[A comparative study of transperitoneal transmesenteric approach versus paracolic sulci approach laparoscopic adrenal tumorectomy for treatment of primary hyperaldosteronism on left side].

Objective: To compare the therapeutic effect of transperitoneal transmesenteric approach versus paracolic sulci approach laparoscopic adrenal tumorectomy for treatment of left-sided primary hyperaldosteronism. Methods: From January 2017 to July 2019, the clinical data of 70 patients with left-sided primary hyperaldosteronism (PHA) who underwent surgery in the First Hospital of Lanzhou University and five other hospitals in Gansu Province were retrospectively analyzed. There are 43 male and 27 female patients. Among them,28 patients were performed transperitoneal transmesenteric approach laparoscopic adrenal tumorectomy and 42 patients were performed transperitoneal paracolic sulci approach laparoscopic adrenal tumorectomy. The general information and perioperative data of the two groups were compared. Results: All 70 cases of surgery were successfully completed. As compared with the paracolic sulci approach group, the operation time was significantly shorter in the transmesenteric approach group[(26.7±8.8)vs (38.9±7.1)min,P<0.001)], and the estimated blood loss was less in the transmesenteric approach group[45(30,50) vs 50(40,60)ml,P=0.042]. There was no statistically significant difference in the postoperative hospitalization days between the two groups[(4.4±1.0)vs(4.5±1.0)d, P=0.669)]. The electrolytes and aldosterone to renin ratio returned to a healthy level in the postoperative one month, and the blood pressure also returned to a healthy level in 53 (75.7%) patients. Conclusion: Transperitoneal transmesenteric approach laparoscopic adrenal tumorectomy is safe and feasible, with a short operation time and relatively less estimated blood loss.

[Adenosine inhibits spontaneous and glutamate induced discharges of hippocampal CA1 neurons].

Effects of adenosine (Ado) on spontaneous and glutamate induced discharges of neurons in CA1 area of hippocampal slices were examined using extracelluar recording technique. The results are as follows. (1) In response to the application of Ado (0.01 0.1 micromol/L, n=20) into the superfusate, spontaneous discharge rates (SDR) of 20 neurons decreased significantly in a dose dependent manner. (2) Both Ado non selective receptor antagonist 8 phenyltheophylline (8-PT, 0.5 mmol/L) and Ado selective A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 50 nmol/L), completely blocked the inhibitory effects of Ado in 22 CA1 units. (3) In 10 units, ATP sensitive K(+) channel blocker glibenclamide (Gli, 15 mmol/L) also abolished the effect of Ado. (4) Application of glutamate (Glu, 0.2 mmol/L) into the superfusate for 2 min led to a marked increase in the discharge rate of 15 neurons in an epileptiform pattern; the epileptiform discharges induced by glutamate (Glu, 0.2 mmol/L) in 15 neurons were suppressed significantly by application of Ado (10 micromol/L) into the superfusate. (5) 8-PT (2 mmol/L), DPCPX (200 nmol/L) and Gli (7 mmol/L) were all capable of abolishing the inhibiting effect of Ado on the action of glutamate. Taken together, it is suggested that Ado can bind with adenosine A1-receptors on CA1 neurons, resulting in an activation of K(ATP) channels and inhibition of neuronal activity. The inhibitory effect of Ado on glutamate induced epileptiform activities in rat hippocampal neurons is also mediated by adenosine A1-receptor with involvement of ATP-sensitive potassium channels.

[Modulatory effects of 17beta-estradiol on the electrical activity of subfornical organ neurons].

The effects of 17beta-estradiol (E(2) ) on electrical activity of neurons in subfornical organ (SFO) slices were examined using extracelluar recording technique. The results are as follows. (1) In 15 SFO units, a low dose of E(2) (0.1 nmol/L) applied into superfusate induced an increase in discharge rate from 3.21+/-0.37 to 6.79+/-0.71 Hz (P<0.001), whereas a high dose of E(2) (100 nmol/L ) caused a decrease in discharge rate from 3.44+/-0.40 to 1.44+/-0.36 Hz (P<0.01); (2) glutamate NMDA receptor antagonist MK-801 (50 pmol/L) blocked the excitatory effects induced by low dose of 17beta-estradiol in 7 units; (3) L-arginine (L-arg, 1 mmol/L), a physiological precursor of NO, abolished the excitatory effects induced by low dose of 17beta-estradiol in 7 units; (4) application of N-omega-nitro-L-arginine methyl ester (L-NAME, 10 mmol/L), an inhibitor of NOS, blocked the inhibitory effects induced by high dose of 17beta-estradiol in 6 units. The above results suggest that the estrogen exerts dual action on SFO neuron. E(2) at low dosage increases the discharge rate of SFO neuron, an effect which may be related to the activation of NMDA receptors, whereas E(2) at high dosage decreases the discharge rate, an effect which may be attributed to the activation of NOS with resultant production of NO.

