Autophagy: a multifaceted player in the fate of sperm.

BACKGROUND: Autophagy is an intracellular catabolic process of degrading and recycling proteins and organelles to modulate various physiological and pathological events, including cell differentiation and development. Emerging data indicate that autophagy is closely associated with male reproduction, especially the biosynthetic and catabolic processes of sperm. Throughout the fate of sperm, a series of highly specialized cellular events occur, involving pre-testicular, testicular and post-testicular events. Nonetheless, the most fundamental question of whether autophagy plays a protective or harmful role in male reproduction, especially in sperm, remains unclear. OBJECTIVE AND RATIONALE: We summarize the functional roles of autophagy in the pre-testicular (hypothalamic-pituitary-testis (HPG) axis), testicular (spermatocytogenesis, spermatidogenesis, spermiogenesis, spermiation) and post-testicular (sperm maturation and fertilization) processes according to the timeline of sperm fate. Additionally, critical mechanisms of the action and clinical impacts of autophagy on sperm are identified, laying the foundation for the treatment of male infertility. SEARCH METHODS: In this narrative review, the PubMed database was used to search peer-reviewed publications for summarizing the functional roles of autophagy in the fate of sperm using the following terms: 'autophagy', 'sperm', 'hypothalamic-pituitary-testis axis', 'spermatogenesis', 'spermatocytogenesis', 'spermatidogenesis', 'spermiogenesis', 'spermiation', 'sperm maturation', 'fertilization', 'capacitation' and 'acrosome' in combination with autophagy-related proteins. We also performed a bibliographic search for the clinical impact of the autophagy process using the keywords of autophagy inhibitors such as 'bafilomycin A1', 'chloroquine', 'hydroxychloroquine', '3-Methyl Adenine (3-MA)', 'lucanthone', 'wortmannin' and autophagy activators such as 'rapamycin', 'perifosine', 'metformin' in combination with 'disease', 'treatment', 'therapy', 'male infertility' and equivalent terms. In addition, reference lists of primary and review articles were reviewed for additional relevant publications. All relevant publications until August 2021 were critically evaluated and discussed on the basis of relevance, quality and timelines. OUTCOMES: (i) In pre-testicular processes, autophagy-related genes are involved in the regulation of the HPG axis; and (ii) in testicular processes, mTORC1, the main gate to autophagy, is crucial for spermatogonia stem cell (SCCs) proliferation, differentiation, meiotic progression, inactivation of sex chromosomes and spermiogenesis. During spermatidogenesis, autophagy maintains haploid round spermatid chromatoid body homeostasis for differentiation. During spermiogenesis, autophagy participates in acrosome biogenesis, flagella assembly, head shaping and the removal of cytoplasm from elongating spermatid. After spermatogenesis, through PDLIM1, autophagy orchestrates apical ectoplasmic specialization and basal ectoplasmic specialization to handle cytoskeleton assembly, governing spermatid movement and release during spermiation. In post-testicular processes, there is no direct evidence that autophagy participates in the process of capacitation. However, autophagy modulates the acrosome reaction, paternal mitochondria elimination and clearance of membranous organelles during fertilization. WIDER IMPLICATIONS: Deciphering the roles of autophagy in the entire fate of sperm will provide valuable insights into therapies for diseases, especially male infertility.

Melatonin regulates the cross-talk between autophagy and apoptosis by SIRT3 in testicular Leydig cells.

Autophagy and apoptosis, as major modes of cell death, play critical roles in cellular homeostasis. Our previous study demonstrated that the cross-talk between autophagy and apoptosis regulated cadmium-induced testicular injury and self-recovery, influencing male fertility. However, the underlying mechanism remains blurry. Herein, our subfertility rat model indicated that cadmium-induced autophagy and apoptosis were ameliorated by the activation of SIRT3 and blunted by the inhibition of SIRT3 in rat testis. Further, generating SIRT3 overexpression and knockdown models in TM3 mouse Leydig cells, we found that melatonin (SIRT3 activator) and overexpression of SIRT3 rescued cadmium-induced autophagy and apoptosis in TM3 cells. Knockdown of SIRT3 induced autophagy and apoptosis, which failed to be reversed by melatonin in TM3 cells. Taken together, SIRT3 functions as a pivotal protective factor in testicular Leydig cells injury, and melatonin regulates the cross-talk between autophagy and apoptosis by SIRT3, ameliorating cadmium-induced testicular injury.

