Optimized nitrogen (N) management (OPT), with reduced total N input and more N applied during panicle development, has been proved to increase grain yield of rice through panicle enlargement. However, the changes in panicle architecture and source of variation are not well understood. A hybrid rice variety named Tianyou 3618 was subjected to OPT and farmer\'s fertilizer practice (FFP) in early cropping seasons of 2016 and 2017. With 16.7 % less N input, OPT increased panicle size by 8.6 % and 27.4 %, and grain yield by 13.8 % and 12.3 % for 2016 and 2017, respectively. OPT had greater dry matter accumulation and N uptake from panicle initiation to heading, which bolstered panicle enlargement. The number of surviving florets per branch was quite constant under different N treatments for all primary, secondary, and tertiary branches, implying that panicle size was mainly determined by the number of branches rather than the number of florets per branch. Little change was observed between OPT and FFP in differentiation, degeneration and survival of primary branches and their florets. Surviving secondary and tertiary branches and their florets were significantly more under OPT than those under FFP. The increase in surviving secondary branches under OPT resulted from both enhanced differentiation and reduced degeneration. While the increase in surviving tertiary branches under OPT was merely from enhanced differentiation though their degeneration was also dramatically increased. Among the increased differentiated florets under OPT, 32.4%-36.3 % and 61.6%-67.7 % came from secondary and tertiary branches, respectively. Among the increased surviving florets under OPT, 62.2%-65.2 % and 32.5%-37.8 % came from secondary and tertiary branches, respectively. Both secondary branches and tertiary branches were principal contributors to the increase in panicle size of OPT. To our knowledge, this is the first report on the detailed changes in panicle architecture and their involvement in panicle enlargement and yield gain under OPT.

BACKGROUND: Aberrant occlusion and aging are two main risks for temporomandibular joint (TMJ) degeneration.
OBJECTIVE: To assess the combined impact of occlusion and age on TMJ disc.
METHODS: To avoid the confounding impact of gender, presently, 126 female C57BL/6J mice, 63 youngsters, 6-week old and 63 adults, 28-week old, were used. An experimental bilateral anterior crossbite (BAC) relation was created by installing metal tubes onto the mandibular incisors. Mice were sacrificed at 3, 7 and 11 weeks (n = 9). Additionally, the installed tubes were removed at 7 weeks in removal groups and the TMJs were sampled after another 4 weeks (n = 9). Disc changes were detected by histomorphology, immunohistochemistry, and western blot assays.
RESULTS: Disc deformation was obvious in BAC groups. The typical change was hyperplasia at the posterior region of the disc where there was significant infiltration of inflammatory cells. Expressions of the inflammatory markers, including tumour necrosis factor-α and interleukin-1β, and the catabolic markers, including fibronectin (FN), FN N-terminal fragments, and vascular endothelial growth factor-A, were all increased. The changes were more obvious in adults than in youngsters. Removal of BAC attenuated inflammatory and catabolic changes in the youngsters, but the inflammatory markers recovered little in the adults.
CONCLUSIONS: TMJ disc responds to BAC by degeneration and inflammation, and respond to BAC removal by rehabilitation. Adult discs show severer degeneration responses to BAC and a lower level of anti-inflammatory capability to BAC removal than the youngster\'s discs. Animals cannot be equated with humans. The human disc response to occlusion changes worth further exploration.

The silkworm is an incredibly valuable insect that produces silk through its silk gland. Within this organ, Fibroinase has been identified and named due to its ability to fibroin degradation. The expression of Fibroinase in the silk gland significantly increases during the larval-pupal stage, which might be associated with the degeneration of the silk gland. In this study, Fibroinase was overexpressed and knocked down specifically both in the middle and posterior silk glands, respectively, using transgenic technology. The investigation of silk gland development in these transgenic silkworms showed that Fibroinase plays a direct role in accelerating silk gland degeneration. The staining analyses performed in the silk glands of transgenic silkworms suggest that Fibroinase is involved in the processes of autophagy and apoptosis during silk gland degeneration. Further experiments demonstrated that Fibroinase, acting as a lysosomal regulator, negatively regulates autophagy via the mTOR (mechanistic target of rapamycin) pathway. Moreover, during apoptosis, Fibroinase could activate Caspase3 by increasing the activity of BmCaspase1, ultimately accelerating the apoptosis process. These findings enhance our understanding of the physiological role of Fibroinase in promoting silk gland degeneration, which plays a role in breaking down proteins in the silk gland and coordinating the regulation of autophagy and apoptosis.

