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PubMed1985

M protein instability and lack of H protein processing associated with nonproductive persistent infection of HeLa cells by measles virus.

Persistent infections such as subacute sclerosing panencephalitis (SSPE) which do not produce infectious virus particles (nonproductive persistence) are often accompanied by a reduced steady-state amount of the viral matrix (M) protein and/or reduced hemadsorption activity. The possible causes of these aberrations associated with nonproductive persistence were investigated by following changes in the viral proteins with time in pulse-chase experiments. Three HeLa cell lines persistently infected with measles virus; K11, K11A, and HG111; were compared to each other and to acutely infected HeLa cells. K11 produces infectious virions at a low level (productive persistence). K11A and HG111 are both nonproductive persistently infected cell lines derived from K11. K11A cells have a reduced steady-state amount of viral M protein and reduced hemadsorption activity. HG111 cells have reduced hemadsorption but a normal level of viral M protein. As such, these cell lines serve as good model systems for the study of nonproductive persistent infection associated with SSPE. The reduced amount of M protein in K11A was found to result from rapid degradation of the protein. Degradation of the protein resulted from changes in the protein itself rather than from cellular changes. The hemagglutination (H) protein was found to be present at a low level in K11A cells. In addition, in both K11A and HG111 cells, conversion of the sugar moiety of the H glycoprotein from the high mannose form to the complex sugar form did not take place. Such modification usually occurs concomitant with transport of glycoproteins onto the cell surface. As such, lack of processing could preclude the appearance of functional H proteins on the cell surface. This could account for the reduced hemadsorption activity in these cells. The roles that these changes may play in the generation of nonproductive persistence are discussed.

Cell Transformation, Viral↗
PubMed1986

Persistent infection of Aedes albopictus C6/36 cells by Bunyamwera virus.

Two cell lines persistently infected with Bunyamwera virus have been established from the C6/36 clone of Aedes albopictus cells. The cells express Bunyamwera virus antigens as detected by immunofluorescence and are resistant to superinfection with Bunyamwera virus and other bunyaviruses, but not Dugbe virus (Nairovirus) nor vesicular stomatitis virus. The virus released from the persistently infected cells developed an altered cloudy or "bull's-eye" plaque morphology with increasing passage level, and a greater temperature sensitivity at 39.5 degrees than standard virus. The persistent virus interfered strongly with the replication of standard Bunyamwera virus in normal C6/36 cells and to a much lesser extent in BHK cells. Interference was not noted with other bunyaviruses or vesicular stomatitis virus. The persistent virus from one cell line, C6/36-PI LO, had a slower migrating nucleocapsid protein on polyacrylamide gels. Analysis of the RNA in persistently infected cells or in persistent virus by Northern blot hybridization with cloned cDNA probes showed that the major viral RNA species was the S segment, while the L and M RNA segments were barely detectable. Our results indicate that Bunyamwera virus can readily establish persistent infections in mosquito cells, and that persistence is accompanied by the generation of viruses with variable genetic and phenotypic characteristics.

Aedes↗
PubMed1982

Role of the S4 gene in the establishment of persistent reovirus infection in L cells.

We have studied the viral genes playing a role in persistence of reovirus in L cells. We established persistent infections by coinfecting L cells using wild-type reovirus type 2 and defective reovirus type 3. An analysis of the genomic double-stranded RNA pattern of the virus population selected during persistent infection revealed that the S4 gene was derived from the defective parent in three independently established lines, suggesting that the S4 gene plays an essential role in the establishment of persistent infection. The selection of recombinant viruses containing the S4 gene derived from the defective virus was specific for persistent infection, since it was not selected in lytic infections. Following the establishment of persistent infection, mutations in the S1 gene appeared in two of three cell lines. Thus mutations in the S4 gene play a critical role in the establishment of persistent infection, while mutations in the S1 gene play a role in the maintenance of the persistent infection.

Animals↗
PubMed1986

Vero cells persistently infected with Tacaribe virus: role of interfering particles in the establishment of the infection.