TAZ-regulated expression of IL-8 is involved in chemoresistance of hepatocellular carcinoma cells.

Chemotherapy resistance is one of the major challenges for the treatment of hepatocellular carcinoma (HCC). In order to investigate the mechanisms involved in chemoresistance of HCC, we established cisplatin (CDDP) and doxorubicin (Dox) resistant HCC cells. The expression of transcriptional coactivator with PDZ-binding motif (TAZ), one of the major downstream effectors of Hippo pathway, was upregulated in chemoresistant HCC cells. Targeted inhibition of TAZ via its siRNAs can restore CDDP and Dox sensitivity of chemoresistant HCC cells. The upregulation of TAZ increased the expression of IL-8 in HCC/CDDP and HCC/Dox cells. Recombinant IL-8 (rIL-8) antagonized the increased chemosensitivity mediated by TAZ knockdown. Mechanistically, TAZ can directly bind with the promoter of IL-8 to activate its transcription in chemoresistant HCC cells. Collectively, our data showed that TAZ-regulated expression of IL-8 was involved in chemoresistance of HCC cells. It indicated that targeted inhibition of TAZ/IL-8 axis might be helpful to improve chemotherapy efficiency for HCC.

Maternal Folic Acid Supplementation Mediates Offspring Health via DNA Methylation.

The clinical significance of periconceptional folic acid supplementation (FAS) in the prevention of neonatal neural tube defects (NTDs) has been recognized for decades. Epidemiological data and experimental findings have consistently been indicating an association between folate deficiency in the first trimester of pregnancy and poor fetal development as well as offspring health (i.e., NTDs, isolated orofacial clefts, neurodevelopmental disorders). Moreover, compelling evidence has suggested adverse effects of folate overload during perinatal period on offspring health (i.e., immune diseases, autism, lipid disorders). In addition to several single-nucleotide polymorphisms (SNPs) in genes related to folate one-carbon metabolism (FOCM), folate concentrations in maternal serum/plasma/red blood cells must be considered when counseling FAS. Epigenetic information encoded by 5-methylcytosines (5mC) plays a critical role in fetal development and offspring health. S-adenosylmethionine (SAM), a methyl donor for 5mC, could be derived from FOCM. As such, folic acid plays a double-edged sword role in offspring health via mediating DNA methylation. However, the underlying epigenetic mechanism is still largely unclear. In this review, we summarized the link across DNA methylation, maternal FAS, and offspring health to provide more evidence for clinical guidance in terms of precise FAS dosage and time point. Future studies are, therefore, required to set up the reference intervals of folate concentrations at different trimesters of pregnancy for different populations and to clarify the epigenetic mechanism for specific offspring diseases.

Cross-talk between autophagy and apoptosis regulates testicular injury/recovery induced by cadmium via PI3K with mTOR-independent pathway.

Autophagy and apoptosis are two major modes of cell death. A balanced interplay between both is vital for phagocytic clearance of apoptotic testicular cells. Here, generating a SD rats model-treated with cadmium (Cd) to mimic environmental exposure on human, we show that autophagy and apoptosis present synchronous change trends in Cd-induced testicular injury/self-recovery. Further, the cross-talk of autophagy and apoptosis is investigated in four testicular cell lines (GC-1/GC-2/TM3/TM4 cells) respectively. Results reveal that Cd-exposure for five consecutive weeks induces reproductive toxicity in male rats. After one cycle of spermatogenesis within 8 weeks without Cd, toxic effects are ameliorated significantly. In vitro, we find that PI3K inhibitor 3-MA regulates apoptosis by inhibiting autophagy with mTOR-independent pathway in Cd-treated testicular cells. Conclusively, cross-talk between autophagy and apoptosis regulates testicular injury/recovery induced by Cd via PI3K with mTOR-independent pathway.

