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At present, COVID-19 is a global pandemic and is seriously harmful to humans. In this retrospective study, the aim was to investigate the interaction between CVD and COVID-19.A total of 180 patients diagnosed with COVID-19 in Yichang Central People's Hospital from 29 January to 17 March 2020 were initially included. The medical history, clinical manifestations at the time of admission, laboratory test results, hospitalization time and complications were recorded. According to the medical history, the patients were assigned to the nonsevere group with non-CVD (In the severe group, compared with non-CVD patients, CVD patients had a significantly higher incidence of fever (CVD affects the severity of COVID-19. COVID-19 also increases the risk of severe CVD.La infección por SARS-CoV-2 está provocando graves consecuencias en la humanidad. El objetivo de este estudio retrospectivo fue investigar el impacto de las enfermedades cardiovasculares (ECV) en la gravedad de dicha infección.Entre el 29 de enero y el 17 de marzo de 2020, se diagnosticaron 180 pacientes con neumonía por SARS-CoV-2 en el Hospital Popular Central de Yichang. Se registraron los antecedentes, manifestaciones clínicas, resultados de laboratorio, tiempo de hospitalización y complicaciones. Los pacientes se dividieron en cuatro grupos: 1) infección no grave sin ECV (n = 90), 2) infección no grave con ECV (n = 22), 3) infección grave sin ECV (n = 40) y 4) infección grave con ECV (n = 28).La prevalencia de fiebre en los pacientes con ECV fue significativamente mayor que en aquellos sin ECV (P 0,05). Sin embargo, en comparación con los pacientes no graves, la proporción de pacientes con hipertensión, diabetes mellitus tipo 2, cardiopatía coronaria e insuficiencia cardíaca en los pacientes graves fue significativamente mayor (p 0,05). Los niveles de recuento de leucocitos, IL-6, PCR, dímero D, NT-proBNP y glucemia en ayunas (GA) en pacientes con ECV fueron significativamente mayores que en los de pacientes sin ECV, aunque los niveles de Hb fueron significativamente menores que los de los pacientes sin ECV (p 0,05). Sin embargo, los valores de NT-proBNP en pacientes con ECV fueron significativamente mayores que en los pacientes sin ECV (P 0,05). Además, el recuento de leucocitos y los niveles de IL-6, PCR, dímero D, CK-MB, ALT, AST, creatinina, NT-proBNPy GA en el grupo de pacientes graves fueron significativamente mayores que en el grupo no grave, mientras que los valores de Hb fueron significativamente menores que en el grupo no grave (p 0,05). La prevalencia de lesión miocárdica aguda, lesión renal aguda, arritmia y muerte súbita en el grupo con ECV fue significativamente mayor que en el grupo sin ECV (p 0,05). Los mismos resultados se encontraron al comparar los pacientes no graves con aquellos con infección grave. Entre los pacientes no graves, la duración media de la estancia hospitalaria fue de 25,25 (DE: 7,61) días en los pacientes sin ECV, mientras que la duración media de la estancia hospitalaria fue de 28,77 (DE: 6,11) días en los pacientes con ECV (p 0,05). Los mismos resultados se observaron al comparar los dos grupos con infección grave.La infección por SARS-CoV-2 es de evolución más grave en los pacientes con ECV.

Background: Hereditary spastic paraplegia (HSP) caused by mutations in ALDH18A1 have been reported as spastic paraplegia 9 (SPG9), with autosomal dominant and autosomal recessive transmission (SPG9A and SPG9B). SPG9 is rare and has shown phenotypic and genotypic heterogeneity in previous reports. Methods: This study screened ALDH18A1 mutations in autosomal recessive HSP patients using combined whole exome sequencing and RNA splicing analysis. We conducted in silico investigations, co-segregation analysis, and ELISA-based analysis of P5CS (Δ1-pyrroline-5-carboxylate synthetase; encoded by ALDH18A1) concentration to validate the pathogenicity of the detected ALDH18A1 variants. All previously reported bi-allelic ALDH18A1 mutations and cases were reviewed to summarize the genetic and clinical features of ALDH18A1-related HSP. Results: A novel missense mutation c.880T>C, p.S294P and an intronic splicing mutation c.-28-13A>G were both detected in ALDH18A1 in an autosomal recessive family presenting with a complicated form HSP. ELISA assays revealed significantly decreased P5CS concentration in the proband's plasma compared with that in the healthy controls. Moreover, review of previously reported recessive cases showed that SPG9B patients in our cohort presented with milder symptoms, i.e., later age at onset and without cognitive impairment. Conclusion: The present study expands the genetic and clinical spectrum of SPG9B caused by ALDH18A1 mutation. Our work defines new genetic variants to facilitate future diagnoses, in addition to demonstrating the highly informative value of splicing mutation prediction in the characterization of disease-related intronic variants.

