bluuebunny/crossref_metadata_2025_split huggingface dataset:
The cost of clinically significant urinary storage symptoms for community dwelling adults in the UK
Authors: Turner D.A. , Shaw C. , McGrother C.W. , Dallosso H.M. , Cooper N.J. , The MRC Incontinence Team  
Published: May 2004

OBJECTIVESTo estimate the cost of clinically significant urinary storage symptoms (CSUSS), including costs borne by the National Health Service (NHS) and individuals, in terms of the use of goods and services in community‐dwelling adults.SUBJECTS AND METHODSThe subjects were community‐dwelling adults aged ≥ 40 years and living in Leicestershire. The prevalence of CSUSS was estimated using a postal questionnaire with a randomly selected sample of 23 182 respondents. The costs associated with CSUSS were estimated using home interviews with 613 cases with and 523 subjects without CSUSS. Cases were defined on the basis of urinary symptoms of leakage, urgency, frequency and nocturia. Willingness‐to‐pay was used to measure intangible costs as an indicator of the value of alleviating symptoms.RESULTSThe estimated total annual cost to the NHS for treating CSUSS cases in community‐dwelling adults was £536 million at 1999/2000 prices (£303 million and £233 million for men and women, respectively). The total value of costs borne by individuals was estimated to be £207 million (£29 million and £178 million for men and women, respectively). This gives total annual costs related to the use of services of £743 million. There were large intangible costs borne by individuals estimated to be £669 million (£301 and £368 million for men and women) for the UK in terms of willingness‐to‐pay.CONCLUSIONSThe costs of CSUSS in the community amounted to ≈ 1.1% of overall NHS spending for 1999/2000. Personally borne and intangible costs are also large and important components of the costs of CSUSS. There are large gender differences in the proportion of costs borne by the NHS, i.e. 91% of male and 57% of female costs.
The expression of thrombospondin‐1 in benign prostatic hyperplasia and prostatic intraepithelial neoplasia is decreased in prostate cancer
Authors: Vallbo C. , Wang W. , Damber J.‐E. 
Published: May 2004

OBJECTIVETo evaluate the immunohistochemical expression of thrombospondin (TSP), a potent inhibitor of angiogenesis, in human benign prostatic hyperplasia (BPH) and prostate cancer.MATERIALS AND METHODSThe expression of TSP‐1, TSP‐2 and CD36 receptor was assessed in 73 tissue specimens using immunohistochemistry; specimens were from 32 patients with BPH, seven with prostatic intraepithelial neoplasia (PIN) and 34 with cancer.RESULTSImmunohistochemistry showed that all 39 patients with BPH and PIN had TSP‐1‐positive glands. In contrast, none of the 34 patients with cancer had positive TSP‐1 staining in the cancer tissue. All 73 patients were positive for TSP receptor CD36 and negative for TSP‐2.CONCLUSIONSTSP is expressed in BPH, down‐regulated in PIN and absent in prostate cancer tissue. This may indicate that TSP is important in prostate cancer progression. Further studies are needed to understand the significance of these findings for the malignant transformation of the prostate gland.
P2X2 and P2X3 receptor expression in human bladder urothelium and changes in interstitial cystitis
Authors: Tempest H.V. , Dixon A.K. , Turner W.H. , Elneil S. , Sellers L.A. , Ferguson D.R. 
Published: May 2004

OBJECTIVETo investigate whether the expression of P2X3 receptors (implicated in the pathophysiology of pain) is altered in human bladder urothelium from patients with interstitial cystitis (IC, a major symptom of which is pain), and as P2X2 receptors can be co‐expressed with P2X3 receptors, to assess their expression also.PATIENTS AND METHODSBladder tissue samples were collected from patients undergoing cystectomy or radical prostatectomy. Patients with IC were diagnosed using the international criteria. RNA protein expression levels of both receptors were evaluated using reverse transcription‐polymerase chain reaction (PCR), real‐time quantitative PCR and Western blot analysis.RESULTSP2X2 was expressed in the human urothelium, in a glycosylated form. There was less gene expression of P2X3 in IC urothelium, whereas P2X2 gene expression was unchanged. This contrasted with the protein expression, which was increased for both P2X2 and P2X3.CONCLUSIONThis is the first report of the expression of the P2X2 receptor in human bladder urothelium. There was greater protein expression of both P2X2 and P2X3 in IC bladder urothelium which did not directly correlate with the gene expression. Changes in expression of P2X2 and P2X3 receptors may contribute to the pain that patients with IC have, and might provide novel drug targets.
Original semiologic standardized evaluation of stratum corneum hydration by Diagnoskin® stripping sample
Authors: Gasser P. , Peno‐Mazzarino L. , Lati E. , Djian B. 
Published: May 2004

