Miracle-dz/UniFAR-FTUs huggingface dataset:
Prognostic significance of cytoplasmic SOX9 in invasive ductal carcinoma and metastatic breast cancer

SOX9, a high mobility group (HMG) box transcription factor, is required for development, differentiation and lineage commitment. It is known to exert its effects through nuclear translocation, such as cell cycle changes in response to retinoic acid treatment in breast cancer cells. However, it is not known whether SOX9 has prognostic significance in human breast cancer. Over-expression and cytoplasmic sequestration of nuclear proteins are implicated in tumor progression. To determine whether SOX9 has any prognostic significance in human breast cancer, its expression and subcellular localization were analyzed in more than 200 human breast carcinomas (BCs). SOX9 mRNA expression data for human BCs were computed from microarray studies available in public databases and correlated with known poor prognostic parameters of BCs. SOX9 protein expression and its correlation with Ki-67 staining in human BCs were assessed using immunohistochemistry. Higher SOX9 mRNA levels were significantly associated with estrogen receptor negative (P ≤ 0.001) and higher grade (P ≤ 0.01) human breast tumors. Patients with higher SOX9 mRNA level had significantly shorter overall survival (P ≤ 0.0001). SOX9 protein, which is normally nuclear, was instead localized in the cytoplasm of 25–30% invasive ductal carcinomas (IDCs) and lymph node metastases. Its cytoplasmic accumulation significantly correlated with enhanced proliferation in breast tumors (Kendall's tau = 0.337 with a P value < 0.0001). Cytoplasmic SOX9 can serve as a valuable prognostic marker for IDCs and metastatic breast cancer. Its significant correlation with breast tumor cell proliferation implies that SOX9 directly contributes to the poor clinical outcomes associated with invasive breast cancer.
Speed Control of the Surface-Mounted Permanent-Magnet Synchronous Motor Based on Takagi–Sugeno Fuzzy Models

The speed control of the surface-mounted permanent-magnet synchronous motor (SPMSM) based on Takagi-Sugeno (T-S) fuzzy models is designed and implemented in this paper. In motor drive speed control, proportional-integral controller is generally applied. However, the tracking performance and load regulation capability should be compromised in the designing process of the controller. This study develops a speed controller based on the T-S fuzzy model with good tracking ability and load variation regulation. First, the dynamic model of an SPMSM is demonstrated and the load torque variation is treated as disturbances. Accordingly, the speed control strategy is developed based on the T-S fuzzy model. The defuzzification process and parallel distributed compensation are introduced. The ability of disturbance suppression and the Lyapunov stability of this system are established and analyzed. The controller gains are obtained via the linear matrix inequality toolbox. The speed control and all essential procedures are realized by the microcontroller Renesas RX62T. The tracking performance and load regulation capability are verified by the experimental results.
Primary Placement of Osseointegrated Implants in Microvascular Mandibular Reconstruction

The goal of mandibular reconstruction is to rehabilitate the patient by restoring occlusal relationships, lower facial contour, oral continence, and a denture-bearing surface. One of the major advantages of the use of vascularized bone over all other methods of mandibular reconstruction is its ability to achieve dental rehabilitation rapidly. The use of osseointegrated dental implants is a valuable adjunct in oral rehabilitation. It provides the most rigid form of stabilization to withstand the forces of mastication. In situations In which soft tissue reconstruction or the height of the alveolar ridge is not sufficient for a tissue-borne denture, implants offer the most suitable alternative. Mandibular reconstruction with free tissue transfer techniques is Ideally suited for the placement of implants. These can be inserted at the time of mandibular reconstruction. Four months after surgery, when the integration process has occurred, the implants are unroofed, loaded, and ready for prosthetic placement. We will present several representative patients who underwent mandibular reconstruction with microvascular free bone transfer who have been successfully rehabilitated by osseointegrated implants. The process of osseointegration, different types of dental implants, and issues regarding radiation and Implants are discussed. This is the first report of dental rehabilitation by primary placement of dental implants in patients undergoing microvascular mandibular reconstruction.
Conformational Changes in the Photocycle of Anabaena Sensory Rhodopsin

