Nanostructure characterisation of flow-formed Cr-Mo-V steel using transmission Kikuchi diffraction technique.

Nowadays flow-forming has become a desired near net shape manufacturing method as it provides excellent mechanical properties with improved surface finish and significant manufacturing cost reduction. However, the material is subjected to excessive plastic deformation during flow-forming process, generating a very fine and complex microstructure. In addition, the intense dislocation density and residual stress that is generated in the component during processing makes the microstructure characterisation using conventional micro-analytical tools challenging. Thus, the microstructure/property relationship study in such a material is rather difficult. In the present study a flow-formed Cr-Mo-V steel nanostructure and crystallographic texture were characterised by means of Transmission Kikuchi Diffraction (TKD). Here, TKD is shown to be a powerful technique in revealing very fine martensite laths within an austenite matrix. Moreover, fine precipitates in the order of 20-70 nm on the martensite lath boundaries were clearly imaged and characterised. This greatly assisted in understanding the preferable site formation of the carbides in such a complex microstructure. The results showed that the actual TKD spatial resolution was in the range of 5-10 nm using 25 kV for flow-formed Cr-Mo-V steel.

Changes in NHS organization of care and management of hospital admissions with COPD exacerbations between the national COPD audits of 2003 and 2008.

BACKGROUND: The 2003 UK Chronic Obstructive Pulmonary Disease (COPD) audit revealed wide variability between hospital units in care delivered. AIMS: To assess whether processes of care, patient outcomes and organization of care have improved since 2003. DESIGN: A UK national audit was performed in 2008 to survey the organization and delivery of clinical care provided to patients admitted to hospital with COPD. METHODS: All UK acute hospital Trusts (units) were invited to participate. Each unit completed cross-sectional resource and organization questionnaires and a prospective clinical audit comprising up to 60 consecutively admitted cases of COPD exacerbation. Comparison between 2003 and 2008 includes aggregated statistics for units participating in both audit rounds. RESULTS: A total of 192 units participated in both audit rounds (6197 admissions in 2003 and 8170 in 2008). In 2008, patients were older and of a poorer functional class. Overall mortality was unchanged but adjusting for age and performance status, inpatient mortality (P = 0.05) and 90-day mortality (P = 0.001) were both reduced in 2008. More patients were discharged under a respiratory specialist (P < 0.01), treated with non-invasive ventilation if acidotic (P < 0.001) and accepted onto early discharge schemes (P < 0.01) while median length of stay fell from 6 to 5 days (P < 0.001). Within these mean data, however, there remains considerable inter-unit variation in organization, resources and outcomes. CONCLUSION: Overall improvements in resources and organization are accompanied by reduced mortality, shorter admissions and greater access to specialist services. There remains, however, considerable variation in the quality of secondary care provided between units.

Acidosis, non-invasive ventilation and mortality in hospitalised COPD exacerbations.

BACKGROUND: Reports of non-invasive ventilation (NIV) use in clinical practice reveal higher mortality rates than in corresponding randomised clinical trials. AIM: To explore factors related to chronic obstructive pulmonary disease (COPD) admissions and NIV use that may explain some of the previously reported high mortality rates. METHODS: National UK audit of clinical care of consecutive COPD admissions from March to May 2008. Retrospective case note audit with prospective case ascertainment. Participating units completed a web-based audit proforma of process and outcomes of clinical care. RESULTS: 232 hospital units collected data on 9716 patients, mean age 73, 50% male. 1678 (20%) of those with gases recorded on admission were acidotic and another 6% became acidotic later. 1077 patients received NIV, 55% had a pH<7.26 and 49% (305/618) had or were still receiving high flow oxygen. 30% (136/453) patients with persisting respiratory acidosis did not receive NIV while 11% (15/131) of acidotic admissions had a pure metabolic acidosis and did. Hospital mortality was 25% (270/1077) for patients receiving NIV but 39% (86/219) for those with late onset acidosis and was higher in all acidotic groups receiving NIV than those treated without. Only 4% of patients receiving NIV who died had invasive mechanical ventilation. CONCLUSIONS: COPD admissions treated with NIV in usual clinical practice were severely ill, many with mixed metabolic acidosis. Some eligible patients failed to receive NIV, others received it inappropriately. NIV appears to be often used as a ceiling of treatment including patient groups in whom efficacy of NIV is uncertain. The audit raises concerns that challenge the respiratory community to lead appropriate clinical improvements across the acute sector.

