Search

Introduction: Transition clinics are conceived as programs dedicated to the active, multidimensional development of a process that addresses the medical, psychosocial, educational, and vocational needs of pediatric patients suffering from a chronic disease that will persist into adulthood. Their understanding is justified in physiological, psychological, and sociocultural terms on the basis of the differential morbidity and mortality associated with a chronic disease that begins in childhood and prevails into adulthood., Materials and Methods: Here, we reflect on the history, structure, and impact of transition clinics in pediatrics, with an emphasis on pediatric rheumatologic diseases. Additionally, we propose comprehensive reflection as an alternative for the patient, their family, and the medical team, outlining guidelines for development, implementation, and evaluation., Results: The transition of care should commence in early adolescence, considering each patient's cognitive ability as a condition for the initiation of an educational process involving introspection into the disease. Interdisciplinarity is defined as a team that addresses the clinical, physical, emotional, and social dimensions of each patient and their interaction with the environment within the framework of individualized care and family support. Despite this, the lack of evidence supporting standardized guidelines for the implementation and overall effectiveness evaluation of these interventions was highlighted., Conclusions: The transition process is considered successful when the patient is adherent and has a positive and informed perception of their health‒disease journey. We urge the generation of evidence documenting the comprehensiveness of processes inherent to transition clinics as the foundation of necessity., Competing Interests: Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: We confirm that the manuscript has been read and approved by all the authors listed. We also confirm that the order of authors listed in the manuscript has been approved by all of us. Finally, this manuscript is original, has not been previously published, and is not currently under consideration for publication elsewhere. Competing interests: The authors have no conflict of interest., (© 2024. The Author(s).)

Objective: The population of adults with single-ventricle congenital heart disease (CHD) is growing. This study explores their lived experiences through an adult developmental psychology framework., Methods: Individuals aged 18 and older with single-ventricle CHD participated in Experience Group sessions and 1:1 interviews. Sessions were transcribed and analysed thematically. Themes were categorized by developmental domains and age group., Results: Of the 29 participants, 18 (62%) were female, 10 (35%) were emerging (18-29 years), 13 (45%) were established (30-45 years), and 6 (21%) were midlife adults (46-60 years). Emerging adults expressed reluctance to initiate romantic relationships and fear of burdening partners, while established adults reported strong relationships with partners deeply involved in caregiving. Emerging adults struggled with finding fulfilling work that meets their health needs, whereas established and midlife adults faced unemployment or early retirement due to health limits. Family dynamics shifted, with established and midlife adults educating their children to become caregivers. Physical limitations and low self-rated health were consistent across life stages, and midlife adults did not worry about traditional chronic conditions. Mental health concerns, including anxiety and depression, persisted across all life stages, but resiliency and positive affect were also evident., Conclusion: Adults with single-ventricle CHD experience developmental milestones differently, indicating the need for early anticipatory guidance in these domains to achieve optimal outcomes in adulthood.

Breast reconstruction using contralateral autologous tissue, also known as breast sharing, is a viable option previously described in the literature, whereby flaps based on perforators of the internal mammary artery (internal mammary artery pedicle) are used. We report a postoncological breast reconstruction case using a microvascular flap taken from the lateral pole of the contralateral breast. We highlight the importance of preserving the medial pole of the donor breast for improving cosmesis, avoiding symmastia, and preserving the intermammary sulcus, as a difference with flaps based on the internal mammary artery pedicle flaps. Breast sensation could be recovered by neurotization of the lateral intercostal nerve, which may be included in the contralateral breast flap to be transferred. Contralateral breast free flaps could be an alternative to reconstruct the breast in selected patients. Oncological risk factors are discussed. Advances in genetic testing and tumor cell biology could help us to select the accurate candidates for this reconstructive technique., Competing Interests: Disclosure: The authors have no financial interest to declare in relation to the content of this article., (Copyright © 2020 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The American Society of Plastic Surgeons.)

