Mechanisms of pulmonary dysfunction after on-pump and off-pump cardiac surgery: a prospective cohort study

Background  

Pulmonary dysfunction following cardiac surgery is believed to be caused, at least in part, by a lung vascular injury and/or atelectasis following cardiopulmonary bypass (CPB) perfusion and collapse of non-ventilated lungs.     

Treatment of myofascial trigger points in common shoulder disorders by physical therapy: A randomized controlled trial [ISRCTN75722066]

Background  

Shoulder disorders are a common health problem in western societies. Several treatment protocols have been developed for the clinical management of persons with shoulder pain. However available evidence does not support any protocol as being superior over others. Systematic reviews provide some evidence that certain physical therapy interventions (i.e. supervised exercises and mobilisation) are effective in particular shoulder disorders (i.e. rotator cuff disorders, mixed shoulder disorders and adhesive capsulitis), but there is an ongoing need for high quality trials of physical therapy interventions. Usually, physical therapy consists of active exercises intended to strengthen the shoulder muscles as stabilizers of the glenohumeral joint or perform mobilisations to improve restricted mobility of the glenohumeral or adjacent joints (shoulder girdle). It is generally accepted that a-traumatic shoulder problems are the result of impingement of the subacromial structures, such as the bursa or rotator cuff tendons. Myofascial trigger points (MTrPs) in shoulder muscles may also lead to a complex of symptoms that are often seen in patients diagnosed with subacromial impingement or rotator cuff tendinopathy. Little is known about the treatment of MTrPs in patients with shoulder disorders.     

A multiparametric index of platelet in vitro aggregation in cerebrovascular disease

148 patients with various forms of cerebrovascular disease (CVD) were studied by means of a multiparametric analysis ofin vitro platelet aggregation, based on the following six parameters: ADP and epinephrine primary and secondary aggregation thresholds and percent maximum aggregation induced by optimal concentrations of ADP and epinephrine. These patients were assigned to four study groups, according to clinical diagnosis supported by CT scan, of transient ischemic attack and reversible neurological deficit (TIA-RIND), or completed stroke, in the presence or absence respectively of antiplatelet medical treatment at the time of the study. A statistically significant increase of thein vitro platelet aggregation was found in 44.4% of the untreated TIA-RIND patients and in 33.9% of the untreated stroke patients. However this last group showed a higher percentage of very marked hyperaggregation. Differences between the two treated study groups and controls were not signicant. No difference was found in collagen-and ristocetin-induced aggregation between the patient groups and the controls.

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Sommario 148 pazienti con varie forme di malattia cerebrovascolare, sono stati studiati con analisi multiparametriche dell'aggregazione piastrinica in vitro sulla base dei seguenti sei parametri: le soglie di aggregazione primaria e secondaria e l'aggregazione massima percentuale indotta da ADP ed Epinefrina. Questi pazienti sono stati suddivisi in 4 gruppi di studio in accordo con la diagnosi clinica confortata dai dati della TAC e cioè: TIA, RIND, o rammollimento in presenza o in assenza rispettivamente di un trattamento antiaggregante nel momento dello studio. è stato trovato un aumento statisticamente significativo dell'aggregazione in vitro delle piastrine nel 44.4% dei casi TIA, RIND non trattati e nel 33,9% dei casi di rammollimento non trattati. Quest'ultimo gruppo, però, ha dimostrato una più alta percentuale di iperaggregazione molto marcata. Le differenze tra i 2 gruppi di studio trattati con antiaggreganti e i controlli non erano significative. Inoltre nessuna differenza è stata riscontrata tra i gruppi e i controlli nell'aggregazione indotta da collageno e ristocetina.

     

S-nitrosoglutathione-containing hydrogel accelerates rat cutaneous wound repair

BACKGROUND: Nitric oxide (NO) plays a key role in wound repair and S-nitrosothiols like S-nitrosoglutathione (GSNO) are well known NO donors. METHODS: Animals were separated in two groups and submitted to excisional wounds on the dorsal surface at the first day. GSNO (100 microm)-containing hydrogels were topically applied on the wound bed in the GSNO group, daily, during the first 4 days. Control group was topically treated with hydrogel without GSNO for the same period. Wound contraction and re-epithelialization were measured. Animals were sacrificed 21 days after wounding. Samples of lesion and normal tissue were formalin-fixed, paraffin embedded for histological analysis. RESULTS: Wound contraction, measured 14 and 21 days after wounding, was greater in the GSNO group than in the control group (P<0.05 for both). The re-epithelialized wound area, measured 14 days after wounding, was higher in the GSNO group than in the control group (P<0.05). A higher amount of inflammatory cells was observed in superficial and deep areas of the granulation tissue of the control group compared to the GSNO group. Twenty-one days after wounding, thin red-yellow collagen fibers arranged perpendicularly to the surface were found in the granulation tissue of the control group, whereas in the GSNO-treated group collagen fibers were thicker and arranged parallel to the surface. Increased number of mast cells was observed in the GSNO group compared with that in the control group. Vascularization and myofibroblast distribution were similar in both groups. CONCLUSION: Topical application of GSNO-containing hydrogel during the early phases of rat cutaneous wound repair accelerates wound closure and re-epithelialization and affects granulation tissue organization.     

