We analyzed viral nucleic acids in stool samples collected from 35 South Asian children with nonpolio acute flaccid paralysis (AFP). Sequence-independent reverse transcription and PCR amplification of capsid-protected, nuclease-resistant viral nucleic acids were followed by DNA sequencing and sequence similarity searches. Limited Sanger sequencing (35 to 240 subclones per sample) identified an average of 1.4 distinct eukaryotic viruses per sample, while pyrosequencing yielded 2.6 viruses per sample. In addition to bacteriophage and plant viruses, we detected known enteric viruses, including rotavirus, adenovirus, picobirnavirus, and human enterovirus species A (HEV-A) to HEV-C, as well as numerous other members of the Picornaviridae family, including parechovirus, Aichi virus, rhinovirus, and human cardiovirus. The viruses with the most divergent sequences relative to those of previously reported viruses included members of a novel Picornaviridae genus and four new viral species (members of the Dicistroviridae , Nodaviridae , and Circoviridae families and the Bocavirus genus). Samples from six healthy contacts of AFP patients were similarly analyzed and also contained numerous viruses, particularly HEV-C, including a potentially novel Enterovirus genotype. Determining the prevalences and pathogenicities of the novel genotypes, species, genera, and potential new viral families identified in this study in different demographic groups will require further studies with different demographic and patient groups, now facilitated by knowledge of these viral genomes.

This study was to evaluate effects of mixed plant oils (identified as mixed oil 1 [MO1] and mixed oil 2 [MO2]) on performance, serum composition, viscera percentages, meat quality, and fatty acid deposition of broilers. A total of 126 one-day-old Arbor Acres male broiler chicks (weighing 44.91±0.92 g) were randomly allocated to 1 of 3 treatments with 7 replicate pens per treatment (6 broilers per pen). Dietary treatments included a corn-soybean basal diet supplemented with 3% soybean oil (CTR), basal diet with 3% MO1 (a mixture of 15% corn oil, 10% coconut oil, 15% linseed oil, 20% palm oil, 15% peanut oil and 25% soybean oil; MO1), or basal diet with 3% MO2 (a combination of 50% MO1 and 50% extruded corn; MO2). The trial consisted of phase 1 (d 1 to 21) and phase 2 (d 22 to 42). Compared to CTR, broilers fed MO (MO1 or MO2) had greater (p<0.05) average daily gain in phase 1, 2, and overall (d 1 to 42), redness in thigh muscle, concentrations of serum glucose, serum albumin, saturated fatty acids (SFA) and n-6/n-3 polyunsaturated fatty acids (PUFA) ratio in breast muscle, while these broilers also showed lower (p≤0.05) drip loss and concentrations of C18:3n-3 and PUFA/SFA ratio in breast muscle. Broilers fed MO2 had higher (p<0.05) liver percentage, while broilers fed MO1 had lower (p≤0.05) feed conversion ratio in phase 1 and increased (p<0.05) contents of C18:2n-6, C20:5n-3, C22:6n-3, and n-3 PUFA in breast muscle compared to CTR. Mixed plant oils had positive effects on performance, serum parameters, meat quality, liver percentage and fatty acid deposition in broilers, which indicates they can be used as better dietary energy feedstocks than soybean oil alone.

Context The evidence of long-term polyethylene glycol recombinant human GH (PEG-rhGH) in pediatric GH deficiency (GHD) is limited. Objective This study aimed to examine the effectiveness and safety of long-term PEG-rhGH in children with GHD in the real world, as well as to examine the effects of dose on patient outcomes. Design A prospective, observational, posttrial study (NCT03290235). Setting, participants and intervention Children with GHD were enrolled from 81 centers in China in 4 individual clinical trials and received weekly 0.2 mg/kg/wk (high-dose) or 0.1 to <0.2 mg/kg/wk (low-dose) PEG-rhGH for 30 months. Main outcomes measures Height SD score (Ht SDS) at 12, 24, and 36 months. Results A total of 1170 children were enrolled in this posttrial study, with 642 patients in the high-dose subgroup and 528 in the low-dose subgroup. The Ht SDS improved significantly after treatment in the total population (P < 0.0001), with a mean change of 0.53 ± 0.30, 0.89 ± 0.48, 1.35 ± 0.63, 1.63 ± 0.75 at 6 months, 12 months, 24 months, and 36 months, respectively. In addition, the changes in Ht SDS from baseline were significantly improved in the high-dose subgroup compared with the low-dose subgroup at 6, 12, 24, and 36 months after treatment (all P < 0.05). A total of 12 (1.03%) patients developed serious adverse events. There was no serious adverse event related to the treatment, and no AEs leading to treatment discontinuation or death occurred. Conclusions PEG-rhGH showed long-term effectiveness and safety in treating children with GHD. Both dose subgroups showed promising outcomes, whereas PEG-rhGH 0.2 mg/kg/wk might show additional benefit.

