[Analysis of complications and learning curve effects related to deep brain stimulation surgery in 822 Parkinson's disesase patients with the same surgeon].

Objective: To analyze the complications related to deep brain stimulation(DBS) surgery in Parkinson's disease(PD) patients and to determine whether there is a learning curve effect in terms of complications. Methods: Retrospective analysis of the DBS surgical data of 822 PD patients performed by the same surgeon at the First Affiliated Hospital of the University of Science and Technology of China (Anhui Provincial Hospital) from December 2012 to December 2022. The complications related to DBS were evaluated and analyzed the complications of every 100 DBS surgery were further analyzed. Results: A total of 822 PD patients, 453 males and 369 females, aged 31-80 years old, were included. The minimum follow-up period after DBS surgery is 6 months. Surgical related complications occurred in 55 patients (6.69%), including 5 patients (0.61%) with slight bleeding around the electrode, 1 patient (0.12%) with cerebral infarction, 4 patients (0.49%) with postoperative epilepsy, 42 patients (5.11%) with postoperative delirium, 2 patients (0.24%) with respiratory distress, and 1 patient (0.12%) with acute cardiac insufficiency. There were 16 cases (1.94%) of hardware related complications in DBS, of which 4 cases (0.48%) had infection, 1 case (0.12%) had a broken angle at the connection between the pulse generator and the extension wire, 8 cases (0.97%) had an excessively tight extension wire, and 3 cases (0.36%) had an IPG bag hematoma. In the infected cases, 2 patients removed IPG and extension wires. There were 7 cases (0.85%) of stimulus related complications, including 4 cases (0.61%) with programmed sensory abnormalities, 1 case (0.12%) with postoperative abnormal movements and dance like movements, and 2 cases (0.24%) with psychiatric symptoms. A comprehensive analysis was conducted on the above complications, among which 8 cases (0.97%) were relatively serious complications. After active treatment, satisfactory results were achieved, and none of them affected the patient's DBS treatment effect and no patients died. For every 100 cases of DBS surgery complications were analyzed, the percentage of complications decreased significantly from 14.50% (58 cases) in the first 400 cases to 4.73% (20 cases) in the last 400 cases (P<0.001). Conclusion: DBS surgery is safe and has an acceptable low incidence of complications. The incidence of complications also decreases with the accumulation of experience, showing a learning curve effect.

Unilateral biportal endoscopic spine surgery for lumbar spinal stenosis: a systematic review and meta-analysis.

OBJECTIVE: Lumbar spinal stenosis is the most common spinal degenerative disease in patients over 60 years, and the unilateral biportal endoscopic (UBE) spine surgery treatment of lumbar spinal stenosis (LSS) has achieved preliminary clinical results. This systematic review and meta-analysis aimed to reveal the clinical efficacy of UBE for LSS and provide evidence for clinical practice. MATERIALS AND METHODS: PubMed, Embase, Web of Science, and Cochrane databases were searched for literature. The papers selected were those published from inception till October 2021. The selected pieces of literature were graded for evidence using the Oxford Centre for Evidence-Based Medicine: Levels of Evidence (March 2009). Outcomes measures were operation time, blood loss, complication rate, admission period, Visual Analogue Scale (VAS)-back, VAS-leg, and Oswestry Disability Index (ODI) score, and radiological outcomes. The mean comparisons were based on VAS and ODI scores. RESULTS: A total of 823 patients with a single LSS segment were included from the selected nine studies. There were nine studies comparing UBE clinical outcomes and micro-endoscopic unilateral laminotomy for bilateral decompression (M-ULBD). The meta-analysis revealed that the UBE group had better VAS-leg and -back scores in the first week postoperatively [total: mean difference (MD) = -0.96, 95% confidence interval (CI): -1.19, -0.74, p < 0.00001; total: MD = -1.69, 95% CI: -1.93, -1.45, p < 0.00001], 1st month postoperatively (total: MD = -0.35, 95% CI: -0.61, -0.08, p = 0.01; total: MD = -0.40, 95% CI: -0.68, -0.12, p = 0.005), 6th month postoperatively (total: MD = -0.22, 95% CI: -0.35, -0.08, p = 0.002; total: MD = -0.24, 95% CI: -0.40, -0.07, p = 0.005), and UBE group also performed better in ODI score at 1st month postoperatively (total: MD = -3.36, 95% CI: -4.26, -2.46, p < 0.00001). There was no significant difference in VAS-leg and -back scores between both groups at the 3rd and 12th month postoperatively, and ODI scores did not significantly differ between both groups at 3, 6, and 12 months postoperatively (all p > 0.05). CONCLUSIONS: UBE has achieved good preliminary clinical results and may be a minimally invasive alternative surgery for patients with single segmental LSS.

