Combined detection of uMCP-1 and uTWEAK for rapid discrimination of severe lupus nephritis.

Reliable markers for the rapid discrimination of severe renal damage remain a vital concern for lupus nephritis (LN). To determine a better tool for kidney damage detection, the present study compared the evaluation ability of novel urinary cytokines and chemokines (namely urinary monocyte chemoattractant protein 1 (uMCP-1), tumor necrosis factor-like weak inducer of apoptosis (uTWEAK)) with traditional serum or urinary markers (namely urinary alpha 1-microgrobulin (uα1-MG), beta 2-microglobulin (uß2-MG) and serum complement C3 (C3), complement C4 (C4), creatinine (Cr), blood urea nitrogen (BUN) and cystatin C (Cys C)) in discriminating LN renal damage. Correlations between markers with Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) renal SLEDAI scores, biopsy activity index (BAI) and biopsy chronicity index (BCI) scores were evaluated. Receiver operating characteristic (ROC) curves were generated to evaluate a single or combined model in discriminating active renal involvement (rSLEDAI scores > 0) and patients with poor pathological outcome (BAI scores ≥ 7). uMCP-1 and uTWEAK possess higher correlation coefficients with renal damage and larger areas under ROC curves (AUCs) than other markers. A combined model of uMCP-1 and uTWEAK showed an AUC of 0.887, sensitivity of 86.67% and specificity of 80.00% to discriminate active LN, and an AUC of 0.778, sensitivity of 75.00% and specificity of 81.82% to discriminate LN with poor outcome, which are better than the utility of any markers individually.

Protein tyrosine kinase regulates α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor trafficking induced by acute hypoxia in cultured brainstem neurons.

This study was performed to investigate the modulation effect of protein tyrosine kinase on postsynaptic a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor trafficking induced by acute hypoxia in cultured brainstem neurons. The cultured neurons were exposed to 1% O2 and the expression of AMPA receptor subunit GluR2 on the cell surface was significantly increased, while total GluR2 was not markedly changed. Furthermore, the hypoxia-induced increase in GluR2 expression on the cell surface was partially blocked by the protein tyrosine kinase membrane-permeable inhibitor genistein. In contrast, both the protein tyrosine kinase agonist nerve growth factor and protein tyrosine phosphatase inhibitor vanadate promoted the hypoxia-induced increase of GluR2 expression on cell surface. Moreover, GluR2 could be phosphorylated by tyrosine under normoxia and hypoxia conditions in vitro on brainstem neurons, and tyrosine phosphorylation of GluR2 was significantly stronger under hypoxia conditions. Our results indicate that acute hypoxia induces the AMPA receptor subunit GluR2 to rapidly migrate to the cell membrane to modify the strength of the synapse. This study indicates that tyrosine phosphorylation of the receptor is an important pathway regulating the rapid migration of GluR2 in the postsynaptic domain induced by hypoxia.

[Changes of brain pain center and default mode network an electro acupuncture in Weizhong and Dachangshu acupoints: a task-fMRI study].

OBJECTIVE: To investigate the functional brain pain center and default mode network response to electro acupuncture stimulate in weizhong acupoints(BL40) and dachangshu acupoints(BL25). METHODS: During January to February 2015, volunteers were enrolled in this study from the staff and student interns of Gansu Province Traditional Chinese Medicine Hospital. A total of 20 healthy, right-handed subjects, male 9, female 11, age (23±3) years, participated in this study. Block design task functional magnetic resonance imaging(fMRI) 3.0 T was performed in all subjects by electro acupuncture stimulating at BL40 and BL25 from the same experienced acupuncturist.The needle connected electric acupuncture apparatus through tow long coaxial-cable. A block design with five 120 s blocks of rest time (OFF block, electric acupuncture turn off ) interspersed between five 60 s blocks of stimulation (ON block, electric acupuncture turn on) fMRI scan. Magnetic resonance data of brain function was collected and FSL(fMRI Software Library) software was used to analyze the data. RESULTS: All subjects' data were analyzed except 2 cases whose head movement were more than 2 mm. Activated brain function regions by electro acupuncture stimulate included temporal lobe lateral sulcus, lobus insularis, thalamus, supramarginal gyrus, prefrontal medial frontal gyrus. Negative activated brain regions included middle frontal gyrus, parahippocampal gyrus, cingulate cortex abdominal segment, parietal cortex.The functional pain central and default mode network were changed when electro acupuncture stimulate in(BL40) and(BL25). CONCLUSION: There are several brain activation regions and negative activated brain regions when administering electro acupuncture stimulation at BL40 and BL25.

