Comparative cone-beam computed tomographic evaluation of maxillary incisor intrusion and associated root resorption: Intrusion arch vs mini-implants.

INTRODUCTION: Various literature has verified that apical root resorption is a common adverse effect of orthodontic treatment, particularly intrusion. Conventional radiographic techniques underestimated root lengths and overestimated tooth lengths. Cone-beam computed tomography (CBCT) is a useful diagnostic tool to detect orthodontically induced external apical root resorption. This prospective study aimed to compare maxillary incisor intrusion and associated root resorption via CBCT. METHODS: Thirty patients aged 16-23 years, having a deepbite of 6-8 mm and excessive gingival display on smiling, were divided into 2 groups: group 1, with 15 patients who were treated with Burstone intrusion arch, and group 2 with 15 patients who were treated with mini-implants applying 100 g of intrusive force for 4 months with activation done every 4 weeks. During this 4-month study period, no treatment was performed other than the intrusion of incisors. CBCT scans were obtained before and after the intrusion phase of treatment to compare the amount of intrusion and associated root resorption among both groups. RESULTS: No significant difference was found in mean incisor intrusion between groups 1 and 2 (P = 0.772), with slightly more proclination of incisors in group 1, resulting in a significant (P = 0.018) increase in the vertical change of incisal edge in group 1. A statistically significant difference was found in root resorption among both groups (P = 0.004), with more root resorption in group 2. CONCLUSIONS: The results of this study indicate intrusion with both the intrusion systems using appropriate intrusive forces is effective in opening the bite with slightly more external apical root resorption in the mini-implant group.

P-selectin can promote thrombus propagation independently of both von Willebrand factor and thrombospondin-1 in mice.

Essentials The main receptor for platelet glycoprotein (GP) Ibα is von Willebrand factor (VWF). P-selectin and thrombospondin-1 (TSP1) have been suggested as counter receptors for GPIbα. In a laser injury model, P-selectin promotes thrombus propagation independently of VWF and TSP1. In a laser injury model, thrombus persists in interleukin-4 receptor α/GPIbα-transgenic mice. SUMMARY: Background P-selectin and thrombospondin-1 (TSP1) have been suggested as counter ligands that may mediate GPIbα-dependent thrombus growth independently of von Willebrand factor (VWF) in vitro. However, residual thrombus formation still persists in Vwf -/- Tsp1-/- mice, suggesting existence of other mechanisms that modulate thrombus propagation. Objective We determined whether P-selectin modulates thrombus propagation in injured arterioles independently of TSP1 and VWF. Methods CD-62P blocking antibody in Vwf -/- Tsp1-/- mice was used to inhibit P-selectin. We determined thrombus growth kinetics in two models of thrombosis: FeCl3 injury-induced and laser injury-induced thrombosis. Results In a 10% FeCl3 injury-induced thrombosis model, the initial platelet adhesion, time to form first thrombus, and non-occlusive residual thrombus growth kinetics were comparable between P-selectin-blocking antibody-treated Vwf -/- Tsp1-/- mice and control IgG-treated Vwf -/- Tsp1-/- mice. On the other hand, in a laser injury-induced thrombosis model, residual thrombus growth kinetics were significantly decreased in P-selectin-blocking antibody-treated Vwf -/- Tsp1-/- mice vs. control IgG-treated Vwf -/- Tsp1-/- mice. Because P-selectin has been suggested as a counter ligand for platelet GPIbα, we determined the role of GPIbα in a laser injury-induced thrombosis model. Surprisingly, in a laser injury model, unlike in a FeCl3 injury model, thrombus formation was not completely inhibited in IL4Rα/GPIbα-tg mice. Residual thrombus growth kinetics were comparable between P-selectin-blocking antibody-treated IL4Rα/GPIbα-tg mice and control IgG-treated IL4Rα/GPIbα-tg mice. Comparison of slopes over time showed that residual thrombus growth kinetics were comparable in P-selectin-blocking antibody-treated Vwf -/- Tsp1-/- and control IgG-treated IL4Rα/GPIbα-tg mice Conclusion In a laser injury-induced thrombosis model, P-selectin modulates thrombus propagation independently of VWF and TSP1.

