Intracardiac embolization of inferior vena cava filter associated with right atrium perforation and cardiac tamponade

Insertion of inferior vena cava filters has been well established in literature, reducing occurrence of pulmonary embolism after an episode of deep venous thrombosis in patients with contraindication to anticoagulation. There are a small number of complications related to procedure and embolization is rare. In this context, we described a case of intracardiac embolization associated with cardiac tamponade.     

Safety of Kidney Transplantation Using Anti-HBc–Positive Donors

BackgroundProspective studies evaluating the risk of hepatitis B virus (HBV) transmission in transplants of kidneys from hepatitis B core antibody (anti-HBc)–positive/hepatitis B surface antibody (anti-HBs)–negative donors are still lacking. The objective of this study was to assess the safety of kidney transplantation with the use of anti-HBc–positive donors.MethodsThis prospective case series study included 50 kidney transplant recipients from anti-HBc–positive donors with or without anti-HBs positivity. Recipients were required to test positive for anti-HBs (titers >10 mUI/mL), regardless of anti-HBc status, and negative for hepatitis B surface antigen (HBsAg). Recipient and donor data were retrieved from medical records, databases, and organ procurement organization sheets. Liver function tests were performed at progressively increasing post-transplantation intervals. Complete serologic tests for HBV were performed before transplantation, 3 and 6 months after transplantation, and annually thereafter.ResultsSix months after transplantation, all recipients were negative for HBsAg, HBeAg, anti-HBe, and anti-HBcIgM. No seroconversion was observed among the 20 patients who received kidneys from anti-HBc–positive/anti-HBs–negative donors. No patient showed elevated liver enzymes during follow-up.ConclusionsKidney transplantation using organs from anti-HBcIgG–positive donors (even when they are concurrently anti-HBs negative) in anti-HBs–positive recipients is a safe procedure and may be considered as a way to expand the donor pool.     

Modulating effect of low level-laser therapy on fibrosis in the repair process of the tibialis anterior muscle in rats

The treatment of muscle injuries is a common practice at rehabilitation centers. Low-level laser therapy (LLLT) has demonstrated positive effects regarding the modulation of the inflammatory response, the enhancement of the tissue repair process and the prevention of fibrosis. The aim of the present study was to evaluate the effects of LLLT on morphological aspects of muscle tissue, collagen remodeling and activity of matrix metalloproteinase 2 (MMP-2) in rat skeletal muscle following acute injury. Wistar rats were divided into five groups: (1) control group (n?=?10), (2) sham group (n?=?10), (3) LLLT group (n?=?30), (4) non-treated injury group (n?=?30) and (5) injury?+?LLLT group (n?=?30). Cryoinjury was performed on the belly of the tibialis anterior (TA) muscle. LLLT was performed daily with an AlGaAs laser (780 nm; beam spot of 0.04 cm², output power of 40 mW, power density of 1 W/cm², energy density of 10 J/cm² and 10-s exposure time). Animals were euthanized at 1, 3 and 7 days. The TA muscles were removed and weighed. Morphological aspects were evaluated using H & E staining. The amount and distribution of collagen fibers were evaluated by picrosirius staining. Characterization and activity of MMP-2 were evaluated by zymography and Western blot techniques, respectively. The results revealed that LLLT induced a reduction in inflammatory infiltrate and myonecrosis after 1 day, an increase in the number of blood vessels after 3 and 7 days as well as an increase in the number of immature muscle fibers and MMP-2 gelatinase activity after 7 days. In conclusion, LLLT has a positive effect on the inflammatory process, MMP2 activity and collagen organization and distribution in the repair process of rat skeletal muscle.     

