Burnout syndrome assessment among Spanish oral surgery consultants: A two populations comparative pilot study.

BACKGROUND: The professional Burnout Syndrome (BOS) or Burnout is considered a professional disease made up of three interrelated dimensions (emotional exhaustion, depersonalization and lack of personal fulfillment). BOS has been documented to most severely affect the healthcare professions, especially dentists. On the other hand, its appearance has been documented at an early age, during dental training. However, there are no studies that analyze its incidence in professionals dedicated to Oral Surgery and Implantology, determining the age of onset and related factors. MATERIAL AND METHODS: The modified Maslach questionnaire was carried out anonymously among the professors and students of the Master of Oral Surgery and Implantology at the Complutense University of Madrid. A total of 36 participants were enrolled in this study and the results of the modified Maslach Questionnaire were established into four groups [1st year (n=6), 2nd year (n=6), 3rd year (n=6) postgraduate students and clinical teachers (n=18)]. The following variables were recorded: Age, sex, years of experience, weekly hours of work, dedication on weekends and scope of work. The statistical analysis performed included Pearson's correlation, analysis of variance, Student's t-test, F-Anova, Chi-Square and Gamma correlation. Statistical Significance of the tests was established of p≤0.05. RESULTS: 36 questionnaires were analyzed, of which 22.2% (n = 8) presented BOS, and 77.8% (n = 28) a medium risk of suffering it. The mean values and standard deviation ​​of emotional exhaustion (7.50 ± 2.43; 9.83 ± 4.12; 15.83 ± 6.21; 30.22 ± 7.86), depersonalization (5.50 ± 1.23; 50 ± 3.27; 11.33 ± 1.75; 17.56 ± 4.13), low personal fulfillment (39.67 ± 3.72; 39.33 ± 2.34; 43.17 ± 3, 55; 37.33 ± 5.51) and professional burnout (54.33 ± 2.66; 61.67 ± 2.88; 70.33 ± 5.43; 85.11 ± 9.05) in the four groups respectively. A significant association was found in the appearance of emotional exhaustion and depersonalization, years of experience, weekly work hours and the work environment. CONCLUSIONS: BOS is a disease that can appear from 30 years of age, after 5 years of professional experience and when there is a clinical consultation of 40 hours a week. Oral Surgery and Implantology seems to be a risk activity for the manifestation of depersonalization.

Semen preservation and artificial insemination in domesticated South American camelids.

Semen preservation and artificial insemination in South American camelids are reviewed giving emphasis to work done in Peru and by the authors. Reports on semen evaluation and the preservation process indicate that semen of alpacas and llamas can be manipulated by making it liquid first. Collagenase appears to be the best enzyme to eliminate viscosity. Tris buffer solution maintains a higher motility than egg-yolk citrate, phosphate buffered saline (PBS), Triladyl, and Merck-I extenders. Cooling of semen took 1h after collected, and equilibrated with 7% glycerol presented a better motility and spermatozoa survival at 1, 7, 15 and 30days after being slowly frozen in 0.25mL plastic straws. Trials of artificial insemination with freshly diluted semen and frozen-thawed semen are encouraging and needs to be tested extensively under field conditions. Recently, fertility rates varied from 3 to 67%. Semen preservation and most important, artificial insemination appear to be a reality, and could be used to improve the genetic quality of alpacas and llamas.

Volatility of radiopharmacy-prepared sodium iodide-131 capsules.

OBJECTIVE: The aims of this study were to quantify the extent of volatilization from 131I-NaI therapeutic capsules prepared in a centralized radiopharmacy and to quantify the amount of volatile 131I released from a dispensing vial containing a compounded 131I-NaI therapy capsule. METHODS: Therapy capsules were prepared by injecting 131I oral solution into capsules containing anhydrous dibasic sodium phosphate. Volatilized activity was obtained by filtering air drawn across samples that were placed open on the bottom of a sample holder cup. Volatile 131I was captured by filtering it through 3 triethylenediamine-impregnated carbon cartridge filters, arranged in series. To quantify the amount of volatile 131I released from a dispensing vial during a simulated patient administration, a vial containing a compounded 131I therapy capsule was opened inside a collapsible plastic bag and all the air was drawn across TEDA-impregnated carbon cartridge filters. RESULTS: The 370-MBq (10-mCi) 131I capsules from the first part of the experiment released an average of 0.035% (SD 0.031%) of the capsule activity on the first day, 0.012% (SD 0.002%) on the second day, and 0.012% (SD < 0.001%) for days 3 through 5. The 37-MBq (1-mCi) 131I capsules released an average of 0.058% (SD 0.025%) on the first day, 0.029% (SD 0.009%) on the second day, and 0.020% (SD 0.004%) on the third day. The activity released from the vial during a simulated patient administration was 0.00093% of the 131I capsule activity. CONCLUSION: The amount of 131I, which volatilized daily from the exposed therapy capsules, was a small percentage of the capsule activity. The volatile 131I that would be released during a patient administration was much less than the activity that volatilized from the exposed therapy capsules.

