Rejected

Whiplash neck injury was described by Crowe in 1928. Whiplash-associated disorder (WAD) is defined as a cervical spinal injury following an acceleration-deceleration mechanism. It is a constellation of symptoms due to psychological factors and neural adaptations, with significant social costs.

The aims were to examine the prevalence of comorbidities and role of oral analgesic use in people with knee pain (KP) compared with those without.

The negative rate of serum HBV DNA, HBeAg, and ALT in the tenofovir group was significantly higher than that in the entecavir group (86.67%, 3.33%, and 80.00%) (all < 0.05). In the tenofovir group, 2cases were considered. . The aim of this study is to analyze the clinical effect and safety of tenofovir in the treatment of chronic hepatitis B (CHB) patients. . A total of 60 patients with CHB who were admitted and treated in Anqing First People's Hospital Affiliated to Anhui Medical University from January 2019 to July 2020 were randomly assigned at a ratio of 1 : 1 into the tenofovir group (treated with tenofovir) and the entecavir group (treated with entecavir) via the random number table method. The clinical therapeutic effect and safety of the two groups were compared. . The serum hepatitis B virus (HBV) DNA levels in the two groups decreased after treatment, but there was no significant difference. Ths (2.50%) had nausea, 1 (1.25%) had headache, and 0 had an elevated creatine kinase. In the tenofovir group,1(3.33%) had nausea, 0 had headache, and 0 had an elevated creatine kinase. In the entecavir group, there were 3 (10.00%) cases of nausea, 2 (6.67%) cases of headache, and 1 (3.33%) case of elevated creatine kinase. The overall incidence of adverse reactions in the tenofovir group (3.33%) was significantly lower than that in the entecavir group (20.00%) (all < 0.05). . Tenofovir is more effective than entecavir in the treatment of patients with CHB due to low incidence of adverse events and a good safety profile.

Lower back pain (LBP) is one of the most common presenting complaints in clinical adult medical patients. While most often diagnosed as "nonspecific mechanical" in etiology, several lesser known, rarer causes of LBP exist, some of which can even cause neuropathic pain. One of these infrequent causes, cluneal neuralgia (CN), is associated most often with damage or entrapment of the cluneal nerves, particularly the superior cluneal nerve (SCN) and/or the middle cluneal nerve (MCN). These nerves supply sensation to the posterior lumbar and buttock area. However, the LBP caused by CN is often difficult to recognize because it can mimic radiculopathy or sacroiliac joint (SIJ) pain or lead to symptoms in the legs. This makes CN significantly important for clinicians and surgeons to include in their differential. A thorough history proves beneficial in the diagnostic workup, as many risk factors for CN have been reported in the literature. If a CN diagnosis is made, several effective conservative measures can alleviate patients' pain, such as nerve blocks, peripheral nerve stimulation, or high frequency thermal coagulation. Additionally, surgical treatments, such as CN release or endoscopic decompression, have resulted in fantastic patient outcomes. The purpose of the present investigation is to investigate the existing literature about CN as a cause for LBP, consider its epidemiology, discuss its pathophysiology and risk factors, elucidate its clinical presentation and diagnosis, and examine the various treatment modalities that have been reported across the world.

Ulcerative colitis is an inflammatory bowel disease. Opposite to Crohn's disease, it affects only the mucosa and submucosa of the large intestine. The disease can have episodes of flares and remissions. Endoscopy studies often disclose pseudopolyps, which are perceived as non-neoplastic and usually do not require removal. Rarely pseudopolyps can become big or even gigantic, leading to abdominal pain, bowel movement dysfunction, or even bowel obstruction. We present a case of a 37-year-old male patient with ulcerative colitis who was operated on because of a gigantic pseudopolyp causing bowel obstruction.

An estimated 20-25% of the population is affected by chronic, non-communicable inflammatory skin diseases. Chronic skin inflammation has many causes. Among the most frequent chronic inflammatory skin diseases are atopic dermatitis, psoriasis, urticaria, lichen planus, and hidradenitis suppurativa, driven by a complex interplay of genetics and environmental factors. Autoimmunity is another important cause of chronic skin inflammation. The autoimmune response may be mainly T cell driven, such as in alopecia areata or vitiligo, or B cell driven in chronic spontaneous urticaria, pemphigus and pemphigoid diseases. Rare causes of chronic skin inflammation are autoinflammatory diseases, or rheumatic diseases, such as cutaneous lupus erythematosus or dermatomyositis. Whilst we have seen a significant improvement in diagnosis and treatment, several challenges remain. Especially for rarer causes of chronic skin inflammation, early diagnosis is often missed because of low awareness and lack of diagnostics. Systemic immunosuppression is the treatment of choice for almost all of these diseases. Adverse events due to immunosuppression, insufficient therapeutic responses and relapses remain a challenge. For atopic dermatitis and psoriasis, a broad spectrum of innovative treatments has been developed. However, treatment responses cannot be predicted so far. Hence, development of (bio)markers allowing selection of specific medications for individual patients is needed. Given the encouraging developments during the past years, we envision that many of these challenges in the diagnosis and treatment of chronic inflammatory skin diseases will be thoroughly addressed in the future.

