Barriers and facilitators to the formation of professional identity among nursing students: A four-year longitudinal qualitative study.

BACKGROUND: Nursing professional identity (NPI) is essential for nurses to develop their nursing profession. It reflects the competencies consistent with the professional practices of nurses and contributes to them providing better healthcare and public health. The formation process of NPI started with undergraduate nursing education and continued throughout the nursing career. OBJECTIVE: To explore nursing students' perceptions of facilitators and barriers to the formation of NPI during their study. METHODS: A 4-year longitudinal, qualitative research design with yearly semi-structured interviews undertaken from 2019 to 2022. The reflexive thematic analysis methodology was applied for the data analysis. RESULTS: Ninety-three nursing students were recruited, joining a group or individual interview. The four-year nursing baccalaureate program revealed a dynamic formation process of NPI: "Outsider of nursing", "Entering the nursing courses", "Building nursing competence", and "Thinking and acting like a nurse". A total of 12 themes were identified to present the barriers and facilitators to the NPI formation at different stages. Specifically, the six barriers include conflict between their ideals and reality, sociocultural stereotypes about nursing, the negative impact of COVID-19, the pre-internship concerns, struggling to meet expectations, and potential danger and discrimination in the healthcare settings. The enablers were: self-motivation and inner belief towards the nursing profession, the power of role models, the improvement of nursing capacity, well integration into the healthcare professional teams, understanding of the clinical environment, and recognition and encouragement from others. CONCLUSIONS: The formation of nursing students' NPI is an ever-changing process, with various intrinsic and extrinsic influences during their four-year study. Nursing educators are suggested to prepare and develop students' professional comportment in their theoretical and clinical practice to develop their professional identity as a nurse.

Realizing zero-order controlled transdermal drug permeation through competing doubly ionic H-bond in patch.

Transdermal drug delivery system (TDDS) was an effective way to realize controlled drug delivery. However, realizing zero-order controlled drug skin delivery was still challenging in the drug-in-adhesive patch. This study provided a strategy to accomplish this delivery form by stabilizing the drug concentration in adhesive through concentration-dependent competitive interaction. Clonidine (CLO) and Granisetron (GRA) were chosen as the model drugs which were of high skin permeability, and polydimethylaminoethyl acrylate (EA) as an excipient to interact with hydroxyphenyl adhesive (HP). Drug release, permeation and pharmacokinetic study were conducted to evaluate the controlled effect of HP-EA. The molecular interaction was characterized by FT-IR, 1H NMR and XPS. Dynamic simulation and molecular docking further clarified the competitive interaction involved in the release process. Both the drug skin permeation study of CLO and GRA patch based on the HP-EA adhesive showed good zero-order fitting with r of 0.994 and 0.998, compared with non-functional adhesive (0-PSA). Furthermore, the pharmacokinetic study of the CLO patch showed a plateau phase for around 52 h without influencing the area under concentration-time curve (AUC), indicating that the HP-EA could realize zero-order drug skin delivery. The mechanism study revealed that EA serving as a 'buffer component' promoted the conversion of the ionic CLO to the neutrals the as the neutrals released, which stabilized '1% neutrals CLO concentration'. In conclusion, the drug delivery system based on the concentration-dependent competitive interaction broadened our understanding of the molecular mechanisms involved in zero-order controlled release in transdermal patches which would promote the development of zero-order drug delivery in TDDS.

The Multimorbidity and Lifestyle Correlates in Chinese Population Residing in Macau: Findings from a Community-Based Needs Assessment Study.

Multimorbidity has become one of the most pressing public health concerns worldwide. The objectives of this study were to understand the prevalence of multimorbidity and its relationship with lifestyle factors among Chinese adults in Macau, and to investigate the combined contribution of common lifestyle factors in predicting multimorbidity. Data were collected through face-to-face interviews using a self-reported questionnaire on common chronic diseases, lifestyle factors and sociodemographics. BMI, physical activity, drinking status, smoking status and sleep quality were assessed, and a composite lifestyle score (0 to 9 points) was calculated, and the higher the score, the healthier the lifestyle. A total of 1443 participants were included in the analysis, of whom 55.2% were female, 51.8% were middle aged or elderly and 30.5% completed tertiary education or higher. The prevalence of multimorbidity was 10.3%. The combination of hypertension and hyperlipidaemia was the most common (22.2%) multimorbidity among the participants with multimorbidity. After the adjustment of the covariates, it was found that the participants who were overweight (OR: 1.95, 95% CI: 1.18-3.20, p = 0.009) or obese (OR: 3.76, 95% CI: 2.38-5.96, p < 0.001), former drinkers (OR: 2.43, 95% CI: 1.26-4.69, p = 0.008), and those who reported poor sleep quality (OR: 2.25, 95% CI: 1.49-3.40, p < 0.001) had a high risk of developing multimorbidity. A one-unit increase in the lifestyle score was associated with a 0.33-times reduction in the risk of developing multimorbidity (OR: 0.67; 95% CI: 0.59-0.77, p < 0.001). A combination of lifestyle factors can influence a variety of multimorbidity among the Chinese adults in Macau. Thus, comprehensively assessing the combined contribution of several lifestyle factors in predicting multimorbidity is important.