Closed-chamber capsulorhexis for cataract extraction combined with penetrating keratoplasty.

We describe a modified closed-chamber capsulorhexis technique that facilitates cataract extraction and intraocular lens insertion combined with penetrating keratoplasty. This technique eliminates most of the risks associated with can-opener capsulotomies, offers the benefits of capsulorhexis, and enhances the safety of the triple procedure.

Cage size and flight speed of the tobacco hawkmoth Manduca sexta

Flight speeds and behaviors of the sphinx moth Manduca sexta were recorded in chambers of four different sizes (0.57, 8.5, 44 and 447 m3). Mean horizontal speed increased linearly with the cube root of chamber volume from 0.57 m s-1 in the smallest chamber to 3.4 m s-1 in the largest. The maximum horizontal speed observed was 5.3 m s-1 in the largest chamber. Speeds decreased linearly with the logarithm of hawkmoth proximity to the wall. In a tunnel chamber (the third largest), moths often flew in a scalloped-shaped path. At the top of the scallop, they glided for 1­5 wing beats. In the largest chamber, moths could be recorded flying at angles other than horizontal (0 °). At flight angles greater or less than 0 °, mean speed decreased linearly with angle until ±40 °. At greater angles, speeds remained between 1 and 2 m s-1. Moths also flew closer to the wall at flight angles deviating from the horizontal. An allometric analysis of the flight speeds of insects and birds suggests that M. sexta may be able to fly at 7­10 m s-1. We conclude that chamber size limits the flight speed and modifies the flight behavior of the tobacco hawkmoth.

Regulation of interferon-alpha-inducible cellular genes in human immunodeficiency virus-infected monocytes.

Cellular mechanisms that control susceptibility to opportunistic infection in human immunodeficiency virus (HIV)-infected individuals remain poorly understood. HIV may induce certain cellular genes that restrict HIV replication and protect cells against other superinfecting viral pathogens. Indeed, HIV-infected monocytes resist infection by vesicular stomatitis virus (VSV). HIV-induced VSV interference in monocytes increases with time after HIV infection. Such interference was evident 6 h after HIV infection and reached maximal levels at 14 days. Monocytotropic but not T cell-tropic HIV strains elicited these effects, signaling a requirement for viral entry and/or replication. Viral interference was independent of interferon (IFN) and was unaffected by addition of neutralizing IFN-alpha and -beta antibodies. The well-described IFN-alpha-inducible antiviral pathways were examined to determine their relationship to the cellular mechanism(s) underlying VSV interference. HIV and IFN-alpha both induced the expression of 2-5A synthetase and Mx gene. In contrast, the guanylate-binding protein (GBP), 6-16, and 9-27 cellular genes were up-regulated by IFN-alpha but not HIV. MxA was detected in HIV-infected monocytes but not in uninfected monocytes. The association between Mx expression and resistance to VSV, coupled with previously described anti-VSV activities by human MxA, suggested that Mx may be an effector molecule for the HIV-induced anti-VSV activities. These results, taken together, suggest that HIV can induce antiviral cellular gene expression, independent of IFN.

Linking empirically based theory and evaluation: the Family Bereavement Program.

Evaluated the effects of a theoretically derived program to prevent mental health problems in children who had experienced the death of a parent. The program was designed to improve variables in the family environment which were specified as mediators of the effects of parental death on child mental health. The evaluation design involved the random assignment of families to either an intervention or control group. The program led to parental ratings of increased warmth in their relationships with their children, increased satisfaction with their social support, and the maintenance of family discussion of grief-related issues. The program also led to parent ratings of decreased conduct disorder and depression problems and overall problems in older children. Significant correlations between the family environment variables and child mental health problems provided further empirical support for the theory underlying the program. Implications for program redesign were derived by reconsidering the adequacy of the program components to change theoretically mediating variables.

Induction of IFN-alpha in peripheral blood mononuclear cells by HIV-infected monocytes. Restricted antiviral activity of the HIV-induced IFN.

