Comparison of Effectiveness of Manual Therapy for Infant Crying: systematic review and meta-analysis of randomized controlled trials.

Objectives: The aim of this systematic review and meta-analysis is to assess and compare the effectiveness of manual therapy in alleviating infant crying, a common symptom of nocturnal crying (NC) and infantile colic (IC). Methods: Total effective rate, crying time and adverse events were used as outcome indicators. To assess the quality, the risk of bias was determined for each study by two authors, using the Cochrane Collaboration's risk of bias tool. RevMan 5.0 was used for data analysis. A total of 98 articles were identified from 6 electronic databases. Results: Among them, twenty-seven studies which included 13 NC and 14 IC were included. Meta-analysis showed favorable effects tuina therapy on total effective rate (TER) of NC (RR 1.20 [95% CI 1.05 to 1.37], p = 0.007), chiropractic therapy on crying time change of IC (SMD -0.83 [95% CI -1.61 to -0.06], p = 0.04) and massage on total crying time of IC (SMD -0.86 [95% CI -1.09 to -0.63], p < 0.00001). This systematic review compares different manual therapies for the treatment of NC and IC. While tuina, chiropractic, and massage show results in alleviating symptoms, the overall evidence remains limited due to the low quality and heterogeneity of the included studies. Conclusion: Therefore, further high-quality research with unified control groups is needed to establish manual therapy as a recommended treatment option for NC and IC. Protocol registration number is CRD42022348143 01/08/2022.

Risk factors of emergency reoperations.

BACKGROUND: Emergency reoperation is considered to be a quality indicator in surgery. We analyzed the risk factors for emergency reoperations. METHODS: Patients who underwent emergency operations from January 1, 2017, to December 31, 2017, at our hospital were reviewed in this retrospective study. Multivariate logistic regression was performed for the perioperative risk factors for emergency reoperation. RESULTS: A total of 1,481 patients underwent emergency operations during the study period. Among them, 79 patients received emergency reoperations. The variables related to emergency reoperation included surgeries involving intracranial and intraoral lesions, highest mean arterial pressure ≥ 110 mmHg, highest heart rate ≥ 100 beats/min, anemia, duration of operation >120 min, and arrival from the intensive care unit (ICU). CONCLUSIONS: The type of surgery, hemodynamics, hemoglobin values, the duration of surgery, and arrival from ICU were associated with emergency reoperations.

Recovery of the Psoas Muscle Index in Living Donors after a Right Lobe Hepatectomy for Liver Transplantation: A Single-Center Experience.

OBJECTIVE: The development of sarcopenia leads to adverse postoperative outcomes. However, no study has investigated perioperative loss in core muscle and the correlation between core muscle and residual liver volume in living donors for liver transplant. PATIENTS AND METHODS: A total of 457 adult healthy donors who underwent a right lobe hepatectomy without the middle hepatic vein for elective liver transplant were retrospectively analyzed. Abdominal computed tomography was performed within 1 month before surgery and the first week and 3 months after the surgery. The average psoas muscle area between lumbar vertebrae 3 and 4 was measured and normalized by height squared (psoas muscle index [PMI] = psoas muscle area/height2). The initial whole liver volume and remnant left lobe volume were measured on computed tomography images. RESULTS: The study cohort included 279 men (61.1%) and 178 women (38.9%). The median preoperative PMIs were 420.9 mm2/m2 (interquartile range, 360.6-487.0 mm2/m2) in men and 280.9 mm2/m2 (interquartile range, 243.5-318.7 mm2/m2) in women. The PMIs in men and women significantly decreased during the first week after surgery, and gradually recovered to preoperative levels during the first 3 months after surgery. Based on the ratio between the remnant left lobe and initial whole liver volume (≥30%), the increase in remnant left lobe volume was not correlated with the decrease in PMI on postoperative day 7. A postoperative U-shaped recovery in the core muscles was present in both male and female donors, independent of the remnant liver ratio. CONCLUSIONS: Despite the requirements of partial liver regeneration and surgical wound repair, healthy donors did not suffer from sustained core muscle loss after surgery.

Iron mediates endothelial cell damage and blood-brain barrier opening in the hippocampus after transient forebrain ischemia in rats.

Blood cells are transported into the brain and are thought to participate in neurodegenerative processes following hypoxic ischemic injury. We examined the possibility that transient forebrain ischemia (TFI) causes the blood-brain barrier (BBB) to become permeable to blood cells, possibly via dysfunction and degeneration of endothelial cells in rats. Extravasation of Evans blue and immunoglobulin G (IgG) was observed in the hippocampal CA1-2 areas within 8 h after TFI, and peaked at 48 h. This extravasation was accompanied by loss of tight junction proteins, occludin, and zonula occludens-1, and degeneration of endothelial cells in the CA1-2 areas. Iron overload and mitochondrial free radical production were evident in the microvessel endothelium of the hippocampus before endothelial cell damage occurred. Administration of deferoxamine (DFO), an iron chelator, or Neu2000, an antioxidant, blocked free radical production and endothelial cell degeneration. Our findings suggest that iron overload and iron-mediated free radical production cause loss of tight junction proteins and degeneration of endothelial cells, opening of the BBB after TFI.

Blood-derived iron mediates free radical production and neuronal death in the hippocampal CA1 area following transient forebrain ischemia in rat.

