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ObjectiveTo investigate the influence of triglyceride （TG）/high-density lipoprotein cholesterol （HDL-C） ratio on the onset of primary liver cancer. MethodsA prospective cohort study was conducted. Physical examination data were collected from 99 750 cases of on-the-job and retired employees of Kailuan Group who participated health examination from July 2006 to December 2007， and they were followed up till December 31， 2021 to observe the onset of primary liver cancer. A one-way analysis of variance was used for comparison of normally distributed continuous data between multiple groups， and the Kruskal-Wallis H test was used for comparison of continuous data with skewed distribution between multiple groups； the chi-square test was used for comparison of categorical data between groups. According to the tertiles of TG/HDL-C ratio， the subjects were divided into Q1， Q2， and Q3 groups， and the incidence density of primary liver cancer was calculated for each group. The Kaplan-Meier method was used to calculate the cumulative incidence rate of primary liver cancer in each group， and the log-rank test was used to compare the difference in cumulative incidence rate between groups. The Cox proportional hazards model was used to analyze the influence of TG/HDL-C ratio on the onset of primary liver cancer. ResultsThere were significant differences between the three groups in age， proportion of male subjects， waist circumference， body mass index， fasting blood glucose， systolic pressure， diastolic pressure， triglyceride， total cholesterol， HDL-C， low-density lipoprotein cholesterol， alanine aminotransferase， high-sensitivity C-reactive protein， chronic liver diseases， hypertension， diabetes， the family history of malignant tumor， drinking， smoking， physical exercise， and educational level （P<0.05）. During the mean follow-up time of 14.06±2.71 years， there were 484 cases of new-onset liver cancer， among whom there were 446 male subjects and 38 female subjects. The incidence density of primary liver cancer was 0.39/1 000 person-years in the Q1 group， 0.35/1 000 person-years in the Q2 group， and 0.30/1 000 person-years in the Q3 group， and the cumulative incidence rates of primary liver cancer in the three groups were 6.03‰， 5.28‰， and 4.49‰， respectively， with a significant difference between the three groups based on the long-rank test （χ2=6.06， P=0.048）. After adjustment for the confounding factors considered， the Cox proportional hazards model showed that compared with the Q3 group， the Q1 group had a hazard ratio of 2.04 （95% confidence interval ［CI］： 1.61 — 2.58， Pfor trend<0.05）， and the Q2 group had a hazard ratio of 1.53 （95%CI： 1.21 — 1.92， Pfor trend<0.05）. ConclusionThe reduction in TG/HDL-C ratio is associated with an increase in the rask of primary liver cancer， especially in people with chronic liver diseases.
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ObjectiveTo investigate the effects of Buyang Huanwutang （BYWHT） on reducing inflammatory injury and improving neurological function after cerebral ischemia-reperfusion in rats via activating the adiponectin （APN） pathway. MethodMale SD rats were randomized into sham， model， BYHWT （16 g·kg-1， twice a day）， and BYHWT + APN inhibitor （GW9662） groups. In the sham group， blood vessels were isolated. The rat model of middle cerebral artery occlusion （MCAO） was established. The rats in the BYHWT+GW9662 group was treated with subcutaneous injection of GW9662 at 4 m·kg-1 30 min before MCAO surgery and BYHWT at 16 g·kg-1 by gavage after MCAO surgery， once in the morning and once in the evening. The immunofluorescence （IF） assay was employed to observe the expression of adiponectin receptor 1 （AdipoR1） and the colocalization of AdipoR1 with neuronal nuclei （NeuN） and ionized calcium binding adaptor molecule 1 （Iba1） in the brain. Enzyme-linked immunosorbent assay （ELISA） was employed to detect the expression of APN in the serum and brain. The balance beam test was carried out to examine the balance ability， and the grasping test to assess the recovery of limb strength. The immunofluorescence assay was used to detect the expression of myeloperoxidase （MPO）. Western blot was employed to determine the expression of tumor necrosis factor-alpha （TNF-α）， interleukin （IL）-1β， IL-6， and IL-10 and in the brain. ResultCompared with the sham group， the modeling promoted the expression of AdipoR1 （P<0.01）， lowered the APN levels in the serum and brain （P<0.05， P<0.01）， increased the score in the balance beam test （P<0.01）， and decreased the grasping strength of forepaw （P<0.01）， which were accompanied with increased MPO， TNF-α， IL-1β， and IL-6 levels （P<0.01） and decreased IL-10 level （P<0.01）. Compared with the model group， BYHWT promoted the expression of AdipoR1 （P<0.01）， elevated APN levels in the serum and brain （P<0.05， P<0.01）， and increased the grasping strength of forepaw （P<0.01）， which were accompanied with lowered MPO， TNF-α， IL-1β， and IL-6 levels （P<0.01） and elevated IL-10 level （P<0.01）. All the above effects were partially blocked by GW9662. ConclusionBYHWT can reduce inflammatory injury and improve neurological function in the rat model of cerebral ischemia-reperfusion by activating the APN pathway.
