A random-effects model was used in all instances


A random-effects model was used in all instances.

Results: Eight trials (n = 774) were identified and subjected to meta-analysis. Statins reduced postoperative atrial fibrillation risk (relative click here risk 0.57, 95% confidence interval 0.45-0.72, P < .0001, risk difference -0.14, 95% confidence interval -0.20 to -0.08, P < .0001, number needed to treat 8) and total hospital stay (weighted mean difference -0.66 days, 95% confidence interval -1.01 to -0.30 days, P = .0004) relative to placebo. Intensive care unit stay was also reduced (weighted mean difference -0.17 days, 95% confidence interval -0.37 to 0.03 days, P = .09) but did not meet prespecified

criteria for statistical significance. Metaregression analysis revealed association between duration

of preoperative statin prophylaxis and postoperative atrial fibrillation risk reduction (3% reduction per day, P = .008). No association was found between statin dose used and risk reduction (P = .47).

Conclusions: Evidence suggests that statins are associated with reduced risk of postoperative atrial fibrillation Selisistat order and shorter hospital stay after cardiac surgery and that earlier therapy results in more profound benefit. (J Thorac Cardiovasc Surg 2010;140:364-72)”
“Objective: This article illustrates our operative technique for pharyngostomy tube placement and describes our clinical experience with pharyngostomy use for gastric conduit decompression after esophagectomy.

Methods: We retrospectively reviewed patients undergoing pharyngostomy this website tube placement for gastric conduit decompression after esophagectomy from January 2008 to August 2009. Patients

were included if they had a pharyngostomy tube placed at esophagectomy (prophylactic placement) or as a means of decompression after post-esophagectomy anastomotic leak (therapeutic placement). We collected operative and clinical data and performed a descriptive statistical analysis.

Results: We placed 25 pharyngostomy tubes for gastric conduit decompression after esophagectomy. Eleven were placed prophylactically (44%); the remaining 14 were placed therapeutically (56%) after anastomotic leak. Prophylactic pharyngostomy tubes remained in place a median of 8 days (range 4-17 days), whereas therapeutic pharyngostomy tubes were left in place a median of 15 days (range 7-125 days). There were 4 infectious complications (16%) unrelated to length of pharyngostomy use: 2 cases of cellulitis (resolved with antibiotics, tube remaining in place) and 2 superficial abscesses after tube removal requiring bedside debridement. Seventy-two percent of patients underwent swallow evaluation; 22% of these patients had radiographic evidence of aspiration.

Conclusions: Pharyngostomy tube placement for gastric conduit decompression after esophagectomy is simple, and tubes can stay in place for prolonged periods.

The debulking continued until the arachnoid plane separating the

The debulking continued until the arachnoid plane separating the nerve and tumor was visualized.

RESULTS: Gross total resection (Simpson I + II) was achieved CB-5083 in all 9 patients. The average VIS was 56.1 in the preoperative period and 26.3 in the postoperative period. Among 9 patients, 8 patients had an improvement of the VIS after surgery. VIS was unchanged in 1 patient, and no patients experienced visual deterioration. Other nonvisual complications, such as rhinoliquorrhea, venous infarction, and permanent anosmia, occurred in 3 patients.

CONCLUSION: Despite the small number of

patients, a high resection rate and favorable visual outcome support the suitability of this approach for resection of TSM.”
“Renin-producing juxtaglomerular cells are connected to each other and to endothelial cells of afferent arterioles by gap junctions containing Connexin

40 (Cx40), abundantly expressed by these two cell types. Here, we generated mice with cell-specific deletion of Cx40 in endothelial and in renin-producing cells, as its global deletion caused local dissociation of renin-producing cells from endothelial cells, renin hypersecretion, and hypertension. In mice lacking endothelial Cx40, the blood pressure, renin-producing cell distribution, and the control of renin secretion were similar to wild-type mice. DihydrotestosteroneDHT cost In contrast, mice deficient for Cx40 in renin-producing cells were hypertensive and these cells were ectopically localized. Although plasma renin activity and kidney renin mRNA levels of these mice were not different from controls, the negative regulation of renin secretion by pressure was inverted to a positive feedback in kidneys lacking Cx40 in renin-producing cells. Thus, our findings show that endothelial Cx40 is not essential for the control of renin expression and/or release. Cx40 in renin-producing cells is required www.selleck.cn/products/VX-770.html for their correct positioning

