Lower paleozoic facies relationships, fossils, and depositional systems of the Northwest Ordos Basin, northern China, are sparsely documented in western world literature (Meng et al., 1997; Kessel, 2005). Recent field work in this area during the summer of 2004 recovered a single specimen of a new chiastoclonellid sponge. That sponge, described here, was collected from a measured section of Lower Paleozoic rocks exposed in the Suhaitu area, in the northern part of the Zhuozi Shan Range, northwestern Ordos Basin (Fig. 1), in southern Inner Mongolia Province. The Zhuozi Shan Range is part of the western Ordos fold and thrust belt, a Late Jurassic–Early Cretaceous tectonic feature, that brought Lower Paleozoic rocks to the surface (Darby and Ritts, 2002; Darby, 2003). Early Paleozoic rocks exposed in the area are dominantly carbonates with minor siliciclastic rocks and they span from the Early Cambrian through the Middle Ordovician (Yang et al., 1992; Meng et al., 1997). They are unconformably overlain by Middle Carboniferous units across the North China Block (Meng et al., 1997).

The cognitive profile of early onset Parkinson’s disease (EOPD) has not been clearly defined. Mutations in the parkin gene are the most common genetic risk factor for EOPD and may offer information about the neuropsychological pattern of performance in both symptomatic and asymptomatic mutation carriers. EOPD probands and their first-degree relatives who did not have Parkinson’s disease (PD) were genotyped for mutations in the parkin gene and administered a comprehensive neuropsychological battery. Performance was compared between EOPD probands with (N = 43) and without (N = 52) parkin mutations. The same neuropsychological battery was administered to 217 first-degree relatives to assess neuropsychological function in individuals who carry parkin mutations but do not have PD. No significant differences in neuropsychological test performance were found between parkin carrier and noncarrier probands. Performance also did not differ between EOPD noncarriers and carrier subgroups (i.e., heterozygotes, compound heterozygotes/homozygotes). Similarly, no differences were found among unaffected family members across genotypes. Mean neuropsychological test performance was within normal range in all probands and relatives. Carriers of parkin mutations, whether or not they have PD, do not perform differently on neuropsychological measures as compared to noncarriers. The cognitive functioning of parkin carriers over time warrants further study. (JINS, 2011, 17, 1–10)

Hepatic fibrosis is a wound-healing response to chronic liver injury, which if persistent can lead to cirrhosis and liver failure. Activation of hepatic stellate cells (HSCs), leading to accumulation of extracellular matrix, is the central event of fibrogenesis. Exciting progress has been made in understanding the molecular basis of this process. Major advances include: (1) elucidation of the effects (and signalling pathways) of key cytokines on HSCs; (2) understanding the transcriptional regulation of HSC activation; (3) characterisation of matrix proteases and their inhibitors; (4) demonstration of apoptosis as an important event in the resolution of hepatic fibrosis, and identification of its mediators; (5) elucidation of the complex and dynamic interaction between HSCs and matrix; and (6) understanding the role of other cellular elements in hepatic fibrosis and their interaction with HSCs. Ongoing research with gene analysis using cDNA or oligonucleotide microarrays, or transcriptional profiling, will further increase our knowledge of the regulation of the process. Ultimately, advances in the understanding of the molecular biology of hepatic fibrosis are critical to the development of effective, targeted antifibrotic therapy that might benefit millions of patients with chronic liver disease worldwide.