[Effects of angiotensin II, atrial natriuretic peptide and arginine vasopressin on activity of subfornical organ neurons in rat brain slices].

The effects of angiotensin II (AG II), atrial natriuretic peptide (ANP) and arginine vasopressin (AVP) on 87 subfornical organ (SFO) neurons from 31 brain slices of rats were observed. After perfusing the brain slices with AG II (10(-7) mol/L, 3 min), spontaneous discharge rate of 40/55 (72.73%) neurons was significantly increased, while that of 3/55 (5.45%) was decreased and 12/55 (21.82%) neurons were non-responsive. The excitatory effects of AG II on neurons in SFO were completely blocked by AG II receptor blocker saralasin (10(-6) mol/L). As the brain slices were perfused with atrial peptide III (AP III) (10(-7) mol/L, 3 min), the firing rate of 7/17 (41.18%) neurons was significantly decreased, while that of 2/17 (11.76%) neurons was increased and 8/17 (47.06%) neurons were non-responsive. By perfusing brain slices with AVP (10(-7) mol/L, 3 min), the firing rate of 8/15 (53.33%) neurons was significantly increased, while that of 3/15 (20.00%) neurons was decreased and 4/15 (26.67%) neurons were non-responsive. Twelve SFO neurons were successively perfused with three peptides. Among them, one was excited by both AG II and AVP, 3 were excited by AG II and inhibited by AP III, and the other one was excited by AVP and inhibited by AP III. The results suggest that the discharge rate of SFO neurons is affected by AG II, ANP and AVP. SFO may be one of the central regions in regulation of water balance and blood pressure.

[Effects of left atrial stretch and carotid occlusion on the single unit activity of anterior and posterior hypothalamus in cat].

The effects of left atrial stretch (AS) and carotid occlusion (CO) on the single unit activity of anterior and posterior hypothalamus (AH and PH) were investigated in 40 urethan-chloralose-anesthetized cats. A total of 185 units with spontaneous discharge were recorded. 46.3% (44/95) of the neurons in AH and 23.3% (21/90) of those in PH were responsive to AS. Majority of the neurons affected by AS exhibited a decrease in firing rate. A few units only showed transient response during the onset and release of AS (on-off response). Out of the 185 units, 85 units were tested by both AS and CO, and 15 units (17.6%) were responsive to both interventions. Among them 11 (73.7%) were inhibited by AS and excited by CO. From the results mentioned above, it is suggested that: (1) AS may exert an inhibitory effect on the activity of neurons in AH. (2) The activity of neurons in PH may be also affected by AS. (3) The inputs from the atrial volume receptor and carotid baroreceptor converge on the same neuron of the hypothalamus.

[Renal responses to left atrial stretch in the cat].

The effects of left atrial stretch (LAS) on urine volume (UV), urinary sodium excretion (UNaV) and potassium excretion (UKV) were studied in 50 anesthetized cats. LAS resulted in a marked increase in UV, UNaV and UKV (all P less than 0.001) in the intact animals. Although LAS still caused an increase in UV and UNaV (P less than 0.01) after vagotomy, the increments were significantly less than those in vagi intact animals (P less than 0.005). LAS also induced an increase in UV, UNaV and UKV (P less than 0.05) in the vagi intact cats with heparin infusion (10U/min/kg), but the increments were significantly less than those in the cats without heparin (P less than 0.05). The responses to LAS were abolished by infusion of heparin after vagotomy (P greater than 0.05). Following left renal denervation, the responses to LAS remained unchanged in the innervated kidney, while those in denervated kidney were attenuated, though still significant. The difference in the response between the innervated and the denervated kidneys was statistically significant (P less than 0.05). These results indicate that LAS can induce a marked increase in UV, UNaV and UKV in anesthetized cats through both neural and humoral mechanisms.

[Effects of angiotensin II, atrial natriuretic peptide III and arginine vasopressin on activity of paraventricular neurons of rat hypothalamic slices].