PBMC cocultured with HIV-infected monocytes for 12 to 48 h released high levels of IFN activity. IFN titers were directly dependent upon time after virus infection and level of HIV replication in infected cells. IFN induction in PBMC was evident with HIV-infected monocytes and PBMC and with myeloid and lymphoblastoid cell lines with at least three different HIV strains. In HIV-infected cell line pairs in which virus infection occurs in both productive and restricted forms, IFN induction in PBMC occurred only with productive infection. IFN activity was acid stable and completely neutralized by antibodies against IFN-alpha. Induction of IFN required cell-cell contact between HIV-infected cells and PBMC, but was independent of MHC compatibility. With PBMC co-cultured with autologous HIV-infected monocytes, IFN induction was highly selective: IL-1 beta, IL-6, or TNF-alpha activity and mRNA were not detected. Cell surface determinants on HIV-infected monocytes that induced IFN in PBMC remained active after fixation in 4% paraformaldehyde. Both adherent and nonadherent PBMC produced IFN after coculture with HIV-infected monocytes. Ability to produce IFN by PBMC was not affected by depletion of T cell, NK cell, B cell, or monocyte subpopulations. The IFN activity produced by PBMC cocultured with HIV-infected cells was about 20-fold less active than equal quantities of rIFN-alpha 2b for inhibition of HIV replication in monocytes and at low concentrations enhanced virus growth. Clinical studies with HIV-infected patients and parallel findings in animal lentivirus disease suggest an adverse role for IFN in disease progression. Conditions for induction of IFN in the culture system described in this report may mimic those in the HIV-infected patient. Defining the molecular basis for IFN induction, the cells that produce IFN, and the altered biologic activity of this important cytokine may provide insight into the pathogenesis of HIV disease.

The use of structural equation modeling in generative research: toward the design of a preventive intervention for bereaved children.

Describes a generative study of processes which may lead to symptomatology in children who have experienced the death of a parent. Based on existing literature, four putative mediating variables were identified: parental demoralization, family warmth, negative family events, and positive stable family events. Structural equation modeling techniques were used to compare several potential causal models involving these variables. The results were most consistent with a model in which bereavement was not directly related to the child symptomatology, but rather its effects were transmitted through these four mediational mechanisms. The implications of the results of the structural modeling for the design and evaluation of preventive interventions are discussed briefly.

The inability of human immunodeficiency virus to infect chimpanzee monocytes can be overcome by serial viral passage in vivo.

Studies of lentivirus infection in ruminants, nonhuman primates, and humans suggest that virus infection of macrophages plays a central role in the disease process. To investigate whether human immunodeficiency virus type 1 (HIV-1) can infect chimpanzee macrophages, we recovered monocytes from peripheral blood mononuclear cells of HIV-1-negative animals and inoculated these and control human monocytes with a panel of four human-passaged monocytotropic virus strains and one chimpanzee-passaged isolate. HIV-1 infected human monocytes synthesized proviral DNA, viral mRNA, p24 antigen, and progeny virions. In contrast, except for the chimpanzee-passaged HIV-1 isolate, chimpanzee monocytes failed to support HIV-1 replication when cultured under both identical and a variety of other conditions. Proviral DNA was demonstrated only at background levels in these cell cultures by polymerase chain reaction for gag- and env-related sequences. Interestingly, the chimpanzee-passaged HIV-1 isolate did not replicate in human monocytes; viral p24 antigens and progeny virions were not detected. The same monocytotropic panel of HIV-1 strains replicated in both human and chimpanzee CD4+ T lymphoblasts treated with phytohemagglutinin and interleukin-2. The failure of HIV-1 to infect chimpanzee monocytes, which can be overcome by serial in vivo viral passage, occurs through a block early in the viral life cycle.

Regulation of cytokine and viral gene expression in monocytes infected with the human immunodeficiency virus.