in the juxtaglomerular area and the control of renin secretion by pressure. Kidney International (2010) 78, 762-768; doi: 10.1038/ki.2010.257; published online 4 August 2010″
“An accurate assessment of iron status in dialysis patients is important because both anemia and overtreatment with erythropoiesis-stimulating agents are associated with poor clinical outcomes. We have previously shown that both analytical and intra-individual (biological) variability in serum ferritin limits its utility as a proxy for iron stores in patients in this setting. As hepcidin is a direct regulator of iron status, its measurement might be useful for monitoring patients with iron dysregulation. We assessed short-term intra-individual variation of serum hepcidin in 28 patients with stable chronic kidney disease on hemodialysis.

Results: At 16 days uroplakin was detectable and it seemed to cor

Results: At 16 days uroplakin was detectable and it seemed to correlate with the loss of Foxa2, while Foxa1 remained at all time points. Androgen receptor was first noted in stroma at day 16. It localized to urothelial nuclei at day 21 and was undetectable at 42 days. Adjacent to the urothelium alpha-smooth

muscle actin was seen on day 16 and it was localized in bundles to the periphery of the graft at later time points. Staining for basilar urothelium with p63 confirmed basilar orientation at all time points.

Conclusions: We report the temporal spatial expression of various genes in early bladder development. This suggests that some proteins may be potential selleck chemicals markers of bladder progenitor cells. Characterizing these markers may potentially identify bladder progenitor cells that have been directed toward a lineage

path destined to become urothelial cells. Ultimately these multipotential progenitor cells could be isolated and used to study and treat diseases that affect the bladder.”
“Purpose: Bladder outlet obstruction can have devastating consequences. Given the poor outcome, intervention in utero has been advocated in an attempt to salvage pulmonary and renal function. We evaluated whether laparoscopic decompression of the obstructed bladder could be performed efficiently by adapting current robot assisted laparoscopic techniques to access the fetus in utero.

Materials and Methods: At 95 days of gestation 20 fetal sheep underwent ligation of the urethra and urachus. Two to 5 days later robot assisted laparoscopic vesicostomy PKC412 was performed. Ultrasound of the kidneys and bladder was performed before each procedure. At 135 days of gestation the urinary tract was evaluated to assess the

adequacy of bladder decompression Trichostatin A and a patent vesicostomy.

Results: After 48 hours of undergoing ligation all fetuses had bilateral moderate hydronephrosis and a markedly distended bladder. In the first 10 fetuses vesicostomy could not be completed laparoscopically due to limited visualization. Additional modifications in trocar placement and gas infusion allowed vesicostomy to be completed laparoscopically in the last 8 fetuses in 2.5 to 4 hours. Urinary tract decompression and a patent vesicostomy were observed in all of these fetuses postoperatively.

Conclusions: We developed specific modifications in current robot assisted laparoscopic techniques and instrumentation to allow the treatment of bladder outlet obstruction in utero. This procedure may be performed efficiently and it may provide advantages over conventional surgery for fetal intervention.”
“Purpose: The laparoscopic surgical approach to unilateral intra-abdominal testis has replaced the open approach at several large centers.

-The algorithm works in three steps Firstly, a first spike detec

-The algorithm works in three steps. Firstly, a first spike detection is made with generic parameters. Secondly, the detected spikes are used to tailor the detection algorithm to the patient; and thirdly,

the resulting patient-specific detection algorithm is used to analyze individual patient with high-quality detection. Therefore, the algorithm produces a patient-specific template-hence exhibiting improved performance metrics, without the need of a priori knowledge from the experts.

Results.-The system was first evaluated for EEG of three patients, against the scoring of three EEG experts, demonstrating similar performance. Later, it was evaluated against the spike and wave percentage evaluation of another expert for 17 additional records. The difference between the two evaluations was 4.4% on average, which is almost the same as the interexpert difference (4.7%).

