Trigger finger at the wrist caused by an intramuscular lipoma within the carpal tunnel: A case report.

BACKGROUND: Trigger finger at the wrist, which occurs with finger movement, is an uncommon presentation. Few reports describing cases of trigger finger at the wrist have been published. Thus, we present a case of an intramuscular lipoma arising from an anomalous flexor digitorum muscle belly in a 48-year-old female patient causing painful finger triggering at the wrist and carpal tunnel syndrome (CTS). CASE SUMMARY: A 48-year-old woman with complaints of a catching sensation during wrist motion and a progressive tingling sensation on the palmar aspect of the right hand for approximately 2 years was referred to our hospital. Triggering of the index to middle finger was evident with a palpable and audible clunk over the carpal tunnel during passive motion. Tinel's sign was positive over the carpal tunnel of the right wrist with a positive Phalen's test. Nerve conduction studies of the median nerve demonstrated a right CTS. Ultrasound examination revealed a 2.5 cm × 2.0 cm subcutaneous hyperechoic mass with no obvious blood flow at the wrist of the right arm. Surgical excision of the tumor and muscle mass led to a resolution of the patient's symptoms, and any triggering or discomfort disappeared. The patient has had no evidence of recurrence at more than 1 year of follow-up. CONCLUSION: Triggering of the fingers at the wrist is rare. It must be noted that there are many possible causes and types of triggering or clicking around the wrist. Accurate diagnosis is mandatory to avoid inaccurate treatment of patients with trigger wrist. During the diagnosis and treatment of CTS, attention should be paid to the variation of tendon tissue in the carpal tunnel, to avoid only focusing on the release of transverse carpal ligament and ignoring the removal of anomalous muscle belly.

LncRNA MEG3 Participates in Caerulein-Induced Inflammatory Injury in Human Pancreatic Cells via Regulating miR-195-5p/FGFR2 Axis and Inactivating NF-κB Pathway.

Acute pancreatitis (AP) is a dysfunctional pancreas disease marked by severe inflammation. Long non-coding RNAs (lncRNAs) involving in the regulation of inflammatory responses have been frequently mentioned. The purpose of this study was to ensure the function and action mode of lncRNA maternally expressed gene 3 (MEG3) in caerulein-induced AP cell model. HPDE cells were treated with caerulein to establish an AP model in vitro. The expression of MEG3, miR-195-5p, and fibroblast growth factor receptor 2 (FGFR2) was measured using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation and apoptosis were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry assay, respectively. The expression of CyclinD1, B cell lymphoma/leukemia-2 (Bcl-2), Bcl-2-associated X protein (Bax), FGFR2, P65, phosphorylated P65 (p-P65), alpha inhibitor of nuclear factor kappa beta (NF-κB) (IκB-α), and phosphorylated IκB-α (p-IκB-α) at the protein level was quantified by western blot. The concentrations of tumor necrosis factor α (TNF-α), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6) were monitored by enzyme-linked immunosorbent assay (ELISA). The targeted relationship between miR-195-5p and MEG3 or FGFR2 was forecasted by the online software starBase v2.0 and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. As a result, the expression of MEG3 and FGFR2 was decreased in caerulein-induced HPDE cells, while the expression of miR-195-5p was increased. MEG3 overexpression inhibited cell apoptosis and inflammatory responses that were induced by caerulein. Mechanically, miR-195-5p was targeted by MEG3 and abolished the effects of MEG3 overexpression. FGFR2 was a target of miR-195-5p, and MEG3 regulated the expression of FGFR2 by sponging miR-195-5p. FGFR2 overexpression abolished miR-195-5p enrichment-aggravated inflammatory injuries. Moreover, the NF-κB signaling pathway was involved in the MEG3/miR-195-5p/FGFR2 axis. Collectively, MEG3 participates in caerulein-induced inflammatory injuries by targeting the miR-195-5p/FGFR2 regulatory axis via mediating the NF-κB pathway in HPDE cells.

Interaction between Schwann cells and other cells during repair of peripheral nerve injury.

Peripheral nerve injury (PNI) is common and, unlike damage to the central nervous system injured nerves can effectively regenerate depending on the location and severity of injury. Peripheral myelinating glia, Schwann cells (SCs), interact with various cells in and around the injury site and are important for debris elimination, repair, and nerve regeneration. Following PNI, Wallerian degeneration of the distal stump is rapidly initiated by degeneration of damaged axons followed by morphologic changes in SCs and the recruitment of circulating macrophages. Interaction with fibroblasts from the injured nerve microenvironment also plays a role in nerve repair. The replication and migration of injury-induced dedifferentiated SCs are also important in repairing the nerve. In particular, SC migration stimulates axonal regeneration and subsequent myelination of regenerated nerve fibers. This mobility increases SC interactions with other cells in the nerve and the exogenous environment, which influence SC behavior post-injury. Following PNI, SCs directly and indirectly interact with other SCs, fibroblasts, and macrophages. In addition, the inter- and intracellular mechanisms that underlie morphological and functional changes in SCs following PNI still require further research to explain known phenomena and less understood cell-specific roles in the repair of the injured peripheral nerve. This review provides a basic assessment of SC function post-PNI, as well as a more comprehensive evaluation of the literature concerning the SC interactions with macrophages and fibroblasts that can influence SC behavior and, ultimately, repair of the injured nerve.

Repair of soft tissue and extensor tendon defects on the dorsum of the hand by transfer of dorsal foot flap and extensor digitorum brevis tendon in a 3-year-old child: A case report.