Extracellular mitochondria drive CD8 T cell dysfunction in trauma by upregulating CD39.

RATIONALE: The increased mortality and morbidity seen in critically injured patients appears associated with systemic inflammatory response syndrome (SIRS) and immune dysfunction, which ultimately predisposes to infection. Mitochondria released by injury could generate danger molecules, for example, ATP, which in turn would be rapidly scavenged by ectonucleotidases, expressed on regulatory immune cells. OBJECTIVE: To determine the association between circulating mitochondria, purinergic signalling and immune dysfunction after trauma. METHODS: We tested the impact of hepatocyte-derived free mitochondria on blood-derived and lung-derived CD8 T cells in vitro and in experimental mouse models in vivo. In parallel, immune phenotypic analyses were conducted on blood-derived CD8 T cells obtained from trauma patients. RESULTS: Isolated intact mitochondria are functional and generate ATP ex vivo. Extracellular mitochondria perturb CD8+ T cells in co-culture, inducing select features of immune exhaustion in vitro. These effects are modulated by scavenging ATP, modelled by addition of apyrase in vitro. Injection of intact mitochondria into recipient mice markedly upregulates the ectonucleotidase CD39, and other immune checkpoint markers in circulating CD8+ T cells. We note that mice injected with mitochondria, prior to instilling bacteria into the lung, exhibit more severe lung injury, characterised by elevated neutrophil influx and by changes in CD8+ T cell cytotoxic capacity. Importantly, the development of SIRS in injured humans, is likewise associated with disordered purinergic signalling and CD8 T cell dysfunction. CONCLUSION: These studies in experimental models and in a cohort of trauma patients reveal important associations between extracellular mitochondria, aberrant purinergic signalling and immune dysfunction. These pathogenic factors with immune exhaustion are linked to SIRS and could be targeted therapeutically.

Supplementation with selenium attenuates autism-like behaviors and improves oxidative stress, inflammation and related gene expression in an autism disease model.

Autism spectrum disorder (ASD) refers to a group of neurodevelopmental disorders. The etiology and pathological mechanisms of ASD are still unknown, and its prognosis is poor. This study investigated the effects of selenium (Se) supplementation on abnormal behavior and cognitive function in ASD model mice, as well as the potential action pathways. BTBR mice were randomly assigned to either a model group (BTBR group), a model selenium supplement group (BTBR+Se group), a normal control group (B6 group) or a normal selenium supplement group (B6+Se group). Sodium selenite, at a dosage of 1 mg/kg/day, was administered to the selenium supplementation groups by gavage. The mice in the BTBR group and the B6 group received the same amount of 0.9% saline by gavage. After 4 weeks of continuous intervention, the social functions and cognitive behaviors of the mice and the selenium concentration in hippocampal tissue were assessed. Hippocampal tissue structures were observed. Changes in neurotransmitter levels, oxidative stress and neuroinflammatory indicators were detected. SelP protein expression was significantly lower in hippocampal tissue from BTBR mice than in hippocampal tissue from B6 mice. The administration of sodium selenite in BTBR mice: (1) increased the expression of SelP; (2) attenuated spatial learning, memory impairment and improved social behaviors; (3) changed the serum levels of 5-HT, DA and Glu; (4) decreased the levels of inflammatory cytokines IL-6, IL-1ß, and TNF-α in serum and hippocampal tissue; (5) reduced the ROS and MDA contents and significantly increased SOD activity, CAT activity, GSH-px activity, and antioxidant GSH levels; and (6) protected against neuronal loss in the hippocampus. Se supplementation significantly improved the social functioning, repetitive stereotyped behavior and cognitive function in BTBR mice. Se may play a protective role in the hippocampus of BTBR mice by regulating neurotransmitter levels, reducing oxidative stress, alleviating neuroinflammation and rescuing neural cell damage.

