Leucocyte apoptosis in patients with acute ischaemic stroke.

1. Inflammation and activated leucocytes are involved in the pathogenesis of acute ischaemic stroke. Leucocyte apoptosis is critical for the efficient resolution of inflammation.

Serial change in platelet activation markers with aspirin and clopidogrel after acute ischemic stroke.

Objectives: Antiplatelet drugs are widely used for secondary prevention after cerebral ischemia of noncardioembolic origin and different antiplatelet drugs exert different pharmacologic effects. This study investigated differences in platelet activation markers in patients taking either aspirin or clopidogrel after acute ischemic stroke.

Methods: A prospective randomized case-control study evaluated 70 patients with noncardioembolic stroke treated with either aspirin (100 mg/d) or clopidogrel (75 mg/d) after acute ischemic stroke.

Treatment with deferiprone for iron overload alleviates bone marrow failure in a Fanconi anemia patient.

Fanconi anemia (FA) is a rare inherited disorder characterized by congenital abnormalities, progressive bone marrow failure and cancer susceptibility. There are no reports in the literature about a specific therapy effective in treating the progressive bone marrow failure of FA except for hematopoietic stem cell transplantation (HSCT). A FA patient started to receive deferiprone (L1) therapy due to iron overload.

Sequential transplants for respective relapse of Hodgkin disease and hemophagocytic lymphohistiocytosis: a treatment dilemma.

The association of hemophagocytic lymphohistiocytosis (HLH) with Hodgkin disease (HD) seems to be uncommon. A 9-year-old boy, diagnosed with HD-HLH, received chemotherapy and remained in complete remission for 21 months. Then the patient received the first autologous transplant and unfortunately died due to multiorgan failure after the second allogeneic transplant because of sequentially respective relapse of HD and HLH.

Compound mutations in human anion exchanger 1 are associated with complete distal renal tubular acidosis and hereditary spherocytosis.

Missense, nonsense, and frameshift mutations in the human anion exchanger 1 have been associated with inherited distal renal tubular acidosis and hereditary spherocytosis. These two disorders, however, are almost always mutually exclusive. We have found an important and unusual exception: a novel combination of heterozygous E522K and G701D mutations in the anion exchanger 1 manifested as complete distal renal tubular acidosis and severe hereditary spherocytosis in an affected patient.

Levels and value of platelet activation markers in different subtypes of acute non-cardio-embolic ischemic stroke.

Introduction: Platelet activation and its interaction with leukocytes are important in the pathophysiology of ischemic stroke. This study aimed to evaluate the value of platelet activation and platelet-leukocyte interaction in different subtypes of acute, non-cardio-embolic ischemic stroke.

Methods: Fifty-four patients with acute, non-cardio-embolic ischemic stroke, including 32 small-vessel and 22 large-vessel diseases, were evaluated.

Dysregulation of Ca2+ movement in platelets from patients with acute ischaemic stroke.

1. Platelets play a pivotal role during acute ischaemic stroke. An increase in cytosolic Ca(2+) concentrations ([Ca(2+)](i)) triggers intracellular signal transduction, leading to platelet aggregation and thrombosis.

CD44 crosslinking-mediated matrix metalloproteinase-9 relocation in breast tumor cells leads to enhanced metastasis.

CD44 plays a major role in multiple physiological processes, including cell-cell adhesion, cell-substrate interaction, lymphocyte homing, and tumor metastasis. It has been reported that highly expressed CD44 in certain types of tumors is associated with the hematogenic spread of tumor cells. The ability of CD44 to bind hyaluronan has been shown to correlate with tumor cell invasiveness, and it is likely that this ability may enhance tumor cell migration at several points during metastasis.

Thoracic vagal efferent nerve stimulation evokes substance P-induced early airway bronchonstriction and late proinflammatory and oxidative injury in the rat respiratory tract.

Electrical stimulation of efferent thoracic vagus nerve (TVN) evoked neurogenic inflammation in respiratory tract of atropine-treated rats by an undefined mechanism. We explored whether efferent TVN stimulation via substance P facilitates neurogenic inflammation via action of nuclear factor-kappaB (NF-kappaB) activation and reactive oxygen species (ROS) production. Our results showed that increased frequency of TVN stimulation concomitantly increased substance P-enhanced hypotension, and bronchoconstriction (increases in smooth muscle electromyographic activity and total pulmonary resistance).

Inducible nitric oxide synthase evoked nitric oxide counteracts capsaicin-induced airway smooth muscle contraction, but exacerbates plasma extravasation.

The contribution of nitric oxide (NO) to capsaicin-evoked airway responses was investigated in rats. The measurement of plasma NO level, airway dynamics, airway smooth muscle electromyogram, and plasma extravasation by India ink and Evans blue leakage technique was adapted. Capsaicin-evoked hypotension, bronchoconstriction, trachea plasma extravasation as well as increases in plasma NO level in a dose-dependent manner.

Role in the inspiratory off-switch of vagal inputs to rostral pontine inspiratory-modulated neurons.

Neurons of the pontine respiratory group (PRG) in the region of the nucleus parabrachialis medialis and the Kolliker-Fuse nucleus are believed to play an important role in promoting the inspiratory (I) off-switch (IOS). In decerebrate gallamine-paralyzed cats ventilated with a cycle-triggered pump system (lung inflation during the neural I phase), we studied the effects of vagal (V) afferent inputs on firing of I-modulated neurons (the most numerous population in PRG) and on I duration. The predominant V effect on unit activity was inhibitory, as shown by two types of test: (a) withholding of inflation during an I phase, which produced increase of unit firing and of its respiratory modulation (58/66 neurons in 14 cats), indicating disinhibition due to removal of phasic V input; (b) delivery of afferent V stimulus trains during a no-inflation I phase, which produced decrease of unit firing and of its respiratory modulation (20 neurons).