Effects of LED phototherapy on relative wound contraction and reepithelialization during tissue repair in hypothyroid rats: morphometric and histological study

The aim of this study was to assess morphometrically and histologically, the effects of light-emitting diode (LED) (λ630?±?20 nm) phototherapy on reepithelialization and wound contraction during tissue repair in hypothyroid rats. Thyroid hormone deficiency has been associated with disorders of tissue repair. LED phototherapy has been studied using several healing models, but their usefulness in the improvement of hypothyroidism wound healing remains unknown. Under general anesthesia, a standard surgical wound (1 cm²) was produced on the dorsum of 48 male Wistar rats divided into four groups of 12 animals each: EC—control euthyroid, ED—euthyroid + LED, HC—control hypothyroid, and HD—Hypothyroid + LED. The irradiation started immediately after surgery and was repeated every other day for 7 and 14 days. Photographs of the wound were taken at the day of the surgical procedure and on days 8 and 15 after surgery, when animals’ deaths occurred. The specimens were removed, routinely processed, and stained with hematoxylin/eosin. Seven days after the surgery, it was possible to observe statistically significant reductions in the wound area of the irradiated euthyroid group, in comparison to hypothyroid group, irradiated and non-irradiated (ANOVA, p?<?0.05). The reepithelialization was significantly higher in the euthyroid and hypothyroid groups irradiated with LED than in the non-irradiated groups (Fisher’s test, p?<?0.05). No significant difference was found in the experimental period of 14 days among the groups. The hypothyroidism delayed wound healing and the LED phototherapy, at these specific parameters, improved the process of reepithelialization in the presence of hypothyroidism.     

Misperceptions of Facial Emotions Among Youth Aged 9–14 Years Who Present Multiple Antecedents of Schizophrenia

