme increased in the mastitic tissue at 24 h and 72 h postinfection, whereas Bcl-2 expression decreased at 24 h but did not differ significantly from the control at 72 h postinfection. Induction of matrix metalloproteinase-9, stromelysin-1 and urokinase-type plasminogen activator was also observed in the mastitic tissue. Moreover, cell proliferation increased in the infected tissue. These results demonstrate that Escherichia coli-induced mastitis promotes apoptosis and cell proliferation.

Animals↗
PubMed2001

Retinoic acid receptor-independent mechanism of apoptosis of melanoma cells by the retinoid CD437 (AHPN).

Retinoic acid (RA) induces differentiation of S91 melanoma cells through activation of RA receptor (RAR)gamma without affecting cell viability. The novel RARgamma-agonist CD437 (AHPN), however, also induces concomitant apoptosis through an unknown mechanism which was investigated here. By utilizing DNA microarray analysis, five apoptosis-associated, CD437-induced transcripts (CITs) were identified. Interestingly, all CITs are also regulated by p53 in a DNA damage response, and consistent with this interpretation, CD437 was found to cause DNA adduct-formation. However, p53 is not required for CD437-dependent regulation of CITs. Among this set of genes, induction of p21(WAF1/CIP1) is likely to be responsible for early S-phase growth-arrest of CD437-treated cells, whereas ei24 is a critical mediator of CD437-induced apoptosis in S91 cells. These data suggest an RAR-independent mechanism in which CD437 causes DNA adduct-formation, resulting in induction of a p53-independent DNA damage response, and subsequent growth-arrest and apoptosis. CD437-mediated DNA adduct-formation may also explain its apoptotic effects in other cell types.

3T3 Cells↗
PubMed2001

A sensitive and rapid method for the determination of protein by the resonance Rayleigh light-scattering technique with Pyrogallol Red.

The resonance Rayleigh light-scattering (RRLS) technique was used to develop a simple, sensitive and selective method for the determination of proteins. The method is based on the interaction between proteins and Pyrogallol Red (PR) in the pH range 3.6-4.2, which causes a substantial enhancement of the resonance scattering signal of PR in the wavelength range 300-450 nm with the maximum scattering peak located at 347 nm. With this method, 0.25-13 microg ml(-1) of bovine serum albumin (BSA), 0.25-10 microg ml(-1) of human serum albumin (HSA) and 0.25-13 microg ml(-1) of human immunoglobulin G (IgG) can be determined, and the detection limits, calculated as three times the standard deviation of nine blank measurements, for BSA, HAS and IgG were 51, 48 and 57 microg l(-1), respectively. Moreover, the method shows almost no protein-to-protein variability and is free from interference from many amino acids and metal ions. The method, with high sensitivity, selectivity and reproducibility, was satisfactorily applied to the determination of the total protein in human serum and saliva samples. Mechanism studies indicated that PR can bind to BSA depending mainly on electrostatic forces, and this interaction can encourage the J-aggregation of PR, which results in enhanced Rayleigh light-scattering in the PR-protein system.

Animals↗
PubMed2001

Immunological characterization of antigens encoded by the RD1 region of the Mycobacterium tuberculosis genome.

Development of immunoassays specific for the diagnosis of tuberculosis requires antigens unique to Mycobacterium tuberculosis. In a search for such antigens we tested six proteins encoded by RD1, a region present in M. tuberculosis and virulent M. bovis genomes but missing from the DNA of all substrains of M. bovis Bacillus Calmette-Guerin (BCG). The six proteins (Rv3871, Rv3872, Rv3873, MTSA-10, ESAT-6 and Rv3878) were purified to near-homogeneity from recombinant Escherichia coli. When tested for the ability to elicit antibody responses and delayed type hypersensitivity in tuberculous guinea pigs, only two of six antigens, ESAT-6 and MTSA-10, elicited strong skin reactions, while vigorous antibody responses were observed to all six proteins. When antibody responses to RD1 antigens were evaluated in sera from patients having pulmonary tuberculosis and from control subjects (patients having mycobacterioses other than tuberculosis, and healthy persons), a sizeable proportion (25%) of tuberculosis patients but none of the control subjects, had antibodies against MTSA-10 and/or ESAT-6. We conclude that MTSA-10 and ESAT-6 are promising candidates for immunodiagnostic assays specific for tuberculosis.

