bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prescription opioid abuse, pain and addiction: Clinical issues and implications
Authors: LING WALTER , MOONEY LARISSA , HILLHOUSE MAUREEN 
Published: May 2011

AbstractIssues. Prescription opioid misuse in the USA has increased over threefold since 1990 to epidemic proportions, with substantial increases in prescription opioid use also reported in other countries, such as Australia and New Zealand. The broad availability of prescription pain medications, coupled with public misconceptions about their safety and addictive potential, have contributed to the recent surge in non‐medical use of prescription opioids and corresponding increases in treatment admissions for problems related to opioid misuse. Given competing pressures faced by physicians to both diagnose and treat pain syndromes and identify individuals at risk for addictive disorders, the use of opioids in the treatment of pain poses a significant clinical challenge. Approach. This paper reviews the interaction between pain and opioid addiction with a focus on clinical management issues, including risk factors for opioid dependence in patients with chronic pain and the use of assessment tools to identify and monitor at‐risk individuals. Treatment options for opioid dependence and pain are reviewed, including the use of the partial µ agonist buprenorphine in the management of concurrent pain and opioid addiction. Implications. Physicians should strive to find a reasonable balance between minimising potential adverse effects of opioid medications without diminishing legitimate access to opioids for analgesia. Conclusions. The article discusses the need to identify methods for minimising risks and negative consequences associated with opioid analgesics and poses research directions, including the development of abuse‐deterrent opioid formulations, genetic risk factors for opioid dependence and opioid‐induced hyperalgesia as a potential target for medication therapy.[Ling W, Mooney L, Hillhouse M. Prescription opioid abuse, pain and addiction: Clinical issues and implications. Drug Alcohol Rev 2011;30:300–305]
Pharmaceutical opioid analgesic and heroin dependence: How do treatment‐seeking clients differ in Australia?
Authors: NIELSEN SUZANNE , BRUNO RAIMONDO , LINTZERIS NICHOLAS , FISCHER JANE , CARRUTHERS SUSAN , STOOVÉ MARK 
Published: May 2011

AbstractIntroduction and Aims. Non‐prescribed use of pharmaceutical opioid analgesics (POA) has been escalating internationally. In Australia, few studies have examined if POA users have similar characteristics and treatment needs to heroin users. The aim of this study was to compare those presenting for treatment where heroin versus POA were the primary drugs of concern. Design and Methods. A convenience sample of 192 treatment entrants were recruited from alcohol and drug treatment services in four Australian jurisdictions. A structured interview collected data on demographic characteristics, substance use, self‐perceived mental and physical health, crime and harms resulting from drug use. Multivariate analyses were performed to identify characteristics which may differentiate those seeking treatment for heroin compared with POA. Results. Most treatment entrants sampled reported a history of injection drug use and use of both heroin and POA. However, those with primary POA problems were less likely to report an overdose history (adjusted odds ratio 0.90, 95% confidence interval 0.81–0.99) and more likely to initiate opioid use for pain (adjusted odds ratio 2.52, 95% confidence interval 1.04–6.12) than those with primary heroin problems. Latent Class Analysis found that, while most of the POA group were similar to heroin users in demographics, health and injecting drug use, there was a small, distinct group of primary POA problem users that did not typically inject and who commonly initiated opioid use for pain and also experienced elevated physical and mental health disability. Discussion and Conclusions. While some differences existed, this study of Australian treatment seekers found many similar characteristics between those with primary problems with heroin and POA. Few non‐injecting POA were recruited in this sample. This finding contrasts with reports of a growing population of opioid‐dependent people with characteristics that are distinct from traditional opioid‐dependent populations, which may reflect the orientation of current treatment systems in Australia towards injection drug users.[Nielsen S, Bruno R, Lintzeris N, Fischer J, Carruthers S, Stoové M. Pharmaceutical opioid analgesic and heroin dependence: How do treatment‐seeking clients differ in Australia? Drug Alcohol Rev 2011;30:291–299]
Margin involvement and clinical pattern of basal cell carcinoma with mixed histology
Authors: Betti R. , Radaelli G. , Crosti C. , Ghiozzi S. , Moneghini L. , Menni S. 
Published: May 2011

