Biomedical subjects

H Liu

Publications and source records attributed to H Liu.

At least 433 records · Page 24Linked to original sources

PubMed2000

Withholding versus withdrawing life-sustaining treatment: patient factors and documentation associated with dialysis decisions.

OBJECTIVE: We evaluated prospectively the use of acute hemodialysis among hospitalized patients to identify demographic and clinical predictors of and chart documentation concerning dialysis withheld and withdrawn. DESIGN: Prospective cohort study. SETTING: Five teaching hospitals. PATIENTS: Five hundred sixty-five seriously ill hospitalized patients who had not previously undergone dialysis who developed renal failure. MAIN OUTCOME MEASURES: Patient demographics, clinical characteristics, preferences, and prognostic estimates associated with having dialysis withheld rather than initiated and withdrawn rather than continued. Differences in chart documentation concerning decision-making for dialysis withheld, withdrawn, and continued. RESULTS: Older patient age, cancer diagnosis, and male gender were associated with dialysis withheld rather than withdrawn. Age and gender differences persisted after adjustment for patients' aggressiveness of care preference. Worse 2-month prognosis was associated with both withholding and withdrawing dialysis. Chart documentation of decision-making was lacking more often for patients with dialysis withheld than for dialysis withdrawn. CONCLUSIONS: Measuring the equity of life-sustaining treatment use will require evaluation of care withheld, not just care withdrawn. Older patients and men, after accounting for prognosis and function, are more likely to have dialysis withheld than withdrawn after a trial. Further exploration is needed into this disparity and the inadequate chart documentation for patients with dialysis withheld.

APACHE↗

PubMed2000

Modifiable risk factors predict functional decline among older women: a prospectively validated clinical prediction tool. The Study of Osteoporotic Fractures Research Group.

OBJECTIVE: To identify modifiable predictors of functional decline among community-residing older women and to derive and validate a clinical prediction tool for functional decline based only on modifiable predictors. DESIGN: A prospective cohort study. SETTING: Four geographic areas of the United States. PARTICIPANTS: Community-residing women older than age 65 recruited from population-based listings between 1986 and 1988 (n = 6632). MEASUREMENTS: Modifiable predictors were considered to be those that a clinician seeing an older patient for the first time could reasonably expect to change over a 4-year period: benzodiazepine use, depression, low exercise level, low social functioning, body-mass index, poor visual acuity, low bone mineral density, slow gait, and weak grip. Known predictors of functional decline unlikely to be amenable to intervention included age, education, medical comorbidity, cognitive function, smoking history, and presence of previous spine fracture. All variables were measured at baseline; only modifiable predictors were candidates for the prediction tool. Functional decline was defined as loss of ability over the 4-year interval to perform one or more of five vigorous or eight basic daily activities. RESULTS: Slow gait, short-acting benzodiazepine use, depression, low exercise level, and obesity were significant modifiable predictors of functional decline in both vigorous and basic activities. Weak grip predicted functional decline in vigorous activities, whereas long-acting benzodiazepine use and poor visual acuity predicted functional decline in basic activities. A prediction rule based on these eight modifiable predictors classified women in the derivation set into three risk groups for decline in vigorous activities (12%, 25%, and 39% risk) and two risk groups for decline in basic activities (2% and 10% risk). In the validation set, the probabilities of functional decline were nearly identical. CONCLUSIONS: A substantial portion of the variation of functional decline can be attributed to risk factors amenable to intervention over the short term. Using eight modifiable predictors that can be identified in a single office visit, clinicians can identify older women at risk for functional decline.

Activities of Daily Living↗

PubMed2000

Design of a dual CCD configuration to improve the signal-to-noise ratio.

The noise of a digital charge coupled device (CCD) detector increases with the readout speed, causing problems in a number of important applications, such as x-ray fluoroscopy and micro-CT. In this paper, we present an approach for the design of a dual-CCD configuration to improve the average signal-to-noise ratio, and hence provide an inexpensive solution within the constraint of the current technology.

