Objective To explore the changes in inflammatory reactions in tail-suspension mice infected by Klebsiella pneumoniae from spaceflight.Methods Tail suspension was used to simulate the physiological effects of microgravity.C57BL/6 mice were randomly divided into control (Con),control+K.pneumoniae T16-169 (Con+T16-169),tail suspension (TS) and tail suspension+K.pneumoniae T16-169 (TS+T16-169) groups.The level of inflammatory cytokines TNF-α,IL-6 and IL-1β mRNA in lung tissue and the plasma cytokine concentration were detected by RT-qPCR and xMAP technology,and HE staining was used to represent the morphological changes in lung tissue.Results Compared with the control group,the expression of inflammatory cytokines in lung tissue and plasma concentrations of all experimental groups were increased,and the difference in TS+T16-169 group was the most significant (P<0.01 or P<0.001).HE staining showed that the lung tissues in Con+T16-169 and TS+T16-169 groups were damaged in different degrees,and the damage of TS+T16-169 group was the most serious.Conclusion The K.pneumoniae from spaceflight significantly increases the expression of inflammatory cytokines in lung tissue and plasma concentrations after infecting tail-suspension mice,and induces more serious damages to the lung tissue,which suggests that inflammatory reactions can be increased in tail suspension mice infected by K.pneumoniae from spaceflight.

Objective To report a case of disseminated cryptococcosis with cutaneous manifestations and osteomyelitis. Methods and Results A 33 year old female was admitted due to multiple nodules and ulcers on the upper arms, shoulders, buttocks and thighs for one year. The patient was pregnant when admitted, and gave birth to a premature baby during her illness. The nodules increased half a month after delivery, which was suspected to be hematogenously disseminated pulmonary tuberculosis and was given anti tuberculous therapy for three months but failed. Physical examination showed there were 39 nodules or ulcers on the face, gum, trunk, buttocks and extre mities. The bone structure of the left tibia and fibula destroyed and a sinus developed on the left fibula. Microbiologic examination showed that lots of spores were seen in the smear of pus and necrotic tissues, which produced yeast like colonies in culture with positive urease and caffeic acid test. Cryptococcus neoformans, serotype A was identified by API yeast reaction band and serology. Inoculation with mice and rats showed that their brains, lungs and livers were involved easily. Further identification as C.neoformans var.neoformans was obtained based on sequence analysis of ribosomal internal transcribed spacer region 2. The anti tuberculous therapy was stopped and anti fungal therapy was initiated at once. Intravenous and topical amphotericin B in combination with fluconazole were chosen in the initial therapy and itraconazole for maintenance. The nodules disappeared after 30 days and the last ulcer in the left tibia healed completely after 200 days. The anti fungal therapy was discontinued after 277 days and the patient was completely cured.

Objective:To analyze the relationship between genotype and clinical phenotype of the MYH7-R453C mutation in five Chinese hypertrophic cardiomyopathy (HCM) families.Methods:A retrospective cohort study was conducted on 527 unrelated HCM probands who were first diagnosed at the First Affiliated Hospital of Air Force Medical University (Xijing Hospital) from February 2014 to July 2018, and the high-throughput whole exome targeted sequencing of 96 genes related to hereditary cardiovascular disease was performed on the probands. The probands carrying the MYH7-R453C mutation were screened out, and their family members carrying the mutation were verified using Sanger sequencing. Healthy individuals without family history of genetic diseases from the same period and ethnicity were recruited as controls. Clinical data such as echocardiography, 12-lead electrocardiogram, and cardiac magnetic resonance imaging of the probands and their family members were collected, and the correlation between patient genotype and clinical phenotype was analyzed. Endpoint or key events were recorded through hospital re-examination or telephone follow-up.Results:The MYH7-R453C mutation was detected in 5 HCM probands, and clinical data and genetic results of 20 family members, including probands, were collected. Among them, 13 carried the MYH7-R453C mutation, of which 12 were diagnosed with HCM, and one child (F1Ⅲ 5) experienced early changes of HCM. The seven family members who did not carry the MYH7-R453C mutation had normal echocardiograms and 12-lead electrocardiograms. Among the 12 patients diagnosed with HCM, 2 experienced (F2Ⅱ 7, F5Ⅰ 2) sudden cardiac death, 2 experienced (F1Ⅲ 1, F3Ⅲ 3) events of sudden cardiac death survival, 2(F1Ⅱ 2, F3Ⅱ 1) died from heart failure during the follow-up period. Combined with the initial visit and follow-up, 4 families (F1, F2, F3, F5) had a family history of sudden death, among which 3 families probands or multiple family members experiencing sudden death before the age of 30 and adverse outcomes such as implantation of implantable cardioverter-defibrillators after sudden death survival. Conclusions:In the five families with HCM carrying MYH7-R453C mutations, genotype is highly correlated with clinical phenotype, and patients have a high risk of sudden death and poor prognosis. Early diagnosis of individuals carrying the MYH7-R453C gene mutation, both within the patient′s family and in the patients themselves, is crucial for initiating early treatment, preventing sudden death, and assessing prognosis.