AbstractBackground  Mixed basal cell carcinoma (BCC) has not been sufficiently and specifically studied.Objective  The aim of this study was to estimate in adults the prevalence of mixed cases observed among primary BCCs and to compare clinical and anatomical features of mixed vs. single BCCs, with focus on the incomplete excision.Patients and methods  A total of 3636 histologically confirmed primary BCCs were examined. Data on gender, age, histological subtype, anatomical location and margin involvement were collected. Mixed type was defined as a combination of two or more single subtypes.Results  Prevalence of single and mixed BCCs was 82.2% and 17.8% respectively. Prevalence of BCCs on the upper limbs was higher in mixed than single cases (8.8% vs. 4.0%; P < 0.001) while prevalence on the back was lower (16.9% vs. 23.7%; P < 0.001). Tumour was aggressive in 59.1% of mixed vs. 16.0% of single BCCs (P < 0.001). Margin involvement was more prevalent in mixed than in single BCCs (16.7% vs. 9.6%; P < 0.0001). At multivariate analysis being mixed vs. single BCC was associated with aggressiveness of tumour (OR = 8.5, 95% CI, 6.9–10.4), lateral margin involvement (OR = 1.98, 95% CI, 1.42–2.76) and subject being man (OR = 1.31, 95% CI, 1.10–1.60) but not with deep involvement of margin or anatomical location.Conclusion  Among BCCs, the mixed type may be observed in adults with relatively high rate and may represent a complex and individual subset of BCCs with potential aggressive behaviour.
Proteomic analysis of metabolic, cytoskeletal and stress response proteins in human heart failure
Authors: Li Weiming , Rong Rong , Zhao Sheng , Zhu Xiaoming , Zhang Ke , Xiong Xin , Yu Xueqing , Cui Qinghua , Li Shuqiang , Chen Li , Cai Jun , Du Jie 
Published: May 2011

AbstractHuman heart failure is a complex syndrome and a primary cause of morbidity and mortality in the world. However, the molecular pathways involved in the remodelling process are poorly understood. In this study, we performed exhaustive global proteomic surveys of cardiac ventricle isolated from failing and non‐failing human hearts, and determined the regulatory pathway to uncover the mechanism underlying heart failure. Two‐dimensional gel electrophoresis (2‐DE) coupled with tandem mass spectrometry was used to identify differentially expressed proteins in specimens from failing (n = 9) and non‐failing (n = 6) human hearts. A total of 25 proteins with at least 1.5‐fold change in the failing heart were identified; 15 proteins were up‐regulated and 10 proteins were down‐regulated. The altered proteins belong to three broad functional categories: (i) metabolic [e.g. NADH dehydrogenase (ubiquinone), dihydrolipoamide dehydrogenase, and the cytochrome c oxidase subunit]; (ii) cytoskeletal (e.g. myosin light chain proteins, troponin I type 3 and transthyretin) and (iii) stress response (e.g. αB‐crystallin, HSP27 and HSP20). The marked differences in the expression of selected proteins, including HSP27 and HSP20, were further confirmed by Western blot. Thus, we carried out full‐scale screening of the protein changes in human heart failure and profiled proteins that may be critical in cardiac dysfunction for future mapping.
Use of a systems approach and evidence‐based One Health for zoonoses research
Authors: Asokan G.V. , Asokan Vanitha , Fedorowicz Zbys , Tharyan Prathap 
Published: May 2011