Conclusions.-We Barasertib ic50 designed a fully automated and efficient spike detection algorithm, which is liable to trim down the specialist’s diagnostic time. (C) 2009 Elsevier A-1210477 purchase Masson SAS. All rights reserved.”
“CCAAT/enhancer-binding protein alpha (C/EBP alpha) is mutated in 10% of acute myeloid leukemias, resulting in either a truncated protein or an altered leucine zipper (C/EBP alpha LZ) that prevents DNA binding. C/EBP alpha induces bcl-2 in cooperation with nuclear factor-kappa B (NF-kappa B) p50 to inhibit apoptosis. We now

demonstrate that C/EBP Flavopiridol (Alvocidib) alpha or a C/EBP alpha LZ oncoprotein binds the bcl-2 P2 promoter in chromatin immunoprecipitation

assays and induces the promoter dependent on the integrity of a kappa B site. C/EBP alpha expressed as a transgene in B cells binds and activates the bcl-2 promoter, but not in nfkb1-/- mice lacking NF-kappa B p50. Bcl-2 is central to the intrinsic apoptotic pathway, whereas FLICE inhibitory protein (FLIP) modulates caspase-8, the initiator caspase of the extrinsic pathway. C/EBP alpha and C/EBP alpha LZ also bind the FLIP promoter and induce its expression dependent upon NF-kappa B p50. Moreover, induction of FLIP by C/EBP alpha protects splenocytes from Fas ligand-induced apoptosis, but only if p50 is present. We also demonstrate the direct interaction between bacterially produced C/EBP alpha and NF-kappa B p50, mediated by the C/EBP alpha basic region. These findings indicate that C/EBP alpha or its oncoproteins activate the bcl-2 and FLIP genes by tethering to their promoters through bound NF-kappa B p50. Targeting their interaction may favor apoptosis of transformed cells.”
“Adult T-cell leukemia/lymphoma (ATLL) develops after infection with human T-cell leukemia virus-1 (HTLV-1) after a long latency period. The negative regulatory programmed death-1/programmed death-1 ligand 1 (PD-1/PD-L1) pathway has been implicated in the induction of cytotoxic T-lymphocyte (CTL) exhaustion during chronic viral infection along with tumor escape from host immunity.

The genes whose expression discriminated between the IgAN patient

The genes whose expression discriminated between the IgAN patients and controls were primarily involved in canonical WNT-beta-catenin and PI3K/Akt pathways. We also tested peripheral blood mononuclear cells and their subpopulations isolated from an independent group of IgAN patients and healthy controls. There were low protein levels of inversin and PTEN, key regulators of WNT-beta-catenin and Givinostat research buy PI3K/Akt, in IgAN patients, suggesting hyperactivation of these pathways. Also, there were increased phospho-Akt protein levels and nuclear beta-catenin accumulation with an enhanced peripheral

blood mononuclear cell proliferation rate. Subpopulation analysis uncovered a major irregularity of WNT signaling in monocytes. Hence, hyperactivation of these pathways may provide insight into mechanisms contributing to the pathogenesis of IgAN. Kidney International (2010) 78, 396-407; doi:10.1038/ki.2010.138; published online 19 May 2010″
“Background/Aims: The correlation between theta activity during wakefulness and slow-wave activity (SWA) during sleep observed after sleep deprivation suggests such patterns can be used as electroencephalogram (EEG) biomarkers of the sleep homeostasis process. Since these EEG components would be very useful objective measures

to assess CNS drug effects, we investigated whether the relationship between sleep homeostatic Amoxicillin EEG biomarkers could be reproduced after an experimental pharmacological intervention. Methods: Seventeen healthy BMS-777607 molecular weight volunteers took part in a phase I randomized, double-blind, crossover design study. To increase sleep propensity, all participants received a single morning oral dose of olanzapine (5 mg) and placebo. Quantitative EEG analysis was done by power spectra calculations: theta activity (3.5-7.5 Hz) during wakefulness and SWA (0.5-4.0 Hz) during sleep. The relationship between the 2 EEG parameters was assessed by correlating

the rise rate (percent/hour) of theta activity in wakefulness and the increase (percent) of SWA in the first non-REM sleep episode. Results: Following olanzapine administration we observed increases in theta activity during wakefulness, and increases in total sleep time, sleep efficiency and slow-wave sleep time during sleep. However, a weak and unreliable correlation was observed between the increases in theta activity and changes in sleep SWA. Conclusions: From these results, we cannot affirm that these waking and sleep EEG variables behave as biomarkers of human sleep homeostasis after drug administration. It is possible that these EEG biomarkers reflect different physiological mechanisms if they are assessed during drug CNS effects. Copyright (C) 2011 S.