Enhanced thermoelectric properties of selenium-deficient layered TiSe(2-x): a charge-density-wave material.

In the present work, we report on the investigation of low-temperature (300-5 K) thermoelectric properties of hot-pressed TiSe2, a charge-density-wave (CDW) material. We demonstrate that, with increasing hot-pressing temperature, the density of TiSe2 increases and becomes nonstoichiometric owing to the loss of selenium. X-ray diffraction, scanning electron microscopy, and transimission electron microscopy results show that the material consists of a layered microstructure with several defects. Increasing the hot-press temperature in nonstoichiometric TiSe2 leads to a reduction of the resistivity and enhancement of the Seebeck coefficient in concomitent with suppression of CDW. Samples hot-pressed at 850 °C exhibited a minimum thermal conductivity (κ) of 1.5 W/m·K at 300 K that, in turn, resulted in a figure-of-merit (ZT) value of 0.14. This value is higher by 6 orders of magnitude compared to 1.49 × 10(-7) obtained for cold-pressed samples annealed at 850 °C. The enhancement of ZT in hot-pressed samples is attributed to (i) a reduced thermal conductivity owing to enhanced phonon scattering and (ii) improved power factor (α(2)σ).

Thermoelectric performance of layered SrxTiSe2 above 300 K.

In this paper we report the thermoelectric performance of Sr intercalated TiSe(2) above 300 K. Refined x-ray diffraction, high resolution transmission electron microscopy and scanning electron microscopy images show well oriented polycrystalline grains along a (0 0 l) direction and layered growth of the sample. Intercalation of Sr in TiSe(2) shows an improved Seebeck coefficient (α) value without altering the polarity of the majority charge carrier. A drastic reduction in the thermal conductivity (κ) from 3.8 W m K(-1) to 1.2 W m K(-1) (at 650 K) was observed which is ascribed to the: (i) scattering of the phonon by natural layer interfaces, grain boundaries and lattice defects and (ii) rattling of intercalated Sr atoms among weakly bound TiSe(2) layers. This led to the maximum ZT of ~0.08 at 650 K for Sr(x)TiSe(2) (x > 0.1) which is almost twice as high as the parent TiSe(2).

ADAMTS13 modulates atherosclerotic plaque progression in mice via a VWF-dependent mechanism.

BACKGROUND: ADAMTS13 reduces the adhesiveness of hyperactive ultra-large von Willebrand factor (ULVWF) multimers by cleaving them into smaller, less active multimers. Recently, we and others have demonstrated that ADAMTS13 reduces atherosclerosis in hypercholesteremic apolipoprotein E (ApoE-/-) deficient mice. It is not known whether ADAMTS13 modulates atherosclerosis directly or indirectly by cleaving ULVWF multimers. OBJECTIVE: We generated triple knockout Adamts13-/-/Vwf-/-/ApoE-/- mice to determine whether ADAMTS13 modulates atherosclerosis through its proteolytic effects on VWF or other potential mechanisms. METHODS: Female mice were fed a high-fat Western diet beginning at 6 weeks of age until they were sacrificed at 4 months. We compared the extent of atherosclerosis in the serial cross-sections of the aortic sinus using the Verhoeff-Van Gieson stain. Macrophage and neutrophil infiltration were quantified by immunohistochemistry. Under plain polarized light interstitial collagen content in the serial cross-sections of the aortic sinus was quantified using picrosirius red stain. RESULTS: Deficiency of VWF in Adamts13-/-/ApoE-/- mice (Adamts13-/-/Vwf-/-/ApoE-/-) completely reversed exacerbated atherosclerosis (P < 0.05 vs. Adamts13-/-/ApoE-/- mice). The lesion size, macrophage and neutrophil infiltration in the aortic sinus of Adamts13-/-/Vwf-/-/ApoE-/- mice were significantly decreased compared with Adamts13-/-/ApoE-/- mice (P < 0.05), but similar to Vwf-/-/ApoE-/- mice. Additionally, interstitial collagen content in the aortic sinus of Adamts13-/-/Vwf-/-/ApoE-/- mice was significantly reduced compared with Adamts13-/-/ApoE-/- mice (P < 0.05), but similar to Vwf-/-/ApoE-/- mice. Total cholesterol and triglyceride levels were similar among groups. CONCLUSIONS: ADAMTS13 modulates inflammatory plaque progression in hypercholesterolemic mice through a VWF-dependent mechanism. These findings provide further evidence on the pathophysiological role for the ADAMTS13/VWF axis in atherosclerosis.

