We elucidated the long-term effects of potassium citrate on urinary metabolic profiles and its impact on stone formation rates.

Materials and Methods: We performed a retrospective cohort study in patients treated at the Comprehensive Kidney Stone Center at our institution between 2000 and 2006. Patients with pre-therapy and post-therapy 24-hour

urinary profiles available who selleck compound remained on potassium citrate for at least 6 months were included in the analysis.

Results: Of the 1,480 patients with 24-hour urinary profiles 503 met study inclusion criteria. Mean therapy duration was 41 months (range 6 to 168). Overall a significant and durable change in urinary metabolic profiles was noted as soon as 6 months after the onset selleck kinase inhibitor of therapy. These changes included increased urinary pH (5.90 to 6.46, p <0.0001) and increased urinary citrate (470 to 700 mg a day, p <0.0001). The stone formation rate also significantly decreased after the initiation of potassium

citrate from 1.89 to 0.46 stones per year (p <0.0001). There was a 68% remission rate and a 93% decrease in the stone formation rate.

Conclusions: Potassium citrate provides a significant alkali and citraturic response. during short-term and long-term therapy with the change in urinary metabolic profiles sustained as long as 14 years of treatment. Moreover, long-term potassium citrate significantly decreases the stone formation rate, confirming its usefulness in patients with recurrent nephrolithiasis.”
“Purpose: We investigated the role of noncontrast computerized tomography in predicting the treatment outcome of shock wave lithotripsy on upper ureteral stones to formulate a clinical algorithm to facilitate clinical management.

Materials and Methods: Adult patients with upper ureteral stones confirmed by noncontrast computerized tomography and scheduled for primary in situ shock wave lithotripsy were prospectively recruited. Standardized treatment was performed on each patient. The primary end point was stone-free status at 3 months. Pretreatment noncontrast

computerized tomography was Casein kinase 1 assessed by a single radiologist blinded to the clinical parameters. Predictive values of computerized tomography measurements on the treatment outcome were then assessed.

Results: Between October 2004 and July 2007 a total of 94 patients (60 male and 34 female) were recruited for the study. Logistic regression showed that stone volume, mean stone density and skin-to-stone distance were potential predictors of successful treatment. From ROC curves the optimum cutoff for predicting treatment outcomes for stone volume, mean stone density and skin-to-stone distance was 0.2 cc, 593 HU and 9.2 cm, respectively. A simple scoring system was constructed based on the 3 factors of stone volume less than 0.2 cc, mean stone density less than 593 HU or skin-to-stone distance less than 9.2 cm. The stone-free rate for patients having 0, 1, 2 and 3 factors was 17.9%, 48.4%, 73.

05. But in GC-resistant cell lines, rapamycin augmented the Selleck H 89 effect of G0/G1 arrest significantly, from 45%

to 58% in CEM-C1-15 cells, 50% to 65% in Jurkat cells, and 57% to 75% in Molt-4 cells, p < 0.05 (Figure 3A). Figure 3 The effect of rapamycin and Dex on cell cycles and the cell cycle regulatory proteins. (A) T-ALL cells were incubated for 48 h with rapamycin(10 nM) and/or Dex (1 μM) and the cell cycle phases were analyzed by PI staining. For all experiments, values of triple experiments were shown as mean plus or minus find more SD. * p < 0.05 as compared with control group or Dex group or Rap group except for CEM-C1-15 cells. (B) Cell-cycle proteins were studied. After 48 h exposure to rapamycin and/or Dex, Molt-4 cells were lysed

and extracts were analyzed learn more by Western blotting. R, rapamycin; D, Dex; RD, rapamycin+Dex; and C, control. To evaluate the molecular basis underlying cell cycle arrest, we investigated the expression of cell cycle regulatory proteins. As shown in Figure 3B, both rapamycin and Dex could induce up-regulation of cyclin-dependent kinase (CDK) inhibitors of p21 and p27, and a synergistic effect of induction was detected when using these two drugs together. Rapamycin did not obviously affect the expression of cyclin A, whereas dexamethasone induced cyclin A expession. Rapamycin prevented dexamethasone-induced expression of cyclin A. Cyclin D1 levels were reduced when treated with rapamycin or dexamethasone alone, or in combination. Compared with Dex, rapamycin had a stronger effect on down-regulation of cyclin D1. Rapamycin sensitizes T-ALL cells to Dex-induced apoptosis Cell cycle arrest could not explain the magic effect on growth inhibition of Dex when co-treated with rapamycin. The main mechanism of Dex in the treatment of lymphoid malignancies is to induce apoptotic cell death. We used Annexin V-PI staining to determine the

