Rapid,Full-Scale Change to Virtual PCIT During the COVID-19 Pandemic: Implementation and Clinical Implications

Health agencies call for the immediate mobilization of existing interventions in response to numerous child and family mental health concerns that have arisen as result of the COVID-19 pandemic. Answering this call, this pilot study describes the rapid, full-scale change from a primarily clinic-based Parent–Child Interaction Therapy (PCIT) model to a virtual service model (i.e., I-PCIT) in an academic and community-based program in Miami, Florida. First, we describe the virtual service training model our program developed and its implementation with 17 therapists (M_Age?=?32.35, 88.2% female, 47.1% Hispanic) to enable our clinic to shift from providing virtual services to a small portion of the families served (29.1%) to all of the families served. Second, we examine the effect of I-PCIT on child and caregiver outcomes during the 2-month stay-at-home period between March 16, 2020, and May 16, 2020, in 86 families (M_ChildAge?=?4.75, 71% Hispanic). Due to the rapid nature of the current study, all active participants were transferred to virtual services, and therefore there was no comparison or control group, and outcomes represent the most recently available scores and not treatment completion. Results reveal that I-PCIT reduced child externalizing and internalizing problems and caregiver stress, and increased parenting skills and child compliance with medium to large effects even in the midst of the COVID-19 pandemic. Finally, the study examined components of our virtual service training model associated with the greatest improvements in child and caregiver outcomes. Preliminary findings revealed that locally and collaboratively developed strategies (e.g., online communities of practice, training videos and guides) had the strongest association with child and caregiver outcomes. Implications for virtual service delivery, implementation, and practice in the midst of the COVID-19 pandemic are discussed.

     

Mitochondrial dysfunction in antiphospholipid syndrome: implications in the pathogenesis of the disease and effects of coenzyme Q(10) treatment

The exact mechanisms underlying the role of oxidative stress in the pathogenesis and the prothrombotic or proinflammatory status of antiphospholipid syndrome (APS) remain unknown. Here, we investigate the role of oxidative stress and mitochondrial dysfunction in the proatherothrombotic status of APS patients induced by IgG-antiphospholipid antibodies and the beneficial effects of supplementing cells with coenzyme Q(10) (CoQ(10)). A significant increase in relevant prothrombotic and inflammatory parameters in 43 APS patients was found compared with 38 healthy donors. Increased peroxide production, nuclear abundance of Nrf2, antioxidant enzymatic activity, decreased intracellular glutathione, and altered mitochondrial membrane potential were found in monocytes and neutrophils from APS patients. Accelerated atherosclerosis in APS patients was found associated with their inflammatory or oxidative status. CoQ(10) preincubation of healthy monocytes before IgG-antiphospholipid antibody treatment decreased oxidative stress, the percentage of cells with altered mitochondrial membrane potential, and the induced expression of tissue factor, VEGF, and Flt1. In addition, CoQ(10) significantly improved the ultrastructural preservation of mitochondria and prevented IgG-APS-induced fission mediated by Drp-1 and Fis-1 proteins. In conclusion, the oxidative perturbation in APS patient leukocytes, which is directly related to an inflammatory and pro-atherothrombotic status, relies on alterations in mitochondrial dynamics and metabolism that may be prevented, reverted, or both by treatment with CoQ(10).     

Regulation by nitric oxide of endotoxin-induced tissue factor and plasminogen activator inhibitor-1 in endothelial cells

The increase in nitric oxide (NO) production in lipopolysaccharide (LPS)-induced sepsis is thought to contribute to the development of shock. However, NO could also play an antithrombotic role. Little is known about the modulating effect of NO on the endothelial overexpression and production of tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) occurring in endotoxemia. We analyzed the effect of N(G)-nitro-L-arginine-methyl-ester (L-NAME), an inhibitor of NO synthases, and S-nitroso-N-acetyl-D,L-penicillamine (SNAP), a NO donor, on the expression and synthesis of TF and PAI-1 by LPS-challenged human umbilical vein endothelial cells (HUVEC): L-NAME enhanced the increase in TF mRNA and antigen levels (P <0.05) observed in LPS-treated HUVEC; SNAP down-regulated the LPS-induced TF increment (p <0.05). However, no effects of NO on regulation of the LPS-dependent increase in PAI-1 could be seen. Thus, NO could play an antithrombotic role in sepsis by down-regulating the endothelial overexpression and production of TF.     

