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ProPride 3P hitch for sale, only used for 4 camping trips about local miles. The hitch was on the travel trailer for about a year covered with Propride covers. I took the hitch off to inspect it, clean it, and paint touch up and ended up upgrading to a 5th wheel.

The hitch is in excellent shape and was used to pull a 30ft travel trailer with an F I upgraded to the Propride from the cheap dealer installed hitch because of issues with sway. This hitch fixed all those issues. The weight distribution bars are Local pick up for the price, will consider shipping but must negotiate the shipping charges.

Includes the custom covers and brake cord extension. Propride lb hitch for sale. Includes extension set and covers. Used 3 times. Sold camper so do not need. Local pick up due to cost of shipping this would be very expensive.

I have an equalizer hitch for sale. It is a combination of a load leveler and anti-sway hitch. About five years old. Used very little. In excellent condition. I even have the original owners manual, as well with installation instructions and diagrams. The stamp on top of the ball says it is rated fo Hitch is too large for my tractor. Make reasonable offer. It's in excellent condition. Always used a nylon plate between the pin box and the hitch head so the paint is not damaged.

The hitch has always been kept out of the weather except when towing. Great for a E2 weight distribution hitch for sale. This hitch is in excellent condition and was only used for a short time. We purchased a new travel trailer in Colorado and needed a hitch to get the trailer home. We already owned a hitch for the trailer, but were 1, miles from home.This banner text can have markup.

Search the history of over billion web pages on the Internet. PREFACE This volume is essentially a cumulation of the monthly bibliography of the Journal of Political Economy and comprises the material published in the separate issues from February,to January,inclusive. The list of titles is thus so nearly coincident with a list of economic pub- lications of the year that it is reasonably accurate to call this volume a Bibliography of Economics for The attempt has been to provide an exhaustive index of all publications of economic interest in the following fields: I.

Books published in the English, French, German, and Italian languages. The government pubhcations of the United States and of Great Britain. Periodical references including book reviews of four or more pages in a selected list of periodicals. Fugitive material, including such items as the more important publications of foreign governments other than Great Britainreports of various organiza- tions, pamphlets, etc.

The limitations of the volume are obvious. It does not index works in all languages; several fruitful fields, such as those of labor union publica- cations, trade and technical journals, etc. Nevertheless, it is hoped that the work as a whole will prove to be serviceable. Its 7, to 7, entries include most of the economic titles of large or permanent value issued inand defects in arrangement and technique are incidental, not vital.

The subject index and cross-references will enable the student to find the material he desires. The value of this material can best be judged by the reader. He alone knows what data are of importance to him. Possibly particular mention should be made of the fact that publications of the various states of the United States are not listed.

Such listing seemed unnecessary in view of the recent establishment of a Monthly List of State Puhlications by the Library of Congress. The heavy work in the compilation and cumulation of this bibliography has been performed largely by Miss Maud Lavery, to whom is due much of whatever merit the result possesses.

Theory i 1. General Works 2. History and Development 3. Scope and Method 4. Teaching of Economics5. Particular Topics II. Economic History. General 2.

Europe 3. The United States 4. Gilds 5. Resources and Economic Conditions. Economic and Commercial Geography 2. Fisheries 3.Hyperglycemia- HG- Amadori-glycated albumin- AGA- induced activation of microglia and monocytes and their adherence to retinal vascular endothelial cells contribute to retinal inflammation leading to diabetic retinopathy DR.

There is a great need for early detection of DR before demonstrable tissue damages become irreversible. Extracellular adenosine, required for endogenous anti-inflammation, is regulated by the interplay of equilibrative nucleoside transporter with adenosine deaminase ADA and adenosine kinase.

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However, because ADA2 gene has not been identified in mouse genome, how diabetes alters adenosine-dependent anti-inflammation remains unclear. Studies of pig retinal microglia and human macrophages revealed a causal role of ADA2 in inflammation. In the vitreous of diabetic patients, decreased miRb-3p is associated with increased ADA2 activity.

These results suggest a regulatory role of miRb-3p in diabetes related retinal inflammation by suppressing ADA2. Diabetic retinopathy DR is a leading cause of blindness among working-age adults.