early stage of apoptosis. Dex, used alone at 1 μM (Dex group), had no apoptotic effect on Jurkat and Molt-4 cells, and there was only a minimal effect on CEM-C1-15 cells at 48 h and a modest effect on CEM-C7-14 cells at 24 h (After 24 h the cells came to the late phase of apoptosis, data not shown.), p > 0.05. Rapamycin, Forskolin in vivo used at 10 nM (Rap group), also had no obvious apoptosis-inducing effect on all 4 cell lines, although at this concentration, significant cell cycle arrest at G1 phase occurred (Figure 3A). However, when combined Dex with rapamycin (Rap+Dex group), a remarkable increase in cell apoptosis was ensued in all 4 cell lines (Figure 4A). Compared with Rap group, the combination treatment group of cells increased the apoptotic rate from 3% to 20% in CEM-C7-14 at 24 h, p < 0.05, from 3% to 16% in CEM-C1-15 cells at 24 h, p < 0.05, from 9% to 18% in Jurkat cells at 72 h, p < 0.05, and from 5% to 14% in Molt-4 cells at 48 h, p < 0.05.

Nested RT-PCR Total RNA in mononuclear cells was extracted by Trizol reagent (Invitrogen, Carlsbad, CA, USA) and RNA concentration was measured by spectrophotometer (BioPhotometer, Eppendorf, Hamburg, German). Approximately 1 μg of total RNA was used for cDNA synthesis using a PrimeScript™ 1st Strand cDNA Synthesis Kit (TaKaRa, Shiga, Japan). PCR reaction was performed in a 25 μl volume comprised of 5 μl of DNA template, 10 × Buffer, 0.15 mM dNTPs, 0.1 mM of each primer

and 0.5U of Ex Taq Hot Start Version (Takara). Primer sequences and amplification conditions are listed in Table 1 and have been described elsewhere [11]. PCR products were identified on a 2% agarose gel containing ethidium bromide.

A resected ESCC tumor tissue and water blank were used as positive and negative control, respectively. Table 1 List of the nested PCR primers CB-839 in vivo Primers Sequences Selleck KPT 330 (5′-3′) Products PCR conditions STC-1 (outer) CTTCACTCAAGCCAGGAGAGGGAAAGAGGAAA 890 bp 94°C for 30s, 62°C for 30s, 72°C for 1 min, 40 cycles QNZ supplier TGGTGTGTCAACACCCCTAAAATGATA STC-1 (inner) GTGGCGGCTCAAAACTCAGCTGAA 645 bp 94°C for 30s, 60°C for 30s, 72°C for 1 min, 40 cycles TTATGCACTCTCATGGGATGTGCGTT β-actin CCCTGGACTTCGAGCAAGAGAT 531 bp 94°C for 30s, 55°C for 30s, 72°C for 1 min, 35 cycles GTTTTCTGCGCAAGTTAGG Statistical analysis Statistical tests were carried out using SPSS version 16.0 (SPSS Inc., Chicago, IL, USA). The differential expressions of STC-1 between tumor and adjacent normal specimens were calculated with Student’s t-test. Differences in frequency were assessed

by Chi-square test or Fisher’s exact test. Overall survival curves were calculated using the Kaplan-Meier method and compared by log-rank testing. Multivariate Cox proportional hazard models were used to define the potential prognostic significance enough of individual parameter. P < 0.05 was taken as statistically significant. Results STC-1 protein expression profiles in ESCC tissue We determined STC-1 protein expression in 85 pairs of ESCC and matched normal tissues by immunohistochemical staining. The representative immunohistochemical results are shown in Figure 1(A-D). In total, there were 71 cases (83.5%) showed a higher level of STC-1 protein expression in tumor tissues than in normal tissues, and the average immunostaining scores in tumor tissues were 3.08 ± 1.81 while in normal tissues was 1.05 ± 1.08 (Figure 1E, P < 0.001). Moreover, distribution of immunostaining scores per sample in tumor tissues and adjacent normal tissues was shown in Figure 1F, the rate of STC-1 protein high/moderate expression in ESCC and normal tissues was 65.9% (56/85) and 7.1% (6/85), respectively, which showed a significant difference (P < 0.001).

