Anatomical relationship between the internal jugular vein and the vertebral artery: An observational study in pre-school children using ultrasound imaging.

Background and Aims: Central venous cannulation is performed in children requiring vasopressor use, long-term antibiotics, chemotherapy or parenteral nutrition. The internal jugular vein is the preferred site for cannulation. Though, there are several studies describing the relation of the common carotid artery (CCA) and internal jugular vein (IJV) in the neck, there is a paucity of data regarding the anatomical relationship between the vertebral artery (VA) and the IJV. This study aims to describe the anatomical relationship between the IJV and the VA using ultrasound imaging in pre-school children in India. Material and Methods: Prospective observational cross-sectional study of 67 randomly selected children (age <5 years) who underwent an ultrasound examination of the right side of the neck, in a position mimicking central venous cannulation, to identify the relationship between the IJV and VA. The skin to the vertebral artery depth (D), width of the VA (W), distance between the IJV and the VA (DIV) was measured. Based on these, children were classified into high risk, moderate risk and low risk category for VA puncture. Results: Of the 67 children, 15 (22.4%) patients belonged to the high-risk group, 25 (37.3%) belonged to the moderate-risk group and 27 (40.23%) belonged to the low-risk group. Conclusion: In addition to localizing the carotid artery, pre-procedural scanning or real-time ultrasound examination to establish the anatomical relation of the IJV to the VA is imperative to alert the clinician of the possible risk of VA puncture.

Interventions to improve adherence to anti-osteoporosis medications: an updated systematic review.

An earlier systematic review on interventions to improve adherence and persistence was updated. Fifteen studies investigating the effectiveness of patient education, drug regimen, monitoring and supervision, and interdisciplinary collaboration as a single or multi-component intervention were appraised. Multicomponent interventions with active patient involvement were more effective. INTRODUCTION: This study was conducted to update a systematic literature review on interventions to improve adherence to anti-osteoporosis medications. METHODS: A systematic literature review was carried out in Medline (using PubMed), Embase (using Ovid), Cochrane Library, Current Controlled Trials, ClinicalTrials.gov , NHS Centre for Review and Dissemination, CINHAL, and PsycINFO to search for original studies that assessed interventions to improve adherence (comprising initiation, implementation, and discontinuation) and persistence to anti-osteoporosis medications among patients with osteoporosis, published between July 2012 and December 2018. Quality of included studies was assessed. RESULTS: Of 585 studies initially identified, 15 studies fulfilled the inclusion criteria of which 12 were randomized controlled trials. Interventions were classified as (1) patient education (n = 9), (2) drug regimen (n = 3), (3) monitoring and supervision (n = 2), and (4) interdisciplinary collaboration (n = 1). In most subtypes of interventions, mixed results on adherence (and persistence) were found. Multicomponent interventions based on patient education and counseling were the most effective interventions when aiming to increase adherence and/or persistence to osteoporosis medications. CONCLUSION: This updated review suggests that patient education, monitoring and supervision, change in drug regimen, and interdisciplinary collaboration have mixed results on medication adherence and persistence, with more positive effects for multicomponent interventions with active patient involvement. Compared with the previous review, a shift towards more patient involvement, counseling and shared decision-making, was seen, suggesting that individualized solutions, based on collaboration between the patient and the healthcare provider, are needed to improve adherence and persistence to osteoporosis medications.

Fever after intraventricular neuroendoscopic procedures in children.

PURPOSE: The purpose of this paper was to study the incidence and clinical significance of fever after intraventricular neuroendoscopic procedures in children. METHODS: We retrospectively assessed all children subjected to an intraventricular neuroendoscopic procedure between 2004 and 2015. Body temperature 6 days postoperatively, symptoms and signs, and eventual cerebrospinal fluid analysis were evaluated. Fever was defined as temperature above 38 °C. RESULTS: Fifty-five children (mean age 4.8 years) had 67 procedures. Forty-three children (47 procedures, 70 %) developed fever, mostly the day of surgery (n = 17; 25 %) or the next day (n = 33; 49 %). All children who were clinically ill (n = 9, including 7 with fever) suffered serious illness, as opposed to none of the children with fever without being clinically ill (n = 36). Fever was unrelated to gender, indication for, and type of procedure and did not influence ETV success rate at 3 months. Children under 1 year less frequently developed fever (p = 0.032). CONCLUSIONS: Fever frequently develops after intraventricular neuroendoscopic procedures in children and follows a rather predictable course, peaking the day of surgery and/or the next day, and rapidly subsiding thereafter. Fever is not a cardinal symptom except when combined with other symptoms in children who are clinically ill (which most of them are not). Close observation avoiding invasive diagnostic tests may suffice for those who are not clinically ill, while extra attention should be paid to those whose temperature rises after day 2 especially when clinically ill, as they likely suffer serious illness. We recommend to closely observe children after any intraventricular neuroendoscopic procedure for at least 5 days.

Comparative kinetic analyses of interaction of inhibitors with Rauscher murine leukemia virus and human immunodeficiency virus reverse transcriptases.