Nunataks or massif de refuge? A phylogeographic study of Rhodiola crenulata (Crassulaceae) on the world's highest sky islands.

BACKGROUND: Quaternary climatic oscillations had tremendous effects on the current distribution of species. Here, we aim to elucidate the glacial history of Rhodiola crenulata, a perennial herb almost exclusively restricted to rock crevices on mountain peaks, and to test whether the nunatak or massif de refuge hypotheses could explain its distribution pattern. RESULTS: Six haplotypes and six ribotypes were detected in the cpDNA data set and the ITS data set, respectively. The divergence of R. crenulata and its closest relatives was dated have occurred ca. 0.65 Mya, during the Naynayxungla glaciation on the QTP. Mismatch distribution analysis suggested that the species experienced a range expansion around 0.31 Mya. Populations with high genetic and haplotype diversity were found on the QTP platform as well in the Hengduan Mountains. The ecological niche modeling results showed that there were suitable habitats on both the QTP platform and in the Hengduan Mountains during the LGM. CONCLUSION: Our results support a scenario that both nunataks and the massif de refuge hypotheses could explain the distribution of R. crenulata. We also confirmed that Quaternary climatic oscillations could promote plant speciation in some circumstances. This study adds to a growing body of evidence suggesting that the QTP plant lineages exhibited diverse reactions to the Quaternary climatic oscillations.

Effect of 2,3',4,4',5-Pentachlorobiphenyl Exposure on Endometrial Receptivity and the Methylation of HOXA10.

Polychlorinated biphenyls (PCBs) are one of the most common endocrine-disrupting chemicals and have obvious toxicity on human reproductive development. The aim of our study was to investigate the toxicity of chronic 2,3',4,4',5-pentachlorobiphenyl (PCB 118) exposure on embryo implantation and endometrial receptivity, with the possible mechanism of DNA methylation involved. Virgin CD-1 female mice (3 weeks old) were housed and orally treated with PCB 118 (0, 1, 10, 100 µg/kg) for a month. After mating with fertile males, the pregnant mice were killed on gestation day 4.5. Compared with the control group, implantation failures were observed in 1 µg/kg PCB 118- and 100 µg/kg PCB 118-treated groups. Abnormal endometrial morphology with open uterine lumens and densely compact stromal cells and poorly developed pinopodes were substantially in response to PCB 118 doses above, as well as the significant downregulation of implantation-associated genes (estrogen receptor 1, homeobox A10 [HOXA10], integrin subunit beta 3) and hypermethylation in the promoter region of HOXA10 further. It was confirmed that chronic exposure to PCB 118 produced an increased number of implantation failures in association with a defective uterine morphology during the implantation period. Alterations in methylation of HOXA10 could explain, at least in part, the mechanism of effects of PCB 118 exposure on the implantation process.

Prognosis of 591 fetuses with ultrasonic soft markers during mid-term pregnancy.