Resonant sheath heating in weakly magnetized capacitively coupled plasmas due to electron-cyclotron motion.

An electron heating mechanism based on a resonance between the cyclotron motion of electrons and the radio frequency sheath oscillations is reported in weakly magnetized capacitively coupled plasmas at low pressure. If half of the electron cyclotron period coincides with the radio frequency period, then electrons will coherently collide with the expanding sheath and gain substantial energy, which enhances the plasma density. A relation between the magnetic field and the driving frequency is found to characterize this resonance effect and the kinetics of electrons are revealed at resonance conditions for various driving frequencies.

Monocyte exocytosis of mitochondrial danger-associated molecular patterns in sepsis suppresses neutrophil chemotaxis.

BACKGROUND: Trauma and sepsis both increase the risk for secondary infections. Injury mobilizes mitochondrial (MT) danger-associated molecular patterns (mtDAMPs) directly from cellular necrosis. It is unknown, however, whether sepsis can cause active MT release and whether mtDAMPs released by sepsis might affect innate immunity. METHODS: Mitochondrial release from human monocytes (Mo) was studied after LPS stimulation using electron microscopy and using fluorescent video-microscopy of adherent Mo using Mito-Tracker Green (MTG) dye. Release of MTG+ microparticles was studied using flow cytometry after bacterial stimulation by size exclusion chromatography of supernatants with polymerase chain reaction (PCR) for mitochondrial DNA (mtDNA). Human neutrophil (PMN), chemotaxis, and respiratory burst were studied after PMN incubation with mtDNA. RESULTS: LPS caused Mo to release mtDAMPs. Electron microscopy showed microparticles containing MT. mtDNA was present both in microvesicles and exosomes as shown by PCR of the relevant size exclusion chromatography bands. In functional studies, PMN incubation with mtDNA suppressed chemotaxis in a dose-dependent manner, which was reversed by chloroquine, suggesting an endosomal, toll-like receptor-9-dependent mechanism. In contrast, PMN respiratory burst was unaffected by mtDNA. CONCLUSION: In addition to passive release of mtDAMPs by traumatic cellular disruption, inflammatory and infectious stimuli cause active mtDAMP release via microparticles. mtDNA thus released can have effects on PMN that may suppress antimicrobial function. mtDAMP-mediated "feed-forward" mechanisms may modulate immune responses and potentially be generalizable to other forms of inflammation. Where they cause immune dysfunction the effects can be mitigated if the pathways by which the mtDAMPs act are defined. In this case, the endosomal inhibitor chloroquine is benign and well tolerated. Thus, it may warrant study as a prophylactic antiinfective after injury or prior sepsis.

Direct Airway Instillation of Neutrophils Overcomes Chemotactic Deficits Induced by Injury.

BACKGROUND: Trauma induces neutrophil migration toward injury sites, both initiating wound healing and protecting against local bacterial infection. We have previously shown that mitochondrial formyl peptides (mtFPs) released by injured tissues act as chemoattractants by ligating neutrophil (PMN) formyl peptide receptor 1 (FPR1). But this process can also internalize multiple neutrophil chemoattractant receptors and thus might limit neutrophil migration to the lung in response to bacteria. Our objective was to better understand susceptibility to pneumonia after injury and thus find ways to reverse it. METHODS AND RESULTS: We modeled the alveolar chemotactic environment in pulmonary infections by incubating Staphylococcus aureus or Escherichia coli with peripheral blood mononuclear cells. Survey of the chemotactic mediators in the resultant conditioned media (CM) showed multiple potent chemoattractants. Pretreating PMN with mtFPs to mimic injury potently reduced net migration toward CM and this net effect was mostly reversed by an FPR1 antagonist. Using an established mouse model of injury-dependent lung infection, we then showed simple instillation of exogenous unstimulated human neutrophils into the airway resulted in bacterial clearance from the lung. CONCLUSION: Injury-derived mtFPs suppress global PMN localization into complex chemotactic environments like infected alveoli. Transplantation of naive exogenous human neutrophils into the airway circumvents that pathologic process and prevents development of post-traumatic pneumonia without injury noted to the recipients.

Formyl Peptide Receptor-1 Blockade Prevents Receptor Regulation by Mitochondrial Danger-Associated Molecular Patterns and Preserves Neutrophil Function After Trauma.