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Objective To describe the clinical features, differential diagnosis and therapeutic method of Madras motor neuron disease (MMND) to improve the understanding of MMND. Methods We retrospectively summarized the clinical data of 3 MMND patients. and conducted the related literature review to compare the similarities and differences on clinical features between our cases and foreign MMND patients. Results Patients in the present study were adult-on?set without definite family history. The main manifestations were multiple lower cranial nerve palsies along with weakness and wasting of proximal limbs. Bifacial palsy and dysarthria were most presented in patients, while definite hearing im?pairment was rarely seen. Two patients had fasciculation and atrophy in tongue and one presented with dysphagia. Weak?ness and atrophy were more frequently presented in upper extremities than in lower limbs. All patients had signs of upper motor neuron damage. The level of creatine kinase (CK) moderately increased in one case. Electromyography (EMG) de?tected a widespread neuronal damage in all patients. MMND should be differentiated from Amyotrophic Lateral Sclerosis, Kennedy Disease and Brown–Vialetto–van Laere Syndrome. Intravenous immunoglobulin therapy showed effective in some cases to some extent. Compare to foreign MMND patients, bifacial weakness at onset was more frequently presented in our patients, but hearing impairment was absent. Conclusion The clinical features of MMND include weakness and at?rophy of limbs, involvement of facial and bulbar muscles, pyramidal dysfunction and hearing impairment. Some clinical manifestations of our patients are different from foreign MMND patient.
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Objective To analyze the clinical features of 35 cases of Kennedy's disease and the correlation be?tween clinical features and CAG repeat size to strengthen the understanding of KD and to avoid misdiagnosis and delayed diagnosis.Methods Clinical data, including clinical signs and symptoms ,serum lipid, serum sex hormone level, electro?myography, the number of CAGs and (amyotrophic lateral sclerosis muscular atrophy,ALS) rating scale were collected from 35 patients genetically diagnosed of Kennedy disease and proceed system analysis. Results Patients with KD were adult onset with the average age of (40.77 ± 8.57) years and the average confirmed course were (8.32 ± 4.17) years. Forty-two point nine percent of the patients had family history. Clinical features included medulla oblongata and spinal muscular atrophy and weakness, limbs tremor, perioral muscles twitch and endocrine function and metabolic disorders in some cases. Creatine kinase, triglyceride, low density lipoprotein, follicle estrogen and prolactin were significantly in?creased compared to healthy adults (P:0.000,0.018,0.000,0.000,0.003). The number of CAG repeat was negatively correlated with the onset age (r=-0.549, P=0.001) but not associated with the illness severity (ALS rating scale) (r=0.001, P=0.998). ALS score was negatively correlated with course of disease(r=-0.540, P=0.001).Conclusions Chinese KD pa? tients share similar clinical phenotypes with those of other races but exhibit slightly different clinical characteristics. The length of the CAG repeat influences age at onset but not the severity of disease. Severity of disease is related to the course of disease.
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Objective To discuss the clinical value of partial splenic embolization in the treatment of schistosomial hypersplenism. Methods Peripheral partial splenic embolization using gelatin sponge (gelfoam) was performed in 17 cases of schistosomial hypersplenism. Results The amount of devascularized parenchyma was 50%~75% (mean, 59%). Postoperative follow-up was conducted for 6~29 months (mean, 16.9 months) in all the 17 cases. The leucocyte count was elevated significantly on the latest follow-up (5.74?1.31?109/L), as compared with the preoperative value (2.19?0.73?109/L) (t=11.86,P=0.000). The platelet count was significantly higher on the latest follow-up (106.18?30.92 ?109/L) than before the embolization (31.29?14.09?109/L) (t=8.28,P=0.000). No severe complications were seen. Conclusions Partial splenic embolization in the treatment of schistosomial hypersplenism is safe and effective, but its long-term effects remain a question to be answered through further research.
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Objective To evaluate the clinical application of partial splenic embolization in the treatment o hypersplenism caused by schistosomiasis. Methods Twenty four patients with hypersplenism caused by schistosomiasis were treated with peripheral partly splenic embolization with gelf.oam. The counts of white blood cell(WBC) and platelet (PLT) were compared between pre-and post-splenic embolization. Results The extent of splenic embolization were 50% - 75%(mean 59.24%) with post-therapeutic follow-up of 6 months ~ 2 years, showing significant increase of WBC count with preoperative, peak and the latest follow-up counts as (2.15?0.67)?109/L, (12.36?3.24)?109/L and (5.65?1.38)?109/L respectively(t = 11.08, P