Primary tuberculosis of parotid gland

A young female presented with complaint of swelling of the parotid region for one year. She was diagnosed as a case of primary tubercular parotiditis. The diagnosis was confirmed by fine needle aspiration cytology. She was managed with antitubercular drugs. After completing the course the swelling resolved completely and there was no recurrence.     

Antitumor components ofAgrocybe cylindracea

To find pharmacologically active components ofAgrocybe cylindracea, its basidiocarps were extracted with water. The extracts were separated by DEAE cellulose column chromatography, Sepharose CL-4B gel filtration, and Concanavalin A-Sepharose 4B affinity chromatography. Among the obtained fractions fromA. cylindracea, fraction IN which was the neutral proteinbound-polysaccharide fraction exhibited a marked antitumor activity and it was tentatively named “Cylindan”. It showed about 70% of tumor inhibition against the solid form of sarcoma 180 when a dose of 30 mg/kg/day was intraperitoneally injected into ICR mice. When each fraction was examined by chemical analysis, Cylindan consisted of 85% polysaccharide, 3% protein and 1% hexosamine. Its polysaccharide moiety contained glucose, mannose, fucose and galactose and its protein moiety contained the comparatively large amounts of aspartic acid and glycine, and other 11 amino acids.     

Spatial learning results in elevated agmatine levels in the rat brain

Accumulating evidence suggests that agmatine, a metabolite of L-arginine by arginine decarboxylase, is a novel neurotransmitter, and exogenous agmatine can modulate behavior functions including learning and memory. However, direct evidence of its involvement in learning and memory processes is currently lacking. This study measured agmatine levels in the hippocampus, parahippocampal region, cerebellum, and vestibular nucleus in rats that were trained to find a hidden escape platform in the water-maze task, or forced to swim in the pool with no platform presented, or kept in the holding-box, using liquid chromatography/mass spectrometry. Compared with the swimming only group and holding-box group, agmatine levels were significantly increased in the CA1 and dentate gyrus subregions of the hippocampus, the entorhinal cortex and the vestibular nucleus in the water-maze training group. These results, for the first time, demonstrate spatial learning-induced region-specific elevation in agmatine, and raise a novel issue of the involvement of agmatine in the processes of learning and memory.     

Coordinated deregulation of cellular receptors, proangiogenic factors and intracellular pathways in acute myeloid leukaemia

Different signaling routes seem to be simultaneously triggered in leukemia, with distinct and overlapping activities. To analyze if altered signals are coordinated and to evaluate their effect on this disease, we have investigated in acute myeloid leukemia samples (AML) the expression and activation status of procoagulant/proangiogenic tissue factor receptor (TF), angiogenic protein VEGF, its cell surface receptor, KDR, and two intracellular proteins involved in their regulation: extracellular regulated kinase (ERK1/2) and nuclear factor kappa-B (NFkappaB). Significantly higher mRNA and protein levels of VEGF, KDR, and TF were found in the AML samples versus controls. Enhanced ERK phosphorylation and NFkappaB activation in most AML samples were also found. In vitro MEK/ERK and NFkappaB-binding activity blockade suppressed the constitutive expression of TF, VEGF, and KDR. Anti-TF antibody treatment significantly suppressed VEGF and KDR expression as well as ERK activation, suggesting that TF expressed by AML cells may be both a regulatory target and a mediator of tumor-associated angiogenesis. Patients showing parallel activation of the studied proteins trended to exhibit higher incidence of fatal outcome. Our results show a coordinated deregulation of cellular receptors, proangiogenic factors, and intracellular pathways in leukemia cells, which may help to design mechanism-based combinations of single transduction-related therapies.