A randomised trial of peer review: the UK National Chronic Obstructive Pulmonary Disease Resources and Outcomes Project.

Peer review has been widely employed within the NHS to facilitate health quality improvement but has not been rigorously evaluated. This article reports the largest randomised trial of peer review ever conducted in the UK. The peer review intervention was a reciprocal supportive exercise that included clinicians, hospital management, commissioners and patients which focused on the quality of the provision of four specific evidence-based aspects of chronic obstructive pulmonary disease care. Follow up at 12 months demonstrated few quantitative differences in the number or quality of services offered in the two groups. Qualitative data in contrast suggested many benefits of peer review in most but not all intervention units and some control teams. Findings suggest peer review in this format is a positive experience for most participants but is ineffective in some situations. Its longer term benefits and cost effectiveness require further study. The generic findings of this study have potential implications for the application of peer review throughout the NHS.

Temperature control of Fano resonances and transmission in superconducting metamaterials.

Losses are the main evil that limits the use of metamaterials in practical applications. While radiation losses may be controlled by design, Joule losses are hereditary to the metamaterial structures. An exception is superconducting metamaterials, where Joule losses can be uniquely controlled with temperature in a very wide range. We put this in use by demonstrating temperature-dependent transmission in the millimeter-wave part of the spectrum in high-Tc superconducting cuprate metamaterials supporting sub-radiant resonances of Fano type.

Clinician perceived good practice in end-of-life care for patients with COPD.

Patients with chronic obstructive pulmonary disease (COPD) have significant end-of-life needs, but are much less likely than patients with cancer to access or receive appropriate palliative care. Little is known about the existing availability or quality of available services within the United Kingdom. We surveyed 100 NHS acute hospitals enquiring into the provision of care for patients with COPD and requesting examples of current good practice that might be used to set standards. Forty-two percent of hospitals had formal palliative care arrangements for patients with COPD, whereas 59% had plans to develop or further develop services. Analysis of qualitative data suggested four strands that highlighted good practice; teams, care pathways, service components and linkages. These data may help to inform the debate leading to the development of standards in end-of-life care for patients with COPD.

Thiazolidinedione insulin sensitizers and the heart: a tale of two organs?

Thiazolidinediones (TZDs) are relatively new agents for the treatment of type 2 diabetes. They act as agonists at the PPAR-gamma nuclear receptor and their therapeutic effects include decreased insulin resistance and hyperglycaemia, an improved plasma lipid, inflammation and pro-coagulant profile, and amelioration of hypertension, microalbuminuria and hepatic steatosis. The most common side effects of TZDs include weight gain and oedema, with occasional reports of congestive heart failure (CHF). This review discusses the benefit-risk profile of TZDs in treating patients with type 2 diabetes, with particular reference to the heart. To provide context, we explore briefly the epidemiology and pathophysiology of heart failure in patients with type 2 diabetes, touch on the association of heart disease and cardiovascular mortality with antihyperglycaemic treatment modalities other than TZDs, and then focus on the effects of TZDs on the heart, cardiovascular risk factors and outcomes. We describe the cluster of host factors, which seems to predispose patients with type 2 diabetes to TZD-induced or TZD-exacerbated oedema and CHF and then provide an overview of the putative mechanisms of these TZD-related side effects. We also propose that certain diuretics (amiloride and spironolactone), by targeting the distal nephron that expresses PPARgamma in collecting duct cells, might be of benefit in ameliorating the fluid retention and oedema associated with TZDs.

Energy restriction enhances therapeutic efficacy of the PPARgamma agonist, rosiglitazone, through regulation of visceral fat gene expression.