ADAMTS13 reduces VWF-mediated acute inflammation following focal cerebral ischemia in mice.

BACKGROUND: ADAMTS13 cleaves hyperactive ultra-large von Willebrand factor (ULVWF) multimers into smaller and less active forms. It remains unknown whether VWF-mediated inflammatory processes play a role in the enhanced brain injury due to ADAMTS13 deficiency. OBJECTIVE: We tested the hypothesis that the deleterious effect of ADAMTS13 deficiency on ischemic brain injury is mediated through VWF-dependent enhanced vascular inflammation. METHODS: Transient focal cerebral ischemia was induced by 60 min of occlusion of the right middle cerebral artery. Myeloperoxidase (MPO) activity and inflammatory cytokines in the infarcted region were evaluated 23 h after reperfusion injury. Neutrophil infiltration within the infarct and surrounding areas was quantitated by immunohistochemistry. RESULTS: We report that ADAMTS13-deficient mice exhibited significantly enlarged infarct size, concordant with increased myeloperoxidase (MPO) activity, neutrophil infiltration and expression of the pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). In contrast, VWF-deficient mice exhibited significantly reduced MPO activity, neutrophil infiltration and inflammatory cytokine induction, demonstrating a role of VWF in these inflammatory processes. Mice deficient for both ADAMTS13 and VWF exhibited an identical reduction of the same inflammatory parameters, demonstrating that the increased inflammation observed in ADAMTS13-deficient mice is VWF dependent. Finally, the increased infarct size observed in ADAMTS13-deficient mice was completely abrogated by prior immunodepletion of neutrophils, demonstrating a causal role for acute inflammation in the enhanced brain injury that occurs in the setting of ADAMTS13 deficiency. CONCLUSION: These findings provide new evidence for ADAMTS13 in reducing VWF-mediated acute cerebral inflammation following ischemic stroke.

Immune complexes and late complement proteins trigger activation of Syk tyrosine kinase in human CD4(+) T cells.

In systemic lupus erythematosus (SLE), the autoantibodies that form immune complexes (ICs) trigger activation of the complement system. This results in the formation of membrane attack complex (MAC) on cell membrane and the soluble terminal complement complex (TCC). Hyperactive T cell responses are hallmark of SLE pathogenesis. How complement activation influences the T cell responses in SLE is not fully understood. We observed that aggregated human γ-globulin (AHG) bound to a subset of CD4(+) T cells in peripheral blood mononuclear cells and this population increased in the SLE patients. Human naive CD4(+) T cells, when treated with purified ICs and TCC, triggered recruitment of the FcRγ chain with the membrane receptor and co-localized with phosphorylated Syk. These events were also associated with aggregation of membrane rafts. Thus, results presented suggest a role for ICs and complement in the activation of Syk in CD4(+) T cells. Thus, we propose that the shift in signalling from ζ-chain-ZAP70 to FcRγ chain-Syk observed in T cells of SLE patients is triggered by ICs and complement. These results demonstrate a link among ICs, complement activation and phosphorylation of Syk in CD4(+) T cells.

Developing biochemical and molecular markers for cyanobacterial inoculants.

Markers for evaluating the establishment of cyanobacteria based on their sensitivity or resistance to antibiotics, saccharide utilization patterns and PCR generated fingerprints were developed. Four selected strains (isolates from rhizosphere soils of diverse agro-ecosystems) have shown potential as diazotrophs and exhibited plant growth promoting abilities. Different responses were obtained on screening against 40 antibiotics, which aided in developing selectable antibiotic markers for each strain. Biochemical profiles generated using standardized chromogenic identification system (including saccharide utilization tests) revealed that 53 % of the saccharides tested were not utilized by any strain, while some strains exhibited unique ability for utilization of saccharides such as melibiose, cellobiose, maltose and glucosamine. PCR based amplification profiles developed using a number of primers based on repeat sequences revealed the utility of 3 primers in providing unique fingerprints for the strains.