Eight Vero cell sublines (Vero T) persistently infected with wild type Tacaribe virus replicated in different hosts were established. In order to unravel the mechanism involved in the initiation and maintenance of persistence, the properties of virus shed by the sublines and the presence of interfering particles (IP) were analyzed. During the course of infection, persistent virus (Tac-pi) underwent mutations although no consistent pattern of virus evolution was observed. ts mutants were isolated from two Vero T sublines, whereas a slow growth variant was shed by another. The remaining sublines released virus resembling wt parental virus. Except for Vero T1 sublines, Vero T cultures shed no detectable IP. These results emphasize the point that neither the emergence of virus mutants nor the synthesis of IP is essential for the maintenance of the persistent state. To define the role of IP in the initiation of persistence, coinfection experiments with a characterized inoculum were performed. For that purpose, attempts were made to obtain IP stocks free from pfu by serial transfers of undiluted virus. Neither enrichment nor amplification of IP occurred, and virus stocks were freed of infectious virus by UV irradiation. If normal Vero cells were infected with Tac-pi virus released by Vero T2, Vero T3, Vero T4, Vero T5, Vero T6, Vero T7 and Vero T10 sublines, a complete destruction of the monolayer without cell recovery was observed. In contrast, parental and Vero T1 viruses always originated persistently infected sublines. Similarly, the addition of IP to virus inocula constituted by Tac-pi viruses released by Vero T2, Vero T3, Vero T4, Vero T5, Vero T6, Vero T7 and Vero T10 sublines gave rise to persistently infected cultures. These results suggest that although IP are not important by themselves in the maintenance of persistence, they play a major role in initiation.

Animals↗
PubMed2006

Persistent depressive symptoms lower aspirin adherence after acute coronary syndromes.

BACKGROUND: Even mild depressive symptoms during hospitalization are an independent risk factor for mortality after acute coronary syndromes (ACS). The mortality risk is highest for patients whose depressive symptoms persist after ACS. Low adherence to medications that reduce the risk of subsequent cardiac events may be one of the mechanisms underlying the relationship between persistent depression and risk of ACS recurrence. We compared electronically monitored adherence to aspirin in 3 groups of patients with ACS: persistently depressed, remittent depressed, and persistently nondepressed. METHODS: Using an electronic device stored in the cap of a pill bottle, we monitored aspirin adherence over a 3-month period in 165 consecutive patients recruited within 1 week of an ACS event. Depressive symptom severity was assessed by using the Beck Depression Inventory at baseline and at 3 months. Adherence was determined by the percentage of days aspirin was taken as prescribed. RESULTS: Among the patients, 10.5% of nondepressed patients, 9.8% of remittent depressed patients, and 42.1% of persistently depressed patients took aspirin < or of the time (P < .001). Examined a different way, the mean percentage of days that the correct aspirin dosage (1 pill per day for all patients) was taken was significantly lower in the persistently depressed patients (76.1%) than in the remittent depressed (87.4%) and persistently nondepressed (89.5%) patients (P < .01). Remittent depressed patients did not differ from nondepressed patients. Results remained unchanged after controlling for baseline depressive symptom severity and medical comorbidity. CONCLUSIONS: Poor medication adherence--a potentially modifiable behavior--may contribute to the high mortality risk observed in patients with persistent symptoms of depression after ACS.

Aged↗
PubMed2005

Persistent diabetic macular edema is associated with elevated hemoglobin A1c.

