Analysis of the Functional Outcome of Arthroscopic Anterior Cruciate Ligament Reconstruction Using the Central Quadriceps Tendon Graft.

INTRODUCTION: Anterior cruciate ligament (ACL) injuries are common, particularly among athletes, and often result in knee instability and decreased functionality. Arthroscopic ACL reconstruction is the standard treatment, typically using a patellar tendon bone graft (PTBG) or hamstring tendon graft (HTG). The central quadriceps tendon graft (QTG) has been proposed as a superior alternative due to its structural properties. METHODOLOGY: This study involved patients undergoing ACL reconstruction using the central quadriceps tendon graft. Functional outcomes were assessed using the Tegner Lysholm knee score were assessed at preoperative and postoperative intervals of two weeks, three months, and six months. Statistical analysis compared these scores over time. RESULTS: Among the subjects, 90.6% were male and 9.4% were female. Injuries primarily resulted from sports activities and road traffic accidents (46.9% each). Right-side injuries were more prevalent (65.6%). The mean time from injury to surgery was 9.37 months. The mean graft size was 8.75 mm, and the mean tourniquet time was 105.94 minutes. Preoperative tests showed positive results for anterior drawer, Lachman, and pivot shift tests in most patients, which were negative postoperatively. Significant improvements in knee flexion and Lysholm knee scores were observed. Preoperative knee flexion ranged from 0-100° to 0-120°, improving to 0-120° to 0-130° six months postoperatively. The mean Lysholm knee score improved from 47.06 preoperatively to 93.16 at six months. Excellent outcomes were seen in 78.1% of the patients, with 21.9% achieving good outcomes. CONCLUSION: The central quadriceps tendon graft is an effective option for ACL reconstruction, offering excellent functional outcomes and low complication rates. It shows promise as a better alternative to traditional graft types, although further research is necessary to confirm these findings.

Myotonic Dystrophy Type 1 (DM1): Clinical Characteristics and Disease Progression in a Large Cohort.

BACKGROUND: DM1 is a multisystem disorder caused by expansion of a CTG triplet repeat in the 3' non-coding region of DMPK. Neuropsychological consequences and sleep abnormalities are important associations in DM1. OBJECTIVE: To describe the clinical phenotype, disease progression and characterize the sleep alterations and cognitive abnormalities in a sub-set of patients. MATERIALS AND METHODS: A retrospective study on 120 genetically confirmed DM1 cases. Findings in neuropsychological assessment and multiple sleep questionnaires were compared with 14 age and sex matched healthy individuals. All 120 patients were contacted through letters/telephonic consultation/hospital visits to record their latest physical and functional disabilities. RESULTS: The mean age at symptom onset was 23.1 ± 11.4 years, M: F = 3.8:1, mean duration of illness = 14.3 ± 9.5 years. Clinically 54.2% had adult onset form, juvenile = 27.5%, infantile = 10.8%, late adult onset = 7.5%. Paternal transmission occurred more frequently. The predominant initial symptoms were myotonia (37.5%), hand weakness (21.7%), lower limb weakness (23.3%) and bulbar (10%). Twenty patients completed sleep questionnaires (SQ). Abnormal scores were noted in Epworth sleepiness scale (55%); Pittsburgh sleep quality index (45%); Berlin SQ (30%); Rapid eye movement sleep Behaviour Disorder SQ (15%); Restless leg syndrome rating scale (10%). Neuropsychological assessment of 20 patients revealed frontal executive dysfunction, attention impairment and visuospatial dysfunction. Frontal lobe was most affected (72%) followed by parietal (16%) and temporal lobe (12%). CONCLUSIONS: The current study provides a comprehensive account of the clinical characteristics in Indian patients with DM1. Hypersomnolence was most commonly seen. Excessive daytime sleepiness and Sleep disordered breathing were the most common sleep related abnormality. Cognitive impairment comprised predominantly of frontal lobe dysfunction.

A Rare Case of Ataxia-Telangiectasia-Like Disorder With MRE11 Mutation.

The prototypical disorder for the early-onset cerebellar ataxia with cerebellar atrophy is ataxia telangiectasia (AT). AT belongs to "DNA-repair defects" or "DNA-repair deficiency" disorders. The ATM (Ataxia-telangiectasia mutated kinase) gene mutated in AT is central to deoxyribonucleic acid (DNA) damage response (DDR) signaling. Other genes implicated in DDR signaling are MRE11A (Meiotic recombination 11). Mutation of this gene results in ataxia-telangiectasia-like disorder (ATLD). We report a boy who presented with mild cerebellar ataxia and dystonia with cerebellar atrophy on brain imaging. Clinical exome sequencing showed compound heterozygous variants in MRE11 gene. He was diagnosed as ATLD, which has not been reported in Indian subcontinent so far.

Effects of (15S)-hydroperoxyeicosatetraenoic acid and (15S)-hydroxyeicosatetraenoic acid on the acute- lymphoblastic-leukaemia cell line Jurkat: activation of the Fas-mediated death pathway.

The antiproliferative effects of 15-LOX (15-lipoxygenase) metabolites of arachidonic acid {(15S)-HPETE [(15S)-hydroperoxyeicosatetraenoic acid] and (15S)-HETE [(15S)-hydroxyeicosatetraenoic acid]} and the mechanism(s) involved were studied in the human T-cell leukaemia cell line Jurkat. (15S)-HPETE, the hydroperoxy metabolite of 15-LOX, inhibited the growth of Jurkat cells 3 h after exposure and with an IC(50) value of 10 microM. The hydroxy metabolite of 15-LOX, (15S)-HETE, on the other hand, inhibited the growth of Jurkat cells after 6 h of exposure and with an IC(50) value of 40 microM. The cells exposed to 10 microM (15S)-HPETE for 3 h or to 40 microM (15S)-HETE for 6 h showed increased expression of Fas ligand and FADD (Fas-associated death domain), caspase 8 activation, Bid (BH3-interacting domain death agonist) cleavage, decrease in mitochondrial membrane potential, cytochrome c release, caspase 3 activation, PARP-1 [poly(ADP-ribose) polymerase-1] cleavage and DNA fragmentation, suggesting the involvement of both extrinsic and intrinsic death pathways. Further studies on ROS (reactive oxygen species) generation revealed the involvement of NADPH oxidase. In conclusion, the present study indicates that NADPH oxidase-induced ROS generation activates the Fas-mediated death pathway.

Isolation of stem cells from human umbilical cord blood.

Umbilical cord blood (UCB) is gaining more prominence in recent times as a source of non-embryonic multipotent stem cells. Global annual human birth rate (100 million) presents UCB as the largest non-controversial stem cell source, with an added advantage of naive immune status. Cord blood stem cells are routinely utilized in stem cell transplantation in leukemia patients and carry huge potential to treat other human diseases with less concern of rejection. Because UCB contains low number of stem cells, their use is associated with significant delays in engraftment of neutrophils and platelets. Development of reliable methods for isolation and expansion of cord blood stem cells is critical for consequent clinical application. The focus of this chapter is to review the methods currently used by different research groups and to recommend an isolation protocol that yields optimal number of UCB stem cells.