Monocytes treated with interferon-alpha (IFN-alpha) at virus challenge show no evidence of human immunodeficiency virus (HIV) infection: no p24 antigen or reverse transcriptase (RT) activity, no viral mRNA and no proviral DNA. Levels of p24 antigen and RT activity in monocytes infected with HIV 1-3 weeks before IFN-alpha treatment gradually decrease to baseline. HIV-induced cytopathic changes are markedly reduced, as are levels of HIV mRNA: the frequency of productively infected cells is less than or equal to 1%. But, levels of proviral DNA in the IFN-alpha-treated and control HIV-infected cells are indistinguishable, and remain so through 3 weeks. Large quantities of proviral DNA in IFN-alpha-treated cells with little active transcription suggest true microbiological latency. The major potential source for IFN-alpha in HIV-infected patients is the macrophage. With any of 15 virus isolates, tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, IFN-omega or IFN-beta are not detected nor the mRNA expressed in HIV-infected or uninfected monocytes. Both uninfected and HIV-infected monocytes produce high levels of these cytokines after treatment with synthetic double-stranded RNA (poly-I:C). Uninfected monocytes also produce high levels of IFN-alpha after treatment with Poly-I:C, Newcastle disease virus or herpes simplex virus. In marked contrast, HIV-infected monocytes express no IFN-alpha activity or mRNA before or after treatment with any of these agents. The markedly diminished capacity of HIV-infected monocyte to produce IFN-alpha reflects a specific transcriptional block and may be an adaptive mechanism of virus to alter basic microbicidal functions of this cell.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhanced HIV replication in macrophage colony-stimulating factor-treated monocytes.

Monocytes cultured 7 to 10 days in recombinant human macrophage CSF (MCSF) were greater than 400-fold more susceptible to HIV infection than an equal number of cells cultured in medium alone. Levels of reverse transcriptase activity and p24 Ag in culture fluids of monocytes treated with MCSF 1 wk before and continuously after HIV infection were significantly greater than those of control cells cultured without MCSF. HIV-induced cytopathic effects in the MCSF-treated cultures also increased in both frequency and extent. At any given viral inoculum, the frequency of HIV-infected cells, the level of HIV mRNA/infected cell, and the level of proviral DNA/infected culture in MCSF-treated monocyte cultures were dramatically greater than those in control cultures. These differences were directly related to MCSF concentration to a maximum between 750 and 1000 U/ml MCSF, and were evident at all time points examined through 5 wk. None of the preceding effects was observed when MCSF was added at the time of or 1 wk after HIV infection. These data suggest that the predominant effect of MCSF for control of HIV infection is on the monocyte itself, not the virus. If these in vitro observations extend to the HIV-infected patient, then the variable levels of MCSF in tissue or blood may determine both the susceptibility of macrophages to virus infection and the extent of virus replication in infected cells.

Neuroleptic malignant syndrome: a unique association with a tricyclic antidepressant.

We report the lst case of neuroleptic malignant syndrome occurring in a patient receiving desipramine, a tricyclic antidepressant, with no exposure to neuroleptics. Our case suggests that this syndrome may be caused by a central imbalance between norepinephrine and dopamine, and not by dopamine depletion alone.

A selective defect of interferon alpha production in human immunodeficiency virus-infected monocytes.

Interferon alpha (IFN-alpha) induces significant antiretroviral activities that affect the ability of human immunodeficiency virus (HIV) to infect and replicate in its principal target cells, CD4+ T cells and macrophages. A major endogenous source of IFN-alpha during any infection is the macrophage. Thus, macrophages have the potential to produce both IFN-alpha and HIV. In this study, we examined the production of IFN-alpha and other cytokines by macrophage colony-stimulating factor (M-CSF)-treated cultured monocytes during HIV infection. Tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), IL-6, IFN-omega, or IFN-beta were not detected nor was the mRNA expressed in either uninfected or HIV-infected monocytes. However, both uninfected and HIV-infected monocytes produced high levels of each of these cytokines after treatment with synthetic double-stranded RNA [poly(I).poly(C)]. Uninfected monocytes also produced high levels of IFN-alpha after treatment with poly(I).poly(C), Newcastle disease virus, or herpes simplex virus. In marked contrast to the preceding observations, HIV-infected monocytes produced little or no IFN-alpha before or after treatment with any of these agents. The absence of detectable IFN-alpha activity and mRNA in poly(I).poly(C)-treated HIV-infected monocytes was coincident with high levels of 2',5' oligoadenylate synthetase and complete ablation of HIV gene expression. The antiviral activity induced by poly(I).poly(C) may be a direct effect of this synthetic double-stranded RNA or secondary to the low levels of IFN-beta and IFN-omega produced by infected cells. The markedly diminished capacity of HIV-infected monocytes to produce IFN-alpha may reflect a specific adaptive mechanism of virus to alter basic microbicidal functions of this cell. The inevitable result of this HIV-induced cytokine dysregulation is virus replication and persistence in mononuclear phagocytes.

Regulation of HIV replication in infected monocytes by IFN-alpha. Mechanisms for viral restriction.

