Miracle-dz/UniFAR-FTUs huggingface dataset:
Increased body mass index makes an impact on brain white-matter integrity in adults with remitted first-episode mania

Background Obesity is increasingly prevalent in bipolar disorder (BD) but data about the impact of elevated body mass index (BMI) on brain white-matter integrity in BD are sparse. Based on extant literature largely from structural magnetic resonance imaging (MRI) studies, we hypothesize that increased BMI is associated with decreased fractional anisotropy (FA) in the frontal, temporal, parietal and occipital brain regions early in the course of BD. Method A total of 26 euthymic adults (12 normal weight and 14 overweight/obese) with remitted first-episode mania (FEM) and 28 controls (13 normal weight and 15 overweight/obese) matched for age, handedness and years of education underwent structural MRI and diffusion tensor imaging scans. Results There are significant effects of diagnosis by BMI interactions observed especially in the right parietal lobe (adjusted F 1,48 = 5.02, p = 0.030), occipital lobe (adjusted F 1,48 = 10.30, p = 0.002) and temporal lobe (adjusted F 1,48 = 7.92, p = 0.007). Specifically, decreased FA is found in the right parietal (F 1,23 = 5.864, p = 0.023) and occipital lobes (F 1,23 = 4.397, p = 0.047) within overweight/obese patients compared with normal-weight patients with FEM. Compared with overweight/obese controls, decreased FA is observed in right parietal (F 1,25 = 6.708, p = 0.015), temporal (F 1,25 = 10.751, p = 0.003) and occipital (F 1,25 = 9.531, p = 0.005) regions in overweight/obese patients with FEM. Conclusions Our findings suggest that increased BMI affects temporo-parietal-occipital brain white-matter integrity in FEM. This highlights the need to further elucidate the relationship between obesity and other neural substrates (including subcortical changes) in BD which may clarify brain circuits subserving the association between obesity and clinical outcomes in BD.
Lymph Node Metastasis From Soft Tissue Sarcoma in Adults Analysis of Data From a Prospective Database of 1772 Sarcoma Patients

To examine the natural history of lymph node metastasis from sarcomas and the utility of therapeutic lymphadenectomy, clinical histories of all adult patients identified by a prospective sarcoma database for the 10-year period July 1982 to July 1991 were examined. Of the 1772 sarcoma patients, 46 (2.6%) were identified with lymph node metastasis. Median follow-up of all patients from diagnosis of lymph node metastasis was 12.9 months (range, 0 to 100 months). Median survival for nonsurvivors was 12.7 months (range, 0 to 40.7). The tumor types with the highest incidence of lymph node metastasis are angiosarcoma (5/37 total cases; 13.5%), embryonal rhabdomyosarcoma (ERMS) (12/88 total cases; 13.6%), and epithelioid sarcoma (2/ 12 total cases; 16.7%). Lymph node metastasis from visceral primary (p = 0.004) and malignant fibrous histiocytomas (p = 0.006) were associated with particularly poor prognosis. Thirty-one patients underwent radical, therapeutic lymphadenectomy with curative intent, whereas 15 patients had less than curative procedures, in most cases biopsy only. Patients not treated with radical lymphadenectomy had a median survival of 4.3 months (range, 1 to 32) whereas radical lymphadenectomy was associated with a 16.3 month median survival and the only long-term survivors (46% 5-year survival by Kaplan-Meier). The authors conclude that lymph node metastases from sarcoma are rare in adults, but vigilance is warranted, especially in angiosarcoma, ERMS, and epithelioid subtypes. Radical lymphadenectomy is appropriate treatment for isolated metastasis to regional lymph nodes and may provide long-term survival.
Lymphocyte beta 2-adrenoceptors mirror precisely beta 2-adrenoceptor, but poorly beta 1-adrenoceptor changes in the human heart.