PURPOSE: To assess the correlation between persistent diabetic macular edema and hemoglobin A1c (HbA1C). DESIGN: Retrospective study. METHODS: Records of type 2 diabetic patients who received eye care for persistent clinically significant macular edema (CSME) from January 2002 to January 2004 were reviewed. Subjects who met one of two criteria were identified: 1) persistent CSME, detected by contact lens biomicroscopy and fluorescein angiography, despite at least two focal laser photocoagulations (FLP) performed at least 3 months before the current diagnosis, or 2) a history of CSME with resolution of macular edema at the time of examination. Patients also needed to have had their HbA1C measured at the Johns Hopkins Hospitals within 3 months of meeting these criteria. RESULTS: The study identified 92 patients (152) eyes with persistent CSME and 32 patients (56 eyes) with resolved CSME. HbA1C values ranged from 5.3% to 15.6% (mean, 8.9%; median, 8.7%) and 5.3% to 9.7% (mean, 6.7%; median, 6.6%) among patients with persistent and resolved edema (P = .0005). Among the 32 patients with persistent unilateral CSME, mean HbA1C was 8.6% (median 8.5%), and among the 60 patients with bilateral CSME, mean HbA1C was 9.1% (median, 8.9%). Of patients with persistent CSME, 74% had HbA1C greater than 7.5% compared with 12.5% of the patients with resolved CSME (P = .0005). CONCLUSIONS: Persons with type 2 diabetes and persistent CSME have higher HbA1C at time of their disease than patients with resolved CSME. Patients with bilateral disease have more elevated HbA1C than those with unilateral disease.

Aged↗
PubMed2005

JNK and PI3k/Akt signaling pathways are required for establishing persistent SARS-CoV infection in Vero E6 cells.

Persistence was established after most of the SARS-CoV-infected Vero E6 cells died. RNA of the defective interfering virus was not observed in the persistently infected cells by Northern blot analysis. SARS-CoV diluted to 2 PFU failed to establish persistence, suggesting that some particular viruses in the seed virus did not induce persistent infection. Interestingly, a viral receptor, angiotensin converting enzyme (ACE)-2, was down-regulated in persistently infected cells. G418-selected clones established from parent Vero E6 cells, which were transfected with a plasmid containing the neomycin resistance gene, were infected with SARS-CoV, resulting in a potential cell population capable of persistence in Vero E6 cells. Our previous studies demonstrated that signaling pathways of extracellular signal-related kinase (ERK1/2), c-Jun N-terminal protein kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3'-kinase (PI3K)/Akt were activated in SARS-CoV-infected Vero E6 cells. Previous studies also showed that the activation of p38 MAPK by viral infection-induced apoptosis, and a weak activation of Akt was not sufficient to protect from apoptosis. In the present study, we showed that the inhibitors of JNK and PI3K/Akt inhibited the establishment of persistence, but those of MAPK/ERK kinase (MEK; as an inhibitor for ERK1/2) and p38 MAPK did not. These results indicated that two signaling pathways of JNK and PI3K/Akt were important for the establishment of persistence in Vero E6 cells.

Animals↗
PubMed2006

Mechanisms of establishment of persistent SARS-CoV-infected cells.

Previously, we reported the establishment of cells with persistent SARS-CoV infection after apoptotic events and showed that both JNK and PI3K/Akt signaling pathways are important for persistence by treatment with inhibitors at the early stages of SARS-CoV infection. However, the mechanisms of establishment of persistent infection are still unclear. In this study, we investigated which signaling pathways play important roles in escape from apoptosis in cells infected with SARS-CoV. In persistently infected cells at 50h.p.i., PI3K/Akt, JNK, p38 MAPK and Bcl-2 were phosphorylated and the protein levels of Bcl-2 and Bcl-xL were increased. When surviving cells were treated with the JNK-specific inhibitor, SP600125, at 50h.p.i., all cells died, suggesting that the JNK signaling pathway is necessary for maintenance of persistently infected cells. Among the signaling pathways in persistently infected cells, Akt and JNK were phosphorylated in SARS-CoV-nucleocapsid (N) protein-expressing Vero E6 cells using vaccinia viral vector (DIs), strongly suggesting that N protein-induced phosphorylation of Akt and JNK are necessary to establish persistence. These results indicated that at least four proteins, Akt, JNK, Bcl-2 and Bcl-xL, are necessary for survival of persistently SARS-CoV-infected cells.

Animals↗
PubMed2005

Histopathology of persistent papules and plaques in adult-onset Still's disease.

