Health Status and Lifestyle Habits of US Medical Students: A Longitudinal Study.

BACKGROUND: Evidence shows that physicians and medical students who engage in healthy lifestyle habits are more likely to counsel patients about such behaviors. Yet medical school is a challenging time that may bring about undesired changes to health and lifestyle habits. AIMS: This study assessed changes in students' health and lifestyle behaviors during medical school. SUBJECTS AND METHODS: In a longitudinal study, students were assessed at both the beginning and end of medical school. Anthropometric, metabolic, and lifestyle variables were measured at a clinical research center. Data were collected from 2006 to 2011, and analyzed in 2013-2014 with SAS version 9.3. Pearson's correlations were used to assess associations between variables and a generalized linear model was used to measure change over time. RESULTS: Seventy-eight percent (97/125) of participants completed both visits. At baseline, mean anthropometric and clinical measures were at or near healthy values and did not change over time, with the exception of increased diastolic blood pressure (P = 0.01), high-density lipoprotein-cholesterol (P < 0.001), and insulin (P < 0.001). Self-reported diet and physical activity habits were congruent with national goals, except for Vitamin D and sodium. Dietary intake did not change over time, with the exceptions of decreased carbohydrate (percent of total energy) (P < 0.001) and sodium (P = 0.04) and increased fat (percent of total energy) and Vitamin D (both P < 0.01). Cardiovascular fitness showed a trend toward declining, while self-reported physical activity increased (P < 0.001). CONCLUSIONS: Students' clinical measures and lifestyle behaviors remain generally healthy throughout medical school; yet some students exhibit cardiometabolic risk and diet and activity habits not aligned with national recommendations. Curricula that include personal health and lifestyle assessment may motivate students to adopt healthier practices and serve as role models for patients.

Ar+ and Xe+ velocities near the presheath-sheath boundary in an Ar/Xe discharge.

The velocities of Ar+ and Xe+ ions near the presheath-sheath boundary in an Ar/Xe discharge are studied by particle-in-cell Monte Carlo simulation. For a pure argon discharge the argon ion has almost the same velocity profile as it does in the mixture of argon and xenon. Similarly, for a xenon discharge the xenon ion has almost the same velocity profile as it does in the mixture of argon and xenon. The ion speed at the sheath-presheath boundary is the same for an ion in a pure argon or xenon discharge and for the same ion in a mixture of argon and xenon. We conclude that, in our simulation, each ion reaches its own Bohm speed at the presheath-sheath interface.

Enhancement of ohmic and stochastic heating by resonance effects in capacitive radio frequency discharges: a theoretical approach.

In low-pressure capacitive radio frequency discharges, two mechanisms of electron heating are dominant: (i) Ohmic heating due to collisions of electrons with neutrals of the background gas and (ii) stochastic heating due to momentum transfer from the oscillating boundary sheath. In this work we show by means of a nonlinear global model that the self-excitation of the plasma series resonance which arises in asymmetric capacitive discharges due to nonlinear interaction of plasma bulk and sheath significantly affects both Ohmic heating and stochastic heating. We observe that the series resonance effect increases the dissipation by factors of 2-5. We conclude that the nonlinear plasma dynamics should be taken into account in order to describe quantitatively correct electron heating in asymmetric capacitive radio frequency discharges.

Upstream ionization instability associated with a current-free double layer.

A low frequency instability has been observed using various electrostatic probes in a low-pressure expanding helicon plasma. The instability is associated with the presence of a current-free double layer (DL). The frequency of the instability increases linearly with the potential drop of the DL, and simultaneous measurements show their coexistence. A theory for an upstream ionization instability has been developed, which shows that electrons accelerated through the DL increase the ionization upstream and are responsible for the observed instability. The theory is in good agreement with the experimental results.

Theory for formation of a low-pressure, current-free double layer.

A diffusion-controlled theory is developed for the formation of a low-pressure, current-free double layer just inside an upstream insulating source chamber connected to a larger diameter, downstream chamber. The double layer is described using four groups of charged particles: thermal ions, monoenergetic accelerated ions flowing downstream, accelerated electrons flowing upstream, and thermal electrons. The condition of particle balance upstream is found to determine the double layer potential. The double layer disappears at very low pressures due to loss of ionization balance upstream and due to energy relaxation processes for ionizing electrons at higher pressures, in good agreement with experiments.