The present study aimed to examine the value of ultrasonic soft markers in prenatal screening by analyzing the clinical outcome of fetuses with ultrasonic soft markers during the second trimester of pregnancy. A retrospective analysis was performed to evaluate the outcome of 591 fetuses with ultrasonic soft markers from January 2015 to August 2016 in Zhongnan Hospital of Wuhan University, China. It was found that 591 fetuses showed ultrasonic soft markers in 4927 cases with the occurrence rate being 12.0%. Among them, 564 fetuses (95.4%) were delivered and the remaining 27 cases (4.6%) were aborted. Five hundred and sixty-seven cases had single ultrasonic soft marker, including echogenic intracardiac focus (n=343), mild renal pelvis dilatation (n=116), short long bones (n=72), single umbilical artery (n=31), mild lateral ventriculomegaly (n=21), choroid plexus cysts (n=19), and echogenic bowel (n=13), with the disappearing rates in pregnancy being 97.1% (333/343), 77.6% (90/116), 0% (0/72), 0% (0/31), 57.1% (12/21), 89.5% (17/19) and 61.5% (8/13) respectively. The rate of pregnancy termination due to single ultrasonic soft marker was 3.4% (19/567), and that was 33.3% (8/24) due to two ultrasonic soft markers with the difference being statistically significant (P<0.05). The reasons of pregnancy termination included malformations (polycystic kidney, cleft lip and palate, congenital heart diseases, pcromphalus, hypospadias, hydrocephalus), chromosome abnormality, and stillbirth. It was concluded that single ultrasonic soft marker is usually transient manifestation in pregnancy. Without the other structural defects, single ultrasonic soft marker usually disappears spontaneously with favorable prognosis in a low-risk population. It is suggested that ultrasonic soft markers should be appropriately interpreted to avoid unnecessary invasive examination.

Prognosis of 591 Fetuses with Ultrasonic Soft Markers during Mid-Term Pregnancy / 华中科技大学学报（医学）（英德文版）

The present study aimed to examine the value of ultrasonic soft markers in prenatal screening by analyzing the clinical outcome of fetuses with ultrasonic soft markers during the second trimester of pregnancy.A retrospective analysis was performed to evaluate the outcome of 591 fetuses with ultrasonic soft markers from January 2015 to August 2016 in Zhongnan Hospital of Wuhan University,China.It was found that 591 fetuses showed ultrasonic soft markers in 4927 cases with the occurrence rate being 12.0％.Among them,564 fetuses (95.4％) were delivered and the remaining 27 cases (4.6％) were aborted.Five hundred and sixty-seven cases had single ultrasonic soft marker,including echogenic intracardiac focus (n=343),mild renal pelvis dilatation (n=116),short long bones (n=72),single umbilical artery (n=31),mild lateral ventriculomegaly (n=21),choroid plexus cysts (n=19),and echogenic bowel (n=13),with the disappearing rates in pregnancy being 97.1％ (333/343),77.6％ (90/116),0％ (0/72),0％ (0/31),57.1％ (12/21),89.5％ (17/19) and 61.5％ (8/13) respectively.The rate of pregnancy termination due to single ultrasonic soft marker was 3.4％ (19/567),and that was 33.3％ (8/24) due to two ultrasonic soft markers with the difference being statistically significant (P＜0.05).The reasons of pregnancy termination included malformations (polycystic kidney,cleft lip and palate,congenital heart diseases,pcromphalus,hypospadias,hydrocephalus),chromosome abnormality,and stillbirth.It was concluded that single ultrasonic soft marker is usually transient manifestation in pregnancy.Without the other structural defects,single ultrasonic soft marker usually disappears spontaneously with favorable prognosis in a low-risk population.It is suggested that ultrasonic soft markers should be appropriately interpreted to avoid unnecessary invasive examination.

CXCR4, CXCR7, and CXCL12 are associated with trophoblastic cells apoptosis and linked to pathophysiology of severe preeclampsia.

Preeclampsia is a pregnancy disorder with sudden onset of maternal hypertension and proteinuria, which is characterized by defective cytotrophoblast invasion, increased apoptosis in cytotrophoblast, and diminished syncytial differentiation. In this study, samples from 11 mild preeclamptic patients, 18 severe preeclamptic patients, and 21 normal pregnant women were collected. The expression level of CXCL12 and its two receptors (CXCR4 and CXCR7) in these samples and their relationship with apoptosis were investigated. Morphological change of trophoblast cells that was observed by scanning electron microscope (SEM) indicated a significant tendency of apoptosis in the preeclamptic placenta. Immunohistochemical staining showed that expression level of three proteins was significantly lower in severe preeclamptic placentas compared with normal placentas (P<0.05), whereas no significant difference was found between mild preeclamptic and normal placentas (P>0.05). Real time quantitative PCR (RT-qPCR) and Western blot showed that both mRNA and protein expression level of CXCR4, CXCR7, and CXCL12 of trophoblasts were lower in the severe preeclampsia group than that in the normal group (P<0.05 for mRNA, P<0.01 for protein). In conclusion, our data revealed that the roles of CXCR4, CXCR7, and CXCL12 are associated with trophoblastic cells apoptosis and may be linked to the occurrence and development of severe preeclampsia.

