Background The current study aimed to determine the impact of SARS-CoV-2 infection on male fertility. Methods This is a single-center, hospital-based observational study that included autopsied testicular and epididymal specimens of deceased COVID-19 male patients ( n =6) and recruited recovering COVID-19 inpatients ( n =23) with an equal number of age-matched controls, respectively. We performed histopathological examinations on testicular and epididymal specimens, and also performed TUNEL assay and immunohistochemistry. Whereas, we investigated the semen specimen for sperm parameters and immune factors. Findings Autopsied testicular and epididymal specimens of COVID-19 showed the presence of interstitial edema, congestion, red blood cell exudation in testes, and epididymides. Thinning of seminiferous tubules was observed. The number of apoptotic cells within seminiferous tubules was significantly higher in COVID-19 compared to control cases. It also showed an increased concentration of CD3+ and CD68+ in the interstitial cells of testicular tissue and the presence of IgG within seminiferous tubules. Semen from COVID-19 inpatients showed that 39.1% ( n =9) of them have oligozoospermia, and 60.9% ( n =14) showed a significant increase in leucocytes in semen. Decreased sperm concentration, and increased seminal levels of IL-6, TNF-α, and MCP-1 compared to control males were observed. Interpretation Impairment of spermatogenesis was observed in COVID-19 patients, which could be partially explained as a result of an elevated immune response in testis. Additionally, autoimmune orchitis occurred in some COVID-19 patients. Further research on the reversibility of impairment and developing treatment are warranted. Funding This study was supported by Ministry of Science and Technology of China Plan, Hubei Science and Technology Plan, National Key Research and Development Program of China, HUST COVID-19 Rapid Response Call, China and National Natural Science Foundation of China; these funding bodies are public institutions, and they had no role in study conception, design, interpretation of results, and manuscript preparation.

Background: The interaction between astrocytes and microglia plays a vital role in the damage and repair of brain lesions due to traumatic brain injury (TBI). Recent studies have shown that exosomes act as potent mediators involved in intercellular communication. Methods: In the current study, the expression of inflammatory factors and miR-873a-5p in the lesion area and oedema area was evaluated in 15 patients with traumatic brain injury. Exosomes secreted by astrocytes were detected by immunofluorescence, Western blot and electron microscopy. A mouse model of TBI and an in vitro model of LPS-induced primary microglia were established to study the protective mechanism of exosomes from miR-873a-5p overexpressing in TBI-induced nerve injury. Results: We discovered that exosomes derived from activated astrocytes promote microglial M2 phenotype transformation following TBI. More than 100 miRNAs were detected in these astrocyte-derived exosomes. miR-873a-5p is a major component that was highly expressed in human traumatic brain tissue. Moreover, miR-873a-5p significantly inhibited LPS-induced microglial M1 phenotype transformation and the subsequent inflammation through decreased phosphorylation of ERK and NF-κB p65. This effect also greatly improved the modified neurological severity score (mNSS) and attenuated brain injury in a strictly controlled cortical impact mouse model. Conclusions: Taken together, our research indicates that miRNAs in the exosomes derived from activated astrocytes play a key role in the astrocyte-microglia interaction. miR-873a-5p, as one of the main components of these astrocyte-derived exosomes, attenuated microglia-mediated neuroinflammation and improved neurological deficits following TBI by inhibiting the NF-κB signalling pathway. These findings suggest a potential role for miR-873a-5p in treating traumatic brain injury.

