Enhanced meningeal lymphatic drainage ameliorates lipopolysaccharide-induced brain injury in aged mice.

BACKGROUND: Sepsis-associated encephalopathy (SAE) is an acute cerebral dysfunction caused by sepsis. Neuroinflammation induced by sepsis is considered a potential mechanism of SAE; however, very little is known about the role of the meningeal lymphatic system in SAE. METHODS: Sepsis was established in male C57BL/6J mice by intraperitoneal injection of 5 mg/kg lipopolysaccharide, and the function of meningeal lymphatic drainage was assessed. Adeno-associated virus 1-vascular endothelial growth factor C (AAV1-VEGF-C) was injected into the cisterna magna to induce meningeal lymphangiogenesis. Ligation of deep cervical lymph nodes (dCLNs) was performed to induce pre-existing meningeal lymphatic dysfunction. Cognitive function was evaluated by a fear conditioning test, and inflammatory factors were detected by enzyme-linked immunosorbent assay. RESULTS: The aged mice with SAE showed a significant decrease in the drainage of OVA-647 into the dCLNs and the coverage of the Lyve-1 in the meningeal lymphatic, indicating that sepsis impaired meningeal lymphatic drainage and morphology. The meningeal lymphatic function of aged mice was more vulnerable to sepsis in comparison to young mice. Sepsis also decreased the protein levels of caspase-3 and PSD95, which was accompanied by reductions in the activity of hippocampal neurons. Microglia were significantly activated in the hippocampus of SAE mice, which was accompanied by an increase in neuroinflammation, as indicated by increases in interleukin-1 beta, interleukin-6 and Iba1 expression. Cognitive function was impaired in aged mice with SAE. However, the injection of AAV1-VEGF-C significantly increased coverage in the lymphatic system and tracer dye uptake in dCLNs, suggesting that AAV1-VEGF-C promotes meningeal lymphangiogenesis and drainage. Furthermore, AAV1-VEGF-C reduced microglial activation and neuroinflammation and improved cognitive dysfunction. Improvement of meningeal lymphatics also reduced sepsis-induced expression of disease-associated genes in aged mice. Pre-existing lymphatic dysfunction by ligating bilateral dCLNs aggravated sepsis-induced neuroinflammation and cognitive impairment. CONCLUSION: The meningeal lymphatic drainage is damaged in sepsis, and pre-existing defects in this drainage system exacerbate SAE-induced neuroinflammation and cognitive dysfunction. Promoting meningeal lymphatic drainage improves SAE. Manipulation of meningeal lymphangiogenesis could be a new strategy for the treatment of SAE.

Low temperature inhibits pectin degradation by PpCBFs to prolong peach storage time.

Low-temperature storage is a widely used method for peach fruit storage. However, the impact of PpCBFs on pectin degradation during low-temperature storage is unclear. As such, in this study, we stored the melting-flesh peach cultivar "Fuli" at low temperature (LT, 6°C) and room temperature (RT, 25°C) to determine the effect of different temperatures on its physiological and biochemical changes. Low-temperature storage can inhibit the softening of "Fuli" peaches by maintaining the stability of the cell wall. It was found that the contents of water-soluble pectin and ionic-soluble pectin in peach fruit stored at RT were higher than those stored at LT. The enzyme activities of polygalacturonase (PG), pectate lyase (PL), and pectin methylesterase (PME) were all inhibited by LT. The expressions of PpPME3, PpPL2, and PpPG were closely related to fruit firmness, but PpCBF2 and PpCBF3 showed higher expression levels at LT than RT. The promoters of PpPL2 and PpPG contain the DER motif, which suggested that PpCBF2 and PpCBF3 might negatively regulate their expression by directly binding to their promoters. These results indicated that LT may maintain firmness by activating PpCBFs to repress pectin-degradation-related enzyme genes during storage.

Exogenous BR delayed peach fruit softening by inhibiting pectin degradation enzyme genes.

