Timothy Grass Pollen Induces Spatial Reorganisation of F-Actin and Loss of Junctional Integrity in Respiratory Cells

Inflammation - Grass pollens have been identified as mediators of respiratory distress, capable of exacerbating respiratory diseases including epidemic thunderstorm asthma (ETSA). It is...     

Does pravastatin therapy affect cardiac enzyme levels after percutaneous coronary intervention?

Serum cardiac enzyme elevation after percutaneous coronary intervention (PCI), a relatively common complication, is a prognostic determinant of long-term outcome in patients who undergo these procedures. Statins are postulated to reduce such complications. This study investigated the short-term effects of pravastatin on serum creatine kinase myocardial isoform (CK-MB) and serum cardiac troponin I (cTpI) levels after elective PCI. Of 93 patients studied, 72 (77.4%) were men, and 21 (22.6%) were women (mean age, 58.9±11.0 y). Patients were randomly divided into 3 groups before they underwent elective PCI. Preoperatively, group 1 patients (n=30) received pravastatin 10 mg/d, and group 2 patients (n=29) received pravastatin 40 mg/d. Control group patients (n=34) received no lipid-lowering medication. Serum CK-MB and serum cTpI levels were measured preoperatively and then again at 6, 24, and 36 h postoperatively. Demographic features of patients and characteristics of the PCI procedure, including number of vessels/lesions and duration and number of inflations, did not differ among groups (P>.05). Mean serum CK-MB and serum cTpI levels were significantly increased after PCI in all patients (P<.001). When compared with control group patients, those given pravastatin did not experience significantly lowered postprocedural serum CK-MB or serum cTpI levels (P>.05). Preprocedural pravastatin therapy at dosages of 10 mg/d and 40 mg/d seems inadequate for preventing serum cardiac enzyme elevations during short-term follow-up after PCI. Additional research on this topic is recommended.     

Effects of hemodialysis on myocardial performance index

The myocardial performance index (MPI) reflects global ventricular function. Chronic hypervolemia and uremia may negatively affect the myocardium of both ventricles. The aims of this study were to investigate how chronic renal failure (CRF) affects biventricular MPI and to determine whether preload reduction by hemodialysis (HD) affects left ventricular MPI (LVMPI) and right ventricular MPI (RVMPI) in CRF. Twenty-one patients with CRF (group 1) were examined 1 hour before and 1 hour after an HD session and 1 7 healthy control patients (group 2) were examined once by echocardiography. The MPI for each ventricle was calculated as the sum of isovolumic time intervals divided by the ejection time. Before HD, the LVMPI of group 1 was similar to that in group 2 (P≫.05), but the RVMPI of group 1 was significantly higher (P=.007). After the HD session, LVMPI and RVMPI remained unchanged (P>.05 for both). The LVMPI and RVMPI were not correlated either before or after HD in group 1 (P>.05 for both), whereas they were correlated in group 2 (r= 0.671, P=.003). Chronic renal failure causes isolated RV dysfunction, as reflected by increased RVMPI values. Preload reduction by HD does not affect LVMPI or RVMPI. Patients with CRF also do not exhibit the correlation of LVMPI and RVMPI that is observed in healthy individuals.     

Diagnostic red flags: steroid‐treated malignant CNS lymphoma mimicking autoimmune inflammatory demyelination

The presence of inflammation and demyelination in a central nervous system (CNS) biopsy points towards a limited, yet heterogeneous group of pathologies, of which multiple sclerosis (MS) represents one of the principal considerations. Inflammatory demyelination has also been reported in patients with clinically suspected primary central nervous system lymphoma (PCNSL), especially when steroids had been administered prior to biopsy acquisition. The histopathological changes induced by corticosteroid treatment can range from mild reduction to complete disappearance of lymphoma cells. It has been proposed that in the absence of neoplastic B cells, these biopsies are indistinguishable from MS, yet despite the clinical relevance, no histological studies have specifically compared the two entities. In this work, we analyzed CNS biopsies from eight patients with inflammatory demyelination in whom PCNSL was later histologically confirmed, and compared them with nine well defined early active multiple sclerosis lesions. In the patients with steroid‐treated PCNSL (ST‐PCNSL) the interval between first and second biopsy ranged from 3 to 32 weeks; all of the patients had received corticosteroids before the first, but not the second biopsy. ST‐PCNSL patients were older than MS patients (mean age: ST‐PCNSL: 62 ± 4 years, MS: 30 ± 2 years), and histological analysis revealed numerous apoptoses, patchy and incomplete rather than confluent and complete demyelination and a fuzzy lesion edge. The loss of Luxol fast blue histochemistry was more profound than that of myelin proteins in immunohistochemistry, and T cell infiltration in ST‐PCNSL exceeded that in MS by around fivefold (P = 0.005). Our data indicate that in the presence of extensive inflammation and incomplete, inhomogeneous demyelination, the neuropathologist should refrain from primarily considering autoimmune inflammatory demyelination and, even in the absence of lymphoma cells, instigate close clinical follow‐up of the patient to detect recurrent lymphoma.     