The effects of angiotensin II (AG II), atrial natriuretic peptide III (ANP III) and arginine vasopressin on 101 paraventricular nucleus (PVN) neurons from 28 brain slices of rats were observed. After perfusing the brain slices with AG II (10(-7) mol/L, 3 min), spontaneous discharge rate of 28/50 (56.0%) neurons was significantly increased, while that of 5/50 (10.0%) was significantly decreased and 17/50 (34.0%) neurons were non-responsive. Both of excitatory and inhibitory effects of AG II on neurons in PVN were completely blocked by AG II receptor blocker saralasin (10(-6) mol/L). As the brain slices were perfused with ANP III (10(-7) mol/L, 3 min), the firing rate of 16/26 (61.54%) neurons was decreased, while that of 1/26 (3.85%) neurons was increased and 9/26 (34.61%) neurons were non-responsive. During perfusing brain slices with AVP (10(-7) mol/L, 3 min), the firing rate of 19/25 (76.0%) neurons was significantly increased, while that of 1/25 (4.0%) neurons was decreased and 5/25 (20.0%) neurons were non-responsive. Twenty-five PVN neurons were successively perfused with three peptides. Among them, 4 were excited by both AG II and AVP, 2 were excited by AG II and inhibited by ANP III, and 7 were excited by AVP and inhibited by ANP III. The results show that the discharge rate of PVN neurons may be affected by AG II, ANP III and AVP. It is likely that PVN acts as an integrative site for neuroendocrine and autonomic functions.

[Effects of no precursor and donor on neuronal activity of rat hippocampal slices].

Using extracellular recording technique, the effects of L-arginine (L-arg), N-nitro-L-arginine (L-NNA), SIN-1 and methylene blue (MB) on spontaneous discharges of neurons in CA1 area of hippocampal slices were examined to determine the role of L-arg: NO pathway and the possible underlying mechanism. The results were as follows: (1) In response to the application of L-arg (1 mmol/L) into the superfusate for 2 min, spontaneous discharge rate (SDR) of 42/54 (77.8%) neurons was decreased significantly, while that of 12/54 (22.2%) neurons showed no change. Following the application of L-NNA (0.15 mmol/L) into the superfusate for 2 min, SDR of 25/29 (86.2%) neurons was increased markedly and that of 4/29 (13.8%) neurons was not affected. The effect of L-NNA might be reversed by pretreatment with L-arg. (2) With application of NO donor SIN-1 (5 mmol/L), SDR of 25 (100%) neurons was decreased in a dose-dependent manner. (3) After superfusing the brain slice with guanylate cyclase inhibitor, MB (3 mumol/L) for 30 min, SDR of 10 units showed significant increase as compared with control. However, MB failed to abolish the effect of L-arg on hippocampal neurons. Taken together, it is likely that NO is released during the resting state of hippocampal neurons and may inhibit the activity of hippocampus, an effect not mediated by the action of guanylate cyclase.

[Inhibitory effects of nitric oxide on glutamate-induced neuronal activity of CA1 area in rat hippocampal slices].

Using extracellular recording technique, the effects of L-arginine (L-arg), SIN-1 and N-nitro-L-arginine (L-NNA) on glutamate-induced discharge of neurons in CA1 area of hippocampal slices were examined to define the role of L-arg:NO pathway in glutamate-induced discharge of hippocampal neurons and its possible underlying mechanism. The results obtained are as follows. (1) In response to the application of glutamate (0.5 mmol/L) into the superfusate for 1 min, the discharge rate of 12 neurons was increased markedly in an epileptiform pattern. (2) The increased discharge induced by glutamate (0.5 mmol/L) in 10 neurons was suppressed significantly by application of L-arg (10 mmol/L) into the superfusate for 2 min. (3) The glutamate-induced increase of discharge in 12 neurons was decreased markedly by superfusing the brain slice with NO donor SIN-1 (5 mmol/L) for 1 min. (4) As the discharge rate of 12 neurons was increased by pretreatment with glutamate (0.5 mmol/L), application of L-NNA (0.15 mmol/L) into superfusate for 2 min might further augment the discharge intensively and in some case eventually led to abrupt suppression of the discharge. Taken together, it is likely that glutamate binding with NMDA receptors in hippocampal neurons not only induces an increase in discharge, but also activates the L-arg: NO pathway to generate NO responsible for neuroprotection via negative feedback mechanisms.

[Collection, evaluation and utilization of local varieties of Fritillaria thunbergii Miq].

Nine local varieties of Fritillaria thunbergii were collected and their plant morphology, phenology, disease resistance yield characters and breeding rate were studied. A new and better variety (Duozhi) was found and put to use.

Revisiting the concept of cancer stem cells in prostate cancer.

The cancer stem cell (CSC) model proposes that cells within a tumor are organized in a hierarchical lineage relationship and display different tumorigenic potential, suggesting that effective therapeutics should target rare CSCs that sustain tumor malignancy. Here we review the current status of studies to identify CSCs in human prostate cancer as well as mouse models, with an emphasis on discussing different functional assays and their advantages and limitations. We also describe current controversies regarding the identification of prostate epithelial stem cells and cell types of origin for prostate cancer, and present potential resolutions of these issues. Although definitive evidence for the existence of CSCs in prostate cancer is still lacking, future directions pursuing the identification of tumor-initiating stem cells in the mouse may provide important advances in evaluating the CSC model for prostate cancer.