A psychoeducation program for stress management and psychosocial problems in multiple sclerosis.

BACKGROUND: Multiple Sclerosis (MS) patients should cope effectively with problems of life and with problems originating from the disease. This is important because it affects the course of the disease, psychiatric morbidity, and quality of life. OBJECTIVE: This study was carried out as an intervention design with a control group to assess the effects of psychoeducation on MS patients' ways of coping with stress, psychiatric symptoms, and qualities of life. SUBJECTS AND METHODS: A total of 80 MS patients affiliated with the MS Association of Turkey were included and randomly assigned into intervention and control groups. An 8-week psychoeducation program was offered to the intervention group, whereas the control group was not given any treatment during the same period. Data were collected using a Descriptive Information Form, the Ways of Coping Inventory, the Brief Symptom Inventory, and the MS Quality of Life-54 scale. RESULTS: Based on the study, among the ways of coping with stress, problem-focused approach increased, whereas the emotional-focused approach decreased statistically significantly in the intervention group. Among the psychiatric symptoms, the levels of anxiety, depression, and somatization decreased. However, there was no significant change in the negative self-concept and hostility symptoms. The total quality-of-life scores increased significantly (P < 0.05). In the intervention group, these effects continued in the three-month-follow-up measurement. The control group showed no statistically significant change in the same parameters during the same periods. It is recommended that group psychoeducation programs should be carried out extensively in order for MS patients to cope with stress effectively and improve their mental health and quality of life.

A novel murine model for chronic inflammatory alveolar bone loss.

BACKGROUND AND OBJECTIVE: Chronic inflammatory bowel disease (IBD) demonstrates some similarities to the dysregulated chronic immunoinflammatory lesion of periodontitis. Trinitrobenzene sulphonic acid (TNBS) and dextran sodium sulphate (DSS) administered to rodents have been shown to elicit inflammatory responses that undermine the integrity of the gut epithelium in a similar manner to IBD in humans. The objective of this study was to evaluate the ability of these chemicals to elicit periodontal inflammation as a novel model for alveolar bone loss. MATERIAL AND METHODS: Mice were treated by oral application of TNBS twice a week, or with DSS in the diet over a period of 18 weeks. Alveolar bone loss was assessed on the defleshed skull using morphometric measures for area of bone resorption. RESULTS: The TNBS-treated animals tolerated oral administration with no clinical symptoms and gained weight at a similar rate to normal control animals. In contrast, DSS exerted a systemic response, including shortening of colonic tissue and liver enzyme changes. Both TNBS and DSS caused a localized action on periodontal tissues, with alveolar bone loss observed in both maxilla and mandibles, with progression in a time-dependent manner. Bone loss was detected as early as week 7, with more severe periodontitis increasing over the 18 weeks (p < 0.001). Young (7-month-old) and old (12-month-old) mice with severe combined immunodeficiency were treated with TNBS for a period of 7 weeks and did not develop significant bone loss. CONCLUSION: These data show that oral administration of TNBS or DSS provokes alveolar bone loss in concert with the autochthonous oral microbiota.

Herpes in the peripartum period: a case report.

BACKGROUND: Despite the tremendous advances made in the management of genital herpes, neonatal herpes has not been completely eradicated. In addition, the time from the onset of symptoms in the neonate to the diagnosis of herpes and institution of antiviral medication has remained unchanged in the past 20 years. CASE: Neonatal herpes infection resulted from primary, first-episode peripartum genital herpes in the mother. Due to a high index of suspicion, herpes testing was performed on the infant and neonatal herpes diagnosed. Subsequently, the mother developed evidence of primary herpes infection. CONCLUSION: This case report illustrates the problems with current management strategies for prevention of neonatal herpes.

Inflammatory 'double hit' model of temporomandibular joint disorder with elevated CCL2, CXCL9, CXCL10, RANTES and behavioural hypersensitivity in TNFR1/R2-/- mice.

