Miracle-dz/UniFAR-FTUs huggingface dataset:
Cross-cultural Comparison of the Scoliosis Research Society Outcomes Instrument Between American and Japanese Idiopathic Scoliosis Patients: Are There Differences?

Study Design. A comparative study. Objective. To report a preliminary evaluation of the Scoliosis Research Society Outcomes Instrument (SRS-24) and determine whether differences in baseline scores exist between American and Japanese patients with idiopathic scoliosis. Summary of Background Data. Because the SRS outcomes instrument was primarily introduced for the American population, baseline scores in the Japanese population might differ from the American population. A comparative study using the SRS instrument between American and Japanese patients with idiopathic scoliosis has not been reported. Methods. Two comparable groups of 100 idiopathic scoliosis patients before spinal fusion were separated into American (A) and Japanese (J). There were no statistically significant differences between the groups for gender (A: 9 men/91 women vs. J: 13 men/87 women), age (A: 15.0 ± 2.4 vs. J: 14.9 ± 3.8), main curve location (A: 77 thoracic/23 lumbar, J: 76 thoracic/24 lumbar), main curve Cobb angle (A: 50.5 ± 5.2 vs. J: 51.1 ± 8.7), and thoracic kyphosis (A: 20.9 ± 14.3 vs. J: 19.9 ± 12.1) (P > 0.05, for all comparisons). Patients were evaluated using the first section of the SRS-24 which was divided into 4 domains: total pain, general self-image, general function, and activity. SRS-24 scores were statistical compared in individual domains and questions using the Mann-Whitney U test. Results. American patients had significantly lower scores in pain (P < 0.0001, A: 3.7 ± 0.8 vs. J: 4.3 ± 0.4), function (P < 0.01, A: 3.9 ± 0.6 vs. J: 4.2 ± 0.5), and activity (P < 0.0001, A: 4.5 ± 0.8 vs. J: 4.9 ± 0.3) domains compared with Japanese patients. Japanese patients had significantly lower scores in the self-image (P < 0.0001, A: 4.0 ± 0.7 vs. J: 3.5 ± 0.5) domain. With regard to individual questions, there were significant differences in the scores between the 2 groups for all questions except 5 and 13 (P < 0.05, for all comparisons). Conclusion. SRS-24 scores in the Japanese idiopathic scoliosis population differed from that of the American population. Japanese patients had less back pain, a negative self-image regarding back deformity, higher general physical function, and daily activity. It is highly probable that patient’s perceptions differ due to cultural differences, which affect SRS-24 scores so a cross-cultural comparison of the SRS instrument content is necessary in the future.
Melatonin synergizes the chemotherapeutic effect of 5‐fluorouracil in colon cancer by suppressing PI3K/AKT and NF‐κB/iNOS signaling pathways

5‐Fluorouracil (5‐FU) is one of the most commonly used chemotherapeutic agents in colon cancer treatment, but has a narrow therapeutic index limited by its toxicity. Melatonin exerts antitumor activity in various cancers, but it has never been combined with 5‐FU as an anticolon cancer treatment to improve the chemotherapeutic effect of 5‐FU. In this study, we assessed such combinational use in colon cancer and investigated whether melatonin could synergize the antitumor effect of 5‐FU. We found that melatonin significantly enhanced the 5‐FU‐mediated inhibition of cell proliferation, colony formation, cell migration and invasion in colon cancer cells. We also found that melatonin synergized with 5‐FU to promote the activation of the caspase/PARP‐dependent apoptosis pathway and induce cell cycle arrest. Further mechanism study demonstrated that melatonin synergized the antitumor effect of 5‐FU by targeting the PI3K/AKT and NF‐κB/inducible nitric oxide synthase (iNOS) signaling. Melatonin in combination with 5‐FU markedly suppressed the phosphorylation of PI3K, AKT, IKKα, IκBα, and p65 proteins, promoted the translocation of NF‐κB p50/p65 from the nuclei to cytoplasm, abrogated their binding to the iNOS promoter, and thereby enhanced the inhibition of iNOS signaling. In addition, pretreatment with a PI3K‐ or iNOS‐specific inhibitor synergized the antitumor effects of 5‐FU and melatonin. Finally, we verified in a xenograft mouse model that melatonin and 5‐FU exerted synergistic antitumor effect by inhibiting the AKT and iNOS signaling pathways. Collectively, our study demonstrated that melatonin synergized the chemotherapeutic effect of 5‐FU in colon cancer through simultaneous suppression of multiple signaling pathways.
Increased Susceptibility of Nrf2 Knockout Mice to Colitis-Associated Colorectal Cancer

