Characterization of the complete mitochondrial genomes of two Critically Endangered wedgefishes: Rhynchobatus djiddensis and Rhynchobatus australiae.

We present the complete mitochondrial genomes of the Critically Endangered whitespotted wedgefish, Rhynchobatus djiddensis (Forsskål, 1775), and bottlenose wedgefish, Rhynchobatus australiae (Whitley, 1939), with the R. djiddensis mitogenome documented for the first time. The genomes for R. djiddensis and R. australiae are 16,799 and 16,805 bp in length, respectively. Both comprise 13 protein-coding regions, 22 tRNA genes, two rRNA genes, and a non-coding control region. All protein-coding regions consistently start with the ATG start codon; however, the alternative start codon GTG is observed at the start of the COX1 gene. NADH2, COX2, and NADH4 have incomplete stop codons: T or TA, and tRNALeu and tRNASer , have atypical codons: UAA, UGA, GCU, and UAG. The phylogenetic analysis places R. djiddensis and R. australiae within the Rhynchobatus genus, separate from other families in the order Rhinopristiformes. We also highlight the most variable gene regions to expedite future primer design, of which NADH2 was the most variable (4.5%) when taking gene length into account. These molecular resources could promote the taxonomic resolution of the whitespotted wedgefish species complex and aid in the genetic characterization of populations of these and related species.

The effect of willow fodder feeding on immune cell populations in the blood and milk of late-lactating dairy goats.

In a previous study, we showed that access to willow fodder decreased somatic cell counts (SCC) in the milk of local Mamber goats grazing in brushland at the end of lactation. To test whether the consumption of willow affects the cells of the immune system, Alpine crossbred dairy goats grazing in the same environment were either offered free access to freshly cut willow fodder (W, n = 24) or not (C, n = 24) for 2 weeks. The willow fodder contained 7.5 g/kg DM of salicin. The other major secondary compounds were catechin, myricitrin, hyperin and chlorogenic acid (2.2, 2.6, 1.0 and 0.75 g/kg DM, respectively). Udder health status was determined before the experiment, and each of the two groups included five (W) or six (C) goats defined as infected, as established by microbial cfu in milk, and 19 (W) or 18 (C) non-infected goats. Goats ingested, on average, 600 g of DM from willow (25% of food intake), resulting in minor changes in dietary quality compared to the controls, as established by faecal near-IR spectrometry. Throughout the 2 weeks of experiment, differences between groups in dietary CP contents were minor and affected neither by infection nor by access to willow; the dietary percentage of neutral detergent fibre (NDF) decreased in C and increased in W; dietary acid detergent fibre (ADF) increased; and the dietary tannin contents decreased for both treatments. However, milking performance and milk quality attributes in both W and C goats were similar. Initial SCC and milk neutrophil (cluster of differentiation (CD)18+ and porcine granulocyte (PG)68) cell counts were higher in infected than in non-infected goats; counts decreased significantly in W but not in C uninfected goats. The percentage of CD8+ T-cells increased in all C goats, while in the W group, a significant increase was found only for infected goats. The consumption of willow mitigated an increase in CD8+ in blood and triggered an increase in CD8+ in milk, suggesting an immune-regulatory effect independent of udder status. To our knowledge, this is the first report of a direct nutraceutical effect of fodder ingestion on the immune status of goats.

Prevalence and location of tobacco smoke exposure outside the home in adults and children in the United States.

OBJECTIVES: Tobacco smoke exposure (TSE) is associated with many adverse health outcomes. The goal of this study was to provide insight into the prevalence and location of self-reported TSE outside the home for US adults and children. STUDY DESIGN: Cross-sectional survey. METHODS: Data from a nationally representative sample of US adults from 2014 were included. Participants who responded that they smelled smoke during the past seven days in various settings were considered to have been exposed to TSE. Parents were asked about TSE exposure of their children. RESULTS: Sixty-nine percent of all adults reported TSE outside their home in the past seven days. The most common exposure location among adults was on a public sidewalk and outside the doorway of a building (both 33%). Thirty-three percent of parents reported outside the home TSE for their children in the past seven days. Most commonly, the reported exposure was 'In some other place(s)' (16%), followed by at a relative's house (10%). CONCLUSIONS: This study reports on TSE outside the home in a wide variety of settings and a broad range of ages in a nationally representative US sample. A high proportion of US adults and children are exposed to TSE outside the home in indoor, outdoor, public, and private settings. Smoke-free laws, clinical interventions, education, and a change in social norms are required to stop TSE.

