SYMPOSIA / SO7-1 : NOVEL SIGNALING PATHWAYS REVEALED THROUGH ANALYSIS OF DEATH INDUCTION AND INFLAMMATION BY RECEPTORS OF THE TNF/NGF FAMILY

(D . Wallach),(M . Boldin),(T . Goncharov),(A . Kovalenko),(D . Landstein),(S . Leu),(N . Malinin),(M . Schuchmann),(A . Watts),(E . Varfolomeev),(S . Zhang) 한국생화학분자생물학회 (구 한국생화학회) 1999 6th IUBMB SEOUL CONFERENCE Vol.- No.-

Special Lecture : Modern Management of Uterine Myomas

( Edward E. Wallach ) 대한산부인과학회 1994 대한산부인과학회 학술대회 Vol.74 No.-

Caspase-8 deficiency in mouse embryos triggers chronic RIPK1-dependent activation of inflammatory genes, independently of RIPK3

Kang, Tae-Bong,Jeong, Ju-Seong,Yang, Seung-Hoon,Kovalenko, Andrew,Wallach, David Nature Publishing Group UK 2018 CELL DEATH AND DIFFERENTIATION Vol.25 No.6

<P>Deletion of the <I>Casp8</I> gene in epithelial tissues of mice results in severe inflammatory pathologies. Its ubiquitous deletion, or its specific deletion in endothelial cells, results in intrauterine death associated with capillary damage. These pathologies are all preventable by co-deletion of <I>Casp8</I> and the genes encoding either the RIPK1 or the RIPK3 protein kinase. Since activation of RIPK3 in Caspase-8-deficient cells can trigger necroptotic cell death, and since RIPK1 can activate RIPK3, it is widely assumed that the inflammatory states resulting from Caspase-8 deficiency occur as a consequence of RIPK3-induced necroptosis. Here, we report that although on a <I>Ripk3</I>-null background C<I>asp8</I> deletion in mice does not result in outright pathological changes, it triggers enhanced expression of a variety of inflammatory genes in utero, which gradually subsides after birth. Deletion of <I>Ripk1</I>, or even of only one of its two alleles, obliterates this activation. Resembling the embryonic pathology observed in RIPK3-expressing cells, the activation of inflammatory genes observed on a <I>Ripk3</I>-null background seems to be initiated in endothelial cells. Analysis of endothelial cells isolated from livers of Caspase-8-deficient embryos revealed neither an increase in the amount of RIPK1 in these cells after <I>Casp8</I> deletion, nor triggering of RIPK1 phosphorylation. These findings indicate that the triggering of inflammation by <I>Casp8</I> deletion in mice occurs, in part, independently of necroptosis or other functions of RIPK3, and rather reflects enhanced RIPK1-dependent signaling for activation of inflammatory genes.</P>

Magnetic Order in YbMn2Si2 - Neutron Scattering Investigation

S. J. Campbell,M. Hofmann,R. A. Mole,K. Prokes,D. Wallacher,J. L. Wang 한국물리학회 2013 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.63 No.3

Several mechanisms have been proposed to account for the structural and magnetic behaviour ofthe rare earth intermetallic compound YbMn2Si2 below the transition that occurs around 30 K. We have carried out detailed neutron diffraction measurements over the temperature range 0.3 -52 K and confirm both an antiferromagnetic structure with ferromagnetic Mn (001) planes coupledantiferromagnetically along the c-axis above 30 K and the absence of ordering of the Yb sublatticedown to 0.3 K. The decrease in intensity of the (111) reflection around 30 K together with theappearance of satellite reflections of propagation vector k = 00 12 confirm that the magnetic unitcell doubles along the c axis below TN2. The resultant molecular field acting on half of the ionsbelow 30 K removes the degeneracy of the Kramers doublets of the Yb3+ ions and accounts forthe additional excitations observed below 30 K compared with the inelastic neutron scatteringabove 30 K.

The effect of Al on the hydrogen sorption mechanism of LiBH₄

Friedrichs, O.,Kim, J. W.,Remhof, A.,Buchter, F.,Borgschulte, A.,Wallacher, D.,Cho, Y. W.,Fichtner, M.,Oh, K. H.,Zü,ttel, A. Royal Society of Chemistry 2009 Physical chemistry chemical physics Vol.11 No.10