SynopsisIn a normal and healthy skin, the regular elimination of the superficial corneocytes, called desquamation, is a fundamental physiologic process intended to protect the barrier function of the skin. This invisible loss of corneocytes, individually or in small groups, is incessantly compensated by the divisions of the proliferative layer and the upward cellular maturation in order to maintain the harmonious renewal of the epidermis and the integrity of the stratum corneum. The harmony of this desquamation process is intimately conditioned by a sufficient hydration of the stratum corneum: (i) an abnormal desquamation leads to a disruption of the water barrier function and consequently to a dehydration tendency of the stratum corneum, and (ii) a cutaneous dryness (whatever the cause) is able to disturb the desquamation process. Protecting the water content of the stratum corneum has always been a major preoccupation of the cosmetic industry scientists. Consequently, the moisturizing properties of a cosmetic product are objectively measured by various explorations directly targeted on the hydration (corneometry) and on the level of the water barrier function (transepidermal water loss (TEWL) measurements), which depends directly on the skin hydration state. This intimate linkage of the desquamation process and the water content of the stratum corneum enable us to suggest an indirect assessment of the hydration from a direct study of the desquamation by examining a skin‐stripping sample (D‐Squames®) by an optical microscope (linked to a computer). We will describe this already known technique and mainly its new and unpublished semiologic exploitation, named Diagnoskin®, whose advantages are its simplicity and its reproducibility particularly interesting in the case of sequential appraisal of dermatologic or cosmetic treatments.
Post‐adolescent acne
Authors: Knaggs H. E. , Wood E. J. , Rizer R. L. , Mills O. H. 
Published: May 2004

SynopsisAlthough acne has traditionally been viewed as predominantly affecting adolescents, a significant and growing body of literature suggests an adult (i.e. post‐adolescent) form of the disease. This review summarizes selected publications on post‐adolescent acne, and discusses possible causes and treatment options. Recent epidemiological studies show that there appears to be an increase in post‐adolescent acne, and that the disease is lasting longer and is requiring treatment well into the mid forties. There is good agreement that, unlike teenage acne, where males tend to show the most severe forms of the disease, post‐adolescent acne mainly affects females (the lesions are frequently perioral and occur premenstrually) and that there are two forms of the disease. The terms ‘persistent’ and ‘late onset’ are now generally accepted as describing these two types. The causes of post‐adolescent acne remain to be fully elucidated and hormones, colonization by resistant bacteria and the use of cosmetics have been put forward and debated in the literature. Additionally, some clues to the cause of post‐adolescent acne may be gleaned from an individual's response to therapy. Perhaps one of the most intriguing explanations for the increase in this disease is the proposed relationship between increasing stress levels, androgen hormones and increasing levels of acne found in women in fast paced jobs.
Amphiphilic association structures in a model skin lotion with hydroxy acids
Authors: Al‐Bawab A. , Friberg S. E. 
Published: May 2004

SynopsisThe phase diagrams were determined of lactic and isohexanoic hydroxy acids as well as salicylic acid with water, a non‐ionic surfactant and a paraffinic oil to outline the influence of the hydroxy acids on the structure in a model for a skin lotion. The results showed the influence of the acid to be similar to that of the oil, but that the difference in chain length between the two alpha acids had only insignificant influence. The results are discussed from two aspects: the structures involved in the lotion as applied and the action of the lotion residue on the skin after the evaporation of the water.
Symposium abstracts
Authors: Grina Diana K. , He Claire Q. , Rawlings Anthony 
Published: May 2004

