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ABSTRACT:Success of propagating sweetbay magnolia (Magnolia virginiana L. [Magnoliaceae]) from cuttings varies considerably. Results presented in the literature are generally conflicting as to which hormone type, concentration, or combination of concentrations and types work best. With labor shortages and labor costs on the rise, growers are looking at more efficient and economical ways to apply auxin. With potential to reduce production costs and increase efficiency, foliar auxin application is a novel and financially viable application method for the nursery and greenhouse industry. Two studies were conducted to assess the best way to propagate sweetbay magnolia commercially using stem cuttings. The first study examined basal wounding and auxin use as methods to improve rooting of sweetbay cuttings. Overall, dipping sweetbay magnolia cuttings in Hortus IBA at 5000, 7500, or 10,000 ppm, regardless of basal wounding, resulted in a higher quality liner. The second study investigated auxin application method and propagation substrate for further improvement of rooting success. Results indicated that sweetbay magnolia cuttings propagated into 100% pine bark with Hortus IBA at 10,000 ppm applied as a basal quick dip resulted in a higher quality liner. While foliar sprays may have the potential to reduce labor cost when propagating some plant species from cuttings, this method was not the most effective in successful cutting propagation of sweetbay magnolias. Overall, sweetbay magnolias rooted best in 100% pine bark after being dipped in 10,000 ppm Hortus IBA.

IntroductionWe investigated whether changes in engagement in home-based creative activities were associated with changes in depressive symptoms, anxiety symptoms and life satisfaction during the COVID-19 pandemic, aiming to replicate findings from the UK in a USA sample.Methods3725 adults were included from the COVID-19 Social Study in the USA, a panel study collecting data weekly during the COVID-19 pandemic. We measured engagement in eight types of creative leisure activities on the previous weekday between April and September 2020. Data were analysed using fixed effects regression models.ResultsIncreased time spent gardening was associated with reductions in depressive and anxiety symptoms and enhanced life satisfaction. Spending more time doing woodwork/DIY and arts/crafts were also associated with enhanced life satisfaction. However, more time watching television, films or other similar media (not for information on COVID-19) was associated with increased depressive symptoms. Other creative activities were not associated with mental health or well-being.ConclusionSome findings differ from evidence obtained in the UK, demonstrating the importance of replicating research across countries. Our findings should also be considered when formulating guidelines for future stay-at-home directives, enabling individuals to stay well despite the closure of public resources.

White drupelet disorder (WDD) in blackberry (Rubus subgenus Rubus) is an abiotic condition resulting from a cultivar and environment interaction. Although high temperatures and light intensities have been implicated, little is known why this disorder manifests. Other factors, such as overall plant stress, may be contributing influences. In this study, three treatments were applied to examine whether the addition of nitrogen (N) can reduce WDD on 'Sweetie Pie' erect blackberry over three seasons. An initial 50 lb/acre (56.0 kg·ha-1) N was applied to all plots at budbreak. Two additional N application treatments of 100 kg·ha-1 were applied at one time (1×) or five, 20-kg·ha-1 applications (5×), spaced 1 week apart for 5 weeks starting at bloom. One control treatment of no additional N (0×) was also included. Berries were harvested and weighed as a total, then berries with white drupelets were separated out and weighed. The two values were divided to create a proportion and were then multiplied by 100 to determine the percentage. Nitrogen application decreased the percentage of white drupelet berries from 13.0% (control) to 10.0% (one additional application) and 9.1% (five additional applications). WDD for the 0× treatment correlated negatively to maximum high daytime temperatures during May (r = -0.58, P = 0.03) over the three seasons. Occurrence of white drupelets by treatments 0×, 1×, and 5× correlated significantly with the cumulative number of rainfall events (r = 0.49, 0.47, and 0.46, respectively). Leaf chlorophyll index and photosynthesis measurements were unaffected by treatment. Although it is likely that multiple factors are involved in the development of white drupelets, additional N may reduce the problem. [ABSTRACT FROM AUTHOR]