The nuclear factor-erythroid 2-related factor 2 (Nrf2) plays a critical role in protecting various tissues against inflammation, which is a potential risk factor for colorectal and other cancers. Our previously published mouse model work showed that Nrf2 helps protect against dextran sulfate sodium (DSS)–induced colitis/inflammation, and others have shown that Nrf2 helps protect against inflammation-associated colorectal carcinogenesis (aberrant crypt foci). The present study extended these important earlier findings by exploring the role of Nrf2 in colitis-associated colorectal cancer in a mouse model involving azoxymethane/DSS–induced colorectal carcinogenesis in Nrf2 knockout mice. Azoxymethane/DSS–treated Nrf2 knockout mice had increased incidence, multiplicity, and size of all colorectal tumors, including adenomas, versus treated wild-type (WT) mice, and the proportion of tumors that were adenocarcinoma was much higher in knockout (80%) versus WT (29%) mice. Compared with WT mice, knockout mice also had increased markers of inflammation in tumor tissue (cyclooxygenase-2 and 5-lipoxygenase expressions and prostaglandin E2 and leukotriene B4 levels) and in inflamed colonic mucosa (nitrotyrosine expression), supporting the association of knockout mouse tumor formation with inflammation. The phase II detoxifying/antioxidant enzymes NAD(P)H-quinone reductase 1 and UDP-glucurosyltransferase 1A1 were elevated in the normal mucosa of WT, but not Nrf 2 knockout, mice treated with azoxymethane/DSS. Our findings show that Nrf2 plays a critical role in protecting against inflammation-associated colorectal cancer.
Robust functional observer design for uncertain fractional-order time-varying delay systems

In this work, existence and design of Robust Functional Observer (RFO) for Uncertain Fractional-Order Systems with Time-Varying-Delay (UFOS-TVD) are addressed. Usually, when the considered system is under the effect of structured uncertainties, this kind of problems, referred as ℓ2-gain rejection, aims at designing a RFO minimizing a given cost function subject to ℓ2-gain rejection constraint, which means, the rejection of the uncertain states effect on the estimated errors. An LMI-based minimization problem for the robust stability is derived based on the indirect Lyapunov and Lyapunov-Krasovskii approaches. Finally, a simulation results are presented to illustrate the performance of the proposed methodology.
A Review of Stereotactic Radiosurgery in the Management of Brain Metastases

This review addresses the epidemiology, historical reports, current issues, data and controversies involved in the management of brain metastases. The literature regarding surgery, whole brain radiation therapy, stereotactic radiosurgery or some combination of those treatments is discussed as well as issues of cost-effectiveness. Ongoing prospective randomized trials will further elucidate the optimal management for patients with brain metastases. Until those data are available, clinicians are encouraged to apply the existing data reviewed here in conjunction with best clinical judgment. A brief clinical guide is as follows. Patients with a solitary metastasis in an operable location and symptomatic mass effect should undergo surgery. Patients with poor performance status (KPS < 70) or more than three brain metastases should receive WBRT alone. Patients with 1-3 brain metastases and KPS ≥ 70, should receive WBRT + SRS. If the patient refuses WBRT or needs salvage after WBRT, then SRS alone is appropriate. Clinicians should not be too dogmatic and should always apply the best clinical judgment.
Predictors of patient self-ratings of quality of life in Alzheimer disease: cross-sectional results from the Canadian Alzheimer's Disease Quality of Life Study.

