Lupus nephritis and pregnancy

AIM: To evaluate effects of pregnancy on the course and prognosis of lupus nephritis and fetal outcome, in particular, in patients with lupus nephritis (LN) and antiphospholipid syndrome (APS). MATERIAL AND METHODS: A retrospective analysis was made of the course of LN in 31 females (44 pregnancies). RESULTS: A favorable outcome of pregnancy is possible in LN women if they had a persistent remission at conception. However, one third of these women had exacerbations of LN in pregnancy and early postpartum period. Pregnancy developing in active LN aggravated LN course in all the women. Fetal outcome was unfavorable. LN was especially severe if it arose in the course of pregnancy or early postpartum period. It seems that the presence of APS affected pregnancy outcome in a less degree than LN activity. CONCLUSION: Both in pregnancy and postpartum period, LN showed frequent exacerbations, but if the conception takes place during a persistent remission of LN, under adequate care and treatment, a delivery of a viable child is possible without an extraordinary risk for the mother.     

The effect of cortisone on renal succinodehydrase activity in experimental cytotoxic nephritis

Summary A study was made of succinodehydrase activity in the kidneys of rats suffering from experimental cytotoxic nephritis and treated with cortisone. In untreated nephritis the activity of the enzyme in the epithelium of the convoluted tubules decreased considerably, and was intensified in some of the glomeruli.Cortisone administration before or two days after the injection of the cytotoxic serum caused activation of succinodehydrase in the tubular epithelium without having any effect upon its activity in the glomeruli.(Presented by Active Member AMN SSSR I. V. Davydovskii) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 50, No. 9, pp, 61–64, September, 1960     

The effect of penetrating radiation on the succinic dehydrogenase activity of the parenchymatous organs of white rats

Summary The succinic dehydrogenase activity was studied on the sections from the heart, liver and kidney of albino rats exposed to repeated x-ray irradiations. The animals were sacrificed during the course of the 1st, 2nd and 3rd radiation sicknesses and during their temporary recovery. It was found that the enzyme activity does not change in 3 hours after the primary and the secondary x-ray irradiations. However, it seems to increase in 24 hours.At the onset of the radiation sickness (i.e. on the 7th day) and during its course the enzyme activity diminishes and remains on the lowered levels after the clinical recovery. The degree of elevations and falls of the enzyme activity depends upon the dose and the number of x-ray irradiations. The theoretical concepts underlying the above-mentioned results are discussed.Presented by Active Member of the AMN SSSR S. R. Mardashev     

抗CD20单抗（Rituximab）作为B细胞淋巴瘤老龄患者初始治疗的新标准

背景侵袭性B细胞淋巴瘤是目前最常见的非霍奇金淋巴瘤类型,主要包括弥漫大B细胞淋巴瘤(DLBCL)和套细胞淋巴瘤(MCL)。超过60%的患者被诊断出B细胞淋巴瘤时年龄都在60岁以上。在过去的30年间,CHOP方案(环磷酰胺、多柔比星、长春新碱、泼尼松)是治疗DLBCL的金标准。年龄较轻的患者     

Expression of vasoactive intestinal polypeptide and calcitonin gene-related peptide in human stellate ganglia after acute myocardial infarction

Using the method of indirect immunofluorescence the distribution of vasoactive intestinal polypeptide (VIP) and calcitonin gene-related peptide (CGRP) was investigated in autopsy specimens of human stellate ganglia following acute myocardial infarction (AMI). The dramatic increase of both VIP- and CGRP-immunoreactivities in principal ganglionic neurons as well as of calcitonin gene-related peptide in perineuronal nets was revealed. It was concluded that hypoxia and myocardial ischaemia following AMI are the main inducing factors for activation of both vasoactive regulatory neuropeptide synthesis. The upregulation of VIP and CGRP expression in sympathetic ganglionic neurons may provide regulatory and trophic support to the ischaemic heart.     

