OBJECTIVE: To review the main fixation methods for proximal tibial extra-articular fractures based on clinical and biomechanical results, and to provide evidence for clinical application. METHODS: Extensive related literature at home and abroad was conducted in recent years, and external fixation systems such as external fixation braces and external locking plates, as well as internal fixation systems such as plates and intramedullary nails, were systematically reviewed regarding their application indications, clinical efficacy, and biomechanical results in proximal tibial extra-articular fractures. RESULTS: External fixation systems have advantages in fractures with open or severe soft tissue injury, facilitating wound management and maintaining stability of the fracture site to some extent. However, in proximal tibial extra-articular fractures with good soft tissue conditions, internal fixation systems such as plates and intramedullary nails are still the first choice. Some studies have found that intramedullary nails allow patients to bear weight early, with shorter fracture healing time and higher rate of malunion, while other studies have found that both intramedullary nails and plates have similar clinical efficacy and can achieve satisfactory treatment results. CONCLUSION The choice of fixation method for proximal tibial extra-articular fractures depends not only on the type of fracture, but also on the surgeon's habits and operational skills. Larger-scale studies are still needed to clarify the advantages and disadvantages of intramedullary nails and locking plates in the treatment of proximal tibial extra-articular fractures.
Humans ; Tibial Fractures/surgery* ; Bone Plates ; Fracture Fixation, Intramedullary/instrumentation* ; Fracture Fixation, Internal/instrumentation* ; Fracture Healing ; External Fixators ; Bone Nails ; Fracture Fixation/instrumentation* ; Treatment Outcome ; Biomechanical Phenomena

The core pathological feature of Parkinson's disease(PD)is the abnormal aggregation of α-synuclein and the result ing neuronal damage.α-Synuclein exhibits toxic effects when it forms oligomers or fibrils,leading to neuronal death via multiple pathways,including mitochondrial dysfunction,impaired vesicular trafficking,dopamine auto-oxidation,and neuroinflammation.In addition,α-synuclein can propagate between cells via exosomes,endocytosis/exocytosis,tunneling nanotubes,or vagal nerve axonal transport,creating a cascade of pathological effects.Animal models of PD that recapitulate the key pathological hallmark of α-synuclein accumulation are indispensable tools for elucidating disease mechanisms and developing novel therapeutic interventions.To date,various strategies,including transgenic techniques,bacterial artificial chromosome(BAC)-mediated expression,viral vector-mediated overexpression,and gene editing,have been employed to develop α-synuclein overexpression animal models.These models have significantly advanced our exploration of the relationship between PD and α-synuclein.This systematic review considers the structure and function of α-synuclein,its mechanisms of toxicity,intercellular propagation pathways,animal models of overexpression,and potential therapeutic targets based on its pathogenic mechanisms.

The core pathological feature of Parkinson's disease(PD)is the abnormal aggregation of α-synuclein and the result ing neuronal damage.α-Synuclein exhibits toxic effects when it forms oligomers or fibrils,leading to neuronal death via multiple pathways,including mitochondrial dysfunction,impaired vesicular trafficking,dopamine auto-oxidation,and neuroinflammation.In addition,α-synuclein can propagate between cells via exosomes,endocytosis/exocytosis,tunneling nanotubes,or vagal nerve axonal transport,creating a cascade of pathological effects.Animal models of PD that recapitulate the key pathological hallmark of α-synuclein accumulation are indispensable tools for elucidating disease mechanisms and developing novel therapeutic interventions.To date,various strategies,including transgenic techniques,bacterial artificial chromosome(BAC)-mediated expression,viral vector-mediated overexpression,and gene editing,have been employed to develop α-synuclein overexpression animal models.These models have significantly advanced our exploration of the relationship between PD and α-synuclein.This systematic review considers the structure and function of α-synuclein,its mechanisms of toxicity,intercellular propagation pathways,animal models of overexpression,and potential therapeutic targets based on its pathogenic mechanisms.