Speech without conscious awareness

Following commissurotomy, it is usually the case that information presented to the left hemisphere can be named and described, while information presented to the mute, right hemisphere cannot be spoken about. In the present study, it was discovered that under special test conditions, an MRI-verified, callosally sectioned adult could name or write about information presented to the right hemisphere. Studies revealed this was not an instance of right hemisphere expression. Rather, the right hemisphere was somehow able to program the left hemisphere for a spoken or written response. Further, the studies also showed that the left hemisphere was not consciously aware that it possessed the information transmitted to it by the right half brain.     

Acetylcholinesterase Staining in Human Auditory and Language Cortices: Regional Variation of Structural Features

Cholinergic innervation of the cerebral neocortex arises fromthe basal forebrain and projects to all cortical regions. Acetylcholinesterase(AChE), the enzyme responsible for deactivating acetylcholine,is found within both cholinergic axons arising from the basalforebrain and a subgroup of pyramidal cells in layers III andV of the cerebral cortex. This pattern of staining varies withcortical location and may contribute uniquely to cortical microcircuitrywithin functionally distinct regions. To explore this issuefurther, we examined the pattern of AChE staining within auditory,auditory association, and putative language regions of whole,postmortem human brains. The density and distribution of acetylcholine-containing axonsand pyramidal cells vary systematically as a function of auditoryprocessing level. Within primary auditory regions AChE-containingaxons are dense and pyramidal cells are largely absent. Adjacentcortical regions show a decrease in the density of AChE-containingaxons and an increase in AChE-containing pyramidal cells. Theposterior auditory and language regions contain a relativelyhigh density of AChE-containing pyramidal cells and AChE-containingaxons. Although right and left posterior temporal regions arefunctionally asymmetrical, there is no apparent asymmetry inthe general pattern of AChE staining between homologous regionsof the two hemispheres. Thus, the pattern of AChE staining covarieswith processing level in the hierarchy of auditory corticalregions, but does not vary between the functionally distinctright and left posterior regions. An asymmetry in the size of layer III AChE-rich pyramidal cellswas present within a number of cortical regions. Large AChE-richpyramidal cells of layer III were consistently greater in sizein the left hemisphere as compared to the right. Asymmetry inlayer III pyramidal cell size was not restricted to language-associatedregions, and could potentially have a variety of etiologiesincluding structural, connectional, and activational differencesbetween the left and right hemisphere.     

Life expectancy in British Marfan syndrome populations

A total of 206 patients with Marfan syndrome were ascertained throughout genetic clinics in Wales and Scotland during the period 1970–1990. There were 45 deaths representing 22% of the cohort. Mean age at death was 45.3 ± 16.5 years. 50% median cumulative survival in the total cohort (n = 206) was 53 years for males and 72 years for females. Multivariate analysis confirmed severity as the best independent indicator of survival. These findings and survival curves will assist in the counselling of British families and individuals with Marfan syndrome.     

Sharing neuroimaging studies of human cognition

After more than a decade of collecting large neuroimaging datasets, neuroscientists are now working to archive these studies in publicly accessible databases. In particular, the fMRI Data Center (fMRIDC), a high-performance computing center managed by computer and brain scientists, seeks to catalogue and openly disseminate the data from published fMRI studies to the community. This repository enables experimental validation and allows researchers to combine and examine patterns of brain activity beyond that of any single study. As with some biological databases, early scientific, technical and sociological concerns hindered initial acceptance of the fMRIDC. However, with the continued growth of this and other neuroscience archives, researchers are recognizing the potential of such resources for identifying new knowledge about cognitive and neural activity. Thus, the field of neuroimaging is following the lead of biology and chemistry, mining its accumulating body of knowledge and moving toward a 'discovery science' of brain function.     

Homozygosity mapping of achromatopsia to chromosome 2 using DNA pooling

Achromatopsia is an autosomal recessive disease of the retina, characterized clinically by an inability to distinguish colors, impaired visual acuity, nystagmus and photophobia. A genome-wide search for linkage was performed using an inbred Jewish kindred from Iran. To facilitate the genome-wide search, we utilized a DNA pooling strategy which takes advantage of the likelihood that the disease in this inbred kindred is inherited by all affected individuals from a common founder. Equal molar amounts of DNA from all affected individuals were pooled and used as the PCR template for short tandem repeat polymorphic markers (STRPs). Pooled DNA from unaffected members of the kindred was used as a control. A reduction in the number of alleles in the affected versus control pool was observed at several loci. Upon genotyping of individual family members, significant linkage was established between the disease phenotype and markers localized on chromosome 2. The highest LOD score observed was 5.4 (theta = 0). When four additional small unrelated families were genotyped, the combined peak LOD score was 8.2. Analysis of recombinant chromosomes revealed that the disease gene lies within a 30 cM interval which spans the centromere. Additional fine-mapping studies identified a region of homozygosity in all affected individuals, narrowing the region to 14 cM. A candidate gene for achromatopsia was excluded from this disease interval by radiation hybrid mapping. Linkage of achromatopsia to chromosome 2 is an essential first step in the identification of the disease-causing gene.