The human microbiome encompasses a variety of microorganisms that change dynamically and are in close contact with the body. The microbiome influences health and homeostasis, as well as the immune system, and any significant change in this equilibrium (dysbiosis) triggers both acute and chronic health conditions. Microbiome research has surged, in part, due to advanced sequencing technologies enabling rapid, accurate, and cost-effective identification of the microbiome. A major prerequisite for stool sample collection to study the gut microbiome in longitudinal prospective studies requires standardized protocols that can be easily replicated. However, there are still significant bottlenecks to stool specimen collection that contribute to low patient retention rates in microbiome studies. These barriers are further exacerbated in solid organ transplant recipients where diarrhea is estimated to occur in up to half the patient population. We sought to test two relatively easy sample collection methods (fecal swab and wipes) and compare them to the more cumbersome “gold” standard collection method (scoop) using two different sequencing technologies (16S ribosomal RNA sequencing and shotgun metagenomics). Our comparison of the collection methods shows that both the swabs and the wipes are comparable to the scoop method in terms of bacterial abundance and diversity. The swabs, however, were closer in representation to the scoop and were easier to collect and process compared to the wipes. Potential contamination of the swab and the wipe samples by abundant skin commensals was low in our analysis. Comparison of the two sequencing technologies showed that they were complementary, and that 16S sequencing provided enough coverage to detect and differentiate between bacterial species identified in the collected samples. Our pilot study demonstrates that alternative collection methods for stool sampling are a viable option in clinical applications, such as organ transplant studies. The use of these methods may result in better patient retention recruitment rates in serial microbiome studies.

Clinical placement for nurse practitioner (NP) students is difficult due to an increase in demand for clinical sites and qualified preceptors, and the nursing faculty shortage. The American Association of Colleges of Nursing supports the use of simulation with standardized patients as an adjunct to traditional clinical placement for NPs. In this article, we describe an innovative standardized patient simulation experience implemented in a family NP master’s of science program. The purposes of this experience were to provide alternative clinical opportunities and formative feedback for NP students and to identify gaps in students' diagnostic reasoning. Lessons learned through this experience are included.

Background:The faculty of an undergraduate nursing program decided to undertake a major curriculum overhaul, transitioning from a curriculum based on the biomedical model to a concept-based curriculum. However, shortly after the new curriculum was implemented, faculty identified many issues with how and when the concepts were being taught.Method:In response to the early implementation issues, a conceptual grid was developed to guide assessment of the new curriculum.Results:The conceptual grid provided a framework for assessment of the new concept-based curriculum. By using this approach, the faculty was able to identify and correct curricular issues that impeded student learning.Conclusion:The conceptual grid has been extremely useful in the assessment of a newly implemented concept-based curriculum. [The conceptual grid has been extremely useful in the assessment of a newly implemented concept-based curriculum. [J Nurs Educ. 2016;55(8):467–470.]

No solvent cage effect could be found in the reduction of 4‐aminocyclohexanone 3by Shvo's hydroxycyclopentadienyl ruthenium hydride 2. No preference was observed in the complex formation from trapping by aminoalcohol product 4over external trapping by aminoketone 3or by Shvo hydride 2. A solvent cage effect has previously been proposed to support an outer‐sphere mechanism in the reduction of imines by 2; this was based on the observation that there was >90% preference for complexation of the newly formed amine over an external amine. Since alcohols form stronger hydrogen bonds than amines a larger cage effect would be expected in the present study. The lack of a cage effect in the present reduction suggests that the previous results from imine reduction require an additional explanation (other than a solvent cage effect).