To study the relationship of changes in human lymphocyte beta-adrenoceptors to changes potentially occurring in solid tissues we studied 16 patients undergoing elective coronary artery bypass grafting and determined the density of lymphocyte beta 2-adrenoceptors [by (-)125I-iodocyanopindolol (ICYP) binding] in comparison to beta-adrenoceptor density and responsiveness (contractile responses to isoprenaline) in the corresponding right atria. Lymphocyte beta 2-adrenoceptor density (with a range of 278-2442 ICYP binding sites/cell) was significantly correlated with beta-adrenoceptor density in the corresponding atria (54.8-171.6 fmol ICYP bound/mg protein, r = 0.784, P less than 0.001). In these atria the levels of beta 1- and beta 2-adrenoceptors (assessed by non-linear regression analysis of competition curves of the selective beta 2-adrenoceptor antagonist ICI 188,551 with ICYP binding) were approximately . 70 and 30%, respectively. Lymphocyte beta 2-adrenoceptor density, however, correlated significantly better with atrial beta 2-adrenoceptor (r = 0.8441; P less than 0.001) than beta 1-adrenoceptor (r = 0.6226, P less than 0.05) density. On 12 of the 16 atria (electrically driven with 1 Hz at 37 degrees C) isoprenaline (10(-9) to 3 X 10(-6) mol/l) caused positive inotropic effects. The maximum increase in contractile force evoked by saturating concentrations of isoprenaline (mean: 3.52 +/- 0.62 mN), however, correlated equally well with beta 1- and beta 2-adrenoceptor density in the corresponding atria (r = 0.6834 and 0.6567, respectively). These results indicate that changes in lymphocyte beta 2-adrenoceptors can be taken as a precise index of changes of beta 2-adrenoceptors in other (solid) tissues; beta 1-adrenoceptor alterations, however, are only poorly reflected in the lymphocytes.
Spectral‐efficient resource allocation for mixed services in OFDMA‐based 5G heterogeneous networks

One of the principal thrusts of proposed fifth‐generation networks is the provisioning of mixed services or heterogeneous quality of service, which includes delay‐sensitive and delay‐tolerant services. Guaranteeing the fairness in data rate among end users in such a complex network brings many challenges. In this paper, we consider heterogeneous quality of service and fairness in the problem of spectrally efficient resource allocation in orthogonal frequency‐division multiple access (OFDMA)‐based fifth‐generation heterogeneous networks with femtocells. We aim to maximize the total capacity of all femtocells while satisfying the following: fairness constraint for delay‐tolerant users, minimum throughput for delay‐sensitive users, cross‐tier interference threshold of femtocell heterogeneous networks, and exclusive property of OFDMA subchannels. The formulated problem is combinatorial and nonconvex due to the integer constraint of OFDMA subchannels and the nonaffine equality constraint of the fairness. To make the problem more tractable, we propose to maximize the overall throughput over instantaneous data rate instead of power and subchannel. By doing this, the fairness equality becomes affine on instantaneous data rate. The feasible domain of the problem is redefined with the constraints of subchannels readily included. The transformed problem takes the standard convex form, which is much simpler and is easily solved using the Lagrangian dual method. The proposed algorithm has a low complexity and provides a higher spectral efficiency compared with existing algorithms.
Bone morphogenetic protein rescues the lack of secondary cartilage in Runx2‐deficient mice

Secondary cartilages including mandibular condylar cartilage have unique characteristics. They originate from alkaline phosphatase (ALP)‐positive progenitor cells of the periosteum, and exhibit characteristic modes of differentiation. They also have a unique extracellular matrix, and coexpress type I, II and X collagens. We have previously shown that there is a total absence of secondary cartilages in Runx2‐deficient (Runx2–/–) mice. To clarify whether Runx2 is essential for chondrocytic differentiation of secondary cartilages, we performed an organ culture system using mandibular explants derived from Runx2–/– mice at embryonic day 18.0. Since mRNA for bone morphogenetic protein 2 (BMP2) was strongly expressed in osteoblasts of condylar anlagen in wild‐type mice, and was down‐regulated in those of Runx2–/– mice, we chose to investigate BMP2 effects on secondary cartilage formation. Condensed mesenchymal cells of mandibular condylar anlagen in precultured explants were ALP‐positive and expressed type I collagen and Sox9. After culture with recombinant human (rh) BMP2, chondrocytic cells showing ALP activity and expressing Sox5, Sox9, and type I and II collagens, appeared from mesenchymal condensation. This expression profile was comparable with the reported pattern of chondrocytes in mouse secondary cartilages. However, chondrocyte hypertrophy was not observed in the explants. These findings indicate that BMP2 partially rescued chondrocyte differentiation but not chondrocyte hypertrophy in secondary cartilage formation in Runx2–/– mice. Runx2 is required for chondrocyte hypertrophy in secondary cartilage formation, and it is likely that BMP2, which is abundantly secreted by osteoblasts in condylar anlagen, contributes to the early process of secondary cartilage formation.
Bone Grafts to the Nose in Binder's Syndrome (Maxillonasal Dysplasia): A Follow‐Up of Eleven Patients with the Use of Profile Roentgenograms