Atherosclerosis is the leading cause of morbidity and mortality worldwide. The underlying pathogenesis involves multiple metabolic disorders, endothelial dysfunction and a maladaptive immune response, and leads to chronic arterial wall inflammation. Numerous normal physiological activities exhibit daily rhythmicity, including energy metabolism, vascular function and inflammatory immunoreactions, and disrupted or misaligned circadian rhythms may promote the progression of atherosclerosis. However, the association between the circadian rhythm and atherosclerosis remains to be fully elucidated. In the present review, the effects of the circadian rhythm on atherosclerosis progression are discussed.

Aim: Acute coronary syndrome (ACS), a leading cause of morbidity and mortality worldwide, is among the most serious cardiovascular diseases. Circadian rhythms are present in almost all organisms. In clinical practice, we have found that ACS is closely related to these circadian rhythms. However, the relationship between circadian rhythms and plaque instability in ACS patients is incompletely understood. The aim of this study is to provide new insights into the relationship between circadian rhythms and plaque instability in ACS patients. Methods: We enrolled patients with ACS and individuals with normal coronary artery function in this study. The Athens Insomnia Scale (AIS), Pittsburgh Sleep Quality Index (PSQI), International Physical Activity Questionnaire (IPAQ) and Healthy Diet Score (HDS) were used to evaluate circadian rhythms. Furthermore, quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess the mRNA expression levels of muscle aryl hydrocarbon receptor nuclear translocator-like protein 1 (Bmal1), circadian locomotor output cycles kaput (Clock), Cryptochrome1 (Cry1), Period2 (Per2), nuclear receptor subfamily 1, group D, member 1 (Rev-erbα), and matrix metalloproteinases MMP2 and MMP9. Results: AIS scores and PSQI scores were significantly higher in patients with ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina pectoris (UA) than in the normal controls (NCs) (P < 0.05). The IPAQ scores of the NCs and patients with UA were significantly higher than in patients with STEMI and NSTEMI (P < 0.05). Notably higher HDS scores were recorded for the NCs compared to those of patients with UA, NSTEMI, and STEMI (P < 0.05). Consistent with these findings, compared with the NCs, the lowest levels of Bmal1, Clock, Cry1, Per2 and Rev-erbα mRNAs were detected in patients with STEMI, followed by patients with NSTEMI and then patients with UA (P < 0.05). Furthermore, the levels of MMP2 and MMP9 mRNA were significantly higher in the patients with STEMI, NSTEMI, and UA than those in the NCs (P < 0.05). In addition, we found that the levels of MMP mRNA negatively correlated with the levels of clock genes mRNAs (P < 0.05, respectively). Conclusions: Based on our data, the circadian rhythms and clock genes are correlatively with the occurrence of ACS, and the expression levels of clock genes are negatively correlated with plaque stability in ACS patients.

Atherosclerosis (AS) is defined as chronic inflammation of the vessel wall. The major objective of the this study was to explore the mechanism of Treg/Th17 imbalance and the role of high mobility group box-1 protein (HMGB1) on the balance in AS.We detected the apoptotic ratios of Treg and Th17 cells in peripheral blood mononuclear cells (PBMCs) from subjects with AS and normal coronary arteries (NCA) by flow cytometry. The effects of recombinant HMGB1 (rHMGB1) on the proportion, apoptosis and differentiation of Treg and Th17 cells were analyzed using flow cytometry, qRT-PCR and ELISA.The frequencies of apoptotic Treg cells in the PBMCs from the subjects with AS were significantly higher than in those with NCA (p0.01). Stimulation of rHMGB1 obviously increased the level of Th17 cells and acid- related orphan receptor C (RORC) mRNA, and markedly decreased Treg cell frequency and the mRNA expression of factor forkhead family protein 3 (Foxp3) in the PBMCs. rHMGB1 played an obvious role in elevating Treg cell apoptosis ratio (p0.01). rHMGB1 treatment significantly decreased Treg cell ratio and IL-10 level, and increased Th17 cell ratio and IL-17A level induced from naïve CD4HMGB1 may modulate Treg/Th17 balance in patients with AS through inducing Treg cell apoptosis and promoting cell differentiation of Th17.

The surface of 3Cr13 martensitic stainless steel was irradiated by high current pulsed electron beam (HCPEB). The microstructures of the irradiation surface were characterized by X-ray diffraction and electron microscopy. After HCPEB irradiation, formation of a melting layer with depth of about 4 μm on the irradiated surface was determined. Further microstructural investigations indicate that the surface melted layer consists of nanoaustenite and ultrafine carbide particles, which primarily appear at grain boundary triple junction. Additionally, the microhardness and corrosion resistance of the irradiated surfaces was improved significantly. The formation of the nanoaustenite layer induced by HCPEB irradiation was believed to be the dominating reasons for the improvement of comprehensive performance of the material surface.

The microstructures and properties of 2024 aeronautical aluminum alloy subjected to thermal cycling were investigated in simulated Low Earth Orbit space environment. The experimental results demonstrate that the microhardness of aluminum alloys changed with the increasing of thermal cycles. The results of X-ray diffraction (XRD) and transmission electron microscopy (TEM) show that the property changes of the 2024 aluminum alloys during the thermal cycling period are closely related to the microstructural evolution. The relationship between the microstructural evolution and the thermal fatigue was also discussed.