BACKGROUND: The contribution of cholinergic degeneration to gait disturbance in Parkinson\'s disease (PD) is increasingly recognized, yet its relationship with dopaminergic-resistant gait parameters has been poorly investigated. We investigated the association between comprehensive gait parameters and cholinergic nucleus degeneration in PD.
METHODS: This cross-sectional study enrolled 84 PD patients and 69 controls. All subjects underwent brain structural magnetic resonance imaging to assess the gray matter density (GMD) and volume (GMV) of the cholinergic nuclei (Ch123/Ch4). Gait parameters under single-task (ST) and dual-task (DT) walking tests were acquired using sensor wearables in PD group. We compared cholinergic nucleus morphology and gait performance between groups and examined their association.
RESULTS: PD patients exhibited significantly decreased GMD and GMV of the left Ch4 compared to controls after reaching HY stage > 2. Significant correlations were observed between multiple gait parameters and bilateral Ch123/Ch4. After multiple testing correction, the Ch123/Ch4 degeneration was significantly associated with shorter stride length, lower gait velocity, longer stance phase, smaller ankle toe-off and heel-strike angles under both ST and DT condition. For PD patients with HY stage 1-2, there were no significant degeneration of Ch123/4, and only right side Ch123/Ch4 were corrected with the gait parameters. However, as the disease progressed to HY stage > 2, bilateral Ch123/Ch4 nuclei showed correlations with gait performance, with more extensive significant correlations were observed in the right side.
CONCLUSIONS: Our study demonstrated the progressive association between cholinergic nuclei degeneration and gait impairment across different stages of PD, and highlighting the potential lateralization of the cholinergic nuclei\'s impact on gait impairment. These findings offer insights for the design and implementation of future clinical trials investigating cholinergic treatments as a promising approach to address gait impairments in PD.

暂无摘要。

The retina, a tissue of the central nervous system, is vital for vision as its photoreceptors capture light and transform it into electrical signals, which are further processed before they are sent to the brain to be interpreted as images. The retina is unique in that it is continuously exposed to light and has the highest metabolic rate and demand for energy amongst all the tissues in the body. Consequently, the retina is very susceptible to oxidative stress. VDAC, a pore in the outer membrane of mitochondria, shuttles metabolites between mitochondria and the cytosol and normally protects cells from oxidative damage, but when a cell\'s integrity is greatly compromised it initiates cell death. There are three isoforms of VDAC, and existing evidence indicates that all three are expressed in the retina. However, their precise localization and function in each cell type is unknown. It appears that most retinal cells express substantial amounts of VDAC2 and VDAC3, presumably to protect them from oxidative stress. Photoreceptors express VDAC2, HK2, and PKM2-key proteins in the Warburg pathway that also protect these cells. Consistent with its role in initiating cell death, VDAC is overexpressed in the retinal degenerative diseases retinitis pigmentosa, age related macular degeneration (AMD), and glaucoma. Treatment with antioxidants or inhibiting VDAC oligomerization reduced its expression and improved cell survival. Thus, VDAC may be a promising therapeutic candidate for the treatment of these diseases.

OBJECTIVE: Choroidal neovascularisation (CNV) in patients with X-linked retinoschisis (XLRS) has been poorly documented. This study aims to investigate the prevalence and clinical characteristics of CNV in patients with XLRS, as well as analyse the preliminary genotype-phenotype correlation.
METHODS: A retrospective case series of patients with genetically confirmed XLRS was included. Demographic, clinical and genetic features were analysed, with a comparison between CNV and non-CNV eyes.
RESULTS: Among 185 eyes of 129 patients with XLRS, the prevalence of CNV was 8.1% (15/185). The mean diagnostic age of all patients with CNV is 5.1±2.56 years. CNV eyes exhibited a mean best-corrected visual acuity (BCVA) (logarithm of the minimal angle of resolution) of 1.37±0.74. All CNVs were classified as subretinal and active. Peripapillary CNVs accounted for 80.0% (12/15), while subfoveal CNVs accounted for 20.0% (3/15). In CNV eyes, the prevalence of macular atrophy (5/15, 33.3%, p=0.013) and bullous peripheral schisis (14/15, 93.3%, p=0.000) was higher compared with non-CNV eyes. Additionally, CNV eyes exhibited poorer integrity of the outer retina and BCVA (p=0.007) compared with non-CNV eyes. All 15 eyes with CNV underwent anti-vascular endothelial growth factor (anti-VEGF) therapy. Genotype analysis revealed that 7 of 10 patients (70.0%, 10 eyes) were predicted to have missense variants, while 3 of 10 patients (30.0%, 5 eyes) exhibited severe variants.
CONCLUSIONS: The prevalence of CNV in XLRS eyes was found to be 8.1%. All CNVs secondary to XLRS were active and classified as type 2. CNV eyes demonstrated poorer visual function and compromised retinal structures. Anti-VEGF therapy demonstrated effectiveness in treating XLRS-CNVs. No significant genotype-phenotype correlation was established.

