Rejected

The Immunoglobulin G4-related disease (IgG4-RD) is a multisystem inflammatory condition. Pancreaticobiliary manifestations often present as mass lesions that mimic malignancies. The diagnosis is confirmed by histopathological examination, that shows lymphoplasmacytic infiltration, storiform fibrosis, obliterative phlebitis, and positive immunohistochemistry for IgG4. We encountered 3 such patients in a tertiary care hospital in India. Two patients presented with obstructive jaundice and the third with pain abdomen. They had resectable lesions involving the pancreatic head, the right hepatic duct, and gallbladder fundus, respectively, on imaging. Tumor markers were not significantly elevated in any of them. All 3 patients underwent radical surgeries, suspecting malignancy. Surgical specimens showed typical features of IgG4-RD on histomorphology. Serum IgG4 level was elevated in first 2 patients but was normal in sclerosing cholecystitis patient. To conclude, IgG4-RD is a malignant mimicker; hence, on clinical suspicion, liberal attempts for tissue diagnosis may avoid radical surgeries.

Artificial intelligence-assisted interactive health promotion systems are useful tools for the management of musculoskeletal conditions.

Adjuvant medical expulsive therapy (MET) for shock wave lithotripsy (SWL) is controversial. With limited use of the computed tomography (CT), the stone free rate (SFR) become overestimated. Herein we evaluate tamsulosin post-SWL for renal stone using the CT to assess SFR. A randomized controlled trial (NCT05032287) was carried out for renal stone patients amenable for SWL. Patients were allocated after 1st session of SWL to receive tamsulosin 0.4 mg or placebo once daily from the 1st day of SWL and for 3-months or becoming stone free. The primary outcome was SFR, defined by presence of residual fragments (RF) ≤ 3 mm (3C-SFR). The 3C-SFR were 73.8% and 59.6% in tamsulosin and placebo groups, respectively (p = 0.03). The median (IQR) pain scores were 3 (3, 5) and 5 (3, 6) in tamsulosin and placebo groups, respectively (p = 0.04), However, the post-SWL complication and add-on analgesia needed showed no significance differences between groups. The median time for stone free were 30 days (95% CI: 27.29-32.71) in tamsulosin arm, and 36 days (95% CI: 31.01-40.99) in placebo arm, HR = 1.42 (95% CI: 1.02-1.98). Tamsulosin has more reversible adverse effect, compared to placebo (p = 0.03). In our study, the use of tamsulosin as MET following SWL facilitates expulsion of retained residual fragments. Tamsulosin shortens time to reach stone free, decreases pain scores. However, tamsulosin does not affect the add-on IV analgesics and have more reversible adverse effect, compared to placebo.

The aetiologic diagnosis of non-traumatic acute myelopathies (AMs), and their differentiation from other mimicking conditions (i.e. 'mimics'), are clinically challenging, especially in the emergency setting. Here, we sought to identify: (i) red flags suggesting diagnoses alternative to AMs and (ii) clinical signs and magnetic resonance imaging (MRI) features differentiating non-compressive from compressive AMs.

In hypertrophied and failing hearts, fuel metabolism is reprogrammed to increase glucose metabolism, especially glycolysis. This metabolic shift favors biosynthetic function at the expense of ATP production. Mechanisms responsible for the switch are poorly understood. We found that inhibitory factor 1 of the mitochondrial FoF1-ATP synthase (ATPIF1), a protein known to inhibit ATP hydrolysis by the reverse function of ATP synthase during ischemia, was significantly upregulated in pathological cardiac hypertrophy induced by pressure overload, myocardial infarction, or α-adrenergic stimulation. Chemical cross-linking mass spectrometry analysis of hearts hypertrophied by pressure overload suggested that increased expression of ATPIF1 promoted the formation of FoF1-ATP synthase nonproductive tetramer. Using ATPIF1 gain- and loss-of-function cell models, we demonstrated that stalled electron flow due to impaired ATP synthase activity triggered mitochondrial ROS generation, which stabilized HIF1α, leading to transcriptional activation of glycolysis. Cardiac-specific deletion of ATPIF1 in mice prevented the metabolic switch and protected against the pathological remodeling during chronic stress. These results uncover a function of ATPIF1 in nonischemic hearts, which gives FoF1-ATP synthase a critical role in metabolic rewiring during the pathological remodeling of the heart.