AIM: Consumption of a palatable diet can induce hyperphagia, leading to weight gain (dietary obesity) and insulin resistance in rats. Thiazolidinediones (TZDs) can also induce hyperphagia in rats but conversely have an insulin-sensitizing effect. The aim of this study was to investigate whether preventing TZD-induced hyperphagia (i.e. energy restriction) in dietary obese (DIO) rats would enhance the insulin-sensitizing effects of treatment at a therapeutic dose; and, within this paradigm, to produce an original survey of candidate TZD-gene targets in the clinically relevant visceral white adipose tissue (WAT) depot. METHODS: DIO rats that were either freely fed or energy restricted (i.e. pair-fed to the level of untreated controls) were treated with rosiglitazone maleate (RSG; 3 mg/kg/day) for 2 weeks, the restricted group controlling for treatment-induced hyperphagia and weight gain. The outcome measures were circulating concentrations of various biochemical markers of insulin resistance, and gene expression was measured in epididymal WAT. RESULTS: In both freely fed and pair-fed groups, compared to untreated DIO controls, RSG reduced plasma levels of insulin (-29% and -43%; p < 0.05 and p < 0.001, respectively), free fatty acids (FFAs; -45% and -48%; p < 0.01 and p < 0.001, respectively) and triglycerides (TGs; -63% and -72%; both p < 0.001), reflected in improved insulin sensitivity, as measured by homeostasis model assessment (-29% and -43%; p < 0.01 and p < 0.0001). RSG also increased the expression of the fatty acid transport/synthesis genes, fatty acid transport protein (2.4-3.2-fold), epidermal fatty acid-binding protein (FABP; 1.7-2.0-fold), heart FABP (25-29-fold) and fatty acid synthase (2.3-2.9-fold; all p < 0.05) in both groups. Adipocyte FABP was also increased by RSG treatment, but only in combination with energy restriction (1.52-fold; p < 0.05) as was hexokinase II expression (p < 0.001). In contrast, the drug had no effect on expression of several genes associated with lipolysis. Although obesity-induced hyperleptinaemia was normalized only in the energy-restricted group, leptin messenger RNA (mRNA) expression was reduced in both treated groups (all p < 0.01). Resistin and tumour necrosis factor-alpha expression was also reduced, though in the latter case, only with energy restriction (p < 0.05). Other adipokines were unaffected by RSG treatment. CONCLUSION: Our results clearly show that energy restriction enhances the therapeutic efficacy of TZDs and suggest that this occurs, at least in part, through a modulatory effect on gene expression in visceral WAT. These findings improve our understanding of the underlying mechanistic basis for the clinical usefulness of dietary restriction as an adjunct to TZD therapy in type 2 diabetes.

Factors associated with condom use among brothel-based female sex workers in Thailand.

This study sought to determine the actual levels of condom use by female sex workers (FSW) in Thailand brothels. Specifically, it examined the influence that the country of origin of the FSW patrons exerted on usage of a condom, and it assessed the relevancy of constructs from the Health Belief Model in predicting FSW requesting condom usage by their clients. A survey was administered to a cross-sectional non-randomized convenience sample of 150 FSW in four geographic locations in Thailand, which included: Bangkok, Chang Mai, Mae Hong Son and Other (comprised mainly of brothels in small villages). Statistical interpretation of the data indicated that Thai FSW requested condom use in 63% of the cases, while the overall mean of condom use was only 51%. Condom use by patrons' country of origin was as follows: westerners 76%, foreign Asians 52% and native Thai men 27%. These results fall considerably short of the Ministry of Health's goal of 100% condom use in Thai brothels. Furthermore, public health education initiatives need to effectively target the native Thai FSW patrons since they represent the clients least likely to use a condom (27%).

Rapid reversal of hepatic steatosis, and reduction of muscle triglyceride, by rosiglitazone: MRI/S studies in Zucker fatty rats.

AIM: This study aimed to chart the time course and durability of the effects of rosiglitazone, a potent thiazolidinedione-based peroxisome proliferator-activated receptor gamma agonist, on hepatic steatosis and intramyocellular lipid in an animal model of obesity, the Zucker Fatty (ZF) rat. METHODS AND RESULTS: Rosiglitazone (3 mg/kg/day p.o.) significantly reduced both liver fat content (by 59%; p < 0.05) and size (11.5%; p < 0.05) in male ZF rats that received between 3 days and 1 week of treatment, and these reductions were maintained for at least 12 weeks. Liver fat content measured by magnetic resonance spectroscopy (MRS) correlated closely and positively with plasma insulin levels (reduced by 89% within a week, r = 0.8) and with postmortem histological fat fractional volume (r = 0.89). Similarly, liver volume measured by magnetic resonance imaging (MRI) correlated closely with postmortem wet weight (r = 0.99). MRS also showed, and numbers of lipid vacuoles counted in transmission electron micrographs confirmed, that rosiglitazone significantly reduced the elevated intramyocellular lipid seen in ZF rat skeletal muscle by at least 40% (p < 0.05). CONCLUSIONS: Localized MRS and MRI showed that rosiglitazone reversed the hepatic steatosis, hepatomegaly and intramyocellular lipid, characteristic of the ZF rat, an animal model of obesity.