Protecting children and families from tobacco and tobacco-related NCDs in the Western Pacific: good practice examples from Malaysia, Philippines and Singapore.

BACKGROUND: Non-communicable diseases (NCDs) are generally considered diseases of adulthood, but NCD risk factors like tobacco use often are taken up during childhood and adolescence, and second-hand smoke exposure affects child survival and development. METHODS: At a regional meeting of the Asia Pacific Child and Family Health Alliance for Tobacco Control, members reviewed existing good practices of child-focused tobacco control approaches using health promotion strategies. These interventions were implemented nationally in Malaysia, the Philippines and Singapore. RESULTS: Three good practice national examples were identified that focused on creating supportive tobacco-free environments and upgrading cessation skills among paediatricians. These country examples highlight strategic areas to protect children and families from the harms of tobacco, as part of NCD prevention and control. Training paediatricians in brief cessation advice has enabled them to address tobacco-using parents. Fully enforcing smoke-free public areas has led to an increase in smoke-free homes. The Tobacco Free Generation is a tobacco control 'endgame' strategy that taps into a social movement to deglamorize tobacco use and empower youth born in and after year 2000 to reject tobacco and nicotine addiction. CONCLUSION: Tobacco control is pivotal in the fight against NCDs; health promotion strategies to protect children and youth from tobacco have a critical role to play in NCD prevention and control. Frontline health workers, including primary care paediatricians, need to step up and actively advocate for full implementation of the WHO Framework Convention on Tobacco Control, including tobacco tax increases and smoke-free areas, while monitoring patients and their parents for tobacco use and second-hand smoke exposure, preventing adolescent smoking uptake, and offering cessation support. A life-course approach incorporating child-focused efforts to prevent initiation of smoking and second-hand smoke exposure with measures promoting cessation among parents will offer the greatest chance of overcoming future tobacco-related NCD burden.

Computational modeling of direct neuronal recruitment during intracortical microstimulation in somatosensory cortex.

OBJECTIVE: Electrical stimulation of cortical tissue could be used to deliver sensory information as part of a neuroprosthetic device, but current control of the location, resolution, quality, and intensity of sensations elicited by intracortical microstimulation (ICMS) remains inadequate for this purpose. One major obstacle to resolving this problem is the poor understanding of the neural activity induced by ICMS. Even with new imaging methods, quantifying the activity of many individual neurons within cortex is difficult. APPROACH: We used computational modeling to examine the response of somatosensory cortex to ICMS. We modeled the axonal arbors of eight distinct morphologies of interneurons and seven types of pyramidal neurons found in somatosensory cortex and identified their responses to extracellular stimulation. We then combined these axonal elements to form a multi-layered slab of simulated cortex and investigated the patterns of neural activity directly induced by ICMS. Specifically we estimated the number, location, and variety of neurons directly recruited by stimulation on a single penetrating microelectrode. MAIN RESULTS: The population of neurons activated by ICMS was dependent on both stimulation strength and the depth of the electrode within cortex. Strikingly, stimulation recruited interneurons and pyramidal neurons in very different patterns. Interneurons are primarily recruited within a dense, continuous region around the electrode, while pyramidal neurons were recruited in a sparse fashion both near the electrode and up to several millimeters away. Thus ICMS can lead to an unexpectedly complex spatial distribution of firing neurons. SIGNIFICANCE: These results lend new insights to the complexity and range of neural activity that can be induced by ICMS. This work also suggests mechanisms potentially responsible for the inconsistency and unnatural quality of sensations initiated by ICMS. Understanding these mechanisms will aid in the design of stimulation that can be used to generate effective sensory feedback for neuroprosthetic devices.