&NA; Bone grafts are used to lengthen the dorsum and elevate the tip of the nose in patients with Binder's syndrome. Disappointing long‐term results in some patients generally have been assumed to be a result of resorption and/or displacement of the grafts. Treatment outcome was studied in 11 patients with the use of serial profile roentgenograms. At 40 months, the mean values after surgery were reduction of the initial transplant length by 28 percent and reduction of the transplant angle by 4 degrees. The initial nose length was increased by 1 mm, and nose tip projection was increased by 2 mm. Although the mean changes of nose length and nose tip projection seemed small, treatment outcome varied considerably between patients. In contrast with earlier assumptions, no correlation could be found between the degree of transplant resorption and/or displacement and the effect of surgery on nose length and nose tip projection. (Plast. Reconstr. Surg. 101: 297, 1998.)
The Role of Cryptopatch‐Derived Intraepithelial Lymphocytes in the Development of Chronic Ileocecitis

Lympho‐haemopoietic progenitors residing in murine gut cryptopatches (CPs) have been shown to generate intestinal extrathymic intraepithelial lymphocytes (IELs). However, the role of CPs in the development of intestinal inflammation remains unclear. To investigate the role of CPs in the development of intestinal inflammation, we examined SAMP1/Yit mice, which spontaneously develop a chronic intestinal inflammation localized to the terminal ileum and cecum. Here, we showed the sharp correlation between the disease onset and the decreased number of CPs, resulting in decreased number of both thymus‐independent IELs including T‐cell receptor γδ+ (TCRγδ+) and CD8αα+TCRαβ+ cells but not thymus‐dependent CD8αβ+TCRαβ+ and CD4+TCRαβ+ cells in SAMP1/Yit mice. These data provide the first suggestion that thymus‐independent IELs derived from CP might play protective role against the onset and the development of intestinal inflammation.
Metabolism of drugs and carcinogens by human liver enzymes.

Human liver contains enzyme systems which catalyze the ring hydroxylation of 3,4-benzpyrene, the side chain oxidation of pentobarbital, the O-dealkylation of acetophenetidin and the N-dealkylation of 3-methyl-4-monomethylaminoazobenzene. The rate of metabolism of these substrates by hepatic enzymes was compared in man and rat. The enzyme system which hydroxylates 3,4-benzpyrene was studied in detail. This enzyme system in man is similar to that found in the rat; both are localized in the microsomal fraction and require reduced triphosphopyridine nucleotide (NADPH) for activity. Methods are described for measuring oxidative microsomal enzyme activity in small samples of human liver.
Differential obesity indices identify the metabolic syndrome in Black men and women in Cape Town: the CRIBSA study.

AIMS To determine the obesity indices, specifically waist circumference (WC), that identified ≥2 other metabolic syndrome (MS) components (2009 criteria) in 25- to 74-year-old Africans in Cape Town. METHODS Data were collected from a cross-sectional sample by administered questionnaires, clinical measurements and biochemical analyses. The obesity cut points were estimated by the Youden Index. Logistic regression analyses determined whether obesity cut points identifying ≥2 MS components occurred at true inflection points. RESULTS Among the 1099 participants, the calculated cut points and 95% confidence intervals (CI) were: men, WC 83.9 cm (81.6-86.2), waist-to-hip ratio (WHR) 0.89 (0.87-0.90), waist-to-height ratio (WHtR) 0.50 (0.48-0.52) and body mass index (BMI) 24.1 kg/m(2) (22.0-26.1); women, WC 94.0 cm (92.6-95.3), WHR 0.85 (0.83-0.87), WHtR 0.59 (0.57-0.60) and BMI 32.1 kg/m(2) (29.7-34.6). Raised WC was significantly associated with ≥2 MS components in men: WC 84.0-93.9 cm (odds ratio (OR): 3.19, 95% confidence interval (CI): 1.73-5.85) and WC ≥94.0 cm (OR: 8.50, 95% CI: 4.44-16.25) compared with WC <84.0 cm, and in women: WC 80.0-93.9 cm (OR: 2.93, 95% CI: 1.32-6.54) and WC ≥94.0 cm (OR: 5.33, 95% CI: 2.40-11.85) compared with WC <80.0 cm. In the logistic model with BMI for women, obesity (OR: 3.60, 95% CI: 1.82-7.10) but not overweight (P = 0.063) was significantly associated with ≥2 MS components. CONCLUSIONS Obesity cut points for Africans should be re-evaluated and adjusted accordingly.
The Cbl family proteins: Ring leaders in regulation of cell signaling