Inductive heating and E to H transitions in capacitive discharges.

Capacitive discharges have classically been modeled in the electrostatic approximation. However, electromagnetic effects become significant if the excitation wavelength lambda and the plasma skin depth delta are not infinite. An electromagnetic model valid in the entire range of lambda and delta of practical interest is solved. We find that the plasma may either be sustained by the usual capacitive (E) field or by an inductive (H) field, and that the discharge experiences E to H transitions as the voltage between the electrodes is raised.

The effects of nursing home placement on family caregivers of patients with Alzheimer's disease.

PURPOSE: This study sought to determine the effects of nursing home placement (NHP) for patients with Alzheimer's disease, compared to maintaining community placement, on changes in family caregiver health and well-being over time. DESIGN AND METHODS: We utilized a 2-year, longitudinal study with one baseline and four follow-up assessments for patients' spouses, adult offspring, and in-laws (married to offspring). Families were recruited from eight clinical outpatient centers, supported by the State of California, and followed in the community over time. A multidisciplinary clinical evaluation was undertaken by the centers, and follow-up assessments included questionnaire and interview data. RESULTS: Family caregiver health and well-being did not improve over time following NHP, and there were no significant differences in health and well-being between family caregivers who placed their ill elder in a nursing home and those who kept the elder at home or in the community. However, female family caregivers and spouses displayed greater declines in health and well-being over time, compared to other family caregivers, regardless of whether or not NHP occurred. IMPLICATIONS: Families considering NHP need to be advised of what may and may not change following NHP. In particular, spouses and female family caregivers may not experience those changes in life satisfaction and well-being that are hoped for. Variation in the effects of NHP may be more related to pre-NHP family processes and relationships than to the severity of the patient's disability, caregiver strain, patient and caregiver demographics, and use of community-based professional services.

Tumor necrosis factor alpha regulates CXC chemokine receptor expression and function.

The alpha chemokine family is central to the participation of neutrophils in the acute inflammatory response. These substances interact with neutrophils through two cell surface receptors, CXCR-1 and CXCR-2 (formally known as IL-8R-1 and IL-8R-2). We investigated the possible regulatory effects of tumor necrosis factor alpha (TNFalpha) pretreatment on CXCR-1 and CXCR-2. To this end, we examined these receptors with flow cytometry, radioligand binding, Northern blot analyzes, calcium mobilization, and chemotaxis experiments on human neutrophils. In flow cytometry experiments, TNFalpha pretreatment substantially decreased cell surface CXCR-2 receptor levels but showed partial recovery at 120 min. On the other hand, CXCR-1 receptor levels had a sharp decline at 15 min and maintained that level to 120 min. Northern blot analyzes showed that mRNA levels of both IL-8 receptors were essentially unchanged after 45 min of TNFalpha pretreatment, but declined markedly following 2 h of pretreatment. Chemotaxis experiments on cells treated with TNFalpha for 5-120 min showed a substantial down-regulation of chemotaxis to IL-8 and GROalpha. This was noted to be much greater than the decline in cell surface receptors. Calcium mobilization experiments revealed minimal inhibition of the IL-8-induced increase in calcium after pretreatment with TNFalpha, but the response to NAP-2 was substantially inhibited. The data demonstrate differential regulation of the IL-8 receptor.

The effects of family conflict resolution and decision making on the provision of help for an elder with Alzheimer's disease.

This study explored how characteristics of multigeneration families of patients with Alzheimer's disease (AD) affected the family's ability to provide help to their ill elder. An intensive patient and family assessment battery was employed with 211 families with an elder with AD, and measures of the amount and kind of help offered by the family group were recorded. Above and beyond control variables, families that used a focused decision-making style and positive conflict resolution methods provided more help than families that did not use these styles and methods. These data suggest the importance of the family system of care in disease management.

A longitudinal study of predictors of nursing home placement for patients with dementia: the contribution of family characteristics.

