The Law of Equitable Distribution: When Is Domestic Violence More Than Just a Factor in Divorce?

(Excerpt) Imagine you are married. After many years there are problems in your marriage. Some of these issues are beyond your control. You find out that your spouse is cheating on you. You plan to come home from work and confront your spouse about their infidelities. You even begin to think about the divorce process, confronting the concerns raised in your mind. I’ll be okay. I have a great career, I have worked my entire life, and I have saved. I will be okay. That night you approach your spouse. After an argument breaks out, you tell your spouse that you are leaving them. But they get angry. They get so enraged that they attack you in the basement of your marital home. “You’re never going to go anywhere [,]” they say, strangling you. “Now you are going to die.” In 2011, Laura Panek’s husband attacked her, tied a rope around her neck, and attempted to strangle her. Miraculously, she survived the near-death ordeal. Laura’s husband pled guilty to first-degree strangulation and was sentenced to eleven years in prison. Soon after, she filed for divorce. Laura’s attempt for justice was met by months of litigation, during which she was forced to relive her harrowing ordeal in civil court. And in the end, justice was not served. Concerning the parties’ marital assets, the judge awarded Laura’s abuser-spouse a significant portion of her pension fund. Therefore, after retiring in 2019, Laura was forced to make monthly pension distributions to her ex-husband while he continued serving his prison sentence for attempting to kill her. Domestic violence comes in many shapes and sizes, devastating all types of communities regardless of age, sex, or economic status. It includes “willful intimidation, physical assault, battery, sexual assault, and/or other abusive behavior as part of a systematic pattern of power and control” by an intimate partner, such as a spouse. Unfortunately, Laura’s story is not unique— 20% of marriages involve domestic violence. In the United States, 25% of women and 10% of men will experience domestic violence by their intimate partner in their lifetime. In addition to the physical and emotional impact, victims also face financial devastation. Medical costs directly related to intimate partner violence are estimated at more than $4 billion per year, and additional economic hardships are attributable to the loss of work survivors face

Transient activation of mucosal effector immune responses by resident intestinal bacteria in normal hosts is regulated by interleukin-10 signalling

Interleukin-10 (IL-10) is a key regulator of mucosal homeostasis. In the current study we investigated the early events after monoassociating germ-free (GF) wild type (WT) mice with an E. coli strain that we isolated previously from the cecal contents of a normal mouse housed under specific pathogen free (SPF) conditions. Our results show that IFN-γ secreted by mesenteric lymph node (MLN) cells from both IL-10 deficient mice and WT mice, stimulated ex vivo with E. coli lysate, was dramatically higher at day 4 after monoassociation compared to IFN-γ secreted by cells from GF mice without E. coli colonization. Production of IFN-γ rapidly and progressively declined after colonization of WT but not IL-10 deficient mice. E. coli lysate-stimulated WT MLN cells also produced IL-10 that peaked at day 4 and subsequently declined, but not as precipitously as IFN-γ. WT cells that express CD4, CD8, and NKp46 produced IFN-γ; WT CD4-positive cells and B cells produced IL-10. Recombinant IL-10 added to E. coli-stimulated MLN cell cultures inhibited IFN-γ secretion in a dose-dependent fashion. MLN cells from WT mice treated in vivo with neutralizing anti-IL-10 receptor antibody produced more IFN-γ compared with MLN cells from isotype control antibody-treated mice. These findings show that a resident E. coli that induces chronic colitis in monoassociated IL-10 deficient mice rapidly but transiently activates the effector immune system in normal hosts, in parallel with induction of protective IL-10 produced by B cells and CD4(+) cells that subsequently suppresses this response to mediate mucosal homeostasis. This article is protected by copyright. All rights reserved

Antigen-Presenting Cell Production of IL-10 Inhibits T-Helper 1 and 17 Cell Responses and Suppresses Colitis in Mice

IL-10 deficient mice develop TH1/TH17-mediated colitis and IL-10-producing regulatory T cells suppress colitis, implicating IL-10 in maintaining mucosal homeostasis. We transferred germ-free (GF) or specific pathogen free (SPF) CD4+ cells from wild-type (wt) or IL-10−/− (ko) mice into wt or IL-10 ko Rag2−/− recipients to assess the relative importance of immunoregulatory IL-10 derived from T cells vs. antigen presenting cells (APC)

Reduced ratio of protective versus proinflammatory cytokine responses to commensal bacteria in HLA-B27 transgenic rats

