Element-resolved thermodynamics of magnetocaloric LaFe(13-x)Si(x).

By combination of two independent approaches, nuclear resonant inelastic x-ray scattering and first-principles calculations in the framework of density functional theory, we demonstrate significant changes in the element-resolved vibrational density of states across the first-order transition from the ferromagnetic low temperature to the paramagnetic high temperature phase of LaFe(13-x)Si(x). These changes originate from the itinerant electron metamagnetism associated with Fe and lead to a pronounced magneto-elastic softening despite the large volume decrease at the transition. The increase in lattice entropy associated with the Fe subsystem is significant and contributes cooperatively with the magnetic and electronic entropy changes to the excellent magneto- and barocaloric properties.

Treatment of refractory obesity in severely obese adults following management of newly diagnosed attention deficit hyperactivity disorder.

OBJECTIVE: To determine whether attention deficit hyperactivity disorder (ADHD) pharmacological treatment of severely obese subjects with newly diagnosed ADHD would result in sustained weight loss. DESIGN: Longitudinal clinical intervention study of the effects of ADHD medication on weight change over 466 days. SUBJECTS: 78 subjects (6 male, 72 female, mean age 41.3 years, BMI 42.7 kg m(-2)) out of 242 consecutively referred severely obese, weight loss refractory individuals were diagnosed as having ADHD. Sixty-five subjects received treatment and 13 remained as controls. METHODS: Standard screening tests identified subjects likely to have ADHD. A diagnosis was made in 78 subjects by semi-structured clinical interview. ADHD subjects were screened for comorbid conditions (binge eating disorder, mood disorder, sleep apnea, chronic pain, gastroesophageal reflux disease). Satisfactory resolution of symptoms of comorbid conditions was achieved prior to the introduction of pharmacotherapy for ADHD. Subjects not accepting, tolerating or remaining on ADHD medication served as controls. Weight was measured at sequential clinic visits after initiation of pharmacotherapy. RESULTS: Comorbid conditions were found to be highly prevalent (sleep apnea 56.4%, binge eating disorder 65.4%, mood disorder 88.4%). After an average of 466 days (s.d.=260) of continuous ADHD pharmacotherapy, weight change in treated subjects was -12.36% of initial weight and in controls +2.78%, P<0.001. Weight loss in treated subjects was 15.05 kg (10.35%) and weight gain 3.26 kg (7.03%) in controls, P<0.001. CONCLUSIONS: ADHD is a highly prevalent condition in the severely obese population. Treatment of ADHD is associated with significant long-term weight loss in individuals with a lengthy history of weight loss failure. This result is likely because of the positive effects of treatment on self-directedness, persistence and novelty-seeking behaviors. ADHD should be considered as a primary cause of weight loss failure in the obese. Individuals seeking medical or surgical weight loss should be evaluated for ADHD and treated appropriately before intervention. This may improve the outcome for medically managed patients and avoid complications in surgical subjects because of poor compliance with diet and supplement requirements.

Probing magnetic coupling between LnPc2 (Ln = Tb, Er) molecules and the graphene/Ni (111) substrate with and without Au-intercalation: role of the dipolar field.

Lanthanides (Ln) bis-phthalocyanine (Pc), the so-called LnPc2double decker, are a promising class of molecules with a well-defined magnetic anisotropy. In this work, we investigate the magnetic properties of LnPc2 molecules UHV-deposited on a graphene/Ni(111) substrate and how they modify when an Au layer is intercalated between Ni and graphene. X-ray absorption spectroscopy (XAS), and linear and magnetic circular dichroism (XLD and XMCD) were used to characterize the systems and probe the magnetic coupling between LnPc2 molecules and the Ni substrate through graphene, both gold-intercalated and not. Two types of LnPc2 molecules (Ln = Tb, Er) with a different magnetic anisotropy (easy-axis for Tb, easy-plane for Er) were considered. XMCD shows an antiferromagnetic coupling between Ln and Ni(111) even in the presence of the graphene interlayer. Au intercalation causes the vanishing of the interaction between Tb and Ni(111). In contrast, in the case of ErPc2, we found that the gold intercalation does not perturb the magnetic coupling. These results, combined with the magnetic anisotropy of the systems, suggest the possible importance of the magnetic dipolar field contribution for determining the magnetic behaviour.