Equipment Design↗

PubMed2000

A localization algorithm and error analysis for stereo x-ray image guidance.

Stereo x-ray radiography attracts increasing attention in major clinical applications. The purpose of this paper is to analyze the 3D localization error for breast biopsy procedures and provide guidelines for improving its accuracy. Our prototype is a CCD based digital stereo x-ray imaging system. The mathematical model consists of two x-ray sources and one stationary detector plane. A closed form least-squares solution is derived for 3D localization of feature points, particularly a biopsy needle tip, from a pair of 2D digital radiographs. Based on the least-squares formula and its first order approximation, the 3D localization error is analyzed in terms of object location, measurement error, separation between the two x-ray sources, and distance from the source to the detector. The stereo imaging and error estimation formulas are numerically simulated and experimentally validated. The data are in agreement with theoretical prediction. These results can be used for the purpose of system design and protocol optimization.

Algorithms↗

PubMed2000

Lens distortion in optically coupled digital x-ray imaging.

UNLABELLED: The objectives of this research are to analyze geometrical distortions introduced by relay lenses in optically coupled digital x-ray imaging systems and to introduce an algorithm to correct such distortions. METHODS: The radial and tangential errors introduced by a relay lens in digital x-ray imaging were experimentally measured, using a lens-coupled CCD (charge coupled device) prototype. An algorithm was introduced to correct these distortions. Based on an x-ray image of a standard calibration grid, the algorithm first identified the location of the optical axis, then corrected the radial and tangential distortions using polynomial transformation technique. RESULTS: Lens distortions were classified and both radial and tangential distortions introduced by lenses were corrected using polynomial transformation. For the specific lens-CCD prototype investigated, the mean positional error caused by the relay lens was reduced by the correction algorithm from about eight pixels (0.69 mm) to less than 1.8 pixels (0.15 mm). Our investigation also shows that the fourth order of polynomial for the correction algorithm provided the best correction result. CONCLUSIONS: Lens distortions should be considered in position-dependent, quantitative x-ray imaging and such distortions can be minimized in CCD x-ray imaging by appropriate algorithm, as demonstrated in this paper.

Algorithms↗

PubMed2000

Polymorphism in the interleukin-4 promoter affects acquisition of human immunodeficiency virus type 1 syncytium-inducing phenotype.

The emergence of syncytium-inducing (SI) variants of human immunodeficiency virus type 1 (HIV-1) in infected individuals is an indicator of poor prognosis and is often correlated with faster CD4(+) cell depletion and rapid disease progression. Interleukin-4 (IL-4) is a pleiotropic cytokine with various immune-modulating functions including induction of immunoglobulin E (IgE) production in B cells, down-regulation of CCR5 (a coreceptor for HIV-1 non-SI [NSI] strains), and up-regulation of CXCR4 (a coreceptor for HIV-1 SI variants). Here we show that homozygosity of a polymorphism in the IL-4 promoter region, IL-4 -589T, is correlated with increased rates of SI variant acquisition in HIV-1-infected individuals in Japan. This mutation was also shown to be associated with elevated serum IgE levels in HIV-1-infected individuals, especially in those at advanced stages of disease. In contrast, neither a triallele polymorphism in IL-10, another Th2 cytokine, nor a biallele polymorphism in the RANTES promoter affected acquisition of the SI phenotype. This finding suggested that IL-4-589T increases IL-4 production in the human body and thus accelerates the phenotypic switch of HIV-1 from NSI to SI and possibly disease progression of AIDS.

Alleles↗

PubMed2000

Identification of conserved residues contributing to the activities of adenovirus DNA polymerase.