Similar to adults with schizophrenia, youth at high risk for developing schizophrenia present difficulties in recognizing emotions in faces. These difficulties might index vulnerability for schizophrenia and play a role in the development of the illness. Facial emotion recognition (FER) impairments have been implicated in declining social functioning during the prodromal phase of illness and are thus a potential target for early intervention efforts. This study examined 9- to 14-year-old children: 34 children who presented a triad of well-replicated antecedents of schizophrenia (ASz), including motor and/or speech delays, clinically relevant internalizing and/or externalizing problems, and psychotic-like experiences (PLEs), and 34 typically developing (TD) children who presented none of these antecedents. An established FER task (ER40) was used to assess correct recognition of happy, sad, angry, fearful, and neutral expressions, and facial emotion misperception responses were made for each emotion type. Relative to TD children, ASz children presented an overall impairment in FER. Further, ASz children misattributed neutral expressions to face displaying other emotions and also more often mislabeled a neutral expression as sad compared with healthy peers. The inability to accurately discriminate subtle differences in facial emotion and the misinterpretation of neutral expressions as sad may contribute to the initiation and/or persistence of PLEs. Interventions that are effective in teaching adults to recognize emotions in faces could potentially benefit children presenting with antecedents of schizophrenia.Key words: emotion recognition, high risk, child and adolescent psychopathology, social functioning, psychotic-like experiencesPeople with schizophrenia display a marked impairment in recognizing emotions in the faces of others, particularly anger, sadness, and fear, and less difficulty recognizing happy expressions.^1,2 Facial emotion recognition (FER) difficulties are associated with poor social functioning³ and have implications for the development, course, and outcome of the disorder.⁴ Yet, interventions to improve FER performance (eg, Training of Affect Recognition)⁵ can reduce these deficits and elicit generalized improvement in other social cognitive domains.⁶FER impairments are apparent not only among individuals with chronic schizophrenia (for review see Kohler et al 2010)² but also among individuals experiencing a first episode of psychosis^7,8 and among unaffected adolescent (though only for neutral facial expressions)⁹ and adult first-degree relatives of individuals with schizophrenia.¹⁰ Thus, abnormalities in FER are present at illness onset and may also index vulnerabil ity for schizophrenia. Prospective studies following individuals at elevated risk for developing schizophrenia are needed to determine the extent to which impairments of FER precede illness and represent potential targets for early intervention. Among symptomatic, help-seeking individuals meeting ultra-high risk (UHR) criteria for psychosis,^7,8,11–13 evidence for FER impairments is mixed. Two studies reported FER impairments relative to healthy participants,^7,11 while another study indicated specific difficulties in correctly identifying neutral expressions.¹³ A study of a large British birth cohort comprising 5267 children reported no association between FER at 8 years and subclinical psychotic symptoms at 12 years.¹⁴ By contrast, a recent cross-sectional study of 748 children aged 10–13 years indicated that those reporting psychotic-like experiences (PLEs) on questionnaires were poorer at recognizing facial emotional expressions, primarily sadness.¹⁵ Unfortunately, as with many previous FER studies, no information was provided about the nature of the facial emotion misperceptions committed when processing facial expressions. Though PLEs in childhood are significantly associated with later psychotic illness,^16,17 they are also associated with an increased risk of anxiety disorders¹⁶ and other psychiatric disorders including affective disorders, drug use disorders, and personality disorders,¹⁸ albeit to a lesser extent. Thus, PLEs constitute a relatively nonspecific marker of risk for subsequent psychiatric disorders. Further, cross-sectional data from the general population indicate significant comorbidity of PLEs with emotional and behavioral problems,^19,20 implying that the observed relationship between PLEs and FER reported by Roddy et al¹⁵ might reflect the presence of unreported internalizing and/or externalizing psychopathology.To better characterize the nature of FER associated with schizophrenia, several studies have examined facial emotion misperceptions. Relative to healthy adults, individuals with schizophrenia more often mislabel negative emotions to faces displaying no or neutral expressions.^21,22 Adolescent relatives of individuals with schizophrenia, compared with adolescents from healthy families, also more often incorrectly label neutral expressions as displaying negative emotions, predominantly mislabeling them as sad.⁹ Among individuals with schizophrenia, and individuals at high risk for psychosis,²³ functional imaging has revealed hyperactivation of the amygdala during the processing of neutral expressions, which could reflect emotional salience being assigned to neutral stimuli.²⁴ It has been suggested that the tendency to misinterpret neutral facial expressions as displaying emotion may contribute to the development of positive symptoms in schizophrenia.²³ Previous research indicates that facial emotion misperceptions might constitute the cognitive mechanism contributing to the social impairment that characterizes UHR samples¹³ and is a critical component to understanding FER difficulties in samples at risk for schizophrenia.Until recently, there has been no practical method for identifying children who are at elevated risk for schizophrenia. Despite the high heritability of schizophrenia, only approximately one-third of individuals with schizophrenia have a first- or second-degree relative with the illness. Consequently, a positive family history identifies only a subset of children who will develop the illness.²⁵ Prospective investigations of birth cohorts have demonstrated consistently that, by middle childhood, individuals who later developed schizophrenia presented delays in motor and language development; disturbances in social, emotional, and behavioral functioning; and PLEs.¹⁷ Based on this evidence, we developed questionnaires, to be completed by children aged 9–12 years and their primary caregiver, to identify children who present a triad of these replicated antecedents of schizophrenia (ASz).^26,27 We defined ASz to include (1) early speech and/or motor developmental delays/abnormalities; (2) social, emotional, and/or behavioral problems in the clinical range; and (3) PLEs. It is thought that the identification of children who present multiple antecedents of schizophrenia that have been replicated in prospective longitudinal studies will offer greater sensitivity and specificity for later development of schizophrenia than any one antecedent.We are currently following the development of ASz children to determine the specificity and sensitivity of the triad of antecedents for later schizophrenia development. We anticipate that some ASz children will develop schizophrenia and spectrum disorders, some will develop other disorders, and others will remain healthy. In the interim, our investigations have shown that ASz children, compared with typically developing (TD) children who present no antecedents and no family history of schizophrenia or a spectrum disorder, are characterized by features observed among adults with schizophrenia including (1) deficits in performance on standardized intelligence and neuropsychological tests of executive function and memory,²⁸ (2) dyskinetic movement abnormalities,²⁹ (3) reduction in the amplitude of the error-related negativity event-related potential component generated in the anterior cingulate that indexes internal monitoring of behavior,³⁰ and (4) structural brain abnormalities in the superior/middle temporal gyri.³¹ Further, among children aged 9–12 years, two-thirds (69%) of those presenting with the triad of antecedents report distress and/or functional impairment associated with their PLEs.²⁷This study sought to determine whether ASz children present FER difficulties similar to those reported among individuals with schizophrenia and at-risk youth, after accounting for intelligence quotient (IQ) differences between ASz and TD groups,²⁸ which may contribute to FER performance. The study examined overall performance on FER tasks, as well as the specific nature of facial emotion misperceptions. We hypothesized that ASz children would be less accurate than TD children in identifying emotions in facial expressions and that they would more often mislabel neutral faces with other emotion expressions. In particular, we anticipated that ASz children would misidentify neutral expressions as sad, as was reported in a study of youth with family histories of schizophrenia using the same FER task.⁹     