International Society of Blood Transfusion Working Party on red cell immunogenetics and blood group terminology: Cancun report (2012).

The International Society of Blood Transfusion Working Party on red cell immunogenetics and blood group terminology convened during the International congress in Cancun, July 2012. This report details the newly identified antigens in existing blood group systems and presents three new blood group systems.

Genetic and functional analyses describe a novel 730delG mutation in the KEL gene causing K0 phenotype in a Taiwanese blood donor.

AIMS/OBJECTIVES: The purpose of this study was to explore the molecular basis of the K0 phenotype of a Taiwanese blood donor found to have anti-Ku alloantibodies. BACKGROUND: With respect to Kell blood group antigens, almost all Taiwanese have the (K-, k+) phenotype. MATERIALS AND METHODS: Alloantibody identification and KEL antigen typing were performed. Enzymatic function assays were carried out to detect the Kell glycoprotein on RBCs. The KEL genes were sequenced to detect genetic variation. To determine the origin of this novel allele, family studies were conducted. RESULTS: The alloantibody was identified as anti-Ku. The donor was typed K0 . The KEL gene-sequencing data revealed that this K0 donor is a compound heterozygote with two different null alleles. He bears a novel 730delG mutation in one allele. Family studies suggested that the donor inherited the 730delG mutation from his father. The endothelin-converting activity assay indicated that his RBCs had no functional Kell glycoprotein. Other family members who had only one null allele with the 730delG mutation had the phenotype (K-, k+). CONCLUSION: For blood transfusion safety, it is important to establish an effective screening algorithm to identify rare phenotypes, such as the K0 phenotype, and to establish a database of rare blood groups.

Enhanced intestinal transepithelial antigen transport in allergic rats is mediated by IgE and CD23 (FcepsilonRII).

We previously reported that active sensitization of rats resulted in the appearance of a unique system for rapid and specific antigen uptake across intestinal epithelial cells. The current studies used rats sensitized to horseradish peroxidase (HRP) to define the essential components of this antigen transport system. Sensitization of rats to HRP stimulated increased HRP uptake into enterocytes (significantly larger area of HRP-containing endosomes) and more rapid transcellular transport compared with rats sensitized to an irrelevant protein or naive control rats. Whole serum but not IgE-depleted serum from sensitized rats was able to transfer the enhanced antigen transport phenomenon. Immunohistochemistry demonstrated that sensitization induced expression of CD23, the low-affinity IgE receptor (FcepsilonRII), on epithelial cells. The number of immunogold-labeled CD23 receptors on the enterocyte microvillous membrane was significantly increased in sensitized rats and was subsequently reduced after antigen challenge when CD23 and HRP were localized within the same endosomes. Finally, pretreatment of tissues with luminally added anti-CD23 antibody significantly inhibited both antigen transport and the hypersensitivity reaction. Our results provide evidence that IgE antibodies bound to low-affinity receptors on epithelial cells are responsible for the specific and rapid nature of this novel antigen transport system.

Acquisition of telomere repeat sequences by transfected DNA integrated at the site of a chromosome break.

Previous analysis of plasmid DNA transfected into 108 cell clones demonstrated extensive polymorphism near the integration site in one clone. This polymorphism was apparent by Southern blot analysis as diffuse bands that extended over 30 kb. In the present study, nucleotide sequence analysis of cloned DNA from the integration site revealed telomere repeat sequences at the ends of the integrated plasmid DNA. The telomere repeat sequences at one end were located at the junction between the plasmid and cell DNA. The telomere repeat sequences at the other end were located in the opposite orientation in the polymorphic region and were shown by digestion with BAL 31 to be at the end of the chromosome. Telomere repeat sequences were not found at this location in the plasmid or parent cell DNA. Although the repeat sequences may have been acquired by recombination, a more likely explanation is that they were added to the ends of the plasmid by telomerase before integration. Comparison of the cell DNA before and after integration revealed that a chromosome break had occurred at the integration site, which was shown by fluorescent in situ hybridization to be located near the telomere of chromosome 13. These results demonstrate that chromosome breakage and rearrangement can result in interstitial telomere repeat sequences within the human genome. These sequences could promote genomic instability, because short repeat sequences can be recombinational hotspots. The results also show that DNA rearrangements involving telomere repeat sequences can be associated with chromosome breaks. The introduction of telomere repeat sequences at spontaneous or ionizing radiation-induced DNA strand breaks may therefore also be a mechanism of chromosome fragmentation.

