Search

Neonatal sepsis is a major global health challenge, leading to significant morbidity and mortality in newborns. The search for precise biomarkers for its early prediction in clinical settings has been ongoing, with heparin-binding protein (HBP) emerging as a promising candidate. Originating from granules in neutrophils, HBP is released into the bloodstream in response to infection and plays a pivotal role in the body's inflammatory response. Its significance extends beyond its inflammatory origins; research indicates dynamic changes in HBP levels are strongly linked to reduce in-hospital mortality, offering a prognostic advantage over existing biomarkers. Furthermore, HBP has demonstrated considerable clinical utility in the early diagnosis and stratification of neonatal sepsis, suggesting its potential as a reliable blood marker for early prediction of the disease and its severity. Its application may extend to guiding the judicious use of antibiotics in treating newborns, addressing a critical aspect of neonatal care. Despite these encouraging results, the precise clinical utility of HBP for diagnosing and treating sepsis in neonates still demands further clarification through extensive research. This review delves into the current scientific understanding of HBP's contribution to diagnosing, prognosticating, and treating neonatal sepsis, while considering its future clinical applications. [ABSTRACT FROM AUTHOR]

Severe neonatal hyponatremia represents a critical electrolyte imbalance with potentially severe neurological outcomes, a condition rarely documented in community-acquired, full-term newborns. This report underscores a unique case of a 23-day-old, previously healthy, full-term male neonate experiencing severe hyponatremia that precipitated seizures, underscoring the urgency of prompt recognition and intervention. The neonate presented with symptoms including vomiting, groaning, chills, fixed staring, and limb tremors. Critical findings upon admission encompassed hypothermia, hypotension, tachycardia, and tachypnea accompanied by significant weight loss. The clinical presentation was marked by dehydration, lethargy, weak crying, a fixed gaze, irregular breathing, and coarse lung sounds, yet a distended abdomen, hypertonic limb movements, and recurrent seizures were observed. Immediate interventions included establishing IV access, rewarming, mechanical ventilation, seizure management, volume expansion, dopamine for circulatory support, and initiation of empirical antibiotics. Diagnostic evaluations revealed a sodium ion concentration of 105.9 mmol/L, while amplitude-integrated electroencephalography (aEEG) detected pronounced seizure activity characterized by a lack of sleep-wake rhythmicity, noticeable elevation in both the lower and upper amplitude margins, and a sustained decrease in the lower margin voltage dropping below 5 μV, presenting as sharp or serrated waveforms. The management strategy entailed rapid electrolyte normalization using hypertonic saline and sodium bicarbonate, anticonvulsant therapy, and comprehensive supportive care, with continuous aEEG monitoring until the cessation of seizures. Remarkably, by the third day, the neonate's condition had stabilized, allowing for discharge in good health 10 days post-admission. At a 16-month follow-up, the child exhibited no adverse neurological outcomes and demonstrated favorable growth and development. Our extensive review on the etiology, clinical manifestations, aEEG monitoring, characteristics of seizures induced by severe neonatal hyponatremia, treatment approaches, and the prognosis for seizures triggered by severe hyponatremia aims to deepen the understanding and enhance clinical management of this complex condition. It stresses the importance of early detection, accurate diagnosis, and customized treatment protocols to improve outcomes for affected neonates. Additionally, this review accentuates the indispensable role of aEEG monitoring in managing neonates at elevated risk for seizures. Yet, the safety and efficacy of swiftly administering hypertonic saline for correcting severe hyponatremia-induced seizures necessitate further investigation through medical research. [ABSTRACT FROM AUTHOR]