Adenovirus codes for a DNA polymerase that is a member of the DNA polymerase alpha family and uses a protein primer for initiation of DNA synthesis. It contains motifs characteristic of a proofreading 3'-5'-exonuclease domain located in the N-terminal region and several polymerase motifs located in the C-terminal region. To determine the role of adenovirus DNA polymerase in DNA replication, 22 site-directed mutations were introduced into the conserved DNA polymerase motifs in the C-terminal region of adenovirus DNA polymerase and the mutant forms were expressed in insect cells using a baculovirus expression system. Each mutant enzyme was tested for DNA binding activity, the ability to interact with pTP, DNA polymerase catalytic activity, and the ability to participate in the initiation of adenovirus DNA replication. The mutant phenotypes identify functional domains within the adenovirus DNA polymerase and allow discrimination between the roles of conserved residues in the various activities carried out by the protein. Using the functional data in this study and the previously published structure of the bacteriophage RB69 DNA polymerase (J. Wang et al., Cell 89:1087-1099, 1997), it is possible to envisage how the conserved domains in the adenovirus DNA polymerase function.

Adenoviridae↗

PubMed2000

Crk1, a novel Cdc2-related protein kinase, is required for hyphal development and virulence in Candida albicans.

Both mitogen-activated protein kinases and cyclin-dependent kinases play a role in hyphal development in Candida albicans. Using an oligonucleotide probe-based screen, we have isolated a new member of the Cdc2 kinase subfamily, designated Crk1 (Cdc2-related kinase). The protein sequence of Crk1 is most similar to those of Saccharomyces cerevisiae Sgv1 and human Pkl1/Cdk9. In S. cerevisiae, CRK1 suppresses some, but not all, of the defects associated with an sgv1 mutant. Deleting both copies of CRK1 in C. albicans slows growth slightly but leads to a profound defect in hyphal development under all conditions examined. crk1/crk1 mutants are impaired in the induction of hypha-specific genes and are avirulent in mice. Consistent with this, ectopic expression of the Crk1 kinase domain (CRK1N) promotes filamentous or invasive growth in S. cerevisiae and hyphal development in C. albicans. The activity of Crk1 in S. cerevisiae requires Flo8 but is independent of Ste12 and Phd1. Similarly, Crk1 promotes filamentation through a route independent of Cph1 and Efg1 in C. albicans. RAS1(V13) can also activate filamentation in a cph1/cph1 efg1/efg1 double mutant. Interestingly, CRK1N produces florid hyphae in ras1/ras1 strains, while RAS1(V13) generates feeble hyphae in crk1/crk1 strains.

Amino Acid Sequence↗

PubMed2000

Macrophages require constitutive NF-kappaB activation to maintain A1 expression and mitochondrial homeostasis.

NF-kappaB is a critical mediator of macrophage inflammatory responses, but its role in regulating macrophage survival has yet to be elucidated. Here, we demonstrate that constitutive NF-kappaB activation is essential for macrophage survival. Blocking the constitutive activation of NF-kappaB with pyrrolidine dithiocarbamate or expression of IkappaBalpha induced apoptosis in macrophagelike RAW 264.7 cells and primary human macrophages. This apoptosis was independent of additional death-inducing stimuli, including Fas ligation. Suppression of NF-kappaB activation induced a time-dependent loss of mitochondrial transmembrane potential (DeltaPsi(m)) and DNA fragmentation. Examination of initiator caspases revealed the cleavage of caspase 9 but not caspase 8 or the effector caspase 3. Addition of a general caspase inhibitor, z-VAD. fmk, or a specific caspase 9 inhibitor reduced DNA fragmentation but had no effect on DeltaPsi(m) collapse, indicating this event was caspase independent. To determine the pathway leading to mitochondrial dysfunction, analysis of Bcl-2 family members established that only A1 mRNA levels were reduced prior to DeltaPsi(m) loss and that ectopic expression of A1 protected against cell death following inactivation of NF-kappaB. These data suggest that inhibition of NF-kappaB in macrophages initiates caspase 3-independent apoptosis through reduced A1 expression and mitochondrial dysfunction. Thus, constitutive NF-kappaB activation preserves macrophage viability by maintaining A1 expression and mitochondrial homeostasis.

