盐酸非索非那定片联合胸腺肽对慢性荨麻疹患者风团及瘙痒情况的影响

目的:研究盐酸非索非那定片联合胸腺肽对慢性荨麻疹患者风团及瘙痒情况的影响分析。方法:选择2012年7月至2013年7月在我院接受治疗的慢性荨麻疹患者108例作为研究对象。以数字法随机分成观察组(54例)和对照组(54例)。对照组患者单纯服用盐酸非索非那定片,观察组在此基础上加用胸腺肽。对比两组疗效,风团和瘙痒症状总积分情况及不良反应。结果:观察组的总有效率为72.22%(39/54),显著高于对照组的53.70%(29/54),差异有统计学意义(P0.05)。两组治疗后的症状总积分均显著下降,但观察组治疗2,4周后的症状总积分均显著小于对照组,差异均有统计学意义(P0.05)。观察组的总不良反应率为9.26%(5/54),与对照组的22.22%(12/54)相比,差异无统计学意义(P0.05)。结论:盐酸非索非那定与胸腺肽联合治疗慢性荨麻疹疗效较好,值得推荐。     

Uroporphyrinogen decarboxylase

Uroporphyrinogen decarboxylase (EC 4.1.1.37) catalyzes the decarboxylation of uroporphyrinogen III to coproporphyrinogen III. The amino acid sequences, kinetic properties, and physicochemical characteristics of enzymes from different sources (mammals, yeast, bacteria) are similar, but little is known about the structure/function relationships of uroporphyrinogen decarboxylases. Halogenated and other aromatic hydrocarbons cause hepatic uroporphyria by decreasing hepatic uroporphyrinogen decarboxylase activity. Two related human porphyrias, porphyria cutanea tarda and hepatoerythropoietic porphyria, also result from deficiency of this enzyme. The roles of inherited and acquired factors, including iron, in the pathogenesis of human and experimental uroporphyrias are reviewed.     

Parasitic mites of medical and veterinary importance – is there a common research agenda?

There are an estimated 0.5–1 million mite species on earth. Among the many mites that are known to affect humans and animals, only a subset are parasitic but these can cause significant disease. We aim here to provide an overview of the most recent work in this field in order to identify common biological features of these parasites and to inform common strategies for future research. There is a critical need for diagnostic tools to allow for better surveillance and for drugs tailored specifically to the respective parasites. Multi-‘omics’ approaches represent a logical and timely strategy to identify the appropriate mite molecules. Recent advances in sequencing technology enable us to generate de novo genome sequence data, even from limited DNA resources. Consequently, the field of mite genomics has recently emerged and will now rapidly expand, which is a particular advantage for parasitic mites that cannot be cultured in vitro. Investigations of the microbiota associated with mites will elucidate the link between parasites and pathogens, and define the role of the mite in transmission and pathogenesis. The databases generated will provide the crucial knowledge essential to design novel diagnostic tools, control measures, prophylaxes, drugs and immunotherapies against the mites and associated secondary infections.     

Sex-related differences in SLIGRL-induced pruritus in mice

Aims

Pruritus is a common symptom of skin diseases, and is associated with impaired sleep quality and a considerable reduction in the patient's quality of life. Recently, it was reported that there are sex-specific differences in scratching behavior in chronic pruritus patients. Namely, female chronic pruritus patients scratch more and have significantly more scratch lesions than male patients. However, few animal studies have examined sex-related differences in scratching behavior. Thus, the present work investigated sex-related differences in animal pruritus using pruritogens, which are often used to create experimental animal models of itching.

Main methods

Acute pruritus was induced in ICR mice by a single intradermal injection of histamine, 4-methylhistamine, serotonin, compound 48/80, substance P (SP), or the proteinase-activated receptor-2 (PAR-2)-activating peptide SLIGRL-NH₂. Chronic pruritus was induced by 5 weeks of the repeated application of 2,4,6-trinitro-1-chlorobenzene (TNCB) to BALB/c mice.

Key findings

Female mice showed significantly higher scratching counts in SLIGRL-NH₂-induced pruritus than male mice. Conversely, there was no obvious sex-related difference in scratching behavior for the other pruritogens examined.

Significance

These results indicate that sex-related differences may exist in the pruritogen-responsive neurons that transmit the itch signal induced by SLIGRL-NH₂, but not by histamine or 5-HT.     

The role of iron in experimental porphyria and porphyria cutanea tarda

Porphyria cutanea tarda (PCT) and experimental porphyria are characterized by a decreased activity of the enzyme uroporphyrinogen decarboxylase, and accumulation of uroporphyrins and heptacarboxylporphyrins in the liver. Iron (Fe) plays an important role in PCT and experimental porphyria. Biochemically and electron microscopically, we examined the relationship between Fe and porphyrins in liver tissue of C57BL/10 mice made porphyric by administration of iron dextran as Imferon^® (IMF), and in liver biopsies of patients with symptomatic PCT. Accumulation of uroporphyrins and heptacarboxylporphyrins, and an increased amount of Fe were observed in livers of mice treated with IMF and in liver biopsies of patients with PCT. In mice treated with IMF, the activity of uroporphyrinogen decarboxylase was decreased. Both in livers of mice treated with IMF and in livers of patients with PCT, needle-like structures, representing uroporphyrin crystals, were observed by electron microscopy. Uroporphyrin crystals and Fe (as ferritin) were observed in the same hepatocyte. Moreover, there was a striking morphological correlation between uroporphyrin crystals and ferritin-Fe, suggesting a role for (ferritin-)Fe in the pathogenesis of porphyria.     

Reduced substrate affinity for human erythrocyte uroporphyrinogen decarboxylase constitutes the inherent biochemical defect in porphyria cutanea tarda

The pathogenesis of human porphyria cutanea tarda (PCT) is associated with an intrinsic abnormality of the uroporphyrinogen decarboxylase enzyme. To characterize this, we studied the kinetic properties of the red cell enzyme procured from patients with various forms of PCT and non-porphyric controls. The enzyme activity (units/mg hemoglobin) in the red cell hemolysate was close to normal in sporadic PCT but about 75% diminished in the familial PCT. The Michaelis constants (Km) of 200-fold purified red cell enzyme preparations, determined by using pentacarboxylic porphyrinogen I and uroporphyrinogen I as substrates, were more than 3.8-4.0 times higher, and the maximum velocity (Vmax) was about 70% diminished in familial PCT, whereas the Km was about 1.7-1.9 times higher and the Vmax was more or less normal for sporadic PCT. These observations suggest for the first time that the primary lesion in familial PCT is a genetically determined kinetic abnormality of uroporphyrinogen decarboxylase which appears to be different from the sporadic form of the disease.