Electrical characterization of self-assembled monolayers of alkyltrichlorosilanes on native oxide of silicon.

The octadecyltrichlorosilane (C18), dodecyltrichlorosilane (C12) and octyltrichlorosilane (C8) monolayers have been deposited on the native oxide of silicon by self-assembly technique. The morphology of the monolayers studied by atomic force microscopy revealed an average roughness of approximately 1.0 A. The Fourier Transform Infra Red Spectroscopic measurements revealed the presence of peaks at approximately 2848 and 2915 cm(-1) indicating the formation of densely packed monolayers. The current density versus voltage (J-V) measurements using mercury drop as counter electrode showed tunneling current between 10(-5) to 10(-8) A/cm2 at 1 V indicating the excellent dielectric behaviour of these monolayers. The J-V data were fitted to Simmons theory of tunneling which yielded an effective electron energy barrier height of 1.6 +/- 0.2 eV and the effective mass of electron tunneling through the barrier was found to be 0.3 +/- 0.03 m(e). The tunneling decay factor beta was estimated from the current density values measured as a function of thickness of the monolayer and was found to be 0.28 +/- 0.02 A(-1).

Measurement of biomarkers in juvenile idiopathic arthritis patients and their significant association with disease severity: a comparative study.

OBJECTIVE: To evaluate in juvenile idiopathic arthritis (JIA) patients a biomarker panel of anti-cyclic citrullinated peptide (anti-CCP) antibodies, cartilage oligomeric matrix protein (COMP), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), IgM rheumatoid factor (RF), IgG RF, and IgA RF and compare to the presence of joint erosions (JE), joint space narrowing (JSN), and synovitis in order to evaluate aggressive disease. METHODS: Sixty-eight JIA patients (19 RF positive polyarthritis, 23 RF negative polyarthritis, 17 persistent oligoarthritis, and 9 systemic-onset) were evaluated using the biomarker panel and compared to 18 healthy controls. All RF isotypes, anti-CCP antibodies, and COMP were measured by enzyme-linked immunosorbent assays (ELISA). Statistically significant differences and associations were assessed for each biomarker in relation to JE, JSN, and synovitis. Multiple regression analysis was used to find the variables associated with joint damage and synovitis. RESULTS: Patients with JE and JSN had significantly elevated levels of IgA RF, IgM RF, and anti-CCP antibodies. COMP levels were higher in early disease, but also later in disease in patients with no JE or JSN. ESR, CRP, and IgA RF were significantly elevated in patients with active synovitis. Regression analysis showed IgM RF and disease duration to be associated with JE and JSN. Anti-CCP antibodies and COMP were also associated with JSN. CRP and IgA RF were associated with synovitis. CONCLUSION: Our findings demonstrate the importance of measuring IgM RF and IgA RF by ELISA and anti-CCP antibodies by ELISA, in addition to COMP in the assessment of JIA patients to determine severity of disease.

Abnormal kappa:lambda light chain ratio in circulating immune complexes as a marker for B cell activity in juvenile idiopathic arthritis.