Peach fruit deteriorates and senesces rapidly when stored at room temperature. Brassinosteroids (BRs) play an important role in regulating plant growth and development and maintaining fruit quality. However, little information is available on the effect of BRs on the senescence of harvested peach fruit. In this study, different concentrations of BR were used to treat 'Hongniang' peach fruit, and the results showed that 10 µM BR was the most beneficial concentration to delay the senescence of peach fruits. BR treatment delayed the decrease of fruit firmness, the release of ethylene, the increase in water-soluble pectin (WSP) and ionic-soluble pectin (ISP) content and the decrease in covalently bound pectin (CBP) content, inhibited the activities of pectin degradation enzymes, and inhibited the gene expression of PpPME1/3, PpPG, PpARF2, and PpGAL2/16. In addition, BR treatment also inhibited the expression of PpBES1-5/6. Cis-acting regulatory element analysis of pectin degradation enzyme promoters showed that many of them contained BES1 binding elements. All the above results showed that BR treatment had a positive effect on delaying the senescence of peach fruit and prolonging its storage period.

Low temperatures inhibit the pectin degradation of 'Docteur Jules Guyot' pear (Pyrus communis L.).

The most remarkable characteristic of European pears is extremely perishable and difficult to store after postharvest softening. Low-temperature storage is one of the most commonly used methods to prolong the shelf life of European pears. However, the regulatory mechanism of the low-temperature delay of the softening of European pears is still unclear. In this study, the fruit firmness, pectin polysaccharide content, pectin-degrading enzyme activity, and pectin degradation gene expression of 'Docteur Jules Guyot' pears under low temperature (LT) and room temperature (RT) were analyzed. It was found that water-soluble pectin (WSP) was significantly negatively correlated with fruit flesh firmness, and the activities of several pectin-degrading enzymes were inhibited under LT storage conditions. In addition, it was also found that the gene expression patterns of PcPME2, PcPME3, PcPG1, PcPG2, PcPL, PcGAL1, PcGAL2, PcGAL4, and PcARF1 were inhibited by LT. The C-repeat binding factors PcCBF1 and PcCBF2 were also inhibited by long-term LT storage. Correlation analysis showed that the expression of PcCBFs was positively correlated with pectin-degradation enzyme genes, and we found that the promoters of many pectin-degradation enzyme genes contain the CRT/DRE motif, which CBF can directly bind. Therefore, it is speculated that long-term low-temperature conditions inhibit pectin degradation through PcCBFs.

Iridescent chiral nematic papers based on cellulose nanocrystals with multiple optical responses for patterned coatings.

Chiral nematic papers (CNPs) with mesopores structure based on cellulose nanocrystals (CNCs) were fabricated successfully via a swelling and freeze-drying method. The order of the original chiral nematic cellulose nanocrystals film was preserved in CNPs, which was proved by scanning electron microscopy (SEM), polarized optical microscopy (POM) measurements and circular dichroism (CD) spectra. The CNPs exhibited excellent optical responsive properties to different solvents. Inspired by this feature, a colorable ink containing amounts of gel particles was prepared by pulverizing CNPs/water mixture into a suspension. Patterns written in suspension ink with various colors can be formed when soaked with different solvents. Moreover, CNPs displayed an irreversible color response to compression. Additionally, the hydrophilicity of CNPs was tuned by polyethyleneimine. Modified CNPs exhibited different colors under the identical solvent environment when compared to the original one. Aqueous PEI can be used as an ink to depict responsive photonic patterns on CNPs.

Exosomal miR-409-3p secreted from activated mast cells promotes microglial migration, activation and neuroinflammation by targeting Nr4a2 to activate the NF-κB pathway.

OBJECTIVE: Neuroinflammation plays a critical role in central nervous system diseases. Exosomal miRNAs released from various cells are implicated in cell-to-cell communication. Prior studies have placed substantial emphasis on the role of cytokines in mast cell-microglia interactions during neuroinflammation. However, it has never been clearly determined whether exosomal miRNAs participate in the interaction between mast cells and microglia and thus mediate neuroinflammation. METHODS: The characteristics of exosomes isolated from cell culture supernatants were confirmed by transmission electron microscopy (TEM), nanoparticle-tracking analysis (NTA) and Western blot. The transfer of PKH67-labelled exosomes and Cy3-labelled miR-409-3p was observed by fluorescence microscopy. Migration and activation of murine BV-2 microglial cells were evaluated through Transwell assays and immunofluorescence staining for Iba1 and CD68. CD86, IL-1ß, IL-6 and TNF-α were assessed via qRT-PCR and ELISA. MiR-409-3p was detected by qRT-PCR. Nr4a2 and NF-κB levels were measured by western blot. Regulatory effects were identified by luciferase reporter assays. RESULTS: Lipopolysaccharide (LPS)-stimulated murine P815 mast cells secreted exosomes that were efficiently taken up by murine BV-2 cells, which promoted murine BV-2 cell migration and activation. LPS-P815 exosomes increased the CD86, IL-1ß, IL-6 and TNF-α levels in murine BV-2 microglia. Furthermore, activated mast cells delivered exosomal miR-409-3p to murine BV-2 microglia. Upregulated miR-409-3p promoted murine BV-2 microglial migration, activation and neuroinflammation by targeting Nr4a2 to activate the NF-κB pathway. CONCLUSION: Exosomal miR-409-3p secreted from activated mast cells promotes microglial migration, activation and neuroinflammation by targeting Nr4a2 to activate the NF-κB pathway, which provides evidence that not only cytokines but also exosomal miRNAs participate in neuroinflammation. In the future, targeting exosomal miRNAs may provide new insights into neuroinflammation.