The caregivers of elderly patients with dementia (N = 164) were followed for 2 years to determine if characteristics of the multigeneration family predicted nursing home placement (NHP) over and above the effects of patient demographics, severity of patient disease, and characteristics of caregivers. Clinical assessment occurred at baseline, and caregivers were assessed by questionnaire and interview at baseline and every 6 months. No patient demographic, severity, or caregiver characteristic significantly predicted NHP. Families scoring high on emotional closeness, high on negative family feelings, and low on family efficiency institutionalized their ill elders at a significantly higher rate than other families, especially at low levels of patient severity. The findings argue that a careful examination of the multigeneration family should increase the prediction of NHP and the relevance of services offered to these families.

Uncoupling of S-phase and mitosis by recombinant cytotoxic necrotizing factor 2 (CNF2).

Cytotoxic necrotizing factor 2 (CNF2) is an exotoxin identified from virulent clinical isolates of Escherichia coli. It has been characterized in adherent cell lines as an inducer of cellular death, hyperploidy (multinucleation), and cytoskeletal reorganization. The molecular mechanism of these actions is unclear. Two cellular mechanisms can be hypothesized to explain the DNA content increase (hyperploidy) induced by the toxin. The first is that the toxin interferes with cytoplasmic division without interfering with normal nuclear cycling, such that DNA is replicated in the absence of cell division. The second is that the toxin drives the nuclear machinery to replicate the DNA multiple times within one cell cycle, without interfering with cytoplasmic division. In order to investigate these phenomena, we have constructed a recombinant CNF2 gene that expresses a toxin with both an epitope tag and a polyhistidine tag. Extracts made from E. coli that express this gene have a high multinucleating activity that colocalizes with the recombinant 115-kDa protein. To distinguish between these hypotheses, we used recombinant CNF2 and several growth conditions (time, partial differentiation, and stage of growth) to establish a relationship between cellular divisions and generation of hyperploidy. It was also determined that the toxin had no effect upon in vitro DNA replication using a Xenopus egg extract system. In aggregate, these data are consistent with the hypothesis that CNF2 is affecting cytoplasmic division and thereby removing the requirement for a completed mitosis before the initiation of another S-phase. These data are discussed in relation to the generation of polyploid cells during megakaryopoeisis and the generation of aneuploid cells during tumorigenesis.

Megakaryocytic cell line-specific hyperploidy by cytotoxic necrotizing factor bacterial toxins.

Cytotoxic necrotizing factor (CNF) toxins, isolated from certain Escherichia coli strains known to cause intestinal and extra intestinal infections, induce reorganization of the actin cytoskeleton and generate hyperploidy in adherent cell lines. We have examined the effect of CNF toxin on one of the few cell types that naturally increase nuclear DNA content, megakaryocytes. Our studies show that only hematopoietic cells capable of differentiating along the megakaryocyte lineage responded to the CNF2 toxin by becoming polyploid and by reorganizing actin. The K562, HEL, and CHRF-288-11 cell lines can be induced with phorbol ester to differentiate along the megakaryocyte lineage, and these cells also respond to the toxin with increased DNA content and actin cytoskeletal rearrangements. Interestingly, treatment of the K562 and HEL cell lines with CNF2 does not result in an increase in production of the megakaryocytic marker glycoprotein IIIa, unlike phorbol ester treatment. Conversely, two T-cell leukemic cell lines, CEM and Molt4, and the promyelocytic HL-60 cell line, which do not differentiate along the megakaryocyte lineage in response to phorbol myristate acetate, do not respond to CNF2, by increased expression of gpIIIa, increased nuclear DNA content, or actin reorganization. A potential target of these toxins, RhoA, is expressed by both megakaryocytic and nonmegakaryocytic cell lines, as shown by reverse transcription-polymerase chain reaction and Western blot. Although it is clear that the CNF toxins can affect a wide variety of adherent nonhematopoietic cell lines, we propose that the response to CNF, in terms of reorganizing actin structure and increase in DNA content in hematologic suspension cells, correlates with the capability of these target cells to differentiate along the megakaryocytic lineage.

Cloning and characterization of rat density-enhanced phosphatase-1, a protein tyrosine phosphatase expressed by vascular cells.