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Treatment options for DR remain limited and with adverse effects. Major complications in DR include blood-retinal barrier dysfunction and loss of retinal neurons [ 1 — 3 ]. Although these changes may be a major vision-threatening complication in diabetes, by the time they become easily demonstrable, tissue damage has already occurred.

Therefore, there is a great need for early detection and intervention of DR during the prediabetic phase. During early diabetes, retinal immune cell activation causes retinal inflammation leading to major DR complications.

These cells are involved in proinflammatory as well as anti-inflammatory processes.

doten nc 3p

A2AAR, a Gs-coupled adenosine receptor, plays a major role in anti-inflammation. Extracellular concentrations of adenosine are regulated by the interplay of the equilibrative nucleoside transporter ENT with intra- and extracellular enzymes of adenosine metabolism.

During inflammation, an increase in ADA2 has been found in macrophage-rich tissues [ 67 ]. ADA2 activity is elevated significantly in pleural fluids of patients with pulmonary tuberculosis [ 8 ], sera from HIV-infected individuals [ 910 ], and from patients with diabetes [ 11 ], making ADA2 activity a convenient marker to improve the diagnosis and follow-up treatment of these disorders.

It was shown that ADA2 is important for monocyte differentiation and stimulation of macrophage proliferation [ 12 ]. The search for a rodent ADA2 gene by analysis at the critical region at or near the human chromosome 22 pericentromere in humans and the region of conserved synteny in mice has not been successful [ 1314 ].

The role of ADA2, therefore, has been understudied in mice as the sequencing probes or antibodies to mouse ADA2 are not available [ 15 ]. These results suggest that retinal inflammation in DR is mediated by ADA2 and that the anti-inflammatory activity of adenosine receptor signaling is impaired in diabetes due to increased ADA2 activity.

A number of factors regulate gene expression at the transcriptional and translational levels during developmental and diseased conditions.

doten nc 3p

Dysregulation of miRNAs has been shown to contribute to many types of human diseases, including neuronal disorders [ 151819 ].

In contrast to the well-studied miRb-5p, the targets of miRb-3p involved in diabetes are not well studied.Metrics details. Esophageal cancer is a high incident cancer worldwide with poor survival and limited therapeutic options. Alterations of microRNAs are common in cancers, and many of these micro RNAs are potential therapeutic and diagnostic targets to treat these cancers.

However, the biological functions, clinical significance and therapeutic implications of miRb-3p in ESCC remain unclear. Ectopic overexpression of miRb-3p in ESCC cells, mouse xenograft model, and metastasis model were used to evaluate the effects of miRb-3p on proliferation, and migration of cancer cells. Luciferase reporter assay and Western blot were performed to validate the potential targets of miRb-3p after the preliminary screening by computer-aided microarray analysis. We found that miRb-3p expression levels were significantly upregulated in the tumor tissues and serum samples of patients with ESCC.

The expression levels of miRb-3p in both tumor tissues and serum samples were inversely associated with lymph node metastasis and clinical stages. We found more frequent hypomethylation of the CpG sites located upstream of the miRb-3p gene in the ESCC tissues compared with in the adjacent normal tissues, and the DNA methylation status of miRb-3p promoter region inversely correlated with the expression levels of miRb-3p.

Ectopic overexpression of miRb-3p promoted cell proliferation, colony formation, migration and invasion in ESCC. While knockdown of miRb-3p had the opposite effects, particularly in promoting apoptosis.

And systemic delivery of miRb-3p antagomir reduced tumor growth and inhibit FOXO3 protein expression in nude mice. Collectively, our findings suggested upregulated expression of miRb-3p caused by promoter hypomethylation contributed to the progression of ESCC; Thus, miRb-3p is a potentially effective biomarker for ESCC that could have further therapeutic implications.

Esophageal carcinoma is a serious malignancy in terms of both mortality and prognosis [ 1 ]. In China, esophageal cancer is the 5th leading cause of cancer-related death, claiming nearly one-quarter million lives every year [ 3 ]. Esophageal squamous cell carcinoma ESCC is the major form of esophageal cancer among Chinese patients [ 4 ].