Furthermore, shifts from the N155H pathway to either the Q148R or

Furthermore, shifts from the N155H pathway to either the Q148R or H pathway or the Y143R pathway were dependent on the amino acid substitution at position 148 and the secondary mutations in Y143R- or Q148R- or H-containing variants and correlated

with reductions in RAL susceptibility and restorations in RC. Our observations in patient viruses were confirmed by analyzing site-directed mutations. In summary, viruses that acquire mutations defining the 143 or 148 escape pathways are less susceptible to RAL and exhibit greater RC than viruses containing 155 pathway mutations. These selective pressures result in the displacement PI3K inhibitor of N155H variants by 143 or 148 variants under continued drug exposure.”
“Salidroside (SDS), a phenylpropanoid glycoside isolated from Rhodiola rosea L., has been reported to be neuroprotective in vitro, which raises the possibility of MM-102 using SDS as a neuroprotective agent after nerve injuries. In the present study, the possibly beneficial effect of SDS on promoting nerve regeneration after sciatic nerve

crush injury in rats was investigated. Rats with sciatic nerve crush injury were administered intraperitoneally daily with 5 or 10mg/kg body weight of SDS for 4 weeks. Rats that received mecobalamin or saline were considered as a positive or a negative control, respectively. Morphometric analysis of regenerated nerves and Fluoro-Gold retrograde tracing was used to evaluate axonal regeneration, whereas walking track analysis, electrophysiological assessment, and histological appearance of target muscles were carried out to evaluate the recovery of motor function. The results showed that SDS achieved functionally successful nerve regeneration in the rat sciatic nerve crush injury model, indicating that SDS holds potential as a neuroprotective agent for peripheral nerve therapies. NeuroReport 24:217-223 (C) 2013 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.”
“Immunocytochemical techniques are used to analyze the effects of both an actin and myosin inhibitor on spindle architecture in PtK1 cells to

understand why both these inhibitors slow or block chromosome motion and detach chromosomes. Cytochalasin J, an actin inhibitor and a myosin C59 inhibitor, 2, 3 butanedione 2-monoxime, have similar effects on changes in spindle organization. Using primary antibodies and stains, changes are studied in microtubule (MT), actin, myosin, and chromatin localization. Treatment of mitotic cells with both inhibitors results in detachment or misalignment of chromosomes from the spindle and a prominent buckling of MTs within the spindle, particularly evident in kinetochore fibers. Evidence is presented to suggest that an actomyosin system may help to regulate the initial and continued attachment of chromosomes to the mammalian spindle and could also influence spindle checkpoint(s).

The observations confirm the impaired kaliuretic potency of sgk1(

The observations confirm the impaired kaliuretic potency of sgk1(-/-) mice and point to a role of SGK1 in renal Na(+) reabsorption by mechanisms other than ENaC. Copyright (c) 2009 Epigenetics inhibitor S. Karger AG, Basel”
“Deferoxamine (DFO) and erythropoietin (EPO) have each been shown to provide neuroprotection in neonatal rodent models of brain injury. In view of the described anti-oxidative actions

of DFO and the antiapoptotic and anti-inflammatory effects of EPO, we hypothesized that the combination of DFO and EPO would increase neuroprotection after neonatal hypoxic-ischemic brain injury as compared to single DFO or EPO treatment. At postnatal day 7 rats underwent right common carotid artery occlusion followed by a 90-min exposure to 8% oxygen. Rats were treated intraperitoneally with DFO (200 mg/kg), recombinant human EPO (I kU/kg), a combination of DFO-EPO or vehicle at 0, 24 and 48 h after hypoxia-ischemia (HI) and were sacrificed at 72 h. DFO-EPO administration reduced the number of cleaved caspase 3-positive cells in the ipsilateral cerebral cortex. Early neuronal damage was assessed by staining for

microtubuli-associated protein (MAP)-2. In our model 63 +/- 9% loss of ipsilateral MAP-2 was observed after HI, indicating extensive brain injury. DFO, EPO or DFO-EPO treatment PD0332991 mouse did not improve neuronal integrity as defined by MAP-2. Cerebral white matter tracts were stained for myelin basic protein (MBP), a constituent of myelin. Hypoxia-ischemia strongly reduced MBP staining which suggests white matter damage. However, DFO, EPO and DFO-EPO treatment had no effect on the loss of MBP staining. Finally, HI-induced loss of striatal tyrosine hydroxylase staining was not attenuated by DFO, EPO or DFO-EPO. Although DFO-EPO treatment reduced the number of cleaved caspase 3(+) cells, treatment with DFO, EPO, or with the

