[Pruritus of the scalp : Simply pulling out your hair?] / Pruritus der Kopfhaut : Einfach zum Haare raufen?

Scalp pruritus is a frequent symptom and can be caused by dermatologic diseases, contact allergies, neurologic, psychiatric/somatoform and systemic diseases. In daily clinical practice scalp pruritus is a diagnostic and therapeutic challenge, especially if no detectable lesions are present. A detailed patient history and the inspection of scalp and the skin of the whole body are essential for diagnosis. Depending on the clinical findings, further dermatological diagnostic tests, laboratory analysis, imaging techniques and, where necessary, an interdisciplinary specific diagnostic check-up should be performed. Therapy comprises the treatment of the underlying disease, symptomatic antipruritic treatments such as topical treatment and if applicable systemic treatment. All this should be performed considering the individual situation especially the patient's hair growth and density.

Levodopa medication improves incidental sequence learning in Parkinson's disease.

Empirical evidence suggests that levodopa medication used to treat the motor symptoms of Parkinson's disease (PD) may either improve, impair or not affect specific cognitive processes. This evidence led to the 'dopamine overdose' hypothesis that levodopa medication impairs performance on cognitive tasks if they recruit fronto-striatal circuits which are not yet dopamine-depleted in early PD and as a result the medication leads to an excess of dopamine. This hypothesis has been supported for various learning tasks including conditional associative learning, reversal learning, classification learning and intentional deterministic sequence learning, on all of which PD patients demonstrated significantly worse performance when tested on relative to off dopamine medication. Incidental sequence learning is impaired in PD, but how such learning is affected by dopaminergic therapy remains undetermined. The aim of the current study was to investigate the effect of dopaminergic medication on incidental sequence learning in PD. We used a probabilistic serial reaction time task (SRTT), a sequence learning paradigm considered to make the sequence less apparent and more likely to be learned incidentally rather than intentionally. We compared learning by the same group of PD patients (n=15) on two separate occasions following oral administration of levodopa medication (on state) and after overnight withdrawal of medication (off state). Our results demonstrate for the first time that levodopa medication enhances incidental learning of a probabilistic sequence on the serial reaction time task in PD. However, neither group significantly differed from performance of a control group without a neurological disease, which indicates the importance of within group comparisons for identifying deficits. Levodopa medication enhanced incidental learning by patients with PD on a probabilistic sequence learning paradigm even though the patients were not aware of the existence of the sequence or their acquired knowledge. The results suggest a role in acquiring incidental motor sequence learning for dorsal striatal areas strongly affected by dopamine depletion in early PD.

Effectiveness of fresh frozen plasma as supplementary treatment in organophosphate poisoning.

With the establishment of the inadequate efficiency of atropines and oximes in reducing morbidity and mortality of patients poisoned by organophosphates, more attention is given to using other methods such as Fresh Frozen Plasma (FFP) as a bioscavenger to mop up organophosphate toxins. This randomized clinical trial was conducted on 56 organophosphate poisoned patients who were randomly assigned to the FFP and control groups in order of admission. The routine treatment in both groups included atropine and, in moderate to severe cases of poisoning, pralidoxime. The FFP group received four packs of FFP as stat dose at the beginning of treatment. No significant difference was seen between the two groups on the atropine and pralidoxime dosage, hospitalization length and mortality. The present study showed that using four packs of FFP as stat dose at the onset of treatment had no significant effect on the clinical course of organophosphate poisoned patients.

Prognostic significance of recurrent chromosomal aberrations detected by comparative genomic hybridization in sporadic colorectal cancer.

