A synopsis of current practices in minimally invasive surgery for adult spinal deformity

To provide a comprehensive summary of the status, indications and developments in the use of minimally invasive surgery in the field of adult spinal deformity. This study was performed by expert review of literature which has been published and is indexed on PubMed. The most appropriate and recent articles were selected to obtain a consolidation of information and knowledge on use and benefits of minimally invasive surgery in adult spinal deformity. Various MIS techniques have been developed to perform the complex ASD surgeries. These include the transforaminal lateral interbody fusion (TLIF), percutaneous segmental fixation as well as the lateral body interbody fusion (LLIF). It is important for a surgeon to obtain a holistic view of current literature and recommended guidelines on the procedures available for ASD surgeries. Overall, minimally invasive spine surgery has resulted in less use of pain medicine, less blood loss, lower infection rates, less requirement for intensive care, less hospitalization, reduction in physiologic stress, reduction in complication rates, reduction in muscle atrophy and preservation of normal motion with fusion rates being as high as 80-95%. More articles consolidating the vast literature on minimally invasive spine surgery need to be published to allow a surgeon to effectively weight the benefits and drawbacks of it. More research needs to be performed to compare the efficacy of sub-types of minimally invasive spine surgery

Lung-specific interleukin 6 mediated transglutaminase 2 activation and cardiopulmonary fibrogenesis

Pulmonary hypertension (PH) pathogenesis is driven by inflammatory and metabolic derangements as well as glycolytic reprogramming. Induction of both interleukin 6 (IL6) and transglutaminase 2 (TG2) expression participates in human and experimental cardiovascular diseases. However, little is known about the role of TG2 in these pathologic processes. The current study aimed to investigate the molecular interactions between TG2 and IL6 in mediation of tissue remodeling in PH. A lung-specific IL6 over-expressing transgenic mouse strain showed elevated right ventricular (RV) systolic pressure as well as increased wet and dry tissue weights and tissue fibrosis in both lungs and RVs compared to age-matched wild-type littermates. In addition, IL6 over-expression induced the glycolytic and fibrogenic markers, hypoxia-inducible factor 1α, pyruvate kinase M2 (PKM2), and TG2. Consistent with these findings, IL6 induced the expression of both glycolytic and pro-fibrogenic markers in cultured lung fibroblasts. IL6 also induced TG2 activation and the accumulation of TG2 in the extracellular matrix. Pharmacologic inhibition of the glycolytic enzyme, PKM2 significantly attenuated IL6-induced TG2 activity and fibrogenesis. Thus, we conclude that IL6-induced TG2 activity and cardiopulmonary remodeling associated with tissue fibrosis are under regulatory control of the glycolytic enzyme, PKM2

The perfect storm: Thrombotic thrombocytopenic purpura (TTP) associated with COVID‐19, a clinical case series and review

Abstract This is a case series of three patients in our hospital system who developed acquired thrombotic thrombocytopenic purpura (aTTP) after testing positive for COVID‐19 infection. Two patients had acute COVID‐19 infections, and one had COVID‐19 IgG antibodies consistent with prior COVID‐19 infection. Twelve additional cases of aTTP after COVID‐19 infection were found in the literature. COVID‐19 creates alterations in the vWF‐ADAMTS‐13 axis with reduced ADAMTS‐13 in acute illness that may lead those patients who are predisposed into fulminant aTTP. Further genetic studies are necessary to uncover why some patients with COVID‐19 can have concurrent aTTP. For those with a prior COVID‐19 infection, molecular mimicry with autoantibodies to ADAMTS‐13 is likely the predominant trigger, but having an underlying predisposition (prior episode of TTP, genetic predisposition to autoimmune conditions, or breast cancer history) creates an environment that could be a possible trigger for aTTP

Splenic infarction due to Epstein-Barr virus infectious mononucleosis: case report and clinical review

Splenic infarction is a rare and likely underdiagnosed complication of Epstein-Barr virus (EBV) associated infectious mononucleosis (IM). Here we describe an 18-year-old male with persistent severe left-sided abdominal pain found to be EBV positive and have a large splenic infarct, along with a transient decrease in protein C, protein S, and antithrombin III activity levels. He was treated with supportive care, and anticoagulated with heparin and apixaban. We review prior reports and perspectives on underlying pathophysiology, diagnosis, and the management of these cases which likely does not require anticoagulation although may be considered on a per case basis.</jats:p

Oncogenic Herpesvirus HHV-8 Promotes Androgen-Independent Prostate Cancer Growth

Abstract Mechanisms underlying progression to androgen-independent prostate cancer following radical ablation therapy remain poorly defined. Although intraprostatic infections have been highlighted as potential cofactors, pathogen influences on pathways that support tumor regrowth are not known. To explore this provocative concept, we derived androgen-sensitive and -insensitive prostate epithelial cells persistently infected with human herpesvirus 8 (HHV-8), an oncogenic herpesvirus that has been detected in normal prostate epithelium, prostate adenocarcinoma, and biologic fluids of patients with prostate cancer, to explore its effects on transition to hormone-refractory disease. Strikingly, we found that HHV-8 infection of androgen-sensitive prostate cancer cells conferred the capacity for androgen-independent growth. This effect was associated with altered expression and transcriptional activity of the androgen receptor (AR). However, HHV-8 infection bypassed AR signaling by promoting enhancer of zeste homolog 2 (EZH2)–mediated epigenetic silencing of tumor-suppressor genes, including MSMB and DAB2IP that are often inactivated in advanced disease. Furthermore, we found that HHV-8 triggered epithelial-to-mesenchymal transition. Although HHV-8 has not been linked etiologically to prostate cancer, virologic outcomes revealed by our study provide mechanistic insight into how intraprostatic infections could constitute risk for progression to androgen-independent metastatic disease where EZH2 has been implicated. Taken together, our findings prompt further evaluations of the relationship between HHV-8 infections and risk of advanced prostate cancer. Cancer Res; 73(18); 5695–708. ©2013 AACR.</jats:p

Supplementary Table 2 from Oncogenic Herpesvirus HHV-8 Promotes Androgen-Independent Prostate Cancer Growth

&lt;p&gt;PDF file - 204K, Microarray analysis of EMT-relevant genes in HHV-8-infected LNCaP-V219 cells cultured in androgen depleted (CSFBS) conditions.&lt;/p&gt;</jats:p

Supplementary Figure 2 from Oncogenic Herpesvirus HHV-8 Promotes Androgen-Independent Prostate Cancer Growth

&lt;p&gt;PDF file - 121K, MSMB induces apoptosis in PC3 cells but reverses HHV-8-induced androgen-independent growth in LNCaP-v219 cells.&lt;/p&gt;</jats:p

Supplementary Table 1 from Oncogenic Herpesvirus HHV-8 Promotes Androgen-Independent Prostate Cancer Growth

&lt;p&gt;PDF file - 112K, Microarray analysis of altered genes in HHV-8-infected LNCaP-V219 cells cultured in androgen depleted (CSFBS) conditions.&lt;/p&gt;</jats:p