This paper reports a pair of siblings with congenital short-bowel syndrome (CSBS) complicated with intestinal malrotation. Case 1 was born with a birth weight of 2 550 g and a length of 48 cm. On September 10, 2017, emergency Ladd's procedure and appendectomy were performed on the infant 23 days after birth due to intestinal obstruction at the Women and Children's Hospital, School of Medicine, Xiamen University. The small intestine of the infant had a total length of 65 cm. Postoperative enteral and parenteral nutrition supports were provided for six months. Whole exome sequencing revealed a homozygous variant (NM 024769; nucleotide deletion in the exon 3-5) in the CLMP gene (chr11:122953792-122955421), with the parents being the heterozygous carriers but without phenotype. Case 2, the younger sibling of Case 1, was born in the same hospital on March 20, 2020, with a birth weight of 2 932 g and a body length of 49 cm. Prenatal single-gene sequencing on the amniotic fluid identified the same gene variation as his sister's. The baby boy received Ladd's procedure and appendectomy on the second day after birth which found the length of his small intestine was 51 cm. Full enteral nutrition was achieved six months after the operation. Both cases were followed up for 12 months. The body weight and length of Case 1 were both below the first percentile (< P1). The body weight of Case 2 was 8.03 kg ( P3- P5) and the length was 76.0 cm ( P25- P50).

Objective To observe the changes of carotid intima-media thickness(CIMT) and vascular endothelia function in patients with geriatric carotid plaque before and after intensive lipid lowering was performed.Methods 102 patients diagnosed with carotid plaque were ramdomly divided into common group (atorvastatin 10 mg/d,n=48) and intensive lipid lowering group (atorvastatin 20 mg/d,n=54).After one year of treatment,the fasting venous blood total cholesterol (TC),low density lipoprotein cholesterol (LDL-C),high density lipeprotein cholesterol (HDL-C) and triglyceride (TG) were assayed,and the thickest and thinnest CIMT and brachial arterial.endothelium dependent diastolic function (FMD) and carotid artery plaque index(PI) were measured by ultrasound.Results Two groups in the thickest CIMT and PI had no significant difference before and after treatment (P＞0.05).The levels of FMD,TC,LDL-C,TG and the thinnest CIMT had significant difference before and after therapy [common group:GIMT(0.85±0.20)mm,(0.83±0.22) mm,FMD(3.85±1.41)%,(7.91±1.05)%,TC(6.46±1.05) mmol/L,(4.82±1.26) mmol/L,LDL-C (4.71±1.00) mmol/L,(3.16±1.00) mmol/L,TG (1.55±0.45) mmol/L,(1.49±0.44) mmol/L;intensive lipid lowering group:CIMT(0.84±0.20) mm,(0.63±0.17) mm,FMD (3.74±1.38) %,(0.25±1.58)%,TC (6.36±1.06) mmol/L,(4.10±1.00) mmol/L,LDL-C (4.73±1.01) mmol/L、(2.28±1.26) mmol/L,TG (1.56±0.53) mmol/L,(1.50±0.49) mmol/L,P＜0.05].After one year's therapy,the difference in intensive lipid lowering group was more obvious than in common group (P＜0.05).Conclusions Intensive lipid lowering therapy is more effective to decrease TC,LDL-C and CIMT and to improve the vascular endothelia function.Atorvastatin is effective to stabilize the plaque and to retard the atheroscleresis development.

Objective To improve the anderstanding of clinical profile of primary plasma cell leukemia.Methods Case report and literature review.Results A rare case of nervous system relapse in primary plasma cell leukemia was reported.Six patients were identified from the literature.The type of immunoglobulin included IgG(3 patients),IgD(2 patients).Clinical manifestations of nervous system were variable.The average interval from initial diagnosis to the development of nervous system relapse was 16.5 months.Plasma cells were found in cerebrospinal fluid in 4 patients.The mean surviaval time was 6.7 months after nervous system relapse.Conlusion Nervous system relapse in primary plasma cell leukemia is rare with poor prognosis.