The racemization of sec‐alcohols catalyzed by pentaphenylcyclopentadienyl–ruthenium complex 3 ahas been investigated. The mechanism involves ruthenium–alkoxide intermediates: reaction of tert‐butoxide ruthenium complex 4with a series of sec‐alcohols with different electronic properties gave ruthenium complexes bearing a secondary alkoxide as a ligand. The characterization of these alkoxide complexes by NMR spectroscopy together with a study of the reaction using in situ IR spectroscopy is consistent with a mechanism in which the alkoxide substitution step and the β‐hydride elimination step occur without CO dissociation. The alkoxide substitution reaction is proposed to begin with hydrogen bonding of the incoming alcohol to the active ruthenium–alkoxide intermediate. Subsequent alkoxide exchange can occur via two pathways: i) an associative pathway involving a η3‐CpRu intermediate; or ii) a dissociative pathway within the solvent cage. Racemization at room temperature of a 1:1 mixture of (S)‐1‐phenylethanol and (S)‐1‐phenyl‐[D4]‐ethanol gave only rac‐1‐phenylethanol, and rac‐1‐phenyl‐[D4]‐ethanol, providing strong support for a mechanism in which the substrate stays coordinated to the metal center throughout the racemization, and does not leave the coordination sphere. Furthermore, racemization of a sec‐alcohol bearing a ketone moiety within the same molecule does not result in any reduction of the original ketone, which rules out a mechanism where the intermediate ketone is trapped within the solvent cage. These results are consistent with a mechanism where η3‐Ph5C5–ruthenium intermediates are involved. Competitive racemization on nondeuterated and α‐deuterated α‐phenylethanols was used to determine the kinetic isotope effect kH/kDfor the ruthenium‐catalyzed racemization. The kinetic isotope effect kH/kDfor p‐ X‐C6H4CH(OH)CH3was 1.08, 1.27 and 1.45 for X=OMe, H, and CF3, respectively.

Power lawnmowers can pose significant danger of injury to both the operator and the bystander, from direct contact with the rotary blades or missile injury. Our objective was to review our experience with paediatric lawnmower-associated trauma, and the safety recommendations available to operators of power lawnmowers.

The unfolded protein response (UPR) regulates the protein-folding capacity of the endoplasmic reticulum (ER) according to cellular demand. In mammalian cells, three ER transmembrane components, IRE1, PERK, and ATF6, initiate distinct UPR signaling branches. We show that these UPR components display distinct sensitivities toward different forms of ER stress. ER stress induced by ER Ca2+release in particular revealed fundamental differences in the properties of UPR signaling branches. Compared with the rapid response of both IRE1 and PERK to ER stress induced by thapsigargin, an ER Ca2+ATPase inhibitor, the response of ATF6 was markedly delayed. These studies are the first side-by-side comparisons of UPR signaling branch activation and reveal intrinsic features of UPR stress sensor activation in response to alternate forms of ER stress. As such, they provide initial groundwork toward understanding how ER stress sensors can confer different responses and how optimal UPR responses are achieved in physiological settings.

Objective: Nuchal edema (NE) is a clinical indicator for aneuploidy, cardiovascular anomalies, and several genetic syndromes. Its etiology, however, is unknown. In the nuchal area, the endothelium of the jugular lymphatic sacs (JLS) develops by budding from the blood vascular endothelium of the cardinal veins. Abnormal distension of the jugular sacs is associated with NE. We hypothesize that a disturbed lymphatic endothelial differentiation and sac formation causes NE. We investigated endothelial differentiation of the jugular lymphatic system in human and mouse species with NE. Methods: Aneuploid human fetuses (trisomy 21; trisomy 18) were compared with euploid controls (gestational age 12 to 18 weeks). Trisomy 16 mouse embryos were compared with wild type controls (embryonic day 10 to 18). Trisomy 16 mice are considered an animal model for human trisomy 21. Endothelial differentiation was investigated by immunohistochemistry using lymphatic markers (prox-1, podoplanin, lymphatic vessel endothelial hyaluronan receptor [LYVE]-1) and en blood vessel markers (neuropilin [NP]-1 and ligand vascular endothelial growth factor [VEGF]-A). Smooth muscle actin (SMA) was included as a smooth muscle cell marker. Results: We report a disturbed venous-lymphatic phenotype in aneuploid human fetuses and mouse embryos with enlarged jugular sacs and NE. Our results show absent or diminished expression of the lymphatic markers Prox-1 and podoplanin in the enlarged jugular sac, while LYVE-1 expression was normal. Additionally, the enlarged fLS showed blood vessel characteristics, including increased NP-1 and VEGF-A expression. The lumen contained blood cells and smooth muscle cells lined the wall. CONCLUSION: A loss of lymphatic identity seems to be the underlying cause for clinical NE. Also, abnormal endothelial differentiation provides a link to the cardiovascular anomalies associated with NE.

