[A multi-center epidemiological study on pneumococcal meningitis in children from 2019 to 2020]. / 2019­2020å¹´160ä¾‹å„¿ç«¥è‚ºç‚Žé“¾çƒèŒè„‘è†œç‚Žä¸´åºŠæµè¡Œç— å­¦å¤šä¸­å¿ƒç ”ç©¶.

OBJECTIVES: To investigate the clinical characteristics and prognosis of pneumococcal meningitis (PM), and drug sensitivity of Streptococcus pneumoniae (SP) isolates in Chinese children. METHODS: A retrospective analysis was conducted on clinical information, laboratory data, and microbiological data of 160 hospitalized children under 15 years old with PM from January 2019 to December 2020 in 33 tertiary hospitals across the country. RESULTS: Among the 160 children with PM, there were 103 males and 57 females. The age ranged from 15 days to 15 years, with 109 cases (68.1%) aged 3 months to under 3 years. SP strains were isolated from 95 cases (59.4%) in cerebrospinal fluid cultures and from 57 cases (35.6%) in blood cultures. The positive rates of SP detection by cerebrospinal fluid metagenomic next-generation sequencing and cerebrospinal fluid SP antigen testing were 40% (35/87) and 27% (21/78), respectively. Fifty-five cases (34.4%) had one or more risk factors for purulent meningitis, 113 cases (70.6%) had one or more extra-cranial infectious foci, and 18 cases (11.3%) had underlying diseases. The most common clinical symptoms were fever (147 cases, 91.9%), followed by lethargy (98 cases, 61.3%) and vomiting (61 cases, 38.1%). Sixty-nine cases (43.1%) experienced intracranial complications during hospitalization, with subdural effusion and/or empyema being the most common complication [43 cases (26.9%)], followed by hydrocephalus in 24 cases (15.0%), brain abscess in 23 cases (14.4%), and cerebral hemorrhage in 8 cases (5.0%). Subdural effusion and/or empyema and hydrocephalus mainly occurred in children under 1 year old, with rates of 91% (39/43) and 83% (20/24), respectively. SP strains exhibited complete sensitivity to vancomycin (100%, 75/75), linezolid (100%, 56/56), and meropenem (100%, 6/6). High sensitivity rates were also observed for levofloxacin (81%, 22/27), moxifloxacin (82%, 14/17), rifampicin (96%, 25/26), and chloramphenicol (91%, 21/23). However, low sensitivity rates were found for penicillin (16%, 11/68) and clindamycin (6%, 1/17), and SP strains were completely resistant to erythromycin (100%, 31/31). The rates of discharge with cure and improvement were 22.5% (36/160) and 66.2% (106/160), respectively, while 18 cases (11.3%) had adverse outcomes. CONCLUSIONS: Pediatric PM is more common in children aged 3 months to under 3 years. Intracranial complications are more frequently observed in children under 1 year old. Fever is the most common clinical manifestation of PM, and subdural effusion/emphysema and hydrocephalus are the most frequent complications. Non-culture detection methods for cerebrospinal fluid can improve pathogen detection rates. Adverse outcomes can be noted in more than 10% of PM cases. SP strains are high sensitivity to vancomycin, linezolid, meropenem, levofloxacin, moxifloxacin, rifampicin, and chloramphenicol.

Dulaglutide, a long-acting GLP-1 receptor agonist, can improve hyperandrogenemia and ovarian function in DHEA-induced PCOS rats.

OBJECTIVE: The purpose of this study was to explore the effect of dulaglutide on DHEA induced PCOS rats and its mechanism, to provide new drugs and research directions for clinical treatment of PCOS. METHODS: In this study, the PCOS model was established by giving female SD rats subcutaneous injection of DHEA for 21 consecutive days. After modeling, the treatment group was injected subcutaneously with three doses of dulaglutide for 3 weeks. The model group was injected with sterile ultrapure water, and the normal group did not get any intervention. The body weight changes of rats in each group were recorded from the first day when rats received the administration of dulaglutide. Three weeks later, the rats were fasted the night after the last treatment, determined fasting insulin and fasting glucose the next day. After the rats were anesthetized by chloral hydrate, more blood was collected from the heart of the rat. The serum insulin, testosterone and sex hormone binding globulin (SHBG) levels were detected by the enzyme-linked immunoassay method. After removing the adipose tissue, the obtained rat ovary tissue was used for subsequent experimental detection, using HE staining for morphology and follicular development analysis; qRT-PCR for the detection of 3ßHSD, CYP17α1, CYP19α1, and StAR gene expression in ovarian tissue; and western blotting analysis of CYP17α1, CYP19α1, StAR protein expression and insulin level to verify whether dulaglutide has a therapeutic effect on PCOS in rats. RESULTS: After treated with different concentrations of dulaglutide, we found that the body weight of rats in the treatment groups were reduced. Compared with the rats in PCOS group, the serum androgen level of rats in the treatment groups was significantly decreased, and the serum sex hormone binding protein content was significantly increased, and there was statistically significant difference between these groups and PCOS group. In terms of protein expression and gene regulation, the expression of 3ßHSD, CYP19α1 and StAR in the ovarian tissue of rats in treatment groups were decreased significantly after received the treatment of dulaglutide, and there was statistically significant difference between these groups and PCOS group. In addition, dulaglutide reduced the insulin content in the ovarian tissue of PCOS rats. CONCLUSION: Dulaglutide may reduce the hyperandrogenemia of PCOS rats by regulating the content of serum SHBG and the expression of 3ßHSD, CYP19α1, and StAR related genes and proteins, thereby inhibiting the excessive development of small follicles and the formation of cystic follicles in the ovaries of PCOS rats, thereby improving polycystic ovary in PCOS rats. In addition, dulaglutide may reduce the weight of PCOS rats, further reducing the level of high androgen in PCOS rats, and improving the morphology of their polycystic ovaries.