Colorectal carcinomas are characterized by frequent recurrent gains and losses of chromosomal material, especially gains of chromosome arms 20q and 13q, and losses of chromosome arms 18q and 4q. These may be important in the development and progression of colorectal carcinomas. Chromosomal aberrations detected by comparative genomic hybridization in 67 sporadic colorectal carcinomas were examined for their possible associations with patient survival. Dukes' stage, tumor DNA ploidy status, and TP53 genotype/phenotype were also examined for the same. Patients with losses of chromosomal arms 1p, 4q, 8p, 14q, or 18q or gain of chromosomal arm 20q had significantly shorter survival times than those without these aberrations (univariate relative risk 3.45, 2.71, 3.32, 3.26, 3.32, 3.91, respectively), as did patients with more than six chromosomal aberrations per tumor than those with fewer than six aberrations (univariate relative risk 3.26, P = 0.013). DNA aneuploidy and Dukes' stage C + D resulted in poor patient survival (univariate relative risk 3.58, 3.39, respectively). Dukes' stage C + D, 1p loss and 8p loss emerged as the only independent prognostic parameters (relative risk 3.22, 2.53, 2.45, respectively) when entered into multivariate survival analysis together with other significant parameters from univariate survival analysis. Loss of chromosome arm 1p, 4q, 8p, 14q, or 18q or gain of chromosome arm 20q thus results in shortened survival times in colorectal cancer patients. 1p loss and 8p loss were shown to be independent predictors of poor prognosis.

Peripheral lymph node-specific and Peyer's patch-specific homing receptors are differentially regulated following lymphocyte activation.

The MEL-14 receptor (MEL-14 R) expressed by murine lymphocytes represents the peripheral lymph node-specific homing receptor, and is essential for murine lymphocytes to specifically adhere to high endothelial venules (HEV) of the peripheral lymph nodes and to ultimately migrate in vivo into the parenchyma of this lymphoid organ. A Peyer's patch-specific homing receptor, termed LPAM, is now appreciated to mediate murine lymphocyte adhesion to Peyer's patch HEV. We previously demonstrated that the cell surface density of the MEL-14 R was markedly reduced following PMA-induced protein kinase C activation of lymphocytes. In the present study, we investigated the phenotypic and functional expression of LPAM by murine lymphocytes exposed to PMA. The results show that the surface expression of LPAM on activated lymphocytes remains constant under conditions where MEL-14 R is downregulated significantly. Additionally, the surface expression of LPAM is not influenced by calcium ionophore, either alone or in combination with PMA, whereas the PMA-induced loss of MEL-14 R is synergized by calcium ionophore. Therefore, LPAM and MEL-14 R expression are differentially regulated by activated murine lymphocytes. LPAM expressed by TK1 (Peyer's patch HEV-binding murine lymphoma) and MEL-14 R expressed by 38C13 (peripheral lymph node HEV-binding murine lymphoma) were found to be regulated by the consequences of PMA activation in a pattern similar to that of normal lymphocytes. Furthermore, we provide evidence that MEL-14 R internalization is not involved in the loss of the receptor expressed by activated lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Dual effects of pertussis toxin on murine neutrophils in vivo. I. Pertussis toxin inhibits extravasation potential of mature neutrophils while simultaneously stimulating granulopoiesis.

Pertussis toxin (Ptx) has been employed as an adjuvant by many investigators to augment various types of cell-mediated and humoral immune responses. Recent work from our laboratory indicates that the exacerbation of delayed-type hypersensitivity (DTH) and contact hypersensitivity (CH) responses observed in Ptx-treated mice may be mediated by an absolute increase in the number of circulating neutrophils capable of migrating into tissue sites of antigen challenge. The purpose of the present study was to analyze the effects of Ptx on neutrophils and neutrophil function in vivo. Evidence is presented here suggesting that Ptx has both direct and indirect effects on neutrophils following its in vivo administration to normal mice. Mature neutrophils that are directly exposed to the actions of Ptx in vivo exhibit a marked reduction in their ability to extravasate into tissue sites of inflammation. These findings are consistent with those that have been reported following the exposure of isolated neutrophils to the effects of Ptx in vitro (i.e., that Ptx has an inhibitory effect on many of the functional capabilities of isolated neutrophils). Moreover, we have also determined that Ptx can affect the kinetics of neutrophil production indirectly through its ability to stimulate granulopoiesis. Ptx-exposed mice develop a protracted peripheral blood neutrophilia following toxin administration. Although the mechanism(s) involved in stimulating increased neutrophil production is presently unclear, both dexamethasone and indomethacin (cyclooxygenase pathway inhibitors) are able to function synergistically with Ptx to produce a markedly enhanced neutrophilia in exposed mice. We propose that the capacity of Ptx to augment CH and DTH responses and act as a potent adjuvant may relate, in part, to its ability to alter the rate of neutrophil production in vivo.