Comparison of the Heritability of Schizophrenia and Endophenotypes in the COGS-1 Family Study

Background:

Twin and multiplex family studies have established significant heritability for schizophrenia (SZ), often summarized as 81%. The Consortium on the Genetics of Schizophrenia (COGS-1) family study was designed to deconstruct the genetic architecture of SZ using neurocognitive and neurophysiological endophenotypes, for which heritability estimates ranged from 18% to 50% (mean = 30%). This study assessed the heritability of SZ in these families to determine whether there is a “heritability gap” between the diagnosis and related endophenotypes.

Methods:

Nuclear families (N = 296) with a SZ proband, an unaffected sibling, and both parents (n = 1366 subjects; mean family size = 4.6) underwent comprehensive endophenotype and clinical characterization. The Family Interview for Genetic Studies was administered to all participants and used to obtain convergent psychiatric symptom information for additional first-degree relatives of interviewed subjects (N = 3304 subjects; mean family size = 11.2). Heritability estimates of psychotic disorders were computed for both nuclear and extended families.

Results:

The heritability of SZ was 31% and 44% for nuclear and extended families. The inclusion of bipolar disorder increased the heritability to 37% for the nuclear families. When major depression was added, heritability estimates dropped to 34% and 20% for nuclear and extended families, respectively.

Conclusions:

Endophenotypes and psychotic disorders exhibit comparable levels of heritability in the COGS-1 family sample. The ascertainment of families with discordant sibpairs to increase endophenotypic contrast may underestimate diagnostic heritability relative to other studies. However, population-based studies also report significantly lower heritability estimates for SZ. Collectively, these findings support the importance of endophenotype-based strategies and the dimensional view of psychosis.Key words: schizophrenia, psychosis, endophenotypes, cognition, biomarkers, heritability     

Tumor necrosis factor‐α inhibitors alleviation of experimentally induced neuropathic pain is associated with modulation of TNF receptor expression

Inflammation plays a key role in the development of sensitization after peripheral nerve damage. We recently demonstrated that tumor necrosis factor‐α receptor (TNFR) levels in the spinal cord correlate with pain sensation in herniated disc patients in a rat chronic constriction injury (CCI) model. By using the sciatic nerve CCI model, we studied the effect of anti‐TNF‐α treatment on recovery from hypersensitivity and TNFR expression in the dorsal root ganglion (DRG) and dorsal horn (DH). Experimental groups consisted of sham‐operated and CCI‐operated rats that received two s.c. injections (one immediately after surgery, the other 5 days later), both containing saline, etanercept (3 mg/kg body weight), or infliximab (10 mg/kg body weight). Mechanical allodynia (with von Frey filaments) and thermal hyperalgesia (Hargreaves test) were assessed preoperatively and weekly during the first 4 postoperative weeks. DRG and DH samples were collected 2 and 4 weeks after surgery and analyzed for TNFR1 and TNFR2 protein levels by Western blotting and analyzed for mRNA levels by quantitative real‐time polymerase chain reaction. Anti‐TNF‐α treatment resulted in a significant alleviation of pain. TNFR levels were increased five‐ to sixfold in CCI rats compared with sham controls. Both treatments significantly diminished these increased levels. Treated animals that showed a ≥50% alleviation of pain exhibited a significantly reduced TNF R1/R2 mRNA ratio compared with treated animals that recovered less well. These results demonstrate that attenuation of TNFR expression is associated with recovery from nerve injury and suggest that this may be one of the working mechanisms of anti‐TNF therapies. © 2014 Wiley Periodicals, Inc.