The purpose of this study is to compare the relative efficacy and safety of long-acting growth hormone (LAGH) as a growth hormone replacement therapy in prepubertal children with growth hormone deficiency (GHD). We searched the PubMed, Embase, CNKI, and Wanfang databases from inception to July 2023 and identified eleven relevant studies. PEG-LAGH showed better effect on height velocity (mean difference [MD]: − 0.031, 95% credibility interval [CrI]: − 0.278, 0.215) than somatrogon (MD: 0.105, 95% CrI: − 0.419, 0.636), somapacitan (MD: 0.802, 95% CrI: − 0.451, 2.068) and lonapegsomatropin (MD: 1.335, 95% CrI: − 0.3, 2.989) when compared with daily growth hormone (DGH). Furthermore, in terms of height standard deviation score, PEG-LAGH demonstrated better improvement (MD: − 0.15, 95% CrI: − 1.1, 0.66) than somatrogon (MD: − 0.055, 95% CrI: − 1.3, 0.51) and somapacitan (MD: 0.22, 95% CrI: − 0.91, 1.3). PEG-LAGH (risk ratio [RR]: 1.00, 95% CrI: 0.82, 1.2) reduced the risk of adverse events compared with other LAGH (somatrogon, RR: 1.1, 95% CrI: 0.98, 1.2; somapacitan, RR: 1.1, 95% CrI: 0.96, 1.4; lonapegsomatropin, RR, 1.1, 95% CrI: 0.91, 1.3) and was comparable with DGH. This is the first study to indirectly compare the LAGH thorough a network meta-analysis and provide evidence of the optimal efficacy of various LAGH specifically PEG-LAGH and acceptable safety profile in prepubertal children with GHD.

This study aimed to investigate the effects of dietary LY or LY combined with ZnO supplementation on performance and gut health in nursery pigs. 192 Duroc × Landrace × Yorkshire piglets (weaned on d 32 of the age with 9.2 ± 1.7 kg BW) were allocated into four treatments with eight replicate pens, six piglets per pen. The treatments included a basal diet as control (CTR), an antibiotic plus ZnO diet (CTC-ZnO, basal diet + 75 mg/kg of chlortetracycline + ZnO (2000 mg/kg from d 1 to 14, 160 mg/kg from d 15 to 28)), a LY diet (LY, basal diet + 2 g/kg LY), and a LY plus ZnO diet (LY-ZnO, basal diet + 1 g/kg LY + ZnO). The results showed that pigs fed LY or LY-ZnO had increased (p < 0.05) average daily gain, serum IgA, IgG, superoxide dismutase, fecal butyric acid, and total volatile fatty acid concentrations, as well as decreased (p < 0.05) feed conversion ratio and diarrhea rate compared with CTR. In conclusion, pigs fed diets with LY or LY combined with ZnO had similar improvement to the use of antibiotics and ZnO in performance, antioxidant status, immunoglobulins, and gut health in nursery pigs.

Gitelman syndrome (GS) is an autosomal recessive disorder and mild variant of classic Bartter syndrome. The latter is caused by defects in the genes CLCNKB and/or CLCNKA (chloride voltage-gated channel Ka and Kb). Patients with GS usually have loss-of-function mutations in SLC12A3. No patient has been reported with compound heterozygous mutations in these genes. We report a girl with GS with a paternally inherited heterozygous mutation in SLC12A3, and maternally inherited heterozygous variants in both CLCNKB and CLCNKA. In this report, we reported a female patient (8 y and 10 mo) who had growth retardation (111.8 cm, − 1.62 standard deviation height for age) and normal blood pressure, with persistent hypokalemia, hypomagnesemia, hypocalciuria, hypochloremic alkalosis, and elevated levels of plasma renin and aldosterone. Her younger brother, father, and paternal grandmother all had histories of mild low levels of plasma potassium (3.0–3.5 mmol/L), which were rectified by potassium-rich foods. The genomic DNA of the patient, younger brother, parents, and grandparents were screened for gene variations and pedigree analysis using trio whole exome sequencing (WES). The candidate variants were validated by Sanger sequencing. Protein-protein interaction analysis utilized the following databases: Biogrid, MINT, HPRD, STRING, IntAct, iRefIndex, and ppiTrim. The trio WES screening showed that the patient has paternally inherited SLC12A3 p.N359K, and maternally inherited CLCNKB p.L94I. The paternal grandmother and younger brother are both carriers of SLC12A3 p.N359K. According to the STRING database, SLC12A3 and CLCNKB proteins may interact or coexpress with proteins associated with GS. Based on clinical phenotypes, genetic evidence of the pedigree, and previous reported studies, this case of GS indicates a digenetic inheritance of SLC12A3 and CLCNKB that resulted in renal tubular dysfunction perhaps, due to a genetic double-hit mechanism. The putative pathogenicity of the CLCNKB p.L94I variant requires confirmation.