Retinoid signaling controls mouse pancreatic exocrine lineage selection through epithelial-mesenchymal interactions.

BACKGROUND & AIMS: The early embryonic pancreas gives rise to exocrine (ducts and acini) and endocrine lineages. Control of exocrine differentiation is poorly understood, but may be a critical avenue through which to manipulate pancreatic ductal carcinoma. Retinoids have been shown to change the character of pancreatic ductal cancer cells to a less malignant phenotype. We have shown that 9-cis retinoic acid (9cRA) inhibits acinar differentiation in the developing pancreas, in favor of ducts, and we wanted to determine the role of retinoids in duct versus acinar differentiation. METHODS: We used multiple culture systems for the 11-day embryonic mouse pancreas. RESULTS: Retinoic acid receptor (RAR)-selective agonists mimicked the acinar suppressive effect of 9cRA, suggesting that RAR-RXR heterodimers were critical to ductal differentiation. RARalpha was only expressed in mesenchyme, whereas RXRalpha was expressed in epithelium and mesenchyme. Retinaldehyde dehydrogenase 2, a critical enzyme in retinoid synthesis, was expressed only in pancreatic epithelium. 9cRA did not induce ductal differentiation in the absence of mesenchyme, implicating a requirement for mesenchyme in 9cRA effects. Mesenchymal laminin is necessary for duct differentiation, and retinoids are known to enhance laminin expression. In 9cRA-treated pancreas, immunohistochemistry for laminin showed a strong band of staining around ducts, and blockage of laminin signaling blocked all 9cRA effects. Western blot and RT-PCR of pancreatic mesenchyme showed laminin-beta1 protein and mRNA induction by 9cRA. CONCLUSIONS: Retinoids regulate exocrine lineage selection through epithelial-mesenchymal interactions, mediated through up-regulation of mesenchymal laminin-1.

Department of defense eye injuries from fiscal year 1988-1998.

BACKGROUND: The U.S. Army Safety Center, U.S. Navy Safety Center, and U.S. Air Force Safety Center collect data on occupational injuries that occur in each respective military service. METHODS: An 11-year retrospective study of ground eye injuries collected by the Army Safety Center, Navy Safety Center, and Air Force Safety Center, from Fiscal Year (FY) 1988 through FY 1998 was performed. Demographic data analyzed included rank, gender, age, and military/civilian status. Injury data analyzed included severity of injury, eye protection use, injury cost, work days lost due to injury, and days hospitalized due to injury. RESULTS: Statistics for Department of Defense (DoD) eye injuries indicate the average military individual who sustains an eye injury is a 20- to 24-year-old male, E3-E5. This individual is not wearing eye protection and will lose an average of 5.9 days from work at a cost averaging $6,295. The average civil service employee who sustains an eye injury is a WG6-10 who is a 30- to 39-year-old male. This individual is not wearing eye protection and will lose an average of 3.5 days from work at a cost averaging $1,598. Statistically significant differences in the numbers of eye injuries were observed between military occupational groups. In addition, incidence rates between military occupational groups were statistically significant. Category 1, Infantry, Gun Crews, and Seamanship Specialists, has the highest count of injuries and Category 7, Craftsworkers, has the highest incidence. CONCLUSIONS: Proactive vision conservation education at local levels needs to focus on these military occupational groups.

In vivo myocardial protection from ischemia/reperfusion injury by the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone.