BACKGROUND: Persistent plaques and linear pigmentation have been reported as specific skin lesions in some patients with adult-onset Still's disease (AOSD). OBJECTIVE: We sought to characterize the histologic findings of AOSD-associated persistent rash in 11 cases and correlate the histologic findings with the clinical features. METHODS: From 1988 to 2004, 17 cases fulfilling Yamaguchi's criteria for AOSD in our hospital were reviewed and 11 (65%) manifested persistent papules and plaques. The pathology of 13 biopsy specimens of persistent eruption from 9 patients was reviewed. RESULTS: The 11 patients consisted of 3 men and 8 women with age of onset ranging from 19 to 67 years (average 34.7 years). Evanescent Still's rash was recorded in 9 patients. The persistent rash manifested as pruritic, red, violaceous, or brownish scaly or crusted lichenoid papules and plaques usually widely distributed over the trunk, neck, face, and extensor sides of the extremities. Lesions arranged in a bizarre linear pattern resulting from scratching were noted in some patients. Three patients died of severe disease, systemic complications, or both. The histology of persistent papules and plaques was characterized by: (1) multiple individual necrotic keratinocytes, singly or in aggregates, mainly located in the upper epidermis, including the normal or parakeratotic horny layer; and (2) infiltration of lymphocytes and neutrophils in the papillary and middermis. Other less common findings included basal vacuolar alteration, nuclear dust, and subcorneal or intracorneal pustules. CONCLUSIONS: A clinically and pathologically distinct form of persistent lichenoid eruption was commonly observed in our patients with AOSD. The combination of multiple individual necrotic keratinocytes in the upper epidermis and a dermal infiltrate of neutrophils allow for histologic differentiation of this persistent eruption from most other lichenoid and interface dermatitides and may facilitate an earlier diagnosis of AOSD.

Adult↗
PubMed2006

Auditory abilities of speakers who persisted, or recovered, from stuttering.

OBJECTIVE: The purpose of this study was to see whether participants who persist in their stutter have poorer sensitivity in a backward masking task compared to those participants who recover from their stutter. DESIGN: The auditory sensitivity of 30 children who stutter was tested on absolute threshold, simultaneous masking, backward masking with a broadband and with a notched noise masker. The participants had been seen and diagnosed as stuttering at least 1 year before their 12th birthday. The participants were assessed again at age 12 plus to establish whether their stutter had persisted or recovered. Persistence or recovery was based on participant's, parent's and researcher's assessment and Riley's [Riley, G. D. (1994). Stuttering severity instrument for children and adults (3rd ed.). Austin, TX: Pro-Ed.] Stuttering Severity Instrument-3. Based on this assessment, 12 speakers had persisted and 18 had recovered from stuttering. RESULTS: Thresholds differed significantly between persistent and recovered groups for the broadband backward-masked stimulus (thresholds being higher for the persistent group). CONCLUSIONS: Backward masking performance at teenage is one factor that distinguishes speakers who persist in their stutter from those who recover. Education objectives: Readers of this article should: (1) explain why auditory factors have been implicated in stuttering; (2) summarise the work that has examined whether peripheral, and/or central, hearing are problems in stuttering; (3) explain how the hearing ability of persistent and recovered stutterers may differ; (4) discuss how hearing disorders have been implicated in other language disorders.

Adolescent↗
PubMed2004

The role of food plant and pathogen-induced behaviour in the persistence of a nucleopolyhedrovirus.