Prenatal caffeine exposure induced a lower level of fetal blood leptin mainly via placental mechanism.

It's known that blood leptin level is reduced in intrauterine growth retardation (IUGR) fetus, and placental leptin is the major source of fetal blood leptin. This study aimed to investigate the decreased fetal blood leptin level by prenatal caffeine exposure (PCE) and its underlying placental mechanisms. Pregnant Wistar rats were intragastrically administered caffeine (30-120 mg/kg day) from gestational day 9 to 20. The level of fetal serum leptin and the expression of placental leptin-related genes were analyzed. Furthermore, we investigated the molecular mechanism of the reduced placental leptin's expression by treatment with caffeine (0.8-20 µM) in the BeWo cells. In vivo, PCE significantly decreased fetal serum leptin level in caffeine dose-dependent manner. Meanwhile, placental mRNA expression of adenosine A2a receptor (Adora2a), cAMP-response element binding protein (CREB), a short-type leptin receptor (Ob-Ra) and leptin was reduced in the PCE groups. In vitro, caffeine significantly decreased the mRNA expression of leptin, CREB and ADORA2A in concentration and time-dependent manners. The addition of ADORA2A agonist or adenylyl cyclase (AC) agonist reversed the inhibition of leptin expression induced by caffeine. PCE induced a lower level of fetal blood leptin, which the primary mechanism is that caffeine inhibited antagonized Adora2a and AC activities to decreased cAMP synthesis, thus inhibited the expression of the transcription factor CREB and target gene leptin in the placenta. Meantime, the reduced transportation of maternal leptin by placental Ob-Ra also contributed to the reduced fetal blood leptin. Together, PCE decreased fetal blood leptin mainly via reducing the expression and transportation of leptin in the placenta.

Effect of Bisphenol A on invasion ability of human trophoblastic cell line BeWo.

Bisphenol A (BPA) is a kind of environmental endocrine disruptors (EEDs) that interfere embryo implantation. Trophoblast invasion plays a crucial role during embryo implantation. In this study, the effects of BPA on invasion ability of human trophoblastic cell line BeWo and its possible mechanism were investigated. BeWo cells were exposed to BPA and co-cultured with human endometrial cells to mimic embryo implantation in transwell model. The proliferation and invasion capability of BeWo cells were detected. The expression of E-cadherin, DNMT1, MMP-2, MMP-9, TIMP-1 and TIMP-2 were also analyzed. The results showed that the invasion capability of BeWo was reduced after daily exposure to BPA. BPA had biphasic effect on E-cadherin expression level in BeWo cells and expression level of DNMT1 was decreased when treated with BPA. Moreover, BPA treatment also changed the balance of MMPs/TIMPs in BeWo cells by down-regulating MMP-2, MMP-9 and up-regulating TIMP-1, TIMP-2 with increasing BPA concentration. Taken together, these results showed that BPA treatment could reduce the invasion ability of BeWo cells and alter the expression level of E-cadherin, DNMT1, TIMP-1, TIMP-2, MMP-2, and MMP-9. Our study would help us to understand the possible mechanism of BPA effect on invasion ability of human trophoblastic cell line BeWo.

Phytoestrogen intake and risk of ovarian cancer: a meta- analysis of 10 observational studies.