OBJECTIVE: This study analyzed and explored the relationship between isthmic spondylolisthesis and disc degeneration by comparing the degree of disc degeneration in patients with isthmic spondylolisthesis, lumbar disc herniation, and asymptomatic healthy individuals.
METHODS: This study included a total of 138 cases, consisting of L5-S1 single segment lesion patients and a normal lumbar spine population. The cases were divided into 3 groups based on the type of disease: fifty eight cases in the isthmic spondylolisthesis (IS) group, 50 cases in the lumbar disc herniation (LDH) group, and 30 cases in the normal lumbar vertebrae (NLV) group.
RESULTS: The research findings indicate that the proportion of intervertebral disc degeneration in the LDH group is significantly higher than that in the IS group and NLV group (65.3% vs. 33.3% vs. 25.8%, P < 0.05). The Pfirrmann grades of lumbar intervertebral discs (L1-L4) in the LDH group are significantly higher than those in the IS group and NLV group (P < 0.05), and the intervertebral height index (IHI) (L1-L4) of lumbar vertebrae in the LDH group is significantly lower than that in the IS group and NLV group (P < 0.05).
CONCLUSIONS: The results showed that the degree of intervertebral disc degeneration in patients with isthmic spondylolisthesis was lighter than that in patients with LDH, and even similar to that in healthy individuals. The occurrence of IS may have slowed down the degeneration of nonaffected segment intervertebral discs through certain factors.

OBJECTIVE: This study aims to assess the impact of surgical approaches and other factors on the incidence of Adjacent Segment Degeneration (ASD) following Spinal Fusion for Adolescent Idiopathic Scoliosis (AIS).
METHODS: We conducted a comprehensive search of four electronic databases from their inception until March 30, 2023. Two independent reviewers screened titles, abstracts, and full texts and evaluated the methodological quality of the studies. A random-effects model was used to calculate the incidence of ASD.
RESULTS: Our analysis included 14 studies involving 651 individuals. The overall incidence of ASD was 47% (95%CI: 0.37, 0.56). Subgroup analyses revealed that the prevalence of ASD increased with postoperative time (53% (95%CI: 0.31, 0.75) versus 48% (95%CI: 0.36, 0.60) versus 39% (95%CI: 0.22, 0.56)). For the number of fused segments, a group with more than 10 segments had a higher prevalence (49% (95%CI: 0.38, 0.60) versus 44% (95%CI: 0.21, 0.69)). In terms of regions, East Asia had the highest prevalence, followed by Occident and West Asia (52% (95%CI: 0.41, 0.62) versus 43% (95%CI: 0.20, 0.68) versus 37% (95%CI: 0.17, 0.59)). However, the surgical approach, male ratio, and the position of the lowest instrumented vertebra (LIV) did not show significant differences between groups. Funnel plots and Egger\'s test did not reveal any significant publication bias (Egger\'s test: t = 1.62, p-value = .1274).
CONCLUSIONS: This meta-analysis found that nearly half of AIS patients following spinal fusion surgery experienced ASD. Long-term follow-up, regular screening, and timely interventions are essential to reduce the prevalence of ASD.

Aging entails the deterioration of the body\'s organs, including overall damages at both the genetic and cellular levels. The prevalence of age-related ocular disease such as macular degeneration, dry eye diseases, glaucoma and cataracts is increasing as the world\'s population ages, imposing a considerable economic burden on individuals and society. The development of age-related ocular disease is predominantly triggered by oxidative stress and chronic inflammatory reaction. Heme oxygenase-1 (HO-1) is a crucial antioxidant that mediates the degradative process of endogenous iron protoporphyrin heme. It catalyzes the rate-limiting step of the heme degradation reaction, and releases the metabolites such as carbon monoxide (CO), ferrous, and biliverdin (BV). The potent scavenging activity of these metabolites can help to defend against peroxides, peroxynitrite, hydroxyl, and superoxide radicals. Other than directly decomposing endogenous oxidizing substances (hemoglobin), HO-1 is also a critical regulator of inflammatory cells and tissue damage, exerting its anti-inflammation activity through regulating complex inflammatory networks. Therefore, promoting HO-1 expression may act as a promising therapeutic strategy for the age-related ocular disease. However, emerging evidences suggest that the overexpression of HO-1 significantly contributes to ferroptosis due to its dual nature. Surplus HO-1 leads to excessive Fe2+ and reactive oxygen species, thereby causing lipid peroxidation and ferroptosis. In this review, we elucidate the role of HO-1 in countering age-related disease, and summarize recent pharmacological trials that targeting HO-1 for disease management. Further refinements of the knowledge would position HO-1 as a novel therapeutic target for age-related ocular disease.