Apoptosis↗

PubMed2000

Activation of apoptosis signal-regulating kinase 1 (ASK1) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASK1 inhibitor thioredoxin.

The stress-activated protein kinases (SAPKs, also called c-Jun NH(2)-terminal kinases) and the p38s, two mitogen-activated protein kinase (MAPK) subgroups activated by cytokines of the tumor necrosis factor (TNF) family, are pivotal to the de novo gene expression elicited as part of the inflammatory response. Apoptosis signal-regulating kinase 1 (ASK1) is a MAPK kinase kinase (MAP3K) that activates both the SAPKs and p38s in vivo. Here we show that TNF receptor (TNFR) associated factor 2 (TRAF2), an adapter protein that couples TNFRs to the SAPKs and p38s, can activate ASK1 in vivo and can interact in vivo with the amino- and carboxyl-terminal noncatalytic domains of the ASK1 polypeptide. Expression of the amino-terminal noncatalytic domain of ASK1 can inhibit TNF and TRAF2 activation of SAPK. TNF can stimulate the production of reactive oxygen species (ROS), and the redox-sensing enzyme thioredoxin (Trx) is an endogenous inhibitor of ASK1. We also show that expression of TRAF2 fosters the production of ROS in transfected cells. We demonstrate that Trx significantly inhibits TRAF2 activation of SAPK and blocks the ASK1-TRAF2 interaction in a reaction reversed by oxidants. Finally, the mechanism of ASK1 activation involves, in part, homo-oligomerization. We show that expression of ASK1 with TRAF2 enhances in vivo ASK1 homo-oligomerization in a manner dependent, in part, upon the TRAF2 RING effector domain and the generation of ROS. Thus, activation of ASK1 by TNF requires the ROS-mediated dissociation of Trx possibly followed by the binding of TRAF2 and consequent ASK1 homo-oligomerization.

Cell Line↗

PubMed2000

Brain tumor resection: intraoperative monitoring with high-field-strength MR imaging-initial results.

PURPOSE: To investigate the challenges and benefits of magnetic resonance (MR) imaging during brain tumor resection. MATERIALS AND METHODS: A short-bore 1.5-T MR system equipped with echo-planar-capable gradients was used in resection of brain tumors in 30 patients. MR sequences and need for contrast material enhancement were determined on the basis of the targeted lesion. MR images were acquired before, during, and after surgery. Tissue obtained at biopsy or excised as a result of intraoperative MR findings was examined histopathologically. RESULTS: MR images of enhancing lesions proved to be the most challenging to interpret intraoperatively, and relative enhancement at the resection cavity boundary was not specific for residual tumor. The ability to detect residual tumor intraoperatively resulted in a radiologically complete resection in 24 (80%) of 30 patients. The frequency of complications was low, and no untoward effects related to the MR environment were observed. CONCLUSION: Intraoperative MR imaging provided valuable information on the completeness of resection, and resection progress was well demonstrated during surgery.

Adolescent↗

PubMed2000

Hypertonic perfusion inhibits intracellular Na and Ca accumulation in hypoxic myocardium.