Mutation of either arginase structural gene (ARGAH1 or ARGAH2 encoding arginine [Arg] amidohydrolase-1 and -2, respectively) resulted in increased formation of lateral and adventitious roots in Arabidopsis (Arabidopsis thaliana) seedlings and increased nitric oxide (NO) accumulation and efflux, detected by the fluorogenic traps 3-amino,4-aminomethyl-2',7'-difluorofluorescein diacetate and diamino-rhodamine-4M, respectively. Upon seedling exposure to the synthetic auxin naphthaleneacetic acid, NO accumulation was differentially enhanced in argah1-1 and argah2-1 compared with the wild type. In all genotypes, much 3-amino,4-aminomethyl-2',7'-difluorofluorescein diacetate fluorescence originated from mitochondria. The arginases are both localized to the mitochondrial matrix and closely related. However, their expression levels and patterns differ: ARGAH1 encoded the minor activity, and ARGAH1-driven beta-glucuronidase (GUS) was expressed throughout the seedling; the ARGAH2::GUS expression pattern was more localized. Naphthaleneacetic acid increased seedling lateral root numbers (total lateral roots per primary root) in the mutants to twice the number in the wild type, consistent with increased internal NO leading to enhanced auxin signaling in roots. In agreement, argah1-1 and argah2-1 showed increased expression of the auxin-responsive reporter DR5::GUS in root tips, emerging lateral roots, and hypocotyls. We propose that Arg, or an Arg derivative, is a potential NO source and that reduced arginase activity in the mutants results in greater conversion of Arg to NO, thereby potentiating auxin action in roots. This model is supported by supplemental Arg induction of adventitious roots and increased NO accumulation in argah1-1 and argah2-1 versus the wild type.

In Arabidopsis thaliana (L.) Heynh., AtPhr2 and AtNsr1 encode proteins with MYB-like and alpha-helical domains. They resemble CrPsr1, a nuclear-localized MYB protein that is critical for acclimation to phosphorous (P) starvation in the alga Chlamydomonas reinhardtii. Reverse transcription-polymerase chain reaction analysis of the first unique exons indicated that AtPhr2 mRNA increased as early as 6 h after P deprivation (-P), whereas nitrogen deprivation (-N) had no effect. The AtNsr1 mRNA level increased exclusively under -N, an increase first noted by 2 days in -N. In spite of P- and N-specific effects on expression of AtPhr2 and AtNsr1 there appeared to be P-N cross-talk at the whole-plant level. Total non-secreted acid phosphatase activity increased under both -P and -N within 2 days of deprivation. Further, the pho2-1/pho2-1 mutant, reported to be a phosphate accumulator, showed no increase in AtPhr2 mRNA in response to -P and a 70% reduction in the response of AtNsr1 mRNA to -N. Consistent with this pattern, there was no increase in acid phosphatase activity in pho2-1/pho2-1 plants deprived of P or N. However, when deprived of P, pho2-1/pho2-1 plants accumulated much higher levels of nitrate. T-DNA disruption of AtNsr1 resulted in altered expression of at least one nitrate transporter (AtNRT2.5). Further evidence of cross-talk between N and P responses was altered expression of N-responsive genes in pho2-1/pho2-1.

We describe the identification and functional characterization of two Arabidopsis mitochondrial basic amino acid carriers (BAC), AtmBAC1 and AtmBAC2, which are related to the yeast ornithine (Orn) carrier Ort1p, also known as Arg11p. The arg11 mutant requires arginine (Arg) supplementation because it fails to export sufficient ornithine from the mitochondrion to the cytosol where it is converted to arginine. AtmBAC1 and, to a lesser extent, AtmBAC2 partially replaced the function of Ort1p in yeast arg11. The more efficient putative carrier, AtmBAC1, was expressed in E. coli, purified, and reconstituted into phospholipid vesicles, where it transported the basic l-amino acids arginine, lysine, ornithine and histidine (in order of decreasing affinity). AtmBAC1 recognized l-histidine whereas both yeast Ort1p and the mammalian ortholog ORNT1p do not. Also different from ORNT1p, AtmBAC1 did not transport citrulline. AtmBAC1 appeared to be more stereospecific than the yeast and mammalian ornithine carriers, exhibiting greater preference for the l-forms of arginine, lysine and ornithine. By RT-PCR, both AtmBAC1 and AtmBAC2 transcripts were detected in stems, leaves, flowers, siliques, and seedlings. Expression of AtmBAC1 in seedlings is consistent with its involvement in Arg breakdown in early seedling development, i.e. delivery of Arg to mitochondrial arginase. The Km (0.19 mm) for Arg uptake by AtmBAC1 was close to the value we previously determined for the saturable component of Arg uptake into intact mitochondria from soybean seedling cotyledons.

