Minimally Invasive Cytopathology and Accurate Diagnosis: Technical Procedures and Ancillary Techniques.

In recent years, the demand for cytopathological accurate diagnoses has increased as expanding minimally invasive procedures obtain materials from patients with advanced cancer for diagnostic, prognostic, and predictive purposes. However, inadequate knowledge of cytopathological technical procedures and ancillary techniques by clinicians remains the most common reason for the limited availability of cytopathology. The objectives of this review were to understand the technical procedures, ancillary techniques, and application and effectiveness of various types of tests in cytopathology. Each of the many ancillary technologies described in the literature has specific advantages and limitations and laboratories select one or more methods depending on their infrastructure and expertise to achieve the goal from initial screening of the disease to the final diagnosis of the cytopathology. This paper systematically reviews the development of cytopathology, summarizes the existing problems in cytopathology and the new progress of auxiliary examination, to provide a theoretical basis for the advanced development of cytopathological diagnostic technologies and to consolidate the minimally invasive and accurate diagnosis of cytopathologies for clinicians. Cytopathology offers many advantages over other clinical examinations, particularly for minimally invasive and accurate diagnosis.

[Study on mechanism of Fangji Huangqi Decoction on hypouricemic effect and renal protection in hyperuricemia mice].

The aim of this paper was to study the specific mechanism of Fangji Huangqi Decoction(FHT) in decreasing uric acid and improving renal function in mice with hyperuricemia(HUA) induced by potassium oxonate, so as to provide theoretical basis for the research and development of drugs for clinical prevention and treatment of HUA and the modernization of traditional Chinese medicine. Sixty Kunming male mice were randomly divided into 6 groups, with 10 mice in each group, namely normal group, model group(250 mg·kg~(-1) potassium oxonate), FHT high, medium and low-dose groups(10 920, 5 460, and 2 730 mg·kg~(-1)) and positive drug allopurinol group(5 mg·kg~(-1)). Drug administration was given once a day for 7 days. On the 6 th day, mice of each group were kept in metabolic cages, and their urine was collected for 24 hours for determination of uric acid, creatinine, and ß2-microglobulin(ß2-MG) levels. After 7 days, the animals were sacrificed to determine serum uric acid, creatinine ß2-MG and interleukin-1ß(IL-1ß) levels, and their liver and kidney tissues were collected. The liver tissues were used for subsequent determination of xanthine oxidase(XOD) activity, and the kidney tissues were used for subsequent determination of IL-1ß levels, pathological tests and related Western blot experiments. In the cell transfection experiment, the cells were divided into blank group, model group(4.8 mmol·L~(-1) uric acid treatment), FHT administration group(4.8 mmol·L~(-1) uric acid+200 µg·mL~(-1) FHT), leucine-rich repeat kinase 1(LRRK1)-small interfering RNA(siRNA) group(4.8 mmol·L~(-1) uric acid+LRRK1-siRNA transfection) and LRRK1-siRNA+FHT group(4.8 mmol·L~(-1) uric acid+LRRK1-siRNA transfection+200 µg·mL~(-1) FHT). After 24 h incubation, the level of IL-1ß in the cell supernatant was detected, and the cellular proteins were extracted and used to determine LRRK1, epidermal growth factor receptor(EGFR), PDZ kinase 1(PDZK1) and nuclear factor-kappa B(NF-κB) protein expression levels. The results showed that, FHT could significantly reduce the uric acid, creatinine and ß2-MG levels in serum and ß2-MG levels in urine, increase the uric acid and creatinine levels in urine, and improve the renal pathological results of the HUA mice, but showed no effect on liver XOD activity; at the same time, we found that the expression level of IL-1ß in serum and kidney, NF-κB, LRRK1 and EGFR protein levels in kidney of HUA mice were significantly increased, and the expression level of PDZK1 protein was significantly decreased, while FHT could significantly improve the abnormal expression of these proteins, and FHT increased protein expression of renal organic anion transporter 1(OAT1), OAT3 and ATP bin-ding transporter G2(ABCG2) in HUA mice, but FHT had no effect on the expression of urate transporter 1(URAT1). In the cell transfection experiment, after transfection of LRRK1-siRNA, the levels of IL-1ß, EGFR and NF-κB in supernatant were significantly reduced, and the expression of PDZK1 protein was significantly increased. As compared with the LRRK1-siRNA group, the levels of IL-1ß, EGFR, PDZK1 and NF-κB did not change significantly with the additional FHT. This study showed that FHT may regulate the renal uric acid transport system through LRRK1 gene, improve the capacity of uric acid excretion, so as to reduce the level of serum uric acid. At the same time, FHT can not only protect the kidney directly, but also in an indirect manner by reducing the level of uric acid.

Effect of non-genomic actions of thyroid hormones on the anaesthetic effect of propofol.

Hyperthyroidism is a common disease of the endocrine system and it is known that additional propofol anaesthesia is required during surgery for patients with hyperthyroidism compared with those with normal thyroid function. The aim of the present study was to determine the mechanism through which thyroid hormones (THs) inhibit the effect of propofol anaesthesia. Immunofluorescence techniques were used to verify the difference between the expression quantities of γ-aminobutyric acid type A (GABAA) receptor subunits α2 and ß2 in the dorsal root ganglions (DRGs) of rats with hyperthyroidism and those in normal rats. Perforated patch clamp recordings in the whole-cell mode were performed to detect the GABA-activated current in acutely isolated rat DRG neurons from rats with hyperthyroidism and normal rats. This method was also used to evaluate the change in the GABA-activated currents following the pre-perfusion of propofol with and without 3,3',5-L-triiodothyronine (T3). Compared with normal rats, rats with hyperthyroidism expressed same quantities of GABAA receptor α2 and ß2 subunits in DRGs. In addition, no difference in GABA-activated currents in the acutely isolated DRG neurons from the two types of rat was observed (P>0.05). T3 inhibits or minimises the augmentation effect of propofol on the GABA-activated currents (P<0.05). The inhibitory effect of T3 on propofol was minimised by increasing the propofol concentration (P<0.05). The inhibitory effect of T3 on the anaesthetic effect of propofol is achieved through the inhibition of the function of GABAA receptors through the non-genomic actions of the THs, rather than by changing the number of GABAA receptors. This inhibitory effect can be mitigated by increasing the propofol concentration. In conclusion, rats with hyperthyroidism require a larger dose of propofol to induce anaesthesia since the non-genomic actions of THs suppress GABA receptors, which in turn inhibits the anaesthetic action of propofol.