Patients with juvenile idiopathic arthritis (JIA) have been shown to have elevated levels of circulating immune complexes (CICs) which correlated with disease activity. Our aim was to assess B cell activity by measuring the amount of and the kappa:lambda chain immunoglobulin light (L) chain ratio in CICs from JIA patients and to determine potential evidence for either an antigen-driven response or B-cell receptor editing. We used an enzyme-linked immunosorbent assay to measure kappa and lambda chains present in the CICs from the sera of patients with JIA. Statistical analysis was performed using Pearson's correlation, one-way ANOVA and Bonferroni post hoc analysis. Sera from 44 JIA patients were examined for the concentration of L chains in CICs. Healthy controls had a kappa:lambda chain ratio of 1.2:1, whereas this ratio was reversed among JIA subgroups with RF-positive polyarthritis (1:1.2), RF-negative polyarthritis (1:1.3), oligoarthritis (1:2.3) and systemic-onset arthritis (1:2.5). In addition, overall lambda chain selection was not significantly associated with a particular immunoglobulin heavy (H) chain and occurred with all immunoglobulin isotypes. We showed preferential selection of lambda chains contributing to the formation of potentially pathogenic CICs from JIA patients, of all onset types compared to healthy controls, in an H chain-independent manner. The reversal of kappa:lambda chain ratio within the JIA CICs and association with all immunoglobulin isotypes demonstrated the potential for L chain editing. Furthermore, we conclude that a reversal of the normal kappa:lambda chain ratio in JIA CICs may be used as a marker for increased B-cell activity.

Formation of platelet strings and microthrombi in the presence of ADAMTS-13 inhibitor does not require P-selectin or beta3 integrin.

BACKGROUND: Ultra-large von Willebrand factor (ULVWF) and the receptor P-selectin are released from endothelial Weibel-Palade bodies during injury or inflammation. VWF mediates platelet adhesion and P-selectin promotes leukocyte rolling. ADAMTS-13 limits the duration of platelet adhesion by cleaving the ULVWF. In the absence of ADAMTS-13, long VWF filaments decorated with platelets form. Recent in vitro studies suggested that P-selectin might anchor these platelet strings to endothelium, but whether the same mechanism exists in vivo remains to be elucidated. METHODS: We address the role of P-selectin and beta(3) integrin in platelet string formation in vivo using intravital microscopy by infusing inhibitory ADAMTS-13 antibody in P-selectin-/- and beta(3)-deficient mice and activating the endothelium by injecting histamine. RESULTS: We show that inhibition of ADAMTS-13 combined with endothelial activation leads to similar extents of platelet string formation in wild-type, P-selectin- and integrin beta(3)-deficient mice. Further, in venules the platelet strings can coalesce into VWF-platelet aggregates. This process utilizes neither the platelet beta(3) integrin nor P-selectin. We also show in vitro that platelets can act as a bridge between the VWF fibers and that VWF can self-associate even in areas devoid of platelets. CONCLUSIONS: The formation or retention of the platelet strings does not require P-selectin or the endothelial VWF receptor alpha(v)beta(3). Furthermore, in the presence of low ADAMTS-13 activity, VWF-dependent and alpha(IIb)beta(3)-independent platelet clustering occurs in veins, as has been shown at high arterial shear rates. Our study further supports the importance of regulation of VWF multimer size upon secretion from Weibel-Palade bodies.

Presence of plasma complement regulatory proteins clusterin (Apo J) and vitronectin (S40) on circulating immune complexes (CIC).

The complement regulatory (CR) proteins clusterin and vitronectin bind to the membrane attack complex (MAC) and thus prevent cytolysis. In this report, we demonstrate the presence of both of these CR proteins on MAC bound to circulating immune complexes (CIC). We measured the amount of clusterin and vitronectin on MAC in plasma, also referred to as soluble MAC (SMAC), as well as on MAC bound to CIC (MAC-CIC), using antibody directed to polymerized C9 in systemic lupus erythematosus (SLE) patients. We observed a strong correlation among the quantities of SMAC and MAC-CIC. The amount of both clusterin and vitronectin associated with MAC-CIC was two- to threefold higher in comparison to the SMAC. Patients with high levels of clusterin and vitronectin demonstrated renal involvement. We hypothesize that these complement regulatory proteins besides regulating the insertion of MAC play other critical roles, in disease pathogenesis.

A review on potentiality of medicinal plants as the source of new contraceptive principles.

Recently, a review has already been made on the synthetic contraceptive agents whereas this review embraces the natural contraceptives upto year 2001 with 355 references. It also includes the isolation of their active principles, methods of analysis of active ingredients through TLC, HPLC, their side effects and pharmacological action.

Crystallization and initial X-ray crystallographic characterization of recombinant bovine inositol polyphosphate 1-phosphatase produced in Spodoptera frugiperda cells.