OBJECTIVES: Trauma predisposes to systemic sterile inflammation (systemic inflammatory response syndrome) as well as infection, but the mechanisms linking injury to infection are poorly understood. Mitochondrial debris contains formyl peptides. These bind formyl peptide receptor-1, trafficking neutrophils to wounds, initiating systemic inflammatory response syndrome, and wound healing. Bacterial formyl peptides, however, also attract neutrophils via formyl peptide receptor-1. Thus, mitochondrial formyl peptides might suppress neutrophils antimicrobial function. Also, formyl peptide receptor-1 blockade used to mitigate systemic inflammatory response syndrome might predispose to sepsis. We examined how mitochondrial formyl peptides impact neutrophils functions contributing to antimicrobial responses and how formyl peptide receptor-1 antagonists affect those functions. DESIGN: Prospective study of human and murine neutrophils and clinical cohort analysis. SETTING: University research laboratory and level 1 trauma center. PATIENTS: Trauma patients, volunteer controls. ANIMAL SUBJECTS: C57Bl/6, formyl peptide receptor-1, and formyl peptide receptor-2 knockout mice. INTERVENTIONS: Human and murine neutrophils functions were activated with autologous mitochondrial debris, mitochondrial formyl peptides, or bacterial formyl peptides followed by chemokines or leukotrienes. The experiments were repeated using formyl peptide receptor-1 antagonist cyclosporin H, "designer" human formyl peptide receptor-1 antagonists (POL7178 and POL7200), or anti-formyl peptide receptor-1 antibodies. Mouse injury/lung infection model was used to evaluate effect of formyl peptide receptor-1 inhibition. MEASUREMENTS AND MAIN RESULTS: Human neutrophils cytosolic calcium, chemotaxis, reactive oxygen species production, and phagocytosis were studied before and after exposure to mitochondrial debris, mitochondrial formyl peptides, and bacterial formyl peptides. Mitochondrial formyl peptide and bacterial formyl peptides had similar effects on neutrophils. Responses to chemokines and leukotrienes were suppressed by prior exposure to formyl peptides. POL7200 and POL7178 were specific antagonists of human formyl peptide receptor-1 and more effective than cyclosporin H or anti-formyl peptide receptor-1 antibodies. Formyl peptides inhibited mouse neutrophils responses to chemokines only if formyl peptide receptor-1 was present. Formyl peptide receptor-1 blockade did not inhibit neutrophils bacterial phagocytosis or reactive oxygen species production. Cyclosporin H increased bacterial clearance in lungs after injury. CONCLUSIONS: Formyl peptides both activate and desensitize neutrophils. Formyl peptide receptor-1 blockade prevents desensitization, potentially both diminishing systemic inflammatory response syndrome and protecting the host against secondary infection after tissue trauma or primary infection.

Folic acid improves abnormal behavior via mitigation of oxidative stress, inflammation, and ferroptosis in the BTBR T+ tf/J mouse model of autism.

The aim of this study was to examine the effects of folic acid (FA) on the autistic phenotypes in BTBR T+ Itpr3tf/J (BTBR) mice and to investigate underlying mechanisms. Mice received FA (0.2 mg/kg/day) orally from postnatal days 14 to 35. Mice were then tested for stereotyped and repetitive behaviors, social interaction, and spatial learning and memory at the end of FA supplementation. Oxidative stress, neuroinflammatory responses and ferroptosis-related proteins in the brain were also evaluated. FA supplementation in BTBR mice reduced repetitive and stereotyped behavior, improved social communication, and enhanced memory and spatial learning. FA supplementation also reduced neuronal loss in hippocampal CA1 regions of the brain and decreased the levels of the proinflammatory cytokines such as interleukin-1ß (IL-1ß), Iba-1, IL-18, tumor necrosis factor-a, and IL-6 and glial fibrillary acidic protein in the hippocampus. FA supplementation changed the malondialdehyde and glutathione levels and superoxide dismutase (SOD) and glutathione peroxidase activities in the hippocampus. FA supplementation inhibited the elevation of the SOD1 and TFR protein levels and enhanced the relative expression levels of glutathione peroxidase 4 and ferroportin 1 in the hippocampus and increased the relative levels of phospho-Ca2+/calmodulin-dependent protein kinase II and phospho-cAMP-response element binding protein in the hippocampus. FA oral supplementation to BTBR mice rescued stereotyped and repetitive behaviors, social deficit, and spatial learning and memory impairments, likely by improving the oxidative-stress and inflammatory responses by altering the ferroptosis signaling pathways.

