The 'dark phase' in Sr2Ir1-xRhxO4revealed by Seebeck and Hall measurements.

It was found that, although isovalent, Rh substituted for Ir in Sr2IrO4may trap one electron inducing effective hole doping of Ir sites. Transport and thermoelectric measurements on Sr2Ir1-xRhxO4single crystals presented here reveal the existence of an electron-like contribution to transport, in addition to the hole-doped one. As no electron band shows up in ARPES measurements, this points to the possibility that this hidden electron may delocalize in disordered clusters.

Magnetic critical properties and basal-plane anisotropy of Sr2IrO4.

The anisotropic magnetic properties of Sr2IrO4 are investigated, using longitudinal and torque magnetometry. The critical scaling across T(c) of the longitudinal magnetization is that expected for the 2D XY universality class. Modeling the torque for a magnetic field in the basal plane, and taking into account all in-plane and out-of-plane magnetic couplings, we derive the effective fourfold anisotropy K4 ≈ 1 × 10(5) erg mol(-1). Although larger than for the cuprates, it is found to be too small to account for a significant departure from the isotropic 2D XY model. The in-plane torque also allows us to set an upper bound for the anisotropy of a field-induced shift of the antiferromagnetic ordering temperature.

Ordering in Heisenberg spin glasses.

For five different Heisenberg spin glass systems, torque experiments were performed in applied magnetic fields up to 4 T. The Dzyaloshinski-Moriya random anisotropy strengths, the in-field torque onset temperatures, and the torque relaxation were measured. Critical exponents were estimated independently using a standard protocol. The data are strong evidence for a true spin glass ordered state which survives under high applied magnetic fields; they can be interpreted consistently in terms of a chiral ordering model with replica symmetry breaking as proposed by Kawamura and co-workers.

Rheumatoid factors from the peripheral blood of two patients with rheumatoid arthritis are genetically heterogeneous and somatically mutated.

We report the DNA sequences of the heavy and light chain immunoglobulin genes of 11 monoclonal rheumatoid factor (RF)-secreting lines derived from the peripheral blood of two patients with rheumatoid arthritis (RA). It is evident from immunogenetic analysis of these lines that RA-associated RF activity can arise from a wide variety of heavy and light chain genes and gene combinations. Although the RF response from our two patients shows a bias in gene usage toward those genes used to encode monoclonal RF, particularly VkIII, relatively few of these RFs are reactive with the monoclonal antiidiotypes 6B6.6 and 17.109 that define VkIII germline-encoded light chains and the loss of this idiotypic reactivity is clearly related to somatic mutation. Finally, RFs derived from peripheral blood of RA patients show a similar heterogeneity of epitope binding to Fc as that seen for synovium-derived RF and some are clearly different in binding specificity from the restricted RF population found in patients with B cell malignancies. Somatic mutations as well as different VH/VL combinations contribute to the heterogeneity in the binding patterns of these RA-derived RF.

Colchicine suppression of local inflammation due to calcinosis in dermatomyositis and progressive systemic sclerosis.

Two girls, one with progressive systemic sclerosis and a second with dermatomyositis, developed calcinosis in the skin of the prepatellar area. Calcinosis was accompanied by local inflammation and skin ulceration. Oral colchicine therapy in a dosage of 1 mg per day was followed within two months by significant regression of local inflammation and healing of the skin ulcers.

Acquired immunodeficiency with reversed T4/T8 ratios in infants born to promiscuous and drug-addicted mothers.

A new syndrome of acquired immunodeficiency has been identified in seven children who were small for gestational age at birth and subsequently have exhibited failure to thrive, lymphadenopathy, parotitis, hepatosplenomegaly, interstitial pneumonia, and recurrent infections. All have a profound cell-mediated immunodeficiency with reversed T4/T8 ratios. Six are hypergammaglobulinemic and one has low IgG levels. The mothers of five of the seven children are sexually promiscuous and/or drug addicts. Three mothers have an immunodeficiency similar to that found in their infants. One of them died at age 33 years with a diagnosis of acquired immunodeficiency syndrome. In five of the children and in three of their mothers, there is evidence of a persistent Epstein-Barr virus (EBV) infection. We speculate that a perinatal or in utero transmission of EBV can induce an "infectious immunodeficiency." The clinical, histopathologic, and immunologic features resemble those described in adult homosexuals and drug addicts.

Management of recurrent invasive Haemophilus influenzae infection.

A 4 1/2-month-old infant had three separate episodes of invasive Haemophilus influenzae type b infection and did not produce antibody to the capsular polysaccharide of H influenzae b. Immunologic evaluation disclosed normal immunoglobulin and complement concentrations and normal T-cell number and function. In view of the persistent presence of type-specific capsular polysaccharide of H influenzae b (polyribophosphate [PRP]) in blood serum without any detectable anti-PRP antibody for 30 days following H influenzae b meningitis, monthly treatment with immune human serum globulin was undertaken until spontaneous production of anti-PRP antibody occurred. The patient's 4-year-old sibling was found to be a nasopharyngeal carrier and may have been a source for reinfection. A search for possible family carriers should be conducted in evaluating the conditions of patients with recurrent invasive H influenzae b infection. In addition, temporary treatment with immune human serum globulin should be considered.