MiR-150 inhibits proliferation of mantle-cell lymphoma cells via regulation of MET.

OBJECTIVE: The aim of this study was to explore the influences of micro ribonucleic acid (miR)-150 on the proliferation and apoptosis of mantle-cell lymphoma (MCL) cells and to investigate the potential underlying mechanism. PATIENTS AND METHODS: Differentially expressed miRNAs in MCL tissues were excavated via microarray analysis of miRNA expression profiles. Subsequently, the expression of miRNAs were verified by quantitative Reverse Transcription-Polymerase Chain Reaction (RT-qPCR). The influence of miRNA expression on the survival of patients was detected based on clinical data. Besides, the potential targets of miRNAs were determined using Luciferase reporter gene assay combined with qRT-PCR and Western blotting. Primary tumor cells were extracted, and the influences of miR-150 expression on cell proliferation were detected via Cell Counting Kit (CCK)-8 assay and 5-ethynyl-2'-deoxyuridine (EdU) staining assay. Finally, Western blotting and flow cytometry were performed to explore the impact of miR-150 on the apoptosis of primary tumor cells. RESULTS: Microarray analysis of miRNA expression profiles and RT-qPCR verified that the expression levels of hsa-miR-486, hsa-miR-4746, and hsa-miR-3158 rose considerably in MCL tissues, while those of hsa-miR-29b-3p, hsa-miR-150, and hsa-miR-142-5p remarkably declined. According to the results of survival analysis, the survival time was notably prolonged in patients with higher expression levels of miR-150 and miR-486, especially in those with higher expression level of miR-150. Luciferase reporter gene assay and RT-qPCR and Western blotting results demonstrated that miR-150 negatively regulated the expression level of MET. Subsequent CCK-8 assay and EdU staining results revealed that up-regulation of miR-150 significantly suppressed the proliferation of primary MCL cells. Finally, Western blotting and flow cytometry found that increased expression of MET remarkably facilitated the apoptosis of primary MCL cells. CONCLUSIONS: MiR-150 inhibits the proliferation and promotes the apoptosis of MCL cells by negatively regulating MET expression.

Time-dependent alteration of insulin-like growth factor gene expression during nerve regeneration in regions of muscle enriched with neuromuscular junctions.

Insulin-like growth factors (IGFs) increase the rate of motor axon elongation, prevent motoneuron death, and may support the reestablishment of synapses following nerve injury. In situ hybridization was used in the present study to examine the temporal and spatial distribution of IGF gene expression in soleus muscle following sciatic nerve crush in rats. In intact muscle, IGF-II gene expression was generally low, and localized to interstitial cells, possibly fibroblast and Schwann cells. These cells were found in the middle of muscle which is enriched in neuromuscular junctions. IGF-II gene expression, 4-6 days postcrush, was increased in interstitial cells. Thereafter, IGF-II gene expression was also increased in muscle cells or cells closely associated with muscle fibers, such as satellite cells. IGF-II gene expression was increased to a much greater extent in the midregion of muscle enriched in end-plates than in the two ends of muscle, but returned towards normal following the reestablishment of functional synapses. On the other hand, IGF-I gene expression was only slightly increased following nerve crush, and this increase was associated with interstitial, but not muscle cells. These results show that the IGF-I and IGF-II genes are regulated by independent signals and may play separate roles during nerve regeneration. For example, a regional increase in IGF-II gene expression may support preferential nerve terminal sprouting in the middle of muscle enriched in neuromuscular junctions, thereby increasing the probability for the reestablishment of synapses.