combination of DFO and EPO did not protect against Acetophenone gray or white matter damage in the experimental setting applied. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“A thymidine-to-cytosine substitution in the -344 promoter region of the aldosterone synthase gene (CYP11B2) has been associated with essential hypertension in some but not all studies conducted in Chinese. We performed a meta-analysis to evaluate the association of the -344C/T polymorphism with essential hypertension in Chinese. A total of 7,472 individuals (4,259 unselected hypertensive patients and 3,213 normotensive controls) from 9 case-control studies were included in the present investigation. Significant associations between the risk of hypertension and the CC genotype and C allele frequencies were found in a total of 19 studies. Our findings support the notion that the CYP11B2-344C/T polymorphism is associated with essential hypertension.

The duration of the latent period must be known with precision in

The duration of the latent period must be known with precision in order to design effective disease intervention strategies, such as use of antivirals. For a hypothetical influenza pandemic, we thus perform a simulation study to determine the number of cases needed to observe the weekday variation pattern in influenza epidemic incidence data. Our studies suggest that these patterns should be observable at 95% confidence in daily influenza hospitalization data from large cities over 75% of the time.

Using 2009 A(H1N1) daily case data recorded by a large hospital in Santiago, Chile, we show that significant weekday incidence

patterns are evident. From these weekday incidence patterns, we estimate the latent period of influenza to be [0.04, 0.60] days (95% CI). This method for determination of the influenza latent period in MDV3100 mw a community setting is novel, and unique in its approach. (C) 2012 Elsevier Ltd. All rights reserved.”

Current guidelines for the treatment of ST-segment elevation myocardial infarction recommend a door-to-balloon time of 90 minutes or less for patients undergoing primary percutaneous coronary intervention (PCI). Door-to-balloon time has become a performance measure and is the focus of regional and national quality-improvement initiatives. However, it is not known whether national improvements in door-to-balloon

times have been accompanied Danusertib by a decline in mortality.


We analyzed annual trends in door-to-balloon times and in-hospital mortality using data from 96,738 admissions for patients undergoing primary PCI for ST-segment elevation myocardial infarction from July 2005 through June 2009 at

515 Glycogen branching enzyme hospitals participating in the CathPCI Registry. In a subgroup analysis using a linked Medicare data set, we assessed 30-day mortality.


Median door-to-balloon times declined significantly, from 83 minutes in the 12 months from July 2005 through June 2006 to 67 minutes in the 12 months from July 2008 through June 2009 (P<0.001). Similarly, the percentage of patients for whom the door-to-balloon time was 90 minutes or less increased from 59.7% in the first year to 83.1% in the last year (P<0.001). Despite improvements in door-to-balloon times, there was no significant overall change in unadjusted in-hospital mortality (4.8% in 2005-2006 and 4.7% in 2008-2009, P=0.43 for trend) or in risk-adjusted in-hospital mortality (5.0% in 2005-2006 and 4.7% in 2008-2009, P=0.34), nor was a significant difference observed in unadjusted 30-day mortality (P=0.64).


Although national door-to-balloon times have improved significantly for patients undergoing primary PCI for ST-segment elevation myocardial infarction, in-hospital mortality has remained virtually unchanged.

Based on these data, the VEs

from young offspring of preg

Based on these data, the VEs

from young offspring of pregnant rats fed an ethanol-containing or an isocaloric non-alcoholic liquid diet were examined between postnatal day (P) 1 and P31. Studies used enzyme-linked immunosorbent assays and immunoblots to explore the effects of ethanol on the expression of neurotrophins, their receptors, and representative signaling proteins. Ethanol altered the expression of neurotrophins and receptors throughout the first postnatal NSC23766 order month. Expression of NGF Increased, but there was no change in the expression of BDNF. The high affinity receptors (TrkA and TrkB) were unchanged but ethanol decreased expression of the low affinity receptor, p75. One downstream signaling protein, extracellular signal-regulated buy JQ-EZ-05 kinase (ERK), decreased but Akt expression was unchanged. Thus, postnatal cell proliferation in the VE of young rat pups is neurotrophin-responsive and is affected by ethanol. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Metabolically generated acid is the major physiological stimulus

