Application of the medical anti-shock trouser (MAST) increases cardiac output and tissue perfusion in simulated,mild hypovolaemia

We have studied the haemodynamic effects of the application of the medical anti-shock trouser (MAST) in 10 healthy subjects in the semi-upright position in order to simulate mild hypovolaemia. Left ventricular end diastolic dimension (EDD) was measured by M-mode echocardiography and cardiac output (CO) by the Doppler ultrasound technique. Forearm blood flow (FBF) was measured by plethysmography and blood pressure (BP) by the standard cuff technique. Systematic increases in MAST pressure of up to 80 mm Hg were applied. EDD increased to a maximum of 9.3% (p0.01) which was associated with a maximum increase in CO of 31.7% (p0.05). FBF increased by a maximum of 54.2% (p0.001) whilst BP increased by a maximum of 12% (p0.001). These results demonstrate that the application of the MAST is an effective means of transferring blood to the central circulation by compression of the capacitance vessels resulting in significant increases in cardiac output and tissue perfusion. At high pressures there was evidence of compression of resistance vessels, which may be useful in reducing blood loss. The ease and rapidity with which his suit can be applied suggests that it may be useful in the short term treatment of hypovolaemia.     

荨麻疹患者血清特异性IgE的测定与分析

目的 :探讨由 Ig E介导的 型变态反应在荨麻疹发病中的意义及考察 MAST- CAL检测法的临床应用价值。方法 :采用 MAST- CAL法 (多种抗原光化学分析法 )检测了 180例荨麻疹患者血清特异性 Ig E水平 ,分析各种致敏原在荨麻疹发病中的意义。结果 :180例病人中 ,吸入组检出阳性 62例 ,阳性率 34 .4 4 % ,常见的吸入过敏原为粉尘螨、屋尘螨、蟑螂 ;食物组检出阳性为 53例 ,阳性率为 2 9.4 4 % ,最常见的食物过敏原为黄豆、吞拿鱼。结论 :由 Ig E介导的 型变态反应仅占荨麻疹病因的一部分 ,南方地区常见的吸入过敏原为粉尘螨及屋尘螨。 MAST- CAL检测法在检测荨麻疹患者血清特异性 Ig E水平上可提供可靠的实验结果。     

The Michigan Alcoholism Screening Test and Its Shortened Form: A Meta-Analytic Inquiry Into Score Reliability

Meta-analytic methods provide a framework around which an inquiry into MAST and SMAST score reliability was completed. Of the 470 measurement opportunities observed between 1971 and 2005, 62 (13.2%) were coupled with accurate reliability information. Weighted reliability estimates centered on. 80 suggesting that the MAST and SMAST generally produce scores of similar and adequate reliability for most research purposes. However, the variability of internal consistency estimates shows that at times these tools will not produce reliable scores, particularly among female and nonclinical respondents. Multiple regression equations provide practical guidelines to improve reliability estimates for the future use of these instruments.     

酒精依赖者抑郁情绪与酒瘾的相关研究

目的探讨酒精依赖者抑郁情绪与酒瘾的关系。方法对50例酒精依赖、酒精所致精神障碍的患者进行抑郁自评量表(SDS)和密西根酒精依赖调查表(MA ST)评定,比较有抑郁组和无抑郁组的MA ST得分,并对结果进行相关和回归分析。结果酒精依赖者抑郁症状检出率为56%,抑郁组MA ST得分高于无抑郁组(t=3.37,P=0.002),SDS与MA ST相关系数(r=0.621),抑郁情绪对酒瘾的影响度达38.58%。结论酒瘾与抑郁情绪有密切关联,而抑郁情绪与负性生活事件有关。     

PTH‐enhanced structural allograft healing is associated with decreased angiopoietin‐2–mediated arteriogenesis,mast cell accumulation,and fibrosis