BACKGROUND: Patients with temporomandibular joint disorders (TMD), reactive arthritis and rheumatoid arthritis often have combined etiology of hereditary and microenvironmental factors contributing to joint pain. Multiple clinical and animal studies indicate 'double-hit' inflammatory insults can cause chronic inflammation. The first inflammatory insult primes the immune system and subsequent insults elicit amplified responses. The present 'double hit' study produced a chronic orofacial pain model in mice with genetic deletion of both TNFα receptors (TNFR1/R2-/-), investigating the main nociceptive signalling pathways in comparisons to wild type mice. METHODS: An initial inflammatory insult was given unilaterally into the temporomandibular joint (TMJ). Secondary hypersensitivity was tested on the skin over the TMJ throughout the experiment. Three weeks later after complete reversal of hypersensitivity, a second inflammatory insult was imposed on the colon. Pharmacological interventions were tested for efficacy after week 10 when hypersensitivity was chronic in TNFR1/R2-/- mice. Serum cytokines were analysed at Days 1, 14, and Week 18. RESULTS: The double hit insult produced chronic hypersensitivity continuing through the 4-month experimental timeline in the absence of TNFα signalling. P2X7 and NMDA receptor antagonists temporarily attenuated chronic hypersensitivity. Serum cytokine/chemokine analysis on Day 14 when CFA induced hypersensitivity was resolved identified increased levels of pro-inflammatory cytokines CCL2, CXCL9, CXCL10, RANTES and decreased levels of anti-inflammatory cytokines IL-1ra and IL-4 in TNFR1/R2-/- compared to WT mice. CONCLUSIONS: These data suggest a causal feed-forward signalling cascade of these little studied cytokines have the potential to cause recrudescence in this orofacial inflammatory pain model in the absence of TNFα signalling. SIGNIFICANCE: Using a mouse model of chronic inflammatory temporomandibular joint disorder, we determined that absence of functional TNFR1/R2 induces aberrant inflammatory signalling caused by other increased pro-inflammatory and decreased anti-inflammatory cytokines that could serve as blood biomarkers and may predict disease progression.

Percutaneous dilatational tracheostomy.

BACKGROUND: The aim of this study was to investigate the rate, timing, the incidence of complications of percutaneous dilatational tracheostomy (PDT) and its effects by on nosocomial pneumonia. METHODS: The study is a retrospective analysis of 104 patients (56 males, 48 females) > or = 18 years (54 +/- 19) who had undergone a PDT for respiratory failure during the five years 1998-2003. RESULTS: Among 238 patients requiring mechanical ventilation > or = 48 hours, 104 (43.7%) required PDT. PDT was performed after 4.3 +/- 2.3 days of ventilation and the disconnection from mechanical ventilation was 13.6 +/- 8.5 days. Lower airway tract infection was detected in 88 patients: 55 patients (62.5%) before PDT and in 33 patients (37.5%) after PDT. The nosocomial pneumonia was observed after 5.9 +/- 1.67 days of ventilation. CONCLUSIONS: Our results suggest that PDT was performed relatively early, with an acceptable complication rate and that our post-PDT nosocomial pneumonia incidence is low.

CXCR1 Regulates Pulmonary Anti-Pseudomonas Host Defense.

Pseudomonas aeruginosa is a key opportunistic pathogen causing disease in cystic fibrosis (CF) and other lung diseases such as chronic obstructive pulmonary disease (COPD). However, the pulmonary host defense mechanisms regulating anti-P. aeruginosa immunity remain incompletely understood. Here we demonstrate, by studying an airway P. aeruginosa infection model, in vivo bioluminescence imaging, neutrophil effector responses and human airway samples, that the chemokine receptor CXCR1 regulates pulmonary host defense against P. aeruginosa. Mechanistically, CXCR1 regulates anti-Pseudomonas neutrophil responses through modulation of reactive oxygen species and interference with Toll-like receptor 5 expression. These studies define CXCR1 as a novel, noncanonical chemokine receptor that regulates pulmonary anti-Pseudomonas host defense with broad implications for CF, COPD and other infectious lung diseases.