Insect baculoviruses can survive between epidemics as infectious particles external to the host. Many pathogens persist in reservoirs, i.e., microhabitats where survival is enhanced, for example due to protection from the degrading effects of UV irradiation. However, the probability of infecting new susceptible hosts is usually reduced. Persistence of pathogens and their movement in and out of reservoirs is an important, albeit little understood, aspect of insect pathogen ecology. This study investigated interactions between the behaviour of infected insect hosts, virus distribution and plant species on the persistence of the winter moth (Operophtera brumata) nucleopolyhedrovirus. Habitat influenced the persistence of infectious baculovirus in the field: virus on Sitka spruce (Picea sitchensis) and oak (Quercus robur) in forested areas retained more infectivity than virus on heather (Calluna vulgaris) in an unshaded habitat. Plant species per se did not directly affect the persistence of virus on the foliage of potted seedlings. Virally infected insects had altered behaviour and moved down plants relative to control insects, whereas in other systems larvae show height-seeking behaviour. Consequently, the majority of virus particles were distributed on plant stems. In two experiments (one using winter moth NPV and one Mamestra brassicae NPV) virus persisted better on plant stems relative to foliage. Neonate larvae were shown to be able to acquire infections from tree stems contaminated with a low level of virus. These data suggest that plant stems may be important reservoirs for between-year persistence of this pathogen. The observed virus-induced changes in host behaviour in winter moth could enhance the viral persistence by increasing the deposition of occlusion bodies in these reservoirs.

Animals↗
PubMed2005

In vivo efficiency of targeted norfloxacin against persistent, isoniazid-insensitive, Mycobacterium bovis BCG present in the physiologically hypoxic mouse liver.

Persistence of Mycobacterium tuberculosis is a hypoxia-inducible state in which the bacteria are phenotypically insensitive to currently available antituberculous drugs. In humans, persistent M. tuberculosis is found in granulomatous lesions, either inside macrophages or in necrotic tissue, where the partial oxygen pressure (pO(2)) is very low. Persistent bacteria can remain silent for decades before overt tuberculosis develops. Due to insensitivity to classical drugs, M. tuberculosis persistence prevents rapid and definitive clearance of bacteria. Consequently, therapeutic molecules are required that are both active against persistent bacilli and able to reach their intramacrophagic location. In contrast to its native form, norfloxacin is active in vivo against Mycobacterium bovis BCG present in the lungs when temporarily linked to a macromolecular carrier targeted to macrophages. To study the efficiency of this macromolecular prodrug targeted to persistent mycobacteria confined inside macrophages, we established a short-term in vivo model based on the physiological pO(2) differences between lungs, spleen and liver. Whereas lungs and spleen are well oxygenated, the liver has a low pO(2) due to its portal irrigation. Therefore, studying mycobacteria in the liver yields information about in vivo persistent bacilli exposed to low pO(2). To our knowledge, no similar short-term in vivo model has been published to date. Using this model, we demonstrated the insensitivity to isoniazid of M. bovis BCG present in hypoxic sites, and showed that norfloxacin given as a mannosylated macrophage-targeted prodrug was able to kill these isoniazid-insensitive mycobacteria. This demonstrates that intracellular persistent mycobacteria are amenable to antibiotic treatment.

Animals↗
PubMed2005

Persistence, spread and the drift paradox.

We derive conditions for persistence and spread of a population where individuals are either immobile or dispersing by advection and diffusion through a one-dimensional medium with a unidirectional flow. Reproduction occurs only in the stationary phase. Examples of such systems are found in rivers and streams, marine currents, and areas with prevalent wind direction. In streams, a long-standing question, dubbed 'the drift paradox', asks why aquatic insects faced with downstream drift are able to persist in upper stream reaches. For our two-phase model, persistence of the population is guaranteed if, at low population densities, the local growth rate of the stationary component of the population exceeds the rate of entry of individuals into the drift. Otherwise the persistence condition involves all the model parameters, and persistence requires a critical (minimum) domain size. We calculate the rate at which invasion fronts propagate up- and downstream, and show that persistence and ability to spread are closely connected: if the population cannot advance upstream against the flow, it also cannot persist on any finite spatial domain. By studying two limiting cases of our model, we show that residence in the immobile state always enhances population persistence. We use our findings to evaluate a number of mechanisms previously proposed in the ecological literature as resolutions of the drift paradox.

Models, Theoretical↗
PubMed2004

The impact of pharmacogenomic factors on acute persistent rejection in adult lung transplant patients.