OBJECTIVES To assess whether the core symptoms of Alzheimer disease (AD) consistently predict patient self-rated quality of life (QOL) as assessed by a variety of QOL measures in a large national sample of AD patients. DESIGN Cross-sectional. SETTING Fifteen dementia and geriatric clinics across Canada. PARTICIPANTS Community-living patients with AD (n = 370) with Mini-Mental State Exam (MMSE) scores greater than 10. MEASUREMENTS Patients rated their QOL by using two utility indexes, the European QOL-5 Dimensions and the Quality of Well-Being Scale, a global QOL Visual Analog Scale, and the disease-specific QOL-AD instrument. Cognition was assessed with the AD Assessment Scale-Cognitive subscale and MMSE, function with the Disability Assessment for Dementia, and behavioral and psychological symptoms with the Neuropsychiatric Inventory and the Geriatric Depression Scale (GDS). One-way analysis of variance and fully adjusted multiple linear regression were used to assess the relationship between core dementia symptoms and QOL ratings. RESULTS The QOL measures had only small-to-moderate correlations with each other. For all QOL measures, patient ratings were significantly lower among patients with more depressive symptoms. In multivariable analyses, the GDS score was the only significant independent predictor of patient self-ratings for all four QOL measures. CONCLUSIONS Self-rated symptoms of depression were a consistent independent predictor of patient-rated QOL across diverse QOL measures, while performance-based measures of cognition and informant-based functional status were not. These findings confirm the importance of identifying and treating depression in patients with AD and endorse the use of measures of self-rated depressive symptoms and QOL as outcomes in AD clinical trials.
Linking Posttraumatic Stress Disorder and Psychosis: A Look at Epidemiology, Phenomenology, and Treatment

Several recent studies have provided direct evidence for the link between posttraumatic stress disorder (PTSD) and psychosis. Patients with psychotic disorders are known to be at a higher risk of traumatization and PTSD. Additionally, preclinical and clinical data suggest that the effects of trauma exposure on neural networks may provide a common diathesis for disorders like PTSD and schizophrenia. This article reviews evidence on a) the magnitude of association between PTSD and psychosis, b) the causal mechanisms implicated, and c) treatment considerations relevant to this association. A comprehensive MEDLINE search was conducted, and articles pertinent to epidemiological, clinical, and treatment aspects of comorbid PTSD and psychosis were identified. High rates of PTSD characterize patients with severe mental illness. Psychotic phenomena may also be a relatively common manifestation in patients with chronic PTSD. However, in clinical settings, the diagnosis is often missed, and few systematic guidelines exist for the identification and treatment of these comorbidities. Future neurobiological and treatment studies may be useful in better informing the clinical management of these subgroups.
Delayed care-seeking and outcome of dengue-infected patients

A retrospective cohort study was conducted to assess the effect of early (1–4 days after fever onset) and delayed (≥5 days) care-seeking on outcomes of dengue-infected patients. We used data of adult dengue-infected patients treated in Bangkok, Thailand between June 2012 and September 2013. There were 110 patients in the early care-seeking group and 100 in the delayed care-seeking group. There were no deaths. Bleeding complications were not significantly different between the two groups while the latter group had a significantly higher rate of admission compared with the former (98% versus 91.8%, respectively; P = 0.04). Being female was the only factor significantly associated with delayed care-seeking (63.0% versus 45.5%; P = 0.01).
Estrogen receptor- (cid:1) mediates male-female differences in the development of pressure overload hypertrophy

Estrogen receptor- mediates male-female differences in the development of pressure overload hypertrophy. goal of this study was to determine the role of estrogen receptor subtypes in the development of pressure overload hypertrophy in mice. Epidemiological studies have suggested gender differences in the development of hypertrophy and heart disease, but the mechanism and the role of estrogen receptor subtypes are not established. We performed transverse aortic constriction (TAC) and sham operations in male and female wild-type (WT) mice and mice lacking functional estrogen receptor- (cid:2) [ (cid:2) -estrogen receptor knockout ( (cid:2) -ERKO)] and mice lacking estrogen receptor- (cid:1) ( (cid:1) -ERKO). Body, heart, and lung weights were measured 2 wk postsurgery. WT male mice subjected to TAC showed a 64% increase in the heart weight-to-body weight ratio (HW/BW) compared with sham, and WT males have increased lung weight at 2 wk. WT female mice subjected to TAC showed a 31% increase in HW/BW compared with sham, which was signiﬁcantly less than their male counterparts and with no evidence of heart failure. (cid:2) -ERKO females developed HW/BW nearly identical to that seen in WT littermate females in response to TAC, indicating that estrogen receptor- (cid:2) is not essential for the attenuation of hypertrophy observed in WT females. In contrast, (cid:1) -ERKO females responded to TAC with a signiﬁcantly greater increase in HW/BW than WT littermate females. (cid:1) -ERKO females have lower expression of lipoprotein lipase at baseline than WT or (cid:2) -ERKO females. These data suggest an important role for estrogen receptor- (cid:1) in attenuating the hypertrophic response to pressure overload in females.
Why don't they want a male-dominated job? An investigation of young women who changed their occupational aspirations