Identification of two novel mutations in the ATP7B gene that cause Wilson's disease.

BACKGROUND: Wilson's disease is an autosomal recessive disorder characterized by liver disease and/or neurologic deficits due to copper accumulation and is caused by pathogenic mutations in the ATP7B gene. DATA SOURCES: Two unrelated Chinese patients born to nonconsanguineous parents who were diagnosed with earlyonset Wilson's disease. DNA sequencing and bioinformation analysis were conducted. RESULTS: We have identified four mutations in two family trios, of which two were novel, namely, c. 3028A>G (p. K1010E) and c.3992T>G (p.Y1331X), in each patient. CONCLUSIONS: Gene testing is playing an important role in diagnosis of Wilson's disease. The early-onset of Wilson's disease is apparently not associated with P-ATPase domain in the ATP7B protein. Our findings further widen the spectrum of mutations involving the ATP7B gene.

[Changes of N-terminal pro-brain natriuretic peptide in neonates with myocardial ischemic injury].

OBJECTIVE: To investigate the changes of N-terminal pro-brain natriuretic peptide (NT-proBNP) in neonates with hypoxic-ischemic encephalopathy (HIE) complicated by myocardial ischemic injury. METHODS: Thirty-five neonates with HIE (17 cases with concurrent myocardial injury and 18 cases without) were enrolled. Twenty healthy neonates were used as the control group. Plasma NT-proBNP levels were measured using enzyme immunoassay. RESULTS: The mean plasma NT-proBNP levels in patients with myocardial injury (338.8 + or - 76.2 fmol/mL) were significantly higher than those in patients with non-myocardial injury (137.5 + or - 45.1 fmol/mL) and in the control group (113.7 + or - 53.6 fmol/mL) (p<0.01). The NT-proBNP levels in mild, moderate and severe HIE neonates were 141.3 + or - 41.6, 271.8 + or - 118.1 and 347.2 + or - 85.1 fmol/mL, respectively. Compared with the control group, the NT-proBNP levels in the moderate and the severe HIE groups significantly increased (p<0.01). There were significant differences in the NT-proBNP level among the mild, moderate and severe HIE groups (p<0.05). In patients with myocardial injury, the NT-proBNP levels significantly decreased in the convalescent phase compared with those in the acute phase (225.0 + or - 80.0 fmol/mL vs 338.8 + or - 76.2 fmol/mL (p<0.01). CONCLUSIONS: Plasma NT-proBNP levels increase in neonates with HIE complicated by myocardial ischemic injury in the acute phase. Detection of NT-proBNP levels may be useful in the diagnosis of myocardial ischemic injury and the severity evaluation of HIE.

[Correlation of erythrocyte immune function between normal neonates and their mothers].

OBJECTIVE: To study the correlation of erythrocyte immune function between normal neonates and their mothers and the influence of various obstetric factors on neonatal erythrocyte immune function. METHODS: The adherent rate of complement 3b-receptor on the surface of red blood cells (RBC-C3bRR) and the immune complex adherent rate of red blood cells (RBC-ICR) were detected using the erythrocyte saccharomyces rosette test in 104 normal neonates and their mothers. The correlation of erythrocyte immune function between neonates and their mothers was evaluated by the maternal-infant paired test. RESULTS: The levels of RBC-C3bRR (16.80 +/- 1.56% vs 16.23 +/- 1.63%; P < 0.05) and RBC-ICR (5.72 +/- 1.63% vs 5.02 +/- 1.38%; P < 0.01) in neonates were significantly higher than those in their mothers. There was a significantly positive correlation in RBC-ICR levels between neonates and their mothers (r = 0.28, P < 0.05). No correlation was found in RBC-C3bRR levels between the two groups. Neither RBC-C3bRR nor RBC-ICR levels of neonates were associated with various obstetric factors such as amniotic fluid, placenta, umbilical cord, parturient patterns, and puerperal anemia and pregnancy-induced hypertension syndrome. CONCLUSIONS: The erythrocyte immune function in neonates has a relatively mature level and correlates with their mothers' erythrocyte immune function. Various obstetric factors have no influences on neonatal erythrocyte immune function.