Cortico-cortical connections from the prefrontal cortex to the superior temporal sulcal cortex (STs area) were studied in the monkey by means of retrograde axonal transport of horseradish peroxidase (HRP). After injections of 0.15-0.6 microliter of 50% HRP into the STs area, labeled cells were found in various cortical regions. In the prefrontal-STs projections, main features of topographic correlation were revealed; the posterior part of the STs area receives fibers from the superior frontal convexity (areas dorsal to the principal sulcus) and areas 8 and 6, whereas the anterior part of the STs area receives fibers from the inferior frontal convexity (areas ventral to the principal sulcus) and the frontal pole (area FD). The principal sulcus sends fibers to the entire STs area except for its ventral wall of the posterior part. A small cortical area adjacent to the inferior ramus of the arcuate sulcus (area 45 of ref. 41) sends fibers to the entire STs area. In addition, the orbitofrontal cortex projects mainly to the rostral part of the STs area, and the parahippocampal gyrus (areas TF and TH) projects to the deeper part of the entire STs area. 相似文献
MicroRNA‐1 (miR‐1) stands out as the most prominent microRNA (miRNA) in regulating cardiac function and has been perceived as a new potential therapeutic target. Lycium barbarum polysaccharides (LBPs) are major active constituents of the traditional Chinese medicine based on L. barbarum. The purpose of this study was to exploit the cardioprotective effect and molecular mechanism of LBPs underlying heart failure. We found that LBPs significantly reduced the expression of myocardial miR‐1. LBPs improved the abnormal ECG and indexes of cardiac functions in P‐V loop detection in transgenic (Tg) mice with miR‐1 overexpression. LBPs recovered morphological changes in sarcomeric assembly, intercalated disc and gap junction. LBPs reversed the reductions of CaM and cMLCK, the proteins targeted by miR‐1. Similar trends were also obtained in their downstream effectors including the phosphorylation of MLC2v and both total level and phosphorylation of CaMKII and cMyBP‐C. Collectively, LBPs restored adverse structural remodelling and improved cardiac contractile dysfunction induced by overexpression of miR‐1. One of the plausible mechanisms was that LBPs down‐regulated miR‐1 expression and consequently reversed miR‐1‐induced repression of target proteins relevant to myocardial contractibility. LBPs could serve as a new, at least a very useful adjunctive, candidate for prevention and therapy of heart failure. 相似文献
To construct a Bacillus subtilis strain for improved uridine production.
Results
The AAG2846–2848 fragment of the pyrAB gene, encoding carbamoylphosphate synthetase, was deleted in B. subtilis TD246 leading to a 245% increase of uridine production and the conversion from glucose to uridine increased by 10.5%. Overexpression of the pyr operon increased the production of uridine by a further 31% and the conversion rate of glucose to uridine was increased by 18%. In addition, the blocking of arginine synthesis or disabling of glutamate dehydrogenase significantly enhanced the uridine production. The highest-producing strain, B. subtilis TD297, accumulated 11 g uridine/l with a yield of 240 mg uridine/g glucose in shake-flask cultivation.
Conclusion
This is the first report of engineered B. subtilis strains which can produce more than 11 g uridine/l, with a yield reaching 240 mg uridine/g glucose in shake-flask cultivation.
Diel vertical migration (DVM) and diel feeding rhythm of two cladocerans, Daphnia longispina and Bosmina coregoni were investigated at the pelagic area of Lake Toya (Hokkaido, Japan) in May, August and October 1992. Both species performed nocturnal DVM. The amplitude of DVM, however, became smaller from May to October. Such seasonal variations in DVM could not be explained by light penetration and/or water temperature. The two species had a clear feeding rhythm; they fed at night in May and October but also after sunrise in August. These feeding rhythms appeared to be related to the light-dark cycle, but were not necessarily associated with their DVM. We suggest that the diel feeding rhythm and DVM are regulated independently by light cues. 相似文献
A Chinese landrace of barley, Mokusekko 3, is unique in being completely resistant against all strains of barley yellow mosaic
virus (BaYMV). The present investigation revealed that the resistance of Mokusekko 3 is governed by two recessive genes. As
one of the resistance genes was known to be tightly linked with alleles at the Est complex locus, consisting of the Est1, Est2 and Est4 loci for esterase isozymes, each of the resistance genes could be separated by means of marker-assisted selection using an
isozyme allelic combination as a marker. One of the resistance genes, ym1, is linked to K (hooded lemma) and gl3 (glossy leaf 3) with recombination values of 25.3% and 9.7% respectively, and these three genes are located in the order
K-gl3-ym1 on chromosome 4. Another newly designated resistance gene, ym5, is linked to alleles at the Est complex locus and cu2 (curly growth 2), with recombination values of 1.9% and 19.5% respectively, in the order cu2-Est-ym5 from proximal to distal on the long arm of chromosome 3. The complete resistance of Mokusekko 3 is caused by combining two
resistance genes, ym1 and ym5. However, almost all the “resistant” cultivars derived from crosses with Mokusekko 3 are susceptible to the recently detected
strain BaYMV-III in Japan, since they contain only one resistance gene, ym5. Marker-assisted selection to combine resistance genes into a cultivar is discussed for the breeding of stabilizing resistance
to BaYMV.
Received: 23 September 1996 / Accepted: 8 November 1996 相似文献
Several recent studies have suggested seemingly contrasting roles of SIRT2 in inflammation: Our previous cell culture study has indicated that SIRT2 siRNA-produced decrease in SIRT2 levels can lead to significant inhibition of lipopolysaccharides (LPS)-induced activation of BV2 microglia, suggesting that SIRT2 is required for LPS-induced microglial activation. In contrast, some studies have suggested that SIRT2 deficiency can lead to increased inflammation. In our current study, we used a mouse model of neuroinflammation to determine the roles of SIRT2 in LPS-induced inflammation. We found that administration of SIRT2 inhibitor AGK2 can significantly decrease LPS-induced increases in CD11b signals and the mRNA of TNF-α and IL-6. We further found that AGK2 can block LPS-induced nuclear translocation of NFκB. In addition, our study has shown that AGK2 can decrease not only LPS-induced increase in TUNEL signals—a marker of apoptosis-like damage, but also LPS-induced increases in the levels of active Caspase-3 and Bax. Collectively, our current in vivo study, together with our previous cell culture study, has suggested that SIRT2 is required for LPS-induced neuroinflammation and brain injury.