Animals↗
PubMed2001

Mannosylerythritol lipid induces characteristics of neuronal differentiation in PC12 cells through an ERK-related signal cascade.

Rat pheochromocytoma PC12 cells undergo neuronal differentiation in response to nerve growth factor (NGF). The differentiation involves protein kinase cascades that include the kinases MEK and ERK, as well as activation of the transcription factors c-Jun and c-Fos. We show here, that exposure of PC12 cells to mannosylerythritol lipid (MEL), a yeast extracellular glycolipid, enhances the activity of acetylcholinesterase and interrupts the cell cycle at the G1 phase, with resulting outgrowth of neurites and partial cellular differentiation. Treatment with MEL stimulates the phosphorylation of ERK to a similar extent as treatment with NGF, although, the appearance of phosphorylated ERK is somewhat delayed. Both the MEL-induced outgrowth of neurites and the increase in the activity of acetylcholinesterase are prevented by PD98059, a specific inhibitor of MEK. Northern blotting analysis of c-jun transcripts and analysis of transcription in PC12 cells of a c-jun/CAT reporter construct demonstrated a significant increase in the rate of transcription of the c-jun gene upon treatment with MEL. The sequence elements required for the MEL-mediated activation of transcription of the c-jun gene are located between nucleotides -126 and -79 in the 5' flanking region. Our results suggest that MEL induces characteristics of neuronal differentiation in PC12 cells, with transactivation of the c-jun gene, via an ERK-related signal cascade that is partially overlapping the pathways activated in response to NGF. These results might provide the groundwork for the use of microbial extracellular glycolipids as novel reagents for the treatment of cancer cells.

Acetylcholinesterase↗
PubMed2001

Site-directed mutagenesis of human membrane-associated ganglioside sialidase: identification of amino-acid residues contributing to substrate specificity.

Unlike microbial sialidases, mammalian sialidases possess strict substrate specificity, for example the human membrane-associated sialidase, which hydrolyzes only gangliosides. To cast light on the molecular basis of this narrow substrate preference, predicted active site amino-acid residues of the human membrane sialidase were altered by site-directed mutagenesis. When compared with the active site amino-acid residues proposed for Salmonella typhimurium sialidase, only five out of 13 residues were found to be different to the human enzyme, these being located upstream of the putative transmembrane region. Alteration of seven residues, including these five, was followed by transient expression of the mutant enzymes in COS-1 cells and characterization of their kinetic properties using various substrates. Substitution of glutamic acid (at position 51) by aspartic acid and of arginine (at position 114) by glutamine or alanine resulted in retention of good catalytic efficiency toward ganglioside substrates, whereas other substitutions caused a marked reduction. The mutant enzyme E51D exhibited an increase in hydrolytic activity towards GM2 as well as sialyllactose (which are poor substrates for the wild-type) with change to a lower Km and a higher Vmax. R114Q demonstrated a substrate specificity shift in the same direction as E51D, whereas R114A enhanced the preference for gangliosides GD3 and GD1a that are effectively hydrolyzed by the wild-type. The inhibition experiments using 2-deoxy-2,3-didehydro-N-acetylneuraminic acid were consistent with the results in the alteration of substrate specificity. The findings suggest that putative active-site residues of the human membrane sialidase contribute to its substrate specificity.

Amino Acid Sequence↗
PubMed2001

Induction of T cell responses against autologous ovarian tumors with whole tumor cell lysate-pulsed dendritic cells.