Spin-communication channels between Ln(III) bis-phthalocyanines molecular nanomagnets and a magnetic substrate.

Learning the art of exploiting the interplay between different units at the atomic scale is a fundamental step in the realization of functional nano-architectures and interfaces. In this context, understanding and controlling the magnetic coupling between molecular centers and their environment is still a challenging task. Here we present a combined experimental-theoretical work on the prototypical case of the bis(phthalocyaninato)-lanthanide(III) (LnPc2) molecular nanomagnets magnetically coupled to a Ni substrate. By means of X-ray magnetic circular dichroism we show how the coupling strength can be tuned by changing the Ln ion. The microscopic parameters of the system are determined by ab-initio calculations and then used in a spin Hamiltonian approach to interpret the experimental data. By this combined approach we identify the features of the spin communication channel: the spin path is first realized by the mediation of the external (5d) electrons of the Ln ion, keeping the characteristic features of the inner 4 f orbitals unaffected, then through the organic ligand, acting as a bridge to the external world.

The influence of major histocompatibility complex class I antigens on tumor growth and metastasis.

The work described here demonstrates the importance of major histocompatibility complex class I antigens for the control of tumor growth and metastasis by the host's immune system. In certain murine tumor cells which have lost expression of H-2 class I antigens, a de novo expression of H-2 can be achieved by transfection with syngeneic class I genes. In contrast to the parental cells the transfected tumors do not grow any more in syngeneic mice, or in other cases they do not form metastases. The studies suggest that the de novo expression of the H-2 antigens renders the tumors highly immunogenic and leads to effective recognition of a tumor-associated antigen in conjunction with the transfected H-2 antigen. These conclusions were confirmed in other tumor systems. For example, separation of a heterogeneous tumor into clones expressing high or low amounts of H-2 showed that only the tumor cell with low H-2 grew well in syngeneic mice, whereas the H-2 high tumor clones were rejected. In other studies in vitro induction by IFN-gamma of H-2 antigen on H-2 negative tumors led to reduced tumor growth in vivo which was due to the increased immunogenicity. About 10% of human tumors are also low or defective for HLA class I expression and often these tumors appear to be more malignant. The class I negative tumors could either have arisen from class I low or negative tissues or are HLA loss variants which escaped the attack of the immune system. Altogether, our studies and the data of other laboratories demonstrate the important role of class I antigens for anti-tumor immunity and they suggest that modulation of class I expression by gene transfection or by induction with soluble mediators could be a useful tool for the manipulation of tumor immunity.

Fragile X expression in Martin-Bell syndrome, intellectually normal individuals, and neoplasia, interpreted by a viral hypothesis.

We present data on fragile X expression in lymphocytes obtained from the following patients: a university student, an infertile couple, 6 of 22 prostatic cancer patients, a meningioma patient, and members of families with meningioma and familial gliomas. All patients were of normal intelligence. In addition, we report 3 cases of central nervous system (CNS) tumors in more typical fragile X families. We suggest that the fragile X expression as well as the clinical findings may be caused by a viral (or similar) infection. The virus may require a receptor protein coded by one allele of a gene on the X chromosome.

On the meaning of fragile sites in cancer risk and development.

In the last few years, there has been increasing concern about the possible involvement of fragile sites in cancer risk and development. Patients with malignancies and family histories of cancer who presented with constitutional fragile sites are reported here. These findings are discussed with regard to the familial risk for cancer and the tissue specificity of the malignancy in relation to the different fragile sites. The hypothesis is advanced that these may be sites of viral DNA modification, probably representing areas where genes that are important for the metabolism of the virus are located. On the other hand, these genes may well be cellular (proto)oncogenes. We believe that fragile sites may increase the risk for cancer, not by being break-prone points at oncogene locations, but through more complex mechanisms that are not easy to predict.

Familial fragile 8q22 involved as a cancer breakpoint in cells of a large bowel tumor.

A familial fragile 8q22 and an interferon-induced fragile 16q22 were found in two sisters. Eight years previously, both sisters developed an endometrial adenocarcinoma and now one of them presented with an adenocarcinoma of the colon. An 8q22 deletion was found in all the cells of the colonic tumor and seemed to be the primary initiating change. Other nonrandom and possibly promoting aberrations were also present, among others, a 16q22 deletion. The possibility exists that a familial fragile 8q22 may predispose to cancer and a fragile 16q22 may have promoting capacities.