Subjects with conditions associated with vertebral deformity, including osteomalacia, Paget’s disease,

Scheuermann’s disease, hyperparathyroidism, renal bone disease and malignancy with bone metastasis, were excluded. Information on symptoms associated with vertebral fractures was also collected, including difficulty in bending forward, kyphosis (occiput-to-wall >0 cm and/or gap between the costal margin and iliac crest <3 fingerbreadths), low back pain and height loss more than 2 cm since the age of 25 years. These data were collected from interviews conducted by a trained research assistant. All subjects were followed annually via telephone interviews using a structured questionnaire for assessment of the clinical outcome of incident fractures, falls, hospitalization, AZD0530 use of anti-osteoporotic medications,

living status and functional status. Subjects who commenced anti-osteoporosis medication prior to the occurrence of a primary fracture were excluded. Medical history and incident fractures were verified with the computerized patient information system of the Hospital Authority of the Hong Kong Government. For this study, only non-traumatic incident hip fractures and clinical vertebral fractures were Selleckchem Ganetespib included in the analysis. Hip fractures were defined as having a diagnosis coded as International Classification

of Disease, Tenth Revision (ICD-10) S72.0-S72.2 (fracture of the femoral neck, GSK1120212 supplier intertrochanteric, trochanteric, or subtrochanteric), and clinical vertebral fractures were identified in subjects who received medical attention from a physician with a diagnosis coded as ICD-10S22.0-S22.1 (fracture of the thoracic vertebra/multiple thoracic vertebrae), S32.0 or S32.7 (fracture of the lumbar vertebra/multiple lumbar vertebrae). Pathological fractures or fractures caused by traffic accidents or falls from standing heights were Osimertinib clinical trial excluded. The study was approved by the Institutional Review Board of the University of Hong Kong and the Hong Kong West Clusters Hospital of the Hospital Authority. Japan The hip and clinical vertebral fracture incidence rates for the Japanese were obtained from previously published data used to develop the Japanese version of FRAX® [24]. The hip fracture incidence rate was based on data from a census study in Tottori Prefecture, Japan, in 1994 [25]. The incidence of vertebral fracture was based on data obtained from the Adult Health Study in Hiroshima, Japan [26]. Participants were followed through biennial medical examination including radiology assessments since the establishment of the study in 1958.

Nat Genet 41:15–17CrossRefPubMed 8. Duncan EL, Brown MA, Sinsheimer J, Bell J, Carr AJ, Wordsworth BP, Wass JA (1999) Suggestive linkage of the parathyroid receptor type 1 to osteoporosis. J Bone Miner Res 14:1993–1999CrossRefPubMed buy AZD5363 9. Wilson SG, Reed PW, Bansal A, Chiano M, Lindersson M, Langdown M, Prince RL, Thompson D, Thompson E, Bailey M, Kleyn PW, Sambrook P, Shi MM, Spector TD (2003) Comparison of genome

screens for two independent cohorts provides replication of suggestive linkage of bone mineral density to 3p21 and 1p36. Am J Hum Genet 72:144–155CrossRefPubMed 10. Xiao P, Shen H, Guo YF, Xiong DH, Liu YZ, Liu YJ, Zhao LJ, Long JR, Guo Y, Recker RR, Deng HW (2006) Genomic regions identified for BMD in a large sample including epistatic interactions and gender-specific effects. J Bone Miner Res 21:1536–1544CrossRefPubMed 11. Streeten EA, McBride DJ, Pollin TI, Ryan K, Shapiro J, Ott S, Mitchell BD, Shuldiner

AR, O’Connell JR (2006) Quantitative trait loci for BMD identified by autosome-wide linkage scan to chromosomes 7q and 21q in men from the Amish family osteoporosis study. J Bone Miner Res 21:1433–1442CrossRefPubMed 12. Lee YH, Rho YH, selleckchem Choi SJ, Ji JD, Song GG (2006) Meta-analysis of genome-wide linkage studies for bone mineral density. J Hum Genet 51:480–486CrossRefPubMed 13. Ioannidis JP, Ng MY, Sham PC, Zintzaras E, Lewis CM, Deng HW, Econs MJ, Karasik D, Vistusertib Devoto M, Kammerer CM, Spector T, Andrew T, Cupples LA, Duncan EL, Foroud T, Kiel DP, Koller D, Langdahl B, Mitchell BD, Peacock M, Recker R, Shen H, Sol-Church