Upadacitinib is a selective small molecule that inhibits Janus kinase (JAK) type 1. This molecule is administrated orally and is currently approved for the treatment of rheumatoid arthritis, atopic dermatitis, and psoriatic arthritis. Upadacitinib has been approved by the United States Food and Drug Administration for the induction and maintenance therapy of moderate-to-severe ulcerative colitis (UC) and is under investigation by the European Medicines Agency. Data from two induction and two maintenance Phase III randomized controlled trials (RCTs) proved the efficacy of upadacitinib in achieving clinical and endoscopic remission in patients with moderate-to-severe UC, regardless of previous inadequate response to other biologic therapies. The most frequently reported adverse events in the induction trials were acne, creatine phosphokinase increase, nasopharyngitis, headache, and anemia, while in the maintenance studies nasopharyngitis, elevation of creatine phosphokinase, UC exacerbation, upper respiratory tract infection, arthralgia, and anemia were reported. A limited proportion of upadacitinib-treated patients experienced adverse events of special interest, like herpes zoster infections or thromboembolic events, indicating a reliable safety profile. The aim of this review is to summarize the available evidence on upadacitinib in UC providing useful insights about the positioning of this drug in the therapeutic algorithm.

An increase in COVID-19 immunization coverage has been linked to a decrease in the average case fatality rate. As a result, further research is needed to determine the persistence and duration of vaccine-induced protective antibodies in order to assess the effectiveness of COVID-19 vaccinations. The present study aimed to determine the COVID-19 IgG antibodies among healthcare workers (HCWs) before and after the ChAdOx1 nCoV-19 (Covishield™) vaccination. A total of 150 HCWs who had received the Covishield™ vaccine were assessed after obtaining written informed consent. Blood samples were drawn at three time points, namely, within one week prior to first dose of vaccination, prior to second dose of vaccination (28-33 days after the first dose of vaccination), and 90-95 days after the second dose of vaccination for detecting neutralizing antibodies, i.e., IgG antibodies by ELISA. The overall baseline seropositivity among the HCWs was found to be 28% ( = 42), assessed by the sample collected prior to first dose of COVID-19 vaccination. The seroconversion rate was reported to be 80% (  120) one month after the first dosage and increased to 92.7% (  139) three months later. Additionally, there was a significant gradual increase in the IgG concentrations postvaccination in majority of the study participants. In those HCWs who had prior history of SARS-CoV-2 infection, significantly higher antibody level was observed compared to antibody-naive individuals. Fever, pain or swelling at the site of injection, and headache were the most frequently reported adverse events following vaccination among the study participants. Regardless of prior SARS-CoV-2 positivity, two doses of the Covishield vaccine elicited a protective neutralizing antibody response that lasted for three months after the second dose of vaccination.

Chronic ethanol exposure causes neurotoxicity and long-term learning and memory impairment along with hippocampal and frontal cortical dysfunction. Flavonoids possess antioxidant and anti-inflammatory properties believed to be contributory factors in reversing cognitive decline. 6-Methoxyflavone (6-MOF), a flavonoid occurring naturally in medicinal plants, has been reported to instigate neuroprotection by reversing cisplatin-induced hyperalgesia and allodynia. Consequently, this study was designed to investigate 6-MOF activity in models of chronic ethanol-induced cognitive impairment along with neurochemical correlates.

N6-methyladenosine (mA) is the most abundant methylation modification on mRNA in mammals. Fat mass and obesity-related protein (FTO) is the main RNA mA demethylase. FTO is involved in the occurrence and maintenance of neuropathic pain (NP). NP often induces mental disorders. We found that NP downregulated the expression of FTO in the anterior cingulate cortex (ACC), inhibited the expression of matrix metalloproteinase-9 (MMP-9) in the ACC, maladjusted the brain-derived neurotrophic factor precursor (proBDNF) and mature brain-derived neurotrophic factor (mBDNF) levels in the ACC, and induced anxiety- and depression-like behaviors in mice. Blocking the downregulation of FTO in the ACC induced by peripheral nerve injury could reverse the anxiety- and depression-like behaviors of mice. Contrarily, downregulation of simulated FTO induced anxiety- and depression-like behaviors in mice. After peripheral nerve injury, the binding of FTO to MMP-9 mRNA decreased and the enrichment of mA on MMP-9 mRNA increased. In conclusion, downregulation of FTO in ACC by regulating MMP-9 mRNA methylation level contributes to the occurrence of anxiety- and depression-like behaviors in NP mice.