In a survey of 15 different virus isolates, no IFN-alpha or IFN-beta activity was detected in culture fluids of HIV-infected T cells or monocytes. Exogenous rIFN-alpha added to T lymphoblast or monocyte cultures induced restriction in replication of the amphotropic HIV that infect both cell types. With IFN-treated HIV-infected T cells, levels of reverse transcriptase (RT) activity in culture fluids were half those in control cultures, but the frequency of infected cells or the levels of p24 Ag released in culture fluids were unchanged. In contrast to the modest effect of IFN on HIV-infected T cells, IFN-induced antiviral activity in monocytes was quite dramatic. Monocytes treated with IFN at the time of virus challenge showed no evidence of HIV infection: no p24 Ag or RT activity, no viral mRNA, and no proviral DNA. In this system, IFN interrupts one or more early event(s) in the virus replication cycle before formation of proviral DNA. Monocyte cultures infected with HIV 7 days before IFN treatment showed a gradual decrease in levels of p24 Ag and RT activity to baseline by 3 wk. HIV-induced cytopathic changes were markedly reduced, and the frequency of productively infected cells was less than or equal to 1% of total cells. Virus particles released 24 h after IFN treatment were 100- to 1000-fold less infectious than equal numbers of control virions. But, monocytes treated with IFN 7 days after HIV infection were not free of the retroviral pathogen: levels of proviral DNA in the IFN-treated and control HIV-infected cells were indistinguishable. The presence of large quantities of proviral DNA in cells with little or no evidence for active transcription documents a situation approaching true microbiological latency.

Restriction of HIV replication in infected T cells and monocytes by interferon-alpha.

Human recombinant interferon-alpha (IFN alpha) restricted viral replication in human immunodeficiency virus- (HIV) infected T cells and monocytes. With T cells, reverse transcriptase (RT) activity in culture fluids was reduced threefold from that of control infected cells by IFN treatment, but HIV p24 antigen levels were unchanged. In contrast, levels of p24 antigen and RT activity in lysates of IFN-treated infected cells were threefold greater than those of controls. These differences suggest that the mechanism for IFN-induced antiviral effects in HIV-infected T cells resides in the terminal events (assembly and release) of the virus replication cycle. Monocytes treated with IFN at the time of virus challenge showed no p24 antigen or RT activity, no HIV-specific mRNA, and no proviral DNA in cells for up to 3 weeks after infection. IFN treatment of chronically infected monocytes also decreased virus replication, as assessed by p24 antigen, mRNA and RT detection assays. However, levels of proviral DNA in the IFN-treated and control HIV-infected cells were indistinguishable. The presence of large quantities of proviral DNA in cells with little or no evidence for active transcription documents a situation approaching true microbiological latency.

Macrophage-HIV interaction: viral isolation and target cell tropism.

Viral isolates were recovered by cocultivation on macrophage colony-stimulatingfactor (MCSF)-treated monocyte target cells from peripheral blood mononuclear cells (PBMCs) in 25 out of 27 patients seropositive or at risk for HIV infection. Frequency of virus recovery was independent of the patient's age, sex, numbers of CD4+ T cells, clinical stage or zidovudine (azidothymidine) therapy. Sixteen out of 19 HIV isolates were serially passaged in MCSF- treated monocytes. Five out of five virus isolates were also passaged in phytohemagglutinin/interleukin-2 (PHA/IL-2)-treated lymphoblasts. In lymphoblasts, no qualitative or quantitative differences were observed between these isolates and human T-cell leukemia virus IIIB (HTLV-IIIB) for (1) release of p24 antigen reverse transcriptase, and infectious virus, (2) induction of typical cytopathic effects (cell syncytia in 3-10% of cells) and cell lysis, (3) frequency of infected cells (5-20% of PBMC) as detected by in situ hybridization for HIV RNA, (4) down-modulation of T cell plasma membrane CD4, and (5) site of progeny virion assembly and budding (plasma membrane only with no intracytoplasmic accumulation of virus). Progeny virus recovered from infected lymphoblasts was fully infectious for other lymphoblasts, but failed to infect MCSF-treated monocytes. Detailed analysis of target cell tropism among HIV isolates showed that HIV isolated in monocytes infected both monocytes and lymphoblasts; progeny virus isolated in lymphoblasts infected only T cells. HIV interacts differently with monocytes and T cells. Understanding this interaction may more clearly define both the pathogenesis of HIV disease and strategies for therapeutic intervention.