Anabaena sensory rhodopsin (ASR) is a novel microbial rhodopsin recently discovered in the freshwater cyanobacterium Anabaena sp. PCC7120. This protein most likely functions as a photosensory receptor as do the related haloarchaeal sensory rhodopsins. However, unlike the archaeal pigments, which are tightly bound to their cognate membrane-embedded transducers, ASR interacts with a soluble cytoplasmic protein analogous to transducers of animal vertebrate rhodopsins. In this study, infrared spectroscopy was used to examine the molecular mechanism of photoactivation in ASR. Light adaptation of the pigment leads to a phototransformation of an all-trans/15-anti to 13-cis/15-syn retinylidene-containing species very similar in chromophore structural changes to those caused by dark adaptation in bacteriorhodopsin. Following 532 nm laser-pulsed excitation, the protein exhibits predominantly an all-trans retinylidene photocycle containing a deprotonated Schiff base species similar to those of other microbial rhodopsins such as bacteriorhodopsin, sensory rhodopsin II, and Neurospora rhodopsin. However, no changes are observed in the Schiff base counterion Asp-75, which remains unprotonated throughout the photocycle. This result along with other evidence indicates that the Schiff base proton release mechanism differs significantly from that of other known microbial rhodopsins, possibly because of the absence of a second carboxylate group at the ASR photoactive site. Several conformational changes are detected during the ASR photocycle including in the transmembrane helices E and G as indicated by hydrogen-bonding alterations of their native cysteine residues. In addition, similarly to animal vertebrate rhodopsin, perturbations of the polar head groups of lipid molecules are detected.
WNTs in the Neonatal Mouse Uterus: Potential Regulation of Endometrial Gland Development1

The WNTs are secreted proteins that control essential developmental processes, such as embryonic patterning, cell growth, migration, and differentiation. In mice, three members of the Wnt gene family (Wnt4, Wnt5a, and Wnt7a) have been studied extensively in the female reproductive tract. The present study determined effects of postnatal day and exposure to diethylstilbestrol (DES) on Wnt and Fzd gene expression in the mouse uterus as well as the biological role of Wnt11 in postnatal mouse uterine development and function. Wnt4, Wnt5a, Wnt7a, Wnt7b, Wnt11, Wnt16, Fzd6, and Fzd10 were detected by in situ hybridization in the neonatal mouse uterus. In situ hybridization analyses revealed that Wnt4, Wnt5a, and Wnt16 were localized in the endometrial stroma, whereas Wnt7a, Wnt7b, Wnt11, Fzd6, and Fzd10 were in the uterine epithelia of neonatal mice. Exposure of mice to estrogen or estrogen receptor agonists during critical development periods inhibits endometrial adenogenesis. In the present study, DES-induced disruption of endometrial gland development was associated with reduction or suppression of Wnt4, Wnt5a, Wnt7a, Wnt11, Wnt16, and Fzd10. Ablation of Wnt11, an epithelial-expressed, DES-regulated gene, in the neonatal uterus did not affect endometrial adenogenesis or expression of other Wnt genes. Interestingly, Wnt11-deleted uteri had more endometrial glands on Postnatal Day 10. Although CTNNB1 expression was not affected by ablation of Wnt11, Vangl2 was inhibited in the uteri of Wnt11d/d mice. These results support the idea that a number of different Wnt genes are potential regulators for uterine morphogenesis; however, Wnt11 does not have a direct effect on uterine development.
Effects of autonomic activity and changes in heart rate on atrioventricular conduction.

The effects of autonomic neural stimulation and changes in atrial pacing frequency on atrioventricular (AV) conduction were determined in anesthetized open-chest dogs. Increases in vagal stimulation frequency and in pacing rate significantly increased the AV interval, whereas increases in sympathetic stimulation frequency reduced the AV interval. Vagal stimulation (1.4 Hz) prolonged the AV interval by 17 ms when the atrial pacing rate was 2 Hz. On the other hand, the same vagal stimulation increased the AV interval by 29 ms when the pacing rate was 2.73 Hz. In addition, sympathetic stimulation (1.2 Hz) reduced the AV interval by 29 ms when the pacing rate was 2 Hz. In contrast, the same sympathetic stimulation reduced the AV interval 54 ms when the pacing rate was 2.73 Hz. However, the increase in vagal stimulation did not significantly alter the positive dromotropic response of the AV node to sympathetic stimulation. Therefore, the response of AV conduction to combined sympathetic and vagal stimulation was essentially the algebraic sum of the responses to the individual stimulations. Furthermore, the level of activity in one autonomic division did not alter appreciably the interaction between the pacing rate and the activity in the other autonomic division; i.e., the interaction between pacing rate, sympathetic stimulation, and vagal stimulation was not significant.
Adventitial Neuronal Somata