Objective:Nuchal edema (NE) is a clinical indicator for aneuploidy, cardiovascular anomalies, and several genetic syndromes. Its etiology, however, is unknown. In the nuchal area, the endothelium of the jugular lymphatic sacs (JLS) develops by budding from the blood vascular endothelium of the cardinal veins. Abnormal distension of the jugular sacs is associated with NE. We hypothesize that a disturbed lymphatic endothelial differentiation and sac formation causes NE. We investigated endothelial differentiation of the jugular lymphatic system in human and mouse species with NE.Methods:Aneuploid human fetuses (trisomy 21; trisomy 18) were compared with euploid controls (gestational age 12 to 18 weeks). Trisomy 16 mouse embryos were compared with wild type controls (embryonic day 10 to 18). Trisomy 16 mice are considered an animal model for human trisomy 21. Endothelial differentiation was investigated by immunohistochemistry using lymphatic markers (prox-1, podoplanin, lymphatic vessel endothelial hyaluronan receptor [LYVE]-1) and en blood vessel markers (neuropilin [NP]-1 and ligand vascular endothelial growth factor [VEGF]-A). Smooth muscle actin (SMA) was included as a smooth muscle cell marker.Results:We report a disturbed venous-lymphatic phenotype in aneuploid human fetuses and mouse embryos with enlarged jugular sacs and NE. Our results show absent or diminished expression of the lymphatic markers Prox-1 and podoplanin in the enlarged jugular sac, while LYVE-1 expression was normal. Additionally, the enlarged JLS showed blood vessel characteristics, including increased NP-1 and VEGF-A expression. The lumen contained blood cells and smooth muscle cells lined the wall.Conclusion:A loss of lymphatic identity seems to be the underlying cause for clinical NE. Also, abnormal endothelial differentiation provides a link to the cardiovascular anomalies associated with NE.

Increased nuchal translucency in the human fetus is associated with chromosomal abnormalities, enlarged jugular lymphatic sacs, cardiac defects and changed flow through the ductus venosus. The developmental background of this nuchal edema in relation to the associated anomalies remains elusive. We studied the morphologic correlation between neurogenesis and vasculogenesis in neck, heart, and ductus venosus region of wild type and trisomy 16 mice embryos (E10- E18), using an antibody against Neural Cell Adhesion Molecule (NCAM). Trisomy 16 mice are a model for the above described human phenotype. From E12 trisomy 16 mice showed an altered arrangement of cranial nerves IX, X and XI, which are positioned between the carotid artery, jugular vein and enlarged lymphatic sac. The vagal nerve was significantly smaller, compared with wild type embryos. NCAM was over expressed in both neuronal and cardiovascular structures in trisomy 16 mice, being particularly prominent in the 4thand 6thpharyngeal arch arteries, and the ductus venosus. In the 4thand 6thpharyngeal arch arteries, NCAM over expression was located to the part of the vessel wall that is closely related to the vagal and recurrent nerve. In case of 4thpharyngeal arch artery abnormalities NCAM expression, on the other hand, was reduced. In conclusion, the interaction between neurogenesis and vasculogenesis is disturbed in the trisomy 16 mouse model, and might be a common denominator in the spectrum of anomalies associated with increased nuchal translucency.