Calretinin Participates in Regulating Steroidogenesis by PLC-Ca2+-PKC Pathway in Leydig Cells.

Calretinin, a Ca2+-binding protein, participates in many cellular events. Our previous studies found the high expression of calretinin in testicular Leydig cells. In this study, (MLTC-1 cells were infected with LV-calb2, R2C cells with LV-siRNA-calb2. The primary mouse Leydig cells were also used to confirm those data from cell lines. Testosterone level was significantly higher in the MLTC-1 cells with over-expressed calretinin than in the control, while progesterone was lower in the R2C cells in which down-regulated calretinin. The expressions of StAR changed in synchrony with hormones. Cytoplasmic Ca2+ level was significantly increased when calretinin was over-expressed. When MLTC-1 cells were infected with LV-calb2 and then stimulated using Clopiazonic, a Ca2+-releasing agent, testosterone was significantly increased. Interestingly, the expression levels of PLC, p-PKCµ (PKD), p-MARCKS and CREB, were significantly increased in the MLTC-1 cells with over-expressed calretinin, while PLC, p-PKD, p-MARCKS, MARCKS and CREB were decreased in the R2C cells with down-regulated calretinin. We also observed the increased expression of calretinin up-regulated testosterone production and the expressions of StAR and PLC in primary mouse Leydig cells. So, calretinin as a Ca2+-binding protein participates in the regulation of steroidogenesis via the PLC-Ca2+-PKC pathway in Leydig cells.

Protective effect of calretinin on testicular Leydig cells via the inhibition of apoptosis.

The core mechanism of Late-onset hypogonadism (LOH) is the deficiency of androgen due to the functional and quantitative decline of testicular Leydig cells. Here we explored the protective effect of calretinin, a Ca2+-binding protein, on Leydig cells. We found in MLTC-1 cells transfected with LV-calb2, the cell viability and optical density (OD) were higher (p<0.05), cells in the S phase of the cell cycle were increased (p<0.01) and p-ERK1/2 and p-AKT levels were significantly higher (p<0.01 and p<0.05), while in R2C cells transfected with LV-siRNA-calb2, all of the results mentioned above were adverse (p<0.05). The cell apoptotic index after calretinin over-expressed was significantly lower (p<0.001), while the expression levels of mitochondria-related apoptotic factors such as cleaved caspase-9 and cytochrome C (cyto C) were lower and ratio of Bcl2/Bax was higher (p<0.05). After calretinin down-regulated, the apoptotic index was higher (p<0.05), while the expression levels of mitochondria-related apoptotic factors were higher and the ratio of Bcl2/Bax was lower (p<0.05). Therefore, calretinin increases Leydig cell viability and proliferation, possibly via ERK1/2 and AKT pathways, and suppresses apoptosis possibly via the mitochondria-related apoptotic pathway, which could be beneficial in understanding the pathophysiology of LOH and could lead to the study of new treatments.

Peptidome Analysis of Human Serum From Normal and Preeclamptic Pregnancies.

Preeclampsia is a kind of disease that severely harms the health of pregnant women and infants. To better understand the molecular mechanisms involved in preeclampsia, we used liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) to construct a comparative peptidomic profiling of human serum between normal and preeclamptic pregnancies. A total of 201 peptides were confidently identified, with 21 up-regulated and three down-regulated. Further analysis indicated that these differentially expressed peptides correlate with enzyme regulator activity, biological regulation, and coagulation cascades occurring during pathological changes of preeclampsia. The identification of key peptides in serum may serve not only as a basis for better understanding and further exploring the etiology and pathogenesis of PE, but also as potential biomarkers and in providing targets for future therapy in PE, especially in early onset severe PE (sPE). J. Cell. Biochem. 118: 4341-4348, 2017. © 2017 Wiley Periodicals, Inc.

