重症超声在呼吸机撤离中的应用进展和展望

脱机困难在危重症患者中很常见,长时间机械通气及脱机失败均会影响患者的临床结局,如何更好地促成和达成呼吸机的尽早撤离(脱机),是非常重要的课题.重症超声作为重要结构、功能、形态的多维监测手段,可对心脏、肺、膈肌等重要环节的状态和储备能力进行全方位的评估,有助于提升对呼吸环路中核心环节的了解和掌握,在脱机评估及导向治疗中具有重要价值.该文将对重症超声在脱机过程中的应用进行综述.     

儿童异基因造血干细胞移植术后肺急性移植物抗宿主病与感染CT表现

目的 观察儿童异基因造血干细胞移植（allo-HSCT）术后肺部急性移植物抗宿主病（aGVHD）的CT表现,并与感染性病变鉴别。方法 纳入148例allo-HSCT后出现肺部病变患儿,分为aGVHD组（n=85）和感染组（n=63）。比较组间年龄、术后发病时间及肺部CT征象及分布模式差异。结果 aGVHD组与感染组年龄与发病时间差异均具有统计学意义（P均<0.05）。aGVHD组常见CT征象为磨玻璃影（GGO,35/85,41.18%）、实变影（14/85,16.47%）及胸腔积液（12/85,14.12%）,多呈双侧、弥漫分布,可见胸膜下空逸;感染组常见征象包括实变影（33/63,52.38%）、GGO（32/63,50.79%）及支气管壁增厚（23/63,36.51%）,多呈单侧、局限性分布;2组病变分布模式差异均具有统计学意义（P均<0.05）。支气管壁增厚多见于感染组（P<0.05）。结论 儿童肺aGVHD的CT表现具有特征性,结合发病时间等信息可与感染性病变相鉴别。     

Broad and potent neutralizing human antibodies to tick-borne flaviviruses protect mice from disease

Tick-borne encephalitis virus (TBEV) is an emerging human pathogen that causes potentially fatal disease with no specific treatment. Mouse monoclonal antibodies are protective against TBEV, but little is known about the human antibody response to infection. Here, we report on the human neutralizing antibody response to TBEV in a cohort of infected and vaccinated individuals. Expanded clones of memory B cells expressed closely related anti-envelope domain III (EDIII) antibodies in both groups of volunteers. However, the most potent neutralizing antibodies, with IC₅₀s below 1 ng/ml, were found only in individuals who recovered from natural infection. These antibodies also neutralized other tick-borne flaviviruses, including Langat, louping ill, Omsk hemorrhagic fever, Kyasanur forest disease, and Powassan viruses. Structural analysis revealed a conserved epitope near the lateral ridge of EDIII adjoining the EDI–EDIII hinge region. Prophylactic or early therapeutic antibody administration was effective at low doses in mice that were lethally infected with TBEV.     

Associations of Type 2 Diabetes Onset Age With Cardiovascular Disease and Mortality: The Kailuan Study

OBJECTIVEWe aimed to explore the associations between type 2 diabetes onset age and cardiovascular disease (CVD) and all-cause mortality in the Chinese population.RESEARCH DESIGN AND METHODSThis study included 101,080 participants free of prevalent diabetes and CVD at baseline from the Kailuan Study. All participants were monitored biennially until 31 December 2017. During follow-up, 11,384 participants were diagnosed as having type 2 diabetes. For each case subject, one control subject was randomly selected, matched for age (± 1 years) and sex. The final analysis comprised 10,777 case-control pairs. Weighted Cox regression models were used to evaluate the average hazard ratios (AHRs) and 95% CIs of incident CVD and all-cause mortality among patients with new-onset type 2 diabetes versus control subjects across age-groups.ResultsDuring a median follow-up of 5.57 years, 1,794 incident events (907 CVD events, of which there were 725 strokes and 887 deaths) occurred. After adjustment for potential confounders, participants with type 2 diabetes diagnosed at age <45 years had the highest relative risks of CVD and all-cause mortality relative to the matched control subjects, with AHRs of 3.21 (95% CI 1.18–8.72) for CVD, 2.99 (95% CI 1.01–9.17) for stroke, and 4.79 (95% CI 1.95–11.76) for all-cause mortality. The risks gradually attenuated with each decade increase in type 2 diabetes onset age.CONCLUSIONSThe relative risks of CVD and all-cause mortality differed across type 2 diabetes onset age-groups, and the associations were more evident in younger-onset type 2 diabetes.     

Therapeutic Effects of Low-Intensity Pulsed Ultrasound on Premature Ovarian Insufficiency

We explored the therapeutic effects of low-intensity pulsed ultrasound (LIPUS) on a rat model of ovarian damage induced by cyclophosphamide. A total of 44 female rats with premature ovarian insufficiency induced by cyclophosphamide were randomly divided into two groups (an ultrasound group and a control group); 22 normal rats without premature ovarian insufficiency were also included as a third group. The ultrasound group was treated with LIPUS, while the other two groups received the same treatment but without any power output. We monitored the estrous cycles of all rats. Seven days after treatment, 21 rats were selected to mate with male rats. We then recorded the pregnancy rate along with the number and weight of newborn rats per nest. We collected samples of blood, uterus and ovaries from the remaining 45 rats before they were sacrificed. Compared with the normal group, the control group exhibited disordered estrous cycles, more atretic follicles (p < 0.01), higher levels of serum follicle-stimulating hormone (p < 0.01), fewer other follicles (p < 0.01) and lower serum levels of E₂ and anti-Müllerian hormone (p < 0.01). Compared with the control group, the ultrasound group had normal estrous cycles with fewer atretic follicles (p < 0.01), lower levels of serum follicle-stimulating hormone (p < 0.01), more other follicles (p < 0.01) and higher levels of serum E₂ (p < 0.01). No significant difference in the levels of serum anti-Müllerian hormone was noted between the control group and the ultrasound group. No significant differences were observed between the three groups with respect to pregnancy rate or the number and weight of newborns per nest (p > 0.05). In conclusion, our data indicate that LIPUS could improve some ovarian functions of rats with premature ovarian insufficiency.     

Ischemia preconditioning is neuroprotective in a rat cerebral ischemic injury model through autophagy activation and apoptosis inhibition

Sublethal ischemic preconditioning (IPC) is a powerful inducer of ischemic brain tolerance. However, its underlying mechanisms are still not well understood. In this study, we chose four different IPC paradigms, namely 5 min (5 min duration), 5×5 min (5 min duration, 2 episodes, 15-min interval), 5×5×5 min (5 min duration, 3 episodes, 15-min intervals), and 15 min (15 min duration), and demonstrated that three episodes of 5 min IPC activated autophagy to the greatest extent 24 h after IPC, as evidenced by Beclin expression and LC3-I/II conversion. Autophagic activation was mediated by the tuberous sclerosis type 1 (TSC1)-mTor signal pathway as IPC increased TSC1 but decreased mTor phosphorylation. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and hematoxylin and eosin staining confirmed that IPC protected against cerebral ischemic/reperfusion (I/R) injury. Critically, 3-methyladenine, an inhibitor of autophagy, abolished the neuroprotection of IPC and, by contrast, rapamycin, an autophagy inducer, potentiated it. Cleaved caspase-3 expression, neurological scores, and infarct volume in different groups further confirmed the protection of IPC against I/R injury. Taken together, our data indicate that autophagy activation might underlie the protection of IPC against ischemic injury by inhibiting apoptosis.