AbstractThe World Health Organization estimates that 25% of the 57 million annual deaths that occur globally are caused by microbes. A study reported 1415 species of infectious organisms are known to be pathogenic to humans. Zoonoses constitute 61% of all known infectious diseases, with humans serving as the primary reservoir for only 3% of them. Of the 175 infectious species considered to be emerging, 75% are zoonotic. Zoonotic diseases and their impact on human and animal health are not monitored, prevented, and treated in an integrated way, despite the fact that etiologies and treatments are similar across species. The efficacy and resistance of a drug in one species has a bearing on others, in the context of zoonoses. Further, an RCT involving many species is effective in a natural setting, is robust, and may require fewer human volunteers. One Health is based on a systems approach and a collaborative effort of multiple disciplines – working locally, nationally, and globally – to attain optimal health for people, animals, and the environment. Systematic reviews and meta‐analyses have so far been independent and discipline oriented. Pooling of results for diagnostic test accuracies and treatment effects of drugs for zoonoses across species has to be done, since the results of preclinical trials emanate from laboratory animals. The Cochrane Collaboration is the platform of choice to initiate a new group on zoonoses to carry out systematic meta‐analyses of diagnostic tests and drug efficacies without bias, thus underpinning the systems approach and One Health.
Mechanical Disruption of Lysis-Resistant Bacterial Cells by Use of a Miniature, Low-Power, Disposable Device
Authors: Vandeventer Peter E. , Weigel Kris M. , Salazar Jose , Erwin Barbara , Irvine Bruce , Doebler Robert , Nadim Ali , Cangelosi Gerard A. , Niemz Angelika 
Published: May 2011

ABSTRACT

Molecular detection of microorganisms requires microbial cell disruption to release nucleic acids. Sensitive detection of thick-walled microorganisms such as
Bacillus
spores and
Mycobacterium
cells typically necessitates mechanical disruption through bead beating or sonication, using benchtop instruments that require line power. Miniaturized, low-power, battery-operated devices are needed to facilitate mechanical pathogen disruption for nucleic acid testing at the point of care and in field settings. We assessed the lysis efficiency of a very small disposable bead blender called OmniLyse relative to the industry standard benchtop Biospec Mini-BeadBeater. The OmniLyse weighs approximately 3 g, at a size of approximately 1.1 cm
3
without the battery pack. Both instruments were used to mechanically lyse
Bacillus subtilis
spores and
Mycobacterium bovis
BCG cells. The relative lysis efficiency was assessed through real-time PCR. Cycle threshold (

C
T

) values obtained at all microbial cell concentrations were similar between the two devices, indicating that the lysis efficiencies of the OmniLyse and the BioSpec Mini-BeadBeater were comparable. As an internal control, genomic DNA from a different organism was spiked at a constant concentration into each sample upstream of lysis. The

C
T

values for PCR amplification of lysed samples using primers specific to this internal control were comparable between the two devices, indicating negligible PCR inhibition or other secondary effects. Overall, the OmniLyse device was found to effectively lyse tough-walled organisms in a very small, disposable, battery-operated format, which is expected to facilitate sensitive point-of-care nucleic acid testing.
Oncolytic Herpes Simplex Virus 1 Encoding 15-Prostaglandin Dehydrogenase Mitigates Immune Suppression and Reduces Ectopic Primary and Metastatic Breast Cancer in Mice
Authors: Walker Jason D. , Sehgal Inder , Kousoulas Konstantin G. 
Published: May 2011

