The meaning of living with traumatic brain injury in people with moderate or severe traumatic brain injury.

A traumatic brain injury (TBI) extensively affects the injured person's daily life. Research based on the perspectives of people with TBI can increase understanding of the challenges they face and the possibility of supporting them in managing their lives. The aim of this study was to elucidate the meaning of living with TBI as narrated by the people with moderate or severe TBI. The data were collected by means of qualitative research interviews with 12 participants who had lived with TBI for 4-13 years. A phenomenological hermeneutic method was used to interpret the transcribed interviews. The study showed that people with TBI had lost their way and struggled to achieve a new normalcy. Losing one's way included experiences of waking up to unknown, missing relationships and experiencing the body as an enemy. Participants' struggles to attain a new normalcy included searching for an explanation, recovering the self, wishing to be met with respect, and finding a new way of living. Living with TBI seems to mean living with a perpetually altered body that changed the whole life and caused deep suffering, where feelings of shame and dignity competed with each other. Participants seem to be quite alone in their suffering and need more support from healthcare professionals.     

A 2-year follow-up on the clinical and microbiological conditions of periodontium in teenagers

87 teenagers were included in a 2-year follow-up study on clinical and microbiological conditions of the periodontium. The clinical status was determined according to the Community Periodontal Index of Treatment Needs (CPITN) for subjects under 20 years of age. 59% of the subjects had at least 3 healthy sextants at the baseline and 68% at the 2-year examination. The microbiological conditions were assessed by using direct dark-field microscopy, and the culture of Actinobacillus actinomycetemcomitants (A.a.). Subgingival bacterial samples were taken, 2 for the microscopy and 2 for the culture, from the mesial surfaces of the first molars of each subject. The presence of gingival bleeding after probing was separately recorded from the 2 sites sampled for dark-field microscopy. No gingival bleeding at these 2 sites was found at the 2-year examination in 55% of those subjects who were non-bleeding at baseline, in 46% of the subjects initially with 1 bleeding site and in 13% of the subjects with both sites bleeding at baseline. 55% of the subjects with neither fusiforms, motile rods nor spirochetes at baseline maintained their healthy flora for 2 years. A.a. was recovered in 4 subjects at baseline and in 5 subjects 2 years later, in 3 of them at both examinations. Longer follow-up periods are needed to reveal the significance of the constant recovery of A.a. from the same subjects.     

Efficacy of Testosterone Suppression with Sustained-Release Triptorelin in Advanced Prostate Cancer

Introduction

Androgen deprivation therapy (ADT) is a mainstay of treatment against advanced prostate cancer (PC). As a treatment goal, suppression of plasma testosterone levels to <50 ng/dl has been established over decades. Evidence is growing though that suppression to even lower levels may add further clinical benefit. Therefore, we undertook a pooled retrospective analysis on the efficacy of 1-, 3-, and 6-month sustained-release (SR) formulations of the gonadotropin-releasing hormone (GnRH) agonist triptorelin to suppress serum testosterone concentrations beyond current standards.

Methods

Data of 920 male patients with PC enrolled in 9 prospective studies using testosterone serum concentrations as primary endpoint were pooled. Patients aged 42–96 years had to be eligible for ADT and to be either naïve to hormonal treatment or have undergone appropriate washout prior to enrolment. Patients were treated with triptorelin SR formulations for 2–12 months. Primary endpoints of this analysis were serum testosterone concentrations under treatment and success rates overall and per formulation, based on a testosterone target threshold of 20 ng/dl.

Results

After 1, 3, 6, 9, and 12 months of treatment, 79%, 92%, 93%, 90%, and 91% of patients reached testosterone levels <20 ng/dl, respectively. For the 1-, 3-, and 6-month formulations success rates ranged from 80–92%, from 83–93%, and from 65–97% with median (interquartile range) serum testosterone values of 2.9 (2.9–6.5), 5.0 (2.9–8.7), and 8.7 (5.8–14.1) ng/dl at study end, respectively.

Conclusion

In the large majority of patients, triptorelin SR formulations suppressed serum testosterone concentrations to even <20 ng/dl. Testosterone should be routinely monitored in PC patients on ADT although further studies on the clinical benefit of very low testosterone levels and the target concentrations are still warranted.

     

Combined effect of fluoride and 2,3,7,8-tetrachlorodibenzo-<Emphasis Type="Italic">p</Emphasis>-dioxin on mouse dental hard tissue formation in vitro

Fluoride interferes with enamel matrix secretion and mineralization and dentin mineralization. The most toxic dioxin congener, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), also impairs dental hard tissue formation and mineralization in vitro and in vivo. Our aim was to investigate in vitro whether the combined effect of sodium fluoride (NaF) and TCDD on dental hard tissue formation is potentiative. For this purpose, mandibular first and second molar tooth germs of E18 mouse embryos were cultured for 5–12 days with NaF and TCDD alone at various concentrations (2.5, 5, 10, 12.5, 15, and 20 μM and 5, 10, 12.5, and 15 nM, respectively) to determine the highest concentrations, which alone cause no or negligible effects. Morphological changes were studied from the whole tooth photographs and histological tissue sections. The concentrations found were 15 μM for NaF and 10 nM for TCDD. While at these concentrations, the effects of NaF and TCDD alone were barely detectable, the effect of simultaneous exposure on dentin and enamel formation was overt; mineralization of predentin to dentin and enamel matrix secretion and mineralization were impaired. Immunohistochemical analysis revealed that the combined exposure modified amelogenin expression by odontoblasts. Morphology of ameloblasts and the expression of amelogenin indicated that ameloblasts were still secretory. The results show that NaF and TCDD have potentiative, harmful effects on the formation of dental hard tissues. Since children can be exposed to subclinical levels of fluoride and dioxins during early childhood, coincidently with mineralization of the first permanent teeth, this finding may have clinical significance.     

Cognitive/behavioral teratogenetic effects of antiepileptic drugs

The majority of children of mothers with epilepsy are normal, but they are at increased risk for developmental delay. Antiepileptic drugs (AEDs) appear to play a role. Our current knowledge is reviewed, including research design issues and recommendations for future research. In animals, exposure of the immature brain to some AEDs can produce widespread neuronal apoptosis and behavioral deficits. The risks of AEDs in humans are less clear, but recent studies raise concerns, especially for valproate. There is a critical need for well-designed systematic research to improve our understanding of AED effects on the fetal brain.     

Pain- and morphine-associated transcriptional regulation of neuropeptide FF and the G-protein-coupled NPFF2 receptor gene

Neuropeptide FF (NPFF) is involved in pain modulation, especially plasticity during inflammatory and neuropathic pain, and opiate interactions. Its nociceptive functions may be mediated by the NPFF2 receptor. To elucidate the role of the NPFF system in plasticity associated with pathologic pain, we studied the changes of NPFF mRNA and NPFF2 receptor mRNA in rat models of acute colonic inflammation, inflammatory pain, and neuropathic pain. Furthermore, we studied the mRNA levels of both NPFF and NPFF2 receptor in morphine-tolerant rats and after acute morphine injections. We found an activation of spinal NPFF and NPFF2 receptor during early inflammatory pain. Supraspinally, we found an up-regulation of NPFF2 receptor mRNA during acute colonic inflammation and neuropathic pain. Acute, but not chronic, morphine activated the genes supraspinally. The results give further evidence for the involvement of the NPFF system in pain modulation and may provide new therapeutic opportunities for pathologic pain.