Persistent rejection in the face of treatment and multiple episodes of rejection are associated with the development of chronic rejection and graft loss in solid organ transplantation. The factors that create an environment for rejection that persists in the face of treatment are as yet not understood. The objective of this study was to evaluate the risk factors, including human multidrug resistance gene (MDR1), cytochrome P4503A5 (CYP3A5) and cytokine gene polymorphisms, associated with acute persistent rejection (APR) in lung transplant patients. One hundred and twenty-five adult lung transplant patients were studied. MDR1 G2677T, C3435T and CYP3A5 polymorphisms were assessed by direct sequencing of the polymorphic region in patient DNA. Cytokine genotyping for five cytokines was performed using the polymerase chain reaction-sequence specific primers (PCR-SSP) technique. Multivariate regression analysis was used to identify the predictors of acute persistent rejection. The dependent variable was the presence or absence of acute persistent rejection based on lung biopsies during the first postoperative year. The independent variables were MDR1 G2677T and C3435T, CYP4503A5 and cytokine polymorphisms, survival status, age, gender, survival days and HLA mismatches. The MDR1 C3435T polymorphism and age were independently associated with acute persistent rejection (p = 0.025, odds ratio = 0.29, 95% CI 0.1-0.86 and p = 0.016, odds ratio = 0.94, 95% CI 0.89-0.98, respectively). For the MDR1 C3435T polymorphism, 72% of patients with the C allele had acute persistent rejection in comparison to 52% for TT patients (p = 0.04). For age, a significant difference was found between the nonrejection group and the rejection group (mean+/-S.D. 52.1+/-11.2 vs. 44.4+/-12.3, p = 0.01). This is the first report of the association of a drug disposition genotype with drug-resistant acute rejection in organ transplant patients. The major predictor of acute persistent rejection in the first postoperative year for lung transplant patients was the MDR1 C3435T genotype. This association could be due to drug resistance, altered drug disposition or other immunologic effects associated with P-glycoprotein (P-gp) function. Future prospective treatment algorithms should be developed that will incorporate the knowledge of gene polymorphisms into treatment regimens to improve the outcome following lung transplantation.

Adult↗
PubMed2006

Adherent and invasive Escherichia coli are associated with persistent bovine mastitis.

Bovine mastitis caused by Escherichia coli has traditionally been viewed as a transient infection. However, E. coli can also cause clonal persistent intramammary infection (IMI) in dairy cows. In this study, we explored the possibility that E. coli strains associated with persistent IMI are better able to adhere to, invade, survive and replicate in cultured mammary epithelial cells (MAC-T) than transient strains, and examined their serotype, overall genotype, phylogenetic group, and the presence of known virulence genes. Both transient and persistent E. coli strains adhered to MAC-T cells, but persistent strains invaded MAC-T cells 2.6-63.5 times more than transient strains. Blocking the adhesin/invasin FimH with mannose diminished but did not eliminate adhesion and invasion of any strain. Cytoskeletal and protein kinase inhibitors cytochalasin D, colchicine, genistein and wortmannin dramatically reduced invasion of MAC-T cells by both strains. All of the persistent strains, but only one transient strain, were able to survive and replicate intracellularly in MAC-T cells over 48 h. Transient and persistent strains displayed heterogeneous serotypes and overall genotypes, but similar phylogeny (group A), and lacked virulence genes of invasive E. coli. We have found that E. coli strains associated with persistent IMI are better able to invade and replicate within cultured mammary epithelial cells than transient strains. The invasion process involves the host cytoskeleton and signaling cascades and is not FimH dependent. Our findings suggest that the invasion of mammary epithelial cells and intracellular survival play an important role in the pathogenesis of persistent E. coli mastitis.

Analysis of Variance↗
PubMed2006

Defective interfering RNAs of Japanese encephalitis virus found in mosquito cells and correlation with persistent infection.