Ceftriaxone is widely used in pediatric outpatient care for its efficacy against respiratory and digestive system infections, yet its increasing association with severe immune hemolytic reactions requires heightened vigilance from pediatricians. This report details a rare and severe case of ceftriaxone-induced severe immune hemolytic anemia (IHA), hemolytic crisis, myocardial injury, liver injury, renal calculi, and cholecystolithiasis in a previously healthy 3-year-old child. The child, treated for bronchitis, experienced sudden pallor, limb stiffness, and altered consciousness following the fifth day of ceftriaxone infusion, with hemoglobin (Hb) levels precipitously dropping to 21 g/L. Immediate cessation of ceftriaxone and the administration of oxygen therapy, blood transfusion, intravenous immunoglobulin (IVIG), and corticosteroids led to a gradual recovery. Despite initial improvements, the patient's condition necessitated extensive hospital care due to complications including myocardial injury, liver injury, renal calculi, and cholecystolithiasis. After a 12-day hospital stay and a 3-month follow-up, the child showed complete normalization of Hb and liver function and resolution of calculi. In children, ceftriaxone infusion may trigger severe, potentially fatal, hemolytic reactions. Pediatricians must promptly recognize symptoms such as pallor, limb stiffness, and unresponsiveness, indicative of ceftriaxone-induced severe IHA, and immediately discontinue the drug. Effective management includes timely blood transfusion, respiratory support, IVIG administration, and corticosteroids when necessary, along with rigorous vital signs monitoring. Continued vigilance is imperative, even after cessation of ceftriaxone, to promptly address any residual adverse effects. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to analyze the impact of the number and extranodal extension (ENE) of positive parotid lymph nodes (LNs) on distant metastasis in parotid cancer. Methods: Patients with surgically treated parotid cancer were retrospectively enrolled. The hazard ratios (HRs) of the number and ENE of positive parotid LNs on distant metastasis-free survival (DMFS) were evaluated. Results: In the Cox model, the groups with zero and one positive LN had comparable 10-year DMFS, but those with two positive LNs had an HR of 2.11 (95% CI: 1.36-5.29), and those with three or more positive LNs had an HR of 3.31 (95% CI: 2.05-8.43). The presence of ENE in parotid LNs did not impact the DMFS (p = 0.462; HR: 2.17; 95% CI: 0.84-6.17). Conclusion: Parotid LN metastasis was associated with decreased DMFS; this effect was mainly driven by the number of positive LNs rather than ENE. [ABSTRACT FROM AUTHOR]

Paeonia ostii, a widely cultivated tree peony species in China, is a resourceful plant with medicinal, ornamental and oil value. However, fleshy roots lead to a low tolerance to waterlogging in P. ostii. In this study, P. ostii roots were sequenced using a hybrid approach combining single-molecule real-time and next-generation sequencing platforms to understand the molecular mechanism underlying the response to this sequentially waterlogging stress, the normal growth, waterlogging treatment (WT), and waterlogging recovery treatment (WRT). Our results indicated that the strategy of P. ostii, in response to WT, was a hypoxic resting syndrome, wherein the glycolysis and fermentation processes were accelerated to maintain energy levels and the tricarboxylic acid cycle was inhibited. P. ostii enhanced waterlogging tolerance by reducing the uptake of nitrate and water from the soil. Moreover, transcription factors, such as AP2/EREBP, WRKY, MYB, and NAC, played essential roles in response to WT and WRT. They were all induced in response to the WT condition, while the decreasing expression levels were observed under the WRT condition. Our results contribute to understanding the defense mechanisms against waterlogging stress in P. ostii. [ABSTRACT FROM AUTHOR]

Objectives: To determine the predictor for occult neck metastases and the role of elective neck dissection (END) in cT3-4N0 parotid adenoid cystic carcinoma (ACC). Methods: Patients with surgically treated parotid ACC were retrospectively enrolled. Predictors of occult neck metastases and the effect of END on disease specific survival (DSS), overall survival (OS), locoregional control survival (LRC), and distant metastasis free survival (DMS) were analyzed. Results: Occult neck metastases occurred in 35 (19.7%) of the 178 patients undergoing an END. The tumor stage [p=0.011, 4.215 (1.387-10.435)] and intra-parotid lymph node metastasis [p=0.032, 3.671 (1.693-8.775)] were related to the possibility of occult neck metastases independently. The END group had better 10-year LRC than the observation group (56% vs. 43%, p=0.002) and also better 10-year DMS than the observation group (43% vs. 32%, p<0.001). The two groups had similar 10-year DSS (40% vs. 33%, p=0.230) and OS (31% vs. 23%, p=0.094) rates. Furthermore, the Cox model confirmed that END was independently associated with better LRC rate [p=0.022, 2.576 (1.338-6.476)] and better DMS [p=0.011, 2.343 (1.274-7.462)]. Conclusions: Occult neck metastases in cT3-4N0 parotid ACC was not common. A T4 tumor with intra-parotid lymph node metastasis had the highest possibility of occult neck metastases. END had no effect on DSS or OS but significantly decreased the risk of locoregional recurrence and distant metastasis. [ABSTRACT FROM AUTHOR]