Recombinant parathyroid hormone (rPTH) therapy has been evaluated for skeletal repair in animal studies and clinical trials based on its known anabolic effects, but its effects on angiogenesis and fibrosis remain poorly understood. We examined the effects of rPTH therapy on blood vessel formation and osseous integration in a murine femoral allograft model, which caused a significant increase in small vessel numbers, and decreased large vessel formation (p < 0.05). Histology showed that rPTH also reduced fibrosis around the allografts to similar levels observed in live autografts, and decreased mast cells at the graft‐host junction. Similar effects on vasculogenesis and fibrosis were observed in femoral allografts from Col1caPTHR transgenic mice. Gene expression profiling revealed rPTH‐induced angiopoietin‐1 (8‐fold), while decreasing angiopoietin‐2 (70‐fold) at day 7 of allograft healing. Finally, we show anti‐angiopoietin‐2 peptibody (L1‐10) treatment mimics rPTH effects on angiogenesis and fibrosis. Collectively, these findings show that intermittent rPTH treatment enhances structural allograft healing by two processes: (1) anabolic effects on new bone formation via small vessel angiogenesis, and (2) inhibition of angiopoietin‐2–mediated arteriogenesis. The latter effect may function as a vascular sieve to limit mast cell access to the site of tissue repair, which decreases fibrosis around and between the fractured ends of bone. Thus, rPTH therapy may be generalizable to all forms of tissue repair that suffer from limited biointegration and excessive fibrosis. © 2013 American Society for Bone and Mineral Research.     

Mast Cells Trigger Disturbed Bone Healing in Osteoporotic Mice

Mast cells are important tissue-resident sensor and effector immune cells but also play a major role in osteoporosis development. Mast cells are increased in numbers in the bone marrow of postmenopausal osteoporotic patients, and mast cell–deficient mice are protected from ovariectomy (OVX)-induced bone loss. In this study, we showed that mast cell–deficient Mcpt5-Cre R-DTA mice were protected from OVX-induced disturbed fracture healing, indicating a critical role for mast cells in the pathomechanisms of impaired bone repair under estrogen-deficient conditions. We revealed that mast cells trigger the fracture-induced inflammatory response by releasing inflammatory mediators, including interleukin-6, midkine (Mdk), and C-X-C motif chemokine ligand 10 (CXCL10), and promote neutrophil infiltration into the fracture site in OVX mice. Furthermore, mast cells were responsible for reduced osteoblast and increased osteoclast activities in OVX mice callus, as well as increased receptor activator of NF-κB ligand serum levels in OVX mice. Additional in vitro studies with human cells showed that mast cells stimulate osteoclastogenesis by releasing the osteoclastogenic mediators Mdk and CXCL10 in an estrogen-dependent manner, which was mediated via the estrogen receptor alpha on mast cells. In conclusion, mast cells negatively affect the healing of bone fractures under estrogen-deficient conditions. Hence, targeting mast cells might provide a therapeutic strategy to improve disturbed bone repair in postmenopausal osteoporosis. © 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).     

Macrolide susceptibility and molecular characteristics of Bordetella pertussis

ObjectiveTo analyse macrolide resistance and molecular characteristics of Bordetella pertussis clinical isolates from western China, and to explore the relationship between macrolide-resistance and genotypes.MethodsSusceptibilities of B. pertussis clinical isolates to erythromycin, azithromycin and clarithromycin were determined by epsilometer test (E-test). Isolated strains were sequenced to ascertain the presence of the 23S rRNA gene A2047G mutation. Strains were typed using multilocus antigen sequence typing, multilocus variable-number tandem-repeat analysis (MLVA) and pulsed-field gel electrophoresis (PFGE).ResultsOf 58 B. pertussis strains isolated in this study, 46 were macrolide-resistant and 12 were macrolide sensitive. All macrolide-resistant strains carried the A2047G mutation and were the prn1/ptxP1/ptxA1/fim3-1/fim2-1 genotype; the MLVA types were MT195 (19/58), MT55 (13/58) and MT104 (14/58), and the PFGE profiles were classified into BpSR23 (17/58) and BpFINR9 (29/58) types. None of the macrolide-sensitive strains carried the A2047G mutation; genotypes were (prn9 or prn2)/ptxP3/ptxA1/fim3-1/fim2-1, and all were MT27. PFGE profiles differed from the macrolide-resistant strains.ConclusionsB. pertussis clinical isolates from western China were severely resistant to macrolides. Genotypes differed between macrolide-resistant and macrolide-sensitive strains, and there may be a correlation between acquisition of macrolide resistance and changes in specific molecular types.