AISI 304L austenite stainless steel was irradiated by a high-current pulsed electron beam (HCPEB) source in different process. The microstructures were investigated in detail by electron microscopy. The changes of hardness and corrosion resistance induced by irradiation were also tested. The relationship between corrosion resistance and the microstructures has been explored. The experimental results demonstrate the potential of proper HCPEB processing for improving the hardness and corrosion resistance of metallic materials.

To investigate the ultrastructural features of mitochondrial cytopathies and its diagnostic value.Muscle biopsy specimens from 33 cases of mitochondrial cytopathies were examined by routine pathological and electron microscopic examinations.The main pathologic changes included ragged red fibers in modified Gomori staining, hyper-intense staining myofibers in SDH, COX-negative fibers while dark counterstaining with SDH in COX/SDH double staining technique. Ultrastructural findings included subsarcolemmal and intramyofibrillar proliferation of mitochondria and the appearance of abnormal mitochondria, paracrystalline inclusions, concentric dystrophic cristae and excessive subsarcolemmal glycolipid compounds in subsarcolemmal.The presence of proliferation and abnormality of mitochondria, electro-dense granule and paracrystalline inclusions in mitochondria provide key diagnostic evidence for the diagnosis of this disease.

To discuss the surgical treatment of chiari-I malformation complicated with syringomyelia.The surgical treatments of 247 cases were analyzed retrospectively. The indication of operation styles was proposed by various surgical treatment to different MRI (magnetic resonance imaging) findings. MRI findings includes: tonsillar herniation with no or slight syringomyelia (126 cases), tonsillar herniation with syringomyelia above C(2) (second cervical vertebrae) vertebral level (38 cases), serious tonsillar herniation (to C(2) approximately C(3) level) with syringomyelia of isolated spinal segments (67 cases), serious tonsillar herniation (to C(2) approximately C(3) level) with syringomyelia above C(2) vertebral level (16 cases). They were performed by posterior fossa decompression, posterior fossa decompression and incision of the syringomyelia, posterior fossa decompression and resection of the cerebellar tonsils, posterior fossa decompression and incision of the syringomyelia combined with resection of the cerebellar tonsils respectively.The clinical signs and symptoms had been markedly improved or improved in 197 cases (79.8%) until patients were discharged from hospital, unchanged in 39 cases (15.8%), deteriorated in 7 cases (2.8%). there were 4 death in all cases after surgery. 107 cases were followed up from 5 months to 9 years. The postoperative MRI findings in the 107 patients demonstrated that the cavities in spinal cords disappeared completely or nearly in 78 cases, reduced in 14 cases, unchanged in 15 cases.Posterior fossa decompression, posterior fossa decompression and incision of the syringomyelia, posterior fossa decompression and resection of the cerebellar tonsils, posterior fossa decompression and incision of the syringomyelia combined with resection of the cerebellar tonsils should be an effective method for treatment of chiari-I malformation complicated with syringomyelia. Surgical treatment may fully ameliorate the clinical syndromes.

To analyze the impact of hematoma location and vascular territory on the clinical symptoms and signs, neuroimaging findings, and clinical prognosis of striatocapsular hemorrhage.The data of 181 cases of striatocapsular hemorrhage, 124 males and 57 females, aged 28 - 89, including medical history, symptoms, and signs were analyzed. On the basis of hematoma locations and arterial territories, the striatocapsular hemorrhage was divided into six types: anterior type (with the blood supply from Heubner's artery), middle type (with the blood supply from medial lenticulostriate artery), posteromedial type (with the blood supply from anterior choroidal artery), posterolateral type (with the blood supply from posteromedial branches of lateral lenticulostriate artery), lateral type (with the blood supply from the most of lateral branches of lenticulostriate artery), and massive type (with the hematoma occupying the whole or greater part of striatocapsular region). The short-term clinical outcome and prognosis were evaluated by Modified Rankin Scale (MRS). The relationship between the type and outcome was analyzed.There were 22 cases of anterior type, accounting for 12.15%, of which 68.18% showed an excellent outcome (MRS = 0 - 2) and only 1 case died. There were 12 cases of middle type, accounting for 6.63%, of which 6 cases (50%) showed a poor outcome (MRS = 5) but without dead case. There were 19 cases of posteromedial type (10.50%), of which 52.63% had excellent outcome (MRS = 0 - 2) without dead case. There were 19 cases of posterolateral type (18.78%), of which 76.47% were with poor outcome (MRS = 5) and 17.65% died. Accounting for 39.23%, lateral type was the most common condition, of which 38.03% patients had a poor outcome (MRS = 5) and 8.45% cases died. The incidence rate of massive type was also high (12.71%), of which 47.82% showed a poor outcome (MRS = 5) and 47.83% cases died.Hematoma location and vascular territory are the determinating factors of prognosis of striatocapsular hemorrhage. The six-type classification system provides a simple and reliable means to predict the clinical outcomes and to guide therapeutic options of striatocapsular hemorrhage.