for increasing proximal tubule citrate reabsorption, which leads to a decrease in citrate excretion. The activity of the Na-citrate cotransporter, NaDC-1, is increased in vivo by acid ingestion and in vitro by an acidic pH medium. In opossum kidney cells the acid stimulatory effect and the ability of endothelin-1 (ET-1) to stimulate NaDC-1 activity are both blocked by the endothelin B (ET(B)) receptor antagonist, BQ788. Acid feeding had no effect on brush border membrane NaDC-1 activity in mice in which ET(B) receptor expression was knocked out, whereas a stimulatory effect was found in wild-type mice. Using ET(A)/ET(B)

chimeric and ET(B) C-terminal tail truncated constructs, ET-1 stimulation of NaDC-1 required a receptor C-terminal tail from either ET(A) or ET(B). The ET-1 effect was greatest when either the ET(B) transmembrane domain and C-terminal tail were present or the ET(B) C-terminal tail was linked to the ET(A) transmembrane domain. This effect was smaller when the ET(B) because transmembrane domain was linked to the ET(A) C-terminal tail. Thus, the acid-activated pathway mediating stimulation of NaDC-1 activity requires a functional ET(B) receptor in vivo and in vitro, as does acid stimulation of NHE3 activity. Since increased NaDC-1 and NHE3 activities constitute part of the proximal tubule adaptation to an acid load, these studies indicate that there are similarities in the signaling pathway mediating these responses. Kidney International (2010) 78, 895-904; doi:10.1038/ki.2010.264; published online 11 August 2010″
“Thyroid hormone (TH) plays an essential role in growth and differentiation of the central nervous system. Deficiency of TH during perinatal period results in abnormal brain development known as cretinism in human.

These neurochemical and glial alterations are accompanied by impa

These neurochemical and glial alterations are accompanied by impairment in locomotor activity. (C) 2012 Elsevier Inc. All rights reserved.”
“The aim of our study was to develop specific enzyme-linked immunosorbent assays (ELISAs) and apply these to assess mold antigen exposure in composting plants. Sandwich ELISAs based on polyclonal antibodies to Aspergillus fumigatus (Af), Penicillium chrysogenum (Pc),

and Cladosporium herbarum (Ch) antigens were developed and validated. Reactivity to 18 different mold species was tested. To optimize extraction procedure, inhalable dust samples taken by a parallel sampler were extracted with or without homogenization. In 31 composting plants stationary pumps were installed at 4 sites to collect 124 inhalable dust samples. The newly developed ELISAs were used in addition to an anti beta-1,3-glucan ELISA to quantify learn more mold antigens. The Cladosporium ELISA showed less than 0.04% reactivity to extracts from other fungal genera, while the Af ELISA demonstrated a reactivity of up to 3.6% and the Pc ELISA reacted up to 11% to ZD1839 other mold species. Extraction of parallel sampled filters gave higher antigen amounts with homogenization. The increase was highest

for Pc-antigens, followed by Af-antigens, and lowest for Ch-antigens. Mean lower detection limits of homogenized inhalable dust samples were 5 ng/m(3) (Af), 0.6 ng/m(3) (Pc), 0.2 ng/m(3) (Ch), and 0.6 ng/m(3) (beta-1,3-glucan). The ELISAs were able to detect antigens in 43% (Af), 37% (Pc), 94% (Ch), or 100% (beta-1,3-glucan) of the 124 airborne dust samples. Inhalable dust, FAD beta-1,3-glucan, and Af-, Pc-, and Ch-antigen concentrations were significantly correlated. The newly developed mold antigen ELISAs are thus able to measure airborne exposure

levels in composting plants and differentiate between distinct fungi genera.”
“Introduction: Orthostatic hypotension (OH) is associated with troublesome symptoms and increased mortality. It is treatable and deserving of accurate diagnosis. This can be time consuming. The current reference standard for its diagnosis is head-up tilt (HUT) testing with continuous beat-to-beat plethysmography. Our objective was to assess the accuracy of sit-stand testing with semi-automatic sphygmomanometry for the diagnosis of OH.

Design: Retrospective test of diagnostic accuracy.

Methods: This was a retrospective study performed using a database maintained by a busy syncope unit. HUT testing was performed using an automated tilt table with Finometer monitoring. A 3 min 70 degrees HUT was performed following 5 min supine. Sitting blood pressure (BP) was measured following 3 min rest. Standing BP was measured within 30 s of assuming the upright posture. The results of sit-stand testing were compared with HUT testing as a reference standard.