ObjectiveZambia is among the world’s top 10 countries with higher fertility rate (5.5 births/woman); unmet family planning need for births spacing (14%) and limiting births (7%). Women in rural Zambia (24%) are reported to have unmet need for family planning than those in urban areas (17%). This study was conducted to ascertain factors associated with modern contraceptive use among rural Zambian women.DesignCross-sectional study.SettingRural Zambia.ParticipantsSecondary data of 4903 married or cohabiting rural women (15–49 years) after filtering out the pregnant, urban based and unmarried women from 2013 to 2014 Zambian Demographic and Health Survey (ZDHS) were analysed using SPSS V.22. Multiple logistic regression, Pearson’s χ2and descriptive statistics were performed to examine factors associated with modern contraceptive use.ResultsFactors that were positively associated with contraceptive use were respondent’s education (secondary adjusted ORs (AOR = 1.61, p≤0.002); higher (AOR = 2.39, p≤0.050)), wealth index (middle class, (AOR = 1.35, p≤0.005); rich (AOR = 2.04, p≤0.001) and richest (AOR = 1.95, p≤0.034)), high parity (1–2 (AOR = 5.31, p≤0.001); 3–4 (AOR = 7.06, p≤0.001); 5+ (AOR = 8.02, p≤0.001)), men older than women by <10 years (AOR = 1.50, p≤0.026) and women sensitised about family planning at health facility (AOR = 1.73, p≤0.001). However, old age (40–49 years (AOR = 0.49, p≤0.001)), other religions (Protestants, African traditionalists and Muslims) (AOR = 0.77, p≤0.007), ever had pregnancy miscarried, aborted or stillbirth (AOR = 0.78, p≤0.026) and women without knowledge of number of children husband desires (AOR = 0.71, p≤0.001) were negatively associated with contraceptive use.ConclusionModern contraceptive use in rural Zambia among currently married women of reproductive age group is relatively low (43%). We recommend that appropriate interventions are instituted to increase contraceptive access and use especially among uneducated older rural Zambian women.

Since December 2019, an outbreak of coronavirus disease 2019 (COVID-19) has posed significant threats to the public health and life in China. Unlike the other 6 identified coronaviruses, the SARS-Cov-2 has a high infectious rate, a long incubation period and a variety of manifestations. In the absence of effective treatments for the virus, it becomes extremely urgent to develop scientific and standardized proposals for prevention and control of virus transmission. Hereby we focused on the surgical practice in Neurosurgery Department, Tongji Hospital, Wuhan, and drafted several recommendations based on the latest relevant guidelines and our experience. These recommendations have helped us until now to achieve 'zero infection' of doctors and nurses in our department, we would like to share them with other medical staff of neurosurgery to fight 2019-nCoV infection.

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For the first time, we provide evidence that loss of endothelial PDCD10 activates GBM cells and promotes tumor growth, most likely via a paracrine mechanism. PDCD10 shows a tumor-suppressor-like function in the cross talk between ECs and tumor cells and is potentially implicated in GBM progression.

Infections of the reproductive tract are known to contribute to testicular inflammatory impairment, leading to an increase of pro-inflammatory cytokines such as IL-1β, and a decline in sperm quality. Prokineticin 2 (PK2), a secretory protein, is closely associated with the secretion of pro-inflammatory cytokines in inflamed tissue. It was reported that increased PK2 is related to the upregulation of IL-1β, but the underlying mechanism remains elusive. Here, we illustrated that PK2 was upregulated in testicular macrophages (TM) in a rat model of uropathogenic Escherichia coli (UPEC) infection, which induced the activation of the NLRP3 inflammasome pathway to boost IL-1β secretion. Administration of PK2 inhibitor alleviated the inflammatory damage and suppressed IL-1β secretion. Moreover, PK2 promoted NLRP3 expression and the release of cleaved IL-1β from TM to the supernatants after the challenge with UPEC in vitro . IL-1β in the supernatants affected Leydig cells by suppressing the expression of genes encoding for the enzymes P450scc and P450c17, which are involved in testosterone production. Overall, we revealed that increased PK2 levels in TM in UPEC-induced orchitis may impair testosterone synthesis via the activation of the NLRP3 pathway. Our study provides a new insight into the mechanisms underlying inflammation-associated male infertility and suggests an anti-inflammatory therapeutic target for male infertility.

This study aimed to determine the value of ARL9 expression or methylation as a biomarker for LGG survival. We investigated the expression, methylation, prognosis and immune significance of ARL9 through bioinformatics analysis. ARL9 is negatively regulated by ARL9 methylation, leading to its low expression in LGG tissues. Both low ARL9 expression and hypermethylation predicted favorable OS and PFS in LGG patients, according to the TCGA database. Cox regression demonstrated that low ARL9 expression and ARL9 hypermethylation were independent biomarkers for OS. Moreover, three other glioma databases were utilized to verify the prognostic role of ARL9 in LGG, and the similar results were reached. A meta-analysis revealed that low ARL9 expression was closely relevant to better OS. Finally, ARL9 expression exhibited a close correlation with some immune cells, especially CD8+ T cells. ARL9 could constitute a promising prognostic biomarker, and probably plays an important role in immune cell infiltration in LGG.