Involvement of chromosome 22 in a Merkel cell carcinoma in a patient with a previous meningioma.

The relatively simple cytogenetic findings in an aggressive metastatic Merkel cell carcinoma are reported. Deletion 2p was found in 100% of the cells. Nevertheless, this was considered a secondary (metastatic?) change because the same aberration has been found in several other kinds of malignancy. The involvement of chromosome 22 [del(22q) and -22] in 85% of the cells seemed more intriguing, considering the fact that the Merkel cell carcinoma followed a previous meningioma.

Inversion (16)(p13q22) in tumor cells of sigmoid colon.

We report on the cytogenetic findings in direct preparations of two tumors of the sigmoid colon. Respectively, they had a near-triploid and a near-tetraploid constitution and relative numerical and other inconstant chromosomal imbalances. The only constant chromosomal structural anomaly apparently was inversion of chromosome #16, inv(16)(p13q22), which was found in all the cells examined. This rearrangement has been found to be associated with a type of acute myelomonocytic leukemia type M4. We suggest that an etiologic clastogenic (and oncogenic) agent responsible for this rearrangement may eventually be the cause of various kinds of malignancy.

Marker chromosomes in a family with high incidence of cancer.

Two young sisters presenting with malignant or premalignant conditions inherited two marker chromosomes (a 13p- and a 16 with a fragile site at q22). Malignancy was reported in the family on both the mother's and father's side. According to data from the literature on similar markers and from our personal observations, a possible significance may be suggested for these markers. Search for markers must be encouraged in families with high incidence of cancer. Eventually, we may find markers which will help in understanding the processes of carcinogenesis and possibly indicate individuals at risk.

Cytogenetic study of patients with carcinoma of the colon and rectum: particular C-band variants as possible markers for cancer proneness.

A possible involvement of chromosomal heterochromatic polymorphisms in propensity to cancer has been considered and discussed by several investigators who studied groups of patients presenting with different forms of malignancy. We report a cytogenetic study on the circulating lymphocytes of patients suffering from colorectal carcinoma, most of whom were of European origin. Significantly increased incidence of polymorphisms of chromosomes #1 and #9 was found, especially partial inversions (PI). Emphasis is given to the problem of selecting adequate controls, which must be as homogeneous as possible.

Juxta-centromeric fragility of chromosomes 1, 2, 9, 16, and immunodeficiency. Special reference to the fragility of chromosome 2 and its oncogenic potential.

Juxta-centromeric fragility of chromosomes 1, 2, 9, 16, has been described at least thrice in unrelated patients in association with combined immunodeficiency. This association has been confirmed by our findings in both immunodeficient and cancer patients. In our opinion, both the fragility and the immunodeficiency are the results of persistent viral infections by certain DNA (i.e.: Herpes-, Papova-) viruses or RNA (retro-) viruses (i.e. HTLV), which are lymphotropic. The immunodeficiency may be due to virus-cell, cell to cell, or virus-virus interactions. According to our findings, centromeric fragility of chromosome 2 appears to have a particular oncogenic potential probably because of its location in proximity to immunoglobulins genes. We suggest that centromeric fragility of chromosomes 1, 2, 9, 16, may be one of the symptoms of an incipient Acquired Immunodeficiency Syndrome (AIDS) which will not necessarily develop fully.

Using theory to understand the multiple determinants of low participation in worksite health promotion programs.

Low participation at the employee or worksite level limits the potential public health impact of worksite-based interventions. Ecological models suggest that multiple levels of influence operate to determine participation patterns in worksite health promotion programs. Most investigations into the determinants of low participation study the intrapersonal, interpersonal, and institutional influences on employee participation. Community- and policy-level influences have not received attention, nor has consideration been given to worksite-level participation issues. The purpose of this article is to discuss one macrosocial theoretical perspective--political economy of health--that may guide practitioners and researchers interested in addressing the community- and policy-level determinants of participation in worksite health promotion programs. The authors argue that using theory to investigate the full spectrum of determinants offers a more complete range of intervention and research options for maximizing employee and worksite levels of participation.

Induction of assembly of MHC class I heavy chains with beta 2microglobulin by interferon-gamma.