An investigation of thermal comfort inside a bus during heating period within a climatic chamber.

By this study, it was aimed to define a testing and calculation model for thermal comfort assessment of a bus HVAC design and to compare effects of changing parameters on passenger's thermal comfort. For this purpose, a combined theoretical and experimental work during heating period inside a coach was carried out. The bus was left under 20 °C for more than 7 h within a climatic chamber and all heat sources were started at the beginning of a standard test. To investigate effects of fast transient conditions on passengers' physiology and thermal comfort, temperatures, air humidity and air velocities were measured. Human body was considered as one complete piece composed of core and skin compartments and the Transient Energy Balance Model developed by Gagge et al. in 1971 was used to calculate changes in thermal parameters between passenger bodies and bus interior environment. Depending on the given initial and environmental conditions, the graphs of passengers Thermal Sensation and Thermal Discomfort Level were found. At the end, a general mathematical model supported with a related experimental procedure was developed for the use of automotive HVAC engineers and scientists working on thermal comfort as a human dimension.

Effect of angiotensin II receptor blockers, candesartan, on osteoprotegerin level in hypertensive patients: Link between bone and RAAS.

INTRODUCTION: The renin-angiotensin-aldosterone system (RAAS) has recently been considered as a possible link between bone and vascular disease. The present study was designed to determine the effect of the angiotensin II receptor blocker candesartan on circulating osteoprotegerin (OPG) in hypertensive patients with multiple cardiovascular risk factors. MATERIAL AND METHODS: A total of 69 hypertensive patients were randomized to two groups: Group 1 included patients treated with oral candesartan in doses of 16 mg to 32 mg per day in addition to routine standard of care (routine care + ARB), and Group 2 included patients who received routine standard of care other than ARBs or ACEIs, with no change to their treatment (routine care). Patients were evaluated for lipid profile, HbA1C, insulin, C-peptide, CRP, aldosterone, renin, homeostasis model assessment-insulin resistance (HOMA-IR) and OPG. RESULTS: Baseline OPG levels did not differ significantly by treatment group. Post-treatment serum OPG levels were marginally lower in Group1 compared with Group 2; however, this decrease did not reach statistical significance (p = 0.077). CONCLUSIONS: In the present study, treatment with the ARB candesartan had no significant effect on circulating OPG levels in hypertensive patients with multiple cardiovascular risk factors. To the best of our knowledge, the present study is the first to estimate an effect of candesartan on bone remodeling marker such as OPG.

Dysregulated TNFα promotes cytokine proteome profile increases and bilateral orofacial hypersensitivity.

BACKGROUND: Tumor necrosis factor alpha (TNFα) is increased in patients with headache, neuropathic pain, periodontal and temporomandibular disease. This study and others have utilized TNF receptor 1/2 (TNFR1/2) knockout (KO) animals to investigate the effect of TNFα dysregulation in generation and maintenance of chronic neuropathic pain. The present study determined the impact of TNFα dysregulation in a trigeminal inflammatory compression (TIC) nerve injury model comparing wild-type (WT) and TNFR1/2 KO mice. METHODS: Chromic gut suture was inserted adjacent to the infraorbital nerve to induce the TIC model mechanical hypersensitivity. Cytokine proteome profiles demonstrated serology, and morphology explored microglial activation in trigeminal nucleus 10weeks post. RESULTS: TIC injury induced ipsilateral whisker pad mechanical allodynia persisting throughout the 10-week study in both TNFR1/2 KO and WT mice. Delayed mechanical allodynia developed on the contralateral whisker pad in TNFR1/2 KO mice but not in WT mice. Proteomic profiling 10weeks after chronic TIC injury revealed TNFα, interleukin-1alpha (IL-1α), interleukin-5 (IL-5), interleukin-23 (IL-23), macrophage inflammatory protein-1ß (MIP-1ß), and granulocyte-macrophage colony-stimulating factor (GM-CSF) were increased more than 2-fold in TNFR1/2 KO mice compared to WT mice with TIC. Bilateral microglial activation in spinal trigeminal nucleus was detected only in TNFR1/2 KO mice. p38 mitogen-activated protein kinase (MAPK) inhibitor and microglial inhibitor minocycline reduced hypersensitivity. CONCLUSIONS: The results suggest the dysregulated serum cytokine proteome profile and bilateral spinal trigeminal nucleus microglial activation are contributory to the bilateral mechanical hypersensitization in this chronic trigeminal neuropathic pain model in the mice with TNFα dysregulation. Data support involvement of both neurogenic and humoral influences in chronic neuropathic pain.