ABSTRACTOncolytic herpes simplex virus 1 (HSV-1) viruses armed with immunomodulatory transgenes have shown potential for enhanced antitumor therapy by overcoming tumor-based immune suppression and promoting antitumor effector cell development. Previously, we reported that the new oncolytic HSV-1 virus, OncSyn (OS), engineered to fuse tumor cells, prevented tumor growth and metastasis to distal organs in the 4T1/BALB/c immunocompetent breast cancer mouse model, suggesting the elicitation of antitumor immune responses (Israyelyan et al., Hum. Gen. Ther. 18:5, 2007, and Israyelyan et al., Virol. J. 5:68, 2008). The OSV virus was constructed by deleting the OS viral host shutoff gene (vhs; UL41) to further attenuate the virus and permit dendritic cell activation and antigen presentation. Subsequently, the OSVP virus was constructed by inserting into the OSV viral genome a murine 15-prostaglandin dehydrogenase (15-PGDH) expression cassette, designed to constitutively express 15-PGDH upon infection. 15-PGDH is a tumor suppressor protein and the primary enzyme responsible for the degradation of prostaglandin E2 (PGE2), which is known to promote tumor development. OSVP, OSV, and OS treatment of 4T1 tumors in BALB/c mice effectively reduced primary tumor growth and inhibited metastatic development of secondary tumors. OSVP was able to significantly inhibit the development and accumulation of 4T1 metastatic tumor cells in the lungs of treated mice.Ex vivoanalysis of immune cells following treatment showed increased inflammatory cytokine production and the presence of mature dendritic cells for the OSVP, OSV, and OS viruses. A statistically significant decrease in splenic myeloid-derived suppressor cells (MDSC) was observed only for OSVP-treated mice. These results show that intratumoral oncolytic herpes is highly immunogenic and suggest that 15-PGDH expression by OSVP enhanced the antitumor immune response initiated by viral infection of primary tumor cells, leading to reduced development of pulmonary metastases. The availability of the OSVP genome as a bacterial artificial chromosome allows for the rapid insertion of additional immunomodulatory genes that could further assist in the induction of potent antitumor immune responses against primary and metastatic tumors.
Multiploid Inheritance of HIV-1 during Cell-to-Cell Infection
Authors: Del Portillo Armando , Tripodi Joseph , Najfeld Vesna , Wodarz Dominik , Levy David N. , Chen Benjamin K. 
Published: May 2011

ABSTRACT

During cell-to-cell transmission of human immunodeficiency virus type 1 (HIV-1), many viral particles can be simultaneously transferred from infected to uninfected CD4 T cells through structures called virological synapses (VS). Here we directly examine how cell-free and cell-to-cell infections differ from infections initiated with cell-free virus in the number of genetic copies that are transmitted from one generation to the next, i.e., the genetic inheritance. Following exposure to HIV-1-expressing cells, we show that target cells with high viral uptake are much more likely to become infected. Using T cells that coexpress distinct fluorescent HIV-1 variants, we show that multiple copies of HIV-1 can be cotransmitted across a single VS. In contrast to cell-free HIV-1 infection, which titrates with Poisson statistics, the titration of cell-associated HIV-1 to low rates of overall infection generates a constant fraction of the newly infected cells that are cofluorescent. Triple infection was also readily detected when cells expressing three fluorescent viruses were used as donor cells. A computational model and a statistical model are presented to estimate the degree to which cofluorescence underestimates coinfection frequency. Lastly, direct detection of HIV-1 proviruses using fluorescence
in situ
hybridization confirmed that significantly more HIV-1 DNA copies are found in primary T cells infected with cell-associated virus than in those infected with cell-free virus. Together, the data suggest that multiploid inheritance is common during cell-to-cell HIV-1 infection. From this study, we suggest that cell-to-cell infection may explain the high copy numbers of proviruses found in infected cells
in vivo
and may provide a mechanism through which HIV preserves sequence heterogeneity in viral quasispecies through genetic complementation.
RNA Sequence Determinants of a Coupled Termination-Reinitiation Strategy for Downstream Open Reading Frame Translation in Helminthosporium victoriae Virus 190S and Other Victoriviruses (Family Totiviridae)
Authors: Li Hua , Havens Wendy M. , Nibert Max L. , Ghabrial Said A. 
Published: May 2011