Distinct expression profiles of lncRNAs between early-onset preeclampsia and preterm controls.

Early-onset preeclampsia (EOPE), which is the most severe form of the syndrome, confers a high risk of neonatal morbidity and perinatal death. We aim to study the roles of long non-coding RNAs (lncRNAs) in the pathogenesis of early-onset preeclampsia (EOPE). Therefore, we examined the expression profiles of lncRNAs between early-onset preeclampsia and preterm controls using microarray analysis. Quantitative real-time PCR (qRT-PCR) was performed to verify the selected differentially expressed lncRNAs. In total, we identified 15,646 upregulated and 13,178 downregulated lncRNAs in the placenta of EOPE patients compared to the preterm controls. Gene ontology and pathway analysis revealed that compared to the preterm controls, many of the processes over-represented in the EOPE patients were related to cell migration and cell motility. A selection of the differentially expressed lncRNA transcripts was confirmed using qRT-PCR, particularly RP11-465L10.10, which is associated with the MMP9 gene. These data may offer a background/reference resource for future functional studies of lncRNAs related to EOPE.

Lithium ameliorates lipopolysaccharide-induced microglial activation via inhibition of toll-like receptor 4 expression by activating the PI3K/Akt/FoxO1 pathway.

BACKGROUND: Lithium, an effective mood stabilizer for the treatment of bipolar disorders, has been recently suggested to have a role in neuroprotection during neurodegenerative diseases. The pathogenesis of neurological disorders often involves the activation of microglia and associated inflammatory processes. Thus, in this study, we aimed to understand the role of lithium in microglial activation and to elucidate the underlying mechanism(s). METHODS: Primary microglial cells were pretreated with lithium and stimulated with lipopolysaccharide (LPS). The cells were assessed regarding the responses of pro-inflammatory cytokines, and the associated signaling pathways were evaluated. RESULTS: Lithium significantly inhibited LPS-induced microglial activation and pro-inflammatory cytokine production. Further analysis showed that lithium could activate PI3K/Akt signaling. Analyses of the associated signaling pathways demonstrated that the lithium pretreatment led to the suppression of LPS-induced toll-like receptor 4 (TLR4) expressions via the PI3K/Akt/FoxO1 pathway. CONCLUSIONS: This study demonstrates that lithium can inhibit LPS-induced TLR4 expression and microglial activation through the PI3K/Akt/FoxO1 signaling pathway. These results suggest that lithium plays an important role in microglial activation and neuroinflammation-related diseases, which may lead to a new therapeutic strategy for the treatment of neuroinflammation-related disorders.

Targeted metabolomic study indicating glycyrrhizin's protection against acetaminophen-induced liver damage through reversing fatty acid metabolism.

The present study aimed to give a short report on a possible mechanism of glycyrrhizin to acetaminophen-induced liver toxicity. Seven-day intraperitoneal administration of glycyrrhizin (400 mg/kg/day) to 2- to 3-month-old male C57BL/6N mice (mean weight 27 g) significantly prevents acetaminophen-induced liver damage, as indicated by the activity of alanine transaminase and aspartate aminotransferase. Metabolomics analysis and principal component analysis (PCA) using ultra-fast liquid chromatography coupled to triple time-of-flight mass spectrometer were performed. PCA separated well the control, glycyrrhizin-treated, acetaminophen-treated, and glycyrrhizin+acetaminophen-treated groups. Long-chain acylcarnitines were listed as the top ions that contribute to this good separation, which include oleoylcarnitine, palmitoylcarnitine, palmitoleoylcarnitine, and myristoylcarnitine. The treatment of glycyrrhizin significantly reversed the increased levels of long-chain acylcarnitines induced by acetaminophen administration. In conclusion, this metabolomic study indicates a significant glycyrrhizin protection effect against acetaminophen-induced liver damage through reversing fatty acid metabolism.

Expression of the SET protein in testes of mice at different developmental stages.