The loading of dendritic cells (DCs) with whole tumor cell lysates may circumvent the facts that few tumor-specific antigens have been identified in human solid tumors. The present study was designed to investigate whether ovarian cancer cells lysate-pulsed DCs activate T cell responses against autologous ovarian tumors. Incubation of T cells with autologous tumor cell lysate-pulsed DCs stimulated proliferation of autologous T cells. T cells primed by autologous tumor cell lysate-pulsed DCs showed significant killing activity against autologous tumor cells, which could be blocked by anti-MHC-class-I and anti-CD8 mAb. By contrast, T cells primed by autologous unpulsed DCs alone or tumor lysates alone failed to exhibit significant killing activity. In addition, T cells primed by DCs pulsed with allogeneic tumor cell lysates or with autologous normal cell lysate or by these cell lysates alone did not induce the increase in the autologous tumor killing activity. As additional controls, T cells stimulated with autologous tumor lysate-pulsed DCs express no increase in the lysis of autologous monocytes, allogeneic ovarian tumor cells and other cell lines including K562, Daudi and Molt-4. Furthermore, T cells stimulated with autologous tumor lysate-pulsed DCs could produce the considerable amounts of cytokines such as GM-CSF, TNF-alpha and IFN-gamma. The data in the present study suggest that whole tumor cell lysates-pulsed DCs could activate T cell responses against autologous ovarian tumor cells, and that these pulsed DCs may be used as a new approach for the specific immunotherapy of ovarian cancer patients.

Adenocarcinoma↗
PubMed2001

DNA hypermethylation is a mechanism for loss of expression of the HLA class I genes in human esophageal squamous cell carcinomas.

The three human leukocyte antigen (HLA) class I antigens, HLA-A, HLA-B and HLA-C, play important roles in the elimination of transformed cells by cytotoxic T cells. Frequent loss of expression of these antigens at the cell surface has been observed in many human cancers. Various mechanisms for post-transcriptional regulation have been proposed and tested but the molecular mechanisms for transcriptional regulation are not clear. We show by immunohistochemistry that the HLA class I antigens are absent in 26 of 29 (89%) samples of human esophageal squamous cell carcinomas (ESCC). Eleven of the 26 ESCC samples lost mRNA expression for at least one of the HLA genes, as shown by RT-PCR. DNA from the 29 pairs of ESCC and neighboring normal epithelium were examined for CpG island hypermethylation, homozygous deletion, microsatellite instability (MSI) and loss of heterozygosity (LOH). DNA from normal epithelial tissues had no detectable methylation of the CpG islands of any of these gene loci. Thirteen of 29 ESCC samples (45%) exhibited methylation of one or more of the three HLA loci and six samples (21%) exhibited methylation of all three loci. The HLA-B gene locus was most frequently methylated (38%). HLA-B mRNA expression in an ESCC cell line, where HLA-B was hypermethylated and did not express mRNA, was activated after treatment with 5-aza-2'-deoxycytidine. Homozygous deletion of these three gene loci was not observed. Relatively low rates of LOH and MSI were observed for the microsatellite markers D6S306, D6S258, D6S273 and D6S1666, close to the HLA-A, -B and -C loci, although a high ratio of LOH was observed at a nearby locus (represented by the markers D6S1051 and D6S1560), where the tumor suppressor gene p21(Waf1) resides. A strong correlation between genetic alterations and mRNA inactivation was observed in the ESCC samples. Our results indicate that HLA class I gene expression was frequently down-regulated in ESCC at both the protein and mRNA levels and that hypermethylation of the promoter regions of the HLA-A, -B and -C genes is a major mechanism of transcriptional inactivation.

Azacitidine↗
PubMed2001

Applied anatomy of the axillary nerve for selective neurotization of the deltoid muscle.

Morphologic and internal topographic features of the axillary nerve were studied in 40 cadaveric shoulders to provide anatomic data for selective neurotization of the deltoid muscle in axillary nerve injury. The axillary nerve can be divided into three segments. Proximal to the subscapularis muscle, the axillary nerve is a single nerve trunk. Nerve fascicles to the deltoid muscle are identified at its lateral part. In front of the subscapularis muscle, the axillary nerve forms into the lateral and medial fasciculi groups. Distal to the subscapularis muscle, the nerve divides into anterior and posterior branches, which are continuations of the lateral and medial fasciculi groups, respectively. The anterior branch contains all fibers that innervate to the anterior and middle deltoid muscle. In 90% of cases, the posterior branch contains part or all nerve fibers to the posterior deltoid muscle. Nerve fibers to the teres minor and cutaneous sensory fibers are found in the posterior branch. In neurotization of the deltoid muscle, the best approach is to match the donor nerve to the lateral fasciculi group, which will give the highest percentage of reinnervation of the deltoid muscle.

Adult↗
PubMed2001

Concurrent assessment of calpain and caspase-3 activation after oxygen-glucose deprivation in primary septo-hippocampal cultures.