Increased hepatic lipid peroxidation in aged mice.

In recent years, the free radical theory of aging has attained great interest. Many studies on aging using tissue homogenates and subcellular fractions have provided evidence for the occurrence of lipid peroxidation. However, there are studies which report decrease or no significant change in parameters of lipid peroxidation. In our study, we investigated whether hepatic lipid peroxidation levels in male Swiss-Albino mice change with age. Three groups of animals, 3, 6 and 18 months old, were used. The diene conjugate and malondialdehyde levels of liver homogenates, mitochondria and microsomes were measured. Significant increases in both diene conjugate and malondialdehyde levels of liver homogenates and mitochondria have been observed in 18-month-old mice when compared with those aged 3 and 6 months. As for microsomes, only malondialdehyde levels were elevated in the old group when compared with young and adult groups. Both parameters were significantly increased in aged mice which indicate that lipid peroxidation is important in advancing age in mice.

Acute fulminating babesiosis in hamsters infected with Babesia microti.

In this study, Babesia microti (ATCC30222) from mice was adapted to golden hamsters. The parasite was passaged to immunosuppressed and then adapted to normal hamsters. When 30 normal hamsters were inoculated with this strain, parasitaemia increased to 74% of erythrocytes by day 7 and 70% of the hamsters died. By day 12, parasitaemia extended to 90%, with 97% mortality. Hearts and kidneys from infected animals were enlarged. Histopathology revealed acute myocarditis, hepatitis, pneumonitis, glomerulonephritis and splenomegaly. Giemsa, Acridine Orange and Rhodamine staining of the parasite were compared. Scanning electron microscopy of blood from infected hamsters revealed from 1 to 5 intra-erythrocytic parasites.

Evidence for guanosine triphosphate--binding proteins in Trypanosoma cruzi.

The transformation of the parasite Trypanosoma cruzi from the blood-borne trypomastigote to the intracellular amastigote constitutes a key clinical feature in the pathophysiology of Chagas' disease. That this transition occurs without change in the integrity of the plasma membrane of the parasite suggests the presence of biochemical structures, i.e., signal transduction systems, that convey information regarding the external milieu of the host so as to facilitate this transformation. In higher eukaryotes, it has been found that a heterotrimeric GTP-binding protein (G-protein), composed of alpha beta gamma subunits, constitutes a critical component of this complex. Two closely related groups of G-proteins are substrates for cholera toxin (CT)- (Gs) and pertussis toxin (PT)- (Gi1-3 and Go) dependent ADP ribosylation. In concert, they link plasma membrane receptors to adenylate cyclase, resulting in the stimulation or inhibition, respectively, of cAMP generation. In this report, we demonstrate the presence of both groups of G-proteins. Cholera toxin-dependent ADP ribosylation of 42- and 45-kD proteins was demonstrable in amastigotes (AMAST), in the cytosol of epimastigotes (EPI), and weakly in trypomastigotes (TRYP), suggesting the presence of the stimulatory GTP-binding protein, Gs, in T. cruzi. Antisera generated against the alpha s subunit of the Gs heterotrimeric protein (anti-alpha s) bound to a 45-kD protein CT substrate in the rank order TRYP >> AMAST approximately EPI cytosol. Immunoprecipitation of CT-32P-ADP-ribosylated membranes with anti-alpha s resulted in 42- and 45-kD proteins. However, no Gs-mediated activation of adenylate cyclase was demonstrable in reconstitution studies using cyc- lymphoma cells, which lack a functional Gs but possess a beta-adrenergic receptor and adenylyl cyclase enzyme. Pertussis toxin-catalyzed ADP ribosylation was demonstrable in 39-40-kD particulate proteins of EPI, less strongly in AMAST, and least in TRYP, consistent with the presence of inhibitory (Gi) and Go GTP-binding proteins. In support of this observation, immunochemical analysis of the PT substrates identified the presence of alpha o and alpha i1-2-3 in EPI, AMAST and TRYP, although, with the exception of alpha i3, both toxin and associated immunochemical PT substrates are decreased in AMAST and TRYP relative to EPI. Although the functions of these putative G-proteins in T. cruzi are still unclear, their expression may be regulated by the state of parasite differentiation.(ABSTRACT TRUNCATED AT 400 WORDS)