The proto‐oncogenic protein c‐Cbl was discovered as the cellular form of v‐Cbl, a retroviral transforming protein. This was followed over the years by important discoveries, which identified c‐Cbl and other Cbl‐family proteins as key players in several signaling pathways. c‐Cbl has donned the role of a multivalent adaptor protein, capable of interacting with a plethora of proteins, and has been shown to positively influence certain biological processes. The identity of c‐Cbl as an E3 ubiquitin ligase unveiled the existence of an important negative regulatory pathway involved in maintaining homeostasis in protein tyrosine kinase (PTK) signaling. Recent years have also seen the emergence of novel regulators of Cbl, which have provided further insights into the complexity of Cbl‐influenced pathways. This review will endeavor to provide a summary of current studies focused on the effects of Cbl proteins on various biological processes and the mechanism of these effects. The major sections of the review are as follows: Structure and genomic organization of Cbl proteins; Phosphorylation of Cbl; Interactions of Cbl; Localization of Cbl; Mechanism of effects of Cbl: (a) Ubiquitylation‐dependent events: This section elucidates the mechanism of Cbl‐mediated downregulation of EGFR and details the PTK and non‐PTKs targeted by Cbl. In addition, it addresses the functional requirements for E3 Ubiquitin ligase activity of Cbl and negative regulation of Cbl‐mediated downregulation of PTKs, (b) Adaptor functions: This section discusses the mechanisms of adaptor functions of Cbl in mitogen‐activated protein kinase (MAPK) activation, insulin signaling, regulation of Ras‐related protein 1 (Rap1), PI‐3′ kinase signaling, and regulation of Rho‐family GTPases and cytoskeleton; Biological functions: This section gives an account of the diverse biological functions of Cbl and includes the role of Cbl in transformation, T‐cell signaling and thymus development, B‐cell signaling, mast‐cell degranulation, macrophage functions, bone development, neurite growth, platelet activation, muscle degeneration, and bacterial invasion; Conclusions and perspectives. J. Cell. Physiol. 209: 21–43, 2006. © 2006 Wiley‐Liss, Inc.
Commentary: 'Diseases of the world': from epidemiology to etiology of child and adolescent psychopathology--a commentary on Polanczyk et al. (2015).

If you are an epidemiologist, professionally interested in patterns of the distribution of disease in time and space, the first question you will be asked is ‘how many? ’ What is the ‘prevalence rate’ of ADHD? How many children have autism? The second question will be ‘are there more nowadays? ’ Is there an epidemic of childhood depression? Is the rate of conduct disorder increasing? This seems to be the main use that clinicians and clinical researchers make of epidemiology. So epidemiology is seen as important for some purposes but, somehow, not scientifically relevant to the real job of treatment. According to this view, epidemiology's value lies in telling us how bad a problem is (the ‘burden of disease’), how many affected people are getting treatment, and what the likely costs are. All useful stuff, but not getting us any nearer to the holy grail of understanding causes and cures of the ‘diseases of the world’1. In their ‘meta-analysis of the worldwide prevalence of mental disorders in children and adolescents’, Polanczyk and colleagues (Polanczyk et al., 2015, this issue) demonstrate just how partial and mistaken this view of epidemiology is. Polanczyk et al. have indeed provided a most valuable and thorough review of the descriptive issues that bureaucrats obsess about. But in the process they have illuminated several areas that are of real importance for the etiologic questions that scientists need to have answered if we are to make breakthroughs in the treatment and prevention of child and adolescent psychopathology.
Clear‐cell papillary renal cell carcinoma: 24 cases of a distinct low‐grade renal tumour and a comparative genomic hybridization array study of seven cases

Adam J, Couturier J, Molinié V, Vieillefond A & Sibony M (2011) Histopathology58, 1064–1071 Clear‐cell papillary renal cell carcinoma: 24 cases of a distinct low‐grade renal tumour and a comparative genomic hybridization array study of seven cases
An Exception to the Apparent Relationship Between Stress and Fluctuating Dental Asymmetry