The inhibitory effects of several nucleoside triphosphate analogs on Rauscher murine leukemia virus (RMuLV) and human immunodeficiency virus (HIV) type 1 reverse transcriptases (RTs) were studied. With RNA as the template, the apparent K(m) and apparent K(i) values of HIV RT toward its substrates and inhibitors are 12 to 500 times lower than the corresponding values for RMuLV RT. However, the k(i)/k(m) ratios (inhibition efficiencies) for HIV and RMuLV RTs'are similar for AZTTP (zidovudine triphosphate), d4TTP [3'-deoxythymidine-2'-ene-(3'-deoxy-2',3'-didehydrothymidine) triphosphate], PMEADP [9-(2-phosphonylmethoxyethyl)adenine diphosphate], FIAUTP [1-(2-fluoro-2-deoxy-beta-D-arabinofuranosyl)-5-iodouracil triphosphate], and HPMPCDP [(S)-1-(3-hydroxy-2-phosphylmethoxypropyl) cytosine diphosphate]. With DNA as the template, the K(m) values are similar for HIV and RMuLV RTs. However, the K(i)/K(m) values of HIV and RMuLV RTs are significantly different for ddCTP, ddATP, and 3TCTP (2',3'-dideoxy-3'-thiacytidine). The RTs of RMuLV and HIV are sufficiently different from one another that the kinetic inhibition constants for a particular antiviral compounds should be determined to indicate whether anti-RMuLV activity is likely to be predictive for the anti-HIV activity of the compound. This information, in conjunction with species-specific drug metabolism differences and tissue culture antiviral activity, is important in determining the suitability of a particular animal model.

Protection against murine cytomegalovirus infection in aged mice and mice with severe combined immunodeficiency disease with the biological response modifiers polyribosinic-polycytidylic acid stabilized with L-lysine and carboxymethylcellulose, maleic anhydride divinyl ether and colony stimulating factor 1.

A variety of biological response modifiers (BRMs) have provided antiviral protection to immunocompetent mice, and this prompted us to determine their efficacy against murine cytomegalovirus (MCMV) infection in immunocompromised mice-including the profoundly immunocompromised SCID mice and C57Bl/6 and B6D2F1 aged mice. SCID mice showed a marked decrease (> 20-fold) in resistance to MCMV, while there was a slight decrease (3-fold) in aged mice. In BRM antiviral protection studies, SCID mice were almost completely protected against MCMV infection by the pleiotropic immunomodulators, MVE-2 and pICLC, but much less by the more selective CSF-1. pICLC-induced IFN and NK cell cytotoxicity were maintained in SCID mice, suggesting that pleiotropic immunomodulatory effects may be required for antiviral protection in such a profoundly immunocompromised model. pICLC also effectively protected aged mice against lethal MCMV infection and effectively induced IFN. These results emphasize the potential for BRM treatment in immunocompromised hosts.

Biological response modifier-mediated resistance to herpesvirus infections requires induction of alpha/beta interferon.

The role of interferon alpha/beta (IFN) induction by the immunomodulators pICLC and CL246,738 was investigated in CD-1 mice infected with murine cytomegalovirus (MCMV) or herpes simplex virus type 2 (HSV-2). Mice were treated with either normal sheep serum or anti-alpha/beta IFN antiserum, inoculated with the immunomodulators, and infected with virus. Because anti-IFN treatment also decreased natural resistance to HSV-2 and MCMV, two viral challenge doses were used to ensure that the mice with control serum or anti-IFN antiserum received biologically equivalent infections. Antiviral protection of pICLC and CL246,738 against HSV-2 infection was completely abrogated by treatment with anti-alpha/beta interferon antiserum. Mice treated with pICLC also lost antiviral protection against MCMV when interferon alpha/beta was depleted. These results indicate that induction of interferon alpha/beta appears to be a major mechanism for both natural resistance and pICLC-induced antiviral protection against MCMV and HSV-2 herpesvirus infections.

Role of NK cells in immunomodulator-mediated resistance to herpesvirus infection.

Seven chemically diverse biological response modifiers (BRM) were compared for antiviral activity in intact and NK cell-depleted CD-1 mice. Both spontaneous and BRM-induced splenic NK cell cytotoxicity were depleted for at least 5 days following treatment with the monoclonal antibody NK1.1. Antiviral protection of standard doses of MVE-2, pIC, pICLC, rmIFN-tau and CL246,738 against lethal MCMV or HSV-2 infections was not abrogated by NK cell depletion, demonstrating that NK cells are not required for BRM-induced antiviral activity against these herpesviruses. When mice were treated with 100,000 U of rHuIFN-alpha B/D, NK cells were not required for activity against MCMV, while at a dose of 25,000 U, NK cells appeared to be partially required against MCMV. At lower doses, the activity of rHuIFN-alpha B/D against MCMV appeared dependent upon the presence of NK cells. A similar dose-related requirement for NK cells was observed for activity of OK-432. Thus, at higher doses of rHuIFN-alpha B/D and OK-432, elements of the natural immune system in addition to or other than NK cells are apparently involved, while at lower doses NK cells appear to play a more important role in antiviral protection against MCMV infection.