BACKGROUND: Epidemiology studies have shown an inconclusive relationship between phytoestrogen intake and ovarian cancer risk and there have been no relevant meta-analyses directly regarding this topic. The purpose of the present meta-analysis was therefore to investigate any association between phytoestrogen intake and ovarian cancer in detail. MATERIALS AND METHODS: We conducted a search of PubMed, EMBASE, EBSCO, the Cochrane Library, CNKI and Chinese Biomedical Database (up to April 2014) using common keywords for studies that focused on phytoestrogen and ovarian cancer risk. Study-specific risk estimates (RRs) were pooled using fixed effect or random-effect models. RESULTS: Ten epidemiologic studies were finally included in the meta-analysis. The total results indicated higher phytoestrogen intake was associated with a reduced ovarian cancer risk (RR, 0.70; 95%CI: 0.56-0.87). The association was similar in sensitivity analysis. Meta regression analysis demonstrated sources and possibly types and regions as heterogeneous factors. Subgroup analysis of types, sources and regions showed that isoflavones (RR: 0.63; 95%CI: 0.46, 0.86), soy foods (RR: 0.51; 95%CI: 0.39, 0.68) and an Asian diet (RR: 0.48; 95%CI: 0.37, 0.63) intake could reduce the incidence of ovarian cancer. CONCLUSIONS: Our findings show possible protection by phytoestrogens against ovarian cancer. We emphasize specific phytoestrogens from soy foods, but not all could reduce the risk. The habit of plentiful phytoestrogen intake by Asians is worthy to recommendation. However, we still need additional larger well designed observational studies to fully characterize underlying associations.

[Study of blood flow improvement of topical application of estrogen on low genitourinary tract and its safety].

OBJECTIVE: The study of blood flow improvement of local estrogen on the low genitourinary tract and its safety. METHODS: The color Doppler flow imaging technique was employed to observe the flow spectrum of genitourinary tract. During the period of February 2007 to December 2010, there were 78 cases of postmenopausal females on local estrogen. The Doppler parameters included vaginal wall, urethra resistance index (RI) and systolic/diastolic ratio and others. And the lower genital urinary tract symptoms, such as sexual satisfaction, vulvovaginitis, urinary frequency, nocturia and other improvements, as well as adverse drug reactions before treatment and after 1 month, 3 months were recorded and analyzed. RESULTS: The results before treatment and after 1 month, 3 months, vaginal wall artery RI were 0.9 ± 0.2, 0.6 ± 0.2 and 0.7 ± 0.3; S/D 8.6 ± 3.7, 6.0 ± 2.9 and 6.4 ± 2.1; urethral artery RI 0.7 ± 0.2, 0.6 ± 0.2 and 0.6 ± 0.2, S/D 6.6 ± 1.9, 3.5 ± 0.7 and 3.4 ± 0.5 respectively. When the pre- and post-treatment indices were compared, the differences were statistically significant (P < 0.01). After using local estrogen in postmenopausal women, the resistance of lower genital urinary tract vasodilation decreased. Sexual satisfaction increased while the morbidities of vulvovaginitis, urinary frequency and nocturia decreased. The difference was statistically significant (P < 0.01). CONCLUSION: Postmenopausal females on topical estrogen may promote the blood circulation of lower genitourinary tract, red.

Trophoblast-derived chemokine CXCL12 promotes CXCR4 expression and invasion of human first-trimester decidual stromal cells.

BACKGROUND: The aim of this study was to investigate the role of the chemokine (C-X-C motif) ligand 12/chemokine (C-X-C motif) receptor 4 (CXCL12/CXCR4) axis on the crosstalk between human first-trimester trophoblast cells (TCs) and decidual stromal cells (DSCs), to contribute to a better understanding of the molecular mechanisms on the interaction between the mother and embryo during pregnancy. METHODS: CXCR4 on human first-trimester DSC membranes was detected by flow cytometry. The effects of exogenous CXCL12 or TC-conditioned medium (TCM) on proliferation and invasion of DSCs were examined by measuring proliferating cell nuclear antigen (PCNA) and an invasion assay, respectively. Finally, a co-culture model was established to investigate the effect of CXCL12 secreted from TCs on motility of DSCs. RESULTS: The mean (±SEM) percentage of DSCs positive for CXCR4 was 32.32 ± 7.18%. Human recombinant CXCL12 induced an increase in CXCR4 levels on DSCs via binding to CXCR4 (P < 0.01) but had no effect on the PCNA expression of DSCs. Moreover, both exogenous CXCL12 and TCM reinforced the invasive ability of DSCs via CXCR4 ligation. A co-culture model further confirmed that the enhanced invasiveness of DSCs in co-culture with TCs was inhibited by anti-CXCR4 or anti-CXCL12 neutralizing antibody (both P< 0.01). CONCLUSIONS: Human first-trimester DSCs express membrane CXCR4 and TC-derived CXCL12 promotes CXCR4 expression and invasion of DSCs via ligation with CXCR4. Our data highlight the role of CXCL12/CXCR4 axis on the co-operation between TCs and DSCs during human first-trimester pregnancy.