Insulin-like growth factor-II increases and IGF is required for postnatal rat spinal motoneuron survival following sciatic nerve axotomy.

The prolonged disconnection of nerve from muscle results in the death of motoneurons and permanent paralysis. Because clinical nerve injuries generally involve postbirth motoneurons, there is interest in uncovering factors that may support their survival. A rich history of research dating back to the time of Santiago Ramon y Cajal and Viktor Hamburger supports the inference that there are soluble neurotrophic factors associated with nerve and muscle. However, the endogenous factors normally required for motoneuron survival following nerve injury have eluded identification. Two interrelated hypotheses were tested: (1) administration of insulin-like growth factor-II (IGF-II) can support the survival of postbirth motoneurons, and (2) endogenous IGFs are essential for motoneuron survival following nerve injury. We report that IGF-II locally administered close to the proximal nerve stump prevented the death of motoneurons (estimated by relative numbers of neuronal profiles) which ordinarily follows sciatic nerve transection in neonatal rats. By contrast, anti-IGF antiserum, as well as IGF binding proteins-4 and -6, significantly increased (P < 0.01) motoneuron death. This report shows that IGF-II can support survival, and contains the novel observation that endogenous IGF activity in or near nerves is required for motoneuron survival. Other studies have determined that IGF gene and protein expression are increased in nerve and muscle following sciatic nerve crush, and that IGFs are required for nerve regeneration. Taken together, these data show that IGFs are nerve- and muscle-derived soluble factors that support motoneuron survival as well as nerve regeneration.

Insulin-like growth factor (IGF) gene expression is reduced in neural tissues and liver from rats with non-insulin-dependent diabetes mellitus, and IGF treatment ameliorates diabetic neuropathy.

Neural disturbances are observed in the peripheral and central nervous systems of patients with insulin-dependent diabetes mellitus (IDDM) and non-IDDM (NIDDM). Insulin-like growth factors (IGFs) are neurotrophic growth factors that can support nerve regeneration and neuronal survival in the types of neurons known to be afflicted in diabetes. We tested the hypotheses that IGF gene expression is reduced in neural tissues and liver of spontaneously diabetic obese Zucker (fa/fa) rats and that IGF treatment can prevent neuropathy. There was a significant early reduction in IGF-II mRNA content as measured per mg of wet tissue or per poly(A)+ RNA in sciatic nerves, spinal cord and brain from spontaneously diabetic obese (fa/fa) vs. nondiabetic lean (+/+) adult rats. In addition, IGF-I mRNA content was reduced in liver but not nerve or spinal cord of NIDDM rats. Pain/pressure thresholds were abnormal (hyperalgesia) in diabetic (fa/fa) vs. nondiabetic (+/+) rats, and subcutaneous infusion of IGF-II restored thresholds toward normal. The low dose of IGF-II that prevented hyperalgesia in contrast had no effect on hyperglycemia or obesity. These data suggest that IGF treatment may provide rational therapy for diabetic neuropathy and that therapy may be effective even in patients unable to adequately control their hyperglycemia.

Insulin-like growth factors reverse or arrest diabetic neuropathy: effects on hyperalgesia and impaired nerve regeneration in rats.

Diabetic neuropathy is a debilitating disorder whose causation is poorly understood. A new theory proposes that neuropathy may arise as a consequence of loss of neurotrophic insulin-like growth factor (IGF) activity due to diabetes, superimposed on a slow continual loss due to aging. The prediction that IGF-I and IGF-II gene expression are reduced in diabetic nerves was recently tested and validated. Here we tested the prediction that IGF administration can prevent or reverse diabetic sensory neuropathy. Subcutaneous infusion of IGF-I or IGF-II, but not vehicle, halted (P < 0.01) the progression of hyperalgesia in streptozotocin-diabetic rats. Moreover, impaired sensory nerve regeneration was partially reversed within 2 weeks after treatment of diabetic rats with IGFs (P < 0.01). Impaired regeneration could also be prevented by daily subcutaneous IGF injections. The low replacement doses of IGFs were effective despite unabated hyperglycemia and weight loss. These results show that IGF replacement therapy can reverse or prevent diabetic sensory neuropathy independently of hyperglycemia or weight loss.