Although diagnostic technologies and therapies have continuously advanced, the overall five-year survival rate is still far from satisfactory [ 56 ]. Therefore, it is crucial to identify oncogenes or tumor suppressive genes that can serve as biomarkers for ESCC to develop more efficient therapeutic strategies for ESCC patients.

In cancer cells miRNAs can act as either oncogenes or tumor suppressors according to their target genes [ 8 ]. Several studies have shown that miRNAs could be used as diagnostic and prognostic biomarkers for cancers. For example, miR expression was shown to be lower in ESCC tissues and to be associated with poor survival outcome [ 9 ].

In colorectal cancer, high levels of miRb expression and low levels of miRp expression are associated with clinical stages and survival progression [ 1011 ]. The coding gene of miRb is located in chromosome region 2q The mammalian miRb family includes miRb-3p and miRb-5p.

Although miRb-3p and miRb-5p have identical seed sequences, they probably regulate different pathways. Recent research has demonstrated that the expression of miRb-3p in serum maybe used as a biomarker for the diagnosis of hepatocellular carcinoma HCCand in the prediction of survival in patients treated with sorafenib by its association with macrovascular invasion MVI [ 17 ].

However, the exact biological functions and regulatory mechanisms of miRb-3p in human cancer are largely unknown. In the present study, we set up to examine the expression profiles and prognostic value of miRb-3p in ESCC. This study was carried out after obtaining approval from the ethics committee of the hospital and informed consent from all subjects.Metrics details. Triple-negative breast cancer TNBC is highly invasive and aggressive and lacks specific molecular targets to improve the prognosis.

MiRp promotes proliferation of many tumors and its role and underlying mechanisms in TNBC remain to be well elucidated. The tumor growth in vivo was observed in xenograft model. MiRp promoted TNBC cell proliferation in vitro and tumor growth in xenograft model, while suppression of miRp induced cell apoptosis.

The luciferase reporter assay confirmed that B-cell translocation gene 2 BTG2 might be a direct target of miRp, and its expression was negatively regulated by miRp. This study demonstrates that miRp promotes proliferation by targeting tumor suppressor BTG2 and may identify new diagnostic and therapeutic targets in TNBC.

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Breast cancer is the most common malignancy in women nowadays with nearly 1. According to the expression status of hormone receptors and human epidermal growth factor receptor-2 HER2breast cancer consists of luminal A-like, luminal B-like, HER2-positive and triple-negative molecular subtypes respectively [ 2 ]. Chemotherapy remains the standard treatment strategy for TNBC due to the absence of specific therapeutic targets and patients with TNBC may have increased risk of early tumor relapse [ 4 ].

It is urgent to discover new molecular targets to improve the relative poor prognosis of TNBC. MiRNAs play important roles in a series of tumor biological processes, including tumor proliferation, differentiation, apoptosis, migration and invasion [ 6 ]. Dysregulated miRNAs may act as tumor suppressors or oncogenic miRNAs by targeting oncogenes or tumor suppressors [ 7 ].

doten nc 3p

MiR, along with miRb and miR, is a member of the cluster located in intron 13 of the MCM7 oncogene on chromosome 7q Previous studies report that miR is associated with several tumor types, including gastric cancer, prostate cancer, liver cancer, colon cancer and anaplastic thyroid carcinoma [ 910111213 ].

It can be oncogenic or a tumor suppressor depending on different cancer types. However, as the isoform of mature miR, the biological role and underlying mechanisms of miRp in TNBC have not been well elucidated.

As a tumor suppressor in many types of malignancies, BTG2 is involved in proliferation, cell cycle progression, apoptosis, and DNA damage repair [ 17181920 ]. BTG2 expression is downregulated in many human cancers, which is associated with poor prognosis in breast cancer patients [ 21 ]. Breast cancer tissues and adjacent normal tissues were collected from patients who underwent modified breast cancer radical mastectomy or breast conserving surgery in the First Affiliated Hospital of Nanjing Medical University without accepting any chemotherapy prior to tumor resection.

The patients and their relatives provided written informed consent for their clinical information. This study was approved by the ethical committee of Nanjing Medical University. Relative expression level of hsa-miRp was normalized to U6. All procedures were performed in triplicate. Proteins were visualized using a detection system of enhanced chemiluminescence ECL.