Confocal analysis of the whole-mount rat mesenteric branch arteries (MBA) revealed nucleated structures with axonal processes which immunostained for calcitonin gene-related peptide (CGRP). Immunocytochemistry ruled out the possibility that these were immune elements (macrophages and mast or dendritic cells) in close proximity with nerve fibers. To test our hypothesis that β-CGRP is expressed in the rat MBA, we performed RT-PCR using total RNA isolated from the mesenteric artery arcade and intron spanning primers designed to amplify 188 bp of the β-CGRP and 333 bp of α-CGRP cDNA. The PCR yielded an amplicon of the predicted size which was cloned into the pCR 3.1 vector. DNA sequence analysis of the insert showed 100% homology with the β-CGRP cDNA, indicating that mRNA encoding β-CGRP is expressed in the vessel. To learn whether neuronal cell bodies are located in the adventitia of MBA, we performed a limited collagenase digestion of isolated segments and plated the resulting cells in Ham’s F12 medium with 10% horse serum on polyornithine-coated cover glasses. The medium was replaced after 48 h with Ham’s F12 nutrient mixture containing N2 supplement. This resulted in a mixed population of fibroblasts, a small number of smooth muscle cells and a subset of cells that sprouted axons and immunostained positively for neuronal cell adhesion molecule and CGRP antigens. Fibroblasts and smooth muscle cells did not label with these antibodies. These data demonstrate, for the first time, that a population of adventitial neuronal somata (termed ANNIES), possibly of sensory nerve origin, is located in small mesenteric arteries.
MIN and MAX Operators for Fuzzy Intervals and Their Potential Use in Aggregation Operators

This paper aims at expressing MIN and MAX operations when triangular fuzzy intervals are taken as inputs, that is when Zadeh's extension principle is considered. First presented approach consists in representing fuzzy intervals by means of their profiles. In this context, a computation algorithm can be easily derived for implementing the MIN and MAX operations. Another methodology based on interval relations is then proposed for determining a general analytical expression of the MIN and MAX operations. The potential use of these expressions in the framework of uncertain aggregation operators is illustrated with the two-additive Choquet integral.
Coronal and Root Caries in the Dentition of Adults in the United States, 1988–1991

Dental public health policy planning requires accurate and current information about the extent of caries in the United States population. These data are available from the caries examination from Phase 1 of the Third National Health and Nutrition Examination Survey, which found that 94% of adults in the United States show evidence of past or present coronal caries. Among the dentate, the mean number of decayed and filled coronal surfaces per person was 21.5. Dentate females had a lower number of untreated coronal tooth surfaces with caries (1.5), but a higher mean number of treated and untreated surfaces per person (22.7) than males, with scores of 2.1 and 20.2, respectively. Estimates for race-ethnicity groups were standardized by age and gender to control for population differences among them. Dentate non-Hispanic blacks (11.9) and Mexican-Americans (14.1) had half the number of decayed and filled coronal surfaces as non-Hispanic whites (24.3), but more untreated surfaces (non-Hispanic whites, 1.5; non-Hispanic blacks, 3.4; Mexican-Americans, 2.8). Mexican-Americans were most likely to be dentate, had the highest average number of teeth, and had 25% fewer decayed, missing, and filled coronal surfaces (37.6) than non-Hispanic blacks (49.2) and non-Hispanic whites (51.0). Root caries affected 22.5% of the dentate population. Blacks had the most treated and untreated root surfaces with caries (1.6), close to the value for Mexican-Americans (1.4). The score for non-Hispanic whites was 1.1. Untreated root caries is most common in dentate non-Hispanic blacks (1.5), followed by Mexican-Americans (1.2), with non-Hispanic whites (0.6) having the fewest untreated carious root surfaces. Race-ethnicity groups were disparate with respect to dental caries; effort is needed to treat active caries common in some population subgroups.
Amplification of pvmdr1 associated with multidrug-resistant Plasmodium vivax.