SET is a multifunctional protein involved in regulating many biological processes of the cell cycle. It is also a regulator of steroidogenesis in the ovary. However, the expression of SET protein in testis, and its function, still remains ambiguous. In this study, we observed the expression of SET in the testes of mice at different developmental stages, and have discussed its potential function in regulating spermatogenesis and androgen production. Forty-eight male mice at different developmental stages (1 week old as the infancy group; 4 weeks old as the prepubertal group; 12 weeks old as the adult group; over 12 months old as the ageing group) were used. Cellular location of SET protein in the testes was observed by immuno-histochemistry. Expression levels of Set mRNA and SET protein were analyzed by quantitative polymerase chain reaction and Western blotting. SET protein was expressed in spermatogonial cells and spermatocytes; the highest level was mainly in haploid and tetraploid cells of the prepubertal and adult groups, and Leydig cells of the adult and ageing groups. There was a low expression in Sertoli cells. Expression of Set mRNA in the prepubertal group was significantly higher than that in the adult group (P < 0.05), while expression of SET protein was at the highest level in the adult group (P < 0.05). SET protein is mainly expressed in spermatogonial cells and spermatocytes, and poorly expressed in Sertoli cells, suggesting that it is involved in spermatogenesis. Expression of SET protein in Leydig cells suggests a possible role in steroidogenesis.

Cross-linkage effect of cellulose/laponite hybrids in aqueous dispersions and solid films.

Homogenous cellulose/laponite aqueous dispersions and composite films were respectively prepared from the pre-cooling NaOH/urea aqueous systems. Rheological measurements of aqueous dispersions demonstrated a sol-to-gel transition triggered by loading of laponite, reflecting a cross-linkage effect of cellulose/laponite hybrids. Similarly, based on scanning electron microscopy (SEM), Fourier-transform infrared (FTIR) spectroscopy, and X-ray diffraction (XRD) characterizations, as well as mechanical and thermal measurements, the cross-linkage effect of cellulose/laponite hybrids was also found in solid films, which played an important role in improving the tensile strength (σb) of composite films. For instance, the σb exhibited a largest enhancement up to 75.7% at a critical laponite content of 0.100 wt%, indicating that the property of composite film was closely related with the dispersion and interaction state of laponite, i.e. its content in cellulose matrix. These results were expected to provide significant information for fabrication and utility of cellulose-based materials.

Characterisation of cellulose films regenerated from acetone/water coagulants.

A precooled aqueous solution of 7 wt% NaOH/12 wt% urea was used to dissolve cellulose up to a concentration of 2 wt%, which was then coagulated in an acetone/water mixture to regenerate cellulose film. The volume ratio of acetone to water (φ) had a dominant influence on film dimensional stability, film-forming ability, micromorphology, and mechanical strength. The film regenerated at φ=2.0 showed excellent performance in both dimensional stability and film-forming ability. Compared to that from pure acetone, the cellulose film from the acetone/water mixture with φ=2.0 was more densely interwoven, since the cellulosic fibrils formed during regeneration had pores with smaller average diameter. The alkali capsulated in the film during film formation could be released at quite a slow rate into the surrounding aqueous solution. The regenerated cellulose film with adjustable structure and properties may have potential applications in drug release and ultra filtration.

Fabrication of a COF-5 membrane on a functionalized α-Al2O3 ceramic support using a microwave irradiation method.

A novel surface modification strategy was developed using 3-aminopropytriethoxysilane and 4-formylphenylboronic acid successively as covalent linkers between COF-5 and the porous α-Al2O3 ceramic support, and then the COF-5 membrane was further grown successfully on the modified α-Al2O3 support by using a microwave irradiation method.

Prenatal androgen excess programs metabolic derangements in pubertal female rats.