The impact of detoxifying and repair gene polymorphisms on oxidative stress in ischemic stroke

Stroke is a multifactorial disease caused by the combination of certain risk factors and genetic factors. There are possible risk factors having important role in the pathogenesis of stroke. The most important environmental factors are cigarette smoking and oxidative stress which have different sources. GST (M1, T1, P1) have major roles in detoxification of the products of oxidative stress and they are polymorphic. DNA damages can also be repaired by repair enzymes such as OGG1 and XRCC1 which are highly polymorphic and have pivotal roles in repair systems. In the present study, we investigated that polymorphisms in genes involved in detoxification and DNA-repair pathways might modify the individual’s risk for ischemic stroke. Furthermore, the products of oxidative stress and antioxidant capacity were measured and the impact of gene polymorphism on them was evaluated. Our data showed that OGG1 Ser326Cys and XRCC1 Arg399Gln gene polymorphisms had impacts on the development of stroke.     

Histopathologic Features Aid in Predicting Risk for Progression of IgA Nephropathy

Background and objectives: IgA nephropathy (IgAN) is the most common primary glomerular disease worldwide. Accurately identifying patients who are at risk for progressive disease is challenging. The extent to which histopathologic features improves prognostication is uncertain.Design, setting, participants, & measurements: We studied a retrospective cohort with biopsy-proven IgAN in Calgary, Canada. Renal biopsies were reviewed by a nephropathologist with histopathologic data abstracted using a standardized form. The primary outcome was the composite of doubling of serum creatinine, ESRD, or death. Spline models defined significant levels of interstitial fibrosis, glomerulosclerosis, hypertension, proteinuria, and creatinine. The prognostic significances of clinical and histopathologic parameters were determined using Cox proportional hazards models.Results: Data from 146 cases were available for analysis with a median follow-up of 5.8 years. Greater than 25% interstitial fibrosis, >40% glomerular sclerosis, and a systolic BP >150 mmHg were risk thresholds. In univariable analyses, baseline creatinine, proteinuria, systolic BP, glomerular sclerosis, interstitial fibrosis, and crescentic disease were predictors of the primary outcome. In multivariable models adjusted for clinical characteristics, interstitial fibrosis (hazard ratio [HR]2.7; 95% confidence interval [CI] 1.2 to 6.0), glomerular sclerosis (HR 2.6; 95% CI 1.2 to 4.5), and crescents (HR 2.4; 95% CI 1.2 to 5.1) remained independent predictors of the primary outcome and significantly improved model fit compared with clinical characteristics alone.Conclusions: Baseline histopathologic parameters are independent predictors of adverse outcomes in IgAN even after taking into consideration clinical characteristics. Relatively small degrees of interstitial fibrosis confer an increased risk for progressive IgAN.IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Patients with IgAN have a variable clinical course with between 6 and 43% progressing to ESRD over 10 yr (1–5). Given this variability, identifying reliable prognostic factors is important to help stratify clinical monitoring and treatment regimens.Previous studies have identified clinical features including high-grade proteinuria, reduced kidney function, and hypertension at the time of diagnosis as predictors of adverse outcomes (4–7). Studies have identified interstitial fibrosis and glomerular sclerosis as poor prognostic features (8–10). This is not surprising considering that these features are a common final result of damage from glomerulonephritis; however, histopathologic features frequently correlate with serum creatinine, and whether they add prognostic values beyond the measurement of serum creatinine is uncertain. Histopathologic features are commonly categorized on the basis of arbitrary thresholds to denote significant degrees of damage (3,5,11), a factor that may contribute to poor performance in multivariable models of risk prediction in IgAN and result in an underestimation of their ability independently to predict outcomes. We performed a retrospective study using detailed baseline clinical data and quantitative analysis of renal biopsies, including the degree of interstitial fibrosis and glomerulosclerosis, to assess the factors that determine adverse outcomes including chronic kidney disease (CKD) progression and death.     

Thermotherapy in dermatology

Heat has been used as a medicinal and healing modality throughout human history. Today, thermotherapy is being studied in the treatment of many diseases. Although the exact anti-infective mechanism of thermotherapy is yet to be solved, this historically important healing method has shown significant results in the treatments of a variety of dermatological infectious diseases ranging from simple acne to bacterial, parasitic and viral infections, in modern medicine. Induction of cellular apoptosis in medium doses and necrosis in high doses has made thermotherapy an important modality in the treatment of malignant tumors. Especially in dermatology, significant results have been achieved in the treatment of Bowen's disease, melanoma and simple warts. Thermotherapy, which today has also shown advancements in cosmetology, can be delivered by liquid nitrogen in the form of hypothermia and a variety of ways ranging from hot water pads to ultrasound and even to lasers, in the form of hyperthermia. In this article, the place of this historically important treatment method in modern medicine, especially in dermatology, has been reviewed by an extensive search of the literature.     

DNA integrity in patients undergoing hyperbaric oxygen (HBO) therapy

Hyperbaric oxygen (HBO) therapy is successfully applied for a wide variety of diseases. However, recent studies in humans undergoing (HBO) therapy have revealed that HBO is able to induce oxidative DNA damage especially in lymphocytes while the biological significance of this outcome is still not clear. HBO mediated DNA damage in lymphocytes has been determined by using the alkaline version of the comet assay in order to detect DNA strand breakages in patients undergoing HBO therapy. Blood samples were obtained from 100 voluntary patients and were drawn by venipuncture before and immediately after the first session of HBO treatment. The DNA damaging effect of HBO has also been evaluated in the fifth session of HBO therapy. DNA strand breakages were significantly increased after the first session of HBO treatment. However the elevated DNA strand breaks returned to their normal levels in lymphocytes after two hours of in vitro incubation. The elevated DNA strand breaks consistently decreased and reached to the baseline levels after the fifth session of HBO therapy. The results of this study, conducted in patients undergoing HBO therapy, support the existence of the previously reported cellular adaptive response against HBO mediated oxidative DNA damage in experimental studies.