A randomized controlled trial of telephone peer support's influence on breastfeeding duration in adolescent mothers.

PURPOSE: Adolescent mothers breastfeed less often and for a shorter duration than adult mothers. This randomized controlled trial was designed to evaluate the effect of telephone peer support on breastfeeding duration among adolescents. METHODS: Five adolescents who had previously breastfed were trained to provide peer support. Seventy-eight breastfeeding mothers were randomly assigned to an intervention group that received telephone calls from the peer support persons (n = 38) or to a control group that did not receive support (n = 40). An independent interviewer telephoned all new mothers weekly to document feeding patterns. Peer support persons, subjects, and the interviewer were all blinded to the research hypothesis and to group assignment. The primary outcome variable was "any breastfeeding" duration, i.e., the age at complete breastfeeding cessation. A secondary outcome variable was exclusive breastfeeding, i.e., the age at first introduction of any supplement. RESULTS: "Any breastfeeding" duration did not differ significantly between the groups (median 75 days in the intervention group vs. 35 days in the control group, p = 0.26). Among the 13 intervention and 11 control mothers who were exclusively breastfeeding at the time of hospital discharge, the duration of exclusive breastfeeding was increased in the intervention group (median 35 days vs. 10 days, p = 0.004). CONCLUSIONS: This study did not demonstrate a significant effect of peer support on "any breastfeeding" duration. In contrast, exclusive breastfeeding duration appeared to be extended by peer support. This latter finding would benefit from confirmation in future studies. However, unless better methods are developed for retaining peers, this is likely to be a labor-intensive approach to extending exclusive breastfeeding duration among adolescent mothers.

X-chromosome linked inhibitor of apoptosis protein inhibits muscle proteolysis in insulin-deficient mice.

Loss of muscle protein is a serious complication of catabolic diseases and contributes substantially to patients' morbidity and mortality. This muscle loss is mediated largely by the activation of the ubiquitin-proteasome system; however, caspase-3 catalyzes an initial step in this process by cleaving actomyosin into small protein fragments that are rapidly degraded by the proteasome-dependent proteolytic pathway. We hypothesized that X-chromosome linked inhibitor of apoptosis protein (XIAP), an endogenous caspase-3 inhibitor, would block this first step in the cleavage of actomyosin that would make XIAP a candidate for treating muscle wasting. To determine if XIAP could attenuate muscle protein degradation, we used a recombinant lentivirus (Len-XIAP) encoding the full-length human XIAP cDNA to express XIAP in vivo. In muscle of streptozotocin-treated insulin-deficient mice, total muscle protein degradation, caspase-3 activity, and myofibril destruction were increased while XIAP was decreased. Overexpression of XIAP in these mice attenuated the excessive muscle protein degradation. Increased proteasome activity, caspase-3 activity and myofibril protein breakdown were all reduced. The ability of XIAP to prevent the loss of muscle protein suggests that XIAP could be a therapeutic reagent for muscle atrophy in catabolic diseases.

Renal ENaC subunit, Na-K-2Cl and Na-Cl cotransporter abundances in aged, water-restricted F344 x Brown Norway rats.

Renal sodium reabsorption is a key determinant of final urine concentration. Our aim was to determine whether differences existed between aged and young rats in their response to water restriction with regard to the regulation of abundance of any of the major distal renal sodium transporter proteins. Male Fisher 344 x Brown Norway (F344 x BN) rats of 3-, 10-, 24-, or 31 months of age (3M, 10M, 24M, or 31M) were either water restricted (WR) for 5 days or control (ad libitum water). Major renal sodium transporters and channel subunits were evaluated by immunoblotting and immunohistochemistry. Age did not significantly affect plasma arginine vasopressin or aldosterone levels, but renin activity was only 8% in 31M-WR rats relative to 3M-WR (P<0.05). Extreme aging (31M) led to decreased outer medullary abundance of the bumetanide-sensitive Na-K-2Cl cotransporter and decreased cortical abundance of the beta- and gamma-subunits (70-kDa band) of the epithelial sodium channel (ENaC) (P<0.05). Water restriction significantly (P<0.05) increased the abundance of Na-K-2Cl cotransporter (NKCC2) and Na-Cl cotransporter (NCC) across ages. However, these increases were significantly blunted as rats aged. Mean band densities were increased in WR rats (relative to age controls) by 54 and 106% at 3M, but only 25 and 29% at 24M and 0 and 6% at 31M for NKCC2 and NCC, respectively. Aged F344 x BN rats have reduced basal distal tubular renal sodium transporter abundances and blunted upregulation during water restriction, which may contribute to decreased urinary concentrating capacity.