Modulation of sphingosine 1-phosphate (S1P) attenuates spatial learning and memory impairments in the valproic acid rat model of autism.

RATIONALE: Autism spectrum disorders (ASD) are a set of pervasive neurodevelopmental disorders that manifest in early childhood, and it is growing up to be a major cause of disability in children. However, the etiology and treatment of ASD are not well understood. In our previous study, we found that serum levels of sphingosine 1-phosphate (S1P) were increased significantly in children with autism, indicating that S1P levels may be involved in ASD. OBJECTIVE: The objective of this study was to identify a link between increased levels of S1P and neurobehavioral changes in autism. METHODS: We utilized a valproic acid (VPA) -induced rat model of autism to evaluate the levels of S1P and the expression of sphingosine kinase (SphK), a key enzyme for S1P production, in serum and hippocampal tissue. Furthermore, we assessed cognitive functional changes and histopathological and neurochemical alterations in VPA-exposed rats after SphK blockade to explore the possible link between increased levels of S1P and neurobehavioral changes in autism. RESULTS: We found that SphK2 and S1P are upregulated in hippocampal tissue from VPA-exposed rats, while pharmacological inhibition of SphK reduced S1P levels, attenuated spatial learning and memory impairments, increased the expression of phosphorylated CaMKII and CREB and autophagy-related proteins, inhibited cytochrome c release, decreased the expression of apoptosis related proteins, and protected against neuronal loss in the hippocampus. CONCLUSION: We have demonstrated that an increased level of SphK2/S1P is involved in the spatial learning and memory impairments of autism, and this signaling pathway represents a novel therapeutic target and direction for future studies.

Factors influencing sleep disturbances among spouse caregivers of cancer patients in Northeast China.

BACKGROUND: In China, spouse caregivers of cancer patients (SCCPs) are involved in all aspects of patient care and experience psychological distress which could result in sleep disturbance and fatigue. However, few studies have explored the differences between SCCPs and the general population, or what factors affect SCCPs' sleep. This study aims to (1) Compare the differences in sleep disturbances and fatigue severity between SCCPs and the age- and gender-matched general population, and (2) Identify selected personal characteristics, including coping style that affect sleep disturbances in SCCPs. METHODOLOGY/PRINCIPAL FINDINGS: The Stress and Coping Model was used to guide this study. Participants were recruited from the northeast part of China and included 600 people from the general population and 300 SCCPs. Participants completed a socio-demographic form, Fatigue Scale-14, trait Coping Style Questionnaire, and Symptom Checklist-90. RESULTS: The majority of the participants were middle age, most of whom (78.7%) spent more than 8 hours each day taking care of their spouses. Compared to the general population, the SCCPs experienced significant sleep disturbances with a mean of 7.30 (SD = 1.27), and fatigue severity with a mean of 8.11 (SD = 3.25). Among the selected SCCPs' personal characteristics, current poor health status (ß = 0.14, P<0.001), having a spouse under mixed treatment (ß = 0.13, p<0.001), and financial burden (ß = 0.14, P<0.001) are the significant predictors for sleep disturbances. Positive coping is the predictor for fewer sleep disturbances (ß = 0.27, P<0.001). Those who reported sleep disturbances also experienced higher physical and mental fatigue severity (P<0.001). CONCLUSION: Intervention to improve coping style in SCCPs is needed. Further research is also needed to explore the other mediators and moderators that regulate sleep disturbance and health outcomes in the SCCPs.

Carboxyl-terminal amino acids 1052 to 1082 of the latency-associated nuclear antigen (LANA) interact with RBP-Jκ and are responsible for LANA-mediated RTA repression.

Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8, is closely associated with several malignancies, including Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease. KSHV can establish lifelong latency in the host, but the mechanism is not fully understood. Previous studies have proposed a feedback model in which the viral replication and transcription activator (RTA) can induce the expression of the latency-associated nuclear antigen (LANA) during early infection. LANA, in turn, represses transcription and RTA function to establish and maintain KSHV latency. The interaction between LANA and the recombination signal sequence binding protein Jκ (RBP-Jκ, also called CSL), a major transcriptional repressor of the Notch signaling pathway, is essential for RTA repression. In the present study, we show that the LANA carboxyl-terminal amino acids 1052 to 1082 are responsible for the LANA interaction with RBP-Jκ. The secondary structure of the LANA carboxyl terminus resembles the RBP-Jκ-associated module (RAM) of Notch receptor. Furthermore, deletion of the region of LANA residues 1052 to 1082 resulted in aberrant expression of RTA, leading to elevated viral lytic replication. For the first time, we dissected a conserved RBP-Jκ binding domain in LANA and demonstrated that this domain was indispensable for LANA-mediated repression of KSHV lytic genes, thus helping the virus maintain latency and control viral reactivation.