Manipulation of energy and redox states in the C6 glioma cells by buthionine sulfoxamine and N-acetylcysteine and the effect on cell survival to cadmium toxicity.

Changes in cellular energy and redox states were studied in the C6 glioma cells following exposure to chemicals that affect glutathione metabolism. It was demonstrated that treatment with sublethal concentrations (25, 50 and 100 microM) of buthionine sulfoxamine (BSO) did not affect cellular energy state as measured by total adenosine nucleotides (TAN=ATP+ADP+ AMP), ATP:ADP:AMP and energy charge potential (ECP=[ATP + 0.5 (ADP)]/TAN). However, there was a significantly decrease in cellular GSH/GSSG and total glutathione (TG=[GSH+GSSG]/ TAN). The change was due to a significant decrease in intracellular GSH level without significant change in [GSSG]. Cells exposed to BSO for 24 hr were much more sensitive to subsequent injuries caused by Cd (0.6 mM for 3 hr). The results indicated that while a significant reduction of intracellular redox state did not affect cell viability, it could increase the susceptibility of cells to subsequent chemical stress. N-acetylcysteine (NAC), on the other hand, caused a dose (1, 5 and 10 mM)-dependent increase in GSH/GSSG without significant changes in intracellular energy state. Improvement of intracellular GSH/GSSG offered no protection against subsequent Cd induced cell death unless NAC was present at the time Cd was added. The pattern of cell death also correlated with the increase in intracellular free radial generation as measured by the fluorescence labeling with 27- dichlorofluorescin. Results of the present study demonstrated that intracellular redox states could be manipulated by addition of chemicals that affect glutathione metabolism. While the redox state may not be the sufficient condition to cause cell death, it could modulate the response of cells to subsequent Cd treatment. Furthermore, the action of NAC against Cd cytotoxicity may not be related to intracellular redox status.

Glutathione peroxidase and glutathione reductase activities are partially responsible for determining the susceptibility of cells to oxidative stress.

Different cell types response differently to toxic insult. In a previous study, it was demonstrated that the C6 glioma cell is more sensitive to Cd induced oxidative stress than the HepG2 cells. To explain the difference between the two cell lines in their response to oxidative stress, it was hypothesized that the activity of glutathione metabolizing enzymes may be different. The objective of this study is to determine the activities of glutathione peroxidase (GPx) and glutathione reductase (GR) in the two cell lines and to explain how these differences may affect the susceptibility of the two cells to oxidative stress. In the HepG2 cells, the activity of GPx was 2.24+/-0.18 micromol/mg protein/min and that for GR was 5.63+/-0.58 micromol/mg protein/min. For the C6 glioma cells, GPx and GR activities were 1.29+/-0.14 and 1.07+/-0.11 micromol/mg protein/min, respectively. Using the kinetic equilibrium: K(eq)=([GSSG]x[NADPH]x[H(+)])/([GSH](2)x[NADP(+)]), and the GSH/GSSG previously published (HepG2: 2.6 and C6 glioma: 3.6), resting NADPH/NADP(+) for the cell lines were calculated. The results showed that NADPH/NADP(+) for HepG2 cells (17.8) is higher than that in the C6 glioma cells (10.8). These data supported the notion that the reducing power (NADPH/NADP(+)) in the HepG2 cells is higher than that in the C6 glioma cell and thus, the later would be more susceptible to oxidative stress. The results also suggested that besides GSH/GSSG, the activities of GPx and GR are important in predicting tissue redox state. Applying this hypothesis to animal tissues, the ratio of the activities of the two enzymes in mouse liver, cerebral cortex, hippocampus and cerebellum were measured. It was demonstrated that the activities of GPx and GR were different in the different tissues studied. The possible correlation between enzymatic activities and the redox state in the different tissues were discussed.

Energy and redox States in the c6 glioma cells following acute exposure to zn, se(+4), and se(+6) and the correlation with apoptosis.