Adrenalectomy blocks the compensatory increases in UT-A1 and AQP2 in diabetic rat kidney.

In normal rats we showed that glucocorticoids participate in the downregulation of UT-A1 protein abundance in the inner medullary tip and in lowering of basal and vasopressin-stimulated facilitated urea permeability in terminal IMCDs. To examine the relevance of this response to a rat model of human disease, we studied rats with uncontrolled diabetes mellitus (DM) induced by streptozotocin (STZ), since these rats have increased corticosterone production and urea excretion. We found that at 3 days of DM, UT-A1 protein abundance is downregulated in the inner medullary tip compared to pair-fed control rats, while DM for more than 7 days caused an increase in UT-A1. To test whether adrenal steroids could be a mechanism contributing to the latter increase, we studied adrenalectomized rats (ADX), ADX rats given STZ to induce diabetes (ADX + STZ), and ADX + STZ rats receiving exogenous aldosterone or dexamethasone. In contrast to control rats, UT-A1 protein abundance was not increased by prolonged DM in the ADX rats. Aquaporin 2 (AQP2) was not increased in the inner medullas of 10-day DM rats either. However, UT-A1 protein abundance was significantly reduced in the inner medullary tips from both diabetic aldosterone-treated (40 +/- 2%) and dexamethasone-treated (43 +/- 2%) ADX rats compared to diabetic ADX rats without steroid replacement. AQP2 was unaffected by steroid hormone treatments. Thus, both mineralocorticoids and glucocorticoids downregulate UT-A1 protein abundance in rats with uncontrolled diabetes mellitus for 10 days. These results suggest that: 1) the increase in UT-A1 observed in DM is dependent upon having adrenal steroids present; and 2) adrenal steroids are not sufficient to enable the compensatory rise in UT-A1 to a steroid-deficient diabetic animal.

Effect of nitrogen intake on nitrogen recycling and urea transporter abundance in lambs.

Urea recycling in ruminants has been studied extensively in the past, but the mechanisms regulating the amount of urea recycled or excreted remain obscure. To elucidate the role of urea transporters (UT) in N recycling, nine Dorset-Finn ewe lambs (20.8 +/- 0.8 kg) were fed diets containing 15.5, 28.4, and 41.3 g of N/kg of DM for 25 d. Nitrogen balance and urea N kinetics were measured during the last 3 d of the period. Animals were then slaughtered and mucosa samples from the rumen, duodenum, ileum, and cecum, as well as kidney medulla and liver, were collected. Increasing N intake tended to increase N balance quadratically (1.5, 5.1, and 4.4 +/- 0.86 g of N/d, P < 0.09), and linearly increased urinary N excretion (2.4, 10, and 16.5 +/- 0.86 g N/d, P < 0.001) and plasma urea N concentration (4.3, 20.3, and 28.4 +/- 2.62 mg of urea N/dL, P < 0.001), but did not affect fecal N excretion (5.0 +/- 0.5 g of N/d; P < 0.94). Urea N production (2.4, 11.8, and 19.2 +/- 0.83 g of N/d; P < 0.001) and urinary urea N excretion (0.7, 7.0, and 13.4 +/- 0.73 g N/d; P < 0.001) increased linearly with N intake, as well as with the urea N recycled to the gastrointestinal tract (1.8, 4.8, and 5.8 +/- 0.40 g of N/d, P < 0.001). No changes due to N intake were observed for creatinine excretion (518 +/- 82.4 mg/d; P < 0.69) and clearance (46 +/- 10.7 mL/min; P < 0.56), but urea N clearance increased linearly with N intake (14.9, 24.4, and 34.9 +/- 5.9 mL/min; P < 0.04). Urea N reabsorption by the kidney tended to decrease (66.3, 38.5, 29.1 +/- 12.6%; P < 0.06) with increasing N content of the diet. Increasing the level of N intake increased linearly the weight of the liver as a proportion of BW (1.73, 1.88, and 2.22 +/- 0.15%, P < 0.03) but only tended to increase the weight of the kidneys (0.36, 0.37, and 0.50 +/- 0.05%, P < 0.08). Urea transporter B was present in all the tissues analyzed, but UT-A was detected only in kidney medulla, liver, and duodenum. Among animals on the three diets, no differences (P > 0.10) in UT abundance, quantified by densitometry, were found. Ruminal-wall urease activity decreased linearly (P < 0.02) with increasing level of N intake. Urease activity in duodenal, ileal, and cecal mucosa did not differ from zero (P > 0.10) in lambs on the high-protein diet. In the present experiment, urea transporter abundance in the kidney medulla and the gastrointestinal tract did not reflect the increase in urea-N reabsorption by the kidney and transferred into the gut.