Differential spatio-temporal expression of the insulin-like growth factor genes in regenerating sciatic nerve.

Previous studies have demonstrated that the regeneration of mammalian peripheral nerves is dependent on endogenous insulin-like growth factors (IGFs). In the present study, in situ hybridization was used to examine the temporal and spatial expression of the IGF-I and IGF-II genes in rat sciatic nerve after crush. Such expression was characterized in relation to Schwann cell proliferation and the presence of neurofilaments in returning axons during regeneration. The results show that both IGF-I and IGF-II mRNAs were increased in the sciatic nerve distal to the crush site. However, each transcript had a distinctly different temporal and spatial distribution during regeneration. IGF-I gene expression was intensely increased at the crush site within 4 days after nerve crush. Along the portion of the nerve distal to the crush site, a moderate increase was observed to reach maximal levels 10 days postcrush, and was decreased thereafter back towards baseline at 20 days postcrush. Furthermore, this increase was associated with the proliferation of Schwann cells, and the return toward baseline with the regeneration of axons containing neurofilaments. By contrast, IGF-II gene expression was unchanged at or near the site of injury, but unexpectedly was increased in more distal, intramuscular reaches of the nerves. This had a slower time course beginning 10 days postcrush, and was further increased at 20 days postcrush. These results show that the IGF-I and IGF-II genes are regulated by independent signals and probably play different roles during nerve regeneration. They support the hypotheses that IGF-I contributes to the initial sprouting and subsequent elongation of axons in nerves, whereas IGF-II enhances the regeneration of certain axons into neuromuscular branches of nerves, and/or the re-establishment of neuromuscular synapses.

Cholecystokinin octapeptide (CCK-8) antagonizes morphine analgesia in nucleus accumbens of the rat via the CCK-B receptor.

The analgesic effect of systemic morphine (4 mg/kg, s.c.) was antagonized in a dose-dependent manner by cholecystokinin octapeptide (CCK-8) (0.1-0.5 ng) administered bilaterally to the nucleus accumbens of the rat. This effect of CCK-8 could be reversed by devazepide, a CCK-A receptor antagonist, at 50 ng and 200 ng and by L-365,260, a CCK-B receptor antagonist, at 5 ng administered bilaterally to the nucleus accumbens. A marked potentiation of morphine analgesia was achieved by intra-nucleus accumbens injection of 200 ng devazepide or 5 ng L-365,260. Since the effect of L-365,260 in antagonizing the anti-opioid effect of CCK-8 in the nucleus accumbens is 40 times more potent than devazepide, it is suggested that the anti-opioid effect of CCK-8 is mediated by CCK-B receptors. In conclusion, nucleus accumbens is a strategic site where CCK-8 exerts an anti-opioid activity, most probably via the CCK-B receptors.

One-stage total reconstruction of the ear with simultaneous tympanoplasty.

The one-stage total ear reconstruction (auricular reconstruction and tympanoplasty) has a number of merits. 1. Satisfactory esthetic results obtained in one operation. 2. The "super thin" skin flap is elevated on a plane that excludes hair follicles from the flap, so the hair-bearing areas of the scalp can be readily incorporated as part of the ear reconstruction. 3. The reconstructed ear has adequate blood supply and protective sensation. 4. The surgeon may choose to carry out a tympanoplasty and obtain restoration of auditory function or may choose to carry out a pseudomeatus procedure and reduce the operating time. We feel that the "super thin" skin flap and the simultaneous tympanoplasty are valuable supplements to ear reconstruction. The functional results of the tympanoplasty must be considered only a partial success at this time; long-term evaluation as well as technologic improvements are needed.

The use of scrotal septal neurovascular pedicle island skin flap in one-stage repair of hypospadias.

A scrotal septum neurovascular pedicle skin flap was successfully used in one-stage repair of hypospadias in 30 patients with encouraging results. The hairless median scrotal skin flap, with the scrotal septum attached, rich in neurovascular plexus and with the flap tip continuous with the external urethral orifice, is ideal material for creating a new penile urethra without interference to its blood supply. Operative technique and clinical analysis are detailed.