ABSTRACT

The genome-length, dicistronic mRNA of the double-stranded RNA fungal virus
Helminthosporium victoriae
virus 190S (genus
Victorivirus
, family
Totiviridae
) contains two long open reading frames (ORFs) that overlap in the tetranucleotide AUGA. Translation of the downstream ORF, which encodes the RNA-dependent RNA polymerase (RdRp), has been proposed to depend on ribosomal reinitiation following termination of the upstream ORF, which encodes the capsid protein. In the current study, we examined the RNA sequence determinants for RdRp translation in this virus and demonstrated that a coupled termination-reinitiation (stop-restart) strategy is indeed used. Signals for termination-reinitiation are found within a 32-nucleotide stretch of RNA immediately upstream of the AUGA motif, including a predicted pseudoknot structure. The close proximity in which this predicted structure is followed by the upstream ORF's stop codon appears to be especially important for promoting translation of the downstream ORF. The normal strong preferences for an AUG start codon and the canonical sequence context to favor translation initiation appear somewhat relaxed for the downstream ORF. Similar sequence motifs and predicted RNA structures in other victoriviruses suggest that they all share a related stop-restart strategy for RdRp translation. Members of the genus
Victorivirus
thus provide new and unique opportunities for exploring the molecular mechanisms of translational coupling, which remain only partly understood in this and other systems.
Interleukin-6, Produced by Resident Cells of the Central Nervous System and Infiltrating Cells, Contributes to the Development of Seizures following Viral Infection
Authors: Libbey Jane E. , Kennett Nikki J. , Wilcox Karen S. , White H. Steve , Fujinami Robert S. 
Published: May 2011

ABSTRACTCells that can participate in an innate immune response within the central nervous system (CNS) include infiltrating cells (polymorphonuclear leukocytes [PMNs], macrophages, and natural killer [NK] cells) and resident cells (microglia and sometimes astrocytes). The proinflammatory cytokine interleukin-6 (IL-6) is produced by all of these cells and has been implicated in the development of behavioral seizures in the Theiler's murine encephalomyelitis virus (TMEV)-induced seizure model. The assessment, via PCR arrays, of the mRNA expression levels of a large number of chemokines (ligands and receptors) in TMEV-infected and mock-infected C57BL/6 mice both with and without seizures did not clearly demonstrate the involvement of PMNs, monocytes/macrophages, or NK cells in the development of seizures, possibly due to overlapping function of the chemokines. Additionally, C57BL/6 mice unable to recruit or depleted of infiltrating PMNs and NK cells had seizure rates comparable to those of controls following TMEV infection, and therefore PMNs and NK cells do not significantly contribute to seizure development. In contrast, C57BL/6 mice treated with minocycline, which affects monocytes/macrophages, microglial cells, and PMNs, had significantly fewer seizures than controls following TMEV infection, indicating monocytes/macrophages and resident microglial cells are important in seizure development. Irradiated bone marrow chimeric mice that were either IL-6-deficient mice reconstituted with wild-type bone marrow cells or wild-type mice reconstituted with IL-6-deficient bone marrow cells developed significantly fewer behavioral seizures following TMEV infection. Therefore, both resident CNS cells and infiltrating cells are necessary for seizure development.
The Host Phosphoinositide 5-Phosphatase SHIP2 Regulates Dissemination of Vaccinia Virus
Authors: McNulty Shannon , Powell Kimberly , Erneux Christophe , Kalman Daniel 
Published: May 2011

ABSTRACT
After fusing with the plasma membrane, enveloped poxvirus virions form actin-filled membranous protrusions, called tails, beneath themselves and move toward adjacent uninfected cells. While much is known about the host and viral proteins that mediate formation of actin tails, much less is known about the factors controlling release. We found that the phosphoinositide 5-phosphatase SHIP2 localizes to actin tails. Localization requires phosphotyrosine, Abl and Src family tyrosine kinases, and neural Wiskott-Aldrich syndrome protein (N-WASP) but not the Arp2/Arp3 complex or actin. Cells lacking SHIP2 have normal actin tails but release more virus. Moreover, cells infected with viral strains with mutations in the release inhibitor A34 release more virus but recruit less SHIP2 to tails. Thus, the inhibitory effects of A34 on virus release are mediated by SHIP2. Together, these data suggest that SHIP2 and A34 may act as gatekeepers to regulate dissemination of poxviruses when environmental conditions are conducive.
MALIGNANT TRANSFORMATION OF AN ENCHONDROMA OF THE HAND: A CASE REPORT
Authors: Ozcanli H. , Alimoglu E. , Aydin A. T. 
Published: May 2011

Secondary chondrosarcomas according to malignant transformations of the solitary enchondromas were extremely rare in the hand. The aim of this study is to present a case of a 43-year-old male having rare malignant transformation of the solitary enchondroma treated with total excision and replacement with iliac bone graft.