We examined 2 hypotheses regarding why some young women do not maintain their espoused occupational aspirations in male-dominated fields from late adolescence through young adulthood. The first hypothesis concerns attitudes towards math and science; the second concerns the desire for job flexibility. The sample of young women (N = 104) was taken from a larger longitudinal investigation of approximately 1,000 young women from a midwestern metropolitan area in Michigan, USA, who were followed from age 18 (in 1990) to age 25 (1997). Findings suggest that desire for a flexible job, high time demands of an occupation, and low intrinsic value of physical science were the best predictors of women changing their occupational aspirations out of male-dominated fields. These results suggest that despite the women's movement and more efforts in society to open occupational doors to traditional male-jobs for women, concerns about balancing career and family, together with lower value for science-related domains, continue to steer young women away from occupations in traditionally male-dominated fields, where their abilities and ambitions may lie.
A critical role for p59fyn in CD2‐based signal transduction

TCR‐ but not CD2‐triggered IL‐2 production is p56lck dependent. To test the hypothesis that p59fyn, a second src‐family protein tyrosine kinase (PTK) expressed in T lymphocytes, might be an essential upstream component of the CD2 signaling pathway, we generated human (h) CD2 transgenic (tg) fyn+/+ and fyn–/– mice. Clustering of hCD2 molecules on resting peripheral T lymphocytes results in Ca2+ mobilization, activation of MAPK and cellular proliferation. In contrast, in the absence of p59fyn, these CD2‐initiated activities are markedly reduced, while TCR‐triggered proliferation is unaffected. Several CD2 pathway components regulated by p59fyn have been identified including phospholipase C‐γ1 (PLC‐γ1), Vav, protein kinase C‐θ isoform (PKC‐θ), docking protein (Dok), focal adhesion kinase (FAK) and Pyk2. Decreased inducible PKC‐θ catalytic activity and Vav phosphorylation likely account for diminished p38 and JNK activation in hCD2tg fyn–/– mice. Moreover, deficiency in fyn‐dependent PLC‐γ1 catalytic activity may contribute to reduced PKC‐α‐dependent ERK activation. Of note, CD2‐dependent Dok but not linker from activated T cells (LAT) tyrosine phosphorylation requires p59fyn. Furthermore, that FAK and Pyk2 are target substrates implies that p59fyn may be an important regulator of T cell adhesion as well. Collectively, these data identify p59fyn as a key PTK in CD2‐mediated activation of mature T lymphocytes.
The accessory olfactory bulb in the adult rat: A cytological study of its cell types, neuropil, neuronal modules, and interactions with the main olfactory system

The accessory olfactory bulb (AOB) in the adult rat is organized into external (ECL) and internal (ICL) cellular layers separated by the lateral olfactory tract (LOT). The most superficial layer, or vomeronasal nerve layer, is composed of two fiber contingents that distribute in rostral and caudal halves. The second layer, or glomerular layer, is also divided by a conspicuous invagination of the neuropil of the ECL at the junction of the rostral and caudal halves. The ECL contains eight cell types distributed in three areas: a subglomerular area containing juxtaglomerular and superficial short‐axon neurons, an intermediate area harboring large principal cells (LPC), or mitral and tufted cells, and a deep area containing dwarf, external granule, polygonal, and round projecting cells. The ICL contains two neuron types: internal granule (IGC) and main accessory cells (MACs). The dendrites and axons of LPCs in the two AOB halves are organized symmetrically with respect to an anatomical plane called linea alba. The LPC axon collaterals may recruit adjacent intrinsic, possibly γ‐aminobutyric acid (GABA)‐ergic, neurons that, in turn, interact with the dendrites of the adjacent LPCs. These modules may underlie the process of decoding pheromonal clues. The most rostral ICL contains another neuron group termed interstitial neurons of the bulbi (INBs) that includes both intrinsic and projecting neurons. MACs and INBs share inputs from fiber efferents arising in the main olfactory bulb (MOB) and AOB and send axons to IGCs. Because IGCs are a well‐known source of modulatory inputs to LPCs, both MACs and INBs represent a site of convergence of the MOB with the AOB. J. Comp. Neurol. 510:309–350, 2008. © 2008 Wiley‐Liss, Inc.
Adverse Effects of Monosodium Glutamate on Liver and Kidney Functions in Adult Rats and Potential Protective Effect of Vitamins C and E