Bovine inositol polyphosphate 1-phosphatase, a monomeric protein with a molecular mass of 44,000 Da, hydrolyzes the 1-position phosphate from inositol 1,3,4-trisphosphate and inositol 1,4-bisphosphate. The low abundance of inositol polyphosphate 1-phosphatase in tissues has precluded structural studies requiring large quantities of enzyme. We used recombinant Baculovirus harboring the cDNA of bovine inositol polyphosphate 1-phosphatase to infect Spodoptera frugiperda (Sf9) insect cells. Recombinant protein (25 mg per 1 x 10(9) cells) was purified to homogeneity. The enzyme produced in Sf9 cells was similar to the native purified protein as determined by immunoblotting catalytic properties, and inhibition by lithium ions. Crystals of the purified recombinant enzyme were grown by vapor diffusion. Precession photography was used to determine the parameters of inositol polyphosphate 1-phosphatase crystals. The tetragonal crystals belong to the space group P4(1) or P4(3), have unit cell dimensions of a = b = 51.6 A, c = 143.3 A, alpha = beta = gamma = 90 degrees, and contain one molecule per asymmetric unit. We have collected a complete diffraction data set extending to 2.3 A and are currently attempting to solve the three-dimensional structure of bovine inositol polyphosphate 1-phosphatase using a multiple isomorphous replacement strategy.

The significance of serum magnesium in diabetes mellitus.

The mean serum magnesium level in normal individual was found 1.967 +/- mgm/dl. No significant difference in serum magnesium level was found in various age groups. All diabetic patients, having normal renal function, exhibited hypomagnesemia. The hyperglycemia in these cases was inversely related to hypomagnesemia and its restoration towards normal by insulin therapy restored the normal serum magnesium concentration. These existed in inverse correlationship between serum magnesium and cholesterol (r = -0.56). The hypomagnesemia was the result and not the cause of alterations in the cholesterol metabolism. A positive correlation was observed between blood urea level and serum magnesium (r = +0.7) and it was significant. The magnesium correlated with major diabetic complications too, e.g. micro and macroangiopathies. Thus, serum magnesium can be used for prognostic assessment in diabetic individuals.

Pleiotrophin transforms NIH 3T3 cells and induces tumors in nude mice.

The pleiotrophin (PTN) gene (Ptn) encodes an 18-kDa protein that is highly conserved among mammalian species and that functions as a weak mitogen and promotes neurite-outgrowth activity in vitro. To further investigate the role PTN plays in regulating cell growth, we overexpressed the bovine PTN cDNA and now show that PTN phenotypically transforms NIH 3T3 cells, as evidenced by increased cell number at confluence, focus formation, anchorage-independent growth, and tumor formation in the nude mouse. The results demonstrate that the Ptn gene has the potential to regulate NIH 3T3 cell growth and suggest that PTN may influence abnormal cell growth in vivo.

The rne gene is the structural gene for the processing endoribonuclease RNase E of Escherichia coli.

Using T7 RNA polymerase and specific constructs derived from 5S rRNA and RNA I genes, we generated substrates for the RNA processing enzyme RNase E. Using these substrates we have shown that a 3.2 kb DNA fragment that complements the rne-3071 mutation can express RNase E activity. We also found that T7 RNA polymerase terminates within the 5S rRNA gene.

Sequencing and expression of the rne gene of Escherichia coli.

RNase E is a major endonucleolytic RNA processing enzyme in Escherichia coli. We have sequenced a 3.2 kb EcoRI-BamHI fragment encoding the rne gene, and identified its reading frame. Upstream from the gene, there are appropriate consensus sequences for a putative promoter and a ribosome binding site. We have translated this gene using a T7 RNA polymerase/promoter system. We determined 25 amino acids from the N-terminal of the translated product and they are in full agreement with the DNA sequence. The translated product of the rne gene migrates in SDS containing polyacrylamide gels as a 110,000 Da polypeptide, but the open reading frame found in the sequenced DNA indicates a much smaller protein. The entity that migrates as a 110,000 Da contains RNA, which could account, at least partially, for the migration of the rne gene product in SDS containing polyacrylamide gels.