Abnormal brain iron homeostasis has been proposed as a pathological event leading to oxidative stress and neuronal injury under pathological conditions. We examined the possibility that neuronal iron overload would mediate free radical production and delayed neuronal death (DND) in hippocampal CA1 area after transient forebrain ischemia (TFI). Mitochondrial free radicals (MFR) were biphasically generated in CA1 neurons 0.5-8 and 48-60 h after TFI. Treatment with Neu2000, a potent spin trapping molecule, as well as trolox, a vitamin E analogue, blocked the biphasic MFR production and attenuated DND in the CA1, regardless of whether it was administered immediately or even 24 h after reperfusion. The late increase in MFR was accompanied by iron accumulation and blocked by the administration of deferoxamine-an iron chelator. Iron accumulation was attributable to prolonged upregulation of the transferrin receptor and to increased uptake of peripheral iron through a leaky blood-brain barrier. Infiltration of iron-containing cells and iron accumulation were attenuated by depletion of circulating blood cells through X-ray irradiation of the whole body except the head. The present findings suggest that excessive iron transported from blood mediates slowly evolving oxidative stress and neuronal death in CA1 after TFI, and that targeting iron-mediated oxidative stress holds extended therapeutic time window against an ischemic event.

Neu2000, an NR2B-selective, moderate NMDA receptor antagonist and potent spin trapping molecule for stroke.

Excess activation of ionotropic glutamate receptors, primarily N-methyl-D-aspartate (NMDA) receptors and free radicals, evoke nerve cell death following hypoxic-ischemic brain injury in various animal models. However, clinical trials in stroke patients using NMDA receptor antagonists have failed to show efficacy primarily due to the limited therapeutic time window for neuroprotection and a narrow therapeutic index. In comparison, antioxidants prolonged the time window for neuroprotection in animal models of ischemic stroke and showed greater therapeutic potential in clinical trials for ischemic stroke. Excess activation of NMDA receptors and free radicals mediate the two separate pathways of nerve cell death in stroke and a safe and multifunctional drug that can block both routes in the brain will likely provide a better therapeutic outcome in patients with stroke. Derivatives of the lead structures of sulfasalazine and aspirin have led to the discovery of a new molecule, Neu2000, that has demonstrated excellent neuroprotection against NMDA- and free radical-induced cell death. Neu2000 is an NR2B-selective, moderate NMDA receptor antagonist with potent cell-permeable, spin trapping antioxidant action even at nanomolar concentrations. Nonclinical and human phase I studies demonstrated that Neu2000 can be translated to treat patients with stroke with better efficacy and therapeutic time window.

Induction of the unfolded protein response and cell death pathway in Alzheimer's disease, but not in aged Tg2576 mice.

The endoplasmic reticulum (ER) stress results from disrupted protein folding triggered by protein mutation or oxidation, reduced proteasome activity, and altered Ca2+ homeostasis. ER stress is accompanied by activation of the unfolded protein response (UPR) and cell death pathway. We examined if the UPR and cell death pathway would be activated in Alzheimer's disease (AD). RT-PCR experiments revealed increased splicing of X-box binding protein-1 (XBP-1), an UPR transcription factor, in AD compared with age-matched control. Among target genes of XBP-1, expression of protein disulfide isomerase (PDI), but not glucose-regulated protein 78 (GRP78), was increased in AD, suggesting disturbed activation of the UPR in AD. C/EBP homologous protein (CHOP), caspase-3, caspase-4, and caspase-12, downstream mediators of cell death pathway, were activated in AD. Neither the UPR nor cell death pathway was induced in aged Tg2576 mice, a transgenic mouse model of Alzheimer's disease that reveals both plaque pathology and some cognitive deficits. The present study suggests that disturbed induction of the UPR and activation of the pro-apoptotic proteins contribute to neuropathological process in AD irrespective of amyloid beta and senile plaque.

Free radical production in CA1 neurons induces MIP-1alpha expression, microglia recruitment, and delayed neuronal death after transient forebrain ischemia.

Several studies report microglial accumulation and activation in the CA1 area in response to transient forebrain ischemia (TFI). Here we examine the possibility that free radicals and chemokines mediate the transient activation of microglia. Free radicals are produced primarily in CA1 pyramidal neurons within 2 h of TFI. Administration of trolox, a vitamin E analog, led to the inhibition of free radical production and recruitment of microglia in the CA1 area. In addition, intrahippocampal injection of Fe2+ triggered free radical production in CA1 neurons, followed by the recruitment and activation of microglial cells into this area. TFI-induced expression of macrophage inflammatory protein-1alpha (MIP-1alpha) was increased in CA1 neurons before microglial recruitment, and blocked by trolox. Moreover, the MIP-1alpha level was upregulated in cultured hippocampal neurons exposed to Fe2+, suggesting an essential role of free radicals in TFI-induced expression of MIP-1alpha. Intracerebroventricular injection of vMIP-2 (viral macrophage inflammatory protein-2), a broad-spectrum peptide antagonist of chemokine receptors, attenuated microglial recruitment and delayed CA1 neuronal degeneration after TFI. Our data suggest that free radicals produced in CA1 neurons contribute to the recruitment and activation of microglia and neurodegeneration through MIP-1alpha expression.