中药升麻的化学成分

从中药兴安升麻[Cimicifuga dahurica(Turcz.)Maxim.]的干燥根茎中分得五个化合物,其中四个为三萜木糖甙:升麻醇-3-O-β-D-吡喃木糖甙(23R,24S)(Ⅰ),25-O-乙酰升麻醇-3-O-β-D-吡喃木糖甙(23R,24S)(Ⅱ),12-羟基升麻醇-3-O-β-D-吡喃木糖甙(23R,24S)(Ⅲ),升麻醇-3-O-β-D-吡喃木糖基(3→1)-β-D-吡喃木糖甙(23R,24S)(Ⅳ),另一个为异阿魏酸(Ⅴ)。Ⅲ和Ⅳ为新化合物,通过光谱(IR,MS,¹H及¹³C NMR)解析确定了它们的结构,分别命名为升麻甙A(cimiside A)和升麻甙B(cimiside B)。     

Evaluation of Race by Cranial Index of Adult Human Skull in Maharastra Population

Biologists and physical anthropologists attempted to classify human being into races according to phenotypic variations. The latter are based either on one or two phenotypic characters therefore the outcome is unable to givq clear distinction among different races. Cranial index seems to be an important,tool, which may be used to identify the races in different geographical regions. 75 dried skulls collected from different part of Maharashtra were measured to determine the cranial index. Skulls were classified by the method of Montagu (1960)2 Average maximum cranial length and breadth were found to be 17.11 cm and 12.98 cm respectively and maximum & minimum cranial lengths were observed to be 18.50 and 16.60 cm and cranial breadths were noted to be 14.50 and 12.10 cm respectively. Average cranial index (mean ± SD) was 75.49 ± 3.95. In our study most of the skulls were grouped under the Mesocranial (46.66%) and Dolichocranial (42.66%) categorises when based on Montagu and Dolichocranial categorises when 56% based Comas'. As per the conclusion Maharashtrian population belongs to Indo-Dravidian race.     

Periodontal status in oral mucous membrane pemphigoid: initial results of a case‐control study

Oral Diseases (2010) 17 , 90–94 Objective: To evaluate the periodontal status of mucous membrane pemphigoid (MMP) patients and compare it with that of healthy controls. Methods: A prospective study was undertaken to examine the impact of gingival MMP lesions on the human periodontium of 29 patients. Parameters evaluated included full mouth plaque score (FMPS), full mouth bleeding upon probing scores, probing depths (PD), gingival recession, clinical attachment level (CAL), mobility score, furcation involvement, number of missing teeth and Machtei criteria. Results: All periodontal parameters recorded were increased in cases when compared to controls in univariate statistics. The mean differences between groups in PD (0.8 ± 0.2 mm, 95% CI 0.3–1.3), CAL (1.3 ± 0.4 mm, 95% CI 0.4–2.2), FMPS (41.0 ± 6.2%, 95% CI 28.7–53.4), FMBS (16.2 ± 6.6%, 95% CI 3.0–29.4) and tooth loss (2 ± 1 teeth, 95% CI 1–3) were all statistically significant (P < 0.01 for all). Substantial differences in domiciliary oral hygiene routines were observed (P < 0.0001). In multivariate models when FMPS was included as covariate the difference between groups in all clinical periodontal parameters was no longer statistically significant. Conclusions: Our results showed that periodontal status is worse in MMP patients if compared with healthy controls due to a substantial difference in oral hygiene. Oral health should be promoted in MMP.     