Pantoea stewartii subsp. stewartii causes Stewart's wilt of sweet corn. A hypersensitive response and pathogenicity (Hrp) secretion system is needed to produce water-soaking and wilting symptoms in corn and to cause a hypersensitive response (HR) in tobacco. Sequencing of the hrp cluster revealed a putative harpin gene, hrpN. The product of this gene was overexpressed in Escherichia coli and shown to elicit the HR in tobacco and systemic resistance in radishes. The protein was designated HrpN(Pnss). Like other harpins, it was heat stable and protease sensitive, although it was three- to fourfold less active biologically than Erwinia amylovora harpin. We used antibodies to purified HrpN(Pnss) to verify that hrpN mutants could not produce harpin. This protein was secreted into the culture supernatant and was produced by strains of P. stewartii subsp. indologenes. In order to determine the importance of HrpN(Pnss) in pathogenesis on sweet corn, three hrpN::Tn5 mutants were compared with the wild-type strain with 50% effective dose, disease severity, response time, and growth rate in planta as parameters. In all tests, HrpN(Pnss) was not required for infection, growth, or virulence in corn or endophytic growth in related grasses.

Reversible protein phosphorylation/dephosphorylation plays important roles in signaling the plant adaptive responses to salinity/drought stresses. Two protein kinases with molecular masses of 48 and 40 kD are activated in tobacco cells exposed to NaCl. The 48-kD protein kinase was identified as SIPK (salicylic acid-induced protein kinase), a member of the tobacco MAPK (mitogen-activated protein kinase) family that is activated by various other stress stimuli. The activation of the 40-kD protein kinase is rapid and dose-dependent. Other osmolytes such as Pro and sorbitol activate these two kinases with similar kinetics. The activation of 40-kD protein kinase is specific for hyperosmotic stress, as hypotonic stress does not activate it. Therefore, this 40-kD kinase was named HOSAK (high osmotic stress-activated kinase). HOSAK is a Ca(2+)-independent kinase and uses myelin basic protein (MBP) and histone equally well as substrates. The kinase inhibitor K252a rapidly activates HOSAK in tobacco cells, implicating a dephosphorylation mechanism for HOSAK activation. Activation of both SIPK and HOSAK by high osmotic stress is Ca(2+) and abscisic acid (ABA) independent. Furthermore, mutation in SOS3 locus does not affect the activation of either kinase in Arabidopsis seedlings. These results suggest that SIPK and 40-kD HOSAK are two new components in a Ca(2+)- and ABA-independent pathway that may lead to plant adaptation to hyperosmotic stress.

Harpins are bacterial protein elicitors that induce hypersensitive response-like necrosis when infiltrated into nonhost plants such as tobacco (Nicotiana tabacum L.) (Z.-M. Wei, R.J. Laby, C.H. Zumoff, D.W. Bauer, S.Y. He, A. Collmer, S.V. Beer [1992] Science 257: 85-88). Activity of a 49-kD Mg2+-dependent and Ca2+-independent kinase in tobacco leaves increased 50-fold 15 min after infiltration of harpin from Erwinia amylovora (harpinEa). Much less pronounced and more transient activation was detected in water-infiltrated leaves. Biochemical characteristics of the harpinEa-activated protein kinase (HAPK) activity are consistent with those of the mitogen-activated protein kinase family. HAPK is cytosolic and phosphorylates myelin basic protein on serine/threonine residues. Treatment with a protein tyrosine phosphatase completely eliminated HAPK activity, suggesting that tyrosine phosphorylation is required for posttranslational activation. Sustained HAPK activation after cycloheximide treatment implies that HAPK may be negatively regulated by a translation-dependent mechanism. The extracellular Ca2+ chelator EGTA or the protein kinase inhibitor K252a, infiltrated in planta together with harpinEa, partially blocked HAPK activation. The Ca2+-channel blocker La3+ had no effect on HAPK activation, suggesting that phosphorylation events precede and/or do not depend on the entry of extracellular Ca2+ into the cell. These results suggest that early signal transduction events during harpinEa- induced hypersensitive response elicitation depend in part on the activation of HAPK.