We have cloned from cultured vascular smooth muscle cells a protein tyrosine phosphatase, rat density-enhanced phosphatase-1 (rDEP-1), which is a probable rat homologue of DEP-1/HPTP eta. rDEP-1 is encoded by an 8.7-kb transcript and is expressed as a 180- to 220-kD protein. The rDEP-1 gene is located on human chromosome 11 (region p11.2) and on mouse chromosome 2 (region 2E). The cDNA sequence predicts a transmembrane protein consisting of a single phosphatase catalytic domain in the intracellular region, a single transmembrane domain, and eight fibronectin type III repeats in the extracellular region (GenBank accession number U40790). In situ hybridization analysis demonstrates that rDEP-1 is widely expressed in vivo but that expression is highest in cells that form epithelioid monolayers. In cultured cells with epitheliod morphology, including endothelial cells and newborn smooth muscle cells, but not in fibroblast-like cells, rDEP-1 transcript levels are dramatically upregulated as population density increases. In vivo, quiescent endothelial cells in normal arteries express relatively high levels of rDEP-1. During repair of vascular injury, expression of rDEP-1 is downregulated in migrating and proliferating endothelial cells. In vivo, rDEP-1 transcript levels are present in very high levels in megakaryocytes, and circulating plates have high levels of the rDEP-1 protein. In vitro, initiation of differentiation of the human megakaryoblastic cell line CHRF-288-11 with phorbol 12-myristate 13-acetate leads to a very strong upregulation of rDEP-1 transcripts. The deduced structure and the regulation of expression of rDEP-1 suggest that it may play a role in adhesion and/or signaling events involving cell-cell and cell-matrix contact.

Identification of altered gene expression in skeletal muscle during sepsis using differential display.

Different aspects of muscle metabolism are altered during sepsis and there is evidence that some of these changes may be regulated at the gene level. Differential display is a recently described technique to identify genes whose expression has changed during a biological process. This technique utilizes reverse transcriptase-polymerase chain reaction (RT-PCR) to compare mRNA signals in tissues during two different conditions. We used differential display to test the hypothesis that gene expression is altered in skeletal muscle during sepsis. Sepsis was induced in rats by cecal ligation and puncture (CLP). Control rats were sham-operated. Sixteen hours after CLP or sham operation, extensor digitorum longus muscles were harvested and RNA was extracted. Following differential display, 30 fragments (F1-F30) were identified that appeared to be uniquely expressed in muscles from sham-operated or septic rats. These fragments were reamplified by PCR and used as probes in Northern blot analysis. Messenger RNA levels corresponding to 2 of the 30 fragments (F5 and F24) were confirmed to be increased by Northern blot analysis in septic muscle. Following cloning and sequencing, F5 was found to display significant homology to the gene sequence of the guanine nucleotide releasing protein MSS4. The sequence of F24 did not match any reported gene sequence and may therefore represent a previously unidentified gene. The results support the hypothesis that gene expression is altered in skeletal muscle during sepsis.

Cytokine production by a megakaryocytic cell line.

The regulation of megakaryopoeisis by cytokines is not yet well understood. It is possible that autocrine loops are established during megakaryocyte growth and differentiation, aiding in the maturation of these cells. The CHRF-288-11 human megakaryoblastic cell line has been examined for cytokine production in growing cells and cells stimulated to differentiate by the addition of phorbol esters. It has been demonstrated that these cells produce RNA corresponding to the interleukins IL-1 alpha, 1 beta, 3, 7, 8, and 11, granulocyte-macrophage colony stimulating factor (GM-CSF), stem cell factor (SCF), transforming growth factor-beta (TGF-beta), tumor necrosis factor-alpha (TNF-alpha), interferon-alpha (INF-alpha), and basic fibroblast growth factor (bFGF). Additionally, RNA corresponding to the receptors for IL-6, GM-CSF, SCF, INF-alpha, beta, bFGF, and monocyte colony stimulating factor (M-CSF) were also expressed by the cells. The receptor for TNF-alpha was detected immunologically. Analysis at the protein level demonstrated that significant amounts of INF-alpha, TNF-alpha, GM-CSF, SCF, IL-1 alpha, and a soluble form of the IL-6 receptor were produced by the cells. Addition of phorbol esters to CHRF-288-11 cells enhances their megakaryocytic phenotype; such treatment also results in increased secretion of INF-alpha, TNF-alpha, and GM-CSF. These results suggest that potential autocrine loops are established during the differentiation of CHRF-288-11 cells, which may alter the capability of the cell to differentiate. These findings are similar to those recently obtained for marrow-derived megakaryocytes (Jiang et al.) suggesting that CHRF-288-11 cells provide a useful model system for the study of cytokine release during megakaryocyte differentiation.