Changes in cellular energy and redox states in the C6 glioma cells exposed to increasing concentrations of either Zn or Se were studied to examine whether different elements cause different patterns of changes in cellular metabolism. Following a 3-h exposure, both Zn and Se(+4) caused dose-dependent decreases in cell viability and total adenosine nucleotides (TAN = ATP + ADP + AMP). In addition, Zn caused a dose-dependent increase in cellular ATP/TAN and a decrease in the ADP/TAN and AMP/TAN. These changes resulted in a significant increase in energy charge potential (ECP = [ATP + 0.5ADP]/TAN). Se(+4), on the other hand, caused a dose-dependent decrease in ATP/TAN but an increase in both ADP/TAN and AMP/TAN, resulting in a dose-dependent decrease in ECP. Both Zn and Se(+4) caused a dose-dependent decrease in GSH/GSSG and an increase in GSH + GSSG when compared to TAN. In contrast to Zn and Se(+4), the nontoxic Se(+6) caused no significant changes in cellular energy states but reduced the GSH/GSSG ratio from 3.14 +/- 0.49 to 2.05 +/- 0.29, which could be explained by the effect of Se on enzymes responsible for GSH metabolism. As the cellular ATP level has been considered an important element that mediates the mode of cell death, it was suggested that a significant increase in ATP/TAN upon exposure to Zn would indicate that cell death occurred via apoptosis, while Se(+4) caused a different pattern of cell death. This was confirmed by the appearance of cells with fragmented nucleus in cells treated with Zn, but not Se(+4) and Se(+6). The results demonstrated that different chemicals caused different patterns of metabolic changes. The correlation between metabolic changes and the mode of cell death was discussed.

Influences of morphine on the spontaneous and evoked excitatory postsynaptic currents in lateral amygdala of rats.

Acute morphine exposure induces antinociceptive activity, but the underlying mechanisms in the central nervous system are unclear. Using whole-cell patch clamp recordings, we explore the role of morphine in the modulation of excitatory synaptic transmission in lateral amygdala neurons of rats. The results demonstrate that perfusion of 10 microM of morphine to the lateral amygdala inhibits the discharge frequency significantly. We further find that there are no significant influences of morphine on the amplitude of spontaneous excitatory postsynaptic currents (sEPSCs). Interestingly, morphine shows no marked influence on the evoked excitatory postsynaptic currents (eEPSCs) in the lateral amygdala neurons. These results indicate that acute morphine treatment plays an important role in the modulation on the excitatory synaptic transmission in lateral amygdala neurons of rats.

Enhanced Absorption and Diffusion Properties of Lithium on B,N,VC-decorated Graphene.

Systematic first-principles calculations were performed to investigate the adsorption and diffusion of Li on different graphene layers with B/N-doping and/or C-vacancy, so as to understand why doping heteroatoms in graphene anode could significantly improve the performance of lithium-ion batteries. We found that the formation of single or double carbon vacancies in graphene are critical for the adsorption of Li atoms. While the N-doping facilitates the formation of vacancies, it introduces over binding issue and hinders the Li diffusion. The presence of B takes the excessive electrons from Li and N and reduces the energy barrier of Li diffusion on substrates. We perceive that these clear insights are crucial for the further development of graphene based anode materials for lithium-ion batteries.

Stereospecificity of the hydrogen transfer catalyzed by human placental aldose reductase.

Placental aldose reductase (EC 1.1.1.21) was incubated with glucose in the presence of [4A-2H] NADPH prepared in the oxidation of [2-2H] isocitrate by isocitrate dehydrogenase (EC 1.1.1.42) or [4B-2H] NADPH prepared in the oxidation of [1-2H] glucose-6-phosphate dehydrogenase (EC 1.1.1.49). The sorbitol formed from [4A-2H] NADPH contained deuterium and from [4B-2H] NADPH it did not. Therefore, aldose reductase in an A-type enzyme.

A novel reduced-intensity stem cell transplant regimen for nonmalignant disorders.

Bone marrow transplantation (BMT) benefits nonmalignant diseases but is limited by regimen-related toxicity, graft-versus-host disease (GVHD), donor availability, and graft rejection (GR). To overcome some of these barriers, we developed a new conditioning strategy for these patients. In total, 16 patients received Campath-1H (33/48 mg; days -21 to -19), fludarabine (150 mg/m(2); days -8 to -4), melphalan (140/70 mg/m(2); day -3), and transplant using related/unrelated stem cells. GVHD prophylaxis included cyclosporine/methylprednisolone for cord cells. Other recipients also received methotrexate. Risk factors for GR included multiple transfusions (6), low stem cell numbers (1), and immunologic/metabolic disorders (3). Donor engraftment was present in 14/16 recipients. Neutrophils (ANC>0.5 x 10(9)/l) and platelets (>50 x 10(9)/l) engrafted at a median of 13 and 24 days. Two patients died of Pseudomonas sepsis prior to engraftment, one of CMV disease, and another of intracranial hemorrhage. With median follow-up of 281 days (78-907), 12/16 are stable/improved, or cured. Acute GVHD was absent (n=10) or mild and transient (grade1-2 skin) (n=4). There was no chronic GVHD. Toxicities were predominantly early infections within 100 days, and correlated with lymphopenia (CD4+ T and B cells). Stable engraftment and low incidence of significant GVHD, irrespective of age or stem cell source, make this reduced-intensity regimen attractive for nonmalignant disorders.