Search for Pneumocystis carinii DNA in upper and lower respiratory tract of humans.

Recent studies suggest that Pneumocystis carinii DNA may be detected by PCR in oropharyngeal secretions in the majority of patients with P. carinii pneumonitis (PCP). However, the prevalence of P. carinii DNA in patients without PCP has not been well established. A prospective study of 258 nasal, pharyngeal, and salivary specimens from 86 individuals with AIDS, cancer or no underlying disease, and without respiratory infection, found no P. carinii DNA in any of the samples. Separately, to validate the PCR for detection of P. carinii DNA, 45 specimens from the lower respiratory tract (bronchoalveolar lavage [BAL] and sputum) from 31 patients with pneumonitis and AIDS or cancer were studied. Eleven had PCP by conventional stains and 20 did not. All patients with PCP, and none without PCP, had P. carinii DNA in BAL, sputum or both. The study indicates the prevalence of P. carinii DNA is low or absent in oropharyngeal secretions in the absence of PCP.

The effect of chronic ethanol ingestion on hepatic lipid peroxide, glutathione, glutathione peroxidase and glutathione transferase in rats.

Water containing 20% ethanol was given for a period of 3, 6 and 9 weeks to rats, and changes in hepatic lipid peroxide, glutathione, glutathione peroxidase and glutathione transferases were investigated. Lipid peroxide levels and glutathione peroxidase activities remained unchanged after 3 weeks and started to increase thereafter. Glutathione levels and glutathione transferase activities were significantly increased following ethanol consumption. These results show that chronic ethanol consumption stimulates hepatic lipid peroxidation in rats. This stimulation is not dependent on glutathione depletion and the increased glutathione peroxidase and glutathione transferase activities may reflect an adaptive change against ethanol-induced lipid peroxide toxicity.

Thymosin alpha 1 protects liver and aorta from oxidative damage in atherosclerotic rabbits.

The thymus hormones were reported to be effective on lipid peroxidation and the antioxidant system. Thymus plays a broader role than just regulating the immune system. Thymosin alpha 1 is the first subgroup extracted from thymosin F5 and has higher biological activity than thymosin F5. In the present study, we have examined the effects of thymosin alpha 1 on lipid levels and lipid peroxidation and glutathione (GSH) content in the plasma, liver and aorta tissues of atherosclerotic rabbits. At the end of thymosin alpha 1 treatment, we determined the lipid levels and lipid peroxidation of the plasma, liver and aorta tissues and hepatic subcellular fractions in these rabbits. Our results demonstrated that thymosin alpha 1 might normalize changed lipid levels and increased lipid peroxides and also elevate decreased GSH in the plasma, liver and aorta tissues of atherosclerotic rabbits. Results of this study suggest that thymosin alpha 1 may be beneficial to prevent and/or to treat atherosclerosis.