<P>We demonstrate the synthesis of LiBH<SUB>4</SUB> from LiH and AlB<SUB>2</SUB> without the use of additional additives or catalysts at 450 °C under hydrogen pressure of 13 bar to the following equation: 2LiH + AlB<SUB>2</SUB> + 3H<SUB>2</SUB>↔ 2LiBH<SUB>4</SUB> + Al. By applying AlB<SUB>2</SUB> the kinetics of the formation of LiBH<SUB>4</SUB> is strongly enhanced compared to the formation from elemental boron. The formation of LiBH<SUB>4</SUB> during absorption requires the dissociation of AlB<SUB>2</SUB>, <I>i.e.</I> a coupled reaction. The observed low absorption-pressure of 13 bar, measured during hydrogen cycling, is explained by a low stability of AlB<SUB>2</SUB>, in good agreement with theoretical values. Thus starting from AlB<SUB>2</SUB> instead of B has a rather low impact on the thermodynamics, and the effect of AlB<SUB>2</SUB> on the formation of LiBH<SUB>4</SUB> is of kinetic nature facilitating the absorption by overcoming the chemical inertness of B. For desorption, the decomposition of LiBH<SUB>4</SUB> is not indispensably coupled to the immediate formation of AlB<SUB>2</SUB>. LiBH<SUB>4</SUB> may decompose first into LiH and elemental B and during a slower second step AlB<SUB>2</SUB> is formed. In this case, no destabilization will be observed for desorption. However, due to similar stabilities of LiBH<SUB>4</SUB> and LiBH<SUB>4</SUB>/Al a definite answer on the desorption mechanism cannot be given and neither a coupled nor decoupled desorption can be excluded. At low hydrogen pressures the reaction of LiH and Al gives LiAl under release of hydrogen. The formation of LiAl increases the total hydrogen storage capacity, since it also contributes to the LiBH<SUB>4</SUB> formation in the absorption process.</P> <P> </P> <P>Graphic Abstract</P><P>LiBH<SUB>4</SUB> (LiBD<SUB>4</SUB>) is synthesized by hydrogenation of LiH (LiD) and AlB<SUB>2</SUB> without use of additional additives or catalysts. The reversible reaction mechanism is investigated. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=b814282c'> </P>

Clinical findings influencing time to menarche post gonadotropin-releasing hormone agonist therapy in central precocious puberty

Wu Vickie,Zhao Victoria,Issa Rula,Wilkes Meredith,Wallach Elizabeth,Rapaport Robert,Romero Christopher,Yau Mabel 대한소아내분비학회 2021 Annals of Pediatirc Endocrinology & Metabolism Vol.26 No.3

Purpose: This study aimed to evaluate the time interval to menarche after gonadotropin-releasing hormone agonist (GnRHa) treatment in females with central precocious puberty (CPP) and to identify factors contributing to timing of menarche.Methods: We retrospectively reviewed medical records of 39 females with CPP who reached menarche after GnRHa treatment (leuprolide or histrelin). CPP diagnostic criteria were breast development at <8 years old, measurable pubertal luteinizing hormone and/or estradiol concentrations, and bone age advancement. Indications to treat were advanced bone age and psychosocial concerns. Descriptive summaries were reported as frequency and proportion for categorical variables and mean and standard deviation for continuous measures. Linear regression models were developed to evaluate the associations of clinical factors with the time interval to menarche.Results: Mean age was 9.4±1.6 years at treatment onset, and treatment duration was 2.2±1.4 years. Menarche occurred at 12.6±1.1 years, which was 1.04±0.5 years after treatment discontinuation. This was negatively associated with Tanner stage of breast development and bone age at treatment onset and change in bone age during treatment. No association was seen between time interval to menarche and treatment duration, medication, or body mass index.Conclusion: We found the average time interval to menarche after GnRHa treatment in our population of female patients with CPP to be 1.04±0.5 years; this is in agreement with other reports. Tanner stage of breast development, bone age at treatment onset, and change in bone age were negatively associated with time interval to menarche. These data provide clinical correlates that assist providers during anticipatory guidance of patients with CPP after GnRHa treatment.

Role of active and passive smoking in high-risk human papillomavirus infection and cervical intraepithelial neoplasia grade 2 or worse

Rui-Mei Feng,Shang-Ying Hu,Fang-Hui Zhao,Rong Zhang,Xun Zhang,Asya Izraelit Wallach,You-Lin Qiao 대한부인종양학회 2017 Journal of Gynecologic Oncology Vol.28 No.5

Objective: We performed a pooled analysis to examine cigarette smoking and householdpassive smoke exposure in relation to the risk of human papillomavirus (HPV) infection andcervical intraepithelial neoplasia grade 2+ (CIN2+). Methods: Data were pooled from 12 cross-sectional studies for cervical cancer screeningsfrom 10 provinces of China in 1999–2007. A total of 16,422 women were analyzed, alongwith 2,392 high-risk-HPV (hr-HPV) positive women and 381 CIN2+ cases. Pooled odds ratios(ORs) and 95% confidence intervals (CIs) were estimated using logistic regression modelscontrolling for sexual and non-sexual confounding factors. Results: There was an excess risk between active smoking and hr-HPV infection and CIN2+. Adjusted OR for ever smokers vs. never smokers was 1.45 (95% CI=1.10–1.91), for hr-HPVinfection and 1.89 (95% CI=1.03–3.44), for CIN2+. Passive smoking had a slightly increasedrisk on the hr-HPV infection with adjusted OR 1.11 (1.00–1.24), but no statistical associationwas observed between passive smoke exposure and CIN2+. Compared with the neither activenor passive smokers, both active and passive smokers had a 1.57-fold (95% CI=1.14–2.15)increased risk of HPV infection and a 1.99-fold (95% CI=1.02–3.88) risk of CIN2+. Conclusion: Our large multi-center cross-sectional study found active smoking couldincrease the risk of overall hr-HPV infection and CIN2+ adjusted by passive smoking andother factors. Passive smoking mildly increased the risk of HPV infection but not the CIN2+. An interaction existed between passive tobacco exposure and active smoking for hr-HPVinfection and the CIN2+.