BACKGROUND: Diabetes is associated with increased risk of mortality as a consequence of acute myocardial infarction. This study determined whether rosiglitazone (ROSI) could reduce myocardial infarction after ischemia/reperfusion injury. METHODS AND RESULTS: Male Lewis rats were anesthetized, and the left anterior descending coronary artery was ligated for 30 minutes. After reperfusion for 24 hours, the ischemic and infarct sizes were determined. ROSI at 1 and 3 mg/kg IV reduced infarct size by 30% and 37%, respectively (P<0.01 versus vehicle). Pretreatment with ROSI (3 mg. kg(-1). d(-1) PO) for 7 days also reduced infarct size by 24% (P<0.01). ROSI also improved ischemia/reperfusion-induced myocardial contractile dysfunction. Left ventricular systolic pressure and positive and negative maximal values of the first derivative of left ventricular pressure (dP/dt) were significantly improved in ROSI-treated rats. ROSI reduced the accumulation of neutrophils and macrophages in the ischemic heart by 40% and 43%, respectively (P<0.01). Ischemia/reperfusion induced upregulation of CD11b/CD18 and downregulation of L-selectin on neutrophils and monocytes; these effects were significantly attenuated in ROSI-treated animals. Likewise, intercellular adhesion molecule-1 expression in ischemic hearts was markedly diminished by ROSI, as was the ischemia/reperfusion-stimulated upregulation of monocyte chemoattractant protein-1. CONCLUSIONS: ROSI reduced myocardial infarction and improved contractile dysfunction caused by ischemia/reperfusion injury. The cardioprotective effect of ROSI was most likely due to inhibition of the inflammatory response.

A posttermination ribosomal complex is the guanine nucleotide exchange factor for peptide release factor RF3.

The mechanism by which peptide release factor RF3 recycles RF1 and RF2 has been clarified and incorporated in a complete scheme for translation termination. Free RF3 is in vivo stably bound to GDP, and ribosomes in complex with RF1 or RF2 act as guanine nucleotide exchange factors (GEF). Hydrolysis of peptidyl-tRNA by RF1 or RF2 allows GTP binding to RF3 on the ribosome. This induces an RF3 conformation with high affinity for ribosomes and leads to rapid dissociation of RF1 or RF2. Dissociation of RF3 from the ribosome requires GTP hydrolysis. Our data suggest that RF3 and its eukaryotic counterpart, eRF3, have mechanistic principles in common.

Cleavage of colicin D is necessary for cell killing and requires the inner membrane peptidase LepB.

Colicin D is known to kill target cells by cleaving tRNA(Arg). A colicin D-resistant mutant was selected that was altered in the inner membrane leader peptidase, LepB. The substituted residue (Asn274Lys) is located close to the catalytic site. The mutation abolishes colicin D cleavage but not the processing of exported proteins. LepB is required for colicin D cleavage, releasing a small C-terminal fragment that retains full tRNase activity. The immunity protein was found to prevent colicin D processing and furthermore masks tRNase activity, thus protecting colicin D against LepB-mediated cleavage during export. Catalytic colicins share a consensus sequence at their putative processing site. Mutations affecting normal processing of colicin D abolish cytotoxicity without affecting the in vitro tRNase activity.

Insulin-sensitizing action of rosiglitazone is enhanced by preventing hyperphagia.

AIM: We investigated whether pair-feeding to prevent hyperphagia would potentiate the insulin-sensitizing effect of rosiglitazone in chow-fed and insulin-resistant dietary obese rats, and studied the role of leptin and hypothalamic neuropeptide Y as mediators of weight gain during treatment. METHODS: Dietary obese and chow-fed rats (575 +/- 10 vs. 536 +/- 7 g; p < 0.01) were given rosiglitazone (30 mg/kg p.o.) or vehicle daily for 14 days. RESULTS: Energy intake and weight gain were greater in rosiglitazone-treated ad-lib-fed rats (body weight: chow + 24 +/- 2 g, rosiglitazone-treated + 55 +/- 2 g, p < 0.001; dietary obese + 34 +/- 2 g, rosiglitazone-treated + 74 +/- 7 g, p < 0.001). Half of each rosiglitazone-treated group were pair-fed to vehicle-treated controls. Rosiglitazone normalized circulating free fatty acids (FFAs) and insulin sensitivity in dietary obese rats (homeostasis model assessment (HOMA): chow-fed controls, 3.9 +/- 0.3; dietary obese controls, 6.7 +/- 0.7; rosiglitazone-treated, ad lib-fed dietary obese, 4.2 +/- 0.5; both p < 0.01). Insulin sensitivity improved further with pair-feeding (HOMA: 2.9 +/- 0.4; p < 0.05 vs. rosiglitazone-treated, ad lib-fed dietary obese), despite unchanged FFAs. Qualitatively similar findings were made in chow-fed rats. Pair-feeding prevented rosiglitazone-related weight gain in chow-fed, but not dietary obese rats (body weight: + 49 +/- 5 g, p < 0.001 vs. untreated dietary obese controls). Adipose tissue OB mRNA was elevated in dietary obese rats, reduced 49% (p < 0.01) by rosiglitazone treatment, and further (by 16%) with pair-feeding (p < 0.0001). Plasma leptin, however, only fell in the pair-fed group. Hypothalamic neuropeptide Y mRNA was unchanged throughout, suggesting that weight gain associated with high-dose rosiglitazone treatment is independent of hypothalamic neuropeptide Y. CONCLUSIONS: Food restriction potentiates the insulin-sensitizing effect of rosiglitazone in rats, and this effect is independent of a fall in FFAs.