Much evidence supports the view that hypoxic/ischemic injury is largely due to increased intracellular Ca concentration ([Ca](i)) resulting from 1) decreased intracellular pH (pH(i)), 2) stimulated Na/H exchange that increases Na uptake and thus intracellular Na (Na(i)), and 3) decreased Na gradient that decreases or reverses net Ca transport via Na/Ca exchange. The Na/H exchanger (NHE) is also stimulated by hypertonic solutions; however, hypertonic media may inhibit NHE's response to changes in pH(i) (Cala PM and Maldonado HM. J Gen Physiol 103: 1035-1054, 1994). Thus we tested the hypothesis that hypertonic perfusion attenuates acid-induced increases in Na(i) in myocardium and, thereby, decreases Ca(i) accumulation during hypoxia. Rabbit hearts were Langendorff perfused with HEPES-buffered Krebs-Henseleit solution equilibrated with 100% O(2) or 100% N(2). Hypertonic perfusion began 5 min before hypoxia or normoxic acidification (NH(4)Cl washout). Na(i), [Ca](i), pH(i), and high-energy phosphates were measured by NMR. Control solutions were 295 mosM, and hypertonic solutions were adjusted to 305, 325, or 345 mosM by addition of NaCl or sucrose. During 60 min of hypoxia (295 mosM), Na(i) rose from 22+/-1 to 100+/-10 meq/kg dry wt while [Ca](i) rose from 347+/-11 to 1,306+/-89 nM. During hypertonic hypoxic perfusion (325 mosM), increases in Na(i) and [Ca](i) were reduced by 65 and 60%, respectively (P<0.05). Hypertonic perfusion also diminished Na uptake after normoxic acidification by 87% (P<0.05). The data are consistent with the hypothesis that mild hypertonic perfusion diminishes acid-induced Na accumulation and, thereby, decreases Na/Ca exchange-mediated Ca(i) accumulation during hypoxia.

Animals↗

PubMed2000

Role of caspases and NF-kappaB signaling in hydrogen peroxide- and superoxide-induced hepatocyte apoptosis.

Reactive oxygen intermediates (ROI) have been implicated as mediators of hepatocyte death resulting from a variety of forms of liver injury. To delineate the mechanisms that underlie ROI-induced apoptosis, the roles of caspase activation and nuclear factor-kappaB (NF-kappaB) signaling were determined in the rat hepatocyte cell line RALA255-10G after treatment with H(2)O(2) or the superoxide generator menadione. By 8 h, H(2)O(2) and menadione caused 26% and 33% cell death, respectively. Death from both ROI occurred by apoptosis as indicated by morphology under fluorescence microscopy, the induction of caspase activation and DNA fragmentation, and the cleavage of poly(ADP-ribose) polymerase. Despite the presence of caspase activation in both forms of apoptosis, caspase inhibition blocked H(2)O(2)- but not menadione-induced apoptosis. In contrast, inhibition of NF-kappaB activation decreased cell death from both ROI. Different ROI, therefore, induce distinct apoptotic pathways in RALA hepatocytes that are both caspase dependent and independent. In contrast to the known protective effect of NF-kappaB activation in tumor necrosis factor-alpha-induced hepatocyte apoptosis, NF-kappaB promotes hepatocellular death from ROI in these cells.

Animals↗

PubMed2000

Bleomycin-induced pulmonary fibrosis in fibrinogen-null mice.

Mice deleted for the plasminogen activator inhibitor-1 (PAI-1) gene are relatively protected from developing pulmonary fibrosis induced by bleomycin. We hypothesized that PAI-1 deficiency reduces fibrosis by promoting plasminogen activation and accelerating the clearance of fibrin matrices that accumulate within the damaged lung. In support of this hypothesis, we found that the lungs of PAI-1(-/-) mice accumulated less fibrin after injury than wild-type mice, due in part to enhanced fibrinolytic activity. To further substantiate the importance of fibrin removal as the mechanism by which PAI-1 deficiency limited bleomycin-induced fibrosis, bleomycin was administered to mice deficient in the gene for the Aalpha-chain of fibrinogen (fib). Contrary to our expectation, fib(-/-) mice developed pulmonary fibrosis to a degree similar to fib(+/-) littermate controls, which have a plasma fibrinogen level that is 70% of that of wild-type mice. Although elimination of fibrin from the lung was not in itself protective, the beneficial effect of PAI-1 deficiency was still associated with proteolytic activity of the plasminogen activation system. In particular, inhibition of plasmin activation and/or activity by tranexamic acid reversed both the accelerated fibrin clearance and the protective effect of PAI-1 deficiency. We conclude that protection from fibrosis by PAI-1 deficiency is dependent upon increased proteolytic activity of the plasminogen activation system; however, complete removal of fibrin is not sufficient to protect the lung.