Increased nuchal translucency in the human fetus is associated with chromosomal abnormalities, enlarged jugular lymphatic sacs, cardiac defects and changed flow through the ductus venosus. The developmental background of this nuchal edema in relation to the associated anomalies remains elusive. We studied the morphologic correlation between neurogenesis and vasculogenesis in neck, heart, and ductus venosus region of wild type and trisomy 16 mice embryos (E10- E18), using an antibody against Neural Cell Adhesion Molecule (NCAM). Trisomy 16 mice are a model for the above described human phenotype. From E12 trisomy 16 mice showed an altered arrangement of cranial nerves IX, X and XI, which are positioned between the carotid artery, jugular vein and enlarged lymphatic sac. The vagal nerve was significantly smaller, compared with wild type embryos. NCAM was over expressed in both neuronal and cardiovascular structures in trisomy 16 mice, being particularly prominent in the 4thand 6thpharyngeal arch arteries, and the ductus venosus. In the 4thand 6thpharyngeal arch arteries, NCAM over expression was located to the part of the vessel wall that is closely related to the vagal and recurrent nerve. In case of 4thpharyngeal arch artery abnormalities NCAM expression, on the other hand, was reduced. In conclusion, the interaction between neurogenesis and vasculogenesis is disturbed in the trisomy 16 mouse model, and might be a common denominator in the spectrum of anomalies associated with increased nuchal translucency.

Hereditary motor and sensory neuropathy type IIC (HMSN IIC) is an autosomal dominant axonal neuropathy. The cardinal features include distal muscle wasting and weakness, vocal cord paralysis, and mild sensory impairment. Recently, HMSN IIC locus was mapped to chromosome 12q23‐24. Two families affected by HMSN IIC were identified and evaluated for linkage to this region. Segregation analysis in both families was consistent with linkage to chromosome 12q23‐24. Combined analysis generated a multipoint LOD score of 2.1 at marker D12S1583 and refined the HMSN IIC gene interval to The clinical and molecular findings are discussed.Ann Neurol 2005;57:293–297

Fibromatosis is a locally aggressive, proliferative fibroblastic lesion affecting musculoaponeurotic structures, most often in the limbs and trunk. Intracranial fibromatosis is extremely rare and requires aggressive treatment to prevent recurrence. We present the case of a 48 year old woman with aggressive skull base fibromatosis. The lesion extended through the sphenoid sinus, into both pterygoid recesses, destroying the right lateral wall of the sphenoid sinus and invading the cavernous sinus. There was also involvement of the floor of the sella, the clivus, the right petrous temporal bone and the right mastoid. The patient underwent partial resection of the lesion via an extended trans-sphenoidal approach. Postoperative MRI showed residual tissue. A review of the literature shows that intracranial fibromatosis usually appears in the first or second decade. Complete resection is often impossible because of its widely infiltrative nature. Radiotherapy and chemotherapy are often required to improve local control of the lesion. Copyright 2002 Harcourt Publishers Ltd.

ABSTRACTIn vitro experiments have demonstrated intercellular trafficking of the VP22 tegument protein of herpes simplex virus type 1 from infected cells to neighboring cells, which internalize VP22 and transport it to the nucleus. VP22 also can mediate intercellular transport of fusion proteins, providing a strategy for increasing the distribution of therapeutic proteins in gene therapy. Intercellular trafficking of the p53 tumor suppressor protein was demonstrated in vitro using a plasmid expressing full-length p53 fused in-frame to full-length VP22. The p53-VP22 chimeric protein induced apoptosis both in transfected tumor cells and in neighboring cells, resulting in a widespread cytotoxic effect. To evaluate the anti-tumor activity of p53-VP22 in vivo, we constructed recombinant adenoviruses expressing either wild-type p53 (FTCB) or a p53-VP22 fusion protein (FVCB) and compared their effects in p53-resistant tumor cells. In vitro, treatment of tumor cells with FVCB resulted in enhanced p53-specific apoptosis compared to treatment with equivalent doses of FTCB. However, in normal cells there was no difference in the dose-related cytotoxicity of FVCB compared to that of FTCB. In vivo, treatment of established tumors with FVCB was more effective than equivalent doses of FTCB. The dose-response curve to FVCB was flatter than that to FTCB; maximal antitumor responses could be achieved using FVCB at doses 1 log lower than those obtained with FTCB. Increased antitumor efficacy was correlated with increased distribution of p53 protein in FVCB-treated tumors. This study is the first demonstration that VP22 can enhance the in vivo distribution of therapeutic proteins and improve efficacy in gene therapy.