Beta-cell mass dynamics in Zucker diabetic fatty rats. Rosiglitazone prevents the rise in net cell death.

The evolution of diabetes in the male leptin receptor-deficient (fa/fa) Zucker diabetic fatty (ZDF) rat is associated with disruption of normal islet architecture, beta-cell degranulation, and increased beta-cell death. It is unknown whether these changes precede or develop as a result of the increasing plasma glucose, or whether the increased beta-cell death can be prevented. Early intervention with thiazolidinediones prevents disruption of the islet architecture. To determine the specific effects of rosiglitazone (RSG) on beta-cell mass dynamics, male fa/fa (obese) and +/fa or +/+ (lean) rats age 6 weeks were fed either chow (control group [CN]) or chow mixed with rosiglitazone (RSG group) at a dosage of 10 micromol. kg(-1) body wt.day(-1). Rats were killed after 0, 2, 4, 6, or 10 weeks of treatment (at age 6, 8, 10, 12, or 16 weeks). Plasma glucose increased from 8.9 +/- 0.4 mmol/l at 0 weeks to 34.2 +/- 1.8 mmol/l (P = 0.0001) at 6 weeks of treatment in obese CN rats and fell from 8.0 +/- 0.3 to 6.3 +/- 0.4 mmol/l in obese RSG rats (P = 0.02). beta-cell mass fell by 51% from 2 to 6 weeks of treatment (ages 8-12 weeks) in obese CN rats (6.9 +/- 0.9 to 3.4 +/- 0.5 mg; P < 0.05), whereas beta-cell mass was unchanged in obese RSG rats. At 10 weeks of treatment (age 16 weeks), beta-cell mass in obese CN rats was only 56% of that of obese RSG rats (4.4 +/- 0.4 vs. 7.8 +/- 0.3 mg, respectively; P = 0.0001). The beta-cell replication rate fell from a baseline value of 0.95 +/- 0.12% in lean rats and 0.94 +/- 0.07% in obese rats (at 0 weeks) to approximately 0.3-0.5% in all groups by 6 weeks of treatment (age 12 weeks). After 10 weeks of treatment, beta-cell replication was higher in obese RSG rats than in CN rats (0.59 +/- 0.14 vs. 0.28 +/- 0.05%, respectively; P < 0.02). Application of our mass balance model of beta-cell turnover indicated that net beta-cell death was fivefold higher in obese CN rats as compared with RSG rats after 6 weeks of treatment (age 12 weeks). The increase in beta-cell death in obese CN rats during the 6-week observation period was well correlated with the increase in plasma glucose (r2 = 0.90, P < 0.0001). These results suggest that the development of hyperglycemia in ZDF rats is concomitant with increasing net beta-cell death. beta-cell proliferation compensates for the increased beta-cell loss at a time when plasma glucose is moderately elevated, but compensation ultimately fails and the plasma glucose levels increase beyond approximately 20 mmol/l. Treatment with rosiglitazone, previously shown to reduce insulin resistance, prevents the loss of beta-cell mass in obese ZDF rats by maintaining beta-cell proliferation and preventing increased net beta-cell death.

Inner ear fluid volumes and the resolving power of magnetic resonance imaging: can it differentiate endolymphatic structures?

Magnetic resonance imaging (MRI) can accurately recognize minute volumes as small as 1 mm3. The volumes of the utricle and saccule of the inner ear are within the resolving power of MRI, but these structures cannot be recognized because the endolymph and perilymph signals are identical. To clarify the interpretation and description of inner ear structures on MRI, we measured and calculated the volumes of the perilymphatic and endolymphatic spaces of the human ear. We found the total volume of the bony labyrinth to be approximately 192.5 mm3 (endolymph, 34.0 mm3; perilymph, 158.5 mm3).