Assembly of histocompatibility class I heavy chains with beta 2microglobulin (beta 2m) is known to be necessary for cell surface expression. Studies on the H-2 class I deficient but interferon-gamma (IFN-gamma) inducible fibrosarcoma BC2 and the lung carcinoma CMT 64.5 showed that after transfection with allogeneic H-2 class I genes the class I proteins are expressed, but only intracellularly and not on the cell surface. In spite of the presence of beta 2m in the cells no association of the transfected class I chain with beta 2m was observed. However, stimulation with IFN-gamma induced assembly and subsequent surface expression. These findings show that the assembly of class I heavy chains with beta 2m is not a spontaneous event but appears to be regulated by cellular mechanisms the nature of which is still unknown.

Partial monosomy of chromosome 2. Delineable syndrome of deletion 2 (q23-q31).

A malformed, severely retarded 20-year-old female is reported with deletion 2 (q23-q34) in mosaic. The clinical features are compared with those of other reported cases presenting partial monosomy 2q at the segment q23-q31. The stigmata are not very characteristic although a large constellation of features is in common and a definition of a partial monosomy 2 (q23-q31) syndrome seems possible. The features are: poor neurologic development and unresponsiveness to stimulation, growth and mental retardation, low set ears, antimongolian slant, ptosis, cataracts, median cleft of soft palate, severe scoliosis, flexion deformity of fingers, cleft between II and III toes, cardial defect.

[Studies of the nitrogen and carbon content of culture media and of mushrooms, as well as the free amino acid composition of myecelia and fruiting bodies of Lentinus edodes]. / Untersuchungen zum Stickstoff- und Kohlenstoffgehalt von Nährboden und Pilz sowie der Zusammensetzung freier Aminosäuren in Mycel und Fruchtkörpern von Lentinus edodes.

The level contents of nitrogen and carbon in the analysed nature substances may be considered the reason for the good growth of Lentinus edodes on this culture medium (sugar-beet molasses and sawdust). The separate parts of fruit-bodies are showing differences in contents of nitrogen, carbon and free amino-acids; the gills have the highest, the stalk the lowest concentration, that of the hats is taking a middle position. Young and old mycelia as well as the separate parts of fruit bodies are different out of total concentration also in composition of free amino acids. This may be a direction to development and transformations during the change from the vegetative to the reproductive phase.

Familial fragile site found at the cancer breakpoint (1)(q32). Inducibility by distamycin A, concomitance with fragile (16)(q22).

A normal baby was cytogenetically examined immediately after birth for the possible presence of a fragile (16)(q22), which had been found in her mother and in her retarded sister with a 46,XX;46,XX,del(16)(q22) mosaic karyotype. Distamycin A was added to the cultures to enhance the fragile (16)(q22) expression. The response of the baby to the action of distamycin A in vitro was much greater than that of her family members. A fragile (16)(q22) was induced in many cells as well as a fragile (1)(q32), which was also found in her mother. This fragile site, which is known to be a cancer breakpoint, has not been reported so far either to be familial or to be inducible by distamycin A. The concomitance of fragile (1)(q32) with fragile (16)(q22) and their possible significance are considered.

Non-random chromosomal aberrations in a complex leukaemic clone of a Bloom's syndrome patient.

Bloom's syndrome is one of the congenital disorders known to have increased frequency of acute leukaemia. The complex cytogenetic findings in the leukaemic cells of a 39-year-old male with Bloom's syndrome are described. These included a translocation t(7;17), missing 7q and 17p, a reciprocal translocation t(4;22); del 3q, del 8q22, del 20q, missing 12 and missing Y. In the same patient a missing Y had been noted 10 years previously in 15% of his peripheral blood lymphocytes.

Familial syndrome with some features of the Langer-Giedion syndrome, and paracentric inversion of chromosome 8, inv 8 (q11.23----q21.1).

A family is reported with an autosomal dominant inherited syndrome presenting some of the typical features of the tricho-rhino-phalangeal syndrome type II (TRP II) or Langer-Giedion syndrome. The critical region for the expression of the syndrome seems to be at band 8q24.1. In the affected members of the family reported here, anomaly of chromosome 8 was noted, involving however the proximal part of the 8 long arm, which was interpreted as a paracentric inversion. Whether the anomaly is causally or only casually related to the syndrome is a matter of discussion.