The contributions of calpain and caspase-3 to apoptosis and necrosis after central nervous system (CNS) trauma are relatively unexplored. No study has examined concurrent activation of calpain and caspase-3 in necrotic or apoptotic cell death after any CNS insult. Experiments used a model of oxygen-glucose deprivation (OGD) in primary septo-hippocampal cultures and assessed cell viability, occurrence of apoptotic and necrotic cell death phenotypes, and protease activation. Immunoblots using an antibody detecting calpain and caspase-3 proteolysis of alpha-spectrin showed greater accumulation of calpain-mediated breakdown products (BDPs) compared with caspase-3-mediated BDPs. Administration of calpain and caspase-3 inhibitors confirmed that activation of these proteases contributed to cell death, as inferred by lactate dehydrogenase release. Oxygen-glucose deprivation resulted in expression of apoptotic and necrotic cell death phenotypes, especially in neurons. Immunocytochemical studies of calpain and caspase-3 activation in apoptotic cells indicated that these proteases are almost always concurrently activated during apoptosis. These data demonstrate that calpain and caspase-3 activation is associated with expression of apoptotic cell death phenotypes after OGD, and that calpain activation, in combination with caspase-3 activation, could contribute to the expression of apoptotic cell death by assisting in the degradation of important cellular proteins.

Animals↗
PubMed2001

High salt intake and the brain renin--angiotensin system in Dahl salt-sensitive rats.

OBJECTIVES: To assess changes in the activity of the brain renin-angiotensin system during (i) the development of salt-sensitive hypertension; and (ii) the prevention of salt-sensitive hypertension by blocking brain 'ouabain'. METHODS: In protocol I, angiotensin converting enzyme (ACE) mRNA and activity and angiotensin I and II levels were assessed in the hypothalamus and pons of Dahl salt-sensitive (Dahl S) and salt-resistant (Dahl R) rats on regular (120 micromol Na+ per g) or high (1370 micromol Na+ per g) salt diet from 4-6 weeks or 4-9 weeks of age. In protocol II, ACE mRNA and activity were assessed in the hypothalamus and pons in Dahl S on regular or high salt treated with intracerebroventricular (i.c.v.) Fab fragments blocking brain 'ouabain' or gamma-globulins, and in Dahl R on high or regular salt ACE mRNA was assessed by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) assay and angiotensin I and II by radioimmunoassay after high-performance liquid chromatography. In protocol III, effects of i.c.v. angiotensin I and i.c.v. bradykinin on renal sympathetic nerve activity (RSNA), heart rate and blood pressure before and after i.c.v. captopril were assessed in Dahl S and R rats on regular or high salt intake from 4-8 weeks of age. RESULTS: High salt diet caused a gradual, but marked increase in blood pressure in Dahl S but not Dahl R rats. Dahl S rats showed small but significant increases in ACE mRNA in the hypothalamus on regular salt diet. In Dahl S rats on high salt diet for 2 or 5 weeks ACE mRNA levels significantly increased in both hypothalamus and pons, compared with Dahl R rats on either diet or Dahl S rats on regular diet. After 5 weeks of high salt diet, ACE mRNA levels in the hypothalamus in Dahl S rats were almost three-fold higher and in the pons two-fold higher than in Dahl R rats on either diet or Dahl S on regular salt diet. High salt diet also increased ACE activity of the hypothalamus and pons in Dahl S but not Dahl R. Consistent with this increased ACE activity, central responses to angiotensin I were clearly enhanced and to bradykinin markedly diminished in Dahl S on high salt intake. Chronic blockade of brain 'ouabain' by i.c.v. Fab fragments prevented the increases in blood pressure, ACE mRNA and activity in the hypothalamus and pons by high salt intake in Dahl S rats. Angiotensin I levels in the hypothalamus and pons were similar in both groups of rats and there were no significant changes caused by high salt diet in Dahl S and R rats. On regular salt intake angiotensin II levels in the hypothalamus of Dahl S rats showed a significant decrease as compared with Dahl R rats on regular salt diet, and were similar in the pons of the two strains. High salt intake did not affect angiotensin II levels in either hypothalamus or pons in Dahl S and R rats. CONCLUSIONS: These results indicate that high salt intake increases blood pressure, ACE expression and activity in the hypothalamus and pons of Dahl S rats without a parallel increase in angiotensin II levels. Effects of high salt intake on ACE mRNA and activity appear to be secondary to activation of brain 'ouabain'.

