[Trans-oral robotic submandibular gland removal].

Submandibular gland excision was performed on two patients using trans-oral robotic surgery (TORS). Complications such as the injury of marginal mandibular branch of facial nerve, ranula in the floor of the mouth, and postoperative hemorrhage were not observed. Visible cervical scar can be avoided and esthetic outcome can be expected by using this surgical modality.

Stimulation of alpha(1)-adrenoceptors reduces glutamatergic synaptic input from primary afferents through GABA(A) receptors and T-type Ca(2+) channels.

Activation of the descending noradrenergic system inhibits nociceptive transmission in the spinal cord. Although both alpha(1)- and alpha(2)-adrenoceptors in the spinal cord are involved in the modulation of nociceptive transmission, it is not clear how alpha(1)-adrenoceptors regulate excitatory and inhibitory synaptic transmission at the spinal level. In this study, inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs, respectively) were recorded from lamina II neurons in rat spinal cord slices. The specific alpha(1)-adrenoceptor agonist phenylephrine significantly increased the frequency of GABAergic spontaneous IPSCs in a concentration dependent manner, and this effect was abolished by the alpha(1)-adrenoceptor antagonist 2-(2,6-dimethoxyphenoxy)ethylaminomethyl-1,4-benzodioxane (WB4101). Phenylephrine also significantly reduced the amplitude of monosynaptic and polysynaptic EPSCs evoked from primary afferents. The inhibitory effect of phenylephrine on evoked monosynaptic glutamatergic EPSCs was largely blocked by the GABA(A) receptor antagonist picrotoxin and, to a lesser extent, by the GABA(B) receptor antagonist CGP55845. Furthermore, blocking T-type Ca(2+) channels with amiloride or mibefradil diminished the inhibitory effect produced by phenylephrine or the GABA(A) receptor agonist muscimol on monosynaptic EPSCs evoked from primary afferents. Collectively, these findings suggest that activation of alpha(1)-adrenoceptors in the spinal cord increases synaptic GABA release, which attenuates glutamatergic input from primary afferents mainly through GABA(A) receptors and T-type Ca(2+) channels. This mechanism of presynaptic inhibition in the spinal cord may be involved in the regulation of nociception by the descending noradrenergic system.

Effects of ginseng root saponins and ginsenoside Rb1 on immunity in cold water swim stress mice and rats.

The proliferation of splenic lymphocytes, the humoral immune response to sheep red blood cells, and the phagocytotic function of intraperitoneal macrophages were all suppressed by cold water (4 degrees C) swim stress (CWSS) for 5 min in rats and for 3 min in mice. Meanwhile, the levels of serum corticosterone increased. Ginseng root saponins 100 mg.kg-1 or ginsenoside Rb1 10 mg.kg-1 ip or ig completely antagonized the immunosuppression induced by CWSS, and inhibited the increase of serum corticosterone in CWSS rats, but increased the level of serum corticosterone further in CWSS mice.

[Clinical and experimental study of tablet cucumber vine compound in treating essential hypertension].

389 patients with essential hypertension were divided into two groups randomly. 241 patients were treated by tablet of cucumber vine compound and 148 patients by tablet of hypotension compound as control. The symptomatic marked improvement and total effective rate were 63.1% and 81.7% in the treated group and 39.2% and 67.0% (P less than 0.01) in the control group respectively. The marked effective rate in decrease of blood pressure and total effective rate were 52.7%, 90.9% and 58.1%, 92.6% (P greater than 0.05) respectively. Experiments with animals showed that tablet cucumber vine compound possessed persistently decreasing effect on the blood pressure and marked effect on increasing coronary blood flow and improving myocardial contraction. Clinical observation and toxicological test proved that tablet cucumber vine compound had no toxicity and had few side effects and that it was an effective, safe medicine for essential hypertension.

Effects of ginseng root saponins on brain monoamines and serum corticosterone in heat-stressed mice.

The rectal temperature and serum corticosterone increased in mice exposed to 45 degrees C for 15 min; at the same time, the contents of brain 5-HT and NE reduced, brain DA unchanged. Ginseng root saponins (GRS) ip 200 mg/kg inhibited the increase of serum corticosterone and the decrease of brain 5-HT and NE in heat-stressed mice, but did not affect brain DA. GRS lowered mice body temperature at room temperature and inhibited the rise of body temperature under heat environmental conditions in mice. Reserpine eliminated the hypothermia of GRS at room temperature and its inhibitory effect on hyperthermia under heat-stress conditions. PCPA eliminated only the inhibition of GRS on hyperthermia under heat-stress, but had no significant effect on hypothermia at room temperature.