Silvicultural Practices in the Management of (Tendu) Leaf Production: Options and Trade-offs.

Non-timber forest products (NTFPs) are known to provide livelihoods for forest-based communities across the world. While ensuring the sustainability of NTFP harvests is a key challenge, optimizing the production of NTFPs through appropriate silvicultural practices is also critical for forest-based economies. In Central India, the suitability of fire or pruning practices for enhancing the production of leaves of the tendu tree () has been much debated.

Safety and efficacy of mycophenolate in COVID-19: a nonrandomised prospective study in western India.

Background: Antivirals and immunosuppressive agents are used with variable success in the treatment of COVID-19. Mycophenolate, an inhibitor of enzyme inosine monophosphate dehydrogenase, is an immunosuppressant used to prevent allograft rejection and other autoimmune diseases. Few laboratory studies have also reported antiviral properties of mycophenolate.

Using interview surveys and multispecies occupancy models to inform vertebrate conservation.

Species distribution data are an essential biodiversity variable requiring robust monitoring to inform wildlife conservation. Yet, such data remain inherently sparse because of the logistical challenges of monitoring biodiversity across broad geographic extents. Surveys of people knowledgeable about the occurrence of wildlife provide an opportunity to evaluate species distributions and the ecology of wildlife communities across large spatial scales.

Cavernous sinus thrombosis following dental extraction: a rare case report and forgotten entity.

Prior to the advent of efficacious antimicrobial agents, the mortality rate from cavernous sinus thrombosis (CST) was effectively 100%. There have been very few reports of CST associated with tooth extraction. A 40-year-old female presented to the emergency room with swelling over the right side of the face and history of extraction in the upper right region by an unregistered dental practitioner.

CHO-Omics Review: The Impact of Current and Emerging Technologies on Chinese Hamster Ovary Based Bioproduction.

CHO cells are the most prevalent platform for modern bio-therapeutic production. Currently, there are several CHO cell lines used in bioproduction with distinct characteristics and unique genotypes and phenotypes. These differences limit advances in productivity and quality that can be achieved by the most common approaches to bioprocess optimization and cell line engineering.

Osteosarcoma: A Diagnostic Dilemma.

Osteosarcoma is a primeval disease which is still partly understood. It is a malignancy of mesenchymal cells that have the capacity to generate osteoid or immature bone. There have been an abundance of debate and controversies about the nature, aggressiveness, behavior, and various treatment modalities of this entity.

Histone deacetylase inhibitors prevent pulmonary endothelial hyperpermeability and acute lung injury by regulating heat shock protein 90 function.

Transendothelial hyperpermeability caused by numerous agonists is dependent on heat shock protein 90 (Hsp90) and leads to endothelial barrier dysfunction (EBD). Inhibition of Hsp90 protects and restores transendothelial permeability. Hyperacetylation of Hsp90, as by inhibitors of histone deacetylase (HDAC), suppresses its chaperone function and mimics the effects of Hsp90 inhibitors.

p53 protects against LPS-induced lung endothelial barrier dysfunction.

New therapies toward heart and blood vessel disorders may emerge from the development of Hsp90 inhibitors. Several independent studies suggest potent anti-inflammatory activities of those agents in human tissues. The molecular mechanisms responsible for their protective effects in the vasculature remain unclear.

Novel mechanism of attenuation of LPS-induced NF-κB activation by the heat shock protein 90 inhibitor, 17-N-allylamino-17-demethoxygeldanamycin, in human lung microvascular endothelial cells.

Heat shock protein (hsp) 90 inhibition attenuates NF-κB activation and blocks inflammation. However, the precise mechanism of NF-κB regulation by hsp90 in the endothelium is not clear. We investigated the mechanisms of hsp90 inhibition by 17-N-allylamino-17-demethoxygeldanamycin (17-AAG) on NF-κB activation by LPS in primary human lung microvascular endothelial cells.

Heat shock protein 90 inhibitors prevent LPS-induced endothelial barrier dysfunction by disrupting RhoA signaling.

Permeability of the endothelial monolayer is increased when exposed to the bacterial endotoxin LPS. Our previous studies have shown that heat shock protein (Hsp) 90 inhibitors protect and restore LPS-mediated hyperpermeability in bovine pulmonary arterial endothelial cells. In this study, we assessed the effect of Hsp90 inhibition against LPS-mediated hyperpermeability in cultured human lung microvascular endothelial cells (HLMVECs) and delineated the underlying molecular mechanisms.

LPS induces pp60c-src-mediated tyrosine phosphorylation of Hsp90 in lung vascular endothelial cells and mouse lung.

Heat shock protein 90 (Hsp90) inhibitors were initially developed as anticancer agents; however, it is becoming increasing clear that they also possess potent anti-inflammatory properties. Posttranslational modifications of Hsp90 have been reported in tumors and have been hypothesized to affect client protein- and inhibitor-binding activities. In the present study we investigated the posttranslational modification of Hsp90 in inflammation.

Heat shock protein 90 inhibition depletes TrkA levels and signaling in human acute leukemia cells.

Nerve growth factor (NGF) induces autophosphorylation and downstream progrowth and prosurvival signaling from the receptor tyrosine kinase TrkA. Overexpression or activating mutation of TrkA has been described in human acute myeloid leukemia cells. In the present study, we show the chaperone association of TrkA with heat shock protein 90 (hsp90) and the inhibitory effect of the hsp90 inhibitor, 17-DMAG, on TrkA levels and signaling in cultured and primary myeloid leukemia cells.