Fructosamine as a possible monitoring parameter in non-insulin dependent diabetes mellitus patients with periodontal disease.

Fructosamine assay is a new test used in the diagnosis and monitoring of diabetic patients. This assay may be of interest to the periodontist for, while the traditional plasma glucose value would give a general view and information about diabetic control at a certain point, the fructosamine concentration gives an indication of the plasma glucose level over a considerable period of time, such as 1 to 3 weeks. We investigated whether there was any relation between the diseased state of the periodontal tissues and plasma fructosamine and the plasma glucose values in non-insulin dependent diabetes mellitus (NIDDM) patients. We found that fructosamine correlated with the degree of gingival bleeding, however serum glucose levels had little or no correlation.

The effect of heat-stable extract from bovine sublingual salivary glands on the carbohydrate metabolism of the rabbit.

This extract (SLF3) caused hyperglycaemia when injected intraperitoneally (i.p.) into rabbits (20 mg/kg body wt) which was maximal at 0.5 h and took 2 h to return to the initial value. SLF3 also produced a two-fold increase in corticosteroid levels compared to controls, so the increase in blood glucose was probably mediated by adrenal cortical hormone stimulation.

Experimental bovine coccidiosis: control with monensin.

Young Holstein-Friesian bull calves were used in a controlled experiment to evaluate the efficacy of monensin against coccidiosis. The calves were given oocysts of Eimeria bovis and/or E. zurnii. Medication was started 3 days prior to inoculation and continued during the 30-day experimental period. Oocyst shedding was quantified prior to and throughout the experiment and demonstrated that monensin at the rate of 20 or 30 g ton-1 of feed significantly reduced oocyst shedding and clinical coccidiosis. Clinical infection with E. zurnii was very difficult to establish, even when calves were treated with 20 mg dexamethasone IM on Days 12, 15, and 16 post-inoculation.

Pneumocystis carinii infection alters GTP-binding proteins in the lung.

The GTP-binding regulatory proteins (G proteins) in the membranes of the lung parenchyma from normal, uninfected ferrets were compared to those from immunosuppressed animals with and without Pneumocystis carinii pneumonitis. In lung membranes, pertussis toxin (PT) catalyzed ADP ribosylation of a 41-kDa protein; treatment with cholera toxin (CT) led to ribosylation of a 44-kDa polypeptide. Compared to that in the normal ferrets, the level of the 44-kDa protein was dramatically suppressed in the P. carinii-infected animals. Western blot analysis with specific antibodies to alpha s (which recognized CT substrates), alpha common (which reacted to PT substrates), the alpha q/11 epitope, and the beta subunit demonstrated that these proteins were decreased in animals with P. carinii pneumonitis (PCP). Western blotting of PCP-free membranes with a pan-Ras antibody revealed a 21-kDa polypeptide (corresponding to small G proteins). The level of the 21-kDa protein in membranes from PCP-affected animals was only 30% of that in membranes from PCP-free animals. Finally, analogous studies performed with rat lung membranes revealed similar findings. These data suggest that, independent of its exacerbation of immunosuppression, PCP leads to extensive changes in the GTP-binding proteins in the lung.

Search for extrapulmonary Pneumocystis carinii in an animal model.

Pneumocystis carinii-infected immunosuppressed ferrets and rats were searched for P. carinii cysts and trophozoites in extrapulmonary organs, including the heart, liver, stomach, kidney, and spleen. Foci of P. carinii were found in the liver or kidney of 4 (10%) of 40 ferrets but in no extrapulmonary sites of 30 rats with P. carinii pneumonitis. Attempts to identify P. carinii from immunosuppressed rat or ferret blood or propagate the organism intraorbitally in immunosuppressed rats were unsuccessful. Pneumocystis carinii was identified from aspirated stomach contents of ferrets but in none of the rats infected with P. carinii pneumonitis.