Animals↗

PubMed2000

Yohimbine challenge in children with anxiety disorders.

OBJECTIVE: The authors evaluated the neurohormonal and subjective mood response of children with anxiety disorders who were challenged with yohimbine. METHOD: Seventeen children with DSM-IV diagnoses of anxiety disorders and 15 normal comparison children were given yohimbine orally (0.1 mg/kg). Neurohormonal measures and visual analog self-reports of tenseness were recorded over a 150-minute period. RESULTS: Yohimbine was uniformly well tolerated, and it behaviorally differentiated children with anxiety disorders from normal comparison children with higher maximum change (Deltamax) ratings of anxiety in the patients (mean=17.4 mm, SD=29.8) than in the comparison subjects (mean=0.3 mm, SD=4.4). Yohimbine-stimulated Deltamax growth hormone (GH) for children with anxiety disorders (mean=-1.5 ng/ml, SD=5.9) was significantly reduced compared to that of normal comparison children (mean=2.7 ng/ml, SD=4.5). CONCLUSIONS: Yohimbine selectively elevates self-rated anxiety in children with anxiety disorders and is associated with the blunting of GH in those children relative to that of comparison children. Presence of a blunted GH response to yohimbine in children with anxiety disorders is reminiscent of findings in adults with anxiety disorders, particularly panic disorder. These findings support enhanced central adrenergic sensitivity in children with anxiety disorders, as demonstrated by yohimbine-exacerbated anxiety. The findings should be reconciled with the absence of clonidine-related GH blunting in the same cohort.

Administration, Oral↗

PubMed2000

Laryngopharyngeal sensory deficits in patients with laryngopharyngeal reflux and dysphagia.

There are no reliable means of quantifying the edema that results from acid exposure to the posterior larynx in patients with laryngopharyngeal reflux (LPR). However, it is possible to quantify laryngopharyngeal sensitivity in these patients by endoscopic administration of air pulses to the laryngeal mucosa in order to elicit the laryngeal adductor reflex. The purpose of this study was to determine whether patients with LPR have sensory deficits in the laryngopharynx, and whether treatment of these patients with a proton pump inhibitor (PPI) results in resolution of sensory deficits. Flexible endoscopic evaluation of swallowing with sensory testing was prospectively performed in 54 patients with dysphagia without neurologic disease and in 25 healthy controls. The laryngopharyngeal sensory level, posterior laryngeal edema, and LPR were assessed. We defined LPR as passage of food material from the esophageal inlet retrograde into the hypopharynx. Patients with LPR were placed on 3 months of omeprazole or lansoprazole and then retested. Patients without LPR were placed on H2 blockers for 3 months and then retested. In the dysphagia group, 48 of 54 patients (89%) had edema of the posterior larynx, and 42 of 54 (78%) had laryngopharyngeal sensory deficits. We noted LPR in 38 of 54 (70%). In the control group, 1 of 25 subjects (4%) had edema, sensory deficits, and LPR. The differences in incidence of edema, sensory deficits, and LPR between the dysphagia group and the control group were significant (p < .001, chi2 test). Twenty-three patients with LPR placed on a PPI returned for follow-up, with improvement in laryngeal edema in 14 of the 21 (67%) who had pretreatment edema and resolution of sensory deficits in 15 of the 19 (79%) who had pretreatment deficits. In the non-LPR, non-PPI group, 11 of 16 patients returned for follow-up, with improvement in laryngeal edema in none of the 11 and improvement in sensory deficits in 1 of the 11 (9.1%). The differences in improvement in laryngeal edema and sensory deficits between the LPR, PPI group, and the non-LPR, non-PPI group were significant (p < .01, Fisher's exact test). We conclude that patients with dysphagia and edema of the posterior larynx as a result of LPR have sensory deficits in the laryngopharynx. Treatment of these patients with a PPI appears to result in resolution of laryngopharyngeal edema and improvement of sensory deficits, both subjectively and objectively.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed2000

Correlative factors of insulin resistance in essential hypertension.