Doxacurium chloride K, Spotila LD, Uitterlinden AG, Wilson SG, Kung AW, Ralston SH (2007) Meta-analysis of genome-wide scans provides evidence for sex- and site-specific regulation of bone mass. J Bone Miner Res 22:173–183CrossRefPubMed 14. Mullin BH, Prince RL, Dick IM, Hart DJ, Spector TD, Dudbridge F, Wilson SG (2008) Identification of a role for the ARHGEF3 gene in postmenopausal osteoporosis. Am J Hum Genet 82:1262–1269CrossRefPubMed 15. Dvornyk V, Liu XH, Shen H, Lei SF, Zhao LJ, Huang QR, Qin YJ, Jiang DK, Long JR, Zhang YY, Gong G, Recker RR, Deng HW (2003) Differentiation of Caucasians and Chinese at bone mass candidate genes: implication for ethnic difference of bone mass. Ann Hum Genet 67:216–227CrossRefPubMed 16. Bicknell LS, Morgan T, Bonafe L, Wessels MW, Bialer MG, Willems PJ, Cohn DH, Krakow D, Robertson SP (2005) Mutations in FLNB cause boomerang dysplasia. J Med Genet 42:e43CrossRefPubMed 17.

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M. Evidence for an anaplerotic/malonyl-CoA pathway in pancreatic beta-cell nutrient signaling. Diabetes. 1996;45:190–8.PubMedCrossRef 38. Poitout V, Robertson RP. Minireview. Secondary beta-cell failure in

type 2 diabetes–a convergence of glucotoxicity and lipotoxicity. Endocrinology. 2002;143:339–42.PubMed 39. Maedler K, Oberholzer J, Bucher P, Spinas GA, Donath MY. Monounsaturated fatty acids prevent the deleterious effects of palmitate and high glucose on human pancreatic beta-cell turnover and function. Diabetes. 2003;52:726–33.PubMedCrossRef 40. El-Assaad W, Buteau J, Peyot ML, Nolan C, Roduit R, Hardy S, Joly E, Dbaibo G, Rosenberg L, Prentki M. Saturated fatty acids synergize PSI-7977 in vitro with elevated glucose to cause pancreatic beta-cell death. Endocrinology.

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The culture-negative rate in our study was probably not due to the use of empirical antibiotic treatment before the wound culture was available, but it is lower than in other studies

[36, 40, 41]. Unfortunately, contemporary dilemmas about how long to use antibiotics also exist. We recommend continuing with the antibiotic selleck products therapy for 3 to 5 days after the systemic signs and symptoms and most local signs of soft tissue infection have resolved. Other authors suggested the same approach [22, 25, 36, 38]. The emergency surgical debridement of all affected tissue is the primary treatment modality for NSTI and NF. It includes prompt and radical surgical debridement, necrectomy and fasciotomy in cases presenting with the compartment syndrome [8, 37]. Surgical intervention can be life-saving and must be performed buy LY294002 as early as possible. Surgical procedures should be repeated during the next 24 h, 48 h, or longer, depending on the clinical course of the necrotizing infection and vital functions.

Numerous CB-5083 research buy studies [5] have shown that the most important variable for the mortality rate is the timing and extent of the first debridement. In the study of Mock et al. [42] the relative risk of death was 7,5 times greater in cases with improper primary debridement, and in the study of Wong et al. [43] it was 9 times greater when primary surgery was delayed more than 24 hours. Incisions are performed parallel to Langer’s lines to ensure better surgical wound healing and less scaring [6, 36]. We start the incision over the point of maximal fluctuation and then extended

in the direction of Langer’s lines. The surgery also minimizes the overall tissue loss because it cuts the way the infection spreads in course of facial plan and eliminates the need for amputation of the infected limbs [44]. After the release of pus and fluid by performing incisions which are parallel with Langer’s lines we can perform additional perpendicular incisions on the skin [6] to maintain the wound open, and to allow free drainage and to remove additional necrotic tissue. But, skin bridges and flaps generally should be avoided while Thalidomide performing incisions. Every patient who has NSTI and NF needs a regular inspection of the operated wounds during the next 24 hours and later. If there is any concern about the tissue viability, the surgeon must promptly perform a re-operation with additional radical debridement. We maintain that the main reason for the progression of the infection lies in the delay of the first operative debridement, inadequate primary debridement and necrectomy, hemodynamic instability and concomitant illness [36]. The flow of intravascular liquid into third tissue spaces in each presented case was large and therefore hemodynamic resuscitation, nutritional support and enteral feeding in ICU must be started as soon as possible.