Effect of gestational subclinical hypothyroidism on early neurodevelopment of offspring.

OBJECTIVE: To evaluate the effects of gestational subclinical hypothyroidism (SCH) on early neurodevelopment of offspring. STUDY DESIGN: A prospective study included 106 infants born to mothers with gestational SCH and 106 infants born to mothers who were euthyroid during pregnancy. The neurodevelopment of 12 to 24-month-old infants was assessed and compared using the Gesell developmental test (revised version). RESULTS: Infants born to mothers with gestational SCH and those born to euthyroid mothers had similar scores on the Gesell development test. No correlations were observed between maternal TSH concentration and Gesell developmental test scores of offspring. Infants born to mothers who had gestational SCH during the first trimester specifically and those born to euthyroid mothers had similar scores on the Gesell development test. No significant correlations were detected between maternal TSH concentration during the first trimester and offspring neurodevelopment. CONCLUSIONS: No detectable neurodevelopment deficit was observed in offspring up to 24 months old from mothers who had gestational SCH.

LPS receptor subunits have antagonistic roles in epithelial apoptosis and colonic carcinogenesis.

Colorectal carcinoma (CRC) is characterized by unlimited proliferation and suppression of apoptosis, selective advantages for tumor survival, and chemoresistance. Lipopolysaccharide (LPS) signaling is involved in both epithelial homeostasis and tumorigenesis, but the relative roles had by LPS receptor subunits CD14 and Toll-like receptor 4 (TLR4) are poorly understood. Our study showed that normal human colonocytes were CD14(+)TLR4(-), whereas cancerous tissues were CD14(+)TLR4(+), by immunofluorescent staining. Using a chemical-induced CRC model, increased epithelial apoptosis and decreased tumor multiplicity and sizes were observed in TLR4-mutant mice compared with wild-type (WT) mice with CD14(+)TLR4(+) colonocytes. WT mice intracolonically administered a TLR4 antagonist displayed tumor reduction associated with enhanced apoptosis in cancerous tissues. Mucosa-associated LPS content was elevated in response to CRC induction. Epithelial apoptosis induced by LPS hypersensitivity in TLR4-mutant mice was prevented by intracolonic administration of neutralizing anti-CD14. Moreover, LPS-induced apoptosis was observed in primary colonic organoid cultures derived from TLR4 mutant but not WT murine crypts. Gene silencing of TLR4 increased cell apoptosis in WT organoids, whereas knockdown of CD14 ablated cell death in TLR4-mutant organoids. In vitro studies showed that LPS challenge caused apoptosis in Caco-2 cells (CD14(+)TLR4(-)) in a CD14-, phosphatidylcholine-specific phospholipase C-, sphingomyelinase-, and protein kinase C-ζ-dependent manner. Conversely, expression of functional but not mutant TLR4 (Asp299Gly, Thr399Ile, and Pro714His) rescued cells from LPS/CD14-induced apoptosis. In summary, CD14-mediated lipid signaling induced epithelial apoptosis, whereas TLR4 antagonistically promoted cell survival and cancer development. Our findings indicate that dysfunction in the CD14/TLR4 antagonism may contribute to normal epithelial transition to carcinogenesis, and provide novel strategies for intervention against colorectal cancer.

Thin filament activation probed by fluorescence of N-((2-(iodoacetoxy)ethyl)-N-methyl)amino-7-nitrobenz-2-oxa-1,3-diazole-labeled troponin I incorporated into skinned fibers of rabbit psoas muscle.