Youth and tobacco.

Youth around the world take up smoking and use tobacco products at high rates. Young people may not grasp the long-term consequences of tobacco use, although tobacco consumption and exposure has been shown to have significant negative health effects. Youth use a variety of tobacco products that are smoked, chewed, or sniffed, including machine-manufactured cigarettes, cigars, bidis, kreteks, sticks, and snuff. Prevention efforts have focused on countering those aspects that are believed to contribute to smoking uptake, such as tobacco industry advertising and promotion, and access to tobacco. There are many aspects of tobacco promotion through the media that have been more difficult to control, however, such as product placement within popular cinema movies. Once a youth has taken up tobacco, he or she is more likely than an adult to become addicted and should be offered treatment for tobacco cessation. Although there is not yet sufficient evidence to prove efficacy, the same treatments are suggested for youth as are recommended for adults, including nicotine replacement products. Given the severity of the tobacco epidemic worldwide and the devastating health effects on an individual and population basis, there are currently many efforts to curtail the tobacco problem, including the World Health Organization (WHO) sponsored Framework Convention on Tobacco Control. It is through comprehensive and collaborative efforts such as this that the global hazard of tobacco is most likely to be overcome.

Improving adolescent health outcomes.

Adolescent morbidity and mortality are more often due to preventable causes and to risky behavioral choices than to "natural" causes, such as cardiovascular disease or cancer. The leading causes of death among adolescents in Western, industrialized nations are unintentional injuries, especially motor vehicle crashes, homicide, and suicide. The physical and cognitive development of adolescents also results in increased risky behavioral choices, and to high rates of sexually transmitted diseases, substance use and misuse, and inadequate nutrition. These lifestyle choices also have repercussions that last into adulthood. Brief counseling interventions by physicians or other clinicians have been shown to be effective in modifying health risk behaviors in adolescents. Adolescents also have indicated both a belief that physicians should counsel them on risk behaviors and a willingness to discuss risk behaviors if asked about them in a confidential manner. In this paper, we review the leading causes of adolescent morbidity and mortality in the United States and Western Europe, including injuries, violence, depression and suicide, substance use, sexual activity, and nutrition, physical activity, and eating disorders. In addition, we describe the effectiveness of physician counseling for reduction or prevention of specific risk behaviors and the importance of providing comprehensive, confidential care. Additionally, we describe the results of a recent study of implementation of Adolescent Preventive Service Guidelines in community and migrant health centers that increased risky behavior screening and counseling for adolescent patients seen for routine/well care visits.

Teratogen update: Lyme disease.