BACKGROUND Multidrug-resistant strains of Plasmodium vivax are emerging in Southeast Asia. METHODS In vitro drug susceptibility and pvmdr1 genotype were determined in P. vivax field isolates from Indonesia and Thailand. RESULTS Increased pvmdr1 copy number was present in 21% of isolates from Thailand (15/71) and none from Indonesia (0/114; P < .001). Compared with Indonesian isolates, the median IC(50) of Thai isolates was lower for chloroquine (36 vs. 114 nmol/L; P < .001) but higher for amodiaquine (34 vs. 13.7 nmol/L; P = .032), artesunate (8.33 vs. 1.58 nmol/L; P < .001), and mefloquine (111 vs. 9.87 nmol/L; P < .001). In 11 cryopreserved Thai isolates, those with increased pvmdr1 copy number had a higher IC(50) for mefloquine (78.6 vs. 38 nmol/L for single-copy isolates; P = .006). Compared with isolates with the wild-type allele, the Y976F mutation of pvmdr1 was associated with reduced susceptibility to chloroquine (154 nmol/L [range, 4.6-3505] vs. 34 nmol/L [range, 6.7-149]; P < .001) but greater susceptibility to artesunate (1.8 vs. 9.5 nmol/L; P = .009) and mefloquine (14 vs. 121 nmol/L; P < .001). CONCLUSIONS Amplification of pvmdr1 and single-nucleotide polymorphisms are correlated with susceptibility of P. vivax to multiple antimalarial drugs. Chloroquine and mefloquine appear to exert competitive evolutionary pressure on pvmdr1, similar to that observed with pfmdr1 in Plasmodium falciparum.
Binge drinking among Maori secondary school students in New Zealand: associations with source, exposure and perceptions of alcohol use.

AIM Describe factors associated with binge drinking among Maori secondary school students. METHOD Analysis of Maori sample (n=1702) from the 2007 national youth health survey. RESULTS Among current drinkers, 31.5% reported binge drinking (5-9 drinks) and 30.4% reported heavy binge drinking (greater than and equal to 10 drinks) in a 4-hour session in the past four weeks. Compared with non-binge drinkers, binge drinkers more frequently reported 'drinking alcohol was okay for people their age' (OR(binge) =1.9; OR(heavy binge) =2.4), p<0.0001), had friends that drank alcohol (OR(binge) =2.4; OR(heavy binge) =4.0, p<0.0001), had sourced alcohol from friends (OR(binge) =1.7; OR(heavy binge) =1.2, p=0.002) or from 'other adults' (OR(binge) =1.6; OR(heavy binge) =1.7 ; p=0.0004) and buy their own alcohol (OR(binge) =1.7; OR(heavy binge) =2.8, p<0.0001). Binge drinking was associated with poorer school performance, unsafe sex, unwanted sex, an injury, injuring someone else, motor vehicle crashes and 'doing things that could cause trouble'. Binge and heavy binge drinkers reported greater difficulty accessing drug and alcohol services (OR(binge) =2.30; OR(heavy binge) =4.97 p<0.0001). CONCLUSION Binge drinking is associated with a range of poor health and social outcomes for Maori youth. The associated poorer access to drug and alcohol services reveals an inequity requiring priority attention.
Reusing NoC-infrastructure for test data compression

Previous work on testing NoC-based systems has shown that the integrated network can be efficiently reused as test access mechanism (TAM). These approaches exploit the given infrastructure for data transportation. Beyond that, NoC-architectures for nanoscale systems also have to ensure a reliable communication by additional hardware and/or software measures. For example a cyclic redundancy check (CRC) may be added to protect the end-to-end communication between network resources. This paper presents an approach to reuse the CRC hardware for a compression scheme similar to LFSR-reseeding. The experimental results show that competitive compression ratios can be achieved at low extra cost. This way, core testing in NoC-based systems can benefit from test data compression even for standard cores without integrated decompressors.
Feedback regulators in normal and tumour tissues