TP53 is the most commonly altered tumor-suppressor gene in cancer and is currently being tested in Phase II/III gene replacement trials. Many tumors contain wild-type TP53 sequence with elevated MDM2 protein levels, targeting p53 for degradation. These tumors are more refracto-ry to treatment with exogenous wild-type p53. Here we generate a recombinant adenovirus expressing a p53 variant, rAd-p53 (d 13–19), that is deleted for the amino acid sequence neces-sary for MDM2 binding (amino acids 13–19). We compared the apoptotic activity of rAd-p53 (d 13–19) with that of a recombinant adenovirus expressing wild-type p53 (rAd-p53) in cell lines that differ in endogenous p53 status. rAd-p53 (d 13–19) caused higher levels of apoptosis in p53 wild-type tumor lines compared with wild-type p53 treatment, as measured by annexin V-FITC staining. In p53-altered tumor lines, rAd-p53 (d 13–19) showed apoptotic activity similar to that seen with wild-type p53 treatment. In normal cells, no increase in cytopathicity was detected with rAd-p53 (d 13ndash;19) compared with wild-type p53 treatment. This variant protein displayed synergy with chemotherapeutic agents to inhibit proliferation of ovarian and breast cell lines. The p53 variant showed greater antitumor activity in an established p53 wild-type tumor com-pared with treatment with wild-type p53. The p53 variant represents a means of expanding TP53 gene therapy to tumors that are resistant to p53 treatment due to the cellular responses to wild-type p53.Molecular Therapy (2001) 4, 5–12; doi: 10.1006/mthe.2001.0416

Diabetic retinopathy is the leading cause of low vision and blindness in developed countries.1,2Optometrists have an important role in the detection of diabetic‐related eye disease. They are also well‐placed to manage patients with reduced vision due to diabetes. In 1998, visual rehabilitation information was analysed from 590 visually impaired patients attending the multidisciplinary Low Vision Clinic at Kooyong in Melbourne, Australia. Diabetes was the primary cause of vision loss in 43 (7.3 per cent) of the patients. This paper investigates the characteristics of these 43 patients and the strategies employed to assist them. In doing so we hope to assist practitioners in managing patients with low vision due to diabetes.

Diabetic retinopathy is the leading cause of low vision and blindness in developed countries.1,2Optometrists have an important role in the detection of diabetic‐related eye disease. They are also well‐placed to manage patients with reduced vision due to diabetes. In 1998, visual rehabilitation information was analysed from 590 visually impaired patients attending the multidisciplinary Low Vision Clinic at Kooyong in Melbourne, Australia. Diabetes was the primary cause of vision loss in 43 (7.3 per cent) of the patients. This paper investigates the characteristics of these 43 patients and the strategies employed to assist them. In doing so we hope to assist practitioners in managing patients with low vision due to diabetes.

Interleukin-6 is a multifunctional cytokine that is found in high concentrations in intraocular fluids during the uveitic response. Although monocytic cells are a major source of interleukin-6, resident intraocular cells may also contribute to its accumulation in intraocular fluids during uveitis. The purpose of this study was to determine whether interleukin-6 is produced by pigmented ciliary epithelial cells and whether agents known to stimulate interleukin-6 production, such as interleukin-1β, tumor necrosis factor-α, bacterial endotoxin, and stimulators of the adenylyl cyclase/adenosine 3′,5′-cyclic monophosphate system, increase interleukin-6 production by these cells. Primary and first-passage cultures of nontransformed rabbit pigmented ciliary epithelial cells were incubated with the test agents for varying periods of time in serum-free medium and interleukin-6 levels in the cell-conditioned medium were measured by bioassay.