We reviewed the world literature concerning the reproductive effects of Lyme disease (LD). Borrelia burgdorferi, which is the etiology of LD, is a spirochete and, as such, may share the potential for causing fetal infection, which may occur in the setting of maternal spirochetemia. Information concerning the effects of gestational LD derives from case reports and series, epidemiologic studies, and experimental animal models. Although provocative, these studies fail to define a characteristic teratogenic effect. However, skin and cardiac involvement have predominated in some reports. Pregnancy wastage has been suggested primarily by animal studies. Gestational LD appears to be associated with a low risk of adverse pregnancy outcome, particularly with appropriated antibiotic therapy. Suggestions for management of clinical situations are presented.

Growth factors stimulate the Na-K-2Cl cotransporter NKCC1 through a novel Cl(-)-dependent mechanism.

The Na-K-2Cl cotransporter NKCC1 is an important volume-regulatory transporter that is regulated by cell volume and intracellular Cl(-). This regulation appears to be mediated by phosphorylation of NKCC1, although there is evidence for additional, cytoskeletal regulation via myosin light chain (MLC) kinase. NKCC1 is also activated by growth factors and may contribute to cell hypertrophy, but the mechanism is unknown. In aortic endothelial cells, NKCC1 (measured as bumetanide-sensitive (86)Rb(+) influx) was rapidly stimulated by serum, lysophosphatidic acid, and fibroblast growth factor, with the greatest stimulation by serum. Serum increased bumetanide-sensitive influx significantly more than bumetanide-sensitive efflux (131% vs. 44%), indicating asymmetric stimulation of NKCC1, and produced a 17% increase in cell volume and a 25% increase in Cl(-) content over 15 min. Stimulation by serum and hypertonic shrinkage were additive, and serum did not increase phosphorylation of NKCC1 or MLC, and did not decrease cellular Cl(-) content. When cellular Cl(-) was replaced with methanesulfonate, influx via NKCC1 increased and was no longer stimulated by serum, whereas stimulation by hypertonic shrinkage still occurred. Based on these results, we propose a novel mechanism whereby serum activates NKCC1 by reducing its sensitivity to inhibition by intracellular Cl(-). This resetting of the Cl(-) set point of the transporter enables the cotransporter to produce a hypertrophic volume increase.

The care of HIV-infected adults in rural areas of the United States.

OBJECTIVE: This study describes the population of HIV-infected adults receiving care in rural areas of the United States and compares HIV care received in rural and urban areas. METHODS: Interviews were conducted with a nationally representative sample of 367 HIV-infected adults receiving health care in rural areas and 2806 HIV-infected adults receiving health care in urban areas of the contiguous United States. RESULTS: We estimate that 4800 HIV-infected persons received medical care in rural areas during the first half of 1996. Patients in rural HIV care were more likely than patients in urban HIV care to receive care from providers seeing few (<10) HIV-infected patients (38% vs. 3%; p <.001). Rural care patients were less likely than urban care patients to have taken highly active antiretroviral agents (57% vs. 73%; p <.001) or Pneumocystis carinii pneumonia prophylactic medication when indicated (60% vs. 75%; p =.006). CONCLUSIONS: Few American adults received HIV care in rural areas of the United States. Our findings suggest ongoing disparities between urban and rural areas in access to high-quality HIV care.

Cat-scratch disease presenting as multifocal osteomyelitis with thoracic abscess.

The case of a 4-year-old girl who presented with fever and back pain after being scratched by a kitten is presented. The diagnosis of cat scratch disease osteomyelitis was made by the detection of Bartonella henselae DNA by PCR analysis of a rib abscess aspirate.

Localization of the urea transporter UT-B protein in human and rat erythrocytes and tissues.

