Elevated serum concentrations of troponin T in acute stroke: What do they mean?

Elevations in serum troponin T in acute stroke have been suggested as an early marker of a poor outcome. A prospective, case-control study was undertaken to define characteristics associated with elevations in troponin T concentrations. Consecutive admissions to the Royal Adelaide stroke unit were assessed. Stroke outcome was determined using the modified Rankin scale. Elevated serum troponin T was seen in 12/109 (11%) of patients with stroke and was associated with more severe stroke, larger lesion volume and a worse outcome. However, as a prognostic indicator, elevations in troponin T had lower sensitivity for predicting death or dependence at discharge than the National Institute of Health Stroke Scale. Troponin T levels are elevated in a significant proportion of patients with acute stroke, principally those with large infarcts affecting the territory supplied by the middle cerebral artery but their value as a prognostic indicator remains uncertain.     

Short tandem repeat and human leukocyte antigen mutations or losses confound engraftment and typing analysis in hematopoietic stem cell transplants

Clonal chromosomal abnormalities are often found in the tumor cells of patients with malignancies. These abnormalities can cause downregulation of human leukocyte antigen (HLA) and instability of short tandem repeat (STR) DNA sequences, confounding HLA typing and/or engraftment analysis in hematopoietic stem cell transplants (HSCT). We describe here the abnormalities observed during testing of 600 HSCT patients. HLA molecular typing was performed by reference strand conformational analyses and/or sequence-based typing. STR testing was performed with 10 to 16 STR primer sets, following 1 to 4 informative loci in each patient. Eight patients exhibited either loss of heterozygosity (4 STR, 3 HLA) or STR length mutation (n = 1), and 5 of the 8 exhibited correlative cytogenetic abnormalities. Diagnoses were acute myelogenous leukemia (AML; n = 7) or myelofibrosis (MFIB: n = 1), yielding an 11% incidence of these chromosomal abnormalities among the subset of 72 AML/MFIB HSCT patients. These results highlight some of the problems encountered and the possibility for interpretive errors that can arise when analyzing molecular typing and engraftment data, particularly among AML/MFIB patients.     

Dysfunction of the pupillary light reflex in experimental autoimmune autonomic ganglionopathy

Autoimmune autonomic ganglionopathy (AAG) is an antibody-mediated form of severe autonomic failure. AAG is associated with serum antibodies against ganglionic acetylcholine receptors (AChR) and appears to result from impaired synaptic transmission in autonomic ganglia. The rabbit model of experimental AAG (EAAG), induced by immunization, reproduces the cardinal features of the human disease. Pupillary dysfunction is a prominent and defining feature in both AAG and EAAG. We adapted infrared computer-assisted video pupillometry to record direct pupil light responses in control and EAAG rabbits. Offline analysis algorithms were used to determine latency, velocity and amplitude of the constriction and redilation phases of the light reflex. Following immunization, pupillary abnormalities were the earliest sign of evolving autonomic failure. EAAG rabbits showed significant reduction in velocity and amplitude of pupil constriction while redilation parameters were only mildly affected. Fatigue in pupillary constriction, evidenced by premature redilation of the pupil prior to termination of the light stimulus, was observed only in seropositive rabbits. The severity of pupillary abnormalities was significantly correlated with ganglionic AChR antibody level. In chronic EAAG, treatment with pyridostigmine produced a partial recovery of pupil function. We conclude that pupillometry is a robust and sensitive diagnostic tool to assess autonomic dysfunction, distinguish AAG from other disorders, and assess responses to therapy. In EAAG, pupillary dysfunction is partially reversible, parasympathetic pupil function is more severely compromised than sympathetic function, and fatigue of pupillary constriction may be seen. These characteristic abnormalities of the pupillary light reflex may prove to have diagnostic value.     

Metastatic serous carcinoma of the testis: a case report and review of the literature

Serous tumours of the testis and paratestis are rare, with fewer than 50 cases reported in the literature. The majority of the reported cases have been borderline serous tumours, and these tend not to recur or metastasize. Conversely, serous carcinomas can metastasize but this is often a late event. The presence of invasion in an otherwise borderline tumour has also been associated with the development of metastatic disease several years later, thus highlighting the importance of extensive sampling of all cases of borderline serous tumours. We report a case of a young man diagnosed with serous carcinoma of the testis, occurring 18 years after first diagnosis of a testicular germ cell tumour in the contralateral testis. This pattern has not previously been reported.     

A facile synthesis of alpha,alpha'-(EE)-bis(benzylidene)-cycloalkanones and their antitubercular evaluations

An economical and facile synthesis of alpha,alpha'-(EE)-bis(benzylidene)-cycloalkanones was achieved by the reaction of cycloalkanones with different aromatic aldehydes using ethanolic KOH in good yields. Few of the selected compounds were reduced with NaBH(4) to the respective alpha,alpha'-(EE)-bis(benzylidene)-cycloalkanols. All these compounds and our earlier synthesized cyclohexyl phenyl methanols were evaluated for their antitubercular, antifungal and antibacterial activities. Several compounds displayed moderate antitubercular activity with MIC=12.5-1.56 microg/mL. However, none of the compounds displayed any significant antifungal activity.     

Gene therapy to prevent occlusion of venous bypass grafts

Revascularization with vein grafts is standard surgical therapy for occlusive arterial diseases. Autologous saphenous vein grafts are important conduits for repairing blocked coronary arteries and are used in the majority of vein graft procedures. Up to 50% of saphenous vein grafts will be occluded during the first decade after surgery. Vein graft occlusion occurs as a result of neointimal hyperplasia, which takes place in response to hemodynamic changes and vessel wall injury, and is characterized by the migration and proliferation of vascular smooth muscle cells. Intimal hyperplasia is further complicated by the concomitant development of atherosclerosis and thrombosis. In the absence of effective pharmacological interventions for the treatment and prevention of occlusive vein graft disease, gene therapy has emerged as a potential therapeutic alternative. Gene therapy could improve vein graft patency by reducing early thrombosis, neointimal hyperplasia and atherosclerosis. In this review we will summarize the emerging applications of gene therapy as a therapeutic tool in occlusive vein graft disease.