Orthodontic tooth movement following guided tissue regeneration: report of three cases.

This report presents three patients with advanced adult periodontitis and in which orthodontic tooth movement was performed subsequent to guided tissue regeneration procedures. Clinical follow-up showed a mean 3.3-mm attachment gain in the deepest preoperative probing depth sites, and radiographs revealed bone fill following guided tissue regeneration procedures with resorbable and nonresorbable membranes, with and without the use of demineralized freeze-dried bone allograft. Orthodontic tooth movement into the regenerated areas was successful. The feasibility of orthodontic tooth movement following successful regenerative procedures is discussed.

Sepsis stimulates polyamine biosynthesis in the liver and increases tissue levels of ornithine decarboxylase mRNA.

The influence of sepsis on polyamine metabolism in the liver was studied in rats. Sepsis was induced by cecal ligation and puncture; control rats were sham-operated. Sepsis resulted in increased concentrations in liver tissue of putrescine and spermidine and stimulated activity of the enzymes ornithine decarboxylase (ODC) and s-adenosylmethionine decarboxylase. A similar metabolic response was seen following the subcutaneous injection of 1 mg/kg of endotoxin or following the e intraperitoneal injection of 100 micrograms/kg of human recombinant tumor necrosis factor (TNF)-alpha or interleukin-1 alpha (IL-1 alpha). ODC mRNA levels determined by Northern blots were increased in liver tissue of septic rats, suggesting that the increase in ODC activity may be regulated at the transcriptional level although increased stability of the messenger could give rise to similar results. Treatment of rats with either TNF antiserum, recombinant IL-1 receptor antagonist, or the glucocorticoid receptor antagonist RU 38486, did not prevent the sepsis-induced increase in hepatic ODC activity. The data suggest that sepsis stimulates the biosynthesis of polyamines in liver tissue and that this response to sepsis may not primarily be mediated by TNF, IL-1, or glucocorticoids. The biological role of increased liver polyamines during sepsis, in particular their relationship with the synthesis of acute phase proteins, remains to be determined.

Time scale to ergodicity in the Fermi-Pasta-Ulam system.

We study the approach to near-equipartition in the N-dimensional Fermi-Pasta-Ulam Hamiltonian with quartic (hard spring) nonlinearity. We investigate numerically the time evolution of orbits with initial energy in some few low-frequency linear modes. Our results indicate a transition where, above a critical energy which is independent of N, one can reach equipartition if one waits for a time proportional to N(2). Below this critical energy the time to equipartition is exponentially long. We develop a theory to determine the time evolution and the excitation of the nonlinear modes based on a resonant normal form treatment of the resonances among the oscillators. Our theory predicts the critical energy for equipartition, the time scale to equipartition, and the form of the nonlinear modes below equipartition, in qualitative agreement with the numerical results. (c) 1995 American Institute of Physics.

The impact of chronic illness on the health and well-being of family members.

Examined is the impact of dementia on the physical and mental health of all family members caring for an ill parent/spouse. The sample included 97 spouses of patients diagnosed with either Alzheimer's disease or vascular dementia, 186 offspring, and 97 offspring spouses or "in-laws." Multiple regression tested the association between severity of the illness and family member health and well-being. Severity was significantly associated with health and well-being for spouses, offspring, and in-laws, regardless of the amount of caregiving, demonstrating the potential cascading effect of the illness through the family. Use of services displayed no direct association with spouse health and well-being, but service utilization interacted with illness severity. The relationship between severity of illness and spouse health was lower under conditions of high service utilization than under conditions of low service utilization.