Objectives: To explore the possible risk factors of orocutaneous fistula (OCF) development in free flap reconstruction of the tongue/floor of the mouth (TFOM). Methods: Data of patients who underwent free flap reconstruction of the TFOM were retrospectively analyzed. The association between clinicopathologic variables and OCF occurrence was analyzed using univariate and multivariate analyses. Results: Altogether, 469 patients were enrolled. OCF occurred in 43 patients with a rate of 9.2%. The univariate analysis revealed the negative effects of smoking, preoperative albumin level, cachexia, T4 stage, neck dissection, entire resection of the floor of the mouth (FOM), segmental mandibulectomy, and surgical site infection on OCF occurrence. The multivariate analysis confirmed the independence of cachexia (p<0.001, 4.386[1.883–9.472]), tumor stage (p<0.001, 2.738[1.482–6.629]), entire FOM resection (p<0.001, 6.332[2.110– 14.432]), and surgical site infection (p<0.001, 5.376[1.998–11.218]) in affecting the OCF development. Conclusions: OCF development following free flap reconstruction of the TFOM was relatively uncommon, but significantly associated with presence of cachexia, T4 stage, entire FOM resection, and surgical site infection. [ABSTRACT FROM AUTHOR]

Several genes related to mitochondrial functions have been identified as causative genes of neuropathy or ataxia. Cytochrome c oxidase assembly factor 7 (COA7) may have a role in assembling mitochondrial respiratory chain complexes that function in oxidative phosphorylation. Here we identified four unrelated patients with recessive mutations in COA7 among a Japanese case series of 1396 patients with Charcot-Marie-Tooth disease (CMT) or other inherited peripheral neuropathies, including complex forms of CMT. We also found that all four patients had characteristic neurological features of peripheral neuropathy and ataxia with cerebellar atrophy, and some patients showed leukoencephalopathy or spinal cord atrophy on MRI scans. Validated mutations were located at highly conserved residues among different species and segregated with the disease in each family. Nerve conduction studies showed axonal sensorimotor neuropathy. Sural nerve biopsies showed chronic axonal degeneration with a marked loss of large and medium myelinated fibres. An immunohistochemical assay with an anti-COA7 antibody in the sural nerve from the control patient showed the positive expression of COA7 in the cytoplasm of Schwann cells. We also observed mildly elevated serum creatine kinase levels in all patients and the presence of a few ragged-red fibres and some cytochrome c oxidase-negative fibres in a muscle biopsy obtained from one patient, which was suggestive of subclinical mitochondrial myopathy. Mitochondrial respiratory chain enzyme assay in skin fibroblasts from the three patients showed a definitive decrease in complex I or complex IV. Immunocytochemical analysis of subcellular localization in HeLa cells indicated that mutant COA7 proteins as well as wild-type COA7 were localized in mitochondria, which suggests that mutant COA7 does not affect the mitochondrial recruitment and may affect the stability or localization of COA7 interaction partners in the mitochondria. In addition, Drosophila COA7 (dCOA7) knockdown models showed rough eye phenotype, reduced lifespan, impaired locomotive ability and shortened synaptic branches of motor neurons. Our results suggest that loss-of-function COA7 mutation is responsible for the phenotype of the presented patients, and this new entity of disease would be referred to as spinocerebellar ataxia with axonal neuropathy type 3. [ABSTRACT FROM AUTHOR]

Objective: To analyze the serotype distribution and drug resistance of Streptococcus pneumoniae isolated from pediatric patients in a Chinese hospital. Methods: From October 2011 to May 2014, we collected 284 isolates (including 217 noninvasive and 67 invasive strains). We tested the antimicrobial susceptibility of these specimens using the Epsilomer test and disk diffusion method, and the expression of macrolide resistant genes ermB and mefA by polymerase chain reaction. Results: The most common serotype for 217 noninvasive strains was 19F (31.3%). The coverage rates of the 7-, 10-, and 13-valent pneumococcal conjugate vaccines (PCV7, PCV10, and PCV13) were 53.9%, 53.9%, and 86.2%, respectively. For 67 invasive strains, the most common serotype was 23F (22.4%). The coverage rates of PCV7, PCV10, and PCV13 for invasive strains were 77.6%, 82.1%, and 91.0%, respectively. The susceptibility of strains isolated from nonmeningitis specimens to penicillin (PEN) was 97.2%. The rate of multidrug resistance in 284 isolates was 98.7%. All of these isolates were resistant to erythromycin (ERY) and had the ermB gene; 38.6% of those isolates had the mefA gene. Conclusions: Compared with PCV7 and PCV10, the coverage rate of PCV13 was relatively higher for the S. pneumoniae isolates from pediatric patients. This finding suggests that PCV13 probably plays the strongest role in prevention of pneumococcal diseases and control of multidrug resistance. Because pneumococci were sensitive to PEN, this drug is still the preferred choice for clinical treatment of pediatric pneumococcal diseases. [ABSTRACT FROM AUTHOR]