Dietary intake of caffeine has significantly increased in recent years, and beneficial and harmful effects of caffeine have been extensively studied. This paper reviews antioxidant and anti-inflammatory activities of caffeine as well as its protective effects on cardiovascular diseases, obesity, diabetes mellitus, cancers, and neurodegenerative and liver diseases. In addition, we summarize the side effects of long-term or excessive caffeine consumption on sleep, migraine, intraocular pressure, pregnant women, children, and adolescents. The health benefits of caffeine depend on the amount of caffeine intake and the physical condition of consumers. Moderate intake of caffeine helps to prevent and modulate several diseases. However, the long-term or over-consumption of caffeine can lead to addiction, insomnia, migraine, and other side effects. In addition, children, adolescents, pregnant women, and people who are sensitive to caffeine should be recommended to restrict/reduce their intake to avoid potential adverse effects.

To investigate the clinical outcomes of partial sensory root rhizotomy (PSR) on patients with recurrence of multiple sclerosing trigeminal neuralgia(TN-MS) after percutaneous balloon compression (PBC).

The aim of this research was to investigate the effects of telerehabilitation-based remote supervised or unsupervised structured exercise therapy on pain, disability, and quality of life related to chronic nonspecific neck pain.

Calcitonin gene-related peptide (CGRP) was first discovered in the 1980s as a splice variant from the calcitonin gene. Since its discovery, its role in migraine pathophysiology has been well established, first by its potent vasodilator properties and subsequently by its presence and function as a neurotransmitter in the sensory trigeminovascular system. The migraine-provoking ability of CGRP gave support to the pharma industry to develop monoclonal antibodies and antagonists inhibiting the effect of CGRP. A new treatment paradigm has proven effective in the prophylactic treatment of migraine. One of the useful tools to further understand migraine mechanisms is the ex vivo model of CGRP release from the trigeminovascular system. It is a relatively simple method that can be used with various pharmacological tools to achieve know-how to further develop new effective migraine treatments. The present protocol describes a CGRP release model and the technique to quantify the effect of pharmacological agents on the amount of CGRP released from the trigeminovascular system in rodents. A procedure describing the experimental approach from euthanasia to the measurement of protein levels is provided. The essential isolation of the trigeminal ganglion and the trigeminal nucleus caudalis from both mice and rats and the preparation of rat dura mater are described in detail. Furthermore, representative results from both species (rats and mice) are presented. The technique is a key tool to investigate the molecular mechanisms involved in migraine pathophysiology by using various pharmacological compounds and genetically modified animals.

Dexmedetomidine has sedative, sympatholytic, analgesic, and anti-inflammatory effects. We investigated the effects of intraoperative dexmedetomidine infusion without a loading dose in the prevention of pain and inflammation after laparoscopic hysterectomy. In this study, 100 patients undergoing laparoscopic hysterectomy under desflurane anesthesia were randomized to receive either 0.9% saline or dexmedetomidine (0.4 μg/kg/h) after induction to trocar removal. The primary endpoints were postoperative pain and inflammatory response presented by the level of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-10, and C-reactive protein (CRP). The secondary endpoints were hemodynamics during the anesthesia and surgery and postoperative nausea and vomiting. Postoperative pain was decreased in the dexmedetomidine group for every time point, and post-anesthesia care unit (PACU) rescue fentanyl doses were decreased in the dexmedetomidine group. The inflammatory response representing TNF-α, IL-6, IL-10, and CRP were similar across the two groups. Postoperative nausea and vomiting from PACU discharge to 24 h post-surgery were reduced in the dexmedetomidine group. During anesthesia and surgery, the patient's heart rate was maintained lower in the dexmedetomidine-receiving group. Dexmedetomidine of 0.4 μg/kg/h given as an intraoperative infusion significantly reduced postoperative pain but did not reduce the inflammatory responses in patients undergoing laparoscopic hysterectomy.