Dear ReadersSensorially exciting personal care products and regimens appear in the cosmetic arena more and more. The growing consumer delight in this area has sparked a whole new area of research over the last several years to investigate the relationship between aromas, touch, emotion, and general well‐being. This symposium sponsored by Colgate‐Palmolive brought together research leaders in the area and explored some of the latest findings on how specific sensory stimuli may enhance quality of life and the feeling of personal well‐being. Colgate‐Palmolive's leadership in personal care is reflected in the creation of this symposia, the panel of experts chosen, and the topics presented.The International Journal of Cosmetic Science thanks the Colgate‐Palmolive Company for its support of leading‐edge scientific exchange in personal care and for publishing these abstracts.
The
Arabidopsis Cucumovirus Multiplication 1
and
2
Loci Encode Translation Initiation Factors 4E and 4G
Authors: Yoshii Motoyasu , Nishikiori Masaki , Tomita Kayo , Yoshioka Norimichi , Kozuka Reiko , Naito Satoshi , Ishikawa Masayuki 
Published: May 2004

ABSTRACT

The
cum1
and
cum2
mutations of
Arabidopsis thaliana
inhibit cucumber mosaic virus (CMV) multiplication. In
cum1
and
cum2
protoplasts, CMV RNA and the coat protein accumulated to wild-type levels, but the accumulation of the 3a protein of CMV, which is necessary for cell-to-cell movement of the virus, was strongly reduced compared with that in wild-type protoplasts. In
cum2
protoplasts, the accumulation of turnip crinkle virus (TCV)-related RNA and proteins was also reduced. Positional cloning demonstrated that
CUM1
and
CUM2
encode eukaryotic translation initiation factors 4E and 4G, respectively. Unlike most cellular mRNA, the CMV RNA lacks a poly(A) tail, whereas the TCV RNA lacks both a 5′-terminal cap and a poly(A) tail. In vivo translation analyses, using chimeric luciferase mRNA carrying the terminal structures and untranslated sequences of the CMV or TCV RNA, demonstrated that these viral untranslated sequences contain elements that regulate the expression of encoded proteins positively or negatively. The
cum1
and
cum2
mutations had different effects on the action of these elements, suggesting that the
cum1
and
cum2
mutations cause inefficient production of CMV 3a protein and that the
cum2
mutation affects the production of TCV-encoded proteins.
Characterization of the Polymerase and RNase H Activities of Human Foamy Virus Reverse Transcriptase
Authors: Boyer Paul L. , Stenbak Carolyn R. , Clark Patrick K. , Linial Maxine L. , Hughes Stephen H. 
Published: May 2004

ABSTRACT

Foamy virus (FV) replication, while related to that of orthoretroviruses, differs at a number of steps. Several of these differences involve the reverse transcriptase (RT). There appear to be fewer RTs present in FV than in orthoretroviruses; we previously proposed that the polymerase of FV RT was more active than orthoretroviral RTs to compensate for the numerical difference. Here we present further characterization of the RT of FV. The polymerase activity of FV RT was greater than that of human immunodeficiency virus type 1 RT in a variety of assays. We also examined the RNase H activity of FV RT, and we propose that FV RT has a basic loop in the RNase H domain. Although the sequence of the basic loop of FV RT is different from the basic loop of either Moloney leukemia virus RNase H or
Escherichia coli
RNase H, the FV RT basic loop appears to have a similar function.
Differential Antiviral Response of Endothelial Cells after Infection with Pathogenic and Nonpathogenic Hantaviruses
Authors: Kraus Annette A. , Raftery Martin J. , Giese Thomas , Ulrich Rainer , Zawatzky Rainer , Hippenstiel Stefan , Suttorp Norbert , Krüger Detlev H. , Schönrich Günther 
Published: May 2004

ABSTRACTHantaviruses represent important human pathogens and can induce hemorrhagic fever with renal syndrome (HFRS), which is characterized by endothelial dysfunction. Both pathogenic and nonpathogenic hantaviruses replicate without causing any apparent cytopathic effect, suggesting that immunopathological mechanisms play an important role in pathogenesis. We compared the antiviral responses triggered by Hantaan virus (HTNV), a pathogenic hantavirus associated with HFRS, and Tula virus (TULV), a rather nonpathogenic hantavirus, in human umbilical vein endothelial cells (HUVECs). Both HTNV- and TULV-infected cells showed increased levels of molecules involved in antigen presentation. However, TULV-infected HUVECs upregulated HLA class I molecules more rapidly. Interestingly, HTNV clearly induced the production of beta interferon (IFN-β), whereas expression of this cytokine was barely detectable in the supernatant or in extracts from TULV-infected HUVECs. Nevertheless, the upregulation of HLA class I on both TULV- and HTNV-infected cells could be blocked by neutralizing anti-IFN-β antibodies. Most strikingly, the antiviral MxA protein, which interferes with hantavirus replication, was already induced 16 h after infection with TULV. In contrast, HTNV-infected HUVECs showed no expression of MxA until 48 h postinfection. In accordance with the kinetics of MxA expression, TULV replicated only inefficiently in HUVECs, whereas HTNV-infected cells produced high titers of virus particles that decreased after 48 h postinfection. Both hantavirus species, however, could replicate equally well in Vero E6 cells, which lack an IFN-induced MxA response. Thus, delayed induction of antiviral MxA in endothelial cells after infection with HTNV could allow viral dissemination and contribute to the pathogenesis leading to HFRS.
Identification of Synthetic Endothelial Cell-Specific Promoters by Use of a High-Throughput Screen
Authors: Dai Christine , McAninch Robin E. , Sutton Richard E. 
Published: May 2004