Background: Hereditary sensory and autonomic neuropathy (HSAN) type II with WNK1/HSN2 gene mutation is a rare disease characterized by early-onset demyelination sensory loss and skin ulceration. To the best of our knowledge, no cases of an autonomic disorder have been reported clearly in a patient with WNK/HSN2 gene mutation and only one case of a Japanese patient with the WNK/HSN2 gene mutation of HSAN type II was previously reported. Case presentation: Here we describe a 54-year-old woman who had an early childhood onset of insensitivity to pain; superficial, vibration, and proprioception sensation disturbances; and several symptoms of autonomic failure (e.g., orthostatic hypotension, fluctuation in body temperature, and lack of urge to defecate). Genetic analyses revealed compound homozygous mutations in the WNK1/HSN2 gene (c.3237_3238insT; p.Asp1080fsX1). The patient demonstrated sensory loss in the "stocking and glove distribution" but could perceive visceral pain, such as menstrual or gastroenteritis pain. She experienced frequent fainting episodes. She had undergone exenteration of the left metatarsal because of metatarsal osteomyelitis at 18 years. Sural nerve biopsy revealed a severe loss of myelinated and unmyelinated nerves. She complained of severe pain in multiple joints, even on having pain impairment. Although non-steroidal anti-inflammatory drugs are generally more effective than acetaminophen for arthritis, in our case, they were ineffective and acetaminophen (2400 mg/day) adequately controlled her pain and improved quality of life. Over 3 months, the numerical rating scale, pain interference scale of the Brief Pain Inventory, and the Pain Catastrophizing Scale decreased from 6/10 to 3/10, from 52/70 to 20/70, and from 22/52 to 3/52 points, respectively. Conclusions: This is the second reported case of a Japanese patient with WNK/HSN2 gene mutation of HSAN type II and the first reported case of an autonomic disorder in a patient with the WNK/HSN2 gene mutation. Acetaminophen adequately controlled arthropathy related pain in a patient with congenital impairment of pain sensation. [ABSTRACT FROM AUTHOR]

Objective: To explore the clinical significance of 3-phosphoinositide-dependent protein kinase-1 (PDK1) expression in hepatocellular carcinoma (HCC) and its association with clinicopathologic features and prognosis in HCC patients. Materials and methods: A total of 128 HCC patients who received radical resection were enrolled from Wenling Maternal and Child Health Care Hospital between May 2005 and December 2008, and tumor and adjacent tissue samples were collected. Expression of PDK1 was detected by immunohistochemistry method. Correlation of PDK1 expression with clinicopathological features and prognosis was determined by Spearman's correlation analysis. Impact of expression of PDK1 on overall survival and recurrence was determined by Kaplan-Meier analysis. Results: Immunohistochemistry results showed that PDK1 expression in HCC tissues was significantly higher than that in the corresponding adjacent cancer tissues. Univariate analysis showed that PDK1 messenger RNA expression can predict time to recurrence with diagnostic significance (P=0.001). Univariate analysis showed that alpha-fetoprotein level, tumor number, tumor encapsulation, microvascular invasion, and tumor-node-metastasis stage were also unfavorable prognostic variables for recurrence (P<0.05). Kaplan-Meier analysis showed that overexpression of PDK1 correlates with significantly shorter postoperative overall survival and higher recurrence rates (hazard ratio =2.68; 95% confidence interval: 2.46-4.42, P=0.001) in HCC patients after curative resection. Conclusion: Our study indicated that PDK1 may serve as a candidate pro-oncogene and a potential prognostic biomarker for HCC. [ABSTRACT FROM AUTHOR]

To investigate the effects of signal transducer and activator of transcription 3 (STAT3) combined with cisplatin (CDDP) on the growth of human Wilms tumour (WT) SK-NEP-1 cell subcutaneous xenografts in nude mice and the possible mechanisms. Human WT SK-NEP-1 cells were subcutaneously transplanted to establish the BALB/c nude mice xenograft model. Mice were randomly divided into five groups: blank control group, adenovirus control group (NC group), STAT3 group, CDDP group and STAT3 plus CDDP group (combination group). Tumour volume and tumour weight were observed during the therapeutic process. The expression levels of STAT3, glucose regulatory protein 78 (GRP78) and BCL2-associated X protein (BAX) were evaluated by immunohistochemical analysis. Compared with the STAT3 group or CDDP group, the tumour weight and volume was significantly reduced in the combination group (P<0.05). No statistical significance was found in NC group compared with the blank control group (P>0.05). Immunohistochemical analysis showed that STAT3, GRP78 and BAX protein levels in the combination group were significantly higher than those in STAT3 group and CDDP group (P<0.05). Exogenous STAT3 and CDDP may synergistically inhibit the xenograft tumour growth through up-regulation of BAX protein via GRP78. [ABSTRACT FROM AUTHOR]