Germ-free HLA-B27 transgenic (TG) rats do not develop colitis, but colonization with specific pathogen-free (SPF) bacteria induces colitis accompanied by immune activation. To study host-dependent immune responses to commensal caecal bacteria we investigated cytokine profiles in mesenteric lymph node (MLN) cells from HLA-B27 TG versus nontransgenic (non-TG) littermates after in vitro stimulation with caecal bacterial lysates (CBL). Supernatants from CBL-stimulated unseparated T- or B- cell-depleted MLN cells from HLA-B27 TG and non-TG littermates were analysed for IFN-γ, IL-12, TNF, IL-10 and TGF-β production. Our results show that unfractionated TG MLN cells stimulated with CBL produced more IFN-γ, IL-12 and TNF than did non-TG MLN cells. In contrast, CBL-stimulated non-TG MLN cells produced more IL-10 and TGF-β. T cell depletion abolished IFN-γ and decreased IL-12 production, but did not affect IL-10 and TGF-β production. Conversely, neither IL-10 nor TGF-β was produced in cultures of B cell-depleted MLN. In addition, CD4+ T cells enriched from MLN of HLA-B27 TG but not from non-TG rats produced IFN-γ when cocultured with CBL-pulsed antigen presenting cells from non-TG rats. Interestingly, IL-10 and TGF-β, but not IFN-γ, IL-12 and TNF were produced by MLN cells from germ-free TG rats. These results indicate that the colitis that develops in SPF HLA-B27 TG rats is accompanied by activation of IFN-γ-producing CD4+ T cells that respond to commensal bacteria. However, B cell cytokine production in response to components of commensal intestinal microorganisms occurs in the absence of intestinal inflammation

Bifidobacterium animalis causes extensive duodenitis and mild colonic inflammation in monoassociated interleukin-10-deficient mice:

We recently showed that Bifidobacterium animalis is more prevalent within the colons of IL-10 deficient (−/−) mice than in wild type (WT) animals colonized with the same specific pathogen free (SPF) fecal contents. Here we tested the ability of this organism to cause T cell-mediated intestinal inflammation by introducing it into germ-free (GF) IL-10−/− mice

Моделирование стационарных и переходных расходно-частотных характеристик расходомера газа турбинного типа

На підставі розробленої авторами за допомогою CFD технологій комп'ютерної моделі турбінного витратоміра проаналізовані частотно-витратні характеристики в статичних і динамічних умовах, а також помилки вимірювання та запропоновані шляхи їх зменшення.On the basis of CFD technology and developed by authors a computer model for turbine flow meter the frequency-expense static and dynamic characteristics were analyzed as well as the measurement errors and the ways of their reducing are offered.На основе разработанной авторами с помощью CFD технологий компьютерной модели турбинного расходомера проанализированы частотно-расходные характеристики в статических и динамических условиях, а также ошибки измерения и предложены пути их уменьшения

Variable phenotypes of enterocolitis in interleukin 10-deficient mice monoassociated with two different commensal bacteria

BACKGROUND & AIMS: To explore the hypothesis that selective immune responses to distinct components of the intestinal microflora induce intestinal inflammation, we characterized disease kinetics and bacterial antigen-specific T-cell responses in ex germ-free interleukin 10 -/- and wild-type control mice monoassociated with Enterococcus faecalis , Escherichia coli , or Pseudomonas fluorescens . METHODS: Colitis was measured by using blinded histological scores and spontaneous interleukin 12 secretion from colonic strip culture supernatants. Interferon gamma secretion was measured from mesenteric or caudal lymph node CD4 + T cells stimulated with bacterial lysate-pulsed antigen-presenting cells. Luminal bacterial concentrations were measured by culture and quantitative polymerase chain reaction. RESULTS: Escherichia coli induced mild cecal inflammation after 3 weeks of monoassociation in interleukin 10 -/- mice. In contrast, Enterococcus faecalis-monoassociated interleukin 10 -/- mice developed distal colitis at 10-12 weeks that was progressively more severe and associated with duodenal inflammation and obstruction by 30 weeks. Neither bacterial strain induced inflammation in wild-type mice, and germ-free and Pseudomonas fluorescens-monoassociated interleukin 10 -/- mice remained disease free. CD4 + T cells from Enterococcus faecalis- or Escherichia coli-monoassociated interleukin 10 -/- mice selectively produced higher levels of interferon gamma and interleukin 4 when stimulated with antigen-presenting cells pulsed with the bacterial species that induced disease; these immune responses preceded the onset of histological inflammation in Enterococcus faecalis -monoassociated mice. Luminal bacterial concentrations did not explain regional differences in inflammation. CONCLUSIONS: Different commensal bacterial species selectively initiate immune-mediated intestinal inflammation with distinctly different kinetics and anatomic distribution in the same host