Defective interfering (DI) RNAs are deletion mutants of viral genomes that are known in many cases to contribute to persistent infection and modification of viral pathogenesis. Cell type also plays a critical role in the establishment of viral persistence. In this study we have identified for the first time the generation of DI RNAs of Japanese encephalitis virus in C6/36 mosquito cells. A persistent infection was established by replacing growth medium on surviving cells and continued cell passaging. Persistent infection was demonstrated by a continual release of infectious virus, fluorescent antibody staining, and Northern analysis. A population of DI RNAs of approximately 8.2-9.7 kb, not detectable in acutely infected cells, became apparent in the persistently infected cells by 25 days postinfection. Sequence analyses revealed a population of DI RNAs that contained in-frame deletions of 1.3-2.8 kb covering the region of the E gene and some flanking C or prM and NS1 gene sequences. Transcripts from one cDNA clone of a DI RNA replicated in uninfected mosquito cells as demonstrated by RT-PCR. DI RNA-containing virions in supernatant fluids from persistently infected mosquito cells could be used to establish persistent infection in BHK-21 cells. The correlation of DI RNA presence with cell survival suggests that DI RNAs are contributing mechanistically to the establishment of persistent infection in both the mosquito and mammalian cells.

Animals↗
PubMed2003

Circadian variation of arrhythmia onset patterns in patients with persistent atrial fibrillation.

BACKGROUND: The circadian onset patterns and cycle lengths of atrial tachyarrhythmias (AT) were determined in a group of patients with persistent atrial fibrillation. METHODS: Fifteen patients, mean age 63 +/- 14 years and 80% male, were implanted with the Jewel AF atrial defibrillator (Medtronic, Minneapolis, Minn) for persistent atrial fibrillation only. Onset times of AT and median onset atrial cycle lengths were determined from device memory. RESULTS: Over a follow-up period of 23.3 +/- 7 months, 227 episodes of persistent AT were treated by patient-activated atrial defibrillation. The peak onset of persistent AT was nocturnal, with 74% of episodes initiating between 8 pm and 8 am. Eighty-seven percent of the patients experienced an additional 403 paroxysmal AT episodes. These episodes showed a "double-peaked" pattern with the least number of episodes occurring between midnight and 8 am. The mean onset atrial cycle length of persistent AT was significantly shorter than the paroxysmal AT episodes (200 +/- 37 ms vs 240 +/- 39 ms, P <.005). The atrial cycle lengths at arrhythmia onset of both paroxysmal and persistent AT episodes also demonstrated circadian variation. CONCLUSION: There is a circadian distribution of onsets for persistent AT with predominance at night. Patients with persistent AF have >1 type of atrial arrhythmia with differences in the onset patterns and atrial cycle lengths, suggesting different triggers and onset mechanisms.

Adult↗
PubMed1997

Postoperative day 1 serum human chorionic gonadotropin level as a predictor of persistent ectopic pregnancy after conservative surgical management.

OBJECTIVE: To determine characteristics predictive of persistent ectopic pregnancy (EP). DESIGN: Retrospective cohort study. SETTING: Tertiary care, university hospital. PATIENT(S): All women treated surgically for an EP whose postoperative hCG levels were followed until complete resolution or determination of a persistent EP over a 54-month period. MAIN OUTCOME MEASURE(S): Final outcome defined as successful treatment or persistent EP. RESULT(S): Twenty-six (17.7%) of 147 patients were diagnosed with a persistent EP. An inverse relationship was noted between the percent decrease in hCG at postoperative day 1 and the incidence of persistent EP. A significantly greater percentage of persistent EPs were noted when the postoperative day 1 hCG fell < 50% from the initial preoperative hCG level (relative risk = 3.51 [1.25 to 6.68]). No case of persistent EP was noted if the postoperative day 1 hCG declined by > or = 77%. Surgical time differed significantly (129 minutes versus 101 minutes) between cases treated successfully as compared with cases in which conservative treatment failed. No other preoperative or intraoperative variables were found to be significantly different. CONCLUSION(S): Although no single postoperative hCG value is predictive of conservative surgical treatment for EP, a day-1 postoperative hCG value may be used as a predictor of persistent EP.

Chorionic Gonadotropin↗