RATIONALE: Repair of soft tissue defects on the dorsum of the hand with accompanying tendon defects is a challenging problem in clinical practice. PATIENT CONCERNS: Here, we describe the case of a 3-year-old boy with a 1-week old soft tissue injury with infection due to a soft tissue defect on the dorsum of his right hand, and further describe its treatment. DIAGNOSIS: A diagnosis of a soft tissue defect of the dorsum with extensor tendon defects in the fore, middle, ring, and little fingers of the right hand was made. INTERVENTIONS: The defects were repaired using a dorsal foot flap combined with the extensor digitorum brevis tendon, under spinal anesthesia, and a small dose of the sedative phenobarbital (Lumina) was administered via pump injection after the surgery. OUTCOMES: The patient was followed-up for 6 months. The shape of the dorsal hand flap recovered satisfactorily and the skin color was almost normal. Protective sensation was restored and the tendon graft functioned well in vivo. Satisfactory outcomes were achieved in the flexion and extension of each finger. LESSONS: This case study provides evidence that for soft tissue defects on the dorsum of the hand with tendon defects, 1-stage transfer of a dorsal foot flap with the extensor digitorum brevis tendon can be effective for recovery of appearance and extensor function. In case of infant patients, postoperative use of low-dose sedation can effectively reduce the risk of vascular crisis, thus promoting survival of the flap graft, and ensuring the success of the operation.

LPS promotes the progression of sepsis by activation of lncRNA HULC/miR-204-5p/TRPM7 network in HUVECs.

Sepsis is a systemic inflammatory response syndrome caused by infection. Lipopolysaccharide (LPS) has been reported to induce inflammatory responses, and long non-coding RNA highly up-regulated in liver cancer (HULC) expression was associated with the progression of sepsis. But the role and underlying mechanism of HULC in LPS-induced sepsis remain unclear. Cell viability and apoptosis were measured by methyl thiazolyl tetrazolium (MTT) and flow cytometry assays, respectively. The levels of apoptosis-related proteins, inflammatory cytokines and transient receptor potential melastatin7 (TRPM7) were detected by western blot. Reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA) levels were detected by dichloro-dihydro-fluorescein diacetate (DCFH-DA) method using commercial kit. HULC, microRNA-204-5p (miR-204-5p) and TRPM7 expressions in serum of sepsis patients and human umbilical vein endothelial cells (HUVECs) were examined by quantitative real-time polymerase chain reaction (qRT-PCR). Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to confirm the interaction between HULC and miR-204-5p, miR-204-5p and TRPM7. LPS stimulation restrained cell viability and facilitated apoptosis, inflammatory injury and oxidative stress in HUVECs. HULC and TRPM7 were increased and accompanied with decreased miR-204-5p expression in serum of sepsis patients. A significant negative correlation between miR-204-5p and HULC or TRPM7 was observed, and there was a positive relationship between expressions of HULC and TRPM7. Importantly, LPS inhibited the cell viability and induced apoptosis, inflammatory injury and oxidative stress of HUVECs by up-regulating the expressions of HULC and TRPM7, and down-modulating miR-204-5p expression. Mechanically, HULC positively regulated TRPM7 expression by sponging miR-204-5p in HUVECs. LPS impaired cell viability, and promoted cell apoptosis, inflammatory response and oxidative stress in HUVECs by regulating HULC/miR-204-5p/TRPM7 axis.

Case Report: Viral Shedding for 60 Days in a Woman with COVID-19.

Novel coronavirus disease (COVID-19) caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) has become a public health emergency of international concern. This was first noted in Wuhan, Hubei Province, China, and since then has become widespread globally. We report a 71-year-old woman with documented viral shedding (based on reverse transcription-polymerase chain reaction (RT-PCR) testing) of SARS-CoV-2 for 60 days from the onset of symptoms (55 days from her first positive test and 36 days after complete resolution of symptoms). This is to our knowledge the longest duration of viral shedding reported to date. This case demonstrates that viral shedding after COVID-19 diagnosis can be prolonged.

[Study on the clinical epidemiological features of acute cerebral stroke inducing systemic inflammatory response syndrome and multiple organ dysfunction syndrome].

OBJECTIVE: To study the risks on acute cerebral stroke (ACS) inducing systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). METHODS: Data from 1751 patients with acute cerebral stroke were studied by prospective analysis. RESULTS: In all of the ACS patients,the incidence rate (IR) of SIRS was 36.50% with 205 patients having ACS inducing MODS, to which the IR was 11.71%, and 93 deaths. The case fatality ratio (CFR) was 45.37%. The pathogeneses condition of patients and the MR after the occurrence of MODS had positive correlation with the numbers of dysfunction organs. Study on single factor analysis revealed that the incidence of MODS had some related risk factors in the ACS inducing MODS, including age, diseased region close to the mean line, GCS, level of blood sugar, blood white cell count and the chronic disease history etc. The IR of ACS inducing SIRS and MODS was much higher in the condition of the diseased region near the mean line and the ACS of the basilar artery system. CONCLUSION: SIRS seemed the base for MODS while the probability and the development degree were not only involved ACS but also SIRS. MODS induced by ACS could be reduced through the second grade program of disease precaution. The detection of those risk factors in the early period of the ACS course could provide some prediction of the prognosis and turnover, thus some early use of intervention methods might be helpful in the treatment of the disease.