Monosodium glutamate (MSG) was administrated to rats at doses of 0.6 and 1.6 mg/g body weight for 14 days. Body weight and relative liver and kidney weight of rats were significantly increased. On regard to liver functions, the activities of alanine aminotransferase (ALT) and γ glutamyle transferase (GGT) significantly increased in the serum, on MSG administration, meanwhile, serum total protein, albumin and serum total bilirubin significantly decreased. MSG had adverse effects on kidney functions as serum urea and serum creatinine were significantly increased. Vitamin C (0.3 mg/g body weight) and vitamin E (0.2 mg/g body weight) co-adminstrated with MSG, significantly restored the body weight and relative liver and kidney weights to control levels. In the presence of vitamin C and vitamin E the activities of ALT and GGT in the serum were also significantly reduced to become comparable with control trail. Consequently, serum total protein, albumin and serum total bilirubin were significantly increased in the serum, while serum urea and serum creatinine were significantly decreased after administration of each vitamin. The results showed that MSG at doses of 0.6 and 1.6 mg/g of body weight may cause an adverse effect on the hepatic and renal functions which might be due to oxidative stress induced by MSG on the liver and renal tissue. Supplementation of vitamin C and vitamin E was capable of ameliorating MSG-induced oxidative stress on hepatic and renal functions.
Increased Activity of Small GTP-binding Protein-dependent Phospholipase D during Differentiation in Human Promyelocytic Leukemic HL60 Cells*

In response to dibutyryl cyclic AMP (dbcAMP) and all-trans retinoic acid, human promyelocytic leukemic HL60 cells differentiate into granulocyte-like cells. In cell lysate and in vitro reconstitution system, phospholipase D (PLD) activity in response to guanosine 5′-O-(3-thiotriphosphate) (GTPγS) was up-regulated by dbcAMP or all-trans retinoic acid treatment. In the present study, the mechanism(s) for increased PLD activity during differentiation was examined. Western blot analysis revealed that the contents of ADP-ribosylation factor, Rac2, and Cdc42Hs but not RhoA and Rac1 in the cytosolic fraction were elevated during differentiation. However, the cytosolic fraction from undifferentiated cells was almost equally potent as the cytosolic fraction from differentiated cells in the ability to stimulate membrane PLD activity. It was shown that the GTPγS-dependent PLD activity in membranes from differentiated cells was much higher than that in membranes from undifferentiated cells, suggesting that the increased PLD activity during differentiation was due to alterations in some membrane component(s). Clostridium botulinum ADP-ribosyltransferase C3 and C. difficile toxin B, which are known as inhibitors of RhoA and Rho family proteins, respectively, effectively suppressed PLD activity in membranes from differentiated cells. In fact, the amount of membrane-associated RhoA was increased during differentiation. Furthermore, the extent of GTPγS-dependent PLD activity partially purified from membranes from differentiated cells was greater than that from membranes from undifferentiated cells in the presence of recombinant ADP-ribosylation factor 1. The PLD (hPLD1) mRNA level was observed to be up-regulated during differentiation, as inferred by reverse transcription-polymerase chain reaction. Our results suggest the possibility that the increased Rho proteins in membranes and the changed level of PLD itself may be, at least in part, responsible for the increase in GTPγS-dependent PLD activity during granulocytic differentiation of HL60 cells.