A new polyclonal antibody to the human erythrocyte urea transporter UT-B detects a broad band between 45 and 65 kDa in human erythrocytes and between 37 and 51 kDa in rat erythrocytes. In human erythrocytes, the UT-B protein is the Kidd (Jk) antigen, and Jk(a+b+) erythrocytes express the 45- to 65-kDa band. However, in Jk null erythrocytes [Jk(a-b-)], only a faint band at 55 kDa is detected. In kidney medulla, a broad band between 41 and 54 kDa, as well as a larger band at 98 kDa, is detected. Human and rat kidney show UT-B staining in nonfenestrated endothelial cells in descending vasa recta. UT-B protein and mRNA are detected in rat brain, colon, heart, liver, lung, and testis. When kidney medulla or liver proteins are analyzed with the use of a native gel, only a single protein band is detected. UT-B protein is detected in cultured bovine endothelial cells. We conclude that UT-B protein is expressed in more rat tissues than previously reported, as well as in erythrocytes.

Performance of a predictive model for streptococcal pharyngitis in children.

CONTEXT: Group A beta-hemolytic streptococcus (GABHS) pharyngitis is a common childhood illness. The clinical diagnosis is difficult to determine and laboratory tests have limitations; hence, the condition is generally overdiagnosed and overtreated. Several clinical pediatric-specific predictive models have been published but none have been prospectively studied. OBJECTIVE: To test the performance of a previously published predictive model for GABHS pharyngitis in children in different clinical settings and during different seasons. DESIGN: Prospective cohort study. SETTINGS: Pediatric emergency department and 2 pediatric outpatient clinics. PATIENTS: Children aged between 1 and 18 years with pharyngitis on initial examination at study sites between April 1, 1999, and March 31, 2000. INTERVENTIONS: Recording of clinical features during initial evaluation using a standardized form and recovery of GABHS from patients' throats using reference standard methods. MAIN OUTCOME MEASURES: Posttest probability for GABHS positive throat culture associated with the model's positive predictors (moderate to severe tonsillar swelling, cervical lymphadenopathy [moderate to severe tenderness and enlargement of cervical lymph nodes], scarletiniform rash, and the absence of coryza) and the models' negative predictors (absence of the above signs and the presence of coryza). RESULTS: Of 587 patients analyzed, 218 (37%) had a positive throat culture for GABHS. Forty-nine percent were boys. Mean +/- SD age was 6.7 +/- 3.9 years. There was no difference between the subsets within the sample. The posttest probability values for a positive throat culture associated with positive and negative predictors of the model were 79% and 12%, respectively. CONCLUSIONS: A pediatric predictive model for GABHS pharyngitis performed better than physicians' subjective estimates for a positive throat culture and was comparable with a rapid antigen detection test. The model performed consistently well in different populations and across seasons. It can be useful if reliable microbiological testing and/or follow-up are not attainable.

UT-A urea transporter protein in heart: increased abundance during uremia, hypertension, and heart failure.

Urea transporters have been cloned from kidney medulla (UT-A) and erythrocytes (UT-B). We determined whether UT-A proteins could be detected in heart and whether their abundance was altered by uremia or hypertension or in human heart failure. In normal rat heart, bands were detected at 56, 51, and 39 kDa. In uremic rats, the abundance of the 56-kDa protein increased 1.9-fold compared with pair-fed, sham-operated rats, whereas the 51- and 39-kDa proteins were unchanged. We also detected UT-A2 mRNA in hearts from control and uremic rats. Because uremia is accompanied by hypertension, the effects of hypertension per se were studied in uninephrectomized deoxycorticosterone acetate salt-treated rats, where the abundance of the 56-kDa protein increased 2-fold versus controls, and in angiotensin II-infused rats, where the abundance of the 56 kDa protein increased 1.8-fold versus controls. The 51- and 39-kDa proteins were unchanged in both hypertensive models. In human left ventricle myocardium, UT-A proteins were detected at 97, 56, and 51 kDa. In failing left ventricle (taken at transplant, New York Heart Association class IV), the abundance of the 56-kDa protein increased 1.4-fold, and the 51-kDa protein increased 4.3-fold versus nonfailing left ventricle (donor hearts). We conclude that (1) multiple UT-A proteins are detected in rat and human heart; (2) the 56-kDa protein is upregulated in rat heart in uremia or models of hypertension; and (3) the rat results can be extended to human heart, where 56- and 51-kDa proteins are increased during heart failure.