Single-procedure 8Fr rheolytic pharmacomechanical thrombectomy for treatment of acute iliofemoral deep venous thrombosis.

Purpose: We hypothesize that single-procedure venous-specific rheolytic thrombectomy for treatment of acute iliofemoral deep venous thrombosis (DVT) will result in improved clinical symptoms as measured by the venous clinical severity score (VCSS), as well as durable venous patency, with decreased hemorrhagic risks and costs associated with conventional catheter-directed therapy and prolonged lytic exposure.

Materials And Methods: Thirty-three consecutive patients with symptomatic, unilateral, iliofemoral DVT who were treated with single-procedure therapy using the 8Fr rheolytic thrombectomy catheter were retrospectively analyzed from 2012-2021. Abstracted data included technical success (> 95% clearance of acute thrombus), adverse events (AEs), and clinical and imaging outcomes at 1-month and 1-year.

Mitochondria play an essential role in the trajectory of adolescent neurodevelopment and behavior in adulthood: evidence from a schizophrenia rat model.

Ample evidence implicate mitochondria in early brain development. However, to the best of our knowledge, there is only circumstantial data for mitochondria involvement in late brain development occurring through adolescence, a critical period in the pathogenesis of various psychiatric disorders, specifically schizophrenia. In schizophrenia, neurodevelopmental abnormalities and mitochondrial dysfunction has been repeatedly reported.

NDUFV2 pseudogene (NDUFV2P1) contributes to mitochondrial complex I deficits in schizophrenia.

Mitochondria together with other cellular components maintain a constant crosstalk, modulating transcriptional and posttranslational processes. We and others demonstrated mitochondrial multifaceted dysfunction in schizophrenia, with aberrant complex I (CoI) as a major cause. Here we show deficits in CoI activity and homeostasis in schizophrenia-derived cell lines.

Isolated Mitochondria Transfer Improves Neuronal Differentiation of Schizophrenia-Derived Induced Pluripotent Stem Cells and Rescues Deficits in a Rat Model of the Disorder.

Dysfunction of mitochondria, key players in various essential cell processes, has been repeatedly reported in schizophrenia (SZ). Recently, several studies have reported functional recovery and cellular viability following mitochondrial transplantation, mostly in ischemia experimental models. Here, we aimed to demonstrate beneficial effects of isolated active normal mitochondria (IAN-MIT) transfer in vitro and in vivo, using SZ-derived induced pluripotent stem cells (iPSCs) differentiating into glutamatergic neuron, as well as a rodent model of SZ.

Preoperative [Tc]MIBI SPECT/CT Interpretation Criteria for Localization of Parathyroid Adenomas-Correlation with Surgical Findings.

Purpose: Minimally invasive surgery for parathyroid adenomas (PTA) requires precise identification and localization of the diseased gland prior to exploration for optimal surgical planning. The Perrier classification allows for accurate, reproducible, and reliable description of PTA location and communication of clinically significant information to surgeons. The current study compares the Perrier localization of PTA on [Tc]methoxyisobutylisonitrile ([Tc]MIBI) single-photon emission computed tomography (SPECT)/X-ray computed tomography (CT) with the results of surgery.

Dexamethasone in the presence of desipramine enhances MAPK/ERK1/2 signaling possibly via its interference with β-arrestin.

Antidepressant medication is the standard treatment for major depression disorder (MDD). However, the response to these treatments is often incomplete and many patients remain refractory. In the present study, we show that the glucocorticoid receptor (GR) agonist dexamethasone (DEX) increased MAPK/ERK1/2 signaling in the presence of the noradrenergic antidepressant, desipramine (DMI), while no such effect was induced by DEX or DMI alone in human neuroblastoma SH-SY5Y cells.

Abnormal neuronal differentiation and mitochondrial dysfunction in hair follicle-derived induced pluripotent stem cells of schizophrenia patients.

One of the prevailing hypotheses suggests schizophrenia as a neurodevelopmental disorder, involving dysfunction of dopaminergic and glutamatergic systems. Accumulating evidence suggests mitochondria as an additional pathological factor in schizophrenia. An attractive model to study processes related to neurodevelopment in schizophrenia is reprogramming of somatic cells into induced pluripotent stem cells (iPSCs) and differentiating them into different neuronal lineages.

Paraoxonase activity and expression is modulated by therapeutics in experimental rat nonalcoholic Fatty liver disease.

Objective. The objective of the present study is to investigate the effect of rosiglitazone, metformin, ezetimibe, and valsartan (alone or in combinations) on paraoxonase (PON) activity and PON-mRNA expression in nonalcoholic fatty liver disease (NAFLD). Methods.

Half-time SPECT acquisition with resolution recovery for Tc-MIBI SPECT imaging in the assessment of hyperparathyroidism.

Purpose: Reduced SPECT acquisition time protocols have been recently developed based on collimator-detector response compensation reconstruction. The present study aims to evaluate the potential use of a short-time technetium-99m methoxyisobutylisonitrile (Tc99m-MIBI) SPECT algorithm in the investigation of parathyroid adenoma (PTA).