Collisionless bounce resonance heating in dual-frequency capacitively coupled plasmas.

We present the experimental evidence of the collisionless electron bounce resonance heating (BRH) in low-pressure dual-frequency capacitively coupled plasmas. In capacitively coupled plasmas at low pressures when the discharge frequency and gap satisfy a certain resonant condition, the high energy beamlike electrons can be generated by fast sheath expansion, and heated by the two sheaths coherently, thus the BRH occurs. By using a combined measurement of a floating double probe and optical emission spectroscopy, we demonstrate the effect of BRH on plasma properties, such as plasma density and light emission, especially in dual-frequency discharges.

Carbon density and distribution of six Chinese temperate forests.

Quantifying forest carbon (C) storage and distribution is important for forest C cycling studies and terrestrial ecosystem modeling. Forest inventory and allometric approaches were used to measure C density and allocation in six representative temperate forests of similar stand age (42-59 years old) and growing under the same climate in northeastern China. The forests were an aspen-birch forest, a hardwood forest, a Korean pine plantation, a Dahurian larch plantation, a mixed deciduous forest, and a Mongolian oak forest. There were no significant differences in the C densities of ecosystem components (except for detritus) although the six forests had varying vegetation compositions and site conditions. However, the differences were significant when the C pools were normalized against stand basal area. The total ecosystem C density varied from 186.9 tC hm(-2) to 349.2 tC hm(-2) across the forests. The C densities of vegetation, detritus, and soil ranged from 86.3-122.7 tC hm(-2), 6.5-10.5 tC hm(-2), and 93.7-220.1 tC hm(-2), respectively, which accounted for 39.7% +/- 7.1% (mean +/- SD), 3.3% +/- 1.1%, and 57.0% +/- 7.9% of the total C densities, respectively. The overstory C pool accounted for > 99% of the total vegetation C pool. The foliage biomass, small root (diameter < 5mm) biomass, root-shoot ratio, and small root to foliage biomass ratio varied from 2.08-4.72 tC hm(-2), 0.95-3.24 tC hm(-2), 22.0%-28.3%, and 34.5%-122.2%, respectively. The Korean pine plantation had the lowest foliage production efficiency (total biomass/foliage biomass: 22.6 g g(-1)) among the six forests, while the Dahurian larch plantation had the highest small root production efficiency (total biomass/small root biomass: 124.7 g g(-1)). The small root C density decreased with soil depth for all forests except for the Mongolian oak forest, in which the small roots tended to be vertically distributed downwards. The C density of coarse woody debris was significantly less in the two plantations than in the four naturally regenerated forests. The variability of C allocation patterns in a specific forest is jointly influenced by vegetation type, management history, and local water and nutrient availability. The study provides important data for developing and validating C cycling models for temperate forests.

Dynamics of fine roots in five Chinese temperate forests.

We used a minirhizotron method to investigate spatial and temporal dynamics of fine roots (diameter < or =2 mm) in five Chinese temperate forests: Mongolian oak forest, aspen-birch forest, hardwood forest, Korean pine plantation and Dahurian larch plantation. Fine root dynamics were significantly influenced by forest type, soil layer, and sampling time. The grand mean values varied from 1.99 to 3.21 mm cm(-2) (root length per minirhizotron viewing area) for the fine root standing crop; from 6.7 to 11.6 microm cm(-2) day(-1) for the production; and from 3.2 to 6.1 microm cm(-2) day(-1) for the mortality. All forests had a similar seasonal "sinusoidal" pattern of standing crop, and a "unimodal" pattern of production. However, the seasonal dynamics of the mortality were largely unsynchronized with those of the production. The minimum values of standing crop, production and mortality occurred in March for all forests, whereas the maximum values and occurrence time differed among forest types. The standing crop, production and mortality tended to decrease with soil depth. The different spatiotemporal patterns of fine roots among the forests highlight the need for forest-specific measurements and modeling of fine root dynamics and forest carbon allocation.