Nijmegen Breakage Syndrome mutations and risk of breast cancer

Mutations in the NBS1 gene have been identified as disease-causing mutations in patients with Nijmegen Breakage Syndrome (NBS), but their clinical impact on breast cancer susceptibility has remained uncertain. We determined the frequency of 2 NBS mutations, 657del5 and R215W, in two large series of breast cancer cases and controls from Northern Germany and from the Republic of Belarus. The 5-bp-deletion 657del5 was identified in 15/1,588 cases (0.9%) from Belarus and in 1/1,076 cases (0.1%) from Germany but in only 1/1,014 population controls from Belarus and 0/1017 German controls (p < 0.01). The missense substitution R215W was observed in 9/1,588 Byelorussian and 9/1,076 German patients (0.6% and 0.8%, respectively) but was also present in 5/1,014 Byelorussian and 2/1,017 German control individuals (adjusted OR = 1.9, 95%CI 0.8-4.6, p = 0.18). Studies of lymphoblastoid cell lines revealed that NBS1/p95 protein levels were reduced to 70% in cells from a heterozygous breast cancer patient carrying R215W and to 15% in cells from a NBS patient compound heterozygous for 657del5/R215W suggesting that the R215W substitution may be associated with protein instability. Levels of radiation-induced phosphorylation of Nbs1/p95(Ser343) were reduced to 60% and 35% of wildtype, respectively. Neither age at diagnosis nor family history of breast cancer differed significantly between carriers and noncarriers of NBS mutations. The combined data are in line with an about 3-fold increase in breast cancer risk for female NBS heterozygotes (OR 3.1; 95%CI 1.4-6.6) and indicate that the 657del5 deletion and perhaps the R215W substitution contribute to inherited breast cancer susceptibility in Central and Eastern Europe.     

Restoration of thrombolytic potential in plasminogen-deficient mice by bolus administration of plasminogen

Homozygous plasminogen-deficient (Plg-/-) mice had a significantly reduced thrombolytic capacity toward intravenously injected 125I-fibrin labeled plasma clots prepared from Plg-/- murine plasma (9% +/- 3% lysis after 8 hours; (mean +/- SEM, n = 6), as compared with 82% +/- 8% in wild-type mice; P < .0001). Bolus injection of 1 mg purified murine plasminogen in 10- to 17-week-old Plg-/- mice increased the plasminogen antigen and activity levels at 8 hours to normal levels (130 +/- 5 micrograms/mL). Plasminogen administration was associated with significant restoration of thrombolytic potential (64% +/- 7% spontaneous clot lysis; P < .0001 versus lysis without plasminogen injection). Bolus injection of 1 mg plasminogen in homozygous tissue- type plasminogen activator-deficient (t-PA-/-) mice doubled the plasminogen antigen and activity levels after 8 hours and increased 125I-fibrin clot lysis at 8 hours from 13% +/- 3% to 34% +/- 5% (P = .008). Fibrinogen, t-PA antigen and alpha 2-antiplasmin activity levels after 8 hours were not significantly different in the groups with or without plasminogen injection. Injection of plasminogen induced a variable increase (on average 7- to 10-fold) of PAI-1, but no correlation with the extent of spontaneous clot lysis was observed. Histopathologic examination at the end of the experiments revealed that fibrin deposition in the liver of Plg-/- mice was slightly reduced 8 hours after bolus plasminogen injection (P = .007) and markedly reduced after 24 hours (P < .0001). Plasminogen antigen levels in liver extracts were comparable with those found in wild-type mice at 8 hours (130 +/- 20 versus 110 +/- 15 ng/mg protein) and decreased to 25 +/- 3.2 ng/mg protein at 24 hours. Thus, restoration of normal plasminogen levels in Plg-/- mice normalized the thrombolytic potential toward experimentally induced pulmonary emboli, and resulted in removal of endogenous fibrin deposits within 24 hours.