Essential Hypertension (EH) is correlated with a metabolic disturbance characterized by insulin resistance (IR). In this study, there were observed in 47 subjects with EH and 30 subjects with normal blood pressure. Serum levels of insulin-like growth factor-1 (IGF-1), serum levels of growth hormone (GH), the activity of erythrocyte insulin receptors (EIR), and ATP levels in erythrocytes, the insulin sensitivity index (ISI) was used to study the correlative factors of essential hypertension. 1. Among patients with EH, ISI, GH, and low-affinity insulin binding sites of EIRs (RT2) were found to be in significantly lower amounts, IGF-1 levels and the KD2 of the erythrocyte insulin receptors were noted to be significantly higher. Compared with the control group, there was a marked difference between EH group and the control group. However, no statistical difference was observed between the hypertensive group and the group with normal blood pressure as regards erythrocyte ATP levels, high-affinity insulin binding sites of EIRs (RT1), and the KD1 of EIRs. 2. In the hypertensive group, the ISI was negatively correlated with mean arterial blood pressure (MBP), a family history of hypertension, the body mass index (BMI), the waist-hip ratio (WHR) and IGF-1 levels (r=-0.614delta, -0.354**, -0.386**, -0.472**, -0.298*, delta p < 0.001, **p < 0.01, *p < 0.05), were positively correlated with RT2 and GH levels (r=0.301**, 0.275*, **p < 0.01, *p < 0.05). There were no statistically significant differences between ISI and age, sex, smoking history, drinking, RT1, KD1, and ATP levels in erythrocytes. 3. The ISI was used as the dependent variable in multiple linear stepwise regression analysis. MBP (X1), a family history of EH (X2), WHR (X3), GH (X4), IGF-1 (X5), RT2 (X6), and the body mass index (X7) was used as independent variables. X1, X2, X3, X5, X6, and X7 were used in the equations. The results indicate that patients with EH also tend to have IR. We suggest that MBP, a family history of hypertension, BMI, WHR, IGF-1, and RT2 might be independent factors affecting IR in cases of essential hypertension.

Adenosine Triphosphate↗

PubMed2000

Making rats rise to erect bipedal stance for feeding partially prevented orchidectomy-induced bone loss and added bone to intact rats.

The objectives of this study were to investigate the different effects on muscle mass and cancellous (proximal tibial metaphysis [PTM]) and cortical (tibial shaft [TX]) bone mass of sham-operated and orchidectomized (ORX) male rats by making rats rise to erect bipedal stance for feeding. Specially designed raised cages (RC) were used so that the rats had to rise to erect bipedal stance to eat and drink for 12 weeks. Dual-energy X-ray absorptiometry (DEXA) and peripheral quantitative computerized tomography (pQCT) were used to estimate the lean leg mass and bone mineral. Static and dynamic histomorphometry were performed on the triple-labeled undecalcified sections. We found that making the intact rats rise to erect bipedal stance for feeding increased muscle mass, cortical bone volume, and periosteal bone formation. Orchidectomy increased net losses of bone next to the marrow by increasing bone turnover. Making the ORX rats rise to erect bipedal stance increased muscle mass, partially prevented cancellous bone loss in the PTM, and prevented net cortical bone loss in TX induced by ORX by depressing cancellous and endocortical high bone turnover and stimulating periosteal bone formation. The bone-anabolic effects were achieved mainly in the first 4 weeks in the PTM and by 8 weeks in the TX. These findings suggested that making the rats rise to erect bipedal stance for feeding helped to increase muscle mass and cortical bone mass in the tibias of intact rats, increase muscle mass, and partially prevented cancellous and net cortical bone loss in ORX rats.

Animals↗