A 20-nm-thick Au film was then deposited on the samples using e-beam evaporation. Subsequently, the samples PD173074 price were submerged in a HF/H2O2 aqueous Dorsomorphin molecular weight solution for MaCE. As an example, Figure 1c shows the formed Si nanopillars. The molar proportion of HF/H2O2/H2O is X:Y:Z, where (X + Y):Z is kept constant at 1:5, and the molar ratio λ is defined as λ = X / (X + Y). The solutions with different molar ratios, λ, used in this work are listed in

Table 1. During MaCE, only Au contact areas were etched, resulting in vertically aligned arrays of nanoporous Si nanopillars, arrays of nanoporous Si pillars with a nanoporous base, or Si nanopillars with nanoporous shells. The different structural properties are determined

by the molar ratio λ and the doping level of the Si wafer. After MaCE, the samples were investigated using an ultrahigh resolution scanning electron microscope (SEM; Hitachi S-4800). The resist and the Au film were not removed for SEM inspection. Figure 1 Fabrication of the ordered arrays of Si nanopillars. (a) Schematic sketch of the fabrication process for the ordered array of nanoporous Si nanopillars, ordered array of nanoporous Si nanopillars with nanoporous base layer, and ordered LXH254 in vitro array of Si nanopillars with nanporous shells. (b) SEM image of the pattern defined using SCIL. (c) SEM image of the formed Si nanopillars for the lightly doped Si wafer after MaCE (in λ 3 solution

for 10 min). Table 1 List of solutions with different molar ratios, λ , used for the etching solutions Molar ratio Value λ 1 0.5 λ 2 0.7 λ 3 0.85 λ 4 0.92 Results The nanopillars formed from highly doped Si after etching in λ 3 solution for 3, 6, and 10 min, respectively, are shown in Figure 2. After 3-min etching, the nanoporous Si nanopillars had a vertical length of 1.6 μm, accompanied by the formation of a nanoporous base with a homogenous thickness of 1.2 μm below the Au film and the nanopillars (Figure 2a). After 6-min etching, the length of the nanoporous Si nanopillars increased to 6.3 μm, while the thickness of the nanoporous base is clearly reduced to a few hundred nanometers and not being homogenous anymore. After Aurora Kinase 10-min etching, the length of the nanoporous Si nanopillars increased to 15.1 μm, and the thickness of the nanoporous base was reduced even more. The nanoporosity of the nanopillars is more clearly shown in the cracked pillars (Figure 2b,d,f). It is also interesting to note that the nanoporous layer underneath the pillars is thicker than the nanoporous layer directly below the Au film after 6- and 10-min etching (Figure 2d,f). Figure 2 SEM images of nanopillars formed from the highly doped Si in λ 3 solution. After etching for 3 min (a, b), 6 min (c, d), and 10 min (e, f), respectively. Panels b, d, and f show the cracked nanopillars.

Figure 3b,c corresponds to respective images using SF6/O2 and SF6/CHF3 gas mixtures. From the images, it is obvious that the etch rate with the SF6 gas is higher than the etch rate with the two other gases, and as expected, the etching is isotropic, thus resulting in almost full release of the PAA thin film after RIE of the samples for 20 s. Thus,

the nanopatterned Si surface after PAA removal shows quite shallow features. When adding O2 to SF6, the etching process is slowed down and is more anisotropic. Dibutyryl-cAMP solubility dmso As a result, the 20-s etch time does not lead to PAA mask release, but instead, a nanopatterned surface with features well separated by pore walls are formed (Figure 3b image 1). When replacing O2 by CHF3, the RIE process is even slower and more anisotropic, thus resulting in shallower etched features at each pore bottom and thicker pore walls, as clearly depicted in Figure 3c. Figure 3 SEM micrographs of the Si surface of sample 1 after RIE through PAA film and alumina dissolution. Three different gas LY2874455 concentration mixtures were used for etching, which are indicated on top of the images. The etching duration was 20 s. Micrographs 1 of (a), (b), and (c) are cross-sectional images of the PAA layer/Si stack, while micrographs 2 and 3 are plane view SEM images (slightly tilted in images