ABSTRACT

Transcriptional targeting is a desirable property for many gene transfer applications. Because endothelial cells line most blood vessels, they are attractive candidates for the introduction of therapeutic gene products. As a proof-of-concept study, we attempted to identify a synthetic, endothelial cell-specific promoter by use of a high-throughput screen involving self-inactivating (SIN) human immunodeficiency virus type 1 (HIV-1)-based vectors. Select duplex oligodeoxynucleotides recognized by transcription factors and located 5′ of endothelial cell-specific mRNA transcripts were randomly ligated and cloned upstream of a minimal ICAM-2 promoter driving enhanced green fluorescent protein (eGFP) in a SIN HIV-1-based vector. Vesicular stomatitis virus G protein-pseudotyped particles were prepared from a library of >10
6
vector recombinants and used to transduce an endothelial cell line. The highest eGFP expressers were repeatedly sorted, and the synthetic promoters were recovered and retested by a luciferase reporter. Several promoters were active and specific to endothelial cells of varied species, with high selectivity indexes and inducibility under hypoxia-mimetic conditions. One in particular was then introduced back into a SIN HIV-1-based vector to confirm its endothelial cell activity and specificity. This study suggests that SIN vectors may be used in a high-throughput manner to identify tissue-specific promoters of high activity, with potential applications for both transcriptional targeting and gene transfer.
Induction of Suppressor of Cytokine Signaling-3 by Herpes Simplex Virus Type 1 Contributes to Inhibition of the Interferon Signaling Pathway
Authors: Yokota Shin-ichi , Yokosawa Noriko , Okabayashi Tamaki , Suzutani Tatsuo , Miura Shunsuke , Jimbow Kowichi , Fujii Nobuhiro 
Published: May 2004

ABSTRACTWe showed previously that herpes simplex virus type 1 (HSV-1) suppresses the interferon (IFN) signaling pathway during the early infection stage in the human amnion cell line FL. HSV-1 inhibits the IFN-induced phosphorylation of Janus kinases (JAK) in infected FL cells. In the present study, we showed that the suppressor of cytokine signaling-3 (SOCS3), a host negative regulator of the JAK/STAT pathway, is rapidly induced in FL cells after HSV-1 infection. Maximal levels of SOCS3 protein were detected at around 1 to 2 h after infection. This is consistent with the occurrence of HSV-1-mediated inhibition of IFN-induced JAK phosphorylation. The HSV-1 wild-type strain VR3 induced SOCS3 more efficiently than did mutants that are defective in UL41 or UL13 and that are hyperresponsive to IFN. Induction of the IRF-7 protein and transcriptional activation of IFN-α4, which occur in a JAK/STAT pathway-dependent manner, were poorly induced by VR3 but efficiently induced by the mutant viruses. In contrast, phosphorylation of IRF-3 and transcriptional activation of IFN-β, which are JAK/STAT pathway-independent process, were equally well induced by the wild-type strain and the mutants. In conclusion, the SOCS3 protein appears to be mainly responsible for the suppression of IFN signaling and IFN production that occurs during HSV-1 infection.
Intramembrane Proteolysis and Endoplasmic Reticulum Retention of Hepatitis C Virus Core Protein
Authors: Okamoto Kiyoko , Moriishi Kohji , Miyamura Tatsuo , Matsuura Yoshiharu 
Published: May 2004

