Objective To investigate the CT features of the invasion of sublingual space by malignant oropharyngeal tumors in order to provide more accurate information for clinical treatment. Methods Fifty-eight cases of pathologically proven malignant oropharyngeal tumors were collected and retrospectively analyzed. Results Among all the cases, invasion of sublingual space by malignant oropharyngeal tumors could be seen in 14 cases, of which, 7 cases got access to sublingual space through tongue base, 3 cases through parapharyngeal space, 2 cases through pterygomandibular raphe, 2 cases through uncertain routes. Invasion of sublingual space manifested on CT scan as obliteration of fat plane in sublingual space and involvement of the sublingual vessels in the space. Conclusion Malignant oropharyngeal tumors can invade the adjacent sublingual space via tongue base, pterygomandibular raphe, and parapharyngeal space. The invasion of sublingual space by malignant oropharyngeal tumors manifests in CT as effacement of sublingual fat plane and envelopment of hyoid artery.

Objective: To investigate the biological significance of CerbB-2 expression in nasopharyn-geal carcinoma. Methods: The expression of CerbB-2 was detected in 90 nasopharyngeal carcinoma tissues and 22 nasopharyngitis tissues by SP immunohistochemical method. The relationship between CerbB-2 ex-pression and clinicopathological characteristics of nasopharyngeal carcinoma was investigated. Results: The positive expression rate of CerbB-2 protein was 65.56% in nasopharyngeal carcinoma tissues, and 31.82% in nasopharyngitis tissues, with a significant difference (P<0.05). The ratio of expression was 81.0% in patients of N_2 and N_3 lymth node stage, significantly different from that in patients of N_0 and N_1 lymph node stage (52.1%, P<0.05). The expression of CerbB-2 gene was not correlated with age, gender, clinical stage, T stage and distant metastasis of nasopharyngeal carcinoma (P>0.05). Conclusion: There is a high expression of CerbB-2 in nasopharyngeal carcinoma tissues, which might be an important event in the pathogenesis and progression of nasopharyngeal carcinoma.

Objective: To discuss the relationship between lingual tonsil hypertrophy and laryngopharyngeal reflux. Methods: Ninety-two patients who received throat surgery in Nanfang Hospital between October 2015 and October 2016 were enrolled. Twenty-six healthy volunteers were recruited as normal controls. All participants were assessed with the reflux finding score(RFS) and the size of lingual tonsils were evaluated using a clinical grading system proposed by Friedman under electronic laryngoscope. The score of reflux symptom index(RSI), personal history and medical history were gathered. Biopsy specimens of lingual tonsils were taken from all participants for the immunohistochemical stain of pepsin.SPSS 19.0 software was used for statistical analysis. Results: There were 46.2% (12/26) pepsin-positive and 53.8% (14/26) pepsin-negative volunteers in normal controls. There were 87.0% (80/92) pepsin-positive and 13.0% (12/92) pepsin-negative patients in study group. The severity of lingual tonsil hypertrophy and expression intensity of pepsin in patients were significantly higher in volunteers (Z=-3.636, Z=-5.273, P<0.01). The severity of lingual tonsil hypertrophy was positively associated with the pepsin level in patients (r=0.556, P<0.01). The patients with pepsin-positive expression showed significant correlation between lingual tonsil hypertrophy and the positive rate of RSI and RFS (r=0.258, r=0.225, P<0.05). Analysis of correlated factors indicated that lingual tonsil hypertrophy was associated with smoking (χ²=8.502, P<0.05). Conclusions The expression of pepsin can be detected in lingual tonsil tissues. The lingual tonsil hypertrophy is closely related to laryngopharyngeal reflux.

OBJECTIVE To explore the role of clinical pharmacists in identifying paroxysmal spasms caused by drugs， and provide reference for rational drug use. METHODS Retrospective analysis was conducted on pharmaceutical care provided by clinical pharmacists for a patient with ceftazidime-avibactam （CZA-AVI） induced paroxysmal spasms. The clinical pharmacists identified， analyzed and summarized the clinical manifestations， risk factors and treatment methods of the nervous system toxicity caused by antibacterial drugs. According to the patient’s clinical symptoms and test results， the clinical pharmacists recommended temporarily discontinuing the use of polymyxin B and montelukast sodium， and halving the dose of CZA-AVI. The physicians did not adopt the recommendation to halve the dose of CZA-AVI， and when the patient’s neurologic toxicity did not improve， the clinical pharmacists again recommended discontinuing CZA-AVI， which was accepted by the physicians. RESULTS Clinical pharmacists analyzed the condition and checked related drugs that caused paroxysmal spasms of extremities one by one， and finally determined that CZA-AVI might be the drug that caused paroxysmal spasms of extremities in the patient. After stopping the drug， the patient’s symptoms improved and was transferred to a community hospital for rehabilitation treatment. CONCLUSIONS The dose of CZA-AVI should be adjusted according to the renal function and the neurotoxicity should be guarded against， especially for patients with advanced age， renal insufficiency， and the combined use of multiple drugs related to nephrotoxicity and neurotoxicity.

Endocrine-resistance remains a major challenge in estrogen receptor α positive (ERα⁺) breast cancer (BC) treatment and constitutively active somatic mutations in ERα are a common mechanism. There is an urgent need to develop novel drugs with new mode of mechanism to fight endocrine-resistance. Given aberrant ERα activity, we herein report the identification of novel covalent selective estrogen receptor degraders (cSERDs) possessing the advantages of both covalent and degradation strategies. A highly potent cSERD 29c was identified with superior anti-proliferative activity than fulvestrant against a panel of ERα⁺ breast cancer cell lines including mutant ERα. Crystal structure of ERα‒ 29c complex alongside intact mass spectrometry revealed that 29c disrupted ERα protein homeostasis through covalent targeting C530 and strong hydrophobic interaction collied on H11, thus enforcing a unique antagonist conformation and driving the ERα degradation. These significant effects of the cSERD on ERα homeostasis, unlike typical ERα degraders that occur directly via long side chains perturbing the morphology of H12, demonstrating a distinct mechanism of action (MoA). In vivo, 29c showed potent antitumor activity in MCF-7 tumor xenograft models and low toxicity. This proof-of-principle study verifies that novel cSERDs offering new opportunities for the development of innovative therapies for endocrine-resistant BC.