Procedures: Ninety patients (59 women; age range, 21-76 years) with biochemical evidence of hyperparathyroidism were referred for Tc99m-MIBI scintigraphy for diagnosis and localization of PTA.

Induced pluripotent stem cells from hair follicles as a cellular model for neurodevelopmental disorders.

Disease-specific induced pluripotent stem cells (iPSC) allow unprecedented experimental platforms for basic research as well as high-throughput screening. This may be particularly relevant for neuropsychiatric disorders, in which the affected neuronal cells are not accessible. Keratinocytes isolated from hair follicles are an ideal source of patients' cells for reprogramming, due to their non-invasive accessibility and their common neuroectodermal origin with neurons, which can be important for potential epigenetic memory.

Differential expression of genes encoding neuronal ion-channel subunits in major depression, bipolar disorder and schizophrenia: implications for pathophysiology.

Evidence concerning ion-channel abnormalities in the pathophysiology of common psychiatric disorders is still limited. Given the significance of ion channels in neuronal activity, neurotransmission and neuronal plasticity we hypothesized that the expression patterns of genes encoding different ion channels may be altered in schizophrenia, bipolar and unipolar disorders. Frozen samples of striatum including the nucleus accumbens (Str-NAc) and the lateral cerebellar hemisphere of 60 brains from depressed (MDD), bipolar (BD), schizophrenic and normal subjects, obtained from the Stanley Foundation Brain Collection, were assayed.

Growth hormone affects gene expression and proliferation in human prostate cancer cells.

We previously showed that growth hormone (GH) receptors (GHR) are expressed in the most commonly studied human prostate cancer (PCa) cell lines and that GHR isoforms undergo differential, cell-type-specific hormonal regulation. We now report that human GH (hGH) can stimulate/modulate insulin-like growth factor (IGF) and β-oestradiol (E(2) ) receptor (ER(β) ) gene expressions in these cells and interact with IGF-I and E(2) to stimulate androgen-dependent LNCaP cell proliferation. We observed a cell type-dependent, differential regulation of IGF axis gene expression by GH: IGF-I was stimulated in the androgen-dependent LNCaP cells; IGF-II was stimulated in androgen-insensitive (AI) PC3 cells; the IGF-I cognate receptor, IGF-IR, was stimulated in LNCaP cells, but inhibited in PC3 cells; IGF-IIR was stimulated in both LNCaP and PC3 cells.

Leptin affects intestinal epithelial cell turnover in correlation with leptin receptor expression along the villus-crypt axis after massive small bowel resection in a rat.

In this study, we examine the responsiveness of intestinal epithelial cell turnover to leptin (LEP) in correlation with leptin receptor (LEPr) expression along the villus-crypt axis in a rat with short bowel syndrome (SBS). Adult rats underwent either a 75% intestinal resection or a transection. SBS-LEP rats underwent bowel resection and were treated with LEP starting from the fourth postoperative day.

Regulation of growth hormone receptors in human prostate cancer cell lines.

We previously demonstrated the gene expression of two growth hormone (GH) receptor (GHR) isoforms in prostate cancer (PCa) patient tissues and human PCa cell lines. In that initial study, we characterized LNCaP cell GH binding characteristics to GHR and its activation of relevant signal transduction pathways. We now show that GH binding to GHR and GHR mRNA expression in the cell lines studied are hormonally regulated.

Leptin accelerates enterocyte turnover during methotrexate-induced intestinal mucositis in a rat.

Gastrointestinal mucositis occurs as a consequence of cytotoxic treatment. In the present study, we tested whether leptin can protect gut epithelial cells from methotrexate (MTX)-induced intestinal damage. Non-pretreated and pretreated with MTX Caco-2 cells were incubated with increasing concentrations of leptin for 24 h.

Effect of oral glutamine on enterocyte turnover during methotrexate-induced mucositis in rats.

Background/aims: The objective of this study was to evaluate the effects of oral glutamine in preventing intestinal mucosal damage caused by methotrexate (MTX) in rats.

Methods: Male Sprague-Dawley rats were divided into 3 experimental groups: control rats, rats treated intraperitoneally with MTX (MTX rats) and rats treated with oral glutamine in the drinking water (2%) 72 h following intraperitoneal injection of a single dose of MTX (MTX-glutamine rats). Intestinal mucosal damage (Park's injury score), mucosal structural changes, enterocyte proliferation and enterocyte apoptosis were determined 72 h following MTX injection.

Neuroanatomical pattern of mitochondrial complex I pathology varies between schizophrenia, bipolar disorder and major depression.

Background: Mitochondrial dysfunction was reported in schizophrenia, bipolar disorderand major depression. The present study investigated whether mitochondrial complex I abnormalities show disease-specific characteristics.