Angiotensin I↗
PubMed2001

Enhanced renal microvascular reactivity to angiotensin II in hypertension is ameliorated by the sulfonimide analog of 11,12-epoxyeicosatrienoic acid.

OBJECTIVES: Epoxygenase metabolites produced by the kidney affect renal blood flow and tubular transport function and 11,12-epoxyeicosatrienoic acid (11,12-EET) has been putatively identified as an endothelium-derived hyperpolarizing factor. The current studies were performed to determine the influence of 11,12-EET on the regulation of afferent arteriolar diameter in angiotensin II-infused hypertensive rats. MATERIALS AND METHODS: Male Sprague-Dawley rats received angiotensin II (60 ng/min) or vehicle via an osmotic minipump. Angiotensin II-infused hypertensive and vehicle-infused normotensive rats were studied for 2 weeks following implantation of the minipump. Renal microvascular responses to the sulfonimide analog of 11,12-EET (11,12-EET-SI) and angiotensin II were observed utilizing the in-vitro juxtamedullary nephron preparation. Renal cortical epoxygenase enzyme protein levels were quantified by Western blot analysis. Renal microvessels were also isolated and epoxygenase metabolite levels measured by negative ion chemical ionization (NICI)/gas chromatography-mass spectroscopy. RESULTS: Systolic blood pressure averaged 118 +/- 2 mmHg prior to pump implantation and increased to 185 +/- 7 mmHg in rats infused with angiotensin II for 2 weeks. Afferent arteriolar diameters of 2-week normotensive animals averaged 22 +/- 1 microm. Diameters of the afferent arterioles were 17% smaller in hypertensive rats (P< 0.05); however, arterioles from both groups responded to 11,12-EET-SI (100 nmol) with similar 15-17% increases in diameter. As we previously demonstrated, the afferent arteriolar reactivity to angiotensin II was enhanced in angiotensin II-infused animals. Interestingly, elevation of 11,12-EET-SI levels to 100 nmol reversed the enhanced vascular reactivity to angiotensin II associated with angiotensin II hypertension. Renal microvascular EET levels were not different between groups and averaged 81 +/- 9 and 87 +/- 13 pg/mg per 30 min in normotensive and hypertensive animals, respectively. Renal cortical microsomal levels of the epoxygenase CYP2C23 and CYP2C11 proteins were also similar in normotensive and angiotensin II hypertensive rats. CONCLUSIONS: Taken together, these data support the concept that renal microvascular 11,12-EET activity and levels may not properly offset the enhanced angiotensin II renal vasoconstriction during angiotensin II hypertension.

8,11,14-Eicosatrienoic Acid↗
PubMed2001

Visualization of acoustic radiation from a vibrating bowling ball.

This paper presents visualization of acoustic radiation from a vibrating bowling ball using the Helmholtz equation least squares (HELS) method. In conducting the experiments, the ball is excited by a vibration shaker using stationary random signals. The radiated acoustic pressures are measured using two microphones and taken as input to the HELS formulations. The reconstructed acoustic pressures on the bowling ball surface are compared with those measured at the same locations. Also shown are comparisons of the reconstructed and measured acoustic pressure spectra at various locations on the bowling ball surface. Results demonstrate that the accuracy of reconstruction based on measurements over a conformal surface is much higher than that over a finite planar surface. This is because the latter often extends beyond the near-field region, making the accuracy of measurements inconsistent. Nevertheless, satisfactory reconstruction of acoustic pressure fields over the entire bowling ball surface can still be obtained based on the measurements taken over a finite planar surface on one side of the source. In a similar manner, the normal component of the surface velocity is reconstructed. Once these acoustic quantities are determined, the time-averaged acoustic intensity is calculated. Also presented are the formulations for estimating a priori the numbers of expansion functions and measurements required by the HELS method and the guidelines for determining the reconstruction error and optimum measurement locations, given the overall dimensions of the source and the highest frequency of interest in reconstruction.

Journal Article↗