A method is described for the exchange of native troponin of single rabbit psoas muscle fibers for externally applied troponin complexes without detectable impairment of functional properties of the skinned fibers. This approach is used to exchange native troponin for rabbit skeletal troponin with a fluorescent label (N-((2-(iodoacetoxy)ethyl)-N-methyl)amino-7-nitrobenz-2-oxa-1, 3-diazole, IANBD) on Cys(133) of the troponin I subunit. IANBD-labeled troponin I has previously been used in solution studies as an indicator for the state of activation of reconstituted actin filaments (. Proc. Natl. Acad. Sci. USA. 77:7209-7213). In the skinned fibers, the fluorescence of this probe is unaffected when cross-bridges in their weak binding states attach to actin filaments but decreases either upon the addition of Ca(2+) or when cross-bridges in their strong binding states attach to actin. Maximum reduction is observed when Ca(2+) is raised to saturating concentrations. Additional attachment of cross-bridges in strong binding states gives no further reduction of fluorescence. Attachment of cross-bridges in strong binding states alone (low Ca(2+) concentration) gives only about half of the maximum reduction seen with the addition of calcium. This illustrates that fluorescence of IANBD-labeled troponin I can be used to evaluate thin filament activation, as previously introduced for solution studies. In addition, at nonsaturating Ca(2+) concentrations IANBD fluorescence can be used for straightforward classification of states of the myosin head as weak binding (nonactivating) and strong binding (activating), irrespective of ionic strength or other experimental conditions. Furthermore, the approach presented here not only can be used as a means of exchanging native skeletal troponin and its subunits for a variety of fluorescently labeled or mutant troponin subunits, but also allows the exchange of native skeletal troponin for cardiac troponin.

The M.ADP.Pi state is required for helical order in the thick filaments of skeletal muscle.

The thick filaments of mammalian and avian skeletal muscle fibers are disordered at low temperature, but become increasingly ordered into an helical structure as the temperature is raised. Wray and colleagues (Schlichting, I., and J. Wray. 1986. J. Muscle Res. Cell Motil. 7:79; Wray, J., R. S. Goody, and K. Holmes. 1986. Adv. Exp. Med. Biol. 226:49-59) interpreted the transition as reflecting a coupling between nucleotide state and global conformation with M.ATP (disordered) being favored at 0 degrees C and M.ADP.P(i) (ordered) at 20 degrees C. However, hitherto this has been limited to a qualitative correlation and the biochemical state of the myosin heads required to obtain the helical array has not been unequivocally identified. In the present study we have critically tested whether the helical arrangement of the myosin heads requires the M.ADP.P(i) state. X-ray diffraction patterns were recorded from skinned rabbit psoas muscle fiber bundles stretched to non-overlap to avoid complications due to interaction with actin. The effect of temperature on the intensities of the myosin-based layer lines and on the phosphate burst of myosin hydrolyzing ATP in solution were examined under closely matched conditions. The results showed that the fraction of myosin mass in the helix closely followed that of the fraction of myosin in the M.ADP.P(i) state. Similar results were found by using a series of nucleoside triphosphates, including CTP and GTP. In addition, fibers treated by N-phenylmaleimide (Barnett, V. A., A. Ehrlich, and M. Schoenberg. 1992. Biophys. J. 61:358-367) so that the myosin was exclusively in the M.ATP state revealed no helical order. Diffraction patterns from muscle fibers in nucleotide-free and in ADP-containing solutions did not show helical structure. All these confirmed that in the presence of nucleotides, the M.NDP.P(i) state is required for helical order. We also found that the spacing of the third meridional reflection of the thick filament is linked to the helical order. The spacing in the ordered M.NDP.P(i) state is 143.4 A, but in the disordered state, it is 144. 2 A. This may be explained by the different interference functions for the myosin heads and the thick filament backbone.

Assessment of iron status of Zairean women of childbearing age by serum transferrin receptor.

Soluble transferrin receptor (sTfR), previously shown to be a sensitive indicator of tissue iron deficiency, was used to assess iron status of 104 Zairean women (69 lactating, 19 pregnant, and 16 nonpregnant, nonlactating women). Thirteen iron-sufficient female laboratory employees were also studied. Mean sTfR concentrations were higher in pregnant women (9.90 mg/L) than in lactating women (8.55 mg/L), nonlactating women (7.74 mg/L), and laboratory employees (5.11 mg/L) (P < 0.005). Mean serum ferritin and transferrin saturation were lower in pregnant than nonpregnant women. sTfR negatively correlated with hemoglobin (P < 0.05) and transferrin saturation (P < 0.05), and nonsignificantly with ferritin and transferrin. With 7.26 mg sTfR/L (the upper limit of laboratory employees) as the cutoff value, sTfR identified 67% of women with tissue iron deficiency compared with 11.5-57% for transferrin saturation, hemoglobin, or ferritin. Despite the moderate sensitivity (68.5%), 90% of women with sTfR > 7.26 mg/L also had another index below normal and 54% had serum ferritin < or = 50 micrograms/L.