Summary Regulation of cell behaviour and population size is presumed to be not unlike classical regulation in non-biological systems, i.e. it is controlled by the cybernetic principle of negative feedback whereby the performance of progenitor cells depends inversely on a signal from their product, the size of which is proportional to the mass of the product. This signal may be inhibitory, acting directly on the progenitor cells. Alternatively, it may operate via an indirect and integrated inhibitor/stimulator feedback loop in which the one influences the production of the other. Illustrations taken from the various phases of haemopoietic development show the operation of these loops. Haemopoietic stem cells are under the direct influence of both inhibitor and stimulator but it is a feedback signal from the stem cell population that dictates the production of the one rather than the other. A second inhibitor acting at the stem cell level is a low molecular weight tetrapeptide which blocks the entry of cells into DNA synthesis, thus protecting them during a regimen of treatment with an S-phase cytotoxic drug. Proliferation of the maturing cells is also inhibited by feedback products of their fully mature descendants. Here, the effect is one of cell cycle modulation, whereas in the stem cell population the inhibitor and stimulator effect an on/off switch. Attempts to characterize the molecules involved have been limited. A series of tri- to pentapeptides has been described for haemopoietic or epithelial cell inhibitors. A common feature of several is a pGlu-Glu end though whether this has any significance is not known. In tumours it has been shown that some ascites are self-limiting and treatment of small tumours with cell-free fluid from a mature growth blocks their further growth. It appears that many tumour cells produce the feedback signals characteristic of their normal counterparts but are themselves less sensitive to it. The same is true of transforming growth factor-β which is produced and detected by virtually all cell types. In this case, the factor, inhibiting in most cases, is produced in inactive form and achieves its target specificity by a localized capacity to activate it. Some tumours, while responding to exogenous active TGF-β are incapable of activating the latent molecule. It is concluded that the differential sensitivity of normal and neoplastic tissues to physiological feedback regulators is a potentially exploitable property in cancer therapy.
Mild traumatic brain injury is associated with reduced cortical thickness in those at risk for Alzheimer’s disease

Moderate-to-severe traumatic brain injury is one of the strongest environmental risk factors for the development of neurodegenerative diseases such as late-onset Alzheimer's disease, although it is unclear whether mild traumatic brain injury, or concussion, also confers risk. This study examined mild traumatic brain injury and genetic risk as predictors of reduced cortical thickness in brain regions previously associated with early Alzheimer's disease, and their relationship with episodic memory. Participants were 160 Iraq and Afghanistan War veterans between the ages of 19 and 58, many of whom carried mild traumatic brain injury and post-traumatic stress disorder diagnoses. Whole-genome polygenic risk scores for the development of Alzheimer's disease were calculated using summary statistics from the largest Alzheimer's disease genome-wide association study to date. Results showed that mild traumatic brain injury moderated the relationship between genetic risk for Alzheimer's disease and cortical thickness, such that individuals with mild traumatic brain injury and high genetic risk showed reduced cortical thickness in Alzheimer's disease-vulnerable regions. Among males with mild traumatic brain injury, high genetic risk for Alzheimer's disease was associated with cortical thinning as a function of time since injury. A moderated mediation analysis showed that mild traumatic brain injury and high genetic risk indirectly influenced episodic memory performance through cortical thickness, suggesting that cortical thinning in Alzheimer's disease-vulnerable brain regions is a mechanism for reduced memory performance. Finally, analyses that examined the apolipoprotein E4 allele, post-traumatic stress disorder, and genetic risk for schizophrenia and depression confirmed the specificity of the Alzheimer's disease polygenic risk finding. These results provide evidence that mild traumatic brain injury is associated with greater neurodegeneration and reduced memory performance in individuals at genetic risk for Alzheimer's disease, with the caveat that the order of causal effects cannot be inferred from cross-sectional studies. These results underscore the importance of documenting head injuries even within the mild range as they may interact with genetic risk to produce negative long-term health consequences such as neurodegenerative disease.