Role of CAAT/enhancer binding protein homologous protein in panobinostat-mediated potentiation of bortezomib-induced lethal endoplasmic reticulum stress in mantle cell lymphoma cells.

Purpose: Bortezomib induces unfolded protein response (UPR) and endoplasmic reticulum stress, as well as exhibits clinical activity in patients with relapsed and refractory mantle cell lymphoma (MCL). Here, we determined the molecular basis of the improved in vitro and in vivo activity of the combination of the pan-histone deacetylase inhibitor panobinostat and bortezomib against human, cultured, and primary MCL cells.

Experimental Design: Immunoblot analyses, reverse transcription-PCR, and immunofluorescent and electron microscopy were used to determine the effects of panobinostat on bortezomib-induced aggresome formation and endoplasmic reticulum stress in MCL cells.

Treatment with panobinostat induces glucose-regulated protein 78 acetylation and endoplasmic reticulum stress in breast cancer cells.

Increased levels of misfolded polypeptides in the endoplasmic reticulum (ER) triggers the dissociation of glucose-regulated protein 78 (GRP78) from the three transmembrane ER-stress mediators, i.e., protein kinase RNA-like ER kinase (PERK), activating transcription factor-6 (ATF6), and inositol-requiring enzyme 1alpha, which results in the adaptive unfolded protein response (UPR).

Cotreatment with panobinostat and JAK2 inhibitor TG101209 attenuates JAK2V617F levels and signaling and exerts synergistic cytotoxic effects against human myeloproliferative neoplastic cells.

The mutant JAK2V617F tyrosine kinase (TK) is present in the majority of patients with BCR-ABL-negative myeloproliferative neoplasms (MPNs). JAK2V617F activates downstream signaling through the signal transducers and activators of transcription (STAT), RAS/mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3 (PI3)/AKT pathways, conferring proliferative and survival advantages in the MPN hematopoietic progenitor cells (HPCs). Treatment with the pan-histone deacetylase (HDAC) inhibitor panobinostat (PS) is known to inhibit the chaperone function of heat shock protein 90, as well as induce growth arrest and apoptosis of transformed HPCs.

Co-treatment with heat shock protein 90 inhibitor 17-dimethylaminoethylamino-17-demethoxygeldanamycin (DMAG) and vorinostat: a highly active combination against human mantle cell lymphoma (MCL) cells.

Heat shock protein (hsp) 90 inhibitors promote proteasomal degradation of pro-growth and pro-survival hsp90 client proteins, including CDK4, c-RAF and AKT, and induce apoptosis of human lymphoma cells. The pan-histone deacetylase inhibitor vorinostat has also been shown to induce growth arrest and apoptosis of lymphoma cells. Here, we determined the effects of the more soluble, orally bio-available, geldanamycin analogue 17-NN-dimethyl ethylenediamine geldanamycin (DMAG, Kosan Biosciences Inc.

Panobinostat treatment depletes EZH2 and DNMT1 levels and enhances decitabine mediated de-repression of JunB and loss of survival of human acute leukemia cells.

The PRC2 complex protein EZH2 is a histone methyltransferase that is known to bind and recruit DNMT1 to the DNA to modulate DNA methylation. Here, we determined that the pan-HDAC inhibitor panobinostat (LBH589) treatment depletes DNMT1 and EZH2 protein levels, disrupts the interaction of DNMT1 with EZH2, as well as de-represses JunB in human acute leukemia cells. Similar to treatment with the hsp90 inhibitor 17-DMAG, treatment with panobinostat also inhibited the chaperone association of heat shock protein 90 with DNMT1 and EZH2, which promoted the proteasomal degradation of DNMT1 and EZH2.

Akt activates NOS3 and separately restores barrier integrity in H2O2-stressed human cardiac microvascular endothelium.

The integrity of microvascular endothelium is an important regulator of myocardial contractility. Microvascular barrier integrity could be altered by increased reactive oxygen species (ROS) stress seen within minutes after cardiac arrest resuscitation. Akt and its downstream target nitric oxide (NO) synthase (NOS)3 can protect barrier integrity during ROS stress, but little work has studied these oxidant stress responses in human cardiac microvascular endothelial cells (HCMVEC).

NPH4/ARF7 and ARF19 promote leaf expansion and auxin-induced lateral root formation.

Auxin response factors (ARFs) bind auxin response promoter elements and mediate transcriptional responses to auxin. Five of the 22 ARF genes in Arabidopsis thaliana encode ARFs with glutamine-rich middle domains. Four of these can activate transcription and have been ascribed developmental functions.

Plating of the distal radius.

Distal radius fractures are common injuries that can be treated by a variety of methods. Restoration of the distal radius anatomy within established guidelines yields the best short- and long-term results. Guidelines for acceptable reduction are (1) radial shortening < 5 mm, (2) radial inclination > 15 degrees , (3) sagittal tilt on lateral projection between 15 degrees dorsal tilt and 20 degrees volar tilt, (4) intra-articular step-off < 2 mm of the radiocarpal joint, and (5) articular incongruity < 2 mm of the sigmoid notch of the distal radius.

Acute injuries of the distal radioulnar joint and triangular fibrocartilage complex.

Distal radioulnar joint disorders have become increasingly recognized. Over the past decade, advances in functional anatomy, kinematics, advanced imaging, and arthroscopy have improved understanding of distal radioulnar joint disorders and their management. In the past, injuries to the triangular fibrocartilage complex and distal radioulnar joint have been regarded as related but separate entities.