2 of (a), (b), and (c); at vertical e-beam incidence in images 3). By increasing the etching Angiogenesis inhibitor time, the depth of the etched holes at each pore bottom increases, but gradually, the lateral etching results in almost full etching of the inter-hole walls, starting from their top, and finally PAA membrane release. This happens earlier with SF6 (isotropic etching) than with the other two gas mixtures. Figure 4 depicts the SEM images of sample 1 after etching in SF6/O2 (Figure 4a) and in SF6/CHF3 (Figure 4b) for 40 s (images 1 and 2 of Figure 4a, and images 1 and 2 of Figure 4b) and 60 s (images 3 of Figure 4a,b). Already for 40-s etching time, the Epothilone B (EPO906, Patupilone) PAA film is fully released when

using SF6/O2 gas mixture, and the Si inter-hole walls are reduced in height. With SF6/CHF3 gas mixture, well-separated nanofeatures on Si are formed, with the inter-pore Si walls intact at their top surface. Finally, for the 60-s etching time, the PAA layer was fully released in both gas mixtures. Figure 4 SEM micrographs of sample 1 after RIE in two different gas mixtures. Micrographs 1 of (a) and (b) are cross-sectional images, while images 2 and 3 of (a) and (b) are plane view images. Etching was performed in SF6/O2 (images 1 to 3 of (a)) and in SF6/CHF3 (images 1 to 3 of (b)). The etching duration was 40 s in images 1 and 2, and 60 s in images 3. In the cross-sectional images, the PAA mask is present; in the plane view images, it is removed, revealing the nanopatterned Si surface.

Potential confounders that were determined for a time-dependent analysis

during follow-up included age, a history of chronic diseases (including asthma/chronic obstructive pulmonary disease (COPD), rheumatoid arthritis, thyroid disorders, renal failure, cancer, congestive heart failure, cerebrovascular disease, diabetes mellitus, inflammatory bowel disease and secondary osteoporosis (based on the definition of FRAX [28]), a prescription in the 6 months before an interval for CNS medication, anti-parkinson medication, non-steroidal antiinflammatory drugs find more (NSAIDs), oral glucocorticoids and other immunosuppressants (azathioprine, ciclosporin, tacrolimus, mycophenolate mofetil and methotrexate). In this approach it was assumed that no residual effect was left for medication used more than 6 months before an interval. The use of oral glucocorticoids and CNS medication were stratified to average daily dose in 6 months before an interval, and use of oral glucorticoids was also stratified to cumulative dose in the year before an interval. WHO defined daily Selonsertib in vivo dosages were used to add up dose equivalences of various CNS medication and oral glucocorticoid substances. Within the 6 months before each interval, the average daily dose was

calculated by dividing the cumulative dose by the time between the oldest prescription and the start date of the period. In addition, MG disease duration was noted, as measured from the start of follow-up. Statistical Repotrectinib in vivo analysis Time-dependent Cox proportional hazards regression was used in order to estimate hazard ratios (HRs) of fracture risk. The first analysis compared the fracture rate in MG patients with that in control patients, to yield an estimate of the HRs of fracture in MG. The second analysis examined the effect of disease severity and use of oral glucocorticoids, antidepressants, anxiolytics or anticonvulsants Glutathione peroxidase on fracture risk in the MG cohort. For each analysis, the regression model was fitted with the indicators for MG severity and general risk factors. These characteristics were treated as time-dependent variables in the analysis,

in which the total period of follow-up was divided into periods of 30 days, starting at the index date. At the start of each period, the presence of risk factors and indicators of MG severity were assessed by reviewing the computerized prescription and diagnosis records prior to the right censoring date. BMI, alcohol status, smoking status and occurrence of prior fracture were determined at baseline. During follow-up, the presence of a previous record for a chronic disease ever before each period of 30 days was assessed, while the presence of a medical prescription was assessed in the 6 months before each period. All characteristics, except age, were included as categorical variables in the regression models. A priori we tested for interactions between age and gender with fracture risk.