Owing to the heterogeneity in the clinical symptoms of polycystic ovary syndrome (PCOS), the early pathophysiological mechanisms of PCOS remain unclear. Clinical, experimental, and genetic evidence supports an interaction between genetic susceptibility and the influence of maternal environment in the pathogenesis of PCOS. To determine whether prenatal androgen exposure induced PCOS-related metabolic derangements during pubertal development, we administrated 5α-dihydrotestosterone (DHT) in pregnant rats and observed their female offspring from postnatal 4 to 8 weeks. The prenatally androgenized (PNA) rats exhibited more numerous total follicles, cystic follicles, and atretic follicles than the controls. Fasting glucose, insulin, leptin levels, and homeostatic model assessment for insulin resistance were elevated in the PNA rats at the age of 5-8 weeks. Following intraperitoneal glucose tolerance tests, glucose and insulin levels did not differ between two groups; however, the PNA rats showed significantly higher 30- and 60-min glucose levels than the controls after insulin stimulation during 5-8 weeks. In addition, prenatal DHT treatment significantly decreased insulin-stimulated phosphorylation of AKT in the skeletal muscles of 6-week-old PNA rats. The abundance of IR substrate 1 (IRS1) and IRS2 was decreased in the skeletal muscles and liver after stimulation with insulin in the PNA group, whereas phosphorylation of insulin-signaling proteins was unaltered in the adipose tissue. These findings validate the contribution of prenatal androgen excess to metabolic derangements in pubertal female rats, and the impaired insulin signaling through IRS and AKT may result in the peripheral insulin resistance during pubertal development.

Effect of Hsp27 on early embryonic development in the mouse.

Previous studies by this study group have showed that heat shock protein 27 (Hsp27), expressed in the oocyte of growing follicles, is down-regulated in polycystic ovary syndrome ovaries and that down-regulation of Hsp27 improves the maturation of mouse oocytes and increases early apoptosis of oocytes. In this study, the effect of Hsp27 on early embryo development in the mouse was observed. Following microinjection of AdCMV-Hsp27 or AdsiRNA-Hsp27 into the cytoplasm of mouse zygotes, blastocyst morphology was observed and cell apoptosis of blastocysts was detected by TUNEL. After culture in vitro for 96h, blastocysts were analysed for Hsp27 expression by real-time PCR and immunofluorescence. The blastocyst formation rate and embryo quality were evaluated. The expression of Hsp27 was significantly increased in embryos with Hsp27 overexpression (AdCMV-Hsp27), while it was significantly suppressed by 75% in embryos with the gene silenced (AdsiRNA-Hsp27; both P<0.05). Cell apoptosis in blastocysts, blastocyst formation rate and embryo quality were unaffected by Hsp27 overexpression or gene silencing. In conclusion, overexpression or down-regulation of Hsp27 in zygotes, as a single factor, does not significantly affect the subsequent embryonic development.

[Pemetrexed combined DDP in the treatment of advanced non-small cell lung cancer: a case report and literature review].

BACKGROUND AND OBJECTIVE: The aim of this study is to integrate with literature review, and explore the value of treatment of advanced non-small cell lung cancer with second line. METHODS: For the metastatic progressive non-small cell lung adenocarcinoma patient, the evaluation of efficacy for complete response (CR) with endostar combined GC, the sequential treatment with gefitinib, used pemetrexed combined DDP as the second line treatment, followed up and observed with the progression free survival (PFS) and survival time of patient. RESULTS: Pemetrexed combined DDP in the treatment of 5 cycles, the evaluation of lung cancer efficacy for CR, bone metastasis was steady, PFS was 6.6 months, survival time is 22 months now, improved the quality of living life. CONCLUSIONS: For advanced non-small cell lung adenocarcinoma recurrence and metastasis, after the treatment of first line and maintenance therapy, selecting adequately pemetrexed combined DDP, as the second line treatment, can prolong the lifetime and improve the quality of life.

Three-dimensional speckle-tracking imaging for left ventricular rotation measurement: an in vitro validation study.

OBJECTIVE: Left ventricular (LV) twist is manifested in oppositely directed apical and basal rotation. We studied a new 3-dimensional (3D) echocardiography program (wall motion tracking; Toshiba America Medical Systems, Inc, Tustin, CA) for left ventricular rotation. METHODS: We used a rotation model with a variable-speed motor to rotate hearts in a water bath. We studied 10 freshly harvested pig hearts, which were mounted on the rotary actuator of our twist phantom with the heart base rotating and the apex held fixed to avoid translational motion, at rotations of 0 degrees , 15 degrees , 20 degrees , and 25 degrees . Full-volume 3D image loops were acquired on a Toshiba Aplio Artida ultrasound system at a maximized frame rate. RESULTS: As the actual heart rotation increased, computed segmental and global rotation also increased accordingly, with the measured rotations of the basal and middle segments greater than that of the apex (both P < .001). Segmental and global rotation at all 3 levels correlated well with the actual rotation (base: r = 0.93; middle: r = 0.92; apex: r = 0.82; global: r = 0.95; all P < .001). CONCLUSIONS: The new 3D program tracked LV rotation accurately.