ABSTRACT

Hepatitis C virus (HCV) core protein is suggested to localize to the endoplasmic reticulum (ER) through a C-terminal hydrophobic region that acts as a membrane anchor for core protein and as a signal sequence for E1 protein. The signal sequence of core protein is further processed by signal peptide peptidase (SPP). We examined the regions of core protein responsible for ER retention and processing by SPP. Analysis of the intracellular localization of deletion mutants of HCV core protein revealed that not only the C-terminal signal-anchor sequence but also an upstream hydrophobic region from amino acid 128 to 151 is required for ER retention of core protein. Precise mutation analyses indicated that replacement of Leu
139
, Val
140
, and Leu
144
of core protein by Ala inhibited processing by SPP, but cleavage at the core-E1 junction by signal peptidase was maintained. Additionally, the processed E1 protein was translocated into the ER and glycosylated with high-mannose oligosaccharides. Core protein derived from the mutants was translocated into the nucleus in spite of the presence of the unprocessed C-terminal signal-anchor sequence. Although the direct association of core protein with a wild-type SPP was not observed, expression of a loss-of-function SPP mutant inhibited cleavage of the signal sequence by SPP and coimmunoprecipitation with unprocessed core protein. These results indicate that Leu
139
, Val
140
, and Leu
144
in core protein play crucial roles in the ER retention and SPP cleavage of HCV core protein.
A Bidirectional SF2/ASF- and SRp40-Dependent Splicing Enhancer Regulates Human Immunodeficiency Virus Type 1
rev
,
env
,
vpu
, and
nef
Gene Expression
Authors: Caputi Massimo , Freund Marcel , Kammler Susanne , Asang Corinna , Schaal Heiner 
Published: May 2004

ABSTRACT

The integrated human immunodeficiency virus type 1 (HIV-1) genome is transcribed in a single pre-mRNA that is alternatively spliced into more than 40 mRNAs. We characterized a novel bidirectional exonic splicing enhancer (ESE) that regulates the expression of the HIV-1
env
,
vpu
,
rev
, and
nef
mRNAs. The ESE is localized downstream of the
vpu
-,
env
-, and
nef
-specific 3′ splice site no. 5. SF2/ASF and SRp40 activate the ESE and are required for efficient 3′ splice site usage and binding of the U1 snRNP to the downstream 5′ splice site no. 4. U1 snRNP binding to the 5′ splice site no. 4 is required for splicing of the
rev
and
nef
mRNAs and to increase expression of the partially spliced
env
mRNA. Finally, our results indicate that this ESE is necessary for the recruitment of the U1 snRNP to the 5′ splice site no. 4, even when the 5′ splice site and the U1 snRNA have been mutated to obtain a perfect complementary match. The ESE characterized here is highly conserved in most viral subtypes.
Kaposi's Sarcoma-Associated Herpesvirus-Encoded Latency-Associated Nuclear Antigen Inhibits Lytic Replication by Targeting Rta: a Potential Mechanism for Virus-Mediated Control of Latency
Authors: Lan Ke , Kuppers Daniel A. , Verma Subhash C. , Robertson Erle S. 
Published: May 2004

ABSTRACT
Like other herpesviruses, Kaposi's sarcoma-associated herpesvirus (KSHV, also designated human herpesvirus 8) can establish a latent infection in the infected host. During latency a small number of genes are expressed. One of those genes encodes latency-associated nuclear antigen (LANA), which is constitutively expressed in cells during latent as well as lytic infection. LANA has previously been shown to be important for the establishment of latent episome maintenance through tethering of the viral genome to the host chromosomes. Under specific conditions, KSHV can undergo lytic replication, with the production of viral progeny. The immediate-early Rta, encoded by open reading frame 50 of KSHV, has been shown to play a critical role in switching from viral latent replication to lytic replication. Overexpression of Rta from a heterologous promoter is sufficient for driving KSHV lytic replication and the production of viral progeny. In the present study, we show that LANA down-modulates Rta's promoter activity in transient reporter assays, thus repressing Rta-mediated transactivation. This results in a decrease in the production of KSHV progeny virions. We also found that LANA interacts physically with Rta both in vivo and in vitro. Taken together, our results demonstrate that LANA can inhibit viral lytic replication by inhibiting expression as well as antagonizing the function of Rta. This suggests that LANA may play a critical role in maintaining latency by controlling the switch between viral latency and lytic replication.