Methodology/principal Findings: mRNA and protein levels of complex I subunits NDUFV1, NDUFV2 and NADUFS1, were assessed in striatal and lateral cerebellar hemisphere postmortem specimens and analyzed together with our previous data from prefrontal and parieto-occipital cortices specimens of patients with schizophrenia, bipolar disorder, major depression and healthy subjects.

The 18-kDa translocator protein, formerly known as the peripheral-type benzodiazepine receptor, confers proapoptotic and antineoplastic effects in a human colorectal cancer cell line.

Objective: The involvement of the 18-kDa translocator protein (TSPO), formerly known as the peripheral-type benzodiazepine receptor, in apoptosis regulation of HT29 colorectal cancer cells was studied in-vitro. In-vivo TSPO involvement in tumor growth of HT29 cells xenografted into SCID mice was studied.

Methods: Knockdown of TSPO expression in the human HT29 cell line was established by stable transfection with vectors containing the TSPO gene in the antisense direction.

Mitochondrial complex I subunits are altered in rats with neonatal ventral hippocampal damage but not in rats exposed to oxygen restriction at neonatal age.

Several independent lines of evidence suggest mitochondrial dysfunction in schizophrenia in brain and periphery, including mitochondrial hypoplasia, dysfunction of the oxidative phosphorylation system, and altered mitochondrial-related gene expression. In an attempt to decipher whether mitochondrial complex I abnormality in schizophrenia is a core pathophysiological process or is attributable to medication, we studied two animal models of schizophrenia related to the neurodevelopmental hypothesis of this disorder. Protein levels of complex I subunits, 24, 51, and 75 kDa, were assessed in neonatal ventral hippocampal lesion rat model and in rats exposed to hypoxia at a neonatal age.

Urokinase plasminogen activator upregulates paraoxonase 2 expression in macrophages via an NADPH oxidase-dependent mechanism.

Objective: Macrophage foam cells are characterized by increased oxidative stress. Macrophage urokinase plasminogen activator (uPA) was shown to contribute to atherosclerosis progression. We hypothesized that uPA atherogenicity is related to its ability to increase macrophage oxidative stress.

Treatment with glutamine is associated with down-regulation of Toll-like receptor-4 and myeloid differentiation factor 88 expression and decrease in intestinal mucosal injury caused by lipopolysaccharide endotoxaemia in a rat.

Recent evidence suggests that lipopolysaccharide (LPS) endotoxaemia in a rat causes significant mucosal injury. Our objective was to determine the effects of glutamine (Gln) on Toll-like receptor 4 (TLR-4), myeloid differentiation factor 88 (Myd88) and tumour necrosis factor (TNF)-alpha receptor-associated factor 6 (TRAF6) expression in intestinal mucosa following LPS endotoxaemia in a rat. For this purpose, male Sprague-Dawley rats were assigned randomly to one of three experimental groups of 10 rats each: (i) control rats underwent intraperitoneal (i.

Responsiveness of intestinal epithelial cell turnover to TGF-alpha after bowel resection in a rat is correlated with EGF receptor expression along the villus-crypt axis.

Recent evidence suggests that transforming growth factor alpha (TGF-alpha) enhances enterocyte proliferation and stimulates intestinal adaptation after massive bowel resection. In the present study, we evaluated the effects of TGF-alpha on enterocyte turnover and correlated it with epidermal-growth factor (EGF) receptor expression along the villus-crypt axis in a rat model of short bowel syndrome (SBS). Male rats were divided into three groups, sham rats underwent bowel transection (group A); SBS rats underwent a 75% bowel resection (group B); and SBS/TGF-alpha rats underwent bowel resection and were treated with TGF-alpha (75 microg/kg) (group C) from the seventh postoperative day.

Sp1 expression is disrupted in schizophrenia; a possible mechanism for the abnormal expression of mitochondrial complex I genes, NDUFV1 and NDUFV2.

Background: The prevailing hypothesis regards schizophrenia as a polygenic disease, in which multiple genes combine with each other and with environmental stimuli to produce the variance of its clinical symptoms. We investigated whether the ubiquitous transcription factor Sp1 is abnormally expressed in schizophrenia, and consequently can affect the expression of genes implicated in this disorder.

Methodology/principal Findings: mRNA of Sp1 and of mitochondrial complex I subunits (NDUFV1, NDUFV2) was analyzed in three postmortem brain regions obtained from the Stanley Foundation Brain Collection, and in lymphocytes of schizophrenic patients and controls.

Urokinase plasminogen activator (uPA) stimulates cholesterol biosynthesis in macrophages through activation of SREBP-1 in a PI3-kinase and MEK-dependent manner.

Urokinase plasminogen activator (uPA) is expressed in human atherosclerotic lesions, predominantly in macrophages, and contributes to atherosclerosis progression. Since atherogenesis is characterized by the formation of cholesterol-loaded macrophage foam cells, we questioned whether uPA atherogenicity may involve macrophage cholesterol accumulation, and by what mechanisms. uPA increased cellular cholesterol content by 44% (mainly unesterified cholesterol) in THP-1 macrophages, and this effect was inhibited by statins.