[Multicenter randomized controlled clinical study on levornidazole and sodium chloride injection in the treatment of pelvic anaerobic infections].

OBJECTIVE: to evaluate clinical efficacy and safety of levornidazole in the treatment of pelvic anaerobic infections. METHODS: a multicenter randomized controlled clinical study was conducted to evaluate clinical efficacy and safety of levornidazole. One hundred and fourty-three patients with pelvic anaerobic bacteria infection were classified into 70 cases treated by levornidazole in study group and 73 cases treated by Ornidazole in control group. Those patients in two groups were both administered at a dose of 0.5 g twice daily for 5 - 7 days. The rate of clinical efficacy, bacteria clearance and adverse effect were recorded and compared between two groups. RESULTS: at the endpoint, the rate of clinical efficacy were 80% (56/70) in study group and 81% (59/73) in control group, which did not reach significant difference (P > 0.05). The rate of bacteria clearance were 97% (36/37) in study group and 92% (22/24) in control group, which also did not reach significant difference (P > 0.05). The rate of adverse reaction of 3% (20/70) in study group was significantly lower than 22% (16/73) in control group (P < 0.05). CONCLUSION: it is effective and safe to treat pelvic anaerobic infections with levornidazole and sodium chloride injection.

[A comprehensive prevention programs on AIDS, HBV and syphilis among pregnant women and couples experienced premarital medical examination].

OBJECTIVE: To evaluate the effect of comprehensive prevention programs on HIV, HBV and syphilis transmission from mother to child and between premarital couples. METHODS: HIV, HBV and syphilis were screened among pregnant women with interventional measure for infected women; HIV, HBV and syphilis (TP) were screened among premarital couples with medical advice. RESULTS: The HIV, HBsAg and TP positive rates were 8.4‰ (111/13 280), 54‰ (711/13 186) and 12.8‰ (159/12 401) respectively among pregnant women and the total positive rate of the three diseases was 73.8‰ which was significantly higher than HIV positive rate (P < 0.001). The positive rates of HIV, HBsAg and TP were 17.6‰ (464/26 324), 95.3‰ (1826/19 152) and 18.6‰ (355/19 099) respectively among premarital couples and the total positive rate of the three diseases was 131.5‰ which was significantly higher than HIV positive rate alone (P < 0.001). Comprehensive prevention was more economical than prevention for HIV alone. CONCLUSION: The comprehensive strategies for prevention of HIV, HBV and syphilis was feasible, effective and economical that could help to actively conduct the preventive measures.

A case series of 104 women infected with HIV-1 via blood transfusion postnatally: high rate of HIV-1 transmission to infants through breast-feeding.

We investigated transmission of human immunodeficiency virus type 1 (HIV-1) via breast-feeding by 104 Chinese mothers who acquired the infection through blood transfusion postnatally. Of 106 children, 38 (35.8%) were infected. All children survived to age 5 years, and their survival curve was similar to that of their mothers. These findings suggest a high rate of HIV-1 transmission via breast-feeding when mothers were infected postnatally via blood transfusion, perhaps because of the higher viremia expected during the acute phase of infection. The course of disease among infected children was significantly less rapid than that among newborns infected perinatally, suggesting that a brief window of HIV-1-free life often enables the immune system of an infant to stave off rapid disease progression.