Several authors have observed an apparent relationship between the level of environmental stress and the magnitude of fluctuating dental asymmetry. In general, asymmetry has been less in modern human populations compared to earlier hominid populations (Suarez, Am J Phys Anthrop 41:41 1416, 1974; Doyle and Johnston, Am J Phys Anthrop 46:127-134, 1977; Perzigian, Am J Phys Anthrop 47:81-88, 1977). Data presented by Suarez indicate that fluctuating dental asymmetry is less in a modern white population than in a Neanderthal sample. Suarez suggests inbreeding among Neanderthals as a possible explanation. Doyle and Johnston present additional information showing asymmetry in Eskimo and Pueblo Indian samples to be greater than in modern whites. They attribute this to greater stress upon the Eskimos and the Pueblo Indians, who were less able to control their environment than the more technologically advanced modern white population. Perzigian presents data showing greater asymmetry in a hunting and gathering Archaic American Indian population (Indian, Knoll, ca. 4000-2500 B.C.) than in a pooled sample of two agricultural American Indian populations (Campbell and Larson, ca. 1400-1800 A.D.). Asymmetry in the agricultural Amerind population was not significantly different from that in a modern cadaver collection (the Hamann-Todd collection). Perzigian hypothesizes that the reduction in asymmetry is due to the alleviation of metabolic stress resulting from fewer and less plentiful food resources of the non-agricultural Indian Knoll population. Research on the dentition of a population of 208 white children from the University School Growth Study of the University of Michigan has provided data which appear to be at variance with
Muscle Nogo‐A: a marker for amyotrophic lateral sclerosis or for denervation?

Pradat and colleagues in a recent study suggest that the presence of Nogo-A immunoreactivity in muscle biopsies can be used for early detection and diagnosis of amyotrophic lateral sclerosis (ALS). The study represents a continuation and extension of a number of previous studies. Thus, Nogo-A was previously suggested as a potential therapeutic target in ALS because genetic ablation of Nogo-A moderately prolongs life in a mouse model of ALS, and overexpression of Nogo-A in wild-type muscle fibers leads to destabilization of neuromuscular junctions and retraction of the nerve terminals. Previous studies have also suggested that high levels of Nogo-A are expressed in skeletal muscles of patients with ALS and of mice in an animal model of ALS. The levels of Nogo-A expression correlate with the severity of the disease. For Nogo-A to serve as an accurate and specific biomarker for ALS, it is important to show that increased expression is not a mere consequence of muscle denervation. Thus, Pradat and colleagues, as well as Harel and Strittmatter in an editorial comment, refer to a previous study that reports no increased levels of Nogo-A messenger RNA after denervation. We would like to make the scientific and medical communities aware of a study in which we clearly show that Nogo-A messenger RNA and protein are upregulated in denervated mouse hind-limb muscles and in denervated mouse hemidiaphragm muscle. We believe that it is important to make the scientific and medical communities aware of this study because it implies that increased muscle Nogo-A expression in ALS may be a result of the presence of denervated muscle fibers in the muscles. This would explain the correlation of Nogo-A expression with severity of the disease because more muscle fibers are denervated in advanced stages of the disease. The finding that overexpression of Nogo-A in wild-type muscle fibers leads to destabilization of neuromuscular junctions and retraction of the nerve terminals, although interesting in itself, may be biologically insignificant if only denervated muscle fibers express high levels of Nogo-A. Taking all published data into consideration, we conclude that it is premature to suggest Nogo-A as a specific biomarker for ALS or as a therapeutic target in ALS.
Interaction between the premotor processes of eye and hand movements: Possible mechanism underlying eye–hand coordination

Abstract Interaction between the execution process of eye movement and that of hand movement must be indispensable for eye–hand coordination. The present study investigated corticospinal excitability in the hand muscles during the premotor processes of eye and/or hand movement to elucidate interaction between these processes. Healthy humans performed a precued reaction task of eye and/or finger movement and motor-evoked potentials in the hand muscles were evoked in the reaction time. Leftward eye movement suppressed corticospinal excitability in the right abductor digiti minimi muscle only when little finger abduction was simultaneously executed. Corticospinal excitability in the first dorsal interosseous muscle was not suppressed by eye movement regardless of whether or not it was accompanied by finger movement. Suppression of corticospinal excitability in the hand muscles induced by eye movement in the premotor period depends on the direction of eye movement, the muscle tested, and the premotor process of the tested muscle. The suppression may reflect interaction between the motor process of eye movement and that of hand movement particularly active during eye–hand coordination tasks during which both processes proceed.