The miRp mimics and inhibitor lentivirus were constructed by Genechem Shanghai, China to overexpress or knockdown miRp in breast cancer cells. Cells were transfected with appropriate plasmid and miR duplex. Average OD values were used to estimate the number of cells of each group. Cell colony formation ability was measured by plate colony formation assay. Then the plate was gently washed and stained with crystal violet. The number of colonies was counted by observing the proliferation of single cell.

After permeabilization with 0. The cell apoptosis rate of MDA-MB and Sum cells was analyzed after transfection with the miRp inhibitor and negative control. Stably transfected cells were inoculated subcutaneously into the flank of nude mice. Every experiment was repeated at least three times.Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer.

In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. A Nature Research Journal. Regulation of male sexual differentiation by a Y chromosome-linked male determining factor M-factor is one of a diverse array of sex determination mechanisms found in insects. We further demonstrate by both in vitro and in vivo tests that miRp suppresses Bdtra expression. These results indicate that miRp is required for male sex determination in early embryogenesis in B.

Primary signals that initiate sex determination during development appear to be highly divergent among many taxonomic groups 123.

This is exemplified in dipteran insects, such as Drosophila melanogasterin which the primary sex-determining signal consists of the dose of X chromosome-linked signal elements XSE 4. A double XSE dose from XX diploid individuals leads to expression of Sex-lethal Sxlwhich directs female-specific splicing of transformer tra and doublesex dsx pre-mRNA whose gene products sequentially direct female differentiation. Although the Drosophila Y chromosome is necessary for male fertility, it has no apparent role in determining somatic and germline sexual differentiation 89.

This is in contrast to other dipterans, including the mosquitoes Aedes aegyptiAnopheles gambiae and Anopheles stephensiand the housefly, Musca domesticain which a dominant male determining factor M-factor is the primary determinant of male differentiation 101112 However, M-factors identified in these species have no obvious sequence conservation, nor is their mode of function necessarily conserved. For example, in M.

Y-linked M-factors have been inferred for several dipteran insects, but have not yet been identified in tephritid fruit flies, including the Oriental fruit fly, Bactrocera dorsalis Hendelwhich is one of the most devastating and highly invasive agricultural pests of fruits and vegetables throughout the world In contrast to Drosophilathe tra gene in B.

doten nc 3p

As maternal tra transcripts initiate a positive autoregulatory feedback loop in the early zygote, continuous female-specific functional TRA protein is provided and, thus, acts as a cellular memory, maintaining the female-determining signal For male development, the presence of an M-factor, which is required to prevent activation of the tra autoregulatory loop, leads to a male-specific nonfunctional TRA protein.

For B. Understanding the genetic basis of sex determination and male fertility has therefore been central to the development of genetically modified strains for sex separation and sterility. Although Sxl is not involved in tephritid sex determination, orthologs of the Drosophila tratransformer-2 tra-2and dsx genes are functionally homologous 57. Therefore, the discovery of M-factors, or other upstream factors, remains fundamentally important for tephritid species.Willis W.

Allen, Salisbury: Salisbury Printing Co. Allerton, author and publ. Anderson, Cincinnati:W. Ashmead, R. Lippincott Co. Austin, Wilmington:William Cann Inc. House, Ancestry of Priscilla Baker, W. Pauline Kimball Skinner, privately printed, Joseph Gaston Baillie Bulloch, Wash. Cann, Inc. Aitken, N. William Sperry Beinecke. Paul W. Prindle, New Orleans: Polyanthos, Inc.

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BeallLieut. The Bellah Family Papers. Paul Belville Taylor, n. Stanley O. Bennett, Bradenton: Genie Plus, Inc. Edgar J. Josiah Henry Benton, Jr. Ira Elmore Bishop, privately printed. Clemens, The Black Family on the Brandywine. Lewis S. Frederick Horner, Phila: J. Frederick C. Matthew M. Wise, privately printed, Richard Boulden, Esq. And Family. Willis A. Boughton, privately printed, Bowen and Allied Families of Del.


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