Successful treatment of severe subcutaneous insulin resistance with inhaled insulin therapy

van Alfen‐van der Velden AAEM, Noordam C, de Galan BE, Hoorweg‐Nijman JJG, Voorhoeve PG, Westerlaken C. Successful treatment of severe subcutaneous insulin resistance with inhaled insulin therapy. The potential of inhaled insulin therapy for severe resistance to subcutaneous insulin was tested in a 7‐yr old boy with type 1 diabetes mellitus. The efficiency of 1 mg inhaled insulin (Exubera^®) was examined by a 4‐h euglycemic clamp study. During the clamp, the glucose infusion rate started to increase 25 min after inhalation and peaked 120 min after inhalation. Subsequently, a trial of inhaled insulin monotherapy was initiated consisting of pre‐meal inhalations and one inhalation during the night. Since glycemic control remained fair (HbA1c ～8.5%), this therapy was continued. Over the ensuing 18 months, mild keto‐acidosis occurred twice during gastro‐enteritis. Inhaled insulin was well tolerated and pulmonary function did not deteriorate. We conclude that severe resistance to subcutaneous insulin does not preclude sufficient absorption of insulin delivered by pulmonary.     

Small heat shock protein HspB8: its distribution in Alzheimer’s disease brains and its inhibition of amyloid-β protein aggregation and cerebrovascular amyloid-β toxicity

Alzheimer’s disease (AD) is characterized by pathological lesions, such as senile plaques (SPs) and cerebral amyloid angiopathy (CAA), both predominantly consisting of a proteolytic cleavage product of the amyloid-β precursor protein (APP), the amyloid-β peptide (Aβ). CAA is also the major pathological lesion in hereditary cerebral hemorrhage with amyloidosis of the Dutch type (HCHWA-D), caused by a mutation in the gene coding for the Aβ peptide. Several members of the small heat shock protein (sHsp) family, such as αB-crystallin, Hsp27, Hsp20 and HspB2, are associated with the pathological lesions of AD, and the direct interaction between sHsps and Aβ has been demonstrated in vitro. HspB8, also named Hsp22 of H11, is a recently discovered member of the sHsp family, which has chaperone activity and is observed in neuronal tissue. Furthermore, HspB8 affects protein aggregation, which has been shown by its ability to prevent formation of mutant huntingtin aggregates. The aim of this study was to investigate whether HspB8 is associated with the pathological lesions of AD and HCHWA-D and whether there are effects of HspB8 on Aβ aggregation and Aβ-mediated cytotoxicity. We observed the expression of HspB8 in classic SPs in AD brains. In addition, HspB8 was found in CAA in HCHWA-D brains, but not in AD brains. Direct interaction of HspB8 with Aβ_1–42, Aβ_1–40 and Aβ_1–40 with the Dutch mutation was demonstrated by surface plasmon resonance. Furthermore, co-incubation of HspB8 with D-Aβ_1–40 resulted in the complete inhibition of D-Aβ_1–40-mediated death of cerebrovascular cells, likely mediated by a reduction in both the β-sheet formation of D-Aβ_1–40 and its accumulation at the cell surface. In contrast, however, with Aβ_1–42, HspB8 neither affected β-sheet formation nor Aβ-mediated cell death. We conclude that HspB8 might play an important role in regulating Aβ aggregation and, therefore, the development of classic SPs in AD and CAA in HCHWA-D.     

E3 ligase Rad18 promotes monoubiquitination rather than ubiquitin chain formation by E2 enzyme Rad6

In ubiquitin conjugation, different combinations of E2 and E3 enzymes catalyse either monoubiquitination or ubiquitin chain formation. The E2/E3 complex Rad6/Rad18 exclusively monoubiquitinates the proliferating cell nuclear antigen (PCNA) to signal for "error prone" DNA damage tolerance, whereas a different set of conjugation enzymes is required for ubiquitin chain formation on PCNA. Here we show that human E2 enzyme Rad6b is intrinsically capable of catalyzing ubiquitin chain formation. This activity is prevented during PCNA ubiquitination by the interaction of Rad6 with E3 enzyme Rad18. Using NMR and X-ray crystallography we show that the R6BD of Rad18 inhibits this activity by competing with ubiquitin